Oxford Handbook of Critical Care, 2nd Edition

Editors: Singer, Mervyn; Webb, Andrew R. Title: Oxford Handbook of Critical Care, 2nd Edition Copyright ©1997,2005 M...

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Editors: Singer, Mervyn; Webb,

Andrew R.

Title: Oxford Handbook of

Critical Care, 2nd Edition

Copyright ©1997,2005 M. Singer and A. R. Webb

Ovid: Oxford Handbook of Critical Care

file:///C:/Documents%20and%20Settings/MVP/Application%20Data/Mozilla/Firefox/Profiles/2...


Ed itors:

Si nge r, M ervyn; We bb, An dre w R.

Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Resp ir a tor y T h e r ap y T ech n iq u e s

Respiratory Therapy Techniques Oxygen therapy Al l cri t i call y i l l pat i ents shoul d re cei ve add i ti onal i ns pi red oxy gen on a ‘ more not l es s i s b est ’ p hi l os ophy.

Principles Hi g h fl ow , hi gh conce ntrati on oxy gen shoul d b e g i ve n t o any acut el y dy spnoei c or hypoxaem i c pat i e nt unt i l acc urate ti trati on c an be performed usi ng arteri al bl ood gas anal ysi s. In general, mai ntain SaO 2 > 90%, t hough pre ferabl y >95%. Compromi ses may ne ed to be made duri ng acut e on chroni c hyp oxae mi c re spi ratory fai l ure , or p rol ong ed sev ere AR DS, when l owe r v al ues may suffi ce provi d ed ti s sue oxy gen del i v ery i s maint ai ned. Al l p ati ent s p l ac ed on mec hani cal v ent i l a ti on s houl d i ni ti al l y rec ei v e a hi g h FIO 2 unti l ac curat e t i trati on i s pe rforme d usi ng arteri al bl ood gas anal ysi s. Apart from p ati ent s rec ei v i ng hy perbari c O 2 therapy (e.g . for carbon monox i de poi soni ng, di v i ng ac ci d ent s), there i s no nee d t o maint ai n s upranormal l eve l s of PaO 2 .

Cautions A s mal l p rop orti on of pati ent s i n c hroni c Ty pe II (hy poxaemi c, hyp erc apni c ) re spi ratory fai l ure wi l l dev el op apnoea i f the i r ce ntral hyp oxi c d ri v e i s removed by suppl emental ox yge n. How ever, t hi s i s s el d om (i f eve r) abrupt and a pe ri od of det eri orati on and i nc re asi ng drowsi nes s w i l l al ert me di cal and nurs i ng st aff to consi der ei the r (i ) FIO 2 red uct i on i f ove ral l c ond i t i on al l ow s, (i i ) non-i nvasi ve or i nvasi ve m echani cal ve nti l a ti on i f fati gui ng or (i i i ) use of re spi rat ory sti mul ants suc h as d oxep ram. T he corol l ary i s t hat cl ose supervi s i on and m oni tori ng i s nece ssary i n al l cri t i call y i l l pat i ents . A norm al pul se oxi met ry readi ng m ay obs cure d ete ri orat i ng g as exchang e and progre ssi ve hyp erc apni a. Oxy gen toxi c i ty i s de sc ri b ed i n ani mal model s. Normal vol untee rs wi l l b ecome sym ptomat i c aft er sev eral hours of bre athi ng pure oxy gen. Furt hermore, was hout of ni trogen may l ead to mi croate l ec tas i s . Howev er, the rel e vance and rel at i ve i m portance of oxyg en toxi ci ty com pared to other forms of v ent i l a tor t rauma i n c ri ti c al l y i l l pati ent s i s s ti l l far from c l ear. Effort s s houl d nev ert hel ess be made to mi ni mi se FIO 2 whene ver pos si bl e . D ebate conti nues as to whe the r FIO 2 or othe r v ent i l ator s ett i ng s (e.g . PEEP, V T , i nsp i ratory p res sures ) s houl d be red uce d fi rs t. The authors' prese nt vi e w i s t o m i ni mi s e t he ri sks of venti l at or trauma.

Monitoring An oxy gen anal y ser i n the i nsp i ratory l i m b of the v ent i l ator or CPAP/Bi PAP ci rcui t confi rms the p ati ent i s re cei vi ng a known FIO 2 . Mos t m ode rn vent i l ators hav e a bui l t -i n calib rati on d evi ce. Ade quacy and chang es i n art eri al oxy gen saturati on can be conti nuousl y m oni tored by pul se oxi met ry and i nt ermi t tent or c ont i nuous i nvas i ve bl ood gas anal ysi s. P.3

Oxygen masks Huds on-typ e m ask s or nasal ‘ spe ctacl e s’ gi ve an i mpreci se FIO 2 and s houl d onl y b e used when hypoxae mi a i s not a major conce rn. Hudson-t ype mas ks do al l ow del i ve ry of humi di fi e d g as (e.g . v i a an ‘Aq uap ak’ ). Val ves fi tte d t o the Aq uapak s yst em do not del i v er an acc urate FIO 2 unl es s g as fl ow i s at t he rec omm ende d l eve l . Mask s fi tt ed wi t h a Ve nturi val ve del i v er a reasonab l y acc urate FIO 2 (0.24, 0.28, 0. 35, 0. 40, 0. 60) ex cep t i n pati ents wi t h v ery hi gh i ns pi ratory fl ow rate s. The se mas ks do not al l ow del i ve ry of hum i di fi e d g as but are pre ferabl e i n t he s hort term for dys pnoe i c pat i e nts as they e nab l e more p rec i s e moni t ori ng of PaO 2 /F IO 2 rati os. A t i ght-fi tt i ng anaes the ti c mask and re servoi r b ag al l ows 100% oxyg en to be del i ve red .

See also: Venti l at ory support— ind i c ati ons , p 4; Conti nuous pos i ti ve ai rway press ure , p 26; Bas i c res usc i t ati on, p270; Re spi ratory fai l ure, p282 P.4

Ventilatory support—indications Acute ventilatory insufficiency

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Defi ne d b y an ac ut e ri se i n PaC O 2 and a si g ni fi c ant re spi rat ory ac i d osi s. PaCO 2 i s di re ctl y p rop ort i onal to the body' s CO 2 producti on and i nversel y p rop orti onal to al veol ar venti l at i on (m i nute venti l ati on mi nus dead s pac e v ent i l a ti on). Causes i ncl ude: Resp i ratory centre de pre ssi on, e. g. dep res sant d rug s or i ntrac rani al pathol og y Peri pheral neuromuscul ar di sease, e. g. Gui l l ai n–Barré sy ndrome , m yas the ni a gravi s or s pi nal cord pat hol ogy Therape uti c mus cl e paral ysi s, e.g . as p art of balanced anaest hes i a , for m anagem ent of tet anus or s tat us epi l ep ti c us Los s of chest wall i nteg ri t y, e.g . c hes t t rauma, di aphrag m rupt ure Hi g h CO 2 p roduc ti on, e.g . b urns, sep si s or se vere agi t ati on Reduced al veol ar ve nti l at i on, e .g. ai rway obst ruc ti on (ast hma, acut e b ronchi ti s, forei g n b ody), atel ect asi s, pneumoni a, pul monary oede ma (ARD S, cardi ac fai l ure), pl eural pat hol ogy , fi broti c l ung di se ase , ob esi ty Pul monary vas cul ar di sease (pul monary em bol us, cardi ac fai l ure, AR DS)

Oxygenation failure Hyp oxaemi a i s d efi ned by PaO 2 < 11k Pa on F IO 2 ≥0. 4. May be due to: Venti l ati on–perfus i on mi sm atc hi ng (red uce d ve nti l a ti on i n, or pre ferent i al pe rfusi on of, som e l ung areas ), e.g. pneumoni a, pul monary oede ma, pul monary vascul ar di se ase, ex tre mel y hi gh cardi ac out put Shunt (normal pe rfusi on but abs ent ve nti l a ti on i n s ome l ung zones), e. g. pne umoni a , p ul m onary oede ma Di ffus i on l i mi t ati on (re duc ed al v eol ar surfac e area wi th normal ve nti l at i on), e.g . e mphysem a; red uce d i nsp i red oxyg en tensi on, e.g . alti tud e, suffoc ati on Acute vent i l atory i ns uffi ci ency (as above)

To reduce intracranial pressure Red uct i on of PaCO 2 to ap proxi m ate l y 4kPa cause s c ere bral v asoconstri c ti on and the refore re duc es i nt rac rani a l pre ss ure aft er brai n i njury. Rec ent st udi es sug ges t t hi s effec t i s t ransi ent and may i mpair an al read y c ri ti c al cerebral bl ood fl ow.

To reduce work of breathing As si s ted ve nti l at i on ± sed ati on and muscl e rel a xat i on re duc es res pi rat ory muscl e acti vi t y and thus t he work of bre athi ng. In c ardi a c fai l ure or non-c ard i og eni c p ul m onary oed ema the re sul ti ng red uct i on i n my ocardi al oxy gen dem and i s more eas i l y matched to t he sup pl y of ox yge n. P.5

Indications for ventilatory support Venti l at ory support (i nvas i ve or non-i nvas i v e) s houl d be consi d ered i f: Resp i ratory rat e >30/m i n Vi t al cap aci ty 15–20% Exhaust i on Confusi on Seve re shock Seve re LVF Rai s ed ICP

See also: Dys pnoea, p278; Ai rway ob st ruc ti on, p280; R esp i ratory fai l ure, p282; Atel ect asi s and pul monary col l aps e, p 284; Chroni c airfl ow l i mi tat i on, p 286; Ac ut e chest i nfec ti on (1), p288; Acute che st i nfec ti on (2), p290; Acut e res pi ratory di s tress sy ndrome (1), p 292; Acut e resp i ratory di s tre ss syndrome (2), p294; Ast hma—ge neral manage ment , p 296; As thm a—ve nti l a tory m anag eme nt, p298; Inhal ati on i nj ury , p 306; Pul monary e mbol us , p 308; He art fai l ure— ass ess ment, p324; Heart fail ure —manag ement, p326; Acute l i ver fai l ure, p360; Acut e we akness , p 368; Agi tati on/c onfusi on, p370; Generalis ed sei zures , p 372; Int rac rani a l haemorrhag e, p 376; Subarachnoi d haem orrhag e, p378; Stroke , p 380; Rais ed i nt rac rani al pres sure, p382; Gui l l ai n–Barr é s ynd rom e, p384; My ast heni a gravi s , p 386; ICU ne uromus cul ar di s orders, p388; Te tanus, p390; Botul i s m, p 392; Poi soni ng—gene ral p ri nci p l e s, p452; Sed ati ve

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poi soni ng, p 458; T ri c ycl i c anti d epress ant poi soni ng, p460; Coc ai ne, p464; Inhal e d p oi s ons , p 466; Organophosp hat e poi soni ng, p 472; Syst emi c i nfl amm ati on/mul ti -org an fai l ure, p484; Mul t i pl e t rauma (1), p500; Mul ti pl e trauma (2), p502; Head i njury (1), p504; He ad i nj ury (2), p 506; Spi nal cord i nj ury, p 508; Burns—fl ui d m anagem ent , p510; Burns —ge neral managem ent , p 512; N ear-drowni ng , p526; Post-ope rat i ve i ntensi v e c are , p 534 P.6

IPPV—description of ventilators Classification of mechanical ventilators The se may be cl ass i fi ed by the met hod of cy cl i ng from i nsp i rati on to expi rati on. Thi s m ay be w hen a pre set ti me has el a pse d (ti m e-c ycl ed), a preset pres sure reac hed (pres sure-c ycl ed) or a p res et vol ume de l i v ere d (vol ume -cyc l e d). Though the m ethod of c ycl i ng i s c l as si fi e d ac cordi ng to a s i ng l e constant, modern v ent i l a tors all ow a great er deg ree of control . In vol ume -cy cl e d m ode wi t h p res sure l i m i tati on, the up per pres sure alarm l i mi t i s set or the maxi m um i ns pi rat ory press ure control l ed . T he vent i l ator d el i vers a prese t t i d al vol ume (V T ) unl es s t he l ungs are non-c omp l i ant or ai rway re si s tance i s hi gh. Thi s i s use ful to av oi d hi gh peak ai rw ay p res sures . In v ol ume-c ycl ed mod e w i th a ti m e l i mi t , t he i ns pi rat ory fl ow i s reduced ; t he venti l ator d el i vers the prese t V T unl e ss i mp oss i bl e at t he set re spi ratory rat e. If pre ssure l i mi t ati on i s not av ai l abl e t hi s i s useful to l i m i t peak airw ay pre ssures . In t i me -cy cl e d m ode wi th pre ss ure control , prese t p res sure i s del i ve red throughout i ns pi rat i on (unl i ke pre ssure-cyc l ed ve nti l at i on), cyc l i ng bei ng det erm i ne d b y t i me . V T i s d epe nde nt on res pi ratory com pl i ance and ai rway re si s tance . He re, too, hi g h p eak ai rway press ures c an be avoi de d.

Setting up the mechanical ventilator Tidal volume Conventi onal l y set at 7–10m l /k g, t hough rec ent data sug ges t l owe r v al ues (6–7ml /kg ) may b e be tt er i n sev ere acute res pi rat ory failure, re duc i ng barot rauma and i m provi ng outc ome . In s eve re ai rfl ow l i mi tat i on (e .g. as thm a, acute bronchi t i s) sm al l er V T and mi nute vol um e may b e neede d t o allow p rol ong ed exp i rati on.

Respiratory rate Usual l y s et i n acc ordance w i t h V T t o provi de mi nut e ve nti l a ti on of 85–100ml /kg /mi n. In ti m e-c ycl ed or ti m e-l i mi ted mod es the se t resp i ratory rat e de termi nes the ti mi ng of t he venti l at or cyc l es .

Inspiratory flow Usual l y s et bet wee n 40–80l /mi n. A hi ghe r fl ow rate i s more c omfort abl e for alert pat i ents. Thi s al l ows for l ong er exp i rati on i n pat i ents wi t h s eve re ai rfl ow l i mi tat i on but m ay be ass oci ate d wi th hi ghe r p eak ai rway press ures. The fl ow p att ern may be ad jus ted on mos t vent i l ators. A square waveform i s oft en use d b ut dec el e rat i ng fl ow may re duc e peak airw ay p re ssure.

I:E ratio A func ti on of resp i ratory rat e, V T , i ns pi rat ory fl ow and i nspi rat ory ti me. Prol onge d e xpi rat i on i s us eful i n seve re ai rfl ow l i m i tati on w hi l e a prol onge d i nsp i ratory t i m e i s used i n AR DS to al l ow sl ow reac ti ng alve ol i ti me to fi l l . Al ert pat i ents are more com fortab l e wi t h s horter i nsp i ratory t i me s and hi g h i nsp i ratory fl ow rate s.

FIO 2 Set ac cordi ng to art eri al bl ood gas es. Us ual to st art at FIO 2 =0. 6–1 then adjust ac cordi ng t o arte ri a l b l ood g ase s.

Airway pressure In pre ss ure -control l ed or pre ssure-l i mi t ed mode s t he peak airw ay p re ssure (ci rcui t rathe r t han al veol ar press ure ) c an be set (usually ≤35–40cm H 2 O). PEEP i s us ual l y i ncre ase d t o m ai ntai n F RC w hen re spi rat ory compl i ance i s l ow. P.7

Initial ventilator set-up Che ck for l e aks

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Check oxygen is flowing FIO 2

0.6–1

VT

5–10ml/kg

Rate

10–15/min

I:E ratio

1:2

Peak pressure

≤35cmH 2 O

PEEP

3–5cmH 2 O

Key trial Ac ute Res pi rat ory Di stress Synd rom e Ne twork. Ve nti l a ti on wi th l ower ti dal vol um es com pared w i t h t rad i ti onal t i d al vol ume s for acute l ung i njury and the ac ut e resp i ratory d i st re ss syndrome. N Engl J Med 2000; 342:1301–8

See also: IPPV—m ode s of ve nti l a ti on, p8; IPPV—adjusti ng the ve nti l at or, p10; IPPV—failure to tol erate venti l at i on, p 12; IPPV—c omp l i cat i ons of ve nti l a ti on, p14; IPPV—w eani ng te chni ques, p16; IPPV—as ses sm ent of weani ng, p18; Hi gh fre que ncy ve nti l at i on, p 20; Pos i t i ve end ex pi ratory press ure (1), p 22; Pos i t i ve end ex pi rat ory press ure (2), p 24; Lung rec rui tm ent , p 28; Non-i nvas i ve re spi rat ory support, p32; CO 2 moni tori ng, p92; Bl ood gas anal ysi s, p100 P.8

IPPV—modes of ventilation Controlled mechanical ventilation (CMV) A p res et num ber of breat hs are de l i v ere d t o s upp l y al l the p ati ent 's venti l at ory re qui rem ent s. The se bre aths m ay be at a p res et V T (vol um e c ont rol l ed ) or at a prese t i nsp i ratory p res sure (press ure control l ed).

Assist control mechanical ventilation (ACMV) Pat i ents can tri g ger the v ent i l a tor to de termi ne t he res pi rat ory rate b ut , as wi th CMV, a prese t numb er of b re aths are del i ve red i f the s pontaneous resp i ratory rat e fall s b el ow t he p res et l e vel .

Intermittent mandatory ventilation (IMV) A p res et mandat ory rate i s set but p ati ent s are free t o b reathe sp ont ane ous l y bet ween se t v ent i l ator b reaths . Mandat ory breat hs may be synchroni se d wi th pat i e nts ' s pontaneous e fforts (SIMV) t o av oi d mandatory b reaths occ urri ng d uri ng a s pontaneous b reath. Thi s effect , k nown as ‘s tac ki ng’ may l e ad to exc ess i ve ti dal vol um es, hi gh ai rway press ure, i nc ompl et e ex hal ati on and ai r t rappi ng. Press ure support may be add ed to spontaneous bre aths t o ove rcome the work of b reathi ng ass oci ate d w i th op eni ng the ve nti l at or dem and valve .

Pressure support ventilation (PSV) A p res et i nspi rat ory press ure i s adde d t o the v ent i l ator c i rc ui t d uri ng i ns pi rat i on i n sp ont ane ous l y bre athi ng pati e nts . The prese t p res sure s houl d be adj ust ed to ens ure ad equate V T .

Choosing the appropriate mode Pre ssure control l ed venti l ati on avoi ds the d ang ers as soc i at ed wi t h hi gh pe ak ai rway press ure s, al t hough i t may re sul t i n marked chang es i n V T i f com pl i anc e alte rs . Al l owi ng t he pat i ent t o m ake som e s pontaneous resp i ratory e ffort may red uce se dat i on re qui re ment s, re train res pi rat ory muscl es and re duc e m ean ai rway press ures.

Apnoeic patient Use of IM V or ACMV i n pati e nts who are t ot al l y apnoe i c provi des the t otal m i nute vol ume req ui rem ent i f the pres et rat e i s hi g h enoug h (thi s i s effe cti vel y C MV) but allows spontaneous res pi ratory effort on re cov ery .

Patient taking limited spontaneous breaths A g uarant eed mi ni m um mi nute vol um e i s assured wi th bot h ACMV and IMV dep end i ng on the pres et rat e. T he work of spontaneous bre athi ng i s reduced by sup pl yi ng t he p re set V T for spontaneousl y t ri g gered bre aths w i th AC MV, or by add i ng press ure s upp ort to sp ont ane ous breat hs wi t h IMV. Wi th ACM V t he spontaneous ti d al vol ume i s guarante ed whe reas w i th IM V and pre ssure sup port s pontaneous t i dal v ol ume dep end s on l ung compl i ance and may be l e ss than the prese t t i d al vol ume. The advantage of IMV and press ure support i s that gradual reducti on of pre set rate, as spontaneous effort i ncre ase s, al l ows a smooth trans i ti on to pre ss ure support venti l ati on. Subs eque nt weani ng i s b y

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red uct i on of the p res sure s up port l eve l .

See also: IPPV—d esc ri pti on of vent i l ators, p6; IPPV—adjusti ng the ve nti l at or, p10; IPPV—failure to tol erate venti l at i on, p 12; IPPV—c omp l i cat i ons of ve nti l a ti on, p14; IPPV—w eani ng te chni ques, p16; IPPV—as ses sm ent of weani ng, p18; Hi gh fre que ncy ve nti l at i on, p 20; Pos i t i ve end ex pi ratory press ure (1), p 22; Pos i t i ve end ex pi rat ory press ure (2), p 24; Lung rec rui tm ent , p 28; Non-i nvas i ve re spi rat ory support, p32 P.9 P.10

IPPV—adjusting the ventilator Venti l at or adj ust ments are us ual l y mad e i n resp ons e t o bl ood gases , p ul s e oxi m etry or c apnography, pat i ent agi t ati on or di s comfort, or duri ng w eani ng . ‘ Mi g rat i on’ of t he endotracheal tube, ei the r d i st al l y t o t he cari na or be yond, or proxi m al l y s uc h t hat the c uff i s at voc al cord l eve l , may re sul t i n agi tat i on, e xces s coughi ng and a d ete ri orati on i n bl ood gas es. Thi s, and t ube ob struct i on, s houl d be consi dered and rec ti fi e d b efore c hangi ng vent i l ator or s edati on dos e s ett i ng s. The choi c e of v ent i l a tor mode depe nds up on the l e vel of consc i ousne ss, the numb er of s pontaneous b reaths be i ng tak en, and t he b l ood g as val ues . T he spontaneousl y b reathi ng pat i ent c an usual l y c ope ad equate l y wi t h p res sure sup port v ent i l ati on al one. How eve r, on occ asi on, a few i nt erm i t tent m andatory b reaths (SIMV) m ay be nec ess ary to ass i s t g as exchang e or s l ow an exc es si v e s pontaneous rate. The p aralys ed or heavi l y s edated pati e nt wi l l requi re mandat ory breat hs, ei the r v ol ume- or press ure -control l ed. The order of chang e wi l l be di ctated by the s everi t y of re spi ratory fai l ure and i ndi vi d ual op erator prefe rence. Earl i er use of i ncre ase d PEEP i s ad voc ated to re crui t col l a pse d alve ol i and t hus i m prove oxy genati on i n sev ere re spi rat ory fai l ure.

Low PaO 2 considerations Inc rease FIO 2 Revi ew V T and resp i ratory rate Inc rease PEEP (m ay rai se peak ai rway p res sure or reduce CO) Inc rease I:E rat i o Inc rease pre ssure sup port/p res sure c ont rol CMV, i ncreas e s edat i on ± mus cl e re l ax ant s Cons i de r t ol erati ng l ow l ev el (‘p erm i ss i ve hy pox aemi a’) Prone v ent i l ati on, i nhal ed ni t ri c ox i d e

High PaO 2 considerations Dec rease l eve l of p res sure c ont rol /p res sure s upp ort i f V T adeq uat e Dec rease PEEP Dec rease FIO 2 Dec rease I:E rat i o

High PaCO 2 considerations Inc rease V T (i f l ow and p eak ai rway pres sure allows) Inc rease res pi ratory rat e Reduce rat e i f t oo hi g h (to red uce i ntri nsi c PEEP) Reduce dead s pac e CMV, i ncreas e s edat i on ± mus cl e re l ax ant s Cons i de r t ol erati ng hi gh l e vel (‘ permi s si ve hype rcapni a’ )

Low PaCO 2 considerations Dec rease res pi ratory rat e Dec rease V T

See also: IPPV—d esc ri pti on of vent i l ators, p6; IPPV—m ode s of ve nti l a ti on, p8; IPPV—fai l ure to tol erate ve nti l at i on, p 12;

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IPPV—c omp l i cat i ons of ve nti l a ti on, p14; IPPV—w eani ng te chni ques, p16; IPPV—as ses sm ent of weani ng, p18; Hi gh fre que ncy ve nti l at i on, p 20; Pos i t i ve end ex pi ratory press ure (1), p 22; Pos i t i ve end ex pi rat ory press ure (2), p 24; Lung rec rui tm ent , p 28; Non-i nvas i ve re spi rat ory support P.11 P.12

IPPV—failure to tolerate ventilation Agi tati on or ‘ fi g hti ng the ve nti l at or’ m ay occur at any ti m e. Poor t ol e rance may al s o b e i ndi cated by hyp oxaemi a, hyp erc apni a, ve nti l at or al arm s or c ard i ov asc ul a r i ns tab i l i ty.

Poor gas exchange during initial phase of ventilation Inc rease FIO 2 t o 1. 0 and start manual ve nti l at i on. Chec k e ndotrache al tub e i s c orrec tl y posi t i oned and both l ungs are be i ng i nfl a ted . C ons i de r t ube re pl a cem ent , i nt rat rac heal obst ructi on or pne umot horax. Chec k v ent i l a tor ci rc ui t i s b oth i ntac t and pat ent and ve nti l at or i s funct i oni ng correct l y. Check venti l at or set ti ngs i nc l ud i ng FIO 2 , PEEP, I:E rati o, s et ti d al vol ume , resp i ratory rat e and/or p res sure control . Che ck ‘press ure l i mi t’ set ti ngs as the se may be set too l ow, causi ng the venti l at or to ti m e-c ycl e p rem aturel y.

Poor tolerance after previous good tolerance If agi tat i on oc curs i n a p ati ent who has p rev i ousl y tol erat ed m echani cal ve nti l a ti on, ei t her the p ati ent 's condi ti on has det eri orate d or t here i s a probl em i n the venti l at or ci rcui t (i ncl udi ng art i fi ci a l airway) or the v ent i l a tor i t sel f. The pat i ent s houl d be rem ove d from the ve nti l a tor and pl ac ed on m anual venti l ati on wi t h 100% ox ygen whi l e the probl e m i s resol ve d. Resort i ng to i ncre ase d s edati on ± mus cl e rel a xat i on i n thi s ci rcumst anc e i s d ang erous unt i l the cause i s re sol ved . Chec k p ate ncy of the endot rac heal t ube (e .g. wi th a suct i on cathe ter) and re-i nt ubat e i f i n d oub t. Cons i de r m al p osi ti on of t he end otracheal tube (e. g. cuff ab ove vocal cords , t ube ti p at c ari na, tube i n mai n bronchus). Seek and t reat and change s i n t he pat i ent's condi ti on, e.g . t ens i on pneum othorax, sputum pl ug, pain. Where p ati ent s are mak i ng sp ont ane ous re spi ratory effort c ons i d er i nc reasi ng p res sure sup port or addi ng mand atory bre aths. If p ati ent s fai l t o s ync hroni s e w i th IM V b y s tac ki ng s pontaneous and mand atory bre aths, i ncre asi ng pre ssure sup port and red uci ng mandat ory rate m ay hel p; al t ernati vel y, the us e of PSV may be app rop ri a te.

See also: IPPV—d esc ri pti on of vent i l ators, p6; IPPV—m ode s of ve nti l a ti on, p16; IPPV— adj ust i ng the v ent i l a tor, p 10; IPPV—c omp l i cat i ons of ve nti l a ti on, p14; IPPV—w eani ng te chni ques, p16; IPPV—as ses sm ent of weani ng, p18; Hi gh fre que ncy ve nti l at i on, p 20; Pos i t i ve end ex pi ratory press ure (1), p 22; Pos i t i ve end ex pi rat ory press ure (2), p 24; Lung rec rui tm ent , p 28; Non-i nvas i ve re spi rat ory support, p32; Sedati v es, p238; Mus cl e rel a xants, p240; Agi tati on/c onfusi on, p370 P.13 P.14

IPPV—complications of ventilation Haemodynamic complications Venous re turn i s dep end ent on pas si ve fl ow from central v ei ns t o ri ght atri um . As ri ght atri al press ure i ncreas es sec ond ary to the t ransmi tt ed i nc rease i n i nt rat horaci c pre ssure across compl i a nt l ungs, there i s a red uct i on i n ve nous ret urn. Thi s i s l ess of a probl e m i f l ung s are sti ff (e. g. ARD S) alt hough i t wi l l b e e xac erb ate d by the use of i nv ers e I:E rati o and hi gh PEEP. As l ung vol ume i s i ncrease d b y IPPV the p ul m onary vas cul ature i s constri c ted , t hus i nc re asi ng pul monary vas cul ar re si s tance . Thi s wi l l i nc re ase di ast ol i c v ol ume of t he ri ght ventri cl e and, by se ptal shi ft , i mped es fi l l i ng of the l e ft vent ri cl e . T hes e e ffec ts al l c ont ri b ut e to a red uce d s troke vol ume . T hi s re duc ti on c an be mi ni mi sed by re duc i ng ai rw ay p res sures , avoi di ng p rol ong ed i ns pi rat ory ti mes and maint ai ni ng b l ood vol ume.

Ventilator trauma The te rm barotraum a rel a tes to gas e scape i nt o c avi ti e s and i nt ers ti ti a l t i s sue s d uri ng IPPV. Barotrauma i s a mi s nom er si nce i t i s probabl y the d i st end i ng vol um e and hi g h s hear s tre ss that i s res ponsi b l e rat her than pre ss ure . It i s mos t l i k el y to occ ur wi th hi g h V T and hi gh PEEP. It occ urs i n IPPV and condi ti ons ass oc i at ed wi t h l ung ove ri nfl ati on (e. g. ast hma). T ens i on pneum othorax i s l i fe threateni ng and s houl d be sus pec ted i n any p ati ent on IPPV who bec ome s sud denl y agi tat ed, tachy cardi c, hyp otensi ve or e xhi bi ts sud den de teri orati on i n the i r bl ood gas es . An i mmed i ate c hes t drainage tub e s houl d be i ns ert ed i f tensi on p neumot horax dev el ops. Preventi on of v ent i l ator t rauma rel i es on avoi dance of hi gh V T and hi gh ai rway press ure s.

Nosocomial infection

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End otracheal i ntubat i on by pas ses normal d efence mec hani sm s. Ci l i ary act i vi ty and ce l l ul ar morphol ogy i n the tracheobronc hi al tre e are al t ere d. The re qui rem ent for e ndot rache al suc ti on furt her i ncreas es sus cep ti b i l i ty to i nfect i on. In addi ti on, the norm al heat and m oi s ture e xchang i ng me chani s ms are by pas sed re qui ri ng art i fi ci al hum i di fi cat i on of i nspi red gases . F ai l ure to provi de ade quate humi di fi c ati on i nc re ases t he ri s k of sp ut um ret ent i on and i nfec ti on. Mai ntaini ng venti l at ed pat i ents at 30° up ri g ht head t i l t has been shown to re duc e t he i nc i de nce of nos ocomi a l p neumoni a.

Acid–base disturbance Venti l at i ng pati e nts wi th chroni c res pi rat ory fai l ure or hyp erv ent i l a ti on m ay, by rap i d corre cti on of hyp erc apni a, cause res pi rat ory al kal osi s. Thi s reduces pul m onary b l ood fl ow and may c ont ri but e t o hy pox aem i a. A res pi rat ory aci dos i s due t o hy percap ni a may b e d ue t o i nap propri at e v ent i l a tor se tti ng s or may b e d esi red i n an at tem pt to avoi d hi g h V T and venti l at or trauma.

Water retention Vas opres si n re l eased from the ant eri or pi tui tary i s i nc reased due t o a red uc ti on i n i ntrathoraci c b l ood v ol ume and psy chol og i c al stress . R educed uri ne fl ow thus c ont ri b ute s t o w ate r rete nti on. In ad di t i on, t he use of PEEP red uce s l ym phati c fl ow wi t h c ons equent pe ri p heral oed ema, e spe ci a l l y affec ti ng t he upp er bod y. Hig h ai rw ay p res sure red uce s venous re turn, again contri buti ng t o oedem a.

Respiratory muscle wasting Prol onged ve nti l at i on may l ead to di sus e atrophy of the resp i ratory m usc l es .

See also: CO 2 moni t ori ng , p92; Bl ood g as analys i s , p 100; Central venous cat het er—us e, p 114; C ent ral ve nous cat het er—inserti on, p116; Bact eri ol ogy, p158; Acute che st i nfect i on (1), p288; Acut e c hes t i nfe ct i on (2), p 290; Ac ute res pi rat ory di stres s s ynd rom e (1), p292; Acut e resp i ratory di s tre ss syndrome (2), p294; Pne umot horax, p300 P.15 P.16

IPPV—weaning techniques Pat i ents may re qui re al l or part of the i r re spi rat ory support to be provi d ed by a me chani cal venti l at or. We ani ng from mec hani cal v ent i l ati on may fol l ow se veral pat terns. In pati e nts ve nti l a ted for s hort p eri ods (no more than a fe w days) i t i s common to al l ow 20–30mi n breat hi ng on a ‘T ’ p i ec e b efore removi ng t he end otracheal tube. For p ati ent s w ho hav e rece i ve d l ong er term v ent i l a ti on i t i s unl i ke l y that m echani cal support can be wi thd raw n s udd enl y; seve ral met hod s are com monl y used to we an the se p ati ents from me chani c al venti l at i on. T here i s no s trong evi dence that any tec hni que i s s upe ri or i n t erm s of w eani ng succe ss or rat e of we ani ng.

Intermittent ‘T’ piece or continuous positive airway pressure (CPAP) Spontaneous bre athi ng i s al l owed for i ncreas i ng l y prol onged pe ri ods wi t h a re st on mec hani cal v ent i l a ti on i n bet ween. The us e of a ‘T’ pi ec e for l ong er than 30mi n m ay l ead t o basal at el ect asi s s i nc e t he end otracheal tube byp ass es the phy si ol og i c al PEEP effec t of t he l arynx . It i s t herefore com mon to use 5c mH 2 O CPAP as spontaneous bre athi ng pe ri ods get l onge r. In the earl y st age s of we ani ng, me chani c al venti l at i on i s often conti nue d at ni ght t o e ncourage sl e ep, avoi d fat i gue and res t resp i ratory m usc l e s.

Intermittent mandatory ventilation (IMV) The se t m and atory rat e i s g rad ual l y red uce d as t he spontaneous rat e i ncreas es. Sp ont ane ous breat hs are us ual l y pre ss ure supporte d t o ov erc ome ci rc ui t and v ent i l a tor valve re si s tance. Wi th thi s tec hni que i t i s i mportant that t he pat i ent' s requi re d m i nute venti l ati on i s provi ded by the combi nat i on of mandatory b reaths and s pont ane ous breat hs wi t hout an e xce ssi ve spontaneous rat e. The red uc ti on i n m and atory rat e s houl d be s l ow enoug h t o m ai ntai n adeq uat e mi nute ve nti l at i on. It i s al s o i mportant that t he pat i ent c an synchroni se hi s own resp i ratory effort s wi th mandat ory venti l at or bre aths; m any cannot, parti c ul arl y w here t here are freq uent s pontaneous b reaths , s ome of whi ch may ‘st ac k’ w i t h mandatory b reaths causi ng hyp eri nfl at i on.

Pressure support ventilation Al l resp i ratory e fforts are s pontaneous b ut pos i ti ve pre ss ure i s ad ded to eac h b reath, the l eve l b ei ng c hos en to mai ntain an app rop ri ate ti dal vol um e. W eani ng i s pe rforme d b y a gradual red uct i on of the p res sure s upp ort l evel whi l e the re spi ratory rate i s 1 wee k) s houl d generall y be al l ow ed to bre athe s pontaneous l y wi t h C PAP for at l east 24h be fore e xtubat i on.

Indications for re-ventilation If spontaneous res pi rat i on i s di scoord i nate or the pati e nt i s exhaus ted , agi t ate d or c l am my, the v ent i l a tor shoul d b e rec onnect ed. Howev er, cl i ni cal moni tori ng shoul d avoi d e xhaust i on. Succ ess ful we ani ng i s more e asi l y acc omp l i s hed i f exc ess i ve fati g ue i s not al l ow ed to set i n. T achypnoea (>30/mi n), tachy cardi a (> 110/mi n), re spi rat ory ac i dosi s (p H 11k Pa on FIO 2 =0. 4 (PaO 2 /FIO 2 rati o >27.5k Pa) Mi nute vol ume 10ml /kg Maxi mum i nspi ratory forc e (PImax) >20c mH 2 O Resp i ratory rat e/t i dal v ol ume < 100 Qs/Qt 35–40c mH 2 O or s i g ni fi cant red uct i ons i n D O 2 .

See also: IPPV—d esc ri pti on of vent i l ators, p6; IPPV—m ode s of ve nti l a ti on, p8; IPPV—adjusti ng the ve nti l at or, p10; IPPV—c omp l i cat i ons of ve nti l a ti on, p14; Pos i t i ve end ex pi ratory press ure (2), p 24; Conti nuous pos i ti ve ai rway pre ss ure , p 26; Lung recrui tment, p28 P.23 P.24

Positive end expiratory pressure (2) Adjusting PEEP 1. Meas ure bl ood gases and m oni tored haem ody nam i c vari ab l es . 2. If i nd i cated , alte r l eve l of PEEP by 3–5cmH 2 O i ncreme nts . 3. Re-m eas ure gas es and haemodynami c vari abl es aft er 15–20m i n. 4. Cons i de r furthe r c hanges as nec ess ary (i nc l ud i ng ad di t i onal change s i n PEEP, fl ui d c hal l e nge or vas oac ti v e drugs). A numb er of cl i ni cal tri al s have ad jus ted PEEP l eve l s ac cordi ng t o F IO 2 requi re ments (se e t abl e). Al though unl i k el y to consti tute ‘op ti m al PEEP’ for an i ndi v i dual pat i ent, thi s p rovi d es a us eful approxi mat i on and s tarti ng poi nt for further ti trati on of t herapy .

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FIO 2

0.3

0.4

0.4

0.5

0.5

0.6

0.7

0.7

0.7

0.8

0.9

0.9

0.9

1.0

PEEP (cmH 2 O)

5

5

8

8

10

10

10

12

14

14

14

16

18

≥18

Indications Hypoxae mi a re qui ri ng hi g h FIO 2 Opt i mi sat i on of press ure –vol um e c urv e i n s eve re res pi rat ory fai l ure Hypoxae mi a se condary t o l eft heart fai l ure Improve ment of c ard i ac output i n l eft he art failure Reduced work of b reathi ng duri ng w eani ng i n pat i e nts wi th hi g h PEEPi Neuroge ni c p ul m onary oede ma (i . e. non-cardi ogeni c pul monary oe dem a fol l owi ng rel i ef of up per ai rway obst ructi on)

Complications Reduced cardi ac out put . M ay nee d ad di ti onal fl ui d l oadi ng or eve n i not rop es. Thi s shoul d ge neral l y b e avoi ded unl ess hi ghe r PEEP i s ne ces sary t o m ai ntai n adeq uat e arteri a l oxyg enat i on. C aut i on shoul d b e e xerci s ed i n pati ents wi t h m yocard i al i s chaemi a. Inc reased ai rway pres sure (and pot ent i al ri sk of venti l at or trauma). Overi nfl a ti on l ead i ng to ai r t rap pi ng and rai se d PaCO 2 . Use wi th cauti on i n p ati ent s w i t h c hroni c ai rfl ow l i m i tati on or asthma. In press ure- c ont rol l e d ve nti l a ti on overdi s tensi on i s sug ges ted whe n an i ncreas e i n PEEP produc es a si gni fi cant fal l i n ti dal v ol ume. Hi g h l evel s wi l l d ecreas e v enous ret urn, rai s e i nt rac rani al press ure and i nc rease hepati c c ong est i on. PEEP may c hange t he are a of l ung i n whi ch a pul monary artery c athete r t i p i s pos i t i oned from We st Zone III to non-Zone III. Thi s i s sugge ste d b y a ri se i n wedg e p res sure of at l eas t hal f the i ncreas e i n PEEP and requi re s res i ti ng of the PA cathe ter.

See also: IPPV—d esc ri pti on of vent i l ators, p6; IPPV—m ode s of ve nti l a ti on, p8; IPPV—adjusti ng the ve nti l at or, p10; IPPV—c omp l i cat i ons of ve nti l a ti on, p14; Pos i t i ve end ex pi ratory press ure (1), p 22; Conti nuous pos i ti ve ai rway pre ss ure , p 26; Lung recrui tment, p28; Press ure–v ol ume rel ati ons hi p , p 96; Bl ood gas anal y si s , p 100; Inotrop es, p196; Fl ui d chall eng e, p 274; Atel ec tas i s and pul monary c ol l aps e, p284; Rai sed i ntracrani al press ure , p 382 P.25 P.26

Continuous positive airway pressure Conti nuous p osi ti ve airway pre ssure (CPAP) i s the addi ti on of p osi ti v e p res sure t o t he exp i ratory s i de of the b reathi ng ci rcui t of a s pontaneous l y venti l at i ng pati e nt who may or may not b e i nt ubat ed. Thi s se ts the bas el i ne up per ai rway pre ss ure above atm osp heri c pre ss ure , p rev ent s al veol ar c ol l aps e and pos si b l y rec rui ts al ready col l ap sed al veol i . It i s usual l y admi ni ste red i n i ncrements of 2.5cmH 2 O to a maxi mum of 10cmH 2 O and ap pl i ed vi a ei the r a ti ght-fi tt i ng face mas k (face CPAP), nasal mask (nasal CPAP) or exp i ratory l i m b of a ‘T’ pi ece breat hi ng c i rcui t. A hi g h fl ow (i . e. above peak i nsp i ratory fl ow ) i nsp i red air-oxy gen suppl y, or a l arg e rese rvoi r bag i n the i ns pi ratory ci rcui t, i s ne ces sary t o kee p t he val ve open. C PAP i m proves oxy genati on and may re duc e t he work of breat hi ng by reduci ng the al v eol ar-to-mouth pre ssure gradi e nt i n pat i ents wi th hi g h l eve l s of i nt ri nsi c PEEP. Trans i e nt peri od s of hi gh CPAP (e. g. 40c m H 2 O for 40s) may be a useful manoeuv re for re crui t i ng col l aps ed alve ol i and i mprovi ng oxy genati on i n ARD S.

Indications Hypoxae mi a re qui ri ng hi g h resp i ratory rate , e ffort and FIO 2 . Left he art fail ure to i m prove hypoxae mi a and c ard i ac output. Weani ng modal i t y. Reduci ng w ork of breat hi ng i n p ati ent s w i th hi gh PEEPi (e. g. ast hma, c hroni c ai rfl ow l i m i t ati on). NB: use wi t h caut i on and m oni tor c l os el y .

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Complications Wi t h m ask CPAP t here i s an i ncreas ed ri sk of aspi rati on as g ast ri c di l a tat i on may oc cur from swallowed ai r. Ins ert nasog ast ri c tube, es pec i al l y i f consc i ousne ss i s i mp ai red or gas tri c mot i l i ty i s re duc ed. Reduced cardi ac out put due t o reduced ve nous return (raise d i ntra-t horaci c pre ssure). M ay need ad di t i onal fl ui d or e ven i notrope s. Overi nfl a ti on l ead i ng to ai r t rap pi ng and hi gh PaC O 2 . Cauti on i s urged i n pati e nts wi th chroni c ai rfl ow l i mi tat i on or ast hma. Hi g h l evel s wi l l reduce venous re turn and i nc rease i nt racrani a l p res sure. Occ asi onal p oor pati e nt com pl i anc e w i th ti ght -fi tt i ng face m ask due t o feel i ng s of c l austrophobi a and di s com fort on b ri dge of nos e. Ins pi s sat ed sec ret i ons d ue to hi g h fl ow , d ry gas .

Management 1. Meas ure bl ood gases , m oni tor haemodynami c vari abl es and re spi rat ory rate. 2. Prep are ‘T ’ p i e ce c i rcui t w i t h a 5cm H 2 O CPAP valve on the e xpi rat ory l i mb. Conne ct i ns pi rat ory l i mb to fl ow gene rat or/l arge vol ume re servoi r bag. Adjus t ai r-oxy gen mi x t o obtain des i re d F IO 2 (measured by oxy gen anal yse r i n ci rcui t). Us e a he at–moi sture exc hanger to humi d i fy the i nhaled gas . If not i nt ub ated , c ons i d er ei t her nasal or face CPAP. At tac h m ask to fac e b y appropri at e harness and attach ‘T’ pi ece to mas k. Ens ure no ai r l eak around mas k. If usi ng a nasal m ask , encourag e t he pat i ent t o k eep thei r mouth cl ose d. 3. Meas ure gases , resp i ratory rat e, and hae mod ynami c s afte r 15–20mi n. 4. Cons i de r furthe r c hanges i n CPAP (by 2.5cmH 2 O i nc rem ent s) 5. Cons i de r need for (i ) fl ui d challe nge (or v asoact i ve drugs ) i f c i rc ul a tory c omp rom i s e and (i i ) nasog ast ri c t ube i f gast ri c atony p res ent .

See also: Pos i ti ve end ex pi ratory pre ss ure (1), p 22; Pos i t i ve end ex pi rat ory press ure (2), p 24; Inotrope s, p196; Fl ui d chall eng e, p 274; D ysp noe a, p278; Ai rway obs truct i on, p 280; Re spi rat ory failure, p282; At el e ctasi s and p ul m onary col l a pse , p284; Ac ute chest i nfec ti on (1), p288; Acute che st i nfect i on (2), p 290; Acut e resp i ratory d i s tre ss syndrome (1), p 292; Acut e resp i ratory di s tress sy ndrome (2), p 294; Pos t-operati ve i nt ens i ve care, p534 P.27 P.28

Lung recruitment The re has be en consi d erabl e i nterest i n rece nt years i n the conce pt of l ung recrui t ment. The rati onal e i s t hat reopeni ng of col l a pse d alve ol i wi l l re sul t i n i mprove d g as exc hange, wi t h res ul t i ng re duc ti ons i n ai rway p res sures and FIO 2 . Ti m i ng i s c ruc i al as col l aps ed alve ol i are m ore l i kel y t o b e recrui tab l e i n the earl y st age s of resp i ratory fai l ure. It app ears t hat be nefi t i s more l i ke l y i n non-re spi ratory c aus es of ARDS, rat her than i n cas es of d i rect pul monary pat hol ogy such as pne umoni a . Some ani mal st ud i es sugge st that recrui tment p roced ure s m ay e ven be pot ent i a l l y i nj uri ous i n t he l at ter si tuati on. Consi d erati on s houl d be gi v en to l ung recrui tme nt soon after i ntuba-t i on i n p ati ent s w i th se vere resp i ratory fai l ure, and proce dures causi ng d e-recrui tme nt, e. g. e ndotracheal sucti on and ai rway di sc onnect i on.

Recruitment techniques A numb er of tec hni que s are des cri bed to re crui t col l a pse d alve ol i , s uc h as ap pl y i ng 40cmH 2 O PEEP for 40s wi th no venti l at or bre aths; d el i ve ri ng a few l a rge -vol um e, vent i l ator-d el i vered bre aths; or by usi ng a c omb i nati on of varyi ng l ev el s of PEEP and i ncre asi ng pre ssure-del i ve red breat hs to obt ai n op ti mal gas ex change . Al though ane cdotal s ucc ess es are re ported , w i th oc cas i onal l y d ram ati c i mp rov ements i n l ung comp l i anc e and g as exc hange, no com parati ve tri al s have bee n p erform ed, and outc omes have not be en ass ess ed p rospe cti vel y. Hae mod ynam i c compromi se may occ ur duri ng t he proced ure , t hough thi s usually re cov ers on ce ssati on. P.29

Key trial Brower RG, et al for t he ARD S C l i ni c al Tri al s Ne twork. Effec ts of rec rui tme nt maneuv ers i n pati e nts wi th acute l ung i njury and acute res pi rat ory di stres s s ynd rom e ve nti l a ted wi t h hi g h p osi ti v e e nd-e xpi ratory p res sure. Cri t C are Me d 2003; 31:2592–7

P.30

Prone positioning Prone pos i ti oni ng i s us ed to tre at pat i ents wi t h acut e resp i ratory d i s tre ss syndrome (AR DS) to i m prove g as exc hange.

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A numb er of the ori es hav e b een propos ed to exp l ai n w hy t he prone pos i t i on hel ps . T hes e t heori e s i ncl ude : reducti on i n com pre ss i on at el e ctasi s of de pend ent l ung re gi ons (tem porary), red uct i on i n c hes t wall compl i ance i nc reasi ng i nt rathorac i c pre ss ure and al veol ar recrui t ment, bet ter re gi onal di aphragmat i c mov eme nt, be tte r V/Q mat chi ng, i mp rov ed sec ret i on c l earance and l es s al v eol ar di s tensi on l ead i ng to be tte r oxyg enati on.

Indications Prone pos i ti oni ng may be consi dered whe n: PaO 2 10cmH 2 O des pi t e opti mi s at i on of other venti l at ory support.

Technique Pos i ti oni ng the p ati ent takes ti me and pre parati on. Four mem bers of s taff are requi red to t urn t he pat i ent and one person to se cure t he head and e ndotracheal tube. The turn i t sel f i s a tw o-st age proce dure v i a the l a teral pos i t i on. The arm on whi c h t he p ati ent i s t o b e rol l ed i s tuc ked under the hi p wi t h t he other arm l a i d across the c hes t. Pi l l ows are pl ace d unde r t he abd omen and c hes t p ri or to rot ati on to the l a teral pos i ti on. If st abl e, turn may be com pl e ted to prone. Pi l l ows are pl ace d unde r t he shoul d ers and p el v i s . The head of the be d i s rai sed and one arm i s ext end ed at the pati e nt' s s i d e whi l e t he othe r i s fl e xed wi t h t he head faci ng the op pos i te way .

Frequency of turns The re sponse to prone venti l at i on i s di ffi cul t to pre di c t. Som e p ati ent s m ay hav e no i m provem ent i n gas e xchang e; others may have a t emp orary benefi t, req ui ri ng freq uent t urns, and ot hers m ay have di ffi cul ty ret urni ng t o a supi ne pos i t i on. For c omp res si on atel ec tas i s i t i s l i kel y t hat be nefi t wi l l l ast up to 2h be fore resumpt i on of a s upi ne pos i t i on i s re qui red . For other condi t i ons, up to 18h prone pos i t i oni ng may b e requi re d. The head and arm s s houl d be rep osi ti one d 2-hrl y.

Complications The re are probl ems as soc i at ed wi t h p osi ti oni ng the pati e nt prone i nc l ud i ng: faci al oed ema, i ncorre ct pos i t i oni ng of l i mbs l e adi ng to nerve p al s y and acc i de ntal removal of drai ns and cat het ers , p res sure nec ros i s, my osi ti s os si fi c ans . The se probl e ms are preve ntabl e provi ded there i s aw are nes s of thei r p ote nti al .

Contraindications The re are tw o ab sol ut e c ont rai ndi cat i ons to p rone p osi ti on: sev ere he ad, sp i nal or abdomi nal i nj ury and s eve re hae mod ynam i c i nstabi l i t y. Rel a ti ve c ont raind i cati ons i ncl ude: Rece nt abd omi nal surge ry Large abdomen Preg nancy Spi nal i nstabi l i t y (though sp eci al bed s are avai l a bl e for t urni ng affec ted pat i e nts ) Freq uent s ei z ures Mul ti p l e trauma Rai s ed ICP P.31

Key trial Gat ti noni L, e t al for the Prone-Sup i ne Stud y Group. Effe ct of prone pos i ti oni ng on the survi val of pati e nts wi th acute res pi rat ory failure. N Eng l J Med 2001; 345:568–73

See also: Ac ute re spi rat ory di st res s s ynd rom e (1), p292; Acut e resp i ratory d i s tre ss syndrome (2), p294 P.32

Non-invasive respiratory support Dev i ce s of v ary i ng sophi sti cati on are avai l a bl e to aug ment s pontaneous b reathi ng i n the compl i ant p ati ent b y ei ther ass i s ti ng i nsp i rati on (i nspi rat ory support ) and/or p rov i di ng CPAP. Non-i nvas i ve support i s usual l y d el i vered by ti ght fi t ti ng fac e or nasal mask, thoug h a hel met may b e used and i nsp i ratory s upp ort can b e d el i vered by mouthp i ec e. Som e d evi ces al l ow conne cti on to an endotracheal tube for the i ntubat ed b ut spontaneousl y b reathi ng pat i e nt.

Indications Hypoxae mi a re qui ri ng hi g h resp i ratory rate , e ffort and FIO 2 Hype rc apni a i n a fati g ui ng pat i ent Weani ng modal i t y To avoi d e ndotrache al i nt ubati on w here d esi rab l e (e. g. sev ere chroni c ai rfl ow l i mi tati on, i mm unosup pre sse d pati ents) Reduces work of b reathi ng i n pati e nts wi th hi g h PEEPi (e.g . as thma, chroni c ai rfl ow l i mi tat i on). Use wi th cauti on

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and moni tor c l osel y Phys i ot herap y te chni q ue for i mp rovi ng FR C Sl e ep apnoea

Inspiratory support (IS) A p res et i nspi rat ory press ure i s g i ve n whi c h i s t ri ggered by the pati e nt' s b re ath. Thi s tri gg er can be ad jus ted acc ord i ng t o t he d egree of pat i ent e ffort. Some d evi ces wi l l de l i v er bre aths automat i call y at ad jus tab l e rat es and the I:E rati o may also be adj ust abl e. The ti dal vol um e d el i vered for a gi v en l ev el of i ns pi ratory sup port w i l l v ary acc ord i ng t o t he p ati ent 's re spi rat ory compl i a nce . An ex amp l e of an IS devi ce i s the Bi rd ve nti l a tor commonl y use d b y phy si othe rap i s ts for i m provi ng F RC and exp and i ng l ung bas es.

BiPAP (Bi-level Positive Airways Pressure) Thi s d evi ce del i v ers ad jus tab l e l ev el s of press ure support and PEEP. Del i v ere d b reaths can b e ei ther pat i ent-t ri g gered and /or mandat ory. Some Bi PAP d evi ces are dri v en by air; to i ncreas e t he F IO 2 , suppl eme ntal oxyg en c an be gi v en vi a a c i rcui t c onnect i on or through a p ort al i n the mask.

Management 1. Sel ect ty pe and del i v ery mod e of ve nti l a tory s upp ort . 2. Connect pati e nt as per de vi c e i nst ructi ons . 3. Use an app rop ri a te si zed mas k t hat i s comfortabl e and l eak -free. 4. A d el i vered pre ssure of 10–15c mH 2 O i s a usual start i ng poi nt whi ch can b e ad jus ted ac cordi ng to pat i ent res ponse (res pi rat ory rate, de gre e of fati g ue, comfort, bl ood gases …). 5. Expi ratory p res sure s upp ort l evel s are usual l y wi t hi n the 5–12cmH 2 O range. 6. Pati ent s i n res pi ratory di stress may have i ni ti al di ffi c ul ty i n cop i ng wi th the se devi ce s. Cons tant atte nti on and encouragem ent he l p to acc ust om the pati e nt to the de vi c e and/or m ask whi l e di ffe rent l eve l s of sup port, I:E rat i os et c. are be i ng te ste d t o fi nd the op ti mal se tti ng. Cauti ous ad mi ni st rat i on of l ow d ose subcutaneous opi a te i nj ect i ons (e.g. di amorphi ne 2. 5mg ) m ay hel p t o calm the pati e nt wi t hout d epress i ng resp i ratory d ri ve. The ti g ht-fi t ti ng m ask may be found i ncre asi ngl y c l a ust rop hob i c aft er a few d ays ' use. Thi s shoul d be pre-e mpt ed i f poss i b l e by al l owi ng the pat i e nt reg ul a r b reaks. Press ure areas such as the bri dg e of t he nos e s houl d be protec ted . P.33

Key trials Brochard L, et al . Noni nvas i ve venti l at i on for acut e e xac erb ati ons of chroni c obs truct i ve pul monary di se ase. N Engl J Med 1995; 333:817–22

Ant one l l i M, et al . A compari s on of noni nv asi ve p osi ti ve-pre ssure venti l ati on and conve nti onal m echani cal v ent i l ati on i n pat i ents wi t h acut e resp i ratory fai l ure. N Engl J M ed 1998; 339:429–35

P.34

Extracorporeal respiratory support The se tec hni que s have de cl i ned i n popul ari ty ove r rece nt years aft er sev eral t ri al s faile d t o d emonst rat e c l ear out com e b ene fi t i n ad ul t s w i th ve ry sev ere re spi rat ory failure . Surv i val rate s of 50–60% are rep ort ed but cl ear sup eri ori ty ov er convent i onal venti l at i on has not yet bee n d emonst rat ed i n control l ed studi e s. A l arge p ros pec ti ve random i se d s tud y (the ‘C ESAR’ tri al ) i s c urrent l y und er way i n the UK .

Extracorporeal CO 2 removal (ECCO 2 R) An ext rac orporeal veno-v enous ci rcul at i on al l ow s CO 2 cl earanc e v i a a g as exc hang e m emb rane. Bl ood fl ows of 25–33% cardi ac out put are t ypi cal l y us ed w hi c h onl y al l ow for p art i al ox yge nat i on support. Low freq uency (4–5/mi n) pos i t i ve press ure ve nti l at i on i s us ual l y us ed wi t h EC CO 2 R w i th conti nuous oxy genati on throug hout i ns pi rati on and exp i rati on. The l ungs are ‘ hel d open’ w i th hi gh PEEP (20–25c mH 2 O), l i m i te d p eak ai rway press ures (35–40c mH 2 O) and a c ont i nuous fresh gas s upp l y. Thus, ox yge nat i on i s effec ted wi t h l ung rest to ai d recovery. Ant i coagul at i on of the ext rac orp oreal ci rcui t can be re duc ed by usi ng hep ari n-b ond ed tub i ng and m embrane s.

Extracorporeal membrane oxygenation (ECMO) An ext rac orporeal veno-arte ri al ci rcul at i on wi th hi g h b l ood fl ows (approac hi ng c ard i ac outp ut) through a gas exc hange memb rane e nab l es most i f not al l of t he body 's gas ex change re qui rem ent s t o b e m et. The main di s adv ant age s c omp are d t o ECCO 2 R are the ne ed for l a rge bore art eri al punct ure wi th i ts conse que nt ri s ks , and hi gh ext rac orp oreal bl ood fl ows wi t h t he pot ent i al for c el l damag e.

Indications

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Fai l ure of m axi mum i ntensi v e t herapy and ve nti l a tory s upp ort to sustain ade quate gas exc hange as evi denced by the cri te ri a be l ow .

Contraindications Chroni c s yst emi c d i se ase i nvol vi ng any major organ s yst em (e. g. i rreve rsi bl e c hroni c CN S d i se ase , c hroni c l ung di s eas e wi th FEV 1 < 1l , FEV 1 /FVC 6. 0kPa, e mphyse ma or pre vi ous adm i ss i on for chroni c res pi rat ory i nsuffi c i ency, i ncurabl e or rap i dl y fatal m al i gnancy , c hroni c l e ft heart fai l ure, chroni c renal fai l ure, chroni c l i v er fai l ure, HIV re l at ed di seas e). Lung fail ure for >7 days (al though treat ment w i th ex tracorporeal re spi ratory s upp ort may pe rs i st for l ong er than 14 d ays ). Burns (>40% of b ody surfac e). More than 3 organ fai l ure s i n addi ti on to l ung fail ure .

Criteria for ECCO 2 R/ECMO i. Rapi d fai l ure of ve nti l at ory support : i mmed i at e use of the se tec hni que s s houl d be consi d ere d i n t hos e m eet i ng the fol l ow i ng cri t eri a for a p eri od >2h des pi te maxi mum i ntensi ve c are: PaO 2 5cmH 2 O ii. Sl ow fail ure of venti l at ory support: consi der us e afte r 48h maxi mum i ntensi ve c are for t hos e m eet i ng the fol l owi ng gas ex change and me chani cal pul monary func ti on c ri t eri a for a p eri od >12h:

PaO 2 5cmH 2 O

Qs/Qt >30% on FIO 2 = 1.0

FIO 2 >0.6

PaO 2 /FIO 2 30g /l (thi s shoul d be vi ewe d i n t he c ont ext of the p l as ma protei n l eve l )-exud ate —cause s: i nfl am mat ory e. g. pne umoni a , p ul m onary embol us, neop l as m, col l a gen vas cul ar di seases

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Protei n < 30g /l -transudat e—c aus es: (i ) i ncreas ed venous press ure (e. g. heart fai l ure, fl ui d ove rl oad ), (i i ) de cre ase d col l oi d osm oti c p res sure (e.g . c ri t i c al i l l nes s l eadi ng t o reduced pl asm a prot ei n from c api l l ary l e ak and hep ati c dys functi on, he pat i c fai l ure, ne phroti c s ynd rom e)

Technique 1. Confi rm prese nce of effus i on by CXR or ul trasound. 2. Sel ect drai nage si te ei t her by maxi m um are a of st ony dul l ness under pe rc uss i on or under ul trasound gui dance. 3. Use ase pti c t ec hni que . Cl ean area wi t h anti sep ti c and i nfi l t rat e l ocal s ki n and s ubc ut aneous ti ssues wi t h 1% l i d ocaine . Advance i nto dee per ti ssues, as pi rat i ng to confi rm abs enc e of bl ood then i nfi l t rati ng w i th l ocal anae stheti c unt i l pl e ura i s pi erced and fl ui d c an be aspi rated . 4. Adv anc e drai nag e ne edl e/c annul a /drai n sl owl y, app l yi ng gentl e suct i on, t hrough chest wal l and i ntercos tal sp ace (above upp er border of ri b t o av oi d ne urovas cul ar bundl e) unti l fl ui d can be as pi rate d. 5. Wi t hdraw 50ml for m i c rob i ol ogi cal (M , C &S, TB st ai n, e tc. ), bi oche mi c al (prote i n, gl uc ose, et c.) and hi s tol ogi cal /cy tol ogi cal (p neumoc yst i s , mali gnant cel l s, et c.) anal y si s as i ndi cat ed. 6. Ei t her l e ave drai n in s it u conne cte d t o d rai nag e b ag or connec t needl e/c annul a by 3-way tap to drai nage apparat us . 7. Cont i nue aspi rati on/d rai nag e unti l no furt her fl ui d can b e w i thdrawn or i f pat i ent b ecomes sy mpt omat i c (pai n/d ysp noe a). Dys pnoea or hae mody nam i c change s m ay occ ur due to re moval of l arg e v ol umes of fl ui d (>1–2l ) and s ubs equent fl ui d shi ft s; i f thi s i s consi d ere d t o b e a pos si bi l i ty , remove no m ore than 1l at a t i me ei t her by cl amp i ng /dec l a mpi ng drain or rep eat i ng ne edl e aspi rat i on after an eq ui l i b rat i on i nterval (e .g. 4–6h). 8. Remove need l e/drain. Cover punct ure si te wi t h fi rml y app l i ed gauze d re ssi ng.

See also: Che st drain i ns erti on, p42; Ac ute chest i nfec ti on (1), p288; Acute c hes t i nfect i on (2), p 290; Pul monary e mbol us , p308; Heart fai l ure—asse ssm ent , p 324; He art failure —manage ment, p326; Rheumat i c di s orders, p492; Vasc ul i ti des , p494 P.45 P.46

Fibreoptic bronchoscopy Indications Diagnostic Col l ec ti on of mi crobi ol ogi c al ± c ytol og i cal s pec i m ens (by bronc ho- al veol ar l a vag e, p rotec ted brush sp eci men, bi opsy ). Caus e of b ronchi al obs truct i on (e. g. cl ot, forei gn b ody , neop l as m). Exte nt of i nhal a ti on i njury . Di a gnosi s of ruptured trachea/bronchus.

Therapeutic Cl earance of sec ret i ons, i nhal ed v omi tus , e tc . Removal of l umen-obs truct i ng matte r (e.g. mucus pl ug , bl ood cl ot , food, tooth). Proxi m al obs tructi on rat her t han cons ol i dati on i s s ugg est ed by the radi ol og i c al appe arance of a col l ap sed l ung/l ob e and no air bronc hog ram . Cl eansi ng —re movi ng soot or othe r t oxi c m ate ri al s , i rri gati on w i th saline. Di rect ed phy si othe rap y ± saline t o l oos en sec ret i ons. Di rect ed pl a cem ent of bal l oon c at het er to arrest pul monary b l ee di ng. To aid di ffi c ul t e ndotrache al i nt ubati on.

Contraindications/cautions Coag ul opat hy Seve re hyp oxaemi a

Complications Hypoxae mi a —from suc ti on, l os s of PEEP, part i al ob struct i on of endot rac heal t ube and non-d el i ve ry of t i d al vol ume.

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Haem ody nam i c di s turbance i ncl udi ng hype rte nsi on and tachy cardi a (rel a ted to hy pox aemi a, agi tat i on, t rache al sti mul ati on, et c.). Bl e edi ng. Perforati on (unusual t hough more c omm on i f b i opsy tak en).

Procedure It i s di ffi cul t t o p erform fi bre opt i c bronc hos cop y i n a nas al l y i nt ubated pat i e nt. A narrow -l umen sc ope can be us ed but suc ti on i s l i m i t ed. 1. Pre-oxy genate wi t h FIO 2 1.0. Moni t or wi t h p ul s e oxi m etry. 2. Inc rease pre ssure al a rm l i m i t on venti l at or. 3. Lub ri c ate sc ope wi th l ub ri cant g el /sal i ne . 4. If uni ntubat ed, app l y l i doc ai ne g el to nares ± sp ray to phary nx. 5. Cons i de r s hort-term IV s edati on ± paral ysi s. 6. Ins ert sc ope nasal l y (i n a non-i nt ubated pati e nt) or through cat het er mount port i n an i ntubat ed pat i ent. An ass i st ant shoul d s upp ort the e ndotrache al tub e d uri ng the proc edure t o m i ni mi se trauma to bot h t rache a and scope. 7. Inje ct 2% l i doc ai ne i nto trachea to p re vent coughi ng and haem ody nami c effe cts from trache al /cari nal sti mul ati on. 8. Perform thorough i nsp ect i on and any nece ssary proced ure s. If SpO 2 ≤85% or haem odynami c d i s turbance occ urs , remove scope and al l ow re -oxy genati on before conti nui ng. 9. Bronchoal veol ar l a vag e i s p erform ed b y i ns ti l l at i on of at l e ast 60ml of (preferabl y w arm ) i sot oni c s al i ne i nto affe cte d l ung area wi t hout s uct i on, fol l owe d b y as pi rat i on i nto a s teri l e c athete r t rap . Al l bronc hos cop i c sam pl e s shoul d be sent p rom ptl y t o t he l ab . 10. Reducti on of effect i ve end otrac heal t ube l umen and sucti on may affec t t he t i d al vol ume , l eadi ng to hyp oxaemi a and/or hyp erc apni a. 11. Aft er proced ure , rese t v ent i l a tor as ap propri at e. P.47

Chest physiotherapy The ai m i s t o e xpand c ol l ap sed al veol i , mobi l i se chest se creti ons or re -i nfl a te col l ap sed l ung seg ments. No sc i enti fi c val i dati on of e ffe cti veness has b een rep orted . The c urrent v i ew i s that routi ne ‘ prophy l ac ti c’ suc ti oni ng/ bag gi ng shoul d be av oi d ed i n the cri ti cally i l l .

Indications Mobi l i sat i on of se cre ti ons. Re-e xpansi on of c ol l ap sed l ung/l ob es. Prop hyl axi s agai ns t alve ol a r c ol l aps e and sec ond ary i nfec ti on.

Contraindications/cautions Agg res si v e hype ri nfl a ti on i n alread y hy peri nfl a ted l ungs , e .g. ast hma, e mphyse ma—though can be ve ry use ful i n removi ng m ucus p l ugs. Undrai ned pne umothorax . Rai s ed i nt racrani a l p res sure.

Techniques Hyperinflation Hyp eri nfl at i ng to 50% ab ove venti l at or-del i ve red V T , ai mi ng to e xpand col l ap sed al veol i and mobi l i s e s ecreti ons . V T i s rarel y m easure d, s o e i t her exc ess i v e or i nad equate hyp eri nfl at i ons m ay b e g i ve n d epe ndi ng on l ung c ompl i a nce and ope rat or tec hni que. Pres sure-l i m i ti ng dev i ce s (‘bl ow-off val ves ’) or manomet ers c an avoi d e xce ssi ve ai rway pre ss ure s. A recomme nded te chni q ue i s sl ow i nsp i rati on, a 1–2s pl ate au phase and then rap i d rel eas e of the b ag to si mul ate a ‘ huff’ and mobi l i se se creti ons . Pre-oxyg enati on m ay b e need ed as PEEP may b e l ost and t he d el i vered V T may be i nadeq uat e. Cardi a c outp ut oft en fal l s wi t h v ari abl e b l ood p res sure and heart rat e resp ons es. Sedat i on may bl unt the haemodynami c resp ons e. Ful l d efl ati on avoi ds ai r t rap pi ng.

Suction Rem ovi ng sec ret i ons from trachea and mai n b ronchi (usual l y ri ght). A cough refl ex may be st i m ul a ted to mob i l i se

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sec ret i ons furthe r. Tenaci ous se cre ti ons may be l oose ned by i ns ti l l a ti on of 2–5 ml 0.9% s al i ne. Fal l s i n SaO 2 and cardi ovas cul ar di sturb anc e may b e av oi d ed by pre -ox ygenati on.

Percussion and vibration Drummi ng and shaki ng act i ons over chest wall to mob i l i se se cre ti ons.

Inspiratory pressure support (Bird ventilator) The ai m i s t o i ncreas e FRC and exp and col l a pse d alve ol i .

Postural drainage Pat i ent p osi ti oni ng to ass i st drai nage —de pends on affe ct ed l ung area(s).

See also: End otracheal i ntubat i on, p 36; Ches t p hys i othe rap y, p 48; At el ect asi s and pul monary col l a pse , p 284; Haem opt ysi s, p304; Inhal a ti on i njury, p306 P.48

Complications Hypoxae mi a —from suc ti on, l os s of PEEP, et c. Haem ody nam i c di s turbance affect i ng cardi ac out put, heart rat e and b l ood p res sure whi ch may be rel ate d t o hi gh V T , ai rway pres sure, hyp oxae mi a , agi t ati on, trac heal s ti m ul a ti on, etc . Di rect traum a from sucti oni ng. Barotraum a/vol ut rauma i ncl udi ng p neumot horax.

General Ade quat e humi di fi c ati on avoi ds te nac i ous s put um and mucus pl ugs . Pai n rel i ef i s i mp ort ant to encourag e g ood che st exc ursi on and c oug h. Mobi l i sat i on and e ncouragi ng d eep breat hi ng m ay avoi d i nfe cti on.

When to request urgent physiotherapy Col l aps ed l ung/l obe wi th no ai r bronc hog ram vi si bl e , i .e. sugge sti ng proxi m al obs truct i on rathe r t han cons ol i dati on. Mucus p l uggi ng causi ng s ubs egm ent al col l ap se e.g . asthma.

When not to request urgent physiotherapy Cl i ni c al si g ns of che st i nfect i on wi th no sec ret i ons bei ng produc ed. Radi ol ogi cal consol i d ati on wi t h air bronc hog ram but no se creti ons prese nt. P.49

See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; Trache otomy, p38; Mi ni tracheot omy , p 40; Fi b reopti c bronchosc opy , p 46; Ate l ec tas i s and pul monary c ol l aps e, p284; Ac ut e chest i nfec ti on (1), p288; Acute c hes t i nfect i on (2), p290


Ed itors:


Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Car dio vasc u la r Th e r ap y T ech n i qu e s

Cardiovascular Therapy Techniques Defibrillation El e ct ri c al conversi on of a tachy arrhyt hmi a t o rest ore normal s i nus rhy thm . Thi s may be an eme rg enc y proc edure (when t he ci rcul at i on i s ab sent or s eve rel y c omp rom i s ed), se mi -el e cti ve (when t he ci rcul at i on i s c ompromi se d t o a

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l es ser d egree), or el ect i ve (w hen synchroni se d c ard i ov ers i on i s p erform ed t o rest ore s i nus rhyt hm for a non-compromi si ng s uprave ntri c ul a r t achycardi a). Sy nchroni s ati on req ui res i ni ti al connec ti on of ECG l eads from t he pat i ent t o t he defi bri l l at or so that t he shock i s del i ve red on the R wav e t o mi ni mi s e t he ri s k of v ent ri c ul a r fi b ri l l at i on. New er, bi phasi c de fi b ri l l a tors req ui re approxi mat el y half the ene rgy se tti ng of monophasi c d efi bri l l ators.

Indications Comp rom i se d c i rcul ati on, e. g. VF, VT Rest orati on of s i nus rhy thm and more effect i ve cardi ac out put Les sens ri sk of cardi ac thromb us format i on

Contraindications/cautions Aware p ati ent Seve re coagul opathy Caut i on wi th rec ent thrombol ys i s Di g oxi n l eve l s i n tox i c range

Complications Surfac e b urn Peri cardi al tam ponade El e ctrocuti on of b yst and ers

Technique (se e algori t hm opp osi te). The chance s of m ai ntai ni ng s i nus rhy thm are i ncreas ed i n el e cti ve cardi oversi on i f K + >4.5mmol /l and p l as ma Mg 2+ l evel s are normal . Pri or to defi bri l l at i on, e nsure sel f and onl ooke rs are not i n c ont act wi th pat i ent or b ed frame. To reduce the ri sk of sup erfi c i al burns , repl ace ge l /g el l ed pad s afte r e very 3 shocks . Cons i de r res i ti ng pad dl e posi t i on (e .g. anteroposte ri or) i f defi bri l l at i on fails . The ri sk of i nt rac tab l e VF fol l ow i ng de fi b ri l l a ti on i n a pat i e nt rec ei v i ng di gox i n i s small unl es s t he pl a sma di g oxi n l evel s are i n the t oxi c rang e or t he p ati ent i s hypovol aemi c. P.53

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Figure. No Caption Available.

See also: Chronotropes , p 206; Sedati v es, p238; Cardi ac arrest , p 272; Tachy arrhyt hmi as, p316; Hyp okalae mi a , p422 P.54

Temporary pacing (1) Whe n t he heart' s i ntri nsi c pacem aki ng abi l i ty fai l s, te mporary i nte rnal or e xte rnal p aci ng can be i nsti tuted . Inte rnal el e ctrod es c an be end ocardi al (i nserte d vi a a ce ntral vei n) or epi cardi al (pl ace d on the e xte rnal s urface of the he art at thorac otomy). T he e ndocardi al wi re m ay b e p l ac ed und er fl uoroscopi c c ont rol or ‘b l i nd’ us i ng a b al l oon fl ot ati on cat het er. Ex ternal paci ng can be rap i d l y performed by pl a cem ent of two el ect rodes on the front and rear chest wall whe n asys tol e or t hi rd d egree heart bl ock has produced ac ute haemod ynami c compromi se. It i s often us ed as a b ri d ge to tem porary i nternal paci ng. It can al so be use d as a prophyl a cti c m eas ure , e .g. for M obi tz Typ e II s econd-d egree heart bl ock.

Indications Thi rd-deg ree heart bl ock Mobi tz Typ e II s econd-deg ree he art bl ock when t he ci rcul at i on i s compromi sed or an ope rat i on i s p l anned Overpac i ng (rarel y ; more suc ces sful wi t h i nte rnal p aci ng) Asy stol e

Complications Internal pacing As for ce ntral venous cathe ter i nserti on Arrhyt hmi as Infe ct i on (i ncl udi ng end ocardi ti s) Myoc ard i al p erforati on (rare)

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External pacing Di s com fort

Troubleshooting Fai l ure t o p ace may be due t o: 1. No p ace mak er spi kes se en—che ck connec ti ons, check batte ry. 2. No c apt ure (p aci ng spi kes but no QRS com pl e x fol l owi ng)—poor pos i ti oni ng/di s l odgem ent of wi re. Te mporari l y i nc rease out put as thi s may re gai n c apt ure . Re pos i t i on/re pl a ce i nt ernal pac i ng wi re.

General 1. Chec k t hre shol d dai l y as i t wi l l ri s e s l owl y ove r 48–96h, probabl y due t o fi brosi s occurri ng around t he el ec trode s. 2. Overpac i ng i s occasi onal l y i ndi c ate d for a tachy cardi a not res pondi ng t o anti arrhyt hmi c t herapy or cardi ove rs i on. For SVT, pac i ng i s us ual l y att emp ted wi th the wi re si t ed i n the ri ght at ri um. Pace at rat e 20–30bpm ab ove pati ent's he art rate for 10–15s, the n ei ther dec rease rat e i mme di a tel y t o 80bp m or sl owl y, by 20b pm every 5–10s. 3. If overpac i ng fail s, und erp aci ng may be att emp ted wi th the wi re si t uat ed i n ei t her at ri um (for SVT) or, us ual l y , vent ri cl e (for ei t her SVT or VT). A pac ed rat e of 80–100b pm m ay produc e a re fractory peri od suffi ci e nt to sup pre ss the i ntri ns i c tac hyc ard i a. 4. Epi cardi a l p aci ng performed duri ng c ardi a c s urg ery re qui re s s i ti ng of ei t her tw o e pi c ard i al el ect rodes or one epi cardi a l and one ski n el e ctrode (us ual l y a hypodermi c ne edl e). The p aci ng threshol d of ep i cardi al wi res ri ses qui ckl y and m ay bec ome i neffe cti ve aft er 1–2 days. 5. In asys tol e, an el e ctri c al rhy thm produced by paci ng d oes not g uarant ee an adeq uat e c ard i ac output i s b ei ng gene rat ed. P.55

See also: Tem porary paci ng (2), p56; Chronot ropes , p 206; Cardi ac arres t, p272; Brad yarrhy thm i as , p 318 P.56

Temporary pacing (2) Technique (for endocardial electrode placement) 1. If usi ng fl uoroscopy, mov e p ati ent to X-ray sui te or pl ace l e ad shi el d s around bed area. Pl ace pati e nt on ‘sc ree ni ng t abl e’. St aff shoul d w ear l e ad aprons . 2. Use ase pti c t ec hni que throughout. Insert 6Fr she ath i n i nternal jugul ar or subcl avi an vei n. Sut ure i n posi t i on. 3. Connect paci ng w i re el ect rodes to pac i ng box (bl a ck = ne gat i ve pol ari t y = di s tal, red = p osi ti ve pol ari ty = proxi m al ). Set p ace mak ert o d emand. Che ck box i s worki ng and bat tery c harge ade quate. Turn pac i ng rate to ≥30b pm above p ati ent 's i ntri ns i c rhy thm . Set vol tag e t o 4V. 4. Ins ert paci ng w i re through she ath i nto central v ei n. If usi ng b al l oon c atheter, i ns ert to 15–20cm dep th the n i nfl at e b al l oon. Advance cat het er, vi ewi ng ECG moni t or for chang e i n ECG morphol og y and c apt ure of paci ng rat e. If usi ng screeni ng , d i re ct wi re t oward the ap ex of t he ri ght ventri cl e. App rox i mate i ns erti on d ept h from a neck ve i ni s 35–40c m. 5. If p aci ng i m pul ses not c apt ure d, (defl at e b al l oon), wi t hdraw wi re t o 15cm i nserti on d ept h t hen re peat s tep 4. 6. Onc e paci ng cap tured, de cre ase vol tage b y d ecreme nts to de termi ne t hre shol d at whi ch pac i ng i s no l onge r capt ured. Id eal pos i t i on de termi ned by a t hre shol d ≤0. 6V. If not ac hi eved , re-p osi ti on w i re. 7. If p oss i b l e, as k pati ent to cough to che ck that w i re does not di sl odge . 8. Set vol tage at 3 × threshol d and s et des i re d heart rate on ‘d emand’ mod e. Tap e wi re se curel y to pati e nt to pre vent di sl odg ement.

Technique (for external pacing) 1. Connect paci ng w i re ge l l ed e l ec trode s t o pacem ake r. Pl a ce bl a ck (= negati v e p ol a ri t y) el e ctrode on the ante ri or ches t wal l t o t he l eft of the l owe r s ternum and red (= p osi ti ve p ol a ri ty) el e ct rod e t o the c orres pondi ng p osi ti on on t he pos teri or hemi thorax . 2. Connect EC G e l ec trodes from ECG moni t or to exte rnal pac emak er and another set of el e ct rod es from pacem ake r to p ati ent

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3. Set pac emaker to de mand. T urn p aci ng rat e t o ≥30bp m abov e pati ent 's i nt ri nsi c rhyt hm. Se t c urrent t o 70mA. 4. Start pac i ng . Increas e c urrent (b y 5mA i nc re ment s) unt i l paci ng rate captured on moni t or. 5. If p aci ng rate not cap tured at curre nt of 120–130mA re si t e e l ec trodes and repe at ste ps 3–4. 6. Onc e paci ng cap tured, se t c urrent at 5–10m A abov e t hre shol d. P.57

See also: Tem porary paci ng (1), p54; Chronot ropes , p 206; Cardi ac arres t, p272; Brad yarrhy thm i as , p 318 P.58

Intra-aortic balloon counterpulsation Principle A 30–40ml ball oon i s pl ace d i n t he des cendi ng aort a. The bal l oon i s i nfl at ed wi t h hel i um duri ng di ast ol e, t hus i nc re asi ng di a stol i c b l ood pres sure above the b al l oon. T hi s se rve s t o i nc rease c oronary and cerebral perfusi on. The bal l oon i s d efl ate d d uri ng sy stol e, thus dec reasi ng p eri phe ral resi stance and i ncreas i ng s troke v ol ume. No pharmacol ogi cal t echni q ue exi sts whi ch can i ncreas e c oronary b l ood fl ow whi l e re duc i ng pe ri p heral re si s tance. Int ra-aorti c b al l oon count erp ul s ati on may i m prove cardi a c p erform anc e i n s i tuati ons where drugs are i neffec ti ve.

Indications The most obv i ous i ndi cat i on i s t o s upp ort the c i rc ul ati on where a st ruc tural cardi ac defect i s to be re pai red surg i cally . How ever, i t may be use d i n acut e c i rcul atory fai l ure i n any si t uat i on where re sol uti on of the cause of the card i ac dys functi on i s exp ect ed. In ac ute my ocardi al i nfarc ti on, re sol uti on of peri -i nfarct oe dem a may allow s pontaneous i mp rov eme nt i n myocardi a l func ti on; the us e of i ntra-aort i c bal l oon c ounterpul sati on m ay p rov i de te mporary ci rcul at ory support and promote myoc ardi a l heal i ng by i m provi ng m yoc ard i al bl ood fl ow. Ot her i ndi c at i ons i ncl ude acute myocardi t i s and poi s oni ng wi t h my ocardi al de pre ssants . Intra-aort i c bal l oon c ounterpul sati on s houl d not be use d i n aort i c re gurgi t ati on si nce the i ncreas e i n d i as tol i c bl ood press ure woul d i ncre ase re gurgi t ant fl ow.

Insertion of the balloon The us ual route i s vi a a fe moral art ery . Perc utaneous Sel di nger cathe teri s ati on (wi th or wi t hout an i ntroducer sheat h) provi d es a rapi d and safe t echni q ue wi t h m i ni mal arteri a l t rauma and bl eedi ng . Open surgi cal cathe teri s ati on may be nec ess ary i n el derl y pat i e nts wi th atheromat ous di sease. The ball oon pos i t i on shoul d b e c hec ked on a C XR t o e nsure that t he rad i o-opaque ti p i s at t he l ev el of t he 2nd i ntercostal s pac e. Ens ure the l eft radi a l p ul s e i s not l ost.

Anticoagulation The prese nce of a l arge fore i g n body i n the aorta re qui res s yst emi c anti coagul ati on to pre vent t hrombosi s . T he bal l oon s houl d not be l e ft defl at ed for l onge r t han a m i nute whi l e in si tu othe rwi se thromb osi s m ay occ ur des pi t e ant i c oagul at i on.

Control of balloon inflation and deflation Hel i um i s used to i nfl a te t he bal l oon, i t s l ow d ens i t y faci l i t ati ng rapi d trans fer from pum p t o ball oon. Infl ati on i s com monl y ti m ed to the ‘R’ wave of t he ECG, althoug h t i mi ng may be taken from an arte ri a l p res sure wave form. Mi nor adj ust ment m ay b e m ade to the t i mi ng to ens ure that i nfl at i on oc curs i mme di atel y afte r c l osure of the aort i c val ve (after the d i croti c not ch of t he art eri al press ure waveform) and d efl ati on occ urs at the e nd of d i as tol e. The fi l l i ng vol ume of the ball oon can be vari e d up t o t he maxi mum balloon vol ume . T he g re ater t he fi l l i ng v ol ume, the g reater the ci rc ul a tory augm ent ati on. The rate at whi ch bal l oon i nfl at i on oc curs m ay coi nci de wi t h e very c ard i ac be at or eve ry 2nd or 3rd c ard i ac be at. Sl owe r rate s are nec ess ary i n tachy arrhyt hmi as . W eani ng of i nt ra-aorti c b al l oon counte rpul s ati on may be achi ev ed by red uci ng aug mentat i on or the rate of i nfl at i on. P.59

See also: Hyp ote nsi on, p312; He art fai l ure—ass ess ment, p324; Heart fai l ure—manag eme nt, p326; Pos t-operati ve i nt ens i ve care, p534


Ed itors:


Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Ren al Th e r ap y Tec h n i qu e s

Renal Therapy Techniques Haemo(dia)filtration (1)

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The se are al ternat i ve s t o d i al ysi s that requi re a pre ssuri sed , p uri fi e d w ate r s upp l y, more expe nsi ve equi pm ent and ope rat or exp ert i s e, and a g reater ri sk of hae mody nam i c i nstabi l i t y due t o rapi d fl ui d and osm oti c s hi fts . Hae mo(d i a)fi l trati on can be arteri ov enous, us i ng the p ati ent 's bl ood pre ss ure to dri ve bl ood through the hae mofi l t er, or pum ped ve no-v enous. The l att er i s adv ant age ous i n that i t i s not de pendent on t he p ati ent 's bl ood press ure and the pump sys tem i ncorporate s alarms and safet y feature s. Veno-ve nous haem o(di a)fi l t rati on i s i ncreas i ngl y the tec hni que of choi c e. Bl ood i s us ual l y drawn and ret urned vi a a 10–12F r d oub l e l um en central v enous cat het er.

Indications Azotae mi a (uraem i a) Hype rkalae mi a Anuri a /ol i guri a; t o m ake sp ace for nutri ti on Seve re met abol i c ac i d osi s of non-t i s sue hyp ope rfusi on ori gi n Fl ui d overl oad Drug removal Hypothe rmi a/hype rtherm i a

Techniques Num erous i nc l udi ng haemofi l trati on, haemodi a fi l trati on, ul trafi l trati on, conti nuous ul t rafi l trati on w i th i ntermi tte nt di a l ys i s (CUPID ). Fi l trate i s us ual l y rem oved at 1–2l /h and fl ui d bal anc e adjuste d b y varyi ng the fl ui d repl ace ment rat e. Hi g h v ol ume hae mofi l t rat i on i nvol ves much hi g her cl earances (e. g. 35l i n a 4h peri od ) t hough vari ab l e out com es are re ported i n randomi s ed st udi es. Cre ati ni ne and pot ass i um cl earanc es are hi gher wi t h d i afi l t rat i on t houg h fi l trati on alone i s usuall y suffi ci ent provi ded an ade quate ul t rafi l t rate v ol ume i s achi ev ed (1000m l /h = c reati ni ne c l earance of 16ml /mi n).

Membranes Usual l y p ol y acryl oni tri l e , pol yami d e or p ol y sul phone. May b e hol l ow fi bre or fl at -pl at e i n de si gn. Surface are a us ual l y 0.6–1m 2 .

Replacement fluid A b uffere d b al a nce d e l ec trol yt e s ol uti on i s gi v en to buffer aci dae mi a and achi eve the d esi red fl ui d balance. Buffe rs i nc l ude l ac tat e (m etabol i s ed b y l i v er to b i c arb onate), ac etate (me tab ol i sed by mus cl e), and bi carbonat e. Ace tat e causes the m ost haemod ynami c i nst abi l i t y and i s rarel y used i n the c ri t i c al l y i l l . Bi carbonat e s ol uti ons may be more effi ci ent than l ac tat e at reve rsi ng se vere me tab ol i c aci dos i s, but outc ome benefi t has yet to be de mons trate d from i t s use and c are i s ne ede d wi th co-adm i ni st ere d c al c i um si nc e calc i um bi carbonate may crys tal l i s e. In l i ver fai l ure a l ac tat e b uffer may not be ad equate l y met abol i s ed. Si mi l arl y, i n poor perfus i on st ate s, the muscl e m ay not be abl e t o met abol i s e an acet ate buffer. An i ncre asi ng met abol i c al kal osi s m ay be due to exc ess i ve buffe r. In thi s c ase , use a ‘ l ow l a ctate’ (i .e. 30mmol /l ) rep l ac eme nt fl ui d . Potas si um c an be add ed, i f ne ces sary, to mai ntain normokalae mi a . Havi ng 20m mol KCl i n a 4.5l bag provi des a concentrati on of 4.44mmol /l . K + cl earanc e i s i ncreas ed by dec reasi ng t he concentrati on wi t hi n the rep l ac eme nt fl ui d or the di al ysate. P.63

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Key trials Ronco C, e t al. Effect s of d i ffere nt dos es i n conti nuous v eno-venous haemofi l trati on on outc ome s of ac ute re nal fai l ure: a p ros pec ti ve rand omi sed tri a l . Lancet 2000; 356:26–30 Bouman CS, e t al. Effe ct s of earl y hi gh-vol ume conti nuous venovenous he mofi l t rati on on s urv i val and rec overy of renal functi on i n i ntensi v e c are pati e nts wi th acute renal fai l ure: a p ros pec ti v e, random i ze d t ri al . Cri t C are Me d 2002; 30:2205–11

See also: Hae mo(d i a)fi l trati on (2), p64; Coagul ati on moni t ori ng, p156; Ant i c oagul ants , p 248; Ol i guri a, p 330; Ac ute re nal fai l ure—di a gnosi s , p 332; Ac ute re nal fail ure —manage ment, p334; M etabol i c aci dos i s , p 434; Met abol i c alkalos i s, p436; Poi soni ng —ge neral pri nc i pl es p324; Me tab ol i c aci d osi s, p434; Metabol i c al kal osi s, p436; Poi s oni ng—general pri nc i pl es, p452; Rhab dom yol ysi s, p528 P.64

Haemo(dia)filtration (2) Anticoagulation Ant i coagul at i on of the c i rc ui t i s usually wi th unfrac ti onat ed hep ari n (200–2000IU/h), or a pros tanoi d (prost acyc l i n or PG E 1 ) at 2–10ng/kg /mi n, or a c omb i nati on of t he two. Li tt l e exp eri enc e i s avai l ab l e on the us e of l ow mol ecul ar we i ght hepari n, c i t rat e and othe r anti coagul ants suc h as hi rudi n. No anti coagul ant may b e neede d i f t he pat i ent i s auto-anti c oag ul a ted . Prem ature cl ott i ng may be due t o m echani cal ki nki ng/obs truct i on of the ci rc ui t , i nsuffi ci ent anti c oag ul a ti on,

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i nadequate bl ood fl ow rat es or to l ac k of endog enous ant i coagul ants (anti t hrombi n III, hepari n cofac tor II). Usual fi l ter l i fes pan shoul d b e at l eas t 2 days but i s often dec re ased i n s ept i c pat i ents due to de cre ase d endogenous anti c oag ul a nt l ev el s . In t hi s s i tuati on, consi der use of fres h froz en pl a sma, a sy ntheti c p rot eas e i nhi bi tor such as aproti ni n, or ant i throm bi n III rep l ac eme nt (cos tl y).

Filter blood flow Fl ow t hrough the fi l t er i s us ual l y 100–200ml /mi n. Too sl ow a fl ow rat e promotes cl ot ti ng. Too hi gh a fl ow rat e w i l l i nc re ase trans memb rane p res sures and d ecreas e fi l t er l i fesp an wi t hout s i gni fi cant i mp rov eme nt i n cl e arance of ‘mi ddl e m ol e cul es ’ (e .g. urea).

Complications Di s connec ti on l ead i ng to haemorrhage . Infe ct i on ri sk (st eri l e tec hni que must be emp l oy ed). El e ctrol y te, ac i d–bas e or fl ui d i mbalance (ex ces s i nput or removal ). Haem orrhag e (vas cul ar acc ess si te s, pept i c ul cers) rel ate d t o anti coagul ati on therapy or c ons ump ti on coag ul opat hy. He pari n-i nd uc ed t hrombocyt ope ni a may rare l y occ ur.

Cautions Haem ody nam i c i ns tab i l i ty re l at ed to hyp ovol aem i a (es pec i al l y at start ). Vas oac ti v e d rug re moval b y t he fi l ter (e .g. catec hol ami nes ). Memb rane b i oc omp ati bi l i t y p rob l em s (esp eci al l y w i th cuprophane). Drug d osages may ne ed to b e revi sed (c ons ul t pharmaci st ). Ami no aci d l oss es throug h t he fi l ter. Heat l oss l e adi ng to hypothe rmi a. Mask i ng of py rex i a P.65 P.66

Peritoneal dialysis A s l ow form of di a l ys i s, ut i l i si ng the pe ri toneum as the di al y si s me mbrane . Sl ow correct i on of fl ui d and el ect rol yt e di s turbance may be be tte r t ol e rat ed by cri ti cal l y i l l p ati ent s and the te chni que d oes not requi re compl ex equi pm ent . How ever, tre atm ent i s l a bour i nte nsi ve and there i s consi derab l e ri s k of p eri toneal i nfec ti on. It has be en l argel y sup ers ede d b y haem ofi l trati on i n mos t i nt ens i ve care uni ts.

Peritoneal access For ac ute pe ri t one al di a l ys i s a t rochar and cannul a are i ns ert ed throug h a sm al l sk i n i nc i s i on under l ocal anaes the ti c . The sk i n i s prepared and drape d as for any st eri l e proced ure . T he com mone st app roach i s through a s mal l m i dl i ne i nc i s i on 1c m b el ow t he umbi l i cus . T he sub cut ane ous ti ssues and pe ri t one um are punct ure d b y t he trocar whi ch i s wi t hdrawn sl i g htl y b efore t he cannul a i s advance d t owards the p ouc h of Dougl as . In order t o av oi d damag e t o i nt ra-abd omi nal st ructures 1–2l warmed pe ri t one al di a l ys ate may b e i nfused i nto the peri t one um b y a st and ard , s hort i nt ravas cul ar cannul a p ri or t o p l ac eme nt of the trocar and cannul a s yst em. If the mi dl i ne ac ces s s i te i s not avai l ab l e an al t ernati ve i s to use a l at eral approac h, l at eral to a l i ne joi ni ng the umb i l i cus and the anteri or superi or i l i a c s pi ne (av oi d i ng the i nfe ri or e pi g ast ri c v ess el s ).

Dialysis technique Warmed pe ri t one al di a l ys at e i s i nfused i nto the peri t one um i n a vol um e of 1–2l at a t i m e. D uri ng the acut e p has e, fl ui d i s fl ushed i n and drai ned conti nuousl y (i .e. wi th no dwel l ti m e). Onc e b i oc hem i c al control i s achi eve d i t i s usual to l eave fl ui d i n the pe ri t one al cav i ty for 4-6h be fore drai ni ng. Hep ari n (500IU/l ) m ay be adde d t o t he fi rst 6 c ycl es to pre vent fi bri n cat het er bl ock age. There aft er, i t i s onl y nec es sary i f t here i s b l ood or c l oudi ness i n the d rai nag e fl ui d .

Peritoneal dialysate The di al y sat e i s a st eri l e balanced el ect rol yte sol ut i on wi th gl ucose at 75mm ol /l for a s tandard fl ui d or 311m mol /l for a hype rtoni c fl ui d (used for g reater fl ui d remov al ). T he fl ui d i s usual l y p otassi um free s i nce p otass i um exc hanges sl owl y i n pe ri toneal di al y si s , althoug h p otassi um may be add ed i f nec ess ary .

Complications Fl ui d l eak Poor drai nage

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Steroi d therapy Obes e or el de rl y pati e nt Cathete r b l oc kag e Bl ee di ng Omental encas ement Infe ct i on W hi t e c el l s > 50/ml , cl oud y d rai nag e fl ui d Hype rgl yc aemi a Absorpt i on of hy perosm oti c g l uc ose Di a phragm sp l i nti ng

Treatment of infection It i s pos si bl e to st eri l i se the pe ri t one um and cat het er by add i ng ap propri at e anti bi oti c s t o t he di a l ys at e. Sui tab l e reg i me ns i ncl ude: Cefurox i me 500mg /l for 2 c ycl es then 200m g/l for 10 d ays Gent ami ci n 8mg/l for 1 cy cl e dail y P.67

See also: Ol i guri a , p 330; Ac ute re nal failure—di a gnosi s, p332; Ac ute re nal fail ure —manage ment, p334 P.68

Plasma exchange Indications Pl a sma ex change may be us ed to remove ci rcul at i ng toxi ns or t o repl ace mi ss i ng pl asm a fact ors . It m ay b e used i n sep si s (e .g. me ni ngoc occ aem i a). In p ati ent s w i th i m mune me di ated di se ase, pl as ma e xchang e i s usually a tem porary measure w hi l e s yst emi c i mmunos upp res si on take s e ffe ct. There are s ome i mm une me di a ted di seases (e .g. Gui l l ai n–Barré s ynd rom e, t hromboti c t hrombocyt ope ni c purpura) where an i s ol a ted rathe r t han a c ont i nuous ant i body–ant i ge n reac ti on c an be tre ate d w i th earl y pl asm a e xchang e and no fol l ow-up i mmunos upp re ssi on. Most di s eas es req ui re a dail y 3–4l pl asm a ex change re peated for at l eas t 4 further occ asi ons ov er 5–10 d ays .

Techniques Cell separation by centrifugation Bl ood i s se parate d i nto component s i n a ce ntri fuge . Pl as ma (or other spe ci fi c bl ood com ponent s) are di scarde d and a pl a sma re pl a cem ent fl ui d i s i nfused i n eq ual vol ume . C ent ri fugati on m ay be conti nuous w here bl ood i s wi thdrawn and ret urned by sep arate nee dl e s, or i nt erm i t tent where bl ood i s wi thdrawn, sep arated and t hen re turned vi a t he sam e nee dl e .

Membrane filtration Pl a sma i s conti nuous l y fi l tered throug h a l a rge pore fi l ter (m ol e cul ar wei ght cut-off typ i cally 1, 000,000Da). The pl a sma i s di sc ard ed and re pl a ced by i nfus i on of an equal vol ume of rep l ac eme nt fl ui d. The t echni q ue i s si mi l ar to hae mofi l t rat i on and uses the s ame eq ui p ment.

Replacement fluid Mos t p ati ent s w i l l t ol e rat e repl ace ment w i th a pl a sma subst i tute. Our p refere nce i s t o repl ace pl asm a l oss wi th equal vol ume s of 6% hy droxy-ethyl starch and 5% al bumi n. Howev er, some use parti al cry stall oi d re pl a cem ent and ot hers use al l albumi n repl ace ment . Some fresh froze n p l as ma wi l l b e nece ssary aft er the ex change to rep l ac e c oag ul a ti on fac tors. The onl y i nd i c ati on to rep l ac e p l as ma l os s wi th al l fres h frozen pl a sma i s where pl asm a ex change i s be i ng performed to re pl a ce mi s si ng p l asma fac tors.

Complications Ci rcul atory i ns tab i l i ty Intravascul ar vol um e c hanges Re mov al of ci rcul at i ng catec hol ami nes Hypoc al cae mi a Reduced i ntravas cul ar COP If repl ace ment wi th cryst al l oi d

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Infe ct i on Re duc ed pl a sma op soni sati on Bl e edi ng Re mov al of coag ul ati on fac tors P.69

Indications Autoimmune disease Goodpasture' s s ynd rome Gui l l ai n–Barré s ynd rom e Myastheni a g rav i s Pem phi gus Rap i dl y p rog res si ve g l omerul onep hri ti s SLE Thromb oti c t hromb ocyt ope ni c p urp ura

Immunoproliferative disease Cry ogl obul i naem i a Mul ti pl e mye l om a Wal denstrom' s macrog l ob ul i nae mi a

Poisoning Paraquat

Others Meni ng ococcal s ept i c aemi a (pos si bl e benefi t) Sep si s (p oss i b l e benefi t) Rey e's sy ndrome

See also: Coagul ati on moni tori ng, p156; Ant i coagul ants, p248; Gui l l ai n–Barré s yndrome , p 384; Myastheni a g rav i s , p 386; Pl a tel et di sorders, p406; Poi s oni ng—general p ri nci pl e s, p452; Vascul i ti d es, p494


Ed itors:


Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Gas tr oi n te sti n al Th er a py Te ch n iqu es

Gastrointestinal Therapy Techniques Sengstaken-type tube Use d t o m anag e oesophageal v ari ceal haem orrhag e t hat conti nue s d esp i te pharm acol og i cal ± pe r-e ndoscopi c therapy. The de vi c e (Sengst ake n– Bl a kemore or si mi l ar) i s a l arge-bore rubb er tub e usually containi ng two balloons (oe sop hag eal and gastri c ) and t wo furthe r l ume ns (oe sop hag eal and gastri c ) t hat ope n abov e and b el ow t he bal l oons. Thi s d evi ce works usual l y b y t he gas tri c bal l oon al one compress i ng t he vari ce s at t he cardi a . Infl ati on of the oes ophage al bal l oon i s rare l y nec ess ary .

Insertion technique The tubes are usually ke pt i n the fri dg e t o p rov i de ad ded st i ffnes s for easi er i nserti on. 1. The pat i ent ofte n requi res j udi ci ous se dat i on or me chani c al venti l ati on (as warrante d b y c ons ci ous state/l ev el of agi tat i on) pri or t o i nse rti on. 2. Chec k b al l oons i nfl ate prope rl y be forehand. Lubri cate end of tub e. 3. Ins ert vi a m out h. Pl ac e t o d ept h of 55–60cm , i .e. to ens ure gast ri c balloon i s i n st omac h p ri or to i nfl at i on. 4. Infl at e gast ri c balloon wi t h w ate r t o v ol ume i ns tructe d b y m anufact urer (us ual l y ♠200ml ). A s mal l amount of

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rad i o-opaq ue contrast may be add ed. Ne gl i gi bl e re si s tance to i nfl at i on s houl d be fel t . C l am p g ast ri c b al l oon l um en. 5. Pul l t ube bac k unti l res i st anc e i s fel t, i .e . g ast ri c ball oon i s at cardi a. Fi x tub e i n p l ac e b y appl yi ng counter-t rac ti on at t he mout h. Ol d-fashi oned m ethods , s uch as at tac hi ng t he tub e t o a free-hang i ng l i tre b ag of sal i ne , have bee n s upe rse ded by more m anageabl e te chni ques. For e xamp l e, tw o w oode n t ong ue dep res sors, ‘thi ck ene d’ by havi ng El ast opl ast wound around them, are p l ac ed ei t her si de of the tube at t he mouth and then att ached t o e ach ot her at both end s b y more El a stopl ast . T he t ube re mai ns gri pp ed at t he mouth/che ek by t he att ached t ong ue dep res sors b ut can be re tract ed unt i l ade quate b ut not ex ces si ve t rac ti on i s bei ng app l i e d. 6. Perform X-ray to check sati s fac tory p osi ti on of g ast ri c b al l oon. 7. If b l ee di ng c ont i nues (c ont i nued l arge asp i rates from gas tri c or oesophageal l ume ns), i nfl ate oe sop hage al bal l oon (approx 50m l ).

Subsequent management 1. The gas tri c bal l oon i s usuall y ke pt i nfl at ed for 12–24h and defl at ed p ri or to end osc opy ± s cl erothe rap y. T he tracti on on the tube s houl d be tes ted hourl y b y t he nursi ng staff. The oe sop hag eal l umen shoul d b e pl ac ed on cont i nuous d rai nag e whi l e e nte ral nutri ti on and adm i ni st rat i on of drugs can b e g i ve n vi a t he gas tri c l um en. 2. If t he oes ophage al bal l oon i s used , d efl ate for 5–10m i n eve ry 1–2h t o reduce the ri sk of oes ophageal p res sure necros i s. Do not l eav e oe sop hag eal balloon i nfl at ed for l onge r t han 12h after s cl e rot herapy . 3. The tub e m ay need to st ay in si tu for 2–3 days though peri ods of d efl ati on shoul d t hen be al l owe d.

Complications Asp i rati on Perforati on Ul c erati on Oes ophageal necrosi s P.73

See also: Upp er gas troi ntes ti nal hae morrhage, p344; Bl ee di ng v ari ce s, p346 P.74

Upper gastrointestinal endoscopy Oes ophago-gastro-d uod enos cop y i s i de nti cal i n ve nti l at ed and non-v ent i l a ted pati e nts , t hough a p rot ect ed ai rway ± sed ate d s tat us usual l y faci l i tat es the proce dure.

Indications Inve st i gati on of up per gast roi nte sti nal s i gns/s ymp toms . e .g. bl eed i ng , p ai n, m ass , obst ructi on Therape uti c, e. g. s cl erothe rap y for vari ce s, l oc al epi nep hri ne (ad renal i ne) i njec ti on for di s crete bl eed i ng poi nt s, e.g. i n ul ce r b ase Pl ac eme nt of nas ojej unal t ube (w hen gas tri c atony pre vents ent eral feedi ng ) or pe rc utaneous g ast rostomy (PEG) ERCP—unusual i n the IC U p ati ent

Complications Loc al trauma causi ng hae morrhage or p erforati on Abd omi nal di ste nsi on com promi s i ng resp i ratory func ti on

Contraindications/cautions Seve re coagul opathy shoul d i deall y be correct ed

Procedure Upp er gas troi ntes ti nal end osc opy shoul d b e p erform ed b y an e xperi e nce d operator t o mi ni mi s e t he durati on and trauma of the p roc edure, and t o mi ni mi s e g ase ous di ste nsi on of the gut . 1. The pat i ent i s usual l y p l ac ed i n a l ate ral posi t i on t houg h c an be sup i ne i f i ntub ate d. 2. Inc rease FIO 2 and v ent i l ator p res sure alarm s ett i ng s. Consi d er i ncre asi ng sed ati on and ad jus ti ng v ent i l a tor mode .

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3. Moni tor ECG, SPO 2 , ai rway press ures and hae mod ynami c vari a bl e s t hroughout . If p ati ent i s on press ure s upp ort or p re ssure control v ent i l atory m ode s also moni t or ti dal vol ume s. The op erator shoul d c eas e t he proced ure , at leas t temp orari l y, i f the p ati ent be com es comp romi s ed. 4. At the end of the p roc edure the op erator shoul d aspi rat e as m uch ai r as p oss i bl e out of the gastroi ntes ti nal tract to d ecompress the abdomen. P.75

See also: Pul se oxi met ry, p90; Upp er gas troi nt est i nal haem orrhag e, p344; Bl ee di ng v ari ces , p 346


Ed itors:


Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Nu t r iti on

Nutrition Nutrition—use and indications Mal nut ri ti on l ead s t o p oor wound healing, pos t-operati ve com pl i cat i ons and sep si s. Ade quate nut ri t i onal support i s i mp ort ant for c ri ti c al l y i l l pati e nts and s houl d be provi d ed earl y duri ng t he i l l nes s. Evi dence for i m proved outcome from e arl y nutri t i onal sup port e xi s ts for pati e nts wi th traum a and b urns. Ent eral nut ri t i on i s i ndi cat ed whe n swallowi ng i s i nadequate or i m pos si bl e but g ast roi nte sti nal func ti on i s othe rwi se i nt act . Pare nte ral nutri ti on i s i nd i c ate d where the g ast roi nt est i nal t rac t c annot be use d t o p rov i de ad equate nut ri ti onal support , e. g. obs truct i on, i l eus , hi gh sm al l bowel fi stul a or mal abs orp ti on. Parent eral nutri t i on may b e us ed to sup pl e ment e nte ral nutri ti on whe re gas troi nt est i nal functi on al l ows parti al nut ri ti onal support .

Consequences of malnutrition Underfeeding

Overfeeding

Loss of muscle mass Reduced respiratory function Reduced immune function Poor wound healing Gut mucosal atrophy Reduced protein synthesis

Increased VO 2 Increased VCO 2 Hyperglycaemia Fatty infiltration of liver

Calorie requirements Vari ous formul ae e xi s t to c al cul ate the p ati ent 's bas al met abol i c rate but are m i sl ead i ng i n c ri t i c al i l l nes s. Met abol i c rat e c an be meas ured by i nd i re ct cal ori met ry but most pat i e nts are as sumed to req ui re 2000–2700Cal / day, or l es s i f starve d or unde rwe i ght.

Nitrogen requirements Ni t rogen exc ret i on c an b e c al c ul ate d i n t he abs enc e of re nal failure acc ordi ng t o t he 24h urea e xcreti on: Ni t rog en (g/24h) = 2 + Uri nary urea (m mol /24h) × 0. 028 How ever, as w i t h most formul ae, thi s met hod l a cks ac curac y. M ost pati e nts requi re 7–14g /day .

Other requirements The normal requi rements of sub strat es, vi tami ns and t rac e el eme nts are t abl ed opp osi te. Most l ong-t erm cri t i call y i l l pat i ents re qui re fol i c aci d and vi t ami n s upp l em ent ati on duri ng nutri ti onal s up port, e.g . Sol v i to. T rac e e l em ent s are usual l y s up pl e ment ed i n parent eral formul ae b ut shoul d not b e requi red duri ng enteral nut ri ti on. P.79

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Normal daily requirements (for a 70kg adult) Water

2100ml

Energy

2000–2700Cal

Nitrogen

7–14g

Glucose

210g

Lipid

140g

Sodium

70–140mmol

Potassium

50–120mmol

Calcium

5–10mmol

Magnesium

5–10mmol

Phosphate

10–20mmol

Vitamins Thiamine

16–19mg

Riboflavin

3–8mg

Niacin

33–34mg

Pyridoxine

5–10mg

Folate

0.3–0.5mg

Vitamin C

250–450mg

Vitamin A

2800–3300iu

Vitamin D

280–330iu

Vitamin E

1.4–1.7iu

Vitamin K

0.7mg

Trace elements

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Iron

1–2mg

Copper

0.5–1.0mg

Manganese

1–2µg

Zinc

2–4mg

Iodide

70–140µg

Fluoride

1–2mg

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P.80

Enteral nutrition Routes i ncl ude nas o-g ast ri c , naso-duode nal /jej unal, gas trost omy and je junost omy. Nasal tube fee di ng s houl d be vi a a soft, fi ne-b ore tube to aid pat i e nt comfort and avoi d ul ce rat i on of the nose or oes ophagus. Prol onged enteral fee di ng may be acc omp l i she d v i a a pe rc utaneous/p eroperati ve gas trost omy or perope rat i ve je junost omy . Enteral fee di ng provi d es a m ore compl ete di et than p are nte ral nutri ti on, mai nt ai ns s truct ural i nte gri ty of the gut, i mp rov es bow el adaptati on afte r rese cti on and re duc es i nfect i on ri sk .

Feed composition Mos t p ati ent s t ol erate i so-osm ol a r, non-l a ctose fee d. Carbohy drates are p rov i d ed as s ucros e or gl uc ose pol yme rs ; protei n as w hol e p rot ei n or ol i g opep ti des (may b e b ett er abs orb ed than free ami no aci ds i n ‘el eme ntal’ fee ds); fats as med i um chai n or l ong chain tri gl yce ri d es. Me di um c hai n t ri gl y ceri de s are bet ter ab sorbed . Standard feed i s formul ate d at 1Cal /ml . Spec i al fe eds are av ai l ab l e, e.g . hi g h fi bre, hi g h p rot ei n-calori e, re st ri c ted salt, hi gh fat or concentrated (1.5 or 2Cal/ml ) for fl ui d re stri ct i on. Immune-enhanc ed feed s (e.g . g l ut ami ne-enri ched or Imp act ®, a formul a s upp l em ent ed wi t h nucl eot i de s, arg i ni ne and fi sh oi l ) may red uce nosoc omi al i nfect i ons b ut no evi dence of out com e b ene fi t has b een shown from l arg e p ros pec ti v e s tud i es .

Management of enteral nutrition Onc e a de ci s i on i s made to start ent eral nut ri t i on, 30ml /h ful l s treng th standard feed may b e s tarted i m med i at el y . St art er reg i me ns i nc orp orati ng di l ute fe ed are not ne ces sary. Aft er 4h at 30m l /h the feed shoul d b e st opp ed for 30m i n pri or to as pi rati on of the st omac h. Si nce gastri c jui ce producti on i s i nc re ased by the p res enc e of a nas ogastri c tub e, i t i s re asonabl e t o acce pt an asp i rate of 200m l t he i nfusi on rat e i s not i ncre ase d b ut the fee d i s c ont i nued. If as pi rate s remain at hi g h v ol ume des pi t e m eas ure s t o p rom ote gas tri c emp tyi ng (e. g. met ocl oprami de or ery thromy ci n) t hen ei the r b owe l rest , nasoduodenal /nas ojej unal feed i ng or parenteral nut ri ti on shoul d be consi dered.

Complications Tube pl ace ment: trache obronc hi a l i nt ubati on, nas ophary nge al perforati on, i ntracrani al penetrati on (bas al sk ul l frac ture), oe sop hag eal pe rforat i on Refl ux Pul monary asp i rati on Naus ea and vomi t i ng Abd omi nal di ste nsi on i s occ as i onal l y reporte d w i th fe atures i ncl udi ng a te nde r, di ste nde d ab dom en and an i nc reasi ng m etabol i c aci dos i s . Laparot omy and bowel re sec ti on m ay be nece ss ary i n se vere cases Di a rrhoea: l arg e vol ume, bol us fee di ng, hi g h osmol al i t y, i nfect i on, l act ose i ntol erance , anti bi oti c t herapy , hi gh fat content Cons ti pat i on Metabol i c : de hyd rat i on, hype rgl yc aemi a, el e ctrol yte i m bal anc e P.81

Key trial At ki nson S, et al . A prosp ect i ve , rand omi zed , d oub l e-bl i nd, control l ed cl i ni cal t ri a l of e nte ral i m munonutri ti on i n the cri ti cal l y i l l . Cri t C are Me d 1998; 26:1164–72

See also: Nut ri ti on—use and i ndi c ati ons , p 78; El e ctrol ytes , p 146; Calc i um , m agne si um and phosphate , p 148; Gut mot i l i ty age nts , p 226; Vomi t i ng/gast ri c st asi s, p338; Di arrhoe a, p 340; Bowel pe rforat i on and obst ructi on, p348; Hyp ernatraem i a, p416; Hyp onatraemi a, p418; Hyp erk al a emi a, p420; Hypokal aem i a, p422; Hy pom agnesae mi a , p 424; Hypocal cae mi a , p 428; Hypophos phatae mi a , p430 P.82

Parenteral nutrition Feed composition Carbohydrate i s normally provi ded as conce ntrate d g l uc os e. 30–40% of tot al cal ori es are us ual l y gi ven as l i pi d (e. g. soy a b ean emul s i on). T he ni t rogen sourc e i s s ynt het i c, cryst al l i ne L-am i no ac i ds whi ch shoul d c ont ai n ap propri at e quanti ti es of all es senti a l and mos t non-e sse nti al ami no aci ds . Carbohyd rat e, l i pi d and ni troge n s ources are usually mi x ed i nt o a l a rge bag i n a st eri l e pharmacy uni t. Vi tam i ns , t rac e e l em ent s and approp ri a te el e ctrol y te concentrati ons can b e ac hi eved i n a si ngl e i nfus i on, thus avoi di ng m ul t i pl e c onnect i ons. Vol um e, p rotei n and c al ori e content of t he feed shoul d b e d ete rmi ned on a dai l y bas i s i n conjuncti on wi t h t he di e ti ti a n.

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Choice of parenteral feeding route Central venous A d edi cat ed cat het er (or l umen of a m ul ti -l um en cat het er) i s pl ace d unde r s teri l e condi ti ons . F or l ong-t erm fee di ng a sub cut ane ous tunne l i s ofte n used to se parate sk i n and vei n ent ry si t es. Thi s probab l y red uce s t he ri sk of i nfe cti on and cl earl y i d ent i fi es the sp eci al purpos e of t he cat het er. Id eal l y, bl ood sampl es shoul d not b e t aken nor othe r i nj ect i ons or i nfusi ons gi ven vi a t he feed i ng l umen. T he central v enous route al l ows i nfus i on of hy perosm ol a r sol ut i ons, provi d i ng ad equate ene rg y i ntake i n reduced vol um e.

Peripheral venous Parent eral nutri t i on vi a t he peri pheral rout e requi res a s ol uti on w i th os mol al i ty Tab le of Co n te n ts > Spe cial Su pp or t Su r fa ces

Special Support Surfaces Special support surfaces Pressure sores Pre ssure sores oc cur due t o c ompres si on of ti ss ue bet ween bone and the support surface and due to sheari ng force s, fri ct i on and macerat i on of ti ssues agai ns t t he sup port s urface . T he use of spe ci al beds at tem pts t o reduc e t he pre ss ure at the contact i ng sk i n surfac e t o a l e vel l ower than t he cap i l l ary occl usi on pre ss ure . In t he m ajori t y of c ase s i t i s suffi ci e nt to mi ni mi se the ti me that t he sup port s urfac e contact s any one are a of sk i n by pos i ti on change s.

Factors suggesting the need for a special bed

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Pati ent s wi t h s everel y rest ri c ted mobi l i t y d ue t o t racti on or cardi ores pi rat ory i nstabi l i t y c annot be t urned freq uentl y, i f at all . Pati ent s wi t h d ecreas ed s ki n i nte gri ty, e. g. burns, press ure s ore s alre ady prese nt, chroni c ste roi d use , di ab etes mel l i t us. Pati ent s on v asoact i ve drug i nfusi ons.

Types of special support surface Air mattress Thi s e i t her re pl a ces or i s pl ace d on t op of a st and ard hospi tal b ed m att re ss. They p rov i d e mi ni mum red uc ti on i n contac t p res sure but shoul d b e c ons i de red as mi ni m um sup port for any pat i e nt wi t h t he abov e fact ors .

Low air loss bed The se purpos e-b ui l t p res sure-rel i ev i ng be ds al l ow eas i er pati e nt mob i l i ty than othe r s upp ort s urface s. Cont act pre ss ure may st i l l b e hi gher than c api l l ary occ l usi on p res sure s o p osi ti oni ng i s sti l l re qui red . Pati ent s w ho are hae mod ynam i c al l y unst abl e s houl d usual l y b e m anaged on a l ow ai r l oss bed , p art i c ul a rl y i f re cei vi ng v asoconstri c tor drugs . The p res enc e of p res sure s ore s w i th i ntact ski n i s an i ndi cat i on for a l ow air l os s b ed. Rotat i onal l ow ai r l oss bed s allow automat ed l at eral rotati on at v ari abl e t i me i nterval s to faci l i tat e c hes t d rai nag e. The se may al s o b e useful whe re manual pos i t i oni ng i s i mpract i cal.

Air fluidised bed Thi s i s the onl y s up port s urface that consi s tentl y l owers c ont act pres sure t o b el ow capi l l a ry occ l us i on pres sure. Conseq uentl y , p ati ent s w i th se vere c ard i oresp i ratory i ns tab i l i ty , w ho c annot be turned , and pat i ents wi t h p res sure sores wi t h b rok en ski n b ene fi t most. The addi ti onal ab i l i ty to control the te mperat ure of the i m med i at e e nvi ronment i s an adv ant age i n hy pot hermi c pati e nts and t hos e wi th l a rge surface are a b urns. Any ex udat e from the s ki n i s ads orb ed i nt o t he si l i c one be ads on whi ch the pati e nt fl oats . T hi s dryi ng effe ct i s parti cul arl y use ful i n maj or burns (al though i t must be tak en i nt o account for fl ui d repl ace ment t herapy ). T he ai r fl ui di s ed bed al so has a rol e i n p ai n rel i e f.


Ed itors:


Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Resp ir a tor y M on itor in g

Respiratory Monitoring Pulse oximetry Conti nuous non-i nv asi ve moni tori ng of arte ri a l oxyg en sat urati on b y p l ac eme nt of a probe em i tt i ng red and near-i nfrare d l i g ht over t he p ul se on d i gi t, earl obe, cheek or bri dg e of nose. It i s unaffect ed by s ki n p i gm ent ati on, hyp erb i l i rubi naem i a or anaemi a (unl ess profound).

Physics The col our of b l ood v ari es wi t h oxyge n s aturat i on d ue t o t he opt i cal p roperti e s of t he haem moi et y. As the Hb mol ecul e gi v es up O 2 i t bec ome s l ess pe rme abl e t o red l i g ht and takes on a b l ue ti nt . Saturat i on i s de termi ned spe ctrop hot omet ri cal l y by meas uri ng the ‘ bl uene ss’ , uti l i s i ng the abi l i t y of compound s t o absorb l i g ht at a s pec i fi c wav el e ngt h. The us e of tw o wavel eng ths (650 and 940nm) pe rmi ts the rel a ti v e q uant i t i es of re duc ed and oxy hae mogl obi n to b e c al c ul ate d, the reb y de termi ni ng s aturat i on. T he art eri al pul se i s us ed to provi d e t i me poi nt s t o al l ow sub tract i on of the const ant ab sorpt i on of l i ght by ti ssue and venous bl ood. The accurac y of p ul s e oxi m etry i s wi t hi n 2% ab ove 70% SaO 2 .

Indications Cont i nuous moni t ori ng of art eri al ox ygen saturat i on.

Cautions As onl y t wo w ave l engths are use d, pul se oxi met ry meas ures func ti onal rather than frac ti onal ox yhaemog l ob i n sat urati on. Errone ous l y hi g h read i ng s are gi ven wi t h c arb oxy hae mog l ob i n and met hae mog l ob i n. Wi t h p oor peri p heral perfus i on or i ntense vas oconst ri cti on the re adi ng may be i nacc urate (‘fail soft’ ) or, i n newe r mode l s, ab sent (‘fail hard’). Moti on art efacts and hi gh l evel s of ambi ent l i ght i ng m ay affe ct readi ngs.

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Errone ous si gnal m ay b e p rod uce d b y s i gni fi cant venous pul sati on from tri cuspi d reg urg i tati on or v enous cong est i on. Venous pul sati l i t y ac count s for di fferenc es bet ween ear and fi nger SpO 2 i n t he sam e subje ct. Ens ure a g ood LED s i g nal i ndi c ator or a pul se waveform (i f av ai l abl e) i s see n on t he m oni tor. Vi t al dye s (e.g. me thy l thi oni ni um chl ori d e (m ethyl e ne bl ue), i ndoc yani ne green) may affec t SpO 2 re adi ngs . P.91

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; IPPV—ad jus ti ng t he venti l ator, p10; Conti nuous pos i ti ve ai rway press ure, p 26; End otrac heal i ntubat i on, p 36; Trache otomy, p38; F ibreop ti c bronchoscopy, p46; Chest phy si othe rap y, p48; Uppe r g ast roi nte sti nal e ndos copy, p74; Bl ood gas anal ysi s, p100; Basi c res usc i tati on, p270; Dys pnoea, p278; Res pi rat ory fai l ure, p282; Acute che st i nfect i on (1), p288; Acut e c hes t i nfe cti on (2), p 290; Ac ute res pi rat ory di stres s s ynd rom e (1), p292; Acut e resp i ratory di s tre ss syndrome (2), p294; Ast hma—ge neral manage ment , p 296; Ast hma—ve nti l at ory manag ement, p298; Pne umothorax , p300; Poi s oni ng—general p ri nci pl e s, p452; Pos t-op erati ve i nt ens i ve care, p534 P.92

CO 2 monitoring Capnography For capnography , resp i ratory g ase s m ust be sampl ed conti nuousl y and m eas ure d b y a rap i d re sponse dev i c e. Si nce CO 2 has an absorpt i on band i n the i nfrared sp ect rum , m eas ure ment i s faci l i tat ed i n gas mi xtures . Othe r g ase s c an i nt erfere wi th i nfrared ab sorpti on by CO 2 . Thi s m ay b e overcom e b y cali brati ng t he i ns trume nt wi t h known concentrati ons of CO 2 i n the requi re d m eas ure ment rang e, d i l ute d wi th a g as mi x ture s i m i l a r t o e xhaled gas.

The capnogram The CO 2 c onc ent rat i on of exhal ed g as consi sts of 4 p has es (se e fi gure). T he p res enc e of s i gni fi cant concentrati ons of CO 2 i n phase 1 i mp l i e s rebreat hi ng of e xhaled gas. Fai l ure of an ex pi ratory val ve to ope n i s t he most l i ke l y cause of reb reathi ng duri ng m anual vent i l ati on, al though an i nade quate fl ow of fresh gas i nto a reb reathi ng bag i s a com mon cause. The s l op e of phase 3 i s dep end ent on the rate of al v eol ar gas ex change . A st eep sl ope may i ndi cat e venti l at i on-perfus i on mi sm atc h s i nc e alve ol i that are poorl y v ent i l a ted but w el l pe rfused di scharge l at e i n t he res pi rat ory cy cl e . A st eep sl ope i s se en i n pat i ents wi t h s i g ni fi cant aut o-PEEP.

Colorimetric devices The underl yi ng pri nc i pl e i s t hat t he c hange i n pH produc ed by di fferent CO 2 c onc ent rat i ons i n sol uti on wi l l c hange the col our of an i ndi c ator. The se are sm al l de vi c es that fi t ont o an e ndotrache al tub e or t he vent i l ator c i rcui t and res pond rap i d l y (up to 60 bre aths/m i n). T hey can be affec ted by exc ess i ve humi d i t y and g ene ral l y onl y w ork i n the rang e 0–4% C O 2 . They are use ful to confi rm trache al i ntub ati on, duri ng p ati ent trans fer and i n t he cardi ac arrest si tuati on.

End-tidal PCO 2 End -ti dal PC O 2 app rox i mates PaCO 2 i n pati e nts wi th normal l ung funct i on. In ICU p ati ent s pul monary funct i on i s rarel y normal, thus end-ti dal PCO 2 i s a poor approxi mat i on of PaC O 2 . Larg e d i ffere nce s m ay repres ent an i nc re ase d dead s pac e t o t i dal v ol ume rat i o, poor pul monary perfusi on or i ntrapul monary s hunti ng. A progre ssi ve ri s e i n end -ti dal PC O 2 may rep re sent hypov ent i l ati on, ai rway ob st ruc ti on or i ncreas ed C O 2 produc ti on d ue to i nc reased met abol i c rate. End-t i dal PCO 2 falls wi th hyp erv ent i l ati on and i n l ow card i ac output s tat es. It i s ab sent w i th venti l at or di s connec ti on and duri ng cardi ac arres t b ut ri s es wi t h e ffe cti ve CPR or res torat i on of a s pontaneous ci rcul at i on.

Dead space to tidal volume ratio The arteri al t o end-t i dal PCO 2 di fferenc e m ay be use d t o calc ul a te the physi ol ogi c al dead s pac e t o t i dal v ol ume rat i o vi a the Bohr eq uat i on:

In health a val ue bet ween 30 and 45% s houl d be exp ect ed. P.93

The components of the normal capnogram

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Phase 1 Duri ng t he earl y part of the e xhaled breat h anat omi cal de ad s pac e and sam pl i ng dev i ce de ad space gas are s ampl ed. The re i s neg l i gi b l e CO 2 i n phas e 1.

Phase 2 As al veol ar gas be gi ns t o b e s amp l ed there i s a rap i d ri se i n CO 2 conce ntrati on.

Phase 3 Phase 3 i s k nown as the alve ol a r p l at eau and represe nts the CO 2 c onc ent rat i on i n mi xed ex pi red al v eol ar gas . T here i s normal l y a s l i ght i ncrease i n PCO 2 duri ng p has e 3 as al veol ar gas e xchang e conti nues duri ng ex pi rati on. Ai rw ay obs truct i on or a hi g h rate of CO 2 producti on wi l l i nc rease t he sl ope. End-t i dal PCO 2 w i l l b e l ess than t he PCO 2 of i d eal al v eol ar gas si nc e the s amp l ed ex hal ed gas i s mi xed wi th al v eol ar dead sp ace gas.

Phase 4 As i nspi rat i on be gi ns t here i s a rapi d fal l i n sampl e PCO 2 .

See also: Venti l at ory support— ind i c ati ons , p 4; IPPV—adj ust i ng the v ent i l a tor, p 10; End otracheal i ntub ati on, p36; T rac heotom y, p38; F i breop ti c bronc hos cop y, p46; Bl ood gas anal ysi s, p100; Bas i c res usc i t ati on, p270 P.94

Pulmonary function tests Few of the numerous pul monary func ti on t est s c urrentl y avail abl e i mpact upon c l i ni c al managem ent of the cri t i call y i l l , parti c ul arl y i f t he pat i ent has to be m ove d t o a l ab oratory. A numb er of other tes ts req ui re hi g hl y sp eci al i se d equi pm ent and ful fi l a p red omi nant rese arc h rol e.

Clinically relevant tests

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Measurement

Test

Common clinical use

PaO 2 , SaO 2 , PaCO 2

Arterial blood gases

SpO 2

Pulse oximetry

End-tidal PCO 2

Capnography

Vital capacity, tidal volume

Spirometry, electronic flowmetry

Serial measurement of borderline function (VC PV p re ssure >al veol ar press ure and b el ow l eft

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atri a l l eve l on a l at eral CXR. Sus pec t a non-z one III p osi ti on i f (i ) fol l ow i ng a ri s e i n PEEP, t he PAW P ri se s b y > 50% of the i ncre ment, (i i ) t he wed ge trace shows no d ete ctabl e cardi ac pul sati on and/or exce ss re spi rat ory vari a ti on. A non-zone III pos i ti on i s more l i k el y wi th PEEP and/or hypovol aemi a. P.119

Normal values Stroke volume

70–100ml

Cardiac output

4–6l/min

Right atrial pressure

0–5mmHg

Right ventricular pressure

20–25/0–5mmHg

Pulmonary artery pressure

20–25/10–15mmHg

Pulmonary artery wedge pressure

6–12mmHg

Mixed venous oxygen saturation

70–75%

Derived variables

Key trials and studies Connors AF Jr e t al . The effect i ve nes s of ri ght heart c athete ri zat i on i n the i ni t i a l c are of cri ti cal l y i l l p ati ent s. JAM A 1996; 276:889–97 Ri c hard C et al . Earl y use of t he pul monary artery c athete r and out com es i n pat i ents wi t h s hoc k and acute res pi rat ory di s tress sy ndrome : a random i ze d c ont rol l e d t ri a l . JAM A 2003; 290:2713–20 Ibe rt i T J et al . A mul t i ce nte r s tud y of p hys i ci ans ' k now l ed ge of t he pul monary artery c athete r. JAM A 1990; 264:2928–32

See also: Pos i ti ve end ex pi ratory pre ss ure (1), p 22; Pos i t i ve end ex pi rat ory press ure (2), p 24; Bl ood gas anal ysi s, p100; Ext rav asc ul ar l ung water me asurem ent , p 104; Ce ntral venous cathe ter—us e, p114; Cent ral ve nous cat het er— inserti on, p116; Pul monary arte ry cat het er—i nserti on, p120; Cardi ac out put—t hermod i l uti on, p122; C ard i ac out put —ot her i nvas i v e, p 124; Flui d c hal l enge, p274; He art failure—ass ess ment, p324; R out i ne chang es of di s pos abl es , p 478

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P.120

Pulmonary artery catheter—insertion Insertion 1. Ins ert 8Fr c ent ral ve nous i ntroducer sheat h unde r s tri ct as ept i c tec hni que. Pul monary art ery cathe teri s ati on i s easi er vi a i nte rnal j ugul ar or subcl avi an vei ns. 2. Prep are cathe ter pre-i ns ert i on—3-way tap s on all lum ens , fl us h l ume ns wi t h c ry stalloi d, i nfl ate bal l oon w i th 1.6m l air and c hec k for c onc ent ri c i nfl ati on and l e aks , p l ac e t ransparent s l ee ve ove r c athete r t o m ai ntai n future ste ri l i t y, p re ssure transd uce di st al l um en and zero t o a re ferenc e p oi nt (usual l y m i d-axi l l a ry l i ne). De pendi ng on cat het er typ e, othe r p re-i ns erti on c al i brati on ste ps may be req ui red, e. g. oxy gen sat urati on. 3. Ins ert cathe ter 15cm (i . e. beyond the l e ngt h of t he i nt rod uce r s heath) be fore i nfl ati ng bal l oon. Adv anc e c athete r smoothl y t hroug h t he ri g ht heart chambe rs. Pause to rec ord p res sures and note wave form s hap e i n RA, R V and PA. Whe n a characte ri sti c PAWP waveform i s obt ai ned, st op adv anc i ng cathe ter, d efl ate balloon and ensure t hat PA w ave form reap pears. If not , w i thdraw c athete r b y a fe w cm . 4. Sl owl y re -i nfl a te bal l oon, obs erv i ng wav eform trace. The we dge re cordi ng shoul d not b e ob tai ned unti l at l eas t 1.3m l of air has be en i nj ect ed i nt o t he bal l oon. If not , wi thdraw c atheter 1–2c m and repe at. If ‘overwed ged’ (pre ss ure conti nue s t o c l i m b on i nfl ati on), c athete r i s i ns ert ed too far and b al l oon has i nfl ate d forw ard ov er di s tal l umen. Imme di a tel y d efl ate , wi thdraw cathe ter 1–2c m and repe at. 5. Aft er i ns ert i on, a CXR i s usually pe rforme d t o v eri fy cat het er pos i ti on and to ex cl ude pne umot horax.

Contraindications/cautions Coag ul opat hy Tri cus pi d valve prost hes i s or di sease

Complications Prob l e ms of c ent ral ve nous c athete ri sat i on Arrhyt hmi as (es pec i al l y whe n t rav ers i ng tri c usp i d val ve) Infe ct i on (i ncl udi ng end ocardi ti s) Pul monary art ery rupt ure Pul monary i nfarc ti on Knot ti ng of c athete r Val ve d amage (do not wi thd raw cathe ter unl es s b al l oon de fl a ted )

Troubleshooting Exc ess i ve cathe ter l engt h i n a he art chamb er causes coi l i ng and a ri sk of k not ti ng. No more t han 15–20cm shoul d be pas sed be fore t he wave form c hanges . If not, defl at e b al l oon, w i thdraw c athete r, rep eat . A knot can be manage d b y (i ) ‘unknott i ng ’ w i th an i ntral umi nal wi re, (i i ) p ul l i ng taut and re mov i ng cathe ter + i nt rod uce r s heath tog ether, or (i i i ) surgi cal or angi ographi c i nt erv ent i on. If cat het er fai l s to adv anc e t o next chambe r, consi der ‘s ti ffeni ng ’ c athete r b y i nje cti ng i c ed cry stalloi d through di s tal l um en, rol l i ng pati e nt to l eft l ate ral posi t i on or ad vanci ng c at het er sl owl y wi th bal l oon d efl ated . The cathe ter shoul d neve r b e wi thdrawn wi t h t he b al l oon i nfl ate d. Arrhy thm i as on i nserti on usuall y oc cur w hen the cathe ter ti p i s at the tri cuspi d val ve. The se usual l y resol ve on wi t hdrawi ng the cathe ter or, occasi onal l y , after a sl ow b ol us of 1.5m g/kg l i docai ne. P.121

Waveforms

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See also: Central v enous cat het er— ins erti on, p116; Pul monary arte ry cat het er—use , p 118; Pneum othorax, p300; Hae mot horax, p302; Tac hyarrhythmi a s, p316 P.122

Cardiac output—thermodilution The rmodi l ut i on i s the t echni q ue uti l i sed by the pul monary arte ry cat het er to measure ri g ht vent ri cul ar cardi ac out put . The pri nc i p l e i s a m odi fi c ati on of the Fi ck p ri nci pl e where by a b ol us of cool e d 5% g l uc ose i s i njec ted through the proxi m al l umen i nt o t he central ci rcul at i on (ri ght atri um) and t he t emp erature c hange i s det ect ed by a t hermi s tor at the cathe ter ti p, som e 30cm di stal. A modi fi cat i on of the Hami l ton–Stew art eq uat i on, uti l i s i ng the vol ume, tem perature and sp eci fi c he at of the i njec tat e, enab l e s c ard i ac output t o b e c al c ul a ted by an on-l i ne c omp ute r from a curve measuri ng te mpe rat ure chang e i n t he pul monary artery. Conti nuous t hermod i l uti on meas urement uses a mod i fi ed cat het er that e mi t s heat pul se s from a the rmal fi l a ment l yi ng wi t hi n t he ri g ht ventri cl e and ri g ht atri um , 14–25cm from the ti p. 7.5W of he at are ad ded to the bl ood i nt ermi t tentl y ev ery 30–60s and t hes e t emp erature c hanges are m eas ure d b y a the rmi st or 4cm from the ti p. Though upd ate d freq uentl y , t he cardi a c outp ut di s pl ayed i s usually an ave rag e of t he pre vi ous 3–6mi n.

Thermodilution injection technique The computer const ant must be set for t he vol ume and te mpe rat ure of the 5% gl ucose use d. 10m l of i ce-col d g l uc ose provi d es the most acc urate measure. 5ml of room t emp erature i nje ct ate i s suffi ci e ntl y p rec i s e for norm al and hi gh out put st ate s howe ver i t s accurac y d oes worse n at l ow outp ut val ues . 1. Pres s ‘St art ’ b utt on on com put er. 2. Inje ct fl ui d sm oot hl y ove r 2–3s . 3. Repe at at l east twi ce more at rand om p oi nts i n the resp i ratory c ycl e. 4. Averag e 3 measureme nts falli ng wi t hi n 10% of e ach ot her. Re jec t outp uts gaine d from curve s t hat are i rregul ar/non-s mooth.

Erroneous readings Val ve l es i ons—t ri cus pi d re gurgi tat i on wi l l al l ow som e of the i nje ctate to refl ux back i nt o t he ri g ht atri um. Aorti c i nc omp etence produc es a hi gher l e ft v ent ri cul ar out put as a proporti on w i l l regurgi tat e b ack i nto the l e ft vent ri cl e . Sep tal de fect s. Los s of i njec tat e. Che ck that c onnect i ons are ti g ht and do not l eak .

Advantages Most commonl y us ed and fam i l i ar IC U t echni q ue, computer warni ngs of poor c urves .

Disadvantages Non-conti nuous (by i nj ect i on te chni que). 5–10% i nte r- and i ntraobs erver vari a bi l i ty . Errone ous re adi ngs wi th tri cuspi d regurgi tat i on, i nt rac ard i ac s hunts. Freq uentl y repeated me asurem ent s m ay res ul t i n consi derabl e v ol umes of 5% gl ucose b ei ng i nj ect ed. P.123

See also: Pul monary artery c athete r—use, p118; Cardi ac out put —ot her i nvas i ve , p 124; Cardi ac out put—non-i nvasi ve (1), p146; Cardi a c outp ut— non-i nvas i ve (2), p 146; Fl ui d challe nge , p 274; Hy pot ens i on, p 312; Heart fai l ure —as ses sme nt, p324; Sys tem i c i nfl a mmat i on/mul t i -organ fail ure , p 484; Burns —fl ui d manag ement, p510 P.124

Cardiac output—other invasive Dye dilution Mi x i ng of a gi v en vol ume of i nd i cator t o an unknown v ol ume of fl ui d al l ows calcul at i on of thi s vol ume from the de gre e of i nd i cator di l uti on. The ti me el a pse d for the i ndi c ator t o p ass some di s tance i n the cardi ovascul ar s yst em y i el ds a

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cardi ac out put val ue, calc ul a ted as :

…where I i s the amount of i ndi c at or i nj ect ed, C m i s the me an c onc ent rati on of the i ndi cator and t i s the t otal d urati on of the curve . T he t radi t i onal dye di l ut i on t echni q ue i s to i nj ect i ndoc yani ne green i nto a c ent ral ve i n fol l ow ed b y rep eat ed sam pl i ng of art eri al bl ood to enabl e const ruc ti on of a ti me–concentrati on curve wi t h a rap i d up stroke and an exp one nti al dec ay. Pl ott i ng the d ye dec ay c urve s emi l og ari thmi c al l y and ext rap ol a ti ng v al ues to the ori gi n p roduc es the cardi ac out put . T he COLD-Pul s i on de vi c e m eas ure s t he concentrati on d ecay d i rect l y from an i ndwe l l i ng arteri al probe, thus com put i ng card i ac output. Al t ernati vel y, thi s dev i ce may us e t he the rmodi l ut i on app roach, av oi d i ng pul monary artery c athete ri sat i on. T he Li D CO dev i ce i s based on a s i m i l a r p ri nci pl e us i ng l i thi um as the ‘ dye’ .

Advantages Reasonabl y ac curat e, l es s i nvasi v e t han pul monary arte ry cat het er pl a cem ent .

Disadvantages Inv asi ve, re ci rcul at i on of dy e preve nts mul t i pl e repe ate d m easure ment s, l e ngt hy, und erest i mates l ow output v al ues. Inaccurate w i t h moderate / s eve re val vul ar reg urg i tati on. Use of paral ysi ng age nts may i nte rfe re wi t h l i thi um measureme nt.

Direct Fick The am ount of subst anc e p ass i ng i nto a fl ow i ng sy st em i s e qual t o t he di fferenc e i n c onc ent rat i on of the s ubs tance on eac h s i de of the s yst em m ul ti p l i e d b y t he fl ow wi thi n the sy ste m. C ard i ac output i s thus usually calcul a ted by di v i d i ng total body oxyg en consum pti on by the di fference i n oxyg en content b etw een art eri al and m i xe d ve nous bl ood. Al te rnati v el y , CO 2 p rod uct i on can b e used i nste ad of VO 2 as t he i ndi c ator. Art eri al C O 2 can be deri v ed non-i nvas i ve l y from e nd-t i d al CO 2 whi l e mi xed venous CO 2 c an b e d ete rmi ned by rapi d re breathi ng i nto a b ag unt i l CO 2 l e vel s have eq ui l i brate d.

Advantages ‘Gol d st and ard ’ for cardi a c outp ut est i mati on.

Disadvantages For VO 2 : Invasi ve (req ui res measureme nt of mi x ed v enous bl ood), requi re s l eak -free open ci rc ui t or an unwi e l dy cl osed ci rc ui t te chni q ue. Oxy gen consumpt i on me asurem ent s v i a met abol i c cart unrel i ab l e i f FIO 2 i s hi g h. Lung oxy gen consumpt i on not me asured by pul monary arte ry cat het er tec hni que (m ay be hi g h i n ARDS, p neumoni a…). For CO 2 : Non-i nv asi ve but re qui re s norm al l ung func ti on and i s thus not generally ap pl i cab l e i n ICU pati e nts . P.125

See also: CO 2 moni t ori ng , p92; Bl ood g as analys i s , p 100; Ext ravas cul ar l ung w ate r m eas ure ment , p 104; Pul monary arte ry cat het er—us e, p 118; C ard i ac output—t hermod i l uti on, p122; Cardi a c outp ut— non-i nvas i ve (1), p 126; C ard i ac out put —non-i nvasi v e (2), p128; Indi rect calori m etry, p168; Fl ui d chal l enge, p274; Hyp ote nsi on, p312; Heart fai l ure— ass ess ment, p324; Syst emi c i nfl amm ati on/mul ti -org an fai l ure, p484; Burns—fl ui d m anagem ent , p 510 P.126

Cardiac output—non-invasive (1) Doppler ultrasound An ul trasound beam of known fre que ncy i s re fl e ct ed b y m ovi ng red bl ood corpuscl es wi t h a shi ft i n frequenc y proporti onal t o t he b l ood fl ow ve l oc i ty . T he act ual ve l oc i ty can b e c al c ul a ted from the Doppl er equati on whi ch req ui res the c osi ne of t he vec tor be twe en the di rec ti on of t he ul t ras ound b eam and that of bl ood fl ow. T hi s has b een app l i ed t o b l ood fl ow i n the asce ndi ng aorta and aorti c arch (v i a a suprast ernal app roach), d esc end i ng thoraci c aorta (oe sop hag eal app roach) and i ntracard i ac fl ow (e.g . t ransmi tral from an ap i cal approac h). Sp ect ral anal ysi s of t he Dop pl e r freq uency shi ft s p rod uce s v el oci t y–t i me waveforms , t he are a of whi c h represe nts the ‘ stroke di stance ’, i .e . the di st anc e trave l l ed by a col um n of b l ood wi th eac h l eft ve ntri c ul a r s yst ol e (s ee fi g ure op pos i te ). The produc t of stroke di st anc e and aort i c (or mi tral val ve) cross -sec ti onal area i s st rok e v ol ume. Cross -sec ti onal area can be measured echocardi ographi c al l y; howe ver, as b oth op erator exp erti s e and equi pm ent i s re qui red , t hi s ad di ti onal measureme nt can be ei the r i gnored or as sum ed from nomog ram s t o p rov i de a reasonabl e es tim ate of st rok e vol um e.

Advantages Qui ck , s afe, mi ni m al l y i nv asi ve, re asonabl y accurate, conti nuous (vi a oe sop hag eal ap proach), othe r i nform ati on on contract i l i ty, prel oad and afterl oad from wav eform shape (see fi gure opposi t e).

Disadvantages Non-conti nuous (unl es s v i a oes ophagus), l earni ng curve , operator d ependent.

Echocardiography Com bi nes struct ural as wel l as d ynam i c ass es sment of t he heart usi ng ul t rasound refl ec ted off vari ous i nterfac es. Transt horac i c or transoesophageal p rob es provi d e i nformati on on v al v e i nte gri ty, gl obal (di a stol i c and s yst ol i c) and

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reg i onal ventri cul ar funct i on, w al l thi c kne ss, pe ri c ard i al fl ui d or t hi c keni ng , aort i c di sse cti on, ve ntri c ul a r v ol umes and eje cti on fracti on, and p ul m onary pre ssures . Oft en c omb i ne d w i th i nteg ral D opp l er ul trasound for cardi ac out put est i mati on d eri ve d from com bi ned measureme nt of aort i c di ame ter pl us fl ow at vari ous si tes , e .g. l e ft vent ri cul ar out fl ow t rac t, aorta, trans mi tral. Analyt i c software or formul ae can al so enabl e comput at i on of cardi ac out put from est i mati ons of ventri cul ar vol um es.

Advantages Non-i nvas i ve , s afe , rel a ti v el y qui ck . Prov i de s othe r useful i nform ati on on cardi a c s truct ure and func ti on.

Disadvantages Exp ens i ve eq ui p ment, l engthy l earni ng c urve and i nt erobse rve r v ari ab i l i ty. Body hab i tus or p athol ogy (e. g. emp hys ema) may i mpair i mage qualit y. P.127

Doppler blood flow velocity waveform variables


Changes in Doppler flow velocity waveform shape


See also: Cardi a c outp ut— the rmodi l ut i on, p 122; Cardi ac out put —ot her i nvas i ve , p 124; Card i ac output—non-i nv asi ve (2), p128; Fl ui d chall eng e, p 274; Hypotensi on, p312; Heart fai l ure—asse ssm ent , p 324; Sy ste mi c i nfl ammati on/m ul t i -org an fai l ure, p484; Burns— fl ui d manage ment, p510 P.128

Cardiac output—non-invasive (2) Pulse contour analysis The conce pt of thi s t echni q ue i s that t he contour of t he art eri al press ure wav eform i s proporti onal t o s troke vol ume. How ever, i t i s al s o i nfl uenced by aorti c i mpe dance so anothe r c ard i ac output m eas uri ng tec hni que (e .g. comme rci al dev i ce s uti l i s i ng COLD -Pul si on or Li D CO) must be used i n t ande m for i ni ti al cal i brat i on. Al thoug h i t c an the n b e used as a m eans of conti nuous cardi ac out put moni t ori ng, frequent re -calib rat i on s houl d be p erformed agains t t he refere nce te chni que. Thi s i s parti c ul arl y i mportant whe n c hang es i n i m pedance oc cur, e .g. wi th change s i n c ard i ac

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out put , v asc ul a r t one , b ody te mpe rat ure .

Advantages Conti nuous fl ow moni t ori ng, us es dat a from arteri al cannul a al read y in si tu for press ure moni t ori ng.

Disadvantages Change s i n v asc ul a r c omp l i ance wi l l affect ac curac y requi ri ng fre que nt rec al i brati on. Req ui res a good qual i ty , non-ob struct ed and non-d ampe d arte ri al wave form. The re i s deb ate about the re l at i v e qual i ty of si gnal from radi a l v s. fem oral arte ry.

Thoracic bioimpedance Imp edance chang es ori gi nate i n the t horaci c aorta w hen bl ood i s ej ect ed from t he l eft ve ntri c l e. Thi s effect i s us ed to det erm i ne st roke v ol ume from formul a e ut i l i si ng the el ect ri cal fi el d si ze of the thorax, bas el i ne thorac i c i m ped anc e and fl uct uat i on rel a ted to sys tol e, and ve ntri c ul a r e jec ti on t i me . A corre ct i on fac tor for s ex, he i ght and wei ght i s al so i nt roduc ed. The te chni q ue s i m pl y ut i l i se s four pai rs of el ect rod es pl a ced i n prosc ri bed pos i t i ons on t he nec k and thorax ; t hes e are connec ted to a d edi cat ed moni tor w hi c h m eas ure s t horaci c i mp edance to a l ow ampl i t ude , hi gh (70kHz) freq uenc y 2.5m A c urrent appl i ed ac ros s t he el e ctrode s.

Advantages Qui ck , s afe, total l y non-i nvas i ve , reas onabl y ac curate i n normal, spontaneousl y b reathi ng sub jec ts.

Disadvantages Di screpanci es i n cri ti cal l y i l l p ati ent s (esp eci al l y t hos e w i th arrhythmi a s, tac hyc ard i as , i ntrat horaci c fl ui d s hi fts , anatom i cal d eformi ti es, aorti c regurgi tat i on), met al wi t hi n t he t horax, i nabi l i ty to veri fy si gnal. P.129

See also: Cardi a c outp ut— the rmodi l ut i on, p 122; Cardi ac out put —ot her i nvas i ve , p 124; Card i ac output—non-i nv asi ve (1), p126; Fl ui d chall eng e, p 274; Hypotensi on, p312; Heart fai l ure—asse ssm ent , p 324; Sy ste mi c i nfl ammati on/m ul t i -org an fai l ure, p484; Burns— fl ui d manage ment, p510 P.130

Gut tonometry A g as permeabl e si l i cone b al l oon at tac hed to a s amp l i ng t ube i s pass ed i nt o t he l ume n of t he gut . D evi ces ex i st for tonome try i n the s tom ach or si gmoi d col on. The t onomet er al l ows i ndi rect me asurem ent of the PCO 2 of t he g ut muc osa and c al c ul a ti on of t he pH of t he muc osa.

Indications Gut mucos al hyp ope rfusi on i s an e arl y c ons equenc e of hypov ol a emi a. Cove rt ci rcul at ory i nad equacy due to hyp ovol ae mi a may be de tec ted as gut mucos al ac i dosi s and has been rel a ted to pos t-operati ve com pl i cat i ons aft er maj or surgery. In cri ti cal l y i l l p ati ent s t here i s s ome ev i de nce that pre venti on of gut m ucosal ac i d osi s i mprove s out com e. The si gmoi d col on tonomet er i s us eful t o d ete ct i sc hae mi c col i ti s earl y (e .g. aft er abd omi nal vascul ar surgery).

Technique Saline tonometry In the ori gi nal t echni q ue the tonome ter ball oon was prepared by de gas si ng and fi l l i ng w i t h 2. 5ml 0. 9% sal i ne. T he sal i ne was w i thdrawn i nt o a sy ri nge connec ted to the s amp l i ng t ube pri or to i nserti on. After i nserti on the saline w as pas sed back i nt o t he bal l oon. The PCO 2 of t he sal i ne i n the b al l oon eq ui l i b rat ed wi t h t he PC O 2 of t he gut l umen ov er a peri od of 30–90mi n. At s teady state i t was as sum ed that t he PC O 2 of t he gut l umen and g ut muc osa were i n equi l i bri um . T i me corre ct i on fac tors were de ri ved for parti al eq ui l i brat i on bet wee n t he bal l oon s al i ne and the g ut l um en. The m eas ure ment was c omp l et ed by sam pl i ng the saline from the b al l oon and an arteri a l b l ood s amp l e for measureme nt of art eri al [HC O 3 - ].

Gas tonometry Usi ng ai r i n t he tonomet ry bal l oon all ows more rapi d e qui l i brati on b etw een the t onom ete r and the l umi nal PCO 2 . A mod i fi ed cap nom ete r automat i cally fi l l s t he bal l oon wi th ai r and samp l e s t he PCO 2 afte r 5–10mi n eq ui l i b rat i on. Sub seq uent c ycl es of bal l oon fi l l i ng d o not use fresh ai r s o CO 2 equi l i brati on i s qui ck er. Tonome tri c PCO 2 m ay be com pared wi t h e nd-ti d al PCO 2 (m eas ure d w i th the s ame capnom ete r) as an est i mate of art eri al PCO 2 . Wi t h a normal cap nog ram , a balloon PCO 2 si gni fi cantl y hi ghe r t han end-t i dal PCO 2 i mpl i e s g ut muc osal hypop erfusi on.

pH versus regional PCO 2 The pH of the gut m ucosa (pHi) may be cal cul at ed usi ng a modi fi ed He nde rson–Hass el b ach eq uat i on:

whe re K i s t he ti m e d ependent e qui l i brati on c ons tant. How ever, most of the v ari ati on i n the me asurem ent i s due t o vari at i on i n regi onal PCO 2 . Com pari ng re gi onal PCO 2 w i th PaCO 2 gi ves as much i nform ati on as mak i ng the c al c ul a ti on

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of pHi and overcome s t he probl emat i c as sum pti on that arte ri a l [HCO 3 - ] i s equi valent t o m ucosal capi l l a ry [HCO 3 - ]. P.131

See also: CO 2 moni t ori ng , p92; Bl ood g as analys i s , p 100 Ovid: Oxford Handbook of Critical Care

Ed itors:


Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Neu r ol ogi cal Mo n it or i n g

Neurological Monitoring Intracranial pressure monitoring Indications To confi rm t he di a gnosi s of raise d i nt rac rani al press ure (ICP) and moni t or treat ment. May be use d i n c ase s of he ad i nj ury part i cul arl y i f venti l at ed, Gl asg ow C oma Sc ore ≤8, or wi th an abnorm al CT scan. Al s o used i n encep hal opathy , pos t-neurosurge ry and i n se l ec ted cases of i ntracrani al hae morrhage. Al though a rai sed IC P c an b e rel ated to poor prognosi s after he ad i nj ury , t he converse i s not true. Sust ai ned red uct i on of raise d ICP (or mai nte nance of cerebral perfus i on pres sure) i n head i njury m ay i mp rov e outc ome al t hough l arge control l ed tri al s are l ac ki ng.

Methods of monitoring intracranial pressure Ventricular monitoring A c athete r i s i ns ert ed i nt o t he l at eral v ent ri cl e vi a a burr hol e. The cathe ter may be conne cte d t o a press ure trans duc er or may contai n a fi bre opt i c press ure moni t ori ng dev i ce . F ibreop ti c c athete rs req ui re regul ar c al i brati on acc ord i ng t o t he m anufac turer' s i ns truct i ons. Bot h s yst ems shoul d b e t est ed for pat enc y and dam pi ng b y t emp orari l y rai si ng i nt rac rani a l p res sure (e.g . wi th a c oug h or b y occl udi ng a j ugul ar ve i n). C SF may be draine d t hrough the ventri cul ar cathe ter to re duc e i ntrac rani al press ure.

Subdural monitoring The dura i s ope ned vi a a burr hol e and a hol l ow b ol t i nserte d i nto the s kul l . The bol t may be connec ted to a p re ssure trans duc er or admi t a fi breop ti c or hi -fi del i t y pres sure m oni tori ng de vi c e. A s ubd ural b ol t i s e asi er to i ns ert than ventri cul ar moni t ors . T he mai n d i sadvantages of sub dural moni t ori ng are a tendency t o unde res ti mat e ICP and dam pi ng e ffe cts . Agai n c al i brati on and pat enc y t est i ng s houl d be performed reg ul arl y.

Complications Infect i on—part i cul arl y aft er 5 d ays Hae morrhage— parti c ul arl y w i th coagul op athy or d i ffi cul t i nserti on

Using ICP monitoring Normal IC P i s < 10m mHg . A raise d ICP i s usual l y t reated when > 25m mHg i n he ad i nj ury . As ICP i nc reases , t here are oft en sus tai ned ri se s i n ICP t o 50–100m mHg l a sti ng for 5–20m i n, i ncreas i ng wi th fre que ncy as the basel i ne ICP ri s es. Thi s i s ass oci ate d w i th a 60% mortal i t y. Cere bral perfus i on press ure (C PP) i s the di ffe rence bet ween me an BP and mean ICP. Treatm ent ai med at re duc i ng IC P m ay als o reduc e m ean BP. It i s i mport ant to mai ntain CPP >50–60mmHg. P.135

See also: Int racrani a l haem orrhag e, p376; Subarachnoi d haem orrhag e, p378; R ai s ed i nt rac rani a l p res sure, p382; He ad i nj ury (1), p 504; Head i njury (2), p506 P.136

Jugular venous bulb saturation Ret rog rad e p ass age of a fi bre-opti c c athete r from the i nte rnal jugul a r v ei n i nto the jug ul ar bul b e nab l es conti nuous moni tori ng of j ugul ar ve nous b ul b saturati on (SjO 2 ). Thi s can be us ed i n conjuncti on wi t h othe r m oni tors of c ere bral hae mod ynam i c s s uch as mi ddl e c ere bral b l ood fl ow , c ere bral arte ri ovenous l a ct ate di fferenc e and i nt rac rani a l pre ss ure to di rec t m anageme nt.

Principles of SjO 2 management Normal value s are app rox i matel y 65–70%. In the ab sence of anae mi a and w i th maint enance of normal SaO 2 value s, val ues of Sj O 2 >75% sugge st l uxury pe rfusi on or gl obal i nfarcti on wi t h oxyg en not bei ng ut i l i sed ; v al ues Tab le of Co n te n ts > Lab or a tor y M on i tor in g

Laboratory Monitoring Urea and creatinine Measured i n bl ood, uri ne and, occ asi onall y, i n othe r fl ui ds such as abd omi nal drai n fl ui d (e .g. urete ri c di srupt i on, fi s tul ae )

Urea A p rod uc t of the urea cy cl e re sul ti ng from am moni a bre akd own, i t d epends upon adeq uat e l i ve r func ti on for i ts synthe si s and adeq uat e renal func ti on for i ts ex cre ti on. Low l e vel s are thus s een i n ci rrhos i s and hi gh l ev el s i n renal fai l ure. Uraemi a i s a cl i ni cal s ynd rom e i ncl ud i ng l e thargy , d row si ness , c onfusi on, pruri tus and peri cardi ti s resul t i ng from hi gh pl asm a l eve l s of ure a (or, more c orrec tl y , ni troge nous w ast e p rod uct s—azot aem i a). The rati o of uri ne :pl asm a urea may be us eful i n d i st i ngui shi ng ol i guri a of re nal or pre-renal ori g i ns . Hig her rati os (>10:1) are s een i n pre-renal c ond i ti ons , e .g. hy pov ol a emi a, w hereas l ow l eve l s ( 120 µm ol /l s ugg est s a creat i ni ne cl earanc e 40) are see n i n p re-renal condi t i ons and l ow l e vel s ( 0.6

small difference between inspired and expired O 2

Loss of volume

circuit leaks, bronchopleural fistula

Use of indirect calorimetry Hel ps to mat ch nut ri ti onal i ntak e t o e nergy e xpe ndi ture. It i s i m portant t o feed cri ti cal l y i l l p ati ent s approp ri a tel y, avoi di ng bot h unde rfe edi ng and ove rfe edi ng (se e t abl e). Indi rect calori m etry m ay also be us ed to ass ess the work of bre athi ng by as ses si ng the change i n VO 2 duri ng w eani ng from m echani cal ve nti l a ti on. The VO 2 change may al so be use d t o asse ss app rop ri ate l ev el s of se dat i on and anal ges i a. P.169

Respiratory quotients for various metabolic fuels Ketones

0.63

Fat

0.71

Protein

0.80

Carbohydrate

1.00

The whol e bod y R Q d epe nds on the fuel or com bi nati on of fue l s bei ng uti l i sed . N orm al l y a combi nat i on of fat and carbohydrate are uti l i s ed wi t h a RQ of 0.8. Li pog enes i s as soc i at ed wi t h b oth se psi s and overfee di ng m ay gi v e a RQ of 1.1–1. 3

See also: IPPV—asse ss ment of we ani ng, p18; N utri t i on—us e and i nd i cati ons , p78; Ente ral nutri ti on, p80; Parenteral nut ri ti on,

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p82; C O 2 moni tori ng, p92; Cardi ac out put —ot her i nvas i ve , p 124; Opi oi d analge si c s, p234; N on-opi oi d analg esi cs, p236; Sed ati ves , p 238; Py rex i a (1), p 518; Pyre xi a (2), p 520; Pai n, p 532 P.170

Lactate Measurement of blood lactate Analys ers are avai l a bl e to al l ow rap i d measureme nt of bl ood or pl a sma l a ctate on s mal l sam pl e s, usi ng enz yme -bas ed met hod s. The enzymati c c onv ers i on of l a ctate to p yruvat e i s an oxyg en uti l i s i ng reac ti on. The ext racti on of oxyg en from t he sam pl e can b e de tec ted by a sensi t i ve ox yge n fuel cel l sensor and i s d i re ctl y p roporti onal to the s amp l e l ac tat e c onc ent rati on. A w hol e bl ood sampl e (venous or arteri al si nc e t here i s no prac ti c al di fferenc e) i s col l ec te d i nto a hepari n fl uori d e tube to pre vent c oag ul a ti on and gl y col ysi s (l ac tat e p rod uc i ng ). N i t ri t e m ay be used i n t he s amp l e tub e t o c onv ert haemog l obi n to the me t form , t hus av oi d i ng up tak e of ox yge n d uri ng the enzym e reac ti on. The enzymati c me thod i s s pec i fi c for the L-i s omer and w i l l not, there fore, d ete ct D-l act at e (e .g. i n short bowel syndrome). N orm al art eri al whol e bl ood l ac tat e c onc ent rat i on i s Tab le of Co n te n ts > Resp ir a tor y d r u gs

Respiratory drugs Bronchodilators Types β 2 agoni st s: e.g . s al b utamol , e pi nephri ne, terbutal i ne Ant i chol i nergi cs: e. g. i pratropi um Theophy l l i ne s: e .g. am i nophy l l i ne Ste roi ds: e. g. hydroc ort i sone, predni sol one Others : e. g. ket ami ne, i s ofl urane, halot hane

Uses Rel i ef of bronc hos pas m

Routes Inhal e d (s al b ut amol , e pi nephri ne, te rbutal i ne , i pratropi um, i s ofl urane, halot hane) Nebul i sed (s al b utamol , ep i nephri ne, terbut al i ne, i pratropi um) IV (sal butam ol , epi ne phri ne , t erb utali ne, i p rat rop i um , ami nophyl l i ne , hydrocort i sone, ket ami ne) PO (ami nop hyl l i ne, predni sol one)

Side-effects CNS st i mul at i on (s al b utamol , e pi nephri ne, terbut al i ne , am i nophy l l i ne ) Tachycard i a (sal butamol , epi nep hri ne , t erb utaline, ami nop hyl l i ne, ket ami ne) Hypotensi on (sal but amol , terbut al i ne , ami nophyl l i ne , i sofl urane , hal othane) Hype rgl yc aemi a (sal but amol , epi nep hri ne , t erb utaline, hyd roc ort i s one, predni s ol one) Hypokal aem i a (salbutam ol , ep i ne phri ne , t erb utali ne, hyd roc orti s one , p red ni s ol one) Lac ti c ac i dosi s (s al but amol )—rare

Notes Sel ec ti v e β 2 ag oni sts are usuall y gi ven by i nhal ati on vi a a pre ssuri sed aeros ol or a ne bul i z er. Inhal ati on oft en gi v es rap i d re l i e f of bronc hos pas m, al t hough the ae ros ol i s of l es s b ene fi t i n se vere asthma. Neb ul i ze d drug s requi re a mi ni mum v ol ume of 4ml and a dri vi ng g as fl ow of 6–8l /mi n. In ext rem is , ep i ne phri ne may b e used IV, SC or i nje cte d d own the endot rac heal t ube . As e pi nephri ne i s not se l ec ti v e, arrhyt hmi as are more l i kel y. Howe ver, t he α ag oni st effect may reduce muc osal s wel l i ng b y v asoconstri c ti on. Iprat rop i um bromi de has no sys tem i c effect s and doe s not dep res s m ucoci l l i ary cl earanc e. It i s synerg i s ti c wi th β 2 agoni s ts but has a sl owe r onse t of ac ti on. Ami nop hyl l i ne i s synerg i s ti c wi th β 2 agoni s ts . D osages mus t b e adjuste d accordi ng to pl a sma l e vel s (range 10–20m g/l ) s i nc e t oxi c e ffe cts may be se vere. Dos e requi re ments are re duc ed by heart fai l ure, l i v er di seas e, chroni c ai rfl ow l i m i tati on, fev er, ci met i di ne, erythrom yci n. Dos e requi rements are i ncreas ed i n chi l dren, s moke rs and those wi t h a moderate to hi gh al c ohol i ntake.

See also: St eroi ds , p 262; Chroni c ai rfl ow l i mi tati on, p286; Asthma—general m anageme nt, p296; As thm a—v ent i l a tory manage ment , p 298 P.187

Drug dosages

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Aerosol*

Nebuliser*

Salbutamol

100–200µg

2.5–5mg

Terbutaline

250–500µg

5–10mg

Epinephrine

0.5mg

Ipratropium

250µg

IV bolus

IV infusion 3–20µg/min

1.5–5µg/min

Aminophylline

5mg/kg over 20min

Hydrocortisone

200mg qds

0.5mg/kg/h

*Aerosols and nebulisers are usually given 4–6 times daily but may be given more frequently if necessary.

In ext rem is , ep i ne phri ne may b e g i ve n as 0.1–0.5mg s ubc ut aneousl y, i njec ted dow n t he end otracheal tube or by IV i nfusi on. P.188

Respiratory stimulants Types Drug antagoni st s: e.g . nalox one , fl um aze ni l CNS st i mul ants: e. g. d oxapram Al m i tri ne

Uses Acute res pi ratory fai l ure due to fai l ure of v ent i l a tory d ri ve. Drug i nduced ve nti l at ory failure, e. g. as a resul t of exc ess i ve se dat i on or post-operat i ve l y.

Routes IV

Modes of action Nal oxone—s hort acti ng opi at e antag oni st . Fl um aze ni l —s hort acti ng benzod i azepi ne ant agoni s t. Doxapram—g ene ral i s ed c ent ral nerv ous sy ste m s ti m ul a nt wi t h p red omi nant resp i ratory sti mul ati on at l ow er dose s. St i mul at i on of carot i d che morece ptors at very l ow dos es w i t h i ncreas ed ti d al vol ume s. Al m i tri ne—i ncreas es the se nsi ti vi t y of carot i d chemorec ept ors to hyp oxaemi a and hype rc apni a.

Side-effects Sei zures (fl umazeni l , doxap ram ) Tachyarrhythmi a s (nal oxone, fl umazeni l ) Hal l uc i nati ons (doxap ram )

Notes Res pi ratory st i mul ants are mainl y used i n pati e nts wi th chroni c ai rfl ow l i mi tat i on who d evel op acute hyp erc apni c res pi rat ory failure. Effec ts of doxapram are short-l i ved so i nfusi on i s nec es sary. Aft er about 12h i nfus i on the effec ts on venti l atory dri ve are re duc ed. Nal oxone may be use d i n resp i ratory depres si on d ue to opi ate drugs . Si nc e i t reve rse s all opi at e effec ts, i t may b e bet ter to re verse res pi rat ory de pre ssi on wi t h non-spe ci fi c res pi rat ory st i mul ants , l eavi ng pai n rel i ef i ntac t. It may nee d t o b e repeated when l ong acti ng opi ate s are i nv ol v ed.

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As mos t b enz odi aze pi nes are l ong act i ng c ompared to fl umazeni l , repeated doses may b e ne ces sary. Al mi t ri ne d oes not p rod uce ce ntral res pi rat ory st i mul at i on but i t does i mprove venti l at i on–pe rfusi on m atc hi ng b y aug menti ng hypoxi c pul monary v asoconstri ct i on. Effe cts c ont i nue for s eve ral hours after i njec ti on. P.189

Drug dosages IV Infusion

IV bolus

Naloxone

0.1–0.4mg

Flumazenil

0.2mg over 15min (0.1mg/min to max 2mg)

Doxapram

1–1.5mg/kg over 30s

Almitrine

0.25–0.5mg/kg over 30min

IV

2–3mg/min

Key paper Greens tone M , Lass ers on TJ. Doxap ram for ve nti l a tory fai l ure due t o ex ace rbati ons of chroni c obs tructi ve pul monary di s eas e. Coc hrane Dat abase Sys t R ev. 2003; CD000223. Rev i ew

See also: Opi oi d anal ges i cs , p 234; Sed ati ves , p 238; R esp i ratory fai l ure, p 282; Sedat i v e poi s oni ng, p458; Pos t-op erati ve i nt ens i v e c are , p534 P.190

Nitric oxide Ni t ri c oxi d e i s now rec ogni se d as a fundam ent al med i at or i n many p hys i ol ogi cal proc ess es. One of i t s m ost i mportant effect s i s s mooth mus cl e re l ax ati on; ni tri c oxi de i s the maj or l oc al control l er of vas cul ar tone v i a effe ct s on cy cl i c GMP.

Inhaled nitric oxide Ni t ri c oxi d e i s p rov i de d for i nhal a ti on from cy l i nders (1000pp m ni t ri c ox i de i n ni trogen). It i s di l ut ed wi t h i nsp i ratory gas es, ei the r at t he gas suppl y t o t he venti l ator or i n t he i ns pi rat ory l i mb of the venti l at or ci rcui t, to provi de an i nhal ed c onc ent rati on of 1–40p pm, al though most pat i ents req ui re l es s t han 20ppm . Inhal at i on produces vas odi l at ati on at the si te of gas ex change , and m ay i mp rov e ve nti l a ti on–p erfusi on mat chi ng and re duc e p ul m onary art ery pres sures. Random i s ed m ul t i -centre st udi es i n pat i ents wi t h acut e l ung i njury have re vealed no l ong-t erm benefi t or outc ome i m provem ent .

Side-effects Ni t ri c oxi d e i s i mme di a tel y b ound t o haemogl obi n ensuri ng l ocal e ffe cts onl y. There i s no tol eranc e b ut pat i ents can bec ome de pend ent on conti nue d i nhalat i on wi th re bound p ul monary hyp ert ens i on and hypoxae mi a on wi t hdrawal. For thi s reason, wi thdrawal mus t b e g rad ual . Exce ssi ve hum i di fi cat i on of i nspi red gases may form ni tri c aci d wi th NO; the use of he at–moi sture exc hangers rather than w ater b aths i s recomme nded .

Monitoring Ni t ri c oxi d e and ni t rog en di oxi d e c onc ent rat i ons m ay be moni tored conveni entl y wi th portabl e fuel cel l anal yse rs or by che mi l umi nes cence. It i s i mportant to moni tor c onc ent rat i ons of b oth gases i n the i nsp i ratory l i m b of t he venti l at or ci rcui t. Moni t ori ng of ni t rog en di oxi d e i s i mportant to ens ure that tox i c dos es are not form ed wi t h t he oxy gen i n the i nsp i re d g as and subse que ntl y i nhaled by the p ati ent . Al thoug h i t i s ext rem el y rare to s ee tox i c ni t rogen di oxi de c onc ent rati ons (>5p pm) i t i s poss i bl e t o remove ni t rog en d i oxi d e from the i nspi re d g as by usi ng a sod a l i me ad sorber. M ethaem ogl obi n i s form ed when ni tri c oxi de bi nds to hae mogl ob i n. Prol onge d i nhalat i on at hi ghe r dos es may rarel y p rod uce si gni fi cant me thaemogl obi naem i a (>5%) and thi s s houl d the refore be moni t ore d d ai l y.

Achieving the correct dose App roxi m atel y 50% of pat i ents wi t h s eve re res pi ratory fai l ure res pond t o ni tri c oxi de. Howeve r, the most effect i ve dos e v ari es. It i s us ual t o s tart at 1ppm for 10mi n and m oni tor the c hange i n PaO 2 /FIO 2 rati o. An i ncre ase shoul d b e fol l ow ed by an i nc rease i n ni t ri c ox i d e conce ntrat i on to 5p pm for a furt her 10mi n. T hereafter, t he dos e i s adjuste d acc ord i ng t o resp ons e at 10mi n i nte rvals unt i l the most effect i ve dose i s found. Si nce the underl y i ng pathophy si ol og y may chang e, i t i s i mp ort ant to as ses s t he dos e resp ons e at d ai l y i nte rvals, ai mi ng t o k eep the d ose at the l owes t effect i ve l e vel .

Scavenging Si nce the c onc ent rat i ons used are s o s mal l , di l uti on of exhal e d g ase s i nto the at mos phe re i s unl i k el y to produce i mp ort ant envi ronment al concentrati ons . In t he ai r-condi ti oned i ntensi ve c are envi ronment ai r changes are s o

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fre que nt as to make sc ave ngi ng unnece ssary. P.191

Key trials Del l i nge r R P et al , for the Inhal ed Ni t ri c Oxi d e i n ARDS Stud y Group. Effe cts of i nhal ed ni t ri c oxi d e i n p ati ent s w i th acute res pi rat ory di stress s yndrome : resul t s of a random i ze d p has e II t ri a l . Cri t Care Me d 1998; 26:15–23 Lundi n S et al , for t he The Europ ean St udy Group of Inhal ed Ni t ri c Oxi d e. Inhal a ti on of ni tri c oxi de i n acute l ung i nj ury: resul t s of a Europe an mul ti c ent re st udy . Inte nsi ve Care Me d 1999; 25:911–19

See also: Vas odi l a tors, p198; Acut e resp i ratory di s tress sy ndrome (1), p 292; Acute res pi rat ory di stres s s ynd rom e (2), p294 P.192

Surfactant In ARD S t here i s dec reased surfactant produc ti on, bi oche mi c al abnormal i ty of the surfact ant produced and i nhi bi t i on of surfac tant func ti on. The ne t resul t i s al veol ar and sm al l ai rw ay c ol l ap se. Surfactant al s o c ont ri but es to host defenc e agai nst mi cro-organi sm s. Surfac tant rep l ac eme nt woul d b e e xpe cte d t o ex ert t herapeuti c e ffec ts on l ung mec hani cs , g as exc hange and hos t d efe nce . Ins ti l l a ti on of s urfact ant (e i ther as a l i qui d or neb ul i se d) v i a the endot rac heal t ube i nto the l ungs i s as soci a ted wi th i mp rov ed out com e i n neonatal resp i ratory d i s tre ss syndrome. Pot ent i a l i ndi cat i ons i n adul ts i ncl ude ARD S, pne umoni a , c hroni c ai rfl ow l i mi t ati on and as thm a. Mul ti p l e studi es i n ARD S have yet to de monstrate mortalit y benefi t, though thi s may be re l at ed to the typ e of s urfact ant , t he vol ume us ed, or the de l i very s yst em. St udi es have de monstrate d i mprove d oxyg enat i on wi th re comb i nant surfactant protei n C and a trend to i mp rov ed survi val i n pati e nts wi th di rect l ung i njury. Furthe r s tud i es are unde rway usi ng recombi nant s urfact ant prote i n C w i th phosphol i pi ds, and wi th surfactant protei ns B and C. The surfactant i s i ns ti l l e d i nto the l ung s v i a an end otracheal cat het er. Com pl i cat i ons of s urfact ant treat ment have i ncl uded i ncreas ed c oug h, sputum product i on, b ronchospasm, i ncre asd peak airw ay p re ssure and adv ers e e ffe cts on pul monary func ti on. The se can be mi ni mi se d b y ad equate se dat i on and neurom usc ul ar bl ockade b efore i ns ti l l i ng surfac tant. P.193

Key trial Sprag g RG , Lewi s JF, Wal mrath HD et al . Effect of re com bi nant surfact ant prote i n C-based surfactant on the ac ute res pi rat ory di stres s s ynd rom e. N Engl J M ed 2004; 351:884–92

See also: Ac ute re spi rat ory di st res s s ynd rom e (1), p292; Acut e resp i ratory d i s tre ss syndrome (2), p294


Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Car dio vasc u la r Dr u gs

Cardiovascular Drugs Inotropes Types Cate chol am i ne s: e.g . e pi nephri ne, norepi nep hri ne, dobut ami ne, dopam i ne Phos phodi e st erase (PDE) i nhi bi tors: e.g. mi l ri none, enoxi mone Dope xam i ne Cal c i um s ens i ti sers: e.g . l evosi m end an Card i ac gl yc osi des : e. g. di goxi n (weak)

Modes of action Inc rease force of m yoc ard i al contrac ti on, ei t her by st i mul at i ng c ard i ac β 1 ad renore cep tors (cat echol a mi nes), decreas i ng c AMP break down (PDE i nhi bi tors), i ncreas i ng calci um sensi ti v i ty (C a s ens i ti sers), di re ctl y i ncreas i ng cont racti l i ty (di goxi n), or i nhi bi t i ng ne uronal re upt ake of norad renal i ne (dop exami ne). Al l agents exc ept di gox i n

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have , t o g reater or l e sse r d egrees , associ ated di l a tor or const ri ctor p rop ert i es vi a β 1 and β 1 adrenorec ept ors , dopami nerg i c re cep tors, or K AT P channel s . Di g oxi n m ay c aus e s pl a nchni c v asoc ons tri ct i on and, for an i notropi c e ffe ct, re qui re s p l as ma l eve l s at the top of the the rap eut i c range . The i nc re ase i n cardi ac work i s p art i al l y offset i n those drugs posse ss i ng as soc i at ed di l ator e ffe cts . Other than ep i nephri ne (when us ed for i t s v asoconstri c tor effec t i n c ard i op ul m onary res usc i t ati on) or di gox i n (for l ong t erm us e i n c hroni c he art failure), i not rop es are us ual l y gi ven by conti nuous IV i nfusi on ti t rat ed for effec t.

Uses Myoc ard i al fail ure , e .g. pos t-m yoc ard i al i nfarct i on, c ard i om yop athy Myoc ard i al d epress i on, e .g. se psi s Aug ment at i on of oxy gen del i v ery i n hi gh-ri s k s urgi c al pat i ents

Side-effects Arrhyt hmi as (us ual l y ass oci at ed w i th concurrent hy povol ae mi a ) Tachycard i a (usual l y ass oci ate d wi th concurre nt hyp ovol ae mi a ) Hypotensi on (rel ate d t o d i l ator p rop ert i es ± concurrent hypovol aem i a) Hype rt ens i on (rel a ted to const ri c tor prope rt i es ) Ang i nal c hes t p ai n, or ST-s egm ent and T -wav e c hanges on ECG

Notes Epi nep hri ne , nore pi nephri ne, dob utami ne and d opami ne s houl d be gi v en vi a a c ent ral v ei n as ti ssue necrosi s m ay occ ur sec ond ary to pe ri pheral ext ravas ati on. P.197

Drug dosages Epinephrine

Infusion starting from 0.05µg/kg/min

Norepinephrine


Dobutamine

Infusion from 2.5–25µg/kg/min

Dopamine


Dopexamine


Milrinone

Loading dose of 50µg/kg over 10min followed by infusion from 0.375–0.75µg/kg/min

Enoximone

Loading dose of 0.5–1mg/kg over 10min followed by infusion from 5–20µg/kg/min

Digoxin

0.5mg given PO or IV over 10–20min. Repeat at 4–8h intervals until loading achieved (assessed by clinical response). Maintenance dose thereafter is 0.0625–0.25mg/day depending on plasma levels and clinical response.

Levosimendan

12–24µg/kg over 10min followed by 0.1µg/kg/min for 24h

See also: Int ra-aorti c b al l oon count erp ul s ati on, p58; Card i ac output—t hermod i l uti on, p122; Card i ac output—other i nv asi ve, p124; Cardi a c outp ut— non-i nvas i ve (1), p 126; C ard i ac output— non-i nvas i ve (2), p 128; Bas i c res usc i t ati on, p270; Cardi a c arrest , p 272; Fl ui d chal l eng e, p274; Hypotensi on, p312; Sep si s and s ept i c shock —treat ment, p486; Care of the potenti a l organ d onor, p552 P.198

Vasodilators

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Types Ni t rat es: e. g. g l y ceryl tri ni trate, i s osorbi de di ni t rat e Ang i ot ens i n converti ng e nzy me (AC E) i nhi bi tors: e.g . c apt opri l Smooth mus cl e rel a xant s: e.g . s odi um ni t roprussi de, hy dralazine α-ad renerg i c ant agoni sts : e. g. phe ntol am i ne β 2 -adre nergi c ag oni st s: e.g. salb utamol Cal c i um antag oni st s: e .g. ni fed i pi ne , di l t i azem Dopami nergi c ag oni sts : e .g. dop exami ne Phos phodi e st erase i nhi bi tors: e.g . e nox i mone, mi l ri none, si l denafi l Pros tagl a ndi ns: e. g. e pop ros tenol (PGI 2 ), al prost adi l (PGE 1 ) B-t ype nat ri ure ti c pe pti de analog ues , e .g. ne si ri t i de

Modes of action Inc rease cyc l i c GM P c onc ent rat i on (b y ni tri c oxi de donati on or by i nhi b i ti ng cGM P b reakdown), or ac ts di rec tl y on dopami nerg i c re cep tors l ead i ng to vasod i l atat i on Reduce (to varyi ng degrees ) v ent ri cul ar pre l oad and/or afte rl oad . Reduce cardi a c w ork .

Uses Myoc ard i al fail ure , e .g. pos t-m yoc ard i al i nfarct i on, c ard i om yop athy Ang i na/i s chaemi c heart d i se ase Sys tem i c hyp ert ens i on (s pec i fi c c aus es, e. g. phaeoc hromoc ytoma) Vas oconst ri c ti on Peri pheral v asc ul a r d i se ase /hy pop erfusi on Spl anc hni c p erfusi on (dopex ami ne, dop ami ne) Pul monary hyp ert ens i on (i nhaled NO, p ros tag l andi ns, si l de nafi l )

Side-effects/complications Hypotensi on (oft en ass oci ate d w i th concurre nt hyp ovol ae mi a ) Tachycard i a (oft en ass oci ate d w i th concurrent hyp ovol ae mi a ) Symp tom s i nc l ud e headache , fl us hi ng, pos tural hy pot ens i on Renal fai l ure (ACE i nhi bi tors)—es pec i al l y wi t h renal art ery st enos i s , hypovol aemi a, non-st eroi dals

Notes Gl yceryl tri ni trate and i sos orb i de di ni t rate red uce bot h p re l oad and afte rl oad. At hi gher dos e the afte rl oad effect bec ome s m ore promi nent. Tol erance to ni trate s usually commences wi thi n 24–36h unl es s i nte rmi tt ent oral dos i ng i s us ed. Progress i ve i ncreas es i n dos e are req ui red to achi ev e t he sam e effec t. Prol onged (> 24–36h) dose-rel ate d admi ni s trati on of s odi um ni troprussi de can rarel y p roduc e a met abol i c ac i d osi s rel at ed t o c yani de ac cum ul a ti on. ACE i nhi bi t or tab l et s c an be crushe d and gi v en ei t her SL or vi a a nasog ast ri c t ube. Dop ami nergi c d rug s i mprove sp l anchni c bl ood fl ow t hough cl i ni cal be nefi ts are unproved . Hyd ral azi ne has an unpre di c tabl e effect on bl ood press ure and, i f gi v en IV, shoul d b e used wi th cauti on. P.199

Drug dosages Nitrates

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Glyceryl trinitrate 2–40mg/h Isosorbide dinitrate 2–40mg/h

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Sodium nitroprusside

20–400µg/min

Hydralazine

5–10mg by slow IV bolus, repeat after 20–30min. Alternatively, by infusion starting at 200–300µg/min and reducing to 50–150µg/min

ACE inhibitors

Captopril: 6.25mg test dose increasing to 25mg tds Enalapril: 2.5mg test dose increasing to 40mg od Lisinopril: 2.5mg test dose increasing to 40mg od

Nifedipine:

5–20mg PO. Capsule fluid can be injected down nasogastric tube or given sublingually

Phentolamine

2–5mg IV slow bolus. Repeat as necessary.

Dopexamine


Milrinone

Loading dose of 50µg/kg over 10min followed by infusion from 0.375–0.75µg/kg/min

Enoximone

Loading dose of 0.5–1mg/kg over 10min followed by infusion from 5–20µg/kg/min

Epoprostenol, alprostadil

Infusion from 2–30ng/kg/min

Nitric oxide

By inhalation: 2–40ppm

Nesiritide

2µg/kg bolus followed by infusion of 0.01–0.03µg/kg/min

Sildenafil

50mg tds PO

See also: Bl ood press ure moni t ori ng, p110; Card i ac output—the rmodi l uti on, p122; Cardi a c outp ut—other i nvasi ve, p124; Cardi a c outp ut— non-i nvas i ve (1), p 126; Card i ac outp ut—non-i nvasi ve (2), p 128; Hypotensi v e agent s, p202; Ant i a ngi nal ag ent s, p208; N i tri c oxi de , p190; Bas i c res us ci t ati on, p270; F lui d c hal l enge, p274; Hy pertensi on, p314; Ac ute coronary syndrome (1), p 320; Ac ut e c oronary s yndrome (2), p322; Heart fai l ure—as se ssm ent , p 324; Heart fai l ure— managem ent , p 326; Pre-e cl a mps i a and ec l am psi a, p538 P.200

Vasopressors Types α-ad renerg i c : e. g. norepi nep hri ne , ep i nephri ne, dop ami ne, ephedri ne, p henyl e phri ne, m ethoxami ne Drugs red uci ng produc ti on of c ycl i c GM P (i n s ept i c shock ): e .g. me thy l thi oni ni um chl ori de (m ethyl e ne b l ue) Vas opress i n or synthe ti c anal ogue s, e.g . t erl i p res si n

Modes of action Act i ng on pe ri p heral α-adre nergi c or vasop res si n V1 rece ptors Bl ocki ng cGM P p rod uct i on (m ethyl e ne bl ue) Inc rease afte rl oad , mainl y b y arte ri ol a r v asoconstri c ti on and res torati on of vasc ul ar reacti vi t y Venoconst ri c ti on

Uses To i nc rease org an p erfusi on press ure s, parti c ul arl y i n hi gh output, l ow pe ri p heral re si s tance states , e .g. se psi s, anap hyl axi s To rai se c oronary p erfus i on press ure s i n c ard i opul monary re sus ci t ati on (ep i ne phri ne, v asopre ssi n)

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Side-effects/complications Inc reased cardi ac work Dec reased cardi ac out put , e spe ci a l l y wi th age nts where press or effect s p red omi nat e Myoc ard i al and s pl anc hni c i schaem i a Inc reased myocardi al i rri t abi l i t y, esp eci al l y wi t h c onc urrent hy pov ol a emi a, l eadi ng t o arrhythmi a s and tac hyc ard i a Dec reased peri p heral perfus i on and d i st al i s chaemi a/ne crosi s

Notes Pre ssor agents shoul d be av oi d ed, i f possi bl e , i n l ow cardi ac outp ut st ate s as t hey may further com promi s e t he ci rcul at i on. Met hox ami ne and phe nyl ephri ne are the ‘p urest ’ p res sor ag ent s; other α-ad renergi c ag ent s have i notropi c p rop ert i es to gre ate r or l ess er deg re es. Ephedri ne i s s i mi l ar t o ep i nephri ne b ut i ts effec ts are more p rol onged as i t i s not met abol i s ed by monoami ne oxi das e. Effect s of p res sor ag ent s on s pl a nchni c , renal and cerebral ci rcul at i ons are vari a bl e and unpredi ctabl e . Pul monary vascul ar re si stance i s al so rai sed by these ag ent s. Met hyl thi oni ni um chl ori de (me thy l ene b l ue ) i nhi bi t s t he NO–cGM P p athway . It i s c urrent l y unl i c ens ed as a pres sor age nt and i t s use has onl y been reporte d i n a few sm al l case seri es . A mul t i ce ntre s tud y of a NO synthase i nhi b i tor (L-NMM A) was pre mat ure l y di sconti nue d d ue to adve rse outcomes . Vas opres si n (s hort hal f-l i fe, i nfus i on ne ede d) and terl i pre ssi n (l onger half-l i fe, can be gi ven by bol us) may b e effect i ve i n treat i ng catec hol ami ne-res i s tant v asodi l atory shock. Parad oxi cal l y, such pat i ents res pond t o s mal l d ose s that have no press or effe ct i n healt hy p eop l e. Mul ti ce ntre outc ome st udi es are ongoi ng. Exc ess i ve dosi ng of any pre ssor agent m ay l ead to re gi onal i s chaemi a, e.g . c ard i ac , s pl anc hni c. Di g i t al i sc hae mi a may re spond to prompt adm i ni st rat i on of i ntravenous prost anoi ds (e .g. PGE 1 , PGI 2 ). P.201

Drug dosages Norepinephine


Epinephrine


Dopamine

Infusion from 5–50µg/kg/min

Methoxamine

3–10mg by slow IV bolus (rate of 1mg/min)

Ephedrine

3–30mg by slow IV bolus

Methylthioninium chloride (methylene blue)

1–2mg/kg over 15–30min

Vasopressin

0.01–0.04U/min

Terlipressin

0.25–0.5mg bolus, repeated at 30min intervals as necessary to maximum 2mg.

Key paper Lop ez A, et al. Mul ti pl e -ce nte r, random i ze d, pl a ceb o-c ont rol l ed , d oub l e-bl i nd study of the ni tri c oxi de s ynt has e i nhi bi tor 546C88: effe ct on survi v al i n pat i e nts wi th sep ti c shock . C ri t Care Med 2004; 32:21–30

Landry DW , et al . Vas opress i n defi ci enc y c ont ri but es to the vas odi l a ti on of se pti c shock. Ci rcul at i on 1997; 95:1122–5

P.202

Hypotensive agents Types

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Vas odi l at ors α- and β-ad re nergi c bl ock ers In routi ne ICU p rac ti ce β-b l oc kers are use d rel a ti v el y i nfre que ntl y b ecause most hav e a l ong hal f-l i fe and the negati ve i not ropi c effect s are generall y undes i rabl e. Exc ept i ons are esm ol ol and l ab etalol , b oth of whi ch hav e short hal f-l i ve s and v asodi l at i ng prope rti es.

Modes of action Vas odi l at ors re duc e p rel oad and afte rl oad to vari ab l e deg ree s d ependi ng on t ype and d ose β-bl ock ers reduce t he force of myoc ardi a l c ont rac ti l i t y

Uses Hype rt ens i on—sy ste mi c and p ul m onary Heart fai l ure—t o reduce aft erl oad ± p rel oad (c aut i on wi th β-b l oc kers) Cont rol of bl ood press ure, e .g. di ss ect i ng aorti c aneurys m

Side-effects/complications Exce ss i ve hyp ote nsi on Heart fai l ure (w i t h β-bl ocke rs ) Peri pheral hypoperfus i on (wi th β-b l oc kers) Bronchosp asm (wi th β-b l oc kers) Dec reased sym pat het i c re sponse to hyp ogl ycaemi a (wi t h β -bl ock ers )

Notes In cri ti cal l y i l l p ati ent s i t i s oft en advi sab l e to use short -ac ti ng β-bl oc kers b y i nfus i on. P.203

Drug dosages

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Nitrates


Glyceryl trinitrate 2–40mg/h Isosorbide dinitrate 2–40mg/h

Sodium nitroprusside

20–400µg/min.

ACE inhibitors

Captopril: 6.25mg test dose increasing to 25mg tds Enalapril: 2.5mg test dose increasing to 40mg o.d Lisinopril: 2.5 mg test dose increasing to 40mg o.d

Nifedipine:

5–20mg PO. Capsule fluid can be injected down nasogastric tube or given sublingually.

Phentolamine

2–5mg IV slow bolus. Repeat as necessary

Esmolol

A titrated loading dose regimen is commenced followed by an infusion rate of 50–200µg/kg/min.

Propranolol

Initially given as slow IV 1mg boluses repeated at 2min intervals until effect is seen (to maximum 5mg)

Labetalol

0.25–2mg/min

Hydralazine

5–10mg by slow IV bolus, repeat after 20–30min. Alternatively, by infusion starting at 200–300µg/min and reducing to 50–150µg/min.

See also: Bl ood press ure moni t ori ng, p110; Card i ac output—the rmodi l uti on, p122; Cardi a c outp ut—other i nvasi ve, p124; Cardi a c outp ut— non-i nvas i ve (1), p 126; Card i ac outp ut—non-i nvasi ve (2), p 128; Vasodi l at ors , p 198; Basi c res us ci t ati on, p270; Fl ui d challe nge , p 274; Hy pertensi on, p314; Pre -ec l am psi a and ecl amp si a , p 538 P.204

Antiarrhythmics Onl y anti arrhy thm i cs l i kel y t o b e used i n the ICU set ti ng are des cri bed . For supraventri cul ar tachy arrhyt hmi as: adenosi ne, ve rap ami l , ami odarone, di g oxi n, β-b l oc kers, mag nes i um For ve ntri cul a r t achyarrhy thm i as : ami odarone , l i d ocai ne , fl ec ai ni de , b ret yl i um, β-bl ocke rs, magne si um

Uses Correc ti on of supraventri cul ar and v ent ri c ul ar tac hyarrhythmi a s w hi c h e i ther com promi se t he ci rcul at i on or coul d pote nti al l y do so. Di fferent i at i on be twe en s uprave ntri c ul a r and ventri cul ar arrhy thm i as us i ng ad enosi ne

Notes Al l anti arrhyt hmi c agents hav e s i de -effec ts; other than d i g oxi n t hey are ne gat i ve l y i notropi c t o great er or l e sse r deg ree s and may i nduc e profound hy pot ens i on (e .g. verapami l , β-bl oc kers) or b rad ycard i a (e.g . β -bl ock ers , ami odarone, di g oxi n, l i d ocaine). β-b l oc kers i n p art i c ul a r s houl d be use d w i th cauti on bec aus e of these effec ts. Al l A-V bl ocke rs are contrai ndi cat ed i n re-ent ry tac hyc ard i a (e. g. W ol ff–Park i ns on–Whi te sy ndrome). Ade nos i ne : ve ry short-act i ng; m ay rev ert parox ysm al SVT to si nus rhythm. Ine ffe cti ve for at ri a l fl ut te r and fi b ri l l at i on, VT. Contrai ndi c ate d i n 2° and 3° heart bl ock, si ck si nus sy ndrome , as thma. May cause fl ushi ng , bronchosp asm and oc cas i onal sev ere brady cardi a.

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Ami odarone: e ffe cti ve agains t all typ es of tac hyarrhythmi a . Usually gi ven by IV i nfus i on for rapi d e ffe ct but req ui res i ni ti al l oadi ng d ose . W hen converti ng from IV t o oral dosi ng, i ni ti al hi g h oral dosi ng (200mg tds ) i s s ti l l req ui red. Contrai ndi c ate d i n p ati ent s w i t h t hyroi d dy sfunct i on. Has l ow acute tox i c i ty , t hough may cause sev ere bradyc ard i a and bot h c hroni c and acute p ul monary fi b rosi s . Avoi d w i th ot her Cl ass III agents (e. g. sot al ol ). Must be g i ve n v i a central v ei n as cause s p eri phe ral p hl e bi t i s. β-bl ock ers : for SVT, e smol ol i s p referred due to i t s s hort hal f-l i fe though may cause vasod i l atat i on. Ini ti a l l y, i nc reasi ng l oad i ng doses re qui re d; an i nfusi on m ay be need ed the reafte r. Propranol ol can be gi ven by sl ow IV bol use s of 1m g repe ate d at 2mi n i nterval s t o a max i mum of 5mg). Do not g i ve β-bl ocke rs wi t h v erapam i l . Bre tyl i um : m ay t ake 15–20mi n to take e ffe ct; now us ed pre dom i nantl y for res i s tant VF/VT. CPR shoul d be cont i nued for at l east 20mi n. Di g oxi n: s l ow-ac ti ng, re qui res l oadi ng (1–1.5g) t o achi eve therapeuti c pl as ma l eve l s whi ch can be moni t ore d. Load i ng i deally gi ven ove r 12–24h but can b e d one ove r 4–6h. C ont rai ndi cated i n 2° and 3° heart b l oc k. May caus e s eve re bradyc ard i a. Low K + and M g 2+ and marke dl y rai s ed Ca 2+ i ncreas e my ocardi al se nsi ti v i t y to di gox i n. Ami odarone rai s es di g oxi n l eve l s. Li d ocaine : 10ml of 1% sol uti on contai ns 100mg. No effec t on SVT. Loadi ng achi ev ed by 1mg/kg sl ow IV b ol us fol l owe d b y i nfusi on. Contraind i c ated i n 2° and 3° heart b l ock. May cause brady cardi a and C NS si d e-e ffec ts , e. g. drowsi nes s, sei zures. Verapami l : s houl d not be gi ven wi t h β -bl ock ers as profound hy pot ens i on and brad yarrhy thm i as may resul t. Pret re atm ent wi t h 3–5m l 10% cal ci um g l uconate by sl ow IV b ol us p re vent s t he hyp ote nsi ve effect s of ve rap ami l wi t hout affec ti ng i ts anti a rrhythmi c prop ert i es . P.205

Modes of action (Vaughan-Williams classification) Class I

Action

Examples

Reduces rate of rise of action potential: •Ia: increases action potential duration

•Ia: disopyramide

•Ib: shortens duration

•Ib: lidocaine

•Ic: little effect

•Ic: flecainide

II

Reduces rate of pacemaker discharge

β-blockers

III

Prolongs duration of action potential and hence length of refractory period

Amiodarone Sotalol

IV

Antagonises transport of calcium across cell membrane

Verapamil Diltiazem

Drug dosages

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Adenosine

3mg rapid IV bolus. If no response after 1min give 6mg. If no response after 1min give 12mg.

Amiodarone

5mg/kg over 20min (or 150–300mg over 3min in emergency) then IV infusion of 15mg/kg/24h in 5% glucose via central vein. Reduce thereafter to 10mg/kg/24h (approx. 600mg/day) for 3–7 days then maintain at 5mg/kg/24h (300–400mg/day)

β-blockers

Esmolol: a titrated loading dose regimen is commenced followed by an infusion rate of 50–200µg/kg/min. Propranolol: Initially given as slow IV boluses of 1mg repeated at 2min intervals until effect is seen to a maximum of 5mg. Labetalol: 0.25–2mg/min

Bretylium

In emergency 5mg/kg by rapid IV bolus. If no response after 5min, repeat or increase to 10mg/kg.

Digoxin

0.5mg given IV over 10–20min. Repeat at 4–8h intervals until loading achieved (assessed by clinical response). Maintenance dose thereafter is 0.0625–0.25mg/day depending on plasma levels and clinical response.

Lidocaine

1mg/kg slow IV bolus for loading then 2–4mg/min infusion. Should be weaned slowly over 24h.

MgSO 4

10–20mmol over 1–2h. Can be given over 5min in emergency.

Verapamil

2.5mg slow IV. If no response repeat to a maximum of 20mg. An IV infusion of 1–10mg/h may be tried. 10% calcium gluconate solution should be readily available.

See also: Defi bri l l at i on, p 52; ECG moni t ori ng, p108; Bas i c res us ci t ati on, p270; C ard i ac arres t, p272; T achyarrhythmi a s P.206

Chronotropes Types Ant i chol i nergi c: e.g . at ropi ne, gl y cop yrrol a te

Modes of action The ant i c hol i ne rgi c d rugs act by com pet i t i ve ant agoni s m of acet yl c hol i ne at pe ri pheral muscari ni c re cep tors and decreas e atri ov ent ri c ul a r c ond uc ti on t i me .

Uses Al l ty pes of brady cardi a i ncl udi ng 3° heart bl ock. Hi g h d ose atropi ne i s us ed i n cardi opul monary re sus ci tat i on protocol s for tre atm ent of as yst ol e .

Side-effects/complications Ant i chol i nergi c d rug s p rod uce dry m out h, red uct i on and t hi c keni ng of bronc hi al sec ret i ons, and i nhi b i t i on of sweati ng. Uri nary ret ent i on may oc cur b ut parent eral admi ni s trati on does not l ead to gl auc oma.

Notes The anti c hol i nerg i c age nts are usually gi ven by IV bol us , repe ate d as nece ssary. The y are fre que ntl y used as a b ri dge to tem porary paci ng b ut shoul d not b e c ons i de red a sub sti tute. Ex ternal or i nt ernal paci ng s houl d be readi l y acce ssi bl e. At rop i ne ne bul i se rs hav e b een us ed s uc ces sful l y i n pati e nts de vel opi ng sym ptomat i c bradyc ard i a duri ng e ndotrache al suc ti on.

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Neurol ogi cal e ffec ts may be se en w i t h at ropi ne b ut not gl ycopyrrol ate . P.207

Drug dosages Atropine

0.3–0.6mg IV bolus. 3mg is needed for complete vagal blockade.

Glycopyrrolate

0.2–0.4mg IV bolus.

See also: Tem porary paci ng (1), p54; Temp orary pac i ng (2), p56; ECG moni tori ng, p108; Bas i c res usc i t ati on, p270; Cardi ac arres t, p272; Brad yarrhy thm i as , p 318 P.208

Antianginal agents Types Vas odi l at ors : e .g. ni trates , c al c i um antag oni st s β-bl ock ers Potassi um channe l openers : e .g. ni corand i l Asp i ri n, hep ari n, cl opi dog rel

Modes of action Cal c i um c hannel bl ock ers cause compet i t i ve bl ock ade of cel l m emb rane and sl ow c al c i um channel s l e adi ng to decreas ed i nfl ux of calci um i ons i nt o c el l s. Thi s l ead s t o i nhi bi ti on of c ont rac ti on and rel axati on of c ard i ac and smooth mus cl e fi bres res ul t i ng i n c oronary and s yst emi c v asodi l at ati on. Ni t rat es may cause effl ux of calci um i ons from sm oot h musc l e and cardi ac cel l s and al so i nc re ase cGMP s ynt hes i s res ul t i ng i n coronary and s yst emi c v asodi l at ati on. β-bl ock ers i nhi bi t β-adrenorec ept or sti mul at i on, reduci ng m yoc ard i al work and oxy gen consumpt i on. T hi s effec t i s som ewhat offs et by c omp ens atory peri p heral vas oconst ri c ti on. Potassi um channe l openers cause vasod i l atat i on by re l ax ati on of vas cul ar smooth muscl e. The potas si um c hannel openi ng ac ti on w ork s on t he art eri al ci rcul at i on whi l e a ni t rate act i on provi des ad di t i onal vas odi l at ati on. Though asp i ri n, he pari n and cl opi dog rel have no di rect anti a ngi nal effec t, pat i ents wi t h unst abl e angi na benefi t from the reducti on i n pl ate l et ag gre gat i on and t hrombus form ati on.

Uses Ang i na pe ctori s

Side-effects/complications See Di l at ors , Hypotensi v e agents. Ni c orandi l i s c ont raind i cated i n hy pot ens i on and c ard i og eni c s hoc k. It shoul d be av oi d ed i n hyp ovol aem i a. Head ache and fl ushi ng are the m ajor reporte d s i de -effect s. Rap i d and se vere hyperkal aem i a has be en rep ort ed afte r c ardi a c s urg ery .

Notes Com bi nati on the rap y i nvol vi ng i nt ravenous ni t rates , c al c i um antag oni sts , β -bl ock ade and hepari ni sati on has bee n shown to be b ene fi c i a l i n unst abl e angi na; throm bol yti c t herapy confe rs no add ed advantage. Pot ass i um channel ope ners b el ong to a new c l as s of d rug ye t t o b e ex tensi vel y ev al uate d i n c ri ti c al l y i l l pati e nts and shoul d be thus use d w i th cauti on, es pec i al l y whe n hype rkalae mi a i s a concern. Ang i na may occasi onal l y be worsened by a ‘c oronary s teal’ phenom enon w here bl ood fl ow i s di v ert ed away from ste nos ed coronary ves sel s. Thi s d oes not, how ever, occ ur wi t h ni corandi l .

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P.209

Drug dosages Glyceryl trinitrate

0.3mg sublingually, 0.4–0.8mg by buccal spray, 2–40mg/h by IV infusion.

Isosorbide dinitrate

10-20mg tds orally, 2–40mg/h by IV infusion.

Nifedipine

5–20mg PO. The capsule fluid can be aspirated then injected down nasogastric tube or given sublingually.

Propranolol

Given either orally at doses of 10–100mg tds or IV as slow boluses of 1mg repeated at 2min intervals to a maximum of 5mg until effect is seen. This can be repeated every 2–4h as necessary.

Nicorandil

10–20mg PO bd.

Clopidogrel

75mg PO od.

Aspirin

75–150mg PO od.

See also: Ac ute coronary syndorme (1), p 146; Ac ut e c oronary s yndrome (2), p322


Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Ren al Dr u gs

Renal Drugs Diuretics Types Loop di ureti cs: e. g. furose mi d e, bume tani d e Osm oti c d i ureti cs : e. g. manni t ol Thi azi des : e. g. met ol a zone Potassi um sp ari ng di uret i c s: e .g. am i l ori de, sp i ronol act one , p otassi um canrenoat e

Uses To i nc rease uri ne vol ume Cont rol of chroni c oed ema (t hi a zi d es, l oop di uret i c s) Cont rol of hy pertensi on (thi azi des ) To p rom ote re nal ex cre ti on (e.g . forc ed di ures i s, hy percal caemi a)

Routes IV (manni t ol , furosemi de , bumet ani de, potas si um c anrenoate ) PO (met ol a zone, furose mi d e, bume tani d e, ami l ori de , s pi ronol ac tone)

Modes of action Osm oti c d i ureti cs —re duc e d i st al tub ul ar wate r reab sorpt i on

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Thi azi des —i nhi b i t di stal t ubul ar N a + l os s and carboni c anhydrase and i ncreas e N a + and K + ex change . T hi s red uce s t he s up pl y of H + i ons for exc hange wi t h N a + i ons p rod uc i ng and al kal i ne natri uresi s wi t h p otas si um l os s Loop di ureti cs— inhi b i t Na + and Cl - re abs orp ti on i n t he asc end i ng l oop of Henlé Potassi um sp ari ng di uret i c s—i nhi bi t d i st al tub ul a r N a + and K + exc hange

Side-effects Hypovol aem i a Hyponat rae mi a or hy pernat rae mi a Hypokal aem i a Oede ma format i on (manni tol ) Reduced catec hol ami ne effect (thi a zi d es) Hype rgl yc aemi a (thi azi de s) Metabol i c al kal osi s (l oop d i ureti cs ) Hypomag nes aem i a (l oop d i uret i cs ) Panc reati ti s (furosem i de )

Notes It i s i m portant t o c orrect pre-renal c aus es of ol i guri a before re sorti ng to di uret i c use . Di ure ti c s d o not pre vent renal fai l ure but m ay convert ol i g uri c t o p ol y uri c renal fai l ure. If the re i s i nadeq uat e g l om erul ar fi l t rat i on, m anni tol i s ret ai ned and pas ses t o the e xtrace l l ul a r fl ui d t o p rom ote oed ema format i on. Bum etani d e m ay be used i n porp hyri a where t hi azi des and ot her l oop di ure ti c s are contrai ndi c ate d. Pot ass i um sp ari ng di ure ti c s s houl d be avoi de d w i th AC E i nhi bi tors as t here i s an i ncreas ed ri s k of hype rkalae mi a . P.213

Drug dosages Oral Mannitol

IV

Infusion

100g over 20min 6-hrly

Metolazone

5–10mg od

Furosemide

20–40mg 6–24-hrly

5–80mg 6–24-hrly

1–10mg/h

Bumetanide

0.5–1mg 6–24-hrly

0.5–2mg 6–24-hrly

1–5mg/h

Amiloride

5–10mg 12–24-hrly

Spironolactone

100–400mg od

K + canrenoate

200–400mg od

P.214

Dopamine The effec ts of d opami ne are dep end ent on the dose i nfuse d. Dop ami ne was use d w i de l y at l ow dos es i n an att emp t t o sec ure prefe renti al DA 1 sti mul ati on and i ncreas e renal pe rfusi on; how eve r, a l arg e mul t i ce ntre rand omi sed control l ed study com pari ng ‘renal dos e’ d opami ne and di uret i c s s howe d no d i ffere nce i n the i nci dence of renal fai l ure. The wi d esp read use of l ow dos e d opami ne (< 3µg /kg /mi n) has thus d i m i ni she d c ons i de rab l y i n re cent ye ars . Hig her doses i nc re ase cardi ac contracti l i ty vi a β 1 st i m ul a ti on and produc e vasoc ons tri ct i on vi a α st i mul a ti on. Whe re vas oconst ri cti on i s i nappropri a te thi s w i l l reduce renal perfus i on. T here i s, howe ver, e vi d enc e of natri uresi s and di ure si s by enhanc ed Na + trans port i n t he asc end i ng l oop of Henlé. Thi s effe ct i s si mi l ar to that of a l oop di uret i c. In add i ti on to the re nal effec ts of DA 1 sti mul ati on the re may be preferenti a l p erfusi on of the sp l anchni c bed , t hough any benefi ts to pat i ents hav e y et to b e s how n. P.215

Key trial

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Bel l omo R , for the Austral i an and Ne w Zeal and Intensi v e C are Soci e ty (AN ZIC S) Cl i ni c al Tri al s Group. Low -dose dop ami ne i n pat i ents wi t h e arl y renal d ysfunc ti on: a p l ac ebo-control l ed random i se d t ri al . Lance t 2000; 356:2139–43

See also: Di l ureti cs , p212; Ol i guri a , p 330; Ac ute re nal fai l ure—managem ent , p 334


Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Gas tr oi n te sti n al Dr u g s

Gastrointestinal Drugs H 2 blockers and proton pump inhibitors Types H 2 antagoni st s: e.g . rani ti di ne, ci m eti di ne Prot on pum p i nhi bi tors: e.g . om eprazol e

Modes of action The se age nts i nhi b i t se cre ti on of g ast ri c ac i d, reduc i ng b oth vol ume and aci d conte nt, ei the r b y antagoni sm of the hi s tami ne H 2 re cep tor or by i nhi b i t i ng H + K + -AT Pas e whi c h fuel s t he p ari et al cel l p rot on pum p on whi c h ac i d se cre ti on dep end s.

Uses Pept i c ul cerati on, gastri t i s, duode ni t i s Refl ux oes ophagi ti s Prop hyl axi s agai ns t s tre ss ul c erati on Uppe r g ast roi nt est i nal haem orrhag e of p ept i c/stress ul cer ori g i n Wi t h non-s teroi dal anti -i nfl am mat ory ag ent s i n p ati ent s w i th dy spe psi a Gas tri c t onomet ry measureme nt

Side-effects/complications The maj or concern v oi c ed agains t t hes e agents i s the i ncre ase d ri s k of nosoc omi al pne umoni a by re moval of t he aci d b arri er. Howe ver, a mul ti centre RCT compari ng rani ti di ne w i th sucral fate showed no di ffe rence i n pneumoni a rat e and a l ower i nci dence of GI bl e edi ng. H 2 antagoni st s: rare b ut i ncl ude arrhyt hmi as, al tered l i ver funct i on te sts , c onfusi on (i n the e l de rl y ). Prot on pum p i nhi bi tors: al t ere d l i ve r func ti on t es ts.

Notes Al though l i censed and freq uentl y us ed for st res s ul ce r p rop hyl axi s, ove rwhel m i ng support i ve evi dence i s sc ant y. Ent eral nut ri t i on has b een shown to be as effe ct i ve . No ad equate l y powe red st ud y of proton p ump i nhi b i t ors has ye t bee n p erform ed i n ICU pat i ents . Som e s tud i es have shown e ffi cac y i n uppe r g ast roi nt est i nal haem orrhag e s econdary to stress ul cerat i on or pe pti c ul c erati on. Dos age s s houl d be mod i fi ed i n renal fai l ure. Ci m eti di ne c an affect me tab ol i sm of othe r d rugs, i n parti cul ar warfari n, p henytoi n, theophyl l i ne and l i d ocaine (rel a ted to hep ati c c ytochrome P450-l i nked enzym e sy st ems). T hi s does not oc cur wi th rani t i di ne. Ome prazol e c an del ay el i mi nati on of di a zep am, phenyt oi n and w arfari n. P.219

Drug dosages

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Ranitidine

50mg tds by slow IV bolus, 150mg bd PO

Cimetidine

200–400mg qds by slow IV bolus, 400mg bd PO

Omeprazole

40mg IV od (over 20–30min), 20–40mg PO

Key trial Cook D , G uyat t G , M ars hal l J, e t al. A c omp ari son of sucral fate and rani ti d i ne for t he pre venti on of up per gas troi ntes ti nal bl e edi ng i n pat i e nts re qui ri ng m echani cal ve nti l a ti on. Canadi an C ri ti c al Care T ri a l s Group . N Eng l J Med 1998; 338:791–7

See also: Upp er gas troi ntes ti nal end osc opy , p 74; Sucral fat e, p 220; Antaci d s, p222; Uppe r g ast roi nt est i nal haem orrhag e, p344; Bl eedi ng vari c es, p346; Bowe l p erforati on and obs truct i on, p 348 P.220

Sucralfate Modes of action Suc ral fat e i s a basi c al umi ni um s al t of sucrose oct as ul p hat e and i s probab l y not abs orbed from t he gast roi nt est i nal t ract. Exerts a c ytoprotec ti ve effe ct by pre venti ng m ucosal i njury. A p rot ec ti v e b arri er i s forme d b oth ov er normal mucosa and any ul ce r l esi on provi d i ng p rot ect i on ag ai nst penetrati on of gas tri c aci d, bi l e and peps i n as wel l as i rri t ant s s uch as as pi ri n and al cohol . Di rect l y i nhi b i ts pe psi n acti vi ty and abs orb s b i l e s al t s. Weak antac i d act i vi ty .

Uses Pept i c ul cerati on, gastri t i s, duode ni t i s Refl ux oes ophagi ti s Prop hyl axi s agai ns t s tre ss ul c erati on

Side-effects/complications Cons ti pat i on Reduced bi oav ai l abi l i ty of s ome drugs gi ven oral l y, e.g . d i goxi n, p henytoi n. Can b e ov erc ome by gi vi ng agents at l eas t 2h apart. Use wi t h c aut i on i n renal fail ure due t o ri sk of i ncre ase d alum i ni um abs orp ti on.

Notes Al though l i censed and freq uentl y us ed for st res s ul ce r p rop hyl axi s, ove rwhel m i ng support i ve evi dence i s sc ant y. Ent eral nut ri t i on and g ast ri c ac i d bl ock ers have b een shown to be as effect i ve . Evi dence for a red uce d i nci dence of nos ocomi a l p neumoni a c omp are d t o H 2 bl ock er the rap y i s als o c onfl i c ti ng. Si gni fi c ant re duc ti on i n nos ocom i al p neum oni a has bee n s hown compared to a com bi nati on of H 2 bl ock er pl us antaci d but not agai nst H 2 bl ock er al one. Indee d, a l arg e mul t i ce ntre R CT comp ari ng rani t i di ne wi t h s uc ral fat e s howe d no di fferenc e i n p neumoni a rat e and a l ower i nci dence of GI b l ee di ng w i t h rani ti d i ne . Ant ac i ds shoul d not be gi v en for 30m i n before or after sucralfate. P.221

Drug dosages

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Sucralfate


1g six times a day PO or via ng tube.

Key trial Cook D , G uyat t G , M ars hal l J, e t al. A c omp ari son of sucral fate and rani ti d i ne for t he pre venti on of up per gas troi ntes ti nal bl e edi ng i n pat i e nts re qui ri ng m echani cal ve nti l a ti on. Canadi an C ri ti c al Care T ri a l s Group . N Eng l J Med 1998; 338:791–7

See also: Upp er gas troi ntes ti nal end osc opy , p 74; H 2 b l oc kers and proton pump i nhi bi tors, p218; Antaci d s, p222; Uppe r gas troi ntes ti nal hae morrhage, p344; Bl e edi ng vari ce s, p346; Bowel pe rforat i on and obst ruc ti on, p348 P.222

Antacids Types Sod i um bi carbonate Magnesi um-bas ed ant aci ds: e. g. magnesi um tri si l i cat e Al umi ni um -based antac i ds : e .g. al umi ni um hydroxi de (Al udrox) Prop ri etary com bi nati ons : e .g. Gavi s con

Modes of action Neut ralis es gas tri c aci d Prov i d es p rotec ti v e c oat i ng on up per gas troi ntes ti nal muc os a

Uses Symp tom ati c rel i ef of gas tri ti s, duodeni t i s, oe sop hagi ti s Stress ul cer prop hyl axi s (c ont ent i ous)

Side-effects/complications Poss i b l e i nc reased ri sk of nos ocomi a l p neumoni a Al umi ni um toxi c i t y (i f alum i ni um -contai ni ng ant aci ds are us ed l ong-t erm i n pati e nts wi th renal dys functi on) Di a rrhoea (magne si um-b ase d antaci d s) Cons ti pat i on (al umi ni um-b ase d antaci d s) Metabol i c al kal osi s i f l arg e amounts are admi ni s tered Mi l k-al kal i syndrome res ul t i ng i n hy percal caemi a, m etabol i c al kal osi s and renal fai l ure i s v ery rare

Notes As thei r main use i s for s ymp tomati c rel i ef, antac i ds are rare l y nee ded i n me chani c al l y v ent i l ated pati ent s. Conti nual nasog ast ri c i nfusi on of a weak s odi um bi c arb onate sol uti on has be en use d s ucc ess ful l y i n treati ng st res s ul c er-re l at ed haem orrhag e. P.223

Drug dosages

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Magnesium trisilicate

10–30ml qds

Aluminium hydroxide

10–30ml qds

Gaviscon

10–30ml qds

See also: Upp er gas troi ntes ti nal end osc opy , p 74; H 2 b l oc kers and proton pump i nhi bi tors, p218; Sucral fate , p 220; Up per gas troi ntes ti nal hae morrhage, p344; Bl e edi ng vari ce s, p346; Bowel pe rforat i on and obst ruc ti on, p348 P.224

Anti-emetics Types Phenothi az ines: e.g . p roc hl orp erazi ne, chl orp rom azi ne Benzami de s: e .g. me toc l op ram i de Ant i hi st ami nes : e. g. cyc l i zi ne 5HT 3 rece ptor antagoni st s: e.g. ondanset ron, g rani s etron

Modes of action Phenothi az ines i nc rease the thres hol d for vom i ti ng at the chemorec ept or tri gge r z one vi a c ent ral DA 2 -dop ami nergi c bl ock ade ; at hi gher dos es the re may al s o b e s ome effect on the v omi ti ng c ent re. Metocl oprami de act s c ent ral l y and by i ncre asi ng gas tri c mot i l i ty. The exact mec hani sm of cyc l i zi ne acti on i s unknow n. It i nc re ases l ower oe sop hag eal sp hi ncte r t one and m ay i nhi bi t t he mi d brain eme ti c c ent re. Ond ans etron i s a hi ghl y sel ect i ve 5HT 3 re cep tor antag oni st ; i t s pre ci s e m ode of act i on i s unknown but may ac t both ce ntral l y and peri p heral l y.

Uses Naus ea Vomi ti ng

Side-effects/complications Dys toni c or dys ki neti c reac ti ons , oc ul ogy ri c cri s es (prochl orperazi ne, me toc l op ram i de ) Arrhyt hmi as (me toc l op ram i de , p roc hl orp erazi ne) Head aches, fl ushi ng (ondanse tron) Urt i cari a , d row si ness , d ry mouth, bl urred vi si on, uri nary ret ent i on (cy cl i zi ne) Post ural hyp otensi on (prochl orperazi ne, cy cl i zi ne) Rare l y, ne urol ep ti c m al i gnant syndrome (prochl orperazi ne, me toc l op ram i de )

Notes The i ni t i al choi c e s houl d fal l b etw een prochl orperazi ne, me toc l op ram i d e or cy cl i zi ne. Prochl orperaz i ne and c ycl i zi ne are prefe rab l e whe n vomi t i ng i s rel a ted to drugs and m etabol i c di s turbance s acti ng at the chemorec ept or tri gge r z one whi l e met ocl oprami de shoul d be tri e d fi rs t i f a gastroi ntes ti nal cause i s i m pl i cat ed. Met ocl oprami de and prochl orperazine dosag e shoul d b e reduced i n renal and hepati c fail ure . Ond ans etron dos age shoul d b e reduced i n he pat i c fai l ure. P.225

Drug dosages

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Prochlorperazine

5–10mg tds PO, 12.5mg qds IM or by slow IV bolus (note: not licensed for IV use)

Metoclopramide

10mg tds by slow IV bolus, IM or PO

Cyclizine

50mg tds slow IV bolus, IM or PO

Ondansetron

4–8mg tds by slow IV bolus, IM or PO

Granisetron

1–3mg by slow IV bolus up to max 9mg/24h

See also: Ent eral nut ri t i on, p 80; Vom i ti ng/gas tri c stasi s , p 338 P.226

Gut motility agents Types Metocl oprami de Ery thromy ci n

Modes of action Metocl oprami de p robabl y act s b y bl oc ki ng p eri phe ral DA 2 -dop ami nergi c rece ptors Ery thromy ci n i s a mot i l i n agoni st ac ti ng on antral enteri c neurones

Uses Il e us, l a rge nasog ast ri c as pi rat es Vomi ti ng

Side-effects/complications Dys toni c or dys ki neti c reac ti ons , oc ul ogy ri c cri s es (met ocl oprami de ) Arrhyt hmi as (me toc l op ram i de and e ryt hromyc i n) Chol est ati c jaundi ce (ery thromy ci n)

Notes Met ocl oprami de dos i ng shoul d b e reduced i n renal fail ure and he pat i c fai l ure, whi l e erythrom yci n d osi ng shoul d be red uce d i n hepati c fail ure . P.227

Drug dosages Metoclopramide

10mg tds by slow IV bolus, IM or PO

Erythromycin

250mg qds PO or IV

See also: Ent eral nut ri t i on, p 80; Vom i ti ng/gas tri c stasi s , p 338; Bow el perforati on and obs truct i on, p 348 P.228

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Antidiarrhoeals Types Lop erami d e Code i ne phosp hat e

Modes of action Lop erami d e and cod ei ne p hos phate bi nd t o g ut wal l op i ate rec ept ors , reduci ng p rop ul si v e p eri stalsi s and i ncre asi ng anal s phi nc ter tone

Side-effects/complications Abd omi nal cramp s, bl oati ng Cons ti pat i on (i f ex ces si ve amounts gi ven)

Notes Shoul d not b e used when abdomi nal di ste nsi on dev el ops, parti cul arl y wi t h ul ce rat i ve col i t i s or ps eud omem branous col i t i s, or as sol e the rap y i n i nfe cti ve di a rrhoea. Cauti on w i th l operami de i n l i ver fai l ure, and c odei ne i n re nal fai l ure. P.229

Drug dosages Loperamide

2 capsules (20ml) initially, then 1 capsule (10ml) after every loose stool for up to 5 days

Codeine phosphate

30–60mg 4–6hrly PO, IM or by slow IV bolus

See also: Ent eral nut ri t i on, p 80; Di a rrhoea, p 340 P.230

Anticonstipation agents Types Laxati ves : e. g. l ac tul os e, p rop ant hel i ne, mebe veri ne , c ast or oi l Bul ki ng agents: e.g . d i et ary fi bre (b ran), hem i ce l l ul oses (me thy l c el l ul ose, i s pag hul a husk ) Sup pos i tori e s: e.g . g l yc eri ne Enem ata: e .g. warmed normal s al i ne, ol i ve oi l or arac hi s oi l ret ent i on enemata

Modes of action Laxati ves i ncl ude i. anti spasmodi c ag ent s s uch as anti c hol i nerg i cs (e .g. propanthel i ne) and me bev eri ne (a phenyl ethyl a mi ne d eri vat i ve of re serpi ne) ii. non-absorbabl e di sacchari des (e .g. l a ctul os e) whi ch soften the st ool by an os mot i c effect and by l a ct i c aci d p rod uct i on from a b act eri al fermenti ng e ffe ct iii. i rri tants , s uch as castor oi l , whi ch i s hydrol y sed i n the s mal l i nte sti ne rel eas i ng ri ci nol ei c aci d Bul ki ng agents are hy drophi l i c and t hus i ncreas e t he w ate r c ont ent of the s tool .

Side-effects/complications Bl oati ng and ab domi nal d i st ens i on

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Di a rrhoea i f exc es si v e am ounts gi ven

Notes Surgi cal cause s p res ent i ng as const i p ati on suc h as b owel ob st ruc ti on m ust be ex cl uded . Othe r m eas ure s s houl d be tak en i f pos si b l e to i mp rov e b owel func ti on, e.g . reduci ng c onc urrent op i at e d osage, st art i ng enteral nutri ti on. The ag ent of choi c e i s l act ul ose. Larger d oses of l a ctul ose are use d i n hepati c fail ure as the pH of the c ol oni c conte nts i s reduced ; thi s l owers format i on and absorpt i on of amm oni um i ons and other ni t rogenous produc ts i nto the portal c i rcul ati on. Prove n b enefi t i n pat i ents has not b een shown. Ant hraqui none gl y cos i de s (e.g . s enna) and l i q ui d paraffi n are no l ong er rec omm end ed for routi ne use . P.231

Drug dosages Lactulose

15–50ml tds PO

P.232

See also: Ent eral nut ri t i on, p 80; Fai l ure t o op en bow el s , p 342


Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Neu r ol ogi cal Dr u gs

Neurological Drugs Opioid analgesics Types Natural opi a tes : e. g. morphi ne, codei ne Semi sy ntheti c: e.g . d i am orp hi ne, di hydrocodei ne Synthe ti c : e .g. pet hi di ne, fent any l , al fent ani l , re mi fent ani l

Uses Analge si a . Strong analge si c s are ext rac ts from opi um or s ynt het i c subst anc es wi t h s i mi l a r p rop ert i es . T hey are useful for conti nuous pai n rat her than sharp, i ntermi t te nt pai n. Sed ati on Mi l d v asod i l atati on i n heart fai l ure (d i am orp hi ne, morphi ne) Ant i di arrhoeal (codei ne)

Routes IV (morphi ne , di amorp hi ne, papaveretum, pet hi d i ne, fent any l , al fent ani l , rem i fe ntani l ) IM/SC (morphi ne, codei ne, di amorphi ne , d i hy drocod ei ne, pet hi d i ne ) PO (morphi ne, codei ne, di amorphi ne , d i hy drocod ei ne, pet hi d i ne)

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Epi dural (morphi ne , d i am orp hi ne, fentanyl , al fent ani l )

Side-effects Resp i ratory depres si on Cent ral ne rvous sys tem de pre ssi on Add i ct i on (rare i n the c ri ti c al l y i l l ) Wi t hdrawal s ynd rom e (w i thdraw s l ow l y) Sti mul ati on of the vom i t i ng ce ntre App eti te l os s Dry mouth Dec reased gas tri c emp tyi ng and gut m oti l i t y Hi s tam i ne re l ease and i t chi ng Inc reased mus cul ar tone

Notes Morphi ne i s poorl y ab sorbed from the gastroi ntes ti nal tract and i s t herefore usual l y admi ni ste red parenteral l y. It i s met abol i s ed to morphi ne-6-g l uc uroni d e i n t he l i ver whi ch i s si x t i me s m ore potent t han morphi ne and ac cum ul ates i n renal fai l ure. Cod ei ne i s a weak anal ges i c but i s favoured by some i n head i njury s i nce i t i s l es s s edati v e t han morphi ne . Pet hi d i ne has l ocal anae stheti c properti e s associ a ted wi th cardi ac depres si on and vasodi l at ati on. It i s me tab ol i sed to norpet hi di ne whi c h may l ead to se i zures on ac cum ul a ti on. Res pi rat ory dep res si on occ urs de spi te mai nte nance of res pi rat ory rate. Fentanyl and al fent ani l are good, short -act i ng anal ges i cs wi th poor s edati v e q ual i ty . T hey cause se vere resp i ratory dep res si on and mus cul ar ri gi d i t y. R emi fentani l i s ul tra-short -ac ti ng and the pati e nt may suffer from reb ound p ai n i f the i nfus i on i s s top ped tem porari l y . P.235

Drug dosages Intravenous Bolus

Infusion

Morphine

0.1–0.2mg/kg

0.05–0.07mg/kg/h

Diamorphine

0.05–0.1mg/kg

0.03–0.06mg/kg/h

Pethidine

0.5mg/kg

0.1–0.3mg/kg/h

Fentanyl

5–7.5µg/kg

5–20µg/kg/h

Alfentanil

15–30µg/kg

20–120µg/kg/h

Remifentanil

1µg/kg

0.05–2µg/kg/min

Other routes

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Morphine

10mg IM/SC 4-hrly

5–20mg PO 4-hrly

Codeine

30–60mg IM 4-hrly

30–60mg PO 4-hrly

Diamorphine

5mg IM/SC 4-hrly

5–10mg PO 4-hrly

Dihydrocodeine

50mg IM/SC 4–6-hrly

30mg PO 4–6-hrly

Pethidine

25–100mg IM/SC 4-hrly

50–150mg PO 4-hrly

Note that the above doses are a guide only and may need to be altered widely according to individual circumstances. The correct dose of an opiate analgesic is generally enough to ablate pain.

See also: IPPV—fai l ure t o t ol e rat e ve nti l a ti on, p12; Non-op i oi d anal ges i cs , p 236; Sedat i v es, p238; Pai n, p532; Pos t-op erati ve i nt ens i v e c are , p534 P.236

Non-opioid analgesics Types Non-ste roi dal anti -i nfl a mmat ory drug s: e .g. as pi ri n, i ndomet hac i n, di cl ofenac Paracet amol Ketami ne Ni t rous oxi d e Loc al anae st het i cs : e .g. l i doc ai ne, bup i vacai ne

Uses Pai n as soc i a ted wi t h i nfl am matory condi ti ons (as pi ri n, i ndom ethaci n, di cl ofenac) Post -op erati v e p ai n and m usc ul oske l et al pai n (asp i ri n, i ndom ethaci n, di c l ofenac, parace tam ol , ket ami ne, ni trous oxi d e, l i doc ai ne, bup i vacai ne) Opi ate sp ari ng effect (as pi ri n, i ndomet hac i n, di cl ofenac use d w i th st rong anal ges i c s) Ant i py ret i c (as pi ri n, p aracet amol )

Routes IV (ket ami ne) IM (di c l ofenac) PO (asp i ri n, i ndom ethaci n, di c l ofenac, parace tam ol ) PR (asp i ri n, di cl ofenac, parac etam ol ) Loc al /re gi onal (l i docai ne, bupi v acaine ) Inhal e d (ni t rous oxi d e)

Side-effects Gas troi nt est i nal bl e edi ng (asp i ri n, i ndom ethaci n, di c l ofenac) Renal d ysfunc ti on (i nd ome thaci n, d i cl ofe nac i f any hypovol aemi a) Reduced pl ate l et ag gre gat i on (aspi ri n, i nd omet hac i n, d i cl ofe nac ) Reduced prothrom bi n formati on (asp i ri n, i ndom ethaci n, di c l ofenac) Myoc ard i al d epress i on (l i docai ne, bupi v acaine ) Hype rt ens i on and tachy cardi a (k etami ne) Sei zures (l i doc ai ne, bup i vacai ne)

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Hal l uc i nati ons and ps ychoti c t end enc i e s (k etami ne—p rev ent ed by concurrent use of benz odi az epi nes or droperi dol )

Notes Parace tam ol ove rdose can cause sev ere he pat i c fai l ure d ue to the effec ts of alky l at i ng me tab ol i te s. Though normal l y rem ove d b y c onjugat i on wi th gl utathi one , s tores are rapi d l y dep l et ed i n ove rdose. Non-st eroi dal anti -i nfl ammatory agents shoul d be ge neral l y avoi ded i n pati e nts wi th renal dys functi on, GI bl eed i ng or coagul opathy . Ket ami ne i s a d eri vat i ve of phe ncy cl i di ne use d as an i ntrave nous anaes the ti c agent . In s ub anae stheti c dos es i t i s a pow erful analge si c . It has sev eral advantages ove r opi ates i n t hat i t i s as soc i at ed wi t h g ood ai rway maintenanc e, al l ows sp ont ane ous re spi rati on and p rovi d es cardi ovas cul ar sti mul at i on. It i s also a bronchodi l at or. Ni t rous oxi de i s a powerful , s hort act i ng anal g esi c used to cover short , p ai nful proce dures. It may b e useful when del i ve red vi a an i nte rmi tt ent posi t i ve press ure breat hi ng sys tem as an adj unc t t o c hes t p hys i ot herapy . N i trous ox i de shoul d not b e used i n cases of undraine d p neumothorax s i nce i t may di ffus e i nto the p neumot horax res ul t i ng i n tensi on. P.237

Drug dosages Aspirin

600mg PO/PR 4-hrly

Indomethacin

50–100mg PO/PR 12-hrly

Diclofenac

25–50mg PO 8-hrly, 100mg PR 12–24-hrly, 75mg IM 12-hrly

Ketorolac

10mg PO 4–6-hrly, 10–30mg IV, IM 4–6-hrly

Sulindac

200mg PO 12-hrly

Paracetamol

0.5–1g PO/PR 4–6-hrly

Ketamine

5–25µg/kg/min IV

Lidocaine

Maximum 200mg

Bupivicaine

Maximum 150mg*

*Local anaesthetic doses vary according to the area to be anaesthetised. Maximum doses may be increased if epinephrine is used locally.

See also: Opi oi d anal ges i cs , p 234; Sal i c yl a te poi soni ng , p 454; Rhe umati c di sorde rs, p492; Pyrexi a (1), p518; Pyrexi a (2), p520; Pai n, p532; Post -op erati v e i nte nsi ve care, p534 P.238

Sedatives Types Benzod i az epi nes : e. g. di azep am, mi dazol a m, l oraze pam Major t ranqui l l i se rs : e. g. chl orpromazine , hal operi dol Anaest het i c age nts : e. g. propofol , i s ofl urane α 2 agoni st s e.g. cl oni di ne, de xmed etomi d i ne

Uses Sed ati on and anx i ol ysi s

Routes

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IV (di aze pam, mi daz ol a m, l oraze pam , c hl orpromazi ne, hal ope ri dol , p rop ofol , cl oni d i ne , d exm ede tomi di ne) IM (di a zep am, chl orpromaz ine, hal operi d ol ) PO (di a zep am, l oraz epam, chl orp rom azi ne, halop eri dol , cl oni d i ne ) Inhal e d (i sofl urane)

Side-effects Hypotensi on (di a zep am, mi dazol a m, chl orp rom azi ne, halop eri dol , propofol , cl oni di ne, dex mede tom i di ne ) Resp i ratory depres si on (di a zep am, mi d azol am , c hl orp rom azi ne, halop eri dol , p rop ofol ) Arrhyt hmi as (chl orpromaz i ne, hal operi d ol ) Dry mouth (cl oni di ne, dex med etomi d i ne ) Extrap yrami d al di s ord er (chl orpromazine, hal operi d ol ) Fl uori de toxi ci ty (i s ofl urane)

Notes Sed ati on i s nec es sary for m ost IC U p ati ent s. Whi l e the ap propri at e use of s edati v e d rug s c an provi d e c omfort , m ost hav e c ard i ov asc ul a r and res pi rat ory si de-effe cts . Obje ct i ve ass es sment of t he dep th of s edati on i s nec ess ary to ens ure that com fort d oes not g i ve way to ex ces si v el y and d ange rousl y d eep l ev el s of se dat i on. Al l se dat i ve s are pot ent i al l y cumul ati ve so dos es m ust be ke pt to a mi ni mum . Benzod i az epi ne s have the ad vantag e of be i ng am nes i c. Di aze pam i s mainl y admi ni s tered as an emul si on i n i ntralip i d as org ani c s ol vent s are ext rem el y i rri tant t o v ei ns. Mi d azol am i s short er act i ng t han di aze pam al t hough 10% of pat i ents are sl ow met abol i s ers. Al l be nzodi a zep i ne s accumul at e i n renal fail ure ; c are mus t be t ake n t o avoi d exc ess i ve dosag e b y regul ar re ass ess ment of need. Some pat i ents suffer unpre di c tabl e se vere resp i ratory d epress i on wi t h hypotensi on. Propofol use d i n s ubanae stheti c d ose s i s s hort-act i ng thoug h effec ts are cumul ati ve whe n i nfusi ons are prol onge d or wi t h c oex i st i ng hepat i c or re nal failure. It i s gi ven as an em ul s i on i n 10% i ntral i pi d s o l arg e v ol umes may contri b ute si gni fi c ant l y to cal ori e i nt ake. As chl orpromaz ine and hal operi dol antagoni se catec hol ami nes , t hey may cause vasod i l atat i on and hypotensi on. Dys toni c re act i ons and arrhyt hmi as are al so occ asi onall y se en. α 2 ant agoni s ts al s o p rov i d e anal g esi a and are sy nergi s ti c w i th op i at es. De xmed etomi d i ne c aus es m i ni mal resp i ratory dep res si on and the pati e nt i s eas i l y rous abl e. Bradyc ard i a and hy pot ens i on may oc cur, esp eci al l y w i th the l oad i ng dos e. Isofl urane i s l argel y e xhal ed unc hanged and i s t herefore short act i ng. Cumul at i v e effec ts hav e b een rec orded wi t h prol onged us e, carryi ng the t heoret i cal ri s k of fl uori de toxi c i t y. Exhaled i sofl urane shoul d b e s cave nge d. P.239

Drug dosages Bolus

Infusion

Diazepam

0.05–0.15mg/kg

Excessive half-life

Midazolam

50µg/kg

10–50µg/kg/h

Lorazepam

1mg PRN

Propofol

0.5–2mg/kg

1–3mg/kg/h

Chlorpromazine

12.5–100mg

Excessive half-life

Clonidine

100–150µg/min

Dexmedetomidine

Loading infusion of 6.0µg/kg/h over 10min, followed by maintenance infusion of 0.2–0.7µg/kg/h.

Note that the above doses are a guide only and may need to be altered widely according to individual circumstances.

Monitoring sedation

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Fre que nt, ob jec ti v e reas ses sme nt of s edati on d ept h w i th corresp ond i ng ad jus tme nt of i nfusi on d ose s i s nec ess ary to avoi d sev ere cardi ovascul ar and resp i ratory dep res si on. Si m pl e se dat i on sc ores are avail abl e t o ai d asse ss ment .

UCL Hospitals Sedation Score Agitated and restless

+3

Awake and uncomfortable

+2

Aware but calm

+1

Roused by voice, remains calm

0

Roused by movement

-1

Roused by painful or noxious stimuli

-2

Unrousable

-3

Natural sleep

A

Sed ati on dos es are ad jus ted to ac hi e ve a sc ore as cl os e as possi bl e t o 0. Posi t i v e s cores req ui re i ncreas ed sed ati on dos es and ne gat i ve sc ore s requi re re duc ed sed ati on dos es.

See also: IPPV—fai l ure t o t ol e rat e ve nti l a ti on, p12; Opi oi d anal ges i cs , p 234; Ag i tati on/c onfusi on, p370; Sed ati ve poi soni ng , p458; Pos t-op erati ve i nt ens i ve care, p534 P.240

Muscle relaxants Types Depol ari s i ng : e .g. suxame thoni um Non-dep ol a ri s i ng: e .g. pancuroni um, atracuri um, vec uroni um

Mode of action Sux amet honi um i s s tructural l y re l at ed to acet yl chol i ne and causes i ni ti al st i mul at i on of muscul ar contrac ti on seen cl i ni call y as fasci cul at i on. D uri ng thi s proces s, the conti nue d s ti m ul ati on l eads to d ese nsi ti sat i on of the post -sy nap ti c me mbrane of the neuromus cul ar junct i on wi th effl ux of pot ass i um i ons . Subs equent fl acc i d paral y si s i s short ac ti ng (2–3mi n) and cannot be re versed (i s ac tual l y p ote nti ate d) by anti chol i nes terase drugs . Prol onged effect s are see n where there i s c ong eni tal or ac qui red ps eud ochol i nes teras e de fi c i e ncy . Non-dep ol a ri s i ng m usc l e rel axants preve nt ace tyl chol i ne from de pol ari si ng the pos t-s ynapti c memb rane of t he neuromusc ul a r j unc ti on b y c omp eti ti v e b l oc kad e. Reve rsal of p aralys i s i s ac hi e ved by ant i c hol i ne ste ras e d rug s suc h as ne ost i g mi ne. They have a s l owe r onse t and l onger durat i on of ac ti on t han the d epol ari si ng age nts .

Uses To faci l i tat e e ndot rache al i nt ubati on. To faci l i tat e m echani cal ve nti l at i on where op ti m al sed ati on doe s not pre vent pati ent i nterferenc e w i th the func ti on of t he venti l ator.

Routes IV

Side-effects Hype rt ens i on (suxam ethoni um, pancuroni um ) Bradyc ard i a (suxame thoni um)

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Tachycard i a (pancuroni um ) Hype rkalae mi a (s uxamet honi um )

Notes Mod ern i ntensi ve c are pract i c e and d eve l op ments i n venti l at or tec hnol og y have rendered the us e of muscl e rel axants l es s c omm on. Furtherm ore , i t i s rarel y ne ces sary t o ful l y p aralys e m usc l es to faci l i t ate mec hani cal v ent i l ati on. Req ui reme nt for muscl e rel a xants shoul d be re ass ess ed fre que ntl y. Ide al l y, rel axants shoul d b e s top ped i nt ermi t tentl y to al l ow de pth of sed ati on to be ass ess ed. If me chani c al venti l ati on procee ds smoothl y whe n rel a xants hav e b een st oppe d t hey probabl y shoul d not be res tarted . Sux ame thoni um i s c ont rai nd i cated i n sp i nal neurol ogi cal di sease, he pat i c di s eas e and for 5–50 d ays after burns . At rac uri um i s non-cumul ati ve and popul ar for i nfus i on. N on-enzymat i c (Hoffm an) deg rad ati on al l ows c l earance i nd epe nde nt of renal or hep ati c func ti on, al t hough effect s are prol onged i n hy pot hermi a . P.241

Drug dosages Bolus

Infusion

Suxamethonium

50–100mg

2–5mg/min

Pancuronium

4mg

1–4mg/h

Atracurium

25–50mg

25–50mg/h

Vecuronium

5–7mg

Excessive half-life

See also: IPPV—fai l ure t o t ol e rat e ve nti l a ti on, p12; End otrac heal i ntubat i on, p 36; Sed ati ves , p 238; Post -ope rat i ve i ntensi ve care, p534 P.242

Anticonvulsants Types Benzod i az epi nes : e. g. l orazepam , d i azepam, cl onazepam Phenytoi n Carb amazep i ne Sod i um val proat e Magnesi um sul phate Thi opental

Uses Cont rol of st atus e pi l ep ti c us Int erm i tt ent se i zure control Myoc l oni c se i zures (c l onaze pam , s odi um val proate )

Routes IV (l oraz epam, d i az epam, cl onazepam, phe nyt oi n, s odi um val proate , magne si um s ul phate, thi op ent al ) PO (di a zep am, cl onazep am, phenyt oi n, c arbamazap i ne, s odi um val proate ) PR (di a zep am)

Side-effects Sed ati on (benzod i az epi nes , t hi ope ntone) Resp i ratory depres si on (benzodi azepi nes , t hi opentone)

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Naus ea and vomi t i ng (p henytoi n, sodi um valp roate) Ataxi a (pheny toi n, carbam azapi ne) Vi s ual di st urb anc e (p henytoi n, carbamazapi ne) Hypotensi on (di a zep am, thi op ent one ) Arrhyt hmi as (pheny toi n, carbam azapi ne) Panc reati ti s (t hi opentone) Hepati c fail ure (s odi um val proate )

Notes Com mon i nsul ts causi ng s ei zures i nc l ud e c ere bral i sc hae mi c damag e, s pac e occupyi ng l es i ons, drugs or drug/al c ohol wi t hdrawal, met abol i c encep hal o-p athy (i nc l ud i ng hy pog l yc aem i a), and neurosurg ery . Anti convul sants provi de c ont rol of sei zures but do not repl ace re mov al of t he cause whe re thi s i s p oss i b l e. Ons et of sei zure c ont rol m ay b e d el a yed by up to 24h wi th phe nyt oi n but a l oadi ng dos e i s usually gi ven duri ng t he acute phase of s ei zures. Mag nes i um sul phate i s es pec i al l y us eful i n e cl a mpt i c sei zures (and i n t hei r pre venti on). Phe nyt oi n has a narrow t herapeuti c rang e and a non-l i ne ar rel at i onshi p b etw een dos e and pl a sma l e vel s. It i s the refore es senti a l t o m oni tor pl as ma l eve l s freque ntl y. Ent eral feed i ng s houl d be s top ped te mporari l y whi l e oral phe nyt oi n i s ad mi ni s tered. Intravenous us e s houl d onl y oc cur i f t he ECG i s moni t ore d c ont i nuous l y. Carbam aze pi ne has a wi der therapeuti c rang e t han phe nyt oi n and t here i s a l i near rel ati ons hi p be twe en dos e and pl a sma l e vel s. It i s not , t herefore, cri t i cal t o m oni tor pl as ma l eve l s freque ntl y. Pl a sma conce ntrati ons of sodi um v al p roate are not rel a ted to effect s s o m oni tori ng of pl as ma l eve l s i s not us eful . P.243

Intravenous drug dosages Bolus

Infusion

Lorazepam

4mg

Diazepam

2.5mg repeated to 20mg

Phenytoin

18mg/kg at Tab le of Co n te n ts > H ae mato log ica l D r u gs

Haematological Drugs Anticoagulants Types Hepari n Low mol ecul ar we i ght (LMW ) hepari n: e .g. dal te pari n, enoxi pari n Ant i coagul ant p ros tanoi d s: e.g . e pop ros tenol , al prostadi l Sod i um ci trate Warfari n Act i vated Prote i n C

Modes of action Hepari n p otenti ate s natural l y occ urri ng AT-III, re duc es the ad hes i onof pl a tel ets to i njured art eri al wal l s , b i nd s t o pl a tel ets and p rom otes in vi tro ag gre gat i on. LMW hep ari n appe ars t o sp eci fi cal l y i nfl ue nce factor Xa acti vi ty; i t s s i mp l er pharm acoki neti cs al l ow for a smalle r (two thi rd s) dos e t o b e ad mi ni s tered to the same e ffe ct. The effect s of t he p rostanoi ds dep end on the balance bet weenTXA 2 and PGI 2 . Sod i um ci trate che l at es i oni s ed c al ci um. Warfari n produc es a c ont rol l ed de fi c i ency of vi t ami n K dep end ent coagul at i on factors (II, VII, IX and X). Act i vated Prote i n C i s t he act i vated form of t he end oge nous anti coagul ant , Prot ei n C

Uses Mai ntenanc e of an ex tracorporeal c i rc ul ati on Prev ent i on or treat ment of t hromboemb ol i sm Seve re sep si s (act i vated Protei n C)

Routes IV (hep ari ns , anti coagul ant prost anoi ds , s odi um ci trate, ac ti v ate d Prot ei n C, AT -III) SC (hep ari ns) PO (warfari n)

Side-effects Bl e edi ng Hypotensi on (ant i coagul ant p ros tanoi ds) Hepari n i nduced throm boc ytopeni a Hypocal cae mi a and hype rnatraemi a (sod i um ci trate)

Notes Al prostadi l has s i mi l a r e ffec ts to epoprost ani l b ut i s l es s p ote nt. As i t i s m etabol i se d i n t he l ungs, sy st emi c vas odi l at ati on effect s are usual l y m i ni mal . Thi s m ay b e an i mportant adv ant age i n the s hoc ked pat i ent. Maj or use s i n

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i nt ens i v e c are are for anti coagul at i on of fi l te r c i rc ui ts, di gi t al vas cul i t i s/i s chaemi a and p ul m onary hyp ert ens i on. For ex tracorporeal us e c i t rat e has advantages ov er hep ari n i n t hat i t has no k nown anti p l a tel et act i vi ty, i s readi l y fi l te red by a haem ofi l te r (red uci ng sys tem i c ant i c oag ul a ti on), and i s ov erw hel med and neut ral i se d w hen re turned to central venous bl ood. Warfari n i s gi ven oral l y and need s 48–72h to dev el op i ts effect . It c an be reve rs ed b y fres h froz en pl a sma or l ow dos es (1m g) of v i tami n K. Ac ti v ate d Prot ei n C has ant i -i nfl amm atory and pro-fi bri nol yt i c prope rti es i n add i t i on to i t s anti coagul ant ac ti ons. P.249

Drug dosages Heparin Dos e requi rement i s vari ab l e to produc e an APTT of 1.5–3 ti m es control . Thi s usual l y requi re s 500–2000IU/h wi t h an ini ti al l oadi ng d ose of 3000–5000IU.

Low molecular weight heparin For de ep vei n t hrombos i s prophyl a xi s gi ve 2500IU SC 12-hrl y. For anti coagul ati on of an e xtracorporeal c i rcui t a bol us of 35IU/kg i s g i ve n IV fol l owed by an i nfus i on of 13IU/k g. The dose i s adj ust ed to mai ntain ant i -fact or Xa act i vi ty at 0.5–1IU/m l (or 0.2–0. 4IU/ml i f there i s a hi g h ri sk of hae morrhage). For pul monary e mbol i s m g i ve 200IU/kg SC dai l y (or 100IU/kg bd i f at ri sk of b l ee di ng)

Anticoagulant prostaglandins Usual range of 2.5–10ng/k g/m i n. If us ed for an ext rac orporeal ci rcul a ti on t he i nfusi on shoul d be st art ed 30m i n pri or to com mencem ent .

Sodium citrate Infuse d at 5mmol p er l i t re of ext rac orp ore al bl ood fl ow.

Warfarin St art at 10mg/d ay orally for 2 days the n 1–6mg /day accordi ng to INR . For D VT prophyl a xi s , p ul m onary emb ol us, mi t ral s tenosi s, atri al fi bri l l at i on and t i ss ue val ve rep l ac ements the INR s houl d be mai ntaine d b etw een2 and 3. F or rec urrent D VT or pul monary em bol us and mec hani c al val ve repl ac ements the IN R s houl d be kep t b etwe en 3 and 4.5.

Activated Protein C (Drotrecogin α activated) For se psi s, an i nfusi on of 24 µg/kg/h i s gi ven for 96h.

See also: Ext rac orporeal re spi rat ory support , p34; Haemo(di a)fi l t rat i on (2), p 64; Pl as ma e xchang e, p68; C oag ul a ti on moni tori ng, p156; Thromb ol y ti c s, p250; Pul m onary emb ol us, p308; Acute coronary syndrome (1), p320; Ac ute coronary syndrome (2), p322; Cl ot ti ng d i sorde rs , p398; Hyp erosmol ar di abe ti c em erg enc i es , p 444; Se psi s and sep ti c shock— treatm ent , p 248; Post -ope rat i v e i nte nsi ve care, p534 P.250

Thrombolytics Types Al t epl ase (rt-PA) Strept oki nas e Urok i nase

Modes of action Ac ti v ate pl asm i nogen to form p l as mi n whi c h de grades fi bri n

Uses Li fe t hre ate ni ng v enous t hromb osi s Li fe t hre ate ni ng p ul m onary embol us Acute myoc ardi a l i nfarct i on To unbl ock i ndwe l l i ng vas cul ar ac ces s c athete rs

Routes

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IV

Side-effects Bl e edi ng, parti cul arl y from i nvasi v e p roc edures Hypotensi on and arrhyt hmi as Embol i sat i on from pre -exi st i ng cl ot as i t i s broken down Anaphyl ac toi d reac ti ons (ani st rep l ase, st rep tok i nase, uroki nas e)

Contraindications (absolute) Cere brovas cul ar ac ci d ent i n l a st 2 m ont hs Act i ve bl eed i ng i n l a st 10 day s Preg nancy Rece nt pep ti c ul ce rat i on Rece nt surgery

Contraindications (relative) Sys tol i c BP >200mm Hg Aorti c di ss ect i on Prol i ferati v e d i ab eti c reti nopat hy

Notes In acute myocardi a l i nfarc ti on t hey are of most val ue when us ed wi t hi n 12h of t he ons et. The y m ay req ui re adjuvant the rap y (e.g . as pi ri n wi th strep toki nase or hepari n wi th rt -PA) t o maxi m i se the e ffe ct i n acute myoc ardi a l i nfarct i on. rt -PA i s said to be c l ot s el e cti ve and i s there fore useful where a ne ed for i nvas i ve proce dures has be en i denti fi e d. Anaphy l ac toi d reacti ons to st rep tok i nase are not uncommon, p art i c ul a rl y i n t hos e who have had st rep toc oc cal i nfect i ons, and pati ent s s houl d not be exp ose d t wi c e b etw een 5 d ays and 1 year of rece i vi ng the l a st dos e. P.251

Drug dosages Alteplase (rt-PA)

The dose schedule for acute myocardial infarction is 10mgin 1–2min, 50mg in 1h and 40mg over 2h intravenously.

Anistreplase

Single intravenous injection of 30U over 4–5min.

Streptokinase

In acute myocardial infarction (1.5mu over 60min).In severe venous thrombosis (250,000U over 30min followed by 100,000U/h for 24–72h).

Urokinase

For unblocking indwelling vascular catheters 5000–37,500IU are instilled. For thromboembolic disease 4400IU/kg is given over 10min followed by 4400IU/kg/h for 12–24h.

See also: Coagul ati on moni tori ng, p156; C oag ul a nts and anti fi b ri nol yti cs, p254; Pul monary emb ol us, p308; Acute coronary syndrome (1), p320 P.252

Blood products Types Pl as ma: e. g. fre sh frozen pl asm a Pl at el ets Conc ent rat es of coagul ati on fac tors: e.g . c ryopre ci p i t ate , factor VIII c onc ent rat e, fac tor IX compl ex

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Uses Vi t ami n K defi c i ency (fresh frozen pl as ma, fac tor IX c ompl ex) Haem ophi l i a (cryoprec i pi tat e) von Wi l l e brand' s d i se ase (c ryopre ci p i t ate ) Fi bri noge n d efi ci e ncy (c ryopre ci p i tate) Chri st mas di sease (fac tor IX c omp l ex )

Routes IV

Notes A uni t (150m l ) of fre sh frozen pl asm a i s usually col l e ct ed from one d onor and c ont ai ns al l coagul at i on factors i nc l udi ng 200 uni ts fac tor VIII, 200 uni ts fac tor IX and 400m g fi bri nogen. F res h froz en pl a sma i s st ore d at -30° C and shoul d be i nfus ed wi t hi n 2h once defros ted . Pl a tel et concentrate s are v i ab l e for 3 day s w hen st ore d at room tem perature. If they are re fri gerate d v i ab i l i ty dec reases . T hey must be i nfuse d q ui c kl y vi a a short gi vi ng s et wi t h no fi l t er. Indi cat i ons for pl a tel et concentrates i nc l ude pl a tel et count 7 or i n l e ss sev ere hae morrhage 0.5–2m g may b e g i ve n b y s l ow i ntravenous i njec ti on wi th mi ni m um l as ti ng e ffe ct on oral anti coagul ant the rap y. Protam i ne has an anti coagul ant effec t of i t s own i n hi g h d ose s. Protam i ne 1m g neut ral i s es 100IU unfract i onat ed hep ari n i f g i ve n w i thi n 15m i n. Less i s re qui red i f gi ven l a ter s i nc e hepari n i s ex cre ted rapi d l y. Protami ne s houl d be gi v en by sl ow i ntrave nous i nje cti on acc ord i ng t o the APTT . T otal d ose shoul d not exc eed 50m g. Protam i ne i njec ti on may cause se vere hy pot ens i on Tranex ami c aci d has an anti fi b ri nol yti c e ffe ct by antagoni s i ng pl asm i nogen. T he usual dos e i s 1–1. 5g 6–12-hrl y oral l y or by sl ow i ntrave nous i nje cti on. Rec omb i nant fac tor VIIa i s l i censed for use i n haem ophi l i a but a numb er of cas e s eri es i n maj or trauma, orthopaedi c and cardi ac surge ry rep ort be nefi t i n sev ere , i ntract abl e b l ee di ng t hat had not res ponded to st and ard me asures . T he dos e i s 4500IU/kg over 2–5mi n, fol l owed by 3000–6000IU/kg d epe ndi ng on the se veri ty of bl eed i ng . P.255

See also: Coagul ati on moni tori ng, p156; Ant i coagul ants, p248; Thromb ol y ti c s, p250; Aproti ni n, p 256; Bl eed i ng di sorde rs, p396; Cl otti ng di sorders, p398; Post-ope rat i ve i ntensi ve c are, p 534;Pos t-p art um hae morrhage, p542 P.256

Aprotinin The rol e of seri ne prote ase i nhi b i t ors i n coagul at i on and anti coagul ati on i s com pl i cated due t o thei r e ffec ts at vari ous poi nts i n t he c oag ul ati on pat hway . Aproti ni n i s a nat urally oc curri ng, non-s pec i fi c s eri ne protease i nhi b i tor w i th an el i mi nat i on half-l i fe of ab out 2h. Prev ent i on of sys tem i c bl eed i ng wi th aproti ni n does not promote coag ul ati on wi t hi n the ex tracorporeal ci rc ul a ti on and may eve n c ont ri but e t o t he m ai ntenanc e of e xtracorporeal anti coagul ati on.

Modes of action The effec ts of aproti ni n on the c oagul at i on c asc ade are de pendent on t he ci rcul at i ng pl asm a c onc ent rat i ons (ex pre sse d as k al l i krei n i nac ti v ati on uni ts—kIU/ml ) s i nc e t he affi ni ty of aproti ni n for p l as mi n i s si gni fi cantl y great er than t hat for p l as ma kal l i k rei n. At a p l asma l ev el of 125kIU/ml aprot i ni n i nhi bi ts fi b ri nol ysi s and com pl e ment act i vati on. Inhi b i ti on of pl a sma kal l i kre i n req ui res hi ghe r d ose s t o p rov i de pl asm a l eve l s of 250–500kIU/ml . Pl as ma kal l i kre i n i nhi bi ti on—red uce s b l ood c oag ul a ti on m edi ate d v i a contac t wi th ani oni c surfac es and , i n t he cri ti c al l y i l l pati ent , i mproves c i rc ul a tory s tab i l i ty vi a reduced ki ni n ac ti vati on. Prev ent i on of i napp rop ri ate pl ate l et ac ti v ati on—neutrophi l act i vati on (comp l e ment or kall i krei n me di a ted ) c aus es a se condary acti vat i on of pl ate l et s. Imp ort ant i n t hi s pl ate l et –ne utrophi l i nteract i on i s t he rel eas e of Cathe psi n G by ne utrophi l de granul ati on. It has b een dem ons trate d rece ntl y t hat ap rot i ni n c an si g ni fi c ant l y i nhi bi t the pl a tel et act i vati on d ue to puri fi ed Cat hep si n G, thi s mec hani sm formi ng a d i re ct i nhi b i ti on of i nappropri at e neut rophi l m edi ate d p l at el e t acti vat i on.

Uses The mai n rol e of ap rot i ni n i n t he manage ment of the e xtracorporeal c i rcul ati on has be en to pre vent b l ee di ng ass oci ate d wi th hep ari ni sat i on. High dose aproti ni n g i ve n duri ng cardi opul monary by pas s p roc edures has b een show n t o reduce pos t-operati ve bl ood l os s d ram ati cal l y. P.257

Drug dosages Aprotinin—loading dose of 2 × 10 6 kIU followed by 500,000kIU/h

See also: Ext rac orporeal re spi rat ory support , p34; Haemo(di a)fi l t rat i on (2), p 64; Anti coagul ant s, p248; Post -op erati v e i nt ens i v e c are , p534


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Ed itors:



Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Misc ell an e ou s Dr u g s

Miscellaneous Drugs Antimicrobials Types Peni ci l l i ns : e. g. benzyl peni ci l l i n, fl uc l ox aci l l i n, pi peraci l l i n, amp i c i l l i n Cephal ospori ns: e.g . c efotax i me , c eft azi di m e, cefuroxi m e Carb ape nem s: e.g. i mi p enem , m eropenem Ami nog l yc osi des : e .g. gentam i c i n, am i kaci n, t obramy ci n Qui nol one s: e .g. ci profl oxac i n Gl y cop ept i de s: e.g. te i c opl ani n, vancomy ci n Macrol i de s: e.g. erythromyci n, cl ari thromy ci n Other ant i bacte ri a l s :. e .g. cl i ndamy ci n, metroni dazol e, l i nezol i d, c o-t ri moxazol e, ri famp i c i n Ant i fungals: e. g. amphote ri ci n, fl uc ytosi ne, fl uconazol e, caspofungi n, v ori conazol e, i traconazol e Ant i vi ral s: e.g . aci c l ovi r, g anc i cl ovi r

Uses Tre atme nt of i nfect i on. Prop hyl axi s agai ns t i nfe cti on, e. g. peri -operati vel y Loc al choi ce of ant i m i crobi al vari es . Howe ver, as a gui de , t he fol l owi ng choi c es are com mon: Pneumoni a (hospi tal -ac qui red Gram neg ati ve)—ce ftazi d i me , c i profl oxaci n, m eropenem or pi p eraci l l i n/t azobac tam (pi p taz obact am) Pneumoni a (communi t y-ac qui re d)—cefuroxi m e + cl a ri thromy ci n Sys tem i c sep si s —ce furoxi me ± g ent ami ci n (+ met roni d azol e i f anae rob es l i kel y)

Routes Generall y IV i n c ri t i c al l y i l l pati e nts .

Side-effects Hype rs ens i ti vi t y reac ti ons (al l ) Sei zures (hi gh dos e p eni ci l l i ns, hi gh dos e m etroni dazol e , c i profl oxaci n) Gas troi nt est i nal di s turbance (ce phalos pori ns , e ryt hromyc i n, c l i ndam yci n, tei cop l ani n, vancomyc i n, co-t ri moxazol e, ri famp i c i n, me troni d azol e, ci profl oxac i n, am photeri c i n, fl ucy tos i ne ) Ves ti b ul a r d amage (ami nog l yc os i de s) Renal fai l ure (ami nogl ycosi d es, te i c opl ani n, vancomy ci n, ci p rofl ox aci n, ri famp i c i n, amp hot eri ci n, aci cl ovi r) Ery the ma m ul t i form e (c o-t ri m oxazol e) Leucop eni a (c o-t ri moxazol e, met roni dazol e, tei cop l ani n, c i profl oxaci n, fl uc ytosi ne, aci cl ovi r) Thrombocyt ope ni a (l i ne zol i d ) Peri pheral neuropathy (me troni dazol e )

Notes Ant i m i crobi al s s houl d be c hos en acc ordi ng t o mi crobi al sensi ti v i ti es, us ual l y bas ed on adv i ce from the mi crobi ol og y l ab oratory. App ropri ate em pi ri c the rap y for seri ous i nfect i ons s houl d be det erm i ne d b y l i ke l y org ani sms , t aki ng i nt o account known comm uni ty and hospi tal i nfe cti on and re si s tance pat terns. Up to 10% of peni ci l l i n-al l ergi c pati e nts are also ce phalos pori n-al l ergi c .

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P.261

Drug dosages (intravenous)

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Benzylpenicillin

1.2g 6-hrly (2-hrly for pneumococcal pneumonia)

Flucloxacillin

500mg–2g 6-hrly

Ampicillin

500mg–1g 6-hrly

Piptazobactam

4.5g 6–8-hrly

Cefotaxime

1–4g 8-hrly

Ceftazidime

2g 8-hrly

Ceftriaxone

1–4g daily

Cefuroxime

750mg–1.5g 8-hrly

Gentamicin

1.5mg/kg stat then by levels (usually 80mg 8-hrly)

Amikacin

7.5mg/kg stat then by levels (usually 500mg 12-hrly)

Tobramycin

5mg/kg stat then by levels (usually 100mg 8-hrly)

Erythromycin

500mg–1g 6–12-hrly

Metronidazole

500mg 8-hrly or 1g 12-hrly PR

Clindamycin

300–600mg 6-hrly

Ciprofloxacin

200–400mg 12-hrly

Co-trimoxazole

960mg 12-hrly in Pneumocystis carinii pneumonia

Imipenem

1–2g 6–8-hrly

Meropenem

500mg–1g 8-hrly

Rifampicin

600mg daily

Teicoplanin

400mg 12-hrly for 3 doses then 400mg daily

Vancomycin

500mg 6-hrly (monitor levels)

Linezolid

600mg 12-hrly

Chloramphenicol

1–2g 6-hrly

Amphotericin

250µg–1mg/kg daily

Flucytosine

25–50mg/kg 6-hrly

Fluconazole

200–400mg daily

Caspofungin

70mg stat then 50–70mg daily

Voriconazole

400mg 12-hrly on first day then 200–300mg 12-hrly

Itraconazole

200mg 12-hrly for 2 days then 200mg daily

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Common choices for specific organisms Staph. aureus

flucloxacillin

Methicillin-resistant Staph. aureus

teicoplanin, vancomycin, linezolid

Strep. pneumoniae

cefuroxime, benzylpenicillin

N. meningitidis

ceftriaxone, cefotaxime, benzylpenicillin

H. influenzae

cefuroxime, cefotaxime

E. coli

ampicillin, ceftazidime, ciprofloxacin, gentamicin, ciprofloxacin, gentamicin, imipenem, meropenem

Klebsiella spp.

ceftazidime, ciprofloxacin, gentamicin, imipenem, meropenem

Ps. aeruginosa

ceftazidime, ciprofloxacin, gentamicin, imipenem, meropenem, piptazobactam

P.262

Steroids Uses Ant i -i nfl amm atory— ste roi ds are often gi ven i n hi gh dos e for the i r ant i -i nfl amm atory effe ct , e. g. ast hma, alle rgi c and anaphy l ac toi d reac ti ons , vasc ul i ti c di sorde rs, rheum atoi d art hri ti s, i nfl am mat ory bowel di sease, neop l as m-rel a ted ce reb ral oe dem a, the fi bro-prol i ferati ve phase of ARD S, pne umoc oc cal meni ngi t i s, pneumoc yst i s pneumoni a , l arynge al oed ema (e. g. aft er rep eat ed i nt ubati on) and aft er sp i nal c ord i njury. Benefi t i s unp rov ed as y et i n cerebral oed ema fol l owi ng head i njury or c ard i oresp i ratory arrest , and may be harmful i n cerebral mal ari a and sep si s (at hi gh dose). A mul t i ce ntre t ri al has shown i mp roved out com es wi t h ‘ l ow dose’ hy drocorti s one (50mg qd s for one wee k) i n sept i c shock pati e nts wi th dep res sed ad renal functi on (subnormal p l as ma corti s ol re sponse to ACT H, oft en desp i t e ‘ normal ’ or rai s ed pl a sma l e vel s). Some pat i ents wi t h hypotensi on not res pondi ng t o c ate chol am i ne s w i l l i mp rov e wi th corti cos teroi d therapy. Repl ace ment t herapy i s ne ede d for p ati ents wi t h Addi son's di seas e and aft er adrenalec tom y or p i tui tary surge ry. In t he l onger t erm , fl ud roc ort i sone i s usual l y req ui red i n add i ti on for i t s mi neraloc ort i c oi d sodi um-retaini ng effe ct. Hi ghe r repl ac ement d ose s are nee ded i n chroni c ste roi d take rs (i .e. >2 week s w i thi n the l ast year) unde rg oi ng a st res s, e.g . s urg ery , i nfe cti on. Immunos upp res si ve— aft er org an t ransp l antat i on

Side-effects/complications Sod i um and water re tenti on (esp eci al l y w i t h mi neral ocorti coi ds ) Hypoadrenal c ri si s i f st opp ed abrupt l y aft er prol onged treat ment Immunos upp res si ve— pos si b l y i nc re ased i nfec ti on ri s k (q.v .) Neut rophi l i a Impaired gl ucos e t ol e rance/di a bet es mel l i t us Hypokal aem i c al k al osi s Ost eop orosi s , p rox i mal m yop athy (l ong -te rm use ) Inc reased susce pti bi l i t y t o p ept i c ul c er di seas e and GI bl e edi ng

Notes The pe rce i ve d hei g hte ned ri sk of sys tem i c i nfect i on ap pears exagge rat ed. Chroni c ste roi d users g ene ral l y app ear no more affec te d t han the ge neral pop ul a ti on; studi es i n ARD S and sep si s re vealed no great er i nc i de nce of i nfec ti on pos t-s teroi d ad mi ni s trati on. Oral fung al i nfec ti on i s rel a ti vel y common w i th i nhal ed ste roi ds but s yst emi c and pul monary fungal i nfe cti on i s predom i nant l y seen i n t he s eve rel y i mmunoc omp rom i se d (e.g . AIDS, pos t-c hem otherapy) and not t hos e t aki ng hi g h-d ose st eroi ds al one .

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The choi c e of c ort i cost eroi d for short -te rm ant i -i nfl amm atory effe ct i s probab l y i rrel evant provi d ed the dose i s suffi c i e nt. Chroni c hyd roc ort i sone shoul d be av oi d ed for ant i -i nfl am matory use be cause of i ts mi neral ocorti coi d e ffec t but i s ap propri at e for adrenal repl ace ment. Pre dni sone and corti sone are i nac ti ve unt i l met abol i s ed by the l i ver to predni sol one and hyd roc ort i s one res pec ti vel y. Gl ucocorti c oi d s antagoni s e the e ffe cts of ant i c hol i ne ste ras e d rugs. St eroi ds are p rob abl y not l i k el y to cause cri ti cal i l l ness my opathy thoug h t hi s re mai ns a c ont ent i ous i ss ue. P.263

Relative potency and activity Drug

Glucocorticoid activity

Mineralocorticoid activity

Equivalent anti-inflammatory dose (mg)

Cortisone

++

++

25

Dexamethasone

++++

—

0.75

Hydrocortisone

++

++

20

Methylprednisolone

+++

+

4

Prednisolone

+++

+

5

Prednisone

+++

+

5

Fludrocortisone

+

++++

—

Drug dosages Drug

Replacement dose

Anti-inflammatory dose

Dexamethasone

—

4–20mg tds IV

Hydrocortisone

20–30mg daily

100–200mg qds IV

Methylprednisolone

—

500mg–1g IV daily

Prednisolone

2.5–15mg mane

40–60mg od PO

Fludrocortisone

0.05–0.3mg daily

—

Weaning Acute use ( Resu sci tati on

Resuscitation Basic resuscitation In any se vere c ard i oresp i ratory di s turbance the order of pri ori t y s houl d be t o s ecure the ai rway, mai ntain res pi rat i on (i . e. manual venti l at i on i f ne ces sary), re store the ci rc ul a ti on (wi t h e xternal c ard i ac massage i f nec ess ary ) and consi der mec hani c al vent i l ati on. Ini t i al as ses sme nt of t he pat i ent s houl d i ncl ude pat enc y of the airway, palpati on of the pul se s, measureme nt of bl ood p re ssure, presumpt i ve di agnosi s and consi d erati on of t reatme nt of the cause .

Airway protection The ai rway s houl d be opened by l i fti ng t he jaw forward and ti l ti ng the forehead . The m out h and pharynx s houl d be cl eared b y s uct i on and l oos e fi tt i ng d ent ure s removed. If ne ces sary an orop haryng eal (Guede l ) ai rway may be i ns erted .

Manual ventilation Onc e t he ai rway i s prote cte d t he pat i ent w ho i s not breat hi ng requi res manual venti l at i on wi th a s el f-i nfl a ti ng b ag and mask (Amb u b ag). Oxyg en s houl d be del i v ere d i n maxi m um concentrati on (FIO 2 1.0 for manual v ent i l ati on, FIO 2 0.6–1. 0 for spontaneousl y b reathi ng pat i ents). If t he pat i ent b reathe s i nad equate l y (poor art eri al sat urati on, hyp erc apni a, rapi d s hal l ow breat hi ng) v ent i l atory sup port s houl d conti nue.

Circulation If pul ses are not pal pab l e or are we ak or i f t he pat i ent has a s eve re bradyc ard i a ext ernal cardi a c m ass age i s re qui re d and treat ment s houl d conti nue as for a cardi a c arre st . Hy pot ens i on shoul d b e t reated i ni t i al l y wi t h a fl ui d chal l enge al t hough l i fe-t hreate ni ng hypotensi on m ay req ui re b l i nd tre atm ent wi th epi nep hri ne 0.05–0.2m g i ncreme nts at 1–2mi n i nterval s i nt rav enousl y unti l a sati sfac tory bl ood p re ssure i s res tored. Such treat ment s houl d not be prol onged wi thout ci rcul at ory moni t ori ng to ens ure ad equacy of cardi ac out put as wel l as correc ti on of hypotensi on.

Venous access Venous ac ces s m ust be se cured earl y duri ng b asi c resusci tati on. Large-bore c annul a e are nece ssary, e. g. 14G. In cas es of hae morrhage t wo cannul ae are re qui red . Smal l peri pheral v ei ns s houl d be avoi de d; fore arm fl exure vei ns are app rop ri ate i f now here e l se i s av ai l abl e. In very d i ffi cul t pat i e nts a Sel di nger ap proach to the femoral vei n or a central vei n may b e appropri at e. The l a tte r has the ad vant age of provi di ng c ent ral ve nous m oni tori ng. P.271

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Endotrache al i nt ubati on, p36; Ce ntral venous cat het er—inserti on, p116; Col l oi d s, p180; Inot rop es, p196; Vasop res sors, p200; F l ui d c hal l e nge, p274; Hy pot ens i on, p312 P.272

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Cardiac arrest As wi t h b asi c res usc i t ati on the order of pri ori ty i s ai rway, bre athi ng and c i rcul ati on fol l ow ed by d rug t reatment. If the cardi ac arrest i s wi tne sse d a precordi al thump may re vert v ent ri c ul ar tac hyc ard i a or ventri cul ar fi bri l l ati on. Ini ti al manage ment of the airw ay and re spi rat i on i s as for b asi c res usc i tati on. Whe n i ntubat i on i s atte mpt ed i t shoul d be effect ed aft er adeq uat e p re- ox ygenati on and qui ck l y to avoi d hyp oxae mi a . If i ntubat i on i s d i ffi cul t mai ntain manual venti l at i on wi th an Ambu bag, mas k and 100% ox yge n.

Cardiac massage Ext ernal cardi ac mas sag e provi des mi ni mal ci rcul a tory s upp ort duri ng c ard i ac arre st. A com pre ssi on rat e of 80–100/mi n i s l i k el y to provi de t he opt i mum b l ood fl ow duri ng c ard i ac massage wi t h a manual breat h from an ass i s tant for every 5 compress i ons. Av oi d mas sag e d uri ng manual i nsp i rati on i f t he pat i ent i s not i ntub ate d (t o avoi d gas tri c di l atati on); ot herwi s e c ard i ac massage i s more e ffec ti ve i f not synchroni se d t o resp i rati on.

Defibrillation Defi bri l l at i on shoul d b e p erform ed urg ent l y i f VT or VF cannot be ex cl uded . It i s i mportant to res tart cardi a c m ass age i mm edi ate l y aft er defi bri l l at i on wi thout wai ti ng for the EC G t o recover. Ce reb ral d amag e c ont i nues whi l e the re i s no bl ood fl ow.

Drugs Few drugs are neces sary for fi rst l i ne cardi ac arrest manag ement. Drugs shoul d b e gi ven vi a a l a rge ve i n si nce vas oconst ri cti on and poor fl ow creat e d el a y i n i nje cti ons gi ven vi a s mal l p eri pheral v ei ns reac hi ng t he central ci rcul at i on. Acc ess shoul d b e s ecured earl y duri ng t he res usc i t ati on; i f venous ac ces s c annot be sec ure d d oub l e or tri pl e d ose s of drug s may b e g i ve n v i a the end otrac heal t ube.

Epinephrine The α constri c tor effect s pre domi nate d uri ng cardi ac arres t, hel pi ng t o m ai ntai n d i as tol i c bl ood press ure and t hus coronary and ce reb ral pe rfusi on. Epi ne phri ne shoul d b e g i ve n i rre spe cti ve of rhy thm at 1m g (10ml of 1:10, 000 sol ut i on) ev ery 10 CPR se que nce s.

Vasopressin A rec ent random i z ed c ont rol l e d t ri al comp ari ng vas opres si n and e pi nephri ne s how ed i mp rov ed outc ome s w i th vas opress i n for pati ent s i n asys tol e.

Atropine A s i ngl e 3m g dose i s gi ven earl y i n asy st ol e .

Calcium chloride Use d i n e l ec tromec hani c al di s soc i at i on i f there i s hyperkal aem i a, hy poc al c aem i a or cal ci um antagoni st us e. A d ose of 10m l of a 10% sol ut i on i s usual. The mai n di s adv ant age of cal ci um i s the re duc ti on of reperfusi on of i schaemi c brain and promoti on of c ytosol i c cal ci um acc umul at i on duri ng c el l de ath.

Bicarbonate Onl y used i f re sus ci tat i on i s prol ong ed t o c orrec t t emp orari l y a potenti a l l y l e thal p H. A d ose of 50ml of 8.4% sol ut i on i s gi ven. The m ai n di sad vantag e i s t hat i ntracel l ul ar and resp i ratory aci dos i s are ex ace rbated unl es s v ent i l a ti on i s i nc re ase d and t he cause of the met abol i c ac i d osi s i s not corre cte d. P.273

Key trial W enzel V for the Europ ean Re sus ci t ati on Counci l Vas opress or duri ng CPR s tud y. A c omp ari son of vas opress i n and e pi nephri ne for out -of- hosp i tal c ard i op ul monary res us ci t ati on. N Eng l J Med 2004; 350:105–13

P.274

Fluid challenge Hyp ovol ae mi a mus t be t re ated urgentl y t o av oi d the s eri ous c ompl i c ati on of org an fai l ure. An ade quat e c i rcul ati ng vol ume must be provi d ed before consi deri ng ot her me thods of c i rcul atory sup port. Cl i ni cal si gns of hy pov ol a emi a (re duc ed ski n t urg or, l ow C VP, ol i guri a, tac hyc ard i a and hyp ote nsi on) are l ate i ndi cat ors . Li ft i ng t he l egs of a sup i ne pat i ent and wat chi ng for an i m provem ent i n the c i rc ul a ti on i s a us eful i nd i cator of hy povol ae mi a . A hi gh i ndex of sus pi ci on m ust be mai nt ai ned; a norm al heart rat e, bl ood pre ssure and CVP d o not e xcl ud e hy pov ol a emi a and t he CVP i s parti cul arl y unrel i abl e i n p ul m onary vas cul ar di s eas e, ri ght ventri cul ar di se ase , i sol ate d l eft ventri cul ar fail ure and val vul ar heart di seas e. The ab sol ute CVP or PAWP are al so di ffi cul t t o i nte rp ret si nce pe ri p heral venoconst ri cti on may mai ntain the se fi l l i ng pre ssures de spi te hyp ovol ae mi a ; i nde ed, they m ay fal l i n resp ons e t o fl ui d. The re sponse to a fl ui d chal l eng e i s t he safest met hod of as ses sme nt.

Choice of fluid The ai m of a fl ui d chal l eng e i s t o p rod uce a s i g ni fi cant (200ml ) and rap i d i nc rease i n pl a sma vol um e. Col l oi d fl ui ds

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are i d eal ; a ge l at i n sol uti on i s re com mend ed for short te rm pl a sma vol um e e xpansi on i n si m pl e hy povol ae mi a , and hyd rox yet hyl st arc h w here t here i s a probabi l i t y of capi l l a ry l eak. Pack ed red ce l l s have a hi gh haemat oc ri t and d o not ad equate l y expand the pl asm a v ol ume. Cryst al l oi d fl ui d s are rap i d l y l os t from the c i rc ul ati on and do not gi ve a rel i a bl e i ncre ase i n pl asm a v ol ume.

Assessing the response to a fluid challenge Ide al l y, the re sponse of CVP, or stroke vol ume and PAWP, s houl d be moni tored duri ng a fl ui d chal l eng e. Fl ui d chall eng es s houl d be rep eat ed whi l e the re sponse sugge sts conti nui ng hy povol ae mi a . Howe ver, i f s uch moni t ori ng i s not av ai l abl e i t i s reasonabl e t o as ses s t he cl i ni cal resp ons e to up to tw o fl ui d c hal l enges (200m l e ach).

CVP response The chang e i n C VP afte r a 200ml fl ui d c hal l enge depe nds on the s tarti ng bl ood v ol ume (se e fi gure). A 3mm Hg ri se i n CVP re pre sents a s i gni fi cant i nc rease and i s probabl y i ndi cat i ve of an ade quate c i rcul ati ng vol ume . Howe ver, a pos i t i ve re sponse may somet i me s occur i n t he vas oconst ri cte d p ati ent wi th a l ower bl ood vol um e. It i s i mp ort ant t o ass ess the c l i ni c al res ponse i n add i t i on; i f i nade quate, i t i s ap propri at e t o m oni tor st rok e v ol ume and PAW P b efore furthe r fl ui d challe nge s or c ons i de ri ng furthe r c i rc ul atory sup port.

Stroke volume and PAWP response In the i nade quatel y fi l l ed l eft v ent ri cl e a fl ui d challe nge wi l l i ncre ase the s troke v ol ume. Failure to i nc re ase the stroke vol um e w i th a fl ui d challe nge may represe nt an i nadequate chal l enge, parti cul arl y i f t he PAW P fai l s t o ri s e si gni fi c ant l y (3m mHg ). T hi s i ndi cat es that c ard i ac fi l l i ng was i nad equate and the fl ui d c hal l e nge shoul d b e repeated . Suc h a re sponse may also be see n i n ri g ht heart fai l ure, peri c ard i al tamponad e and m i tral st enosi s . It i s i mport ant to moni tor s troke vol ume rathe r t han cardi ac out put duri ng a fl ui d c hal l enge. If the heart rate fal l s ap propri ate l y i n res ponse to a fl ui d c hal l enge the cardi ac out put may not i nc rease des pi t e an i ncreas e i n s troke vol ume . P.275

CVP and stroke volume response to fluid challenge

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See also: Central v enous cat het er— use , p 114; Pul m onary art ery cat het er—us e, p118; C ard i ac output—t hermod i l uti on, p122; Cardi a c outp ut— other i nvasi ve, p124; Cardi ac out put —non-i nvasi v e (1), p126; Cardi a c outp ut—non-i nvas i ve (2), p128; Lac tat e, p170; Col l oi ds, p180; Hyp ote nsi on, p312; Ol i guri a , p 330; Met abol i c aci d osi s, p434; D i ab eti c ket oac i dosi s , p 442; Syst emi c i nfl amm ati on/mul ti organ fai l ure, p 484; Sep si s and s ept i c shock —treat ment, p486; Burns —fl ui d manag ement, p510; Post -op erati v e i nte nsi ve care, p534


Ed itors:


Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Resp ir a tor y D iso r de r s

Respiratory Disorders Dyspnoea Defi ne d as d i ffi cul t y i n b reathi ng. The resp i ratory rate may b e i ncreas ed or dec reased , t hough t he res pi rat ory effort i s us ual l y i nc reased wi th the us e of ac ces sory m usc l e s. The pat i e nt may show s i gns of p rog res si v e fati gue and

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i mp ai red gas ex change .

Commoner ICU causes Respiratory

respiratory failure

Circulatory

heart failure, hypoperfusion, pulmonary embolus, severe anaemia

Metabolic

acidosis

Central

stimulants, e.g. aspirin

Anaphylactic

upper airway obstruction, bronchospasm

Psychiatric

hysterical

Principles of management 1. O 2 the rap y t o maint ai n SaO 2 (i d eal l y >90–95%) 2. Correc t ab normal i t y where possi bl e 3. Sup port t herapy unti l re cov ery m echani cal , e .g. pos i t i ve press ure ve nti l at i on, CPAP p harmac ol ogi c al tre atm ent , e .g. bronc hod i l ators, vas odi l a tors 4. Rel i eve anxi e ty A p syc hi atri c cause of dys pnoea i s onl y made aft er exc l us i on of ot her treat abl e c aus es. Dual c o-e xi s ti ng p athol ogi es shoul d be consi dered, e. g. c hes t i nfect i on and hypov ol a emi a. P.279

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Ai rway obs truct i on, p 280; Res pi rat ory fai l ure, p282; At el e ctasi s and p ul m onary col l ap se, p284; Chroni c ai rfl ow l i m i t ati on, p286; Acute che st i nfect i on (1), p288; Acut e che st i nfect i on (2), p290; Acute res pi rat ory di stress sy ndrome (1), p 292; Ac ute re spi ratory d i st res s s ynd rom e (2), p294; Ast hma—ge neral manage ment , p 296; Pneumot horax, p300; Pul monary em bol us, p308; He art fai l ure—ass ess ment, p324; Heart fail ure —manag ement, p326; Acute weaknes s, p368; Sal i c yl a te poi soni ng , p 454; Anaemi a, p400; Pos t-op erati ve i nt ens i ve care, p534 P.280

Airway obstruction Causes In t he l umen, e. g. forei g n b ody , b l ood c l ot , v omi tus , s put um pl ug In t he wal l , e.g . e pi g l ot ti ti s , l arynge al oed ema, anaphyl a xi s , neop l as m Out si d e t he wal l , e.g . t rauma (fac i al , neck ), thy roi d m ass , haematom a

Presentation In s pontaneousl y breat hi ng pat i ent: s tri dor, dys pnoea, fat i g ue, cy anos i s In v ent i l ate d p ati ent (due t o i ntral umi nal ob struct i on): rai sed ai rway p res sures , d ecreas ed t i d al vol ume , hypoxae mi a , hypercapni a

Diagnosis Ches t and l at eral neck X-ray Fi breop ti c l ary ngoscopy/bronchosc opy CT s can

Management

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Presentation outside ICU/operating theatre: 1. Hi g h FIO 2 2. If c ol l ap sed or i n ext re mi s : i mmed i ate orot rache al i nt ubati on. If i mp oss i bl e, eme rge ncy cri c othyroi dotom y or trache ost omy. 3. If s ymp tom ati c b ut not in ex tre mis : c ons i de r c aus e and tre at as app rop ri a te, e. g. fi b reopti c or ri g i d bronchosc opy for remov al of forei g n b ody, surg ery for t hyroi d mas s. El ect i ve orotracheal i ntub ati on or trache ost omy may be re qui red . 4. Wi t h acut e ep i g l ot ti t i s , t he use of a t ong ue depres sor or nasendos cop y may p rec i pi tate comp l e te obst ructi on so shoul d be und ert ake n i n an operati ng the atre read y t o p erform eme rge ncy trac heos tom y. The re sponsi bl e org ani sm i s usual l y Haemop hil us influenzae and earl y tre atm ent wi th chl orampheni col s houl d be b egun. Ac ute epi gl otti ti s i s recogni sed i n ad ul t s, eve n t hos e of ad vanced ag e. 5. Cons i de r Hel i ox (79%He /21%O 2 ) alone or as a suppl eme nt to oxyg en to red uce vi scosi t y and i mp rov e airfl ow .

Presentation within ICU/operating theatre: 1. If i nt ubated : High FIO 2 Pass sucti on cat het er dow n t he e ndotracheal tube, ass ess ease of pas sag e and t he contents suc ti one d. If t he t ube i s patent, att emp t repe ated suct i on i nterspe rs ed w i th 5m l b ol uses of 0. 9% sal i ne . Urge nt fi b reopti c b ronchoscopy may be nec ess ary for d i ag nos i s and , i f p oss i bl e, rem oval of a forei gn b ody . If t hi s cannot b e removed by fi b reopti c b ronchosc opy , urge nt ri g i d bronchosc opy shoul d b e p erform ed by an e xpe ri e nce d operator. If the end otrac heal t ube i s obs truct ed, re mov e t he t ube , oxyg enate b y face mask t hen rei ntub ate . 2. If not i nt ub ated : As for out -of-ICU prese ntati on. If rece ntl y e xtubat ed, consi der l a ryngeal oede ma. Pos t-e xtubat i on l a ryngeal oede ma i s unpred i ct abl e t hough occ urs more com monl y afte r p rol ong ed or rep eat ed i nt ubati on; the i nci denc e m ay be red uce d b y p rop er tet heri ng of the e ndot rache al tub e and p rev ent i on of ex ces si v e c oug hi ng. If di a gnosed (by nase ndos copy), de xam ethasone 4mg × 3 dos es ove r 24h may re duc e t he s wel l i ng though re -i ntub ati on i s often ne ces sary i n t he i nteri m. P.281

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; Endotrache al i nt ubati on, p36; Trac heot omy , p 38; Mi ni t rac heotom y, p 40; Fi bre opt i c bronc hos cop y, p 46; Bronc hod i l ators, p186; Steroi d s, p262; Ate l ec tas i s and pul monary col l aps e, p 284; Chroni c ai rfl ow l i m i tati on, p286; Ast hma—general m anagem ent , p 296; Haemopty si s , p 304 P.282

Respiratory failure Defi ne d as i mpaire d p ul m onary gas ex change l e adi ng to hypoxae mi a and/or hy percap ni a.

Commoner ICU causes

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Central

Cerebrovascular accident, drugs (e.g. opiates, sedatives), raised intracranial pressure, trauma

Brainstem/spinal cord

Trauma (at or above phrenic level), tetanus, Pickwickian syndrome, motor neurone disease

Neuropathy

Guillain–Barré, critical illness polyneuropathy

Neuromuscular

Muscle relaxants, organophosphorus poisoning, myasthenia gravis

Chest wall/muscular

Flail chest, heart failure, myopathy (including critical illness and disuse myopathy)

Airways

Upper airways obstruction, airway disruption, asthma, anaphylaxis

Parenchymal

Pneumonia, ARDS, fibrosis, pulmonary oedema

Extrapulmonary

Pneumothorax, pleural effusion, haemothorax

Circulatory

Pulmonary embolus, heart failure, Eisenmenger intracardiac shunt

Types of respiratory failure Typ e I: Hypox aem i c— oft en parenc hym al i n ori gi n Typ e II: Hyp oxae mi c , hype rcapni c—ofte n m echani cal i n ori g i n

Principles of management 1. Ens ure SaO 2 com pat i bl e w i th survi val (i .e. us ual l y >80%, pre ferabl y >90–95%) 2. Correc t ab normal i t y where possi bl e, e.g . drai n p neumothorax, rel i e ve/b ypass obs truct i on. 3. Sup port t herapy unti l re cov ery Posi ti v e p res sure v ent i l ati on N on-i nvasi ve res pi ratory sup port Pharmac ol ogi c al tre atm ent , e .g. bronc hod i l ators, ant i b i ot i cs , opi a te ant agoni s ts , resp i ratory s ti mul ant G ene ral me asures , e .g. hyd rat i on, ai rway hum i di fi cat i on, removal of sec re ti ons, physi otherapy, b ronchoscopy 4. Unl ess the pati ent i s sy mpt omat i c (e. g. drowsy , d ysp noe i c) whi l e be i ng me chani c al l y v ent i l a ted , t he PaCO 2 may be l eft el evated to mi ni m i se ve nti l at or traum a (p erm i ss i v e hy percap ni a).Hig her PaCO 2 v al ues may al so be tol erated i f the pati ent i s chroni call y hypercapni c (Type II resp i ratory fai l ure ). P.283

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; C ont i nuous posi t i ve ai rway p res sure, p26; Non-i nvas i ve res pi rat ory support, p32; Endot rache al i nt ubati on, p36; Pul se ox i me try , p 90; Bl ood gas anal y si s, p100; Re spi ratory sti mul ants, p188; Opi oi d anal g esi cs , p 234; Sed ati ves , p 238; Basi c resusc i tati on, p270; Dy spnoea, p278; Ai rw ay obs truct i on, p 280; At el e ctasi s and p ul monary col l a pse , p 284; C hroni c ai rfl ow l i mi t ati on, p286; Ac ute chest i nfec ti on (1), p 288; Acut e c hes t i nfe ct i on (2), p 290; Ac ute re spi ratory d i st res s s ynd rome (1), p292; Acut e resp i ratory di s tress syndrome (2), p294; Asthma— general m anag eme nt, p296; Pneumothorax , p 300; Pul m onary emb ol us, p308; Acute weaknes s, p368; Gui l l ai n–Barré s ynd rom e, p384; My ast heni a gravi s , p 386; IC U neuromuscul ar di sorde rs, p388; Poi soni ng —ge neral pri nc i pl es , p452; Sedati ve p oi s oni ng , p458; Organophosp hat e poi s oni ng, p472; Sys tem i c i nfl am mat i on/mul ti organ fai l ure, p484; HIV rel at ed d i s eas e, p 488; Mul t i pl e t rauma (1), p500; Mul ti pl e trauma (2), p502; Head i njury (1), p504; He ad i nj ury (2), p 506; Spi nal cord i nj ury, p 508; Ne ar drowni ng, p526; Pain, p532; Pos t-operati ve i nt ens i ve care, p534 P.284

Atelectasis and pulmonary collapse A c ol l ap sed l obe or s egm ent i s us ual l y vi si b l e on a CXR. Mac roatel ect as i s i s al s o e vi d ent as vol um e l oss . In mi c roatel ec tas i s the CXR may b e norm al but A-aDO 2 wi l l be hi gh. At el e ctasi s reduc es l ung comp l i anc e and PaO 2 , and i nc re ase s work of bre athi ng . T hi s may resul t i n poor g as exc hange, i ncre ase d airw ay pre ssures , reduced ti dal vol ume and , i f s eve re, ci rcul a tory c ol l aps e.

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Causes Col l aps ed l ob e/s egm ent —bronc hi a l obst ructi on (e. g. sputum re tenti on, forei g n b ody , bl ood cl ot , vomi t us , mi s pl a ced endot rac heal t ube ) Macroat el ect asi s—air space com pre ssi on by heavy, oed ematous l ung ti ss ue, ext ernal com press i on (e. g. pl e ural effusi on, hae mot horax), sp ut um ret ent i on Mi c roatel ect asi s—i nadequate de pth of re spi rat i on, ni t rog en washout by 100% oxyg en wi t h s ubs equent ab sorpti on of oxyg en occ urri ng at a rat e g reater than rep l eni shment.

Sputum retention Exc ess mucous (sputum ) norm al l y s ti m ul a tes coughi ng . If c i l i ary c l earance i s red uc ed (e.g . s mok i ng , s edati v es) or muc ous vol um e i s e xce ssi ve (e.g . asthma, bronc hi ect asi s, cys ti c fi brosi s, chroni c bronchi ti s) sputum re tenti on m ay occ ur. Sput um ret ent i on may al so be the re sul t of i nad equate coughi ng (e .g. chroni c obs truct i ve l ung di s eas e, pai n, neurom usc ul ar di s eas e) or i nc reased muc ous vi sc osi ty (e. g. hypovol aem i a, i nade quate humi di fi c ati on of i ns pi red gas ).

Preventive measures Sputum hyd rati on—m ai ntenanc e of sy ste mi c hy drati on and hum i di fi cat i on of i nspi red gases (e .g. neb ul i ze d sal i ne /bronc hod i l ators, heated water bath, heat m oi s ture exchang i ng fi l t er). Coug h—requi res i ns pi rati on to near t otal l ung c apac i t y, gl otti c c l os ure, contracti on of abd omi nal mus cl es and rap i d openi ng of the g l ot ti s. Dynami c c omp res si on of t he airways and hi gh ve l oc i t y ex pi rat i on exp el s s ecreti ons . The proces s i s l i m i te d i f t otal l ung c apac i t y i s reduced , abdomi nal mus cl e s are weak , p ai n l i mi ts contracti on or smal l ai rway s c ol l aps e on ex pi rat i on. It i s usual t o fl ex the abdomen on coughi ng and thi s shoul d be si mul at ed i n sup i ne pat i e nts by drawi ng the kne es up. Thi s al s o l i m i ts pain i n pat i ents wi t h an uppe r abdomi nal wound. Phys i ot herap y—post ural d rai nag e, percus si on and vi b rat i on hy peri nfl a ti on, i nt erm i t tent p osi ti v e p res sure bre athi ng , i nce nti ve spi rom etry or m anual hyp eri nfl ati on. Mai ntenanc e of l ung vol um es—inc reased V T CPAP, PEEP, pos i t i oni ng to re duc e c omp res si on of l ung ti ss ue b y oede ma.

Management Spe ci fi c manage ment d epe nds on the c aus e and s houl d be correc ti ve. Al l m eas ure s t ake n for p re vent i on s houl d conti nue. If there i s l obar or s egme ntal c ol l ap se wi t h obst ruc ti on of p rox i mal airw ays , b ronchoscopy may be use ful to al l ow di rec ted sucti on, forei gn bod y remov al and saline i ns ti l l at i on. Pati ent s wi t h hi gh FIO 2 m ay det eri orate due to the effec ts of e xce ssi ve l av age or sucti on red uc i ng mi nut e v ent i l a ti on. P.285

See also: Oxy gen therapy, p2; Vent i l a tory s upp ort —i ndi cat i ons, p4; IPPV—compl i cati ons of venti l at i on, p 14; Posi ti v e e nd exp i ratory p res sure (1), p22; Pos i ti ve end exp i ratory pre ssure (2), p24; Conti nuous p osi ti ve airway pre ssure, p26; Non-i nvas i ve re spi rat ory s upp ort , p 32; Lung re crui t ment, p28; Endot rac heal i ntubat i on, p 36; Mi ni t rac heotom y, p 40; Fi b reopti c bronchosc opy , p 46; Ches t p hys i ot herap y, p 48; Bl ood gas anal ysi s, p100; Bronchodi l at ors , p 186; Chroni c ai rfl ow l i m i tati on, p286; Acut e c hes t i nfe ct i on (1), p 288; Ac ute chest i nfec ti on (2), p290; Pos t-operati ve i nt ens i ve care, p534 P.286

Chronic airflow limitation Many p ati ent s requi ri ng IC U ad mi s si on for a c omm uni ty acq ui red pne umoni a have c hroni c resp i ratory fai l ure. An acute exacerbat i on (whi c h m ay or m ay not be i nfect i on-rel a ted ) resul ts i n de com pensat i on and s ympt omati c det eri orati on. Infec ti ons res ul t i ng i n acut e e xace rb ati ons i ncl ude vi rus es, Hae mop hil us influe nzae, Kle bsi ell a and St aph. aureus i n addi ti on t o Strep. pneumoniae, Myc opl asm a pneum oni ae and Legi one lla pneum ophi la. Othe rwi se, pat i ents wi t h c oi nci dental chroni c ai rfl ow l i m i tati on (CAL) are adm i tt ed for ot her re asons or as a prophyl act i c measure i n v i ew of the i r l i mi t ed res pi rat ory funct i on, e .g. for el ec ti v e p ost -ope rat i v e ve nti l a ti on.

Problems in managing CAL patients on the ICU Di s abi l i ty d ue to chroni c i l l he al t h Fati gue , m usc l e weakne ss and dec re ased physi ol ogi cal re serve l eadi ng t o e arl i er ne ed for ve nti l at ory support , i nc reased di ffi cul ty i n weani ng, and great er phy si c al dep end enc y on s upp ort therapi e s Psyc hol ogi cal d epe ndency on sup port t herapi es More prone to pneum othoraces Usuall y have gre ate r l eve l s of sputum producti on Ri ght v ent ri cul ar dys functi on (cor p ul m onale)

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Notes Dec i si ons on whether or not to i ntub ate shoul d b e made i n consul tat i on wi th the pati ent (i f possi bl e), the fami l y, and a resp i ratory phys i c i an wi th knowl e dge of the pati e nt. The p ati ent shoul d b e g i ve n t he b ene fi t of the d oub t and i nt ub ated i n an ac ute si tuati on where a preci se hi story and quali ty of l i fe i s not know n. Tri al s of non-i nvas i v e ve nti l a tory s upp ort ± res pi ratory sti mul ants suc h as d oxep ram have shown c ons i d erabl e suc ces s i n avoi di ng i ntubat i on and m echani cal ve nti l at i on. Acc ept l ower targe t l eve l s of PaO 2 Acc ept hi ghe r t arg et l ev el s of PaCO 2 i f pat i ent i s k now n or s usp ect ed to have chroni c CO 2 retenti on on t he bas i s of e l ev ate d p l as ma bi c arb onate l ev el s on adm i s si on t o hosp i tal.

Weaning the patient with CAL An earl y tri al of ext ubati on m ay b e w ort hwhi l e be fore t he p ati ent b ecom es venti l at or-d epe nde nt. Weani ng may b e a l engt hy p roc edure . D ai l y t ri a l s of spontaneous bre athi ng may reveal fast er-than-anti ci pat ed progre ss. Prov i d e pl ent i ful enc ourage ment and p syc hol ogi cal s upp ort . Sett i ng dail y t arg ets and earl y mobi l i s ati on may be advantageous. Do not ti re by p rol onged spontaneous bre athi ng . C ons i de r g rad ual l y i ncre asi ng peri od s of s pontaneous b reathi ng i nt ers persed by pe ri ods of res t. Ens ure a good ni ght's sl eep . Use pat i ent appe arance and l ack of sym ptoms (e. g. tac hyp noea, fati gue ) rather than s pec i fi c b l ood g as val ues to judg e t he durati on of spontaneous bre athi ng . Earl y trache ost omy may be nefi t when di ffi cul ty i n we ani ng i s exp ect ed. The pat i ent m ay cop e b ett er wi t h a tracheos tom y mask than C PAP. Add i ti on of ext ri nsi c PEEP or CPAP m ay p rev ent earl y ai rways cl osure and thus reduce the work of b reathi ng . Howe ver, t hi s shoul d b e d one wi th cauti on b ecause of the ri sk of i nc re ased ai r trappi ng. Cons i de r heart fai l ure as a cause of di ffi c ul t y i n w eani ng . P.287

Key trials Brochard L, et al . Noni nvas i ve venti l at i on for acut e e xac erb ati ons of chroni c obs truct i ve pul monary di se ase. N Engl J Med 1995; 333:817–22

Ant one l l i M, et al . A compari s on of noni nv asi ve p osi ti ve-pre ssure venti l ati on and conve nti onal m echani cal v ent i l ati on i n pat i ents wi t h acut e resp i ratory fai l ure. N Engl J M ed 1998; 339:429–35

Eps tei n SK, Ci ubotaru RL. Indep end ent effec ts of e ti ol ogy of fai l ure and t i me to re i nt ubati on on outc ome for p ati ents fai l i ng e xtubat i on. Am J Res pi r Cri t Care M ed 1998; 158:489–93

P.288

Acute chest infection (1) Pat i ents may prese nt to i nt ens i ve care as a resul t of an acute c hes t i nfect i on or may de vel op i nfect i on as a com pl i cati on of i nte nsi ve care manag eme nt. Ty pi c al features i nc l ude feve r, cough, purul ent sp utum p rod uct i on, bre athl es sness , p l euri t i c pain and bronc hi a l b reathi ng. Urgent i nve sti gati on i ncl ude s arte ri al gas es, CXR, b l ood c ount and cul ture s of bl ood and s put um. In communi t y acqui re d p neumoni a, ac ute phase ant i body ti t re s s houl d be take n.

Diagnosis and initial antimicrobial treatment Bas i c re sus ci t at i on i s re qui red i f there i s c ard i oresp i ratory c omp rom i s e. App rop ri a te tre atm ent of the i nfe cti on dep end s on CXR and cul ture fi ndi ngs, al though em pi ri c ‘b est guess ’ anti bi oti c t reatment m ay be starte d b efore cul ture res ul ts are avail abl e. Tre atm ent i ncl udes physi otherapy and me thods to aid sp utum c l earance.

Clear CXR Ac ute bronc hi t i s i s as soc i at ed wi t h c oug h, muc oi d sp utum and w hee ze. In previ ous l y healthy p ati ent s a vi ral ae ti ol og y i s mos t l i k el y and there i s often an up per re spi ratory p rod rom e. Symp tom ati c rel i ef i s us ual l y al l t hat i s re qui red . Li kel y organi s ms i n acute on c hroni c b ronchi ti s i ncl ude St rep . p neumoni ae, H. in. uenz ae or Staph. aureus. App ropri ate anti b i ot i c s i ncl ude ce furoxi me or amp i ci l l i n and .ucl oxac i l l i n. Vi ral p neumoni a may be confus ed by the pre sence of bac teri a i n the sp utum b ut sec ond ary bacte ri a l i nfect i on i s common.

Pulmonary cavitation on CXR Cav i tati on s houl d al e rt to the possi bi l i t y of anaerob i c i nfect i on (s put um i s oft en foul s mel l i ng). Staph. aureus, K.

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pne umoniae or t ube rc ul osi s are also as soc i at ed wi t h c avi tat i on. App rop ri a te ant i bi oti cs i ncl ude met roni dazol e or cl i nd amyc i n for anaerobi c i nfect i on, fl uc l ox aci l l i n for Stap h. aureus and ce ftazi d i m e and g ent ami ci n for K. pne umoniae. A fore i gn body or pul monary i nfarct shoul d al so be consi d ered w here t here i s a si ngl e absc ess .

Consolidation on CXR The re cent hi st ory i s i mportant for de ci d i ng the c aus e of a pne umoni a : Hosp i t al acq ui red pne umoni a —enteri c (Gram neg ati ve) organi sm s t reated wi th ceftaz i di me and gentam i c i n, Staph. aureus t reated wi th ceftazidi me and gentam i c i n, St aph. aure us tre ate d w i th fl ucl oxaci l l i n (or tei cop l ani n/vancomy ci n i f mul t i re si stant). Rece nt asp i rati on— anae rob i c or Gram neg ati ve i nfect i on treat ed wi t h c l i ndam yci n or c efurox i me and metroni dazol e. Comm uni ty acq ui red pne umoni a i n a pre vi ousl y heal thy i ndi v i dual —Strep. pneumoniae (oft en l ob ar, ac ute ons et) or atyp i c al pne umoni a (i nsi di ous ons et, known com muni ty outbreak s, renal fai l ure and el e ctrol yte di sturbance i n Leg i onnai re' s d i se ase ). App rop ri ate ant i b i ot i c the rap y i s c efurox i me and c l ari t hromyc i n. Pneumoni a com pl i cat i ng i nfl uenza—Staph. aureus t reated wi th fl ucl oxac i l l i n. Both Staph. aureus and H. infl uenzae are c omm on i n those deb i l i tat ed by chroni c d i s eas e (e .g. al cohol i sm, di abe tes , c hroni c airfl ow l i m i tati on or t he el d erl y). Immunos upp res se d—op portuni s ti c i nfec ti ons (e. g. tub ercul osi s, Pneumocys ti s c ari nii Herpes vi ruses , C MV or fung i ). P.289

Antimicrobial treatment

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Drug

Dose

Organism

Acyclovir

10mg/kg 8-hrly IV

Herpes viruses

Amphotericin B

250mg–1g 6-hrly IV

Fungi

Ampicillin

500mg–1g 6-hrly IV

H. influenzae Gram negative spp.

Benzylpenicillin

1.2g 2–6-hrly IV

Strep. pneumoniae

Ceftazidime

2g 8-hrly IV

K. pneumoniae Ps. aeruginosa Gram negative spp.

Cefuroxime

750mg–1.5g 8-hrly IV

Strep. pneumoniae H. influenzae Gram negative spp.

Clarithromycin

500mg 12-hrly IV (250–500mg 12-hrly PO if less severe)

Atypical pneumonia Strep. pneumoniae

Erythromycin

1g 6–12-hrly (500mg 6-hrly PO if less severe)

Atypical pneumonia Strep. pneumoniae

Clindamycin

300–600mg 6-hrly IV

Anaerobes Gram negative spp.

Cotrimoxazole

120mg/kg/day IV

Pneumocystis carinii

Flucloxacillin

2g 6-hrly IV (500mg–1g 6-hrly PO if less severe)

Staph. aureus

Ganciclovir

5mg/kg 12-hrly IV (over 1h)

CMV

Gentamicin

1.5mg/kg stat IV(thereafter by levels—usually 80mg 8-hrly)

K. pneumoniae, Ps. aeruginosa Gram negative spp.

Metronidazole

500mg 8-hrly IV or 1g 12-hrly PR

Anaerobes

Teicoplanin

400mg 12-hrly for 3 doses then 400mg daily


Vancomycin

500mg 6-hrly (monitor levels)


Linezolid

600mg 12-hrly IV or PO


Key trial Ire gui M et al. Cl i ni cal i m portance of del ays i n the i ni t i at i on of ap propri at e anti bi oti c treat ment for v ent i l ator-associ a ted pneumoni a. C hes t 2002; 122: 262–8

P.290

Acute chest infection (2) Laboratory diagnosis The fol l owi ng s amp l es are requi re d for l ab oratory d i ag nos i s : Sputum (e. g. cough spe ci m en, endot rac heal t ube as pi rate , p rot ect ed brush sp eci men, bronchoal v eol ar l av age spec i m en) Bl ood cul tures Serol ogy (i n com muni t y ac qui re d p neum oni a)

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Uri ne for ant i g en t es ts (i f Leg ionell a, Cand id a or p neumoc occ us sus pec ted ) In sev ere pneum oni a, bl i nd ant i bi oti c the rap y s houl d not be wi t hhe l d whi l e awaiti ng re sul ts. Sp eci mens s houl d , how ever, be t ake n b efore starti ng ant i bi ot i cs . Mi c robi ol og i cal y i el d i s usual l y v ery l ow, e spe ci al l y i f anti bi oti c t herapy has st arted before sampl i ng . Whe re cul tures are p osi ti v e t here i s ofte n m ul t i pl e g row th. Se parati ng pat hog eni c org ani sms from c ol oni si ng org ani sms may b e d i ffi cul t. In hos pi t al ac qui red pneum oni a, k now n nosocom i al pathogens are t he l i kel y s ource, e. g l ocal Gram ne gat i ve fl ora, MRSA.

Continuing treatment Ant i b i ot i cs s houl d be adjuste d accordi ng to sensi ti v i ti es onc e avai l ab l e. Failure to res pond t o t reatme nt i n 72h shoul d prompt consi derat i on of i nfect i ons more c ommon i n t he i mm unocom promi s ed or other di a gnoses . Hos pi t al -acq ui red pneumoni a requi re s t reatme nt wi t h appropri at e anti bi oti cs for 24h after s ympt oms subs i de (us ual l y 3–5 days). Afte r t hi s pe ri od c ul tures shoul d be re peated (off anti bi oti cs i f the re has bee n i mprove ment). Some ICUs wi l l use l onger c ourses —a rec ent mul ti centre s tud y s howe d no d i ffere nce i n outcome b etw een 8 and 15 day s' treatm ent . In aty pi c al or pne umococ cal pneum oni a, 10–14 day s of anti b i oti c treat ment i s usual (though no evi de nce bas e e xi s ts to i nd i c ate the op ti mal durat i on of the rap y). P.291

Key trial C has tre J, for t he PneumA Tri al Group . C ompari son of 8 v s 15 d ays of ant i b i ot i c the rap y for venti l ator-associ a ted p neumoni a i n adul ts : a randomi z ed tri al . JAMA 2003; 290:2588–98

P.292

Acute respiratory distress syndrome (1) ARD S i s the re spi rat ory component of mul t i pl e organ d ysfunc ti on. It may be predom i nant i n the cl i ni cal p i c ture or b e of l es ser cl i ni cal i mport anc e i n rel a ti on t o d ysfunc ti on of ot her organ sy st ems.

Aetiology As part of t he exagge rat ed i nfl am mat ory re sponse fol l owi ng a maj or exog enous i ns ul t w hi c h m ay b e e i ther di rec t (e. g. che st trauma, i nhalat i on i njury) or di s tant (e.g . p eri toni t i s, major hae morrhage, burns ). Hi s tol og y reveals agg reg ati on and ac ti v ati on of neutrophi l s and pl ate l et s, pat chy endot hel i a l and alve ol a r d i s rup ti on, i nt ersti ti al oed ema and fi brosi s. Cl a ssi cal l y , t he acut e p has e i s c haract eri se d b y i ncreas ed cap i l l ary pe rme abi l i ty and the fi b rop rol i ferati v e p has e (afte r 7 days) by a p red omi nant fi brot i c reacti on. Howeve r, more rece nt dat a w oul d s ugg est suc h d i s ti ncti ons are not so cl e ar-cut ; t here m ay be e vi d enc e of m ark ers of fi b rosi s as earl y as day 1.

Definitions Acute lung injury (ALI) PaO 2 /FIO 2 ≤ 300mmHg (40kPa) Regardl ess of l e vel of PEEP Wi t h b i l ateral i nfi l trates on CXR Wi t h p ul m onary art ery wed ge pre ssure Tab le of Co n te n ts > Car dio vasc u la r Diso r d er s

Cardiovascular Disorders Hypotension The ov erall pri nc i pl e i n t he managem ent of hy pot ens i on i s to maint ai n the m i ni mum me an art eri al pre ssure that w i l l ens ure ad equate ti ssue p erfusi on. A normal bl ood press ure d oes not guarante e an adequate cardi ac out put and ci rcul at ory support shoul d ai m t o achi eve ad equate bl ood fl ow as w el l . In ext re mis , t he . rs t l i ne treat ment opti ons shoul d i ncl ude ext ernal cardi ac mas sag e and e pi nephri ne 0.05–0.2m g i ntrave nous b ol uses (1m g i n c ardi a c arre st).

Assessment of hypotension Hyp ote nsi on req ui res treat ment i f t he m ean BP 95mmHg and a sy stol i c p res sure > 180mmHg .

Common causes in intensive care Idi opathi c/e sse nti al Agi tat i on/pain, es pec i al l y whe re mus cl e re l ax ant s are use d Exce ss i ve vas oconst ri cti on, e. g. col d, vas opress or drugs Head i njury, cerebrovascul a r acci dents Drug-rel a ted Di s sec ti ng aneurys m, aorti c c oarctati on Vas cul i ti s, throm bot i c thromb ocy top eni c p urp ura (Pre -)e cl a mps i a Aorti c coarc tat i on (m ay pre sent acut el y i n ad ul t hood) Endocri ne , e .g. phaeoc hromoc ytoma (rare) Renal fai l ure, renal art ery st enosi s (rare ) Spuri ous— und erd amp ed transd uce r s yst em

Indications for acute treatment Hyp ert ens i ve encep hal opathy , heart fai l ure , e cl a mps i a and ac ute di sse cti ng ane urysm are the p ri me i ndi cati ons for rap i d and ag gre ssi ve, al bei t control l e d, red uct i on of bl ood press ure. In other condi t i ons, es pec i al l y chroni c hype rt ens i on and fol l owi ng acut e neurol ogi cal ev ent s, e.g. he ad i nj ury , cerebrovascul a r acci dents, a pre ci p i t ate re duc ti on i n b l ood p res sure m ay adve rs el y affect pe rfusi on l ead i ng t o furt her det eri orati on. Hy pertensi on p ost -ce reb ral ev ent i s not usually treat ed unl ess ve ry hi g h, e.g . m ean BP >140–150m mHg , s yst ol i c BP > 220–230mm Hg. In thi s i ns tance, control l ed and part i al re duc ti on i s mand atory, e. g. usi ng sod i um ni tropruss i d e i nfusi on wi th conti nuous i nv asi ve moni tori ng. In the prese nce of a rai sed IC P, a ce reb ral perfus i on pres sure ≥60–70mm Hg i s usual l y target ed.

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Hypertensive crisis Thi s occ urs when t he pat i ent b ecomes sy mpt omati c (i ncreas i ng drows i ness , s ei z ure s, pap i l l oed ema, reti nop athy) i n the prese nce of el evat ed sys tem i c press ure s. The di ast ol i c BP usual l y e xce eds 120–130mm Hg and the m ean BP >140–150m mHg , al thoug h encep hal opathy can occur at l owe r p res sures .

Principles of management 1. Ade quat e m oni tori ng (i nv asi ve BP, ECG, C VP, CO, uri ne outp ut) 2. Cons i de r p ai n, hypovol aem i a, hy pot hermi a and ag i t ati on, es pec i al l y i f paral y sed . 3. Cons i de r s pec i fi c tre atm ent for, e.g . p haeochromocyt oma, t hyroi d cri s i s, aorti c d i s sec ti on, i nfl am mat ory vasc ul i ti s 4. Sl ow i ntrave nous i nfusi on of ni trate or ni tropruss i de . GTN i s usual l y g i ve n fi rst before consi deri ng sodi um ni t rop rus si de. Ot her op ti ons i nc l ud e l abe tal ol or esm ol ol i nfusi ons , and hydral azi ne (IV or IM ). Sub l i ngual ni fedi pi ne or IV hydral a zi ne m ay som eti mes produce pre ci p i tate fal l s i n BP. Us e c aut i ousl y and s tart wi t h l ow dose s. 5. Ai m to re duc e t o mi l d l y hyp ert ens i ve l e vel s unl e ss a d i ss ect i ng aneurys m i s p res ent where sys tol i c BP shoul d b e l owe red 140ms , axi s 150 i s s ugg est i v e of SVT w hereas sl owe r P wav e rat es may re pre sent a si nus tachy cardi a or at ri al fl utte r w i th bl oc k. T he P w aves are abnormal (fl utte r w aves ) i n atri a l fl ut ter and QRS com pl e xes may be i rreg ul ar i f the bl ock i s vari a bl e . Extreme l y fas t SVT may be due to a re-ent ry pat hway wi th re trograde conduc ti on and pre mat ure ec top i c atri al ex ci tat i on. In W ol ff–Parki ns on–Whi te syndrome the re -entry pathway i nse rt s b el ow the His bundl e al l owi ng rapi d AV c ond uct i on and re-e ntry tac hyarrhyt hmi as. Thi s may be di a gnosed by a s hort PR i nt erv al and a d el t a w ave.

Treatment of tachyarrhythmias Ventricular tachycardia Li doc ai ne, ami odarone or magne si um form the mainstay of drug treatm ent . Overdri ve pac i ng may b e used i f a p aci ng wi re i s i n s itu, c apt uri ng the ve ntri cl e at a paci ng rate hi ghe r t han the arrhythmi a and g rad ual l y red uc i ng the p aci ng rat e. Torsad es de poi nte s m ay be e xac erb ate d b y anti arrhyt hmi cs so mag nes i um or ov erd ri ve p aci ng are safes t.

Supraventricular tachycardia and atrial flutter Caroti d s i nus mass age may b e us ed i n pat i e nts wi th no ri s k of c al c i fi ed atheromat ous carot i d dep osi ts. Ami odarone, ade nos i ne or magne si um are usual l y t he mos t useful drugs i n the cri t i cally i l l . Ve rap ami l m ay be used i f compl exe s are narrow (no ri s k of mi sd i ag nos ed vent ri cul ar tac hyc ardi a ) al though i t and othe r AV nod e bl oc kers s houl d be avoi de d i n re-e ntry t achycardi as.

Atrial fibrillation Ac ute or paroxy smal atri al fi bri l l ati on shoul d be treat ed as for supravent ri cul ar tac hyc ardi a . D i goxi n i s more use ful for chroni c at ri a l fi bri l l at i on and d oes not p rev ent paroxy smal e pi s ode s. P.317

Drug doses and cautions Adenosine

3mg IV as a rapid bolus. If no response in 1min give 6mg followed by 12mg.

Verapamil

2.5mg IV slowly. If no response repeat to a maximum of 20mg. An intravenous infusion of 1–10mg may be used. 10ml CaCl 10% should be available to treat hypotension associated with verapamil. Verapamil should be avoided in re-entry tachyarrhythmias since ventricular response may increase. Life threatening hypotension may occur in misdiagnosed ventricular tachycardia and life threatening bradycardia may occur if the patient has been β-blocked.

Lidocaine

1mg/kg intravenously as a bolus followed by an infusion of 2–4mg/min.

Amiodarone

5mg/kg over 20min then infused at up to 15mg/kg/24h in 5% glucose via a central vein. Avoid with other class III agents (e.g. sotalol) since QT interval may be severely prolonged.

Magnesium

20mmol MgSO 4 over 2–3h. In an emergency it may be given over 5min

See also: Defi bri l l at i on, p 52; ECG moni t ori ng, p108; Ant i arrhythmi c s, p204; Basi c resusci tati on, p270; Cardi ac arrest , p 272; Fl ui d chall eng e, p 274; Hypotensi on, p312; Acute coronary syndrome (1), p320; Hyp erkal aemi a, p420; Hyp okal aem i a, p422; Thy roi d e mergenci e s, p446; Tri cyc l i c anti dep res sant p oi s oni ng, p460; Anaem i a, p400; Py rex i a (1), p518; Pyrexi a (2), p520; Pai n, p532 P.318

Bradyarrhythmias If peri pheral pul ses are not pal pab l e a brady arrhy thm i a req ui res ext ernal cardi ac m ass age and t reatme nt as for asy stol e. For asym ptomat i c bradyc ard i a tre atm ent may not b e requi red other than c l os e moni tori ng and c orrect i on of the cause . T he exc ept i on to thi s i s hi g her de gre es of heart bl ock occ urri ng after an ac ute anteri or my ocardi al i nfarc ti on where p aci ng may be re qui red prophyl a cti cally .

Causes of bradyarrhythmias Whe re pos si b l e the cause of a bradyarrhythmi a shoul d b e t reated . Common c aus es for whi ch sp eci fi c treat ment m ay be req ui red i ncl ude hyp ovol aem i a, hy pot ens i on (m ay also be due t o t he arrhyt hmi a), acute myocardi a l i nfarc ti on, di g oxi n t oxi ci ty, β-b l ocker t oxi ci t y, hyp erk al a emi a, hypothy roi di sm, hy pop i tui tari sm and rai se d i ntracrani al press ure . Di goxi n t oxi ci ty may req ui re tre atm ent wi th ant i di gox i n ant i bodi e s.

Diagnosis of bradyarrhythmias Sinus bradycardia

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Sl ow v ent ri cul ar rat e w i th normal P wav es, normal PR i nte rval and 1:1 AV conducti on.

Heart block Normal P wave s, a p rol ong ed PR i nt erv al and 1:1 AV c ond uct i on sugge st 1° heart bl ock. In 2° he art bl oc k the ventri cl es fai l t o resp ond to at ri a l c ont rac ti on i nt erm i tt ent l y . T hi s may be as soc i at ed wi t h regul ar P wav es and an i nc re asi ng PR i nt erv al unt i l ventri cul ar de pol ari sat i on fail s (M obi tz I or Wenk ebach) or a normal PR i nt erval wi t h reg ul ar fai l ed ventri cul ar de pol ari sati on (Mobi tz II). In the l a tte r c ase the AV c ond uct i on rati o may b e 2:1 t o 5:1. In 3° heart bl ock the re i s compl ete AV di ssoci ati on wi t h a sl ow, i di ove ntri c ul a r rat e.

Absent P wave bradycardia Abs ent P wav es may rep res ent sl ow atri a l fi bri l l at i on or si no-atri al dy sfunct i on. In t he l at te r c ase there wi l l be a sl ow, i di ove ntri c ul a r rate .

Treatment of bradyarrhythmias Hyp oxaemi a must be corre cte d i n all sym ptomat i c bradyc ard i as . F irst l i ne d rug treat ment i s usuall y at ropi ne 0.3m g or gl y cop yrrol ate 200µg i ntravenous l y. If the arrhythmi a fails to re spond, 0. 6mg fol l owed by 1.0mg atropi ne may be gi v en. Failure to res pond t o d rug s requi res tem porary pac i ng. Thi s m ay b e accompl i s hed rapi d l y wi t h an ex ternal sys tem i f there i s haemodynami c c omp rom i se or trans venous l y. Ot her i ndi cat i ons for tem porary pac i ng are shown opp osi te. Hi ghe r d egrees of he art bl ock after an ant eri or my ocardi al i nfarc ti on wi l l usually re qui re permanent paci ng.

Indications for temporary pacing Persi ste nt sym ptomati c bradyc ard i a Bl ack out s as soci a ted wi th 3° heart bl ock 2° heart bl ock RBBB and l eft p ost eri or hem i bl ock Card i ov asc ul ar col l ap se Infe ri or myoc ardi a l i nfarct i on wi th sym ptomat i c 3° heart bl ock Ant eri or myocardi a l i nfarc ti on w i th 3° heart bl ock RBBB and l eft p ost eri or hem i bl ock Al t ernati ng RBBB and LBBB P.319

See also: Tem porary paci ng (1), p54; Temp orary pac i ng (2), p56; ECG moni tori ng, p108; C hronot rop es, p206; Basi c res us ci t ati on, p270; Card i ac arre st, p272; Acute coronary syndrome (1), p320; Thyroi d eme rge nci es, p446; Hyp otherm i a, p516 P.320

Acute coronary syndrome (1) Principles of management of the uncomplicated myocardial infarct Oxyg en— to mai ntain SaO 2 ≥98% Good ve nous acce ss Cont i nuous EC G m oni tori ng Ade quat e p ai n rel i ef Earl y thromb ol y si s pl us asp i ri n (he pari n i f usi ng rt-PA) Earl y β bl oc kade Gradual m obi l i s ati on

Complications of myocardial infarction Card i op ul monary arres t Cont i nui ng c hes t p ai n—may be i s chaemi c or p eri cardi ti c i n ori g i n Pump failure Hypotensi on—apart from cardi og eni c s hoc k c ons i de r hypovol aemi a (e.g . p ost -di ure ti c s) and a thromb ol y si s reac ti on

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Tachyarrhythmi a s/b rad yarrhy thm i as Val ve d ysfunc ti on— pre dom i nantl y m i tral Peri cardi al tam ponade (rare ) Ventri cul ar se ptal d efec t (unusual, oft en pre sents 2–5 days pos t-i nfarct ) Comp l i c at i ons of thrombol yt i c the rap y—arrhythmi a s, bl e edi ng, anaphyl a ctoi d react i on

Management of the complicated myocardial infarct General Oxyg en to mai ntain SaO 2 ≥98% App rop ri a te and promp t m oni tori ng and i nve sti gat i ons as i nd i cated , e .g. ec hoc ard i og ram , p ul m onary art ery cat het er, ang i ography , EC G Earl y thromb ol y si s shoul d s ti l l be gi v en. rt -PA fol l owed by hep ari n s houl d be gi v en i n pre ferenc e t o s tre ptoki nase i f i nv asi ve p roced ure s and/or s urgery are c ont emp l at ed. Art eri al or central venous cannul at i on shoul d not be d el ayed i f cl i ni cally i ndi cat ed. These proced ures shoul d be performed by an expe ri enc ed operat or to m i ni mi se the ri sk of bl e edi ng. The s ubc l av i an route shoul d b e avoi ded. Ang i op l as ty or rev asc ul a ri sat i on surge ry i s benefi ci al i f performed earl y. The c ard i ol og i st shoul d b e i nforme d prompt l y i f a pati ent i s ad mi t ted i n pump fai l ure, conti nui ng p ai n, or v al v ul a r d ysfunc ti on.

Specific Card i op ul monary arres t—c ard i op ul m onary res usc i t ati on Cont i nui ng c hes t p ai n: If i sc hae mi c —IV ni trate and he pari n i nfus i ons, asp i ri n, cl opi dog rel , c al c i um antag oni st and β-bl ocke r (unl ess cont raind i cated ); consi d er urg ent angi ography . If p eri cardi ti c—c ons i de r non-ste roi dal anti -i nfl am mat ory ag ent Managem ent of heart fai l ure—al s o c ons i de r IABP Tachyarrhythmi a —anti a rrhythmi c s, sy nchroni se d D C c ard i ov ers i on Bradyc ard i as —chronotrop e, c ons i d er tem porary pac i ng Val ve d ysfunc ti on— heart fai l ure m anageme nt; consi der surg ery Peri cardi al tam ponade —pe ri c ard i al as pi rat i on Ventri cul ar se ptal d efec t—heart fai l ure m anag eme nt, consi der s urg ery Thrombol ys i s compl i cati ons P.321

Drug dosage

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Diamorphine

2.5mg IV. Repeat prn + anti-emetic

Streptokinase

1.5 million units in 100ml 0.9% saline IV over 1h

rt-PA (alteplase)

100mg IV over 90min (15mg bolus, then 50mg over 30min, then 35mg over 60min

Reteplase

10units IV + further 10units IV 30min later

Aspirin

150mg PO od

Clopidogrel

75mg

Atenolol

50mg PO od (increase to 100mg od if not hypotensive and heart rate exceeds 70bpm) or 5mg slow IV bolus

Propranolol

10–40mg PO qds (titrate to heart rate of 60bpm)

Isosorbide dinitrate

2–40mg/h IV

GTN

10–200µg/min IV or 0.5–1mg SL

Diltiazem

60mg PO tds

Nifedipine

5–10mg sublingual or PO tds

Atropine

0.3mg IV. Repeat to maximum of 2mg

Lidocaine

1mg/kg slow IV bolus then 2–4mg/min

Amiodarone

5mg/kg over 20min then infused up to 15mg/kg/day in 5% glucose via central vein (in emergency give 150–300mg in 10–20ml 5% glucose over 3min)

Key papers Tas k forc e or M anag eme nt of acute myoc ard i al i nfarct i on of the European Soci ety of Cardi ol og y. Manage ment of ac ute myocardi a l i nfarc ti on i n p ati ent s p res ent i ng wi th ST se gment e l ev ati on. Eur Heart J 2003; 24:28–66

See also: Defi bri l l at i on, p 52; Temp orary pac i ng (1), p54; T emp orary pac i ng (2), p 56; Intra-aort i c bal l oon c ounterpul sati on, p58; ECG moni tori ng, p108; Bl ood p res sure m oni tori ng, p110; Ce ntral venous cathe ter—us e, p114; Cent ral ve nous cat het er—inserti on, p116; Pul monary arte ry cat het er—us e, p 118; Pul m onary art ery cathe ter—i nserti on, p120; C ard i ac out put —thermodi l uti on, p122; C ard i ac output—othe r i nvasi v e, p124; Cardi a c outp ut—non-i nvas i ve (1), p 126; C ard i ac out put —non-i nvasi v e (2), p128; Inotrope s, p196; Vas odi l at ors , p 198; Vasop res sors, p200; Ant i arrhythmi c s, p204; Chronotropes , p 206; Anti coagul ant s, p248; Thrombol yt i c s, p250; Basi c res usc i tati on, p270; Cardi ac arrest , p 272; Fl ui d chall eng e, p 274; Hypotensi on, p312; Tac hyarrhythmi a s, p316; Brad yarrhy thm i as , p 318; Acut e c oronary syndrome (2), p322; Heart fail ure —as ses sme nt, p324; Heart fai l ure—m anagem ent , p 326; Pain, p532 P.322

Acute coronary syndrome (2) Angina Isc hae mi c or, rarel y , s pas mod i c constri c ti on of c oronary arte ri e s resul t i ng i n pain, us ual l y pre cordi al , press i ng or crushi ng , and wi t h or wi thout radi a ti on t o j aw, nec k or arms . T he sed ate d, v ent i l ate d p ati ent wi l l not us ual l y com pl a i n of pai n b ut si g ns of di s com fort m ay be apparent, e.g . s weati ng, hyp ert ens i on, t achycardi a. The EC G s houl d be reg ul a rl y s cruti ni s ed for ST seg ment and/or T wave change s. Uns tab l e ang i na encom pas ses a spe ctrum of s ynd romes bet wee n s tab l e ang i na and my ocardi al i nfarcti on. Angi nal att ack s m ay be i nc reased i n frequenc y and/or s eve ri t y, persi st l onger, resp ond l e ss to ni t rates , and occ ur at res t or aft er mi ni mal e xerti on.

Pathophysiology

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Myoc ard i al ox yge n s upp l y–dem and i m bal anc e usually due t o c oronary arte ry atheroma ± di srupt i on of pl aque or new non-oc cl usi v e t hrombus form ati on. Sp asm (Pri nzme tal angi na) i s unc omm on. Vas opress or drugs may compromi se myoc ardi a l p erfusi on by furthe r c ons tri ct i ng an al ready ste nos ed vess el . Vas odi l at or drugs may al so com promi s e m yoc ard i al pe rfusi on b y a ‘c oronary s teal’ phe nom enon where bl ood fl ow i s red i st ri but ed away from ste nos ed vess el s.

Diagnosis Symp tom s, esp eci al l y che st pai n b ut al s o non-s pec i fi c, e. g. sweati ng ECG change s—ST s egm ent el evati on/d epress i on, T wave i nve rs i on No ri s e i n c ard i ac enzym es or troponi n above t he myocardi a l i nfarc ti on t hre shol d Dys ki neti c areas of my ocardi um may be se en on e chocardi ography or angi ography

Treatment Ens ure ade quate oxy genati on Correc t hypot ens i on and t i s sue hyp ope rfusi on Cons i de r d rug c aus es, e.g . v asopre ssors Gl y ceryl tri ni trate 0.5mg SL, or ni trol i ngual spray (0. 4–0.8m g) repe ate d as nece ssary If s ymp tom s are sev ere and/or pe rs i st i ng , m ai ntai n b ed res t Asp i ri n 75mg od PO (unl e ss contraind i c ate d).

For continuing angina: IV Ni t rat e i nfusi on, e.g . g l yc ery l t ri ni t rate, i s osorbi de tri ni trate Cons i de r c al ci um antagoni st , e .g. di l ti azem t hough not al one Cons i de r β -bl ock er (unl es s c ont raind i cated ), e.g . prop ranol ol , ate nol ol LMW hep ari n and cl opi dog rel (unl e ss contraind i c ate d) Cons i de r G P2b 3a i nhi b i tor (IV ept i fi bat i d e or t i rofi b an) i n ad di t i on to as pi ri n and cl opi dogre l i f c ons i de red at hi gh ri s k of MI or de ath If s ymp tom s or ST-s egm ent chang es persi s t d esp i t e op ti mal pharm acol og i cal i nte rve nti on, i nform c ardi ol og i st wi t h a vi e w t o angi ography and p oss i b l e ang i op l as ty or surgery. P.323

Key trial Y us uf S for t he Cl opi d ogrel i n Uns tab l e Angi na t o Preve nt Rec urrent Ev ent s T ri al Inv est i gators. Effect s of c l opi d ogrel i n add i ti on to asp i ri n i n pat i ents wi t h acut e c oronary s ynd rom es wi t hout ST-s egm ent el evat i on. N Engl J Me d. 2001; 345:494–502

P.324

Heart failure—assessment Imp ai red abi l i ty of t he heart to sup pl y ad equate ox ygen and nutri ents to mee t t he dem and s of the b ody 's met abol i s i ng t i ss ues .

Major causes Myoc ard i al i nfarct i on/i s chaemi a Drugs e.g . β -bl ocke rs , c ytotoxi cs Tachy- or bradyarrhythmi a s Val ve d ysfunc ti on Sep si s Sep tal de fect Card i om yop athy/m yocard i ti s Peri cardi al tam ponade

Clinical features

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Decreased forward flow leading to poor tissue perfusion Musc l e fat i g ue l ead i ng ul ti mat el y to hy percap ni a and c ol l aps e Confusi on, ag i tati on, drowsi nes s, coma Ol i guri a Inc reasi ng m etabol i c aci dos i s , arte ri a l hypoxae mi a and dy spnoea

Increased venous congestion secondary to right heart failure Peri pheral oedem a Hepati c c ong est i on Spl anc hni c i sc haem i a Rai s ed i nt racrani a l p res sure

Increased pulmonary hydrostatic pressure secondary to left heart failure Pul monary oed ema, dy spnoea Hypoxae mi a

Investigations Test

Diagnosis

ECG

Myocardial ischaemia/infarction, arrhythmias

CXR

With left heart failure: pulmonary oedema (interstitial perihilar (‘bat's wing’) shadowing, upper lobe blood diversion, Kerley B lines, pleural effusion) ± cardiomegaly

Pulmonary artery catheter

Low cardiac output and stroke volume, low mixed venous oxygen saturation (2mmol/l, hyperlactataemia, low venous O 2 (mixed or central venous), raised cardiac enzymes, troponin, BNP, thyroid function (if indicated)

Echocardiogram

Poor myocardial contractility, pericardial effusion, valve stenosis/incompetence

Notes Peri pheral oede ma i mp l i e s t otal b ody salt and water re tenti on b ut not ne ces sari l y i ntravascul ar fl ui d ov erl oad . P.325

See also: ECG moni t ori ng, p108; Bl ood press ure moni t ori ng, p110; Cent ral ve nous c athete r—use, p114; Ce ntral venous cat het er—inserti on, p116; Pul monary arte ry cat het er—us e, p 118; Pul m onary art ery cathe ter—i nserti on, p120; C ard i ac out put —thermodi l uti on, p122; C ard i ac output—othe r i nvasi v e, p124; Cardi a c outp ut—non-i nvas i ve (1), p 126; C ard i ac out put —non-i nvasi v e (2), p128; Hyp ote nsi on, p312; Tachy arrhyt hmi as, p316; Brady arrhyt hmi as, p318; Acute coronary syndrome (1), p320; Heart fail ure —manag ement, p326 P.326

Heart failure—management Basic measures 1. Det erm i ne l i kel y c aus e and t re at as appropri a te, e. g. anti arrhy thm i c 2. Oxyg en— to mai ntain SaO 2 ≥98% 3. GTN sp ray SL then com menc e IV ni t rat e i nfusi on t i t rat ed rap i dl y unti l g ood cl i ni cal e ffe ct. Be ware hy pot ens i on whi c h, at l ow dosag e, i s sug ges ti v e of l eft ventri cul ar underfi l l i ng, e. g. hyp ovol ae mi a , t amponad e, mi t ral ste nos i s, pul monary e mbol us

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4. If p ati ent i s agi t ate d or i n p ai n, g i ve di amorphi ne IV. 5. Cons i de r e arl y C PAP, Bi PAP and/or IPPV t o reduce work of breat hi ng and provi d e g ood ox ygenati on. Cardi ac outp ut wi l l oft en i mp rov e. D o not del ay unt i l the pati e nt i s i n e xtremi s. 6. Furosem i de i s rare l y need ed as fi rst l i ne the rap y unl e ss i nt rav asc ul ar fl ui d ove rl oad i s causat i ve . Ini t i a l symp tom ati c rel i ef i s provi ded by i t s p rom pt vas odi l at i ng ac ti on; how eve r, sub seq uent d i uresi s m ay res ul t i n mark ed hyp ovol ae mi a l e adi ng to c omp ens atory vas oconst ri cti on, i ncrease d c ard i ac work and worse ni ng myoc ard i al func ti on. Di uret i c s m ay b e i ndi cat ed for ac ute -on-chroni c fai l ure, esp eci al l y i f the pat i e nt i s on l ong term di ureti c t herapy but s houl d not be us ed i f hyp ovol aem i c. If furos emi de i s req ui red , s tart at l ow dos es the n reas se ss.

Directed management 1. Ade quat e m oni tori ng (e .g. pul monary arte ry cat het eri sati on) and i nvest i g ati on (ec hoc ard i og rap hy). 2. If e vi d enc e e xi s ts for hy pov ol a emi a, gi v e 100–200m l c ol l oi d fl ui d c hal l e nges t o ac hi eve opt i mal s troke vol ume . 3. If v asoconstri c ti on p ers i s ts (SVR >1400dyn/s/cm 5 ), t i trat e ni trate i nfus i on further to opt i mi se st rok e vol um e and, i d eal l y , reduce SVR Tab le of Co n te n ts > Ren al Dis or d er s

Renal Disorders Oliguria Defi ne d as a uri ne output < 0.5ml /kg/h and c aus ed by: Post -re nal —uri nary tract ob struc ti on, e.g . b l oc ked cat het er, uret eri c t rauma, prost ati sm , rai s ed i nt ra-abd omi nal pre ssure, bl ood cl ot, bl add er tum our. Renal—e stabl i shed acute renal fai l ure, acute tub ul a r necrosi s, gl omerul one phri ti s. Pre-renal — hyp ovol ae mi a , l ow cardi a c outp ut, hy pot ens i on, i nad equate re nal bl ood fl ow. Obs truct i on and p re-renal causes of ol i guri a must be exc l ud ed before res orti ng t o d i ureti cs .

Urinary tract obstruction A ful l b l ad der shoul d b e ex cl ude d by palpati on. Ens ure a pat ent cathe ter i s pres ent . If ob st ruc ti on i s d ue to bl ood cl ot the bl add er shoul d be i rri gat ed. If ob struct i on i s s usp ect ed hi g her i n the renal t rac t an ul t ras ound s can i s re qui red for di a gnosi s and p oss i b l e urol og i cal i nt erv ent i on (e. g. nep hrostomi e s). Raise d i ntra-abdomi nal pre ssure may cause ol i guri a by i m ped i ng re nal ve nous drai nag e (p art i c ul a rl y i f >20mm Hg). Re l i e f of t he hi g h p res sure ofte n p rom ote s a di ure si s .

Hypovolaemia Onc e renal t ract obs tructi on i s exc l uded , i t i s m and atory to c orrec t hypovol aemi a b y fl ui d c hal l e nge . Ol i g uri a i n hyp ovol ae mi c pati e nts may b e a phy si ol og i c al res ponse or due to a reduced re nal bl ood fl ow.

Inadequate renal blood flow and/or pressure If cardi ac outp ut re mai ns l ow des pi te c orrec ti on of hypov ol a emi a, correc ti on wi t h v asod i l ators and /or i notrope s w i l l be nec ess ary . If t he bl ood pre ssure rem ai ns l ow aft er i mp rov i ng the c ard i ac output, vas opress ors may b e neede d t o achi ev e a mean b l ood p res sure of at l eas t 60mm Hg. In el derl y pat i ents and ot hers w i th pre-e xi s ti ng hype rte nsi on, a

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hi g her me an bl ood pre ssure may be nec ess ary t o maint ai n uri ne outp ut.

Persistent oliguria At temp ts to i ncre ase uri ne output w i th di ure ti cs may fol l ow the abov e me asures i f ol i g uri a p ers i st s. Furos emi de i s gi v en i n a d ose of 5–10mg i ntravenous l y wi t h hi g her i ncre ments at 30m i n i nt erv al s to a max i mum of 250mg . Higher dos es may be nee ded i f the p ati ent has p rev i ousl y re cei ved di ure ti c t herapy . A l ow dose i nfusi on may be st art ed (1–5mg /h IV). Manni tol (20g i nt ravenousl y) may be consi dered al t hough fai l ure t o p rom ote a d i ures i s may i ncre ase oed ema format i on. Fai l ure t o re-es tab l i sh uri ne out put may requi re re nal support i n the form of di a l ys i s or hae mofi l t rat i on. T here i s no p oi nt i n conti nui ng d i uret i c the rap y i f i t i s not effect i ve ; l oop di ure ti c s i n p art i c ul a r m ay be nep hrotox i c. Indi c at i ons for renal sup port i ncl ud e fl ui d ov erl oad , hype rkalae mi a , m etabol i c aci dos i s , c reati on of space for nutri ti on or drugs, pe rsi st ent re nal fai l ure wi t h ri s i ng urea and creat i ni ne, and s ympt omati c urae mi a . P.331

Biochemical assessment Pre-renal cause

Renal cause

Urine osmolality (mOsmol/kg)

>500

40

200µ mol /l ) Hype rkalae mi a Hyponat rae mi a Metabol i c ac i dosi s Persi ste nt ol i guri a may be a feat ure of ac ute re nal fai l ure but non-ol i g uri c renal fai l ure i s not unc omm on; 2–3l of p oor quali ty uri ne per day may occur d esp i te an i nade quate gl omerul a r fi l t rati on rate . T he prognosi s i s be tte r i f uri ne out put i s maint ai ned . Cl i ni cal feat ure s m ay s ug ges t t he c aus e of renal fai l ure and d i ct at e furt her i nves ti g ati on. Ac ut e tub ul ar nec ros i s i s a c omm on aeti ol ogy i n the c ri t i c al l y i l l (e. g. fol l ow i ng hy povol ae mi a , e xte nsi ve burns) but othe r causes must be borne i n mi nd. In sep si s , t he ki d ney often has a normal hi st ol ogi c al app earanc e. Anaemi a i mpl i es chroni c renal fai l ure.

Post-operative renal failure Ri s k fact ors i ncl ude hyp ovol ae mi a , haem odynami c i ns tab i l i ty (parti cul arl y hyp ote nsi on), m ajor ab dom i nal s urgery i n those >50 years , major surg ery i n jaundi ce d pati ent s and b i l i ary and other sep si s . Surgi c al proced ure s (parti cul arl y gynaec ol ogi c al ) may b e compl i c ate d b y damag e t o t he l owe r uri nary t rac t w i th an ob struct i v e ne phropathy . Abd omi nal aort i c ane ury sm surgery m ay b e associ a ted wi th renal art eri al di srupt i on and s houl d be i nve st i gated urg ent l y wi t h renography and p oss i bl e art eri ography or re-e xpl orati on.

Other causes

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Nephrot oxi ns —may cause re nal failure vi a ac ute tubul ar nec rosi s , i nte rs ti t i al ne phri t i s or renal tub ul ar obst ructi on. Al l pot ent i al ne phrotoxi ns s houl d be wi t hdrawn. Rhab dom yol ysi s—s ugg est ed by myogl obi nuri a and rai sed CPK i n p ati ent s w ho have suffe red a c rush i nj ury , c oma or s ei zures. Gl omerul a r d i se ase —re d c el l c ast s, haem aturi a, protei nuri a and sy ste mi c fe atures (e .g. hyp ertensi on, purpura, art hralgi a, vas cul i t i s) are al l sug ges ti v e of g l om erul ar di sease. Re nal bi ops y or s pec i fi c b l ood t est s (e.g . Good pas ture' s s ynd rom e, v asc ul i ti s) are re qui red to confi rm di agnosi s and appropri a te tre atm ent . Haem ol y ti c uraem i c sy ndrome—sugges te d by haemol ys i s, uraem i a, throm boc ytopeni a and ne urol og i cal abnormali ti e s. Crys tal nephrop athy—s ugg est ed b y t he pre sence of cry stals i n the uri nary se di m ent . M i crosc opi c e xam i nati on of the cryst al s confi rms the d i ag nos i s (e. g. urate, ox al a te). Re l ease of p uri ne s and urate are re sponsi bl e for acut e renal fai l ure i n t he tum our l y si s sy ndrome . Renovas cul ar di s orders—l oss of vascul ar suppl y m ay be d i agnos ed by renography. Comp l e te l os s of arteri a l sup pl y may oc cur i n ab dom i nal t rauma or aorti c d i se ase (part i cul arl y di sse cti on). M ore com monl y, the arte ri al sup pl y i s parti al l y c omp rom i s ed (e.g . renal arte ry ste nos i s ) and b l ood fl ow i s further red uce d b y haemodynami c i ns tab i l i ty or l ocal l y vi a drug the rap y (e .g. NSAIDs, AC E i nhi bi tors). Renal vei n obst ruc ti on may be due to thromb osi s or e xte rnal c omp res si on (e.g . rai s ed i nt ra-abd omi nal press ure). P.333

Nephrotoxins The fol l owi ng are som e c ommon nephrot oxi ns:

Allopurinol

Aminoglycosides

Amphotericin

Cephalosporins

Dextran 40

Furosemide

Heavy metals

Herbal medicines

Narcotics

NSAIDs

Organic solvents

Paraquat

Penicillins

Pentamidine

Phenytoin

Radiographic contrast

Sulphonamides

Tetracyclines

Thiazides

Vancomycin

See also: Uri nal ys i s, p166; Fl ui d chall eng e, p 274; Hypotensi on, p312; Ol i guri a, p330; Acute renal fai l ure—m anagem ent , p 334; Bow el perforati on and ob struct i on, p348; Abdomi nal sep si s , p 350; Pancreat i ti s, p354; Acute l i v er fai l ure, p360; Hae mol ysi s, p404; Pl a tel et di s ord ers, p406; Seps i s and se pti c s hoc k—t reatme nt, p486; Mal ari a, p490; R heumat i c di s orders, p492; Vasc ul i ti des , p 494; Mul ti pl e traum a (1), p500; Mul ti p l e trauma (2), p 502; Burns—fl ui d managem ent , p510; Burns— general m anagem ent , p 512; Post-ope rat i ve i ntensi ve c are , p 534 P.334

Acute renal failure—management Ide nti fi cat i on and c orrect i on of re versi b l e causes of re nal failure i s cruci al . Al l cas es req ui re c areful at tenti on to fl ui d manage ment and nutri t i onal sup port. Di al y si s and/or fi l t rat i on t echni q ues wi l l mak e s pac e for adeq uat e fl ui d and nut ri ti onal i ntak e.

Urinary tract obstruction Low er tract obs truct i on re qui re s t he i ns ert i on of a c at het er (sup rapub i c i f the re i s ure thral di srupti on) to al l ow tract dec omp res si on. Ure teri c ob struct i on requi re s uri nary trac t d ecompress i on by nep hrost omy or st ent . A mas si ve di ure si s i s common after d ecom press i on so i t i s i m portant t o e nsure ade quate ci rcul at i ng vol um e t o preve nt sec ond ary pre-renal fai l ure.

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Haemodynamic management Pre -re nal failure i s re versi b l e before i t be com es est abl i shed. Careful fl ui d managem ent to ensure an adeq uat e ci rcul at i ng vol um e and any nec ess ary i not rop e or vasop res sor s upp ort may es tab l i sh a d i uresi s. If ol i guri a pe rsi st s aft er pre -re nal factors hav e b een corre cte d, the us e of di ureti cs (furos emi de, manni tol ) may e stabl i sh a d i ures i s.

Metabolic management Hyp erk al a emi a m ay b e l i fe -threateni ng (> 6.5mmol /l or ECG chang es) and m ay b e p rev ent ed by p otass i um re stri c ti on, earl y di a l ys i s or haemo(di a )fi l trat i on. Hypoc al cae mi a and hy ponatraem i a are be st tre ate d wi th di al y si s and/or hae mo(d i a)fi l trati on, al though calci um suppl ementat i on may b e used . Hyponatraem i a i s us ual l y due to wat er exc ess al t hough sal t-l os i ng ne phropathi es (ac ute tubul ar nec ros i s, ot her renal t ubul ar di sorders) may re qui re sod i um chl ori de suppl eme nts . Hype rphosp hat aemi a m ay be tre ate d wi th di al y si s , fi l trati on or alum i ni um hyd rox i de oral l y. Met abol i c ac i d osi s (not due to ti ss ue hypoperfus i on) m ay be c orrec ted wi th di a l ys i s, fi l t rat i on or 1. 26% sodi um bi c arbonate i nfus i on.

Nephrotoxins and crystal nephropathies Al l nephrot oxi c agents shoul d be wi thhel d i f possi bl e . Al l ne ces sary d rug s s houl d hav e t hei r d osage modi fi ed acc ord i ng t o t he G FR. In some c as es uri nary e xcreti on of nephrotoxi ns and c rys tal s m ay be e ncouraged by uri nary al k al i ni sat i on to maint ai n thei r sol ubi l i ty wi th an i nd uce d d i ures i s (rhabd omyol ys i s , aci d i c cryst al s ). Di a l ys i s may al s o b e useful .

Glomerular disease Imm unosup pre ssi ve the rap y m ay be useful aft er di agnosi s has been confi rme d. Di al y si s i s often re qui red for t he more sev ere forms of gl omerul one phri ti s d esp i t e s teroi d re sponsi veness .

Urgent treatment of hyperkalaemia 10–20ml c al c i um chl ori d e 10% b y s l ow i ntravenous i njec ti on. 100m l 8.4% sodi um b i carb onat e i nt rav enousl y. Gl ucos e (50g) and i nsul i n (10–20IU) i ntrave nousl y wi th careful b l ood g l uc os e moni t ori ng and urge nt haem odi al y si s.

Renal replacement therapy Conti nuous haem ofi l trati on forms the mains tay of re pl a cem ent therapy i n cri ti cal l y i l l pati ent s who ofte n c annot tol erate hae mod i al ysi s d ue to hae mod ynam i c i nstabi l i t y. Peri toneal d i al ysi s i s not com monl y use d t oday. Acute renal fai l ure i n the cri ti cal l y i l l usuall y recovers wi thi n 1–6 wee ks; pe rmanent renal fai l ure i s rare . P.335

General indications for dialysis or haemo(dia)filtration Fl ui d exce ss (e. g. pul monary oe dema) Hype rkalae mi a (> 6.0mmol /l ) Metabol i c ac i dosi s (p H 100µm ol /l /d ay Creati ni ne >300–600µmol /l Urea ri si ng >16–20mmol /l /day To c reate space for nutri ti on or drugs

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Pe ri t one al di al y si s , p 66; Cry stalloi d s, p176; Col l oi d s, p180; Di uret i c s, p212; Dopam i ne , p 214; Basi c resusc i tati on, p270; Fl ui d chal l eng e, p274; Ol i guri a , p330; Acute renal fai l ure—di a gnosi s , p 332; Hy perkal aem i a, p420; Hyp onatraemi a, p418; Hypocal cae mi a , p 428; M etabol i c aci dos i s , p434


Ed itors:


Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Gas tr oi n te sti n al Di sor der s

Gastrointestinal Disorders

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Vomiting/gastric stasis Whi l e vom i ti ng per se i s re l at i v el y rare i n the ICU pati e nt, l arg e vol um e g ast ri c aspi rat es are commonpl ace and probab l y rep res ent t he m ajor reas on for fai l ure of ent eral nutri ti on.

Ileus Il eus affect s t he stomac h m ore frequent l y than t he res t of the g ast roi nt est i nal t rac t. Ab dom i nal s urg ery , d rug s (parti cul arl y opi ate s), gut d ysfunc ti on as a com ponent of mul ti -organ dy sfunct i on, hypoperfus i on and p rol ong ed starvati on m ay al l contri b ute to gas tri c i l eus . Earl y and c ont i nued us e of the b owel for feed i ng ap pears to mai ntain forward p rop ul s i v e ac ti on. Manage ment c ons i st s of t reati ng t he cause whe re pos si b l e, the use of m oti l i ty sti mul ant s suc h as m etocl oprami d e or e ryt hromyc i n and , i n res i st ant cases , b ypassi ng the st omach wi t h a nas oduode nal /nasoje junal tub e or a je junost omy.

Upper bowel obstruction Rel ati vel y unus ual ; apart from pri mary surgi cal cause s s uch as ne opl asm or adhesi ons , t he predom i nant cause i n the ICU i s gastri c outl e t obst ruc ti on. Thi s may be rel ate d t o l ong -st and i ng pe pti c ul c er di s eas e or m ay occur i n the short term from py l ori c and /or duode nal sw el l i ng conse que nt to gas tri ti s or d uod eni ti s . T hi s c an b e d i ag nos ed end osc opi cal l y and treat ed by bow el res t p l us an H 2 antagoni st , p rot on pum p i nhi bi tor or sucralfate.

Gastric irritation Drugs or chemi cal s—e i ther acc i d ent al or adve rs e reac ti on (e .g. st eroi d s, asp i ri n), i ntenti onal (e .g. al cohol , bl eac h) or the rap eut i c (e. g. i pe cac uanaha sy rup ) m ay i nduce vom i ti ng . Treat ment, whe re app rop ri a te, may c omp ri s e (i ) rem oval of the cause , (i i ) di l ut i on wi th cop i ous amounts of fl ui d (i i i ) ne utral i sati on wi th al kal i and/or H 2 ant agoni s t or p rot on pum p i nhi bi tor and (i v) adm i ni st rat i on of ant i -e met i c (e. g. met ocl oprami de).

Neurological St i mul at i on of the em eti c c ent re may fol l ow any neurol ogi cal ev ent (e. g. trauma, C VA), d rug therapy (e.g . che mot herapy ), pai n and m etabol i c di sturbance s. Manage ment i s b y treat i ng t he cause w here p oss i bl e and by jud i ci ous use of anti -em eti cs, i ni t i al l y met ocl oprami de or prochl orperazi ne. Consi der ondanset ron or grani set ron i f the se are unsuc ces sful . P.339

See also: Ent eral nut ri t i on, p 80; El e ctrol y tes , p 146; Opi oi d analge si c s, p234; Anti -em eti cs, p224; Gut moti l i t y agents, p226; Bow el perforati on and obs truct i on, p348; El e ctrol yte manage ment, p414; Poi s oni ng—general p ri nci pl es P.340

Diarrhoea The de fi ni ti on of di a rrhoea i n the ICU pat i ent i s p rob l em ati c as t he amount of st ool pas se d dail y i s d i ffi cul t to measure. Fre que ncy and consi st enc y m ay also vary si g ni fi c ant l y. Loose /wat ery and freq uent ( ≥ 4 × d ay) stool wi l l oft en req ui re i nve sti gati on and/or t re atme nt.

Commoner ICU causes Infe ct i on—Cl ost rid ium di ffi cil e, g ast roent eri ti s (e .g. Sal monell a, Shi gel la), rare r t rop i c al causes (e. g. chol era, dyse ntry, gi ard i as i s, trop i cal s prue). Drugs, e. g. ant i bi oti cs , l axat i v es. Gas troi nt est i nal — feed (e .g. l a ctose i nt ol e rance), c oel i ac di sease, ot her malab sorpti on syndromes , i nfl amm atory bowe l d i se ase , d i ve rti cul i t i s , p el v i c abs ces s, bow el obs tructi on wi t h overfl ow. Ent eral feed i s often i m pl i cat ed but rarel y c aus ati ve. For bl oody di arrhoe a c ons i de r i nfect i on, i schaem i c or i nfl am mat ory bowel di sease.

Diagnosis Rect al exami nati on to rul e out i mp act i on wi th ove rfl ow. Consi der si gmoi doscopy i f col i t i s or C. di ffi cil e s usp ect ed (pse udomem brane seen). Stool sent t o l aborat ory for MC & S, C. diffic ile toxi n. Fat est i mati on (mal abs orp ti on) i s rarel y neces sary i n the ICU pati e nt If i sc hae mi c or i nfl a mmatory b owel di sease sus pec ted , p erform a sup i ne ab dom i nal X-ray and i ns pec t for di l ate d l oop s of b owe l (N B toxi c megacol on), t hi c kened wal l s (i ncrease d s eparat i on be twe en l oops) and ‘t hum bpri nti ng’ (sug ges ti ve of m ucosal oe dema). Fl ui d l ev el s se en on ere ct or l at eral abdomi nal X-ray may be see n i n d i arrhoea or p aral y ti c i l eus and d o not nec ess ari l y i nd i c ate obs truct i on. D i arrhoea i s oft en but not always bl oody . If absc ess s usp ect ed, perform ul t ras onography or CT sc an

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Management 1. Tre at c aus e w here p oss i bl e e .g. for C. di ffi cil e, met roni dazol e p l us c hol esy trami ne (b i nds the toxi n). 2. Cons i de r t emp orary (12–24h) ces sat i on of ent eral feed i f ve ry sev ere . Consi de r c hange i n feed i f ap propri at e, e.g. coel i ac di sease, l a ctose i nt ol e rance. 3. Cons i de r s toppi ng ant i bi oti cs . 4. Gi v e anti di a rrhoeal i f i nfe cti on exc l ud ed. 5. Care ful at tenti on t o fl ui d and el e ctrol yte bal ance (i n parti cul ar Na + , K + , Mg 2 + ). 6. Request surgi cal opi ni on i f i nfarcte d or i nfl ame d b owe l or absc ess suspe cte d. P.341

See also: Ent eral nut ri t i on, p 80; Ant i di arrhoeal s, p228; Anti mi c rob i al s, p260; Abdomi nal sep si s , p 350; Infec ti on—d i ag nos i s , p480 P.342

Failure to open bowels Commoner ICU causes Prol onged i l eus /dec re ase d gut m oti l i ty (e. g. opi ates , p ost -surg ery ) Lac k of enteral nut ri ti on Bowe l obst ructi on— thi s i s a rel a ti v el y uncom mon sec ond ary ev ent and i s m ai nl y see n p ost -ope rat i v el y , ei ther afte r a curat i v e proc edure or w i t h de vel opm ent of adhesi ons

Management 1. Cl i ni c al l y e xcl ude ob struc ti on and c onfi rm p res enc e of st ool pe r rec tum . 2. Ens ure ade quate hyd rat i on. 3. Ant i const i p ati on the rap y may b e g i ve n, usual l y s tarti ng w i t h l axat i v es (e.g . l act ul ose or, for m ore urgent res ponse, mag nes i um sul p hat e), the n p roc eed i ng to gl yce ri ne s upp osi tori e s and, fi nal l y, enemata i f g ent l e r meas ure s p rov e unsucce ss ful . 4. Cons i de r red uci ng/stoppi ng dos e of op i at e i f p oss i b l e. P.343

See also: Ant i c ons ti p ati on age nts , p 230; Op i oi d anal ges i cs , p 234; Bowel perforat i ons and obs tructi on, p348; Abd omi nal se psi s, p350 P.344

Upper gastrointestinal haemorrhage Causes Pept i c ul cerati on Oes ophagi ti s /gastri t i s/duodeni ti s Vari ce s Mal l ory–W ei s s l owe r oesophag eal te ar Neop l as ms

Pathophysiology Pep ti c ul ce rat i on i s re l at ed to protec ti ve b arri e r l oss l e adi ng to aci d or b i l i ary d amage of t he und erl yi ng m ucosa and sub muc osa. Barri e r l oss oc curs sec ond ary to cri ti cal i l l ness , alcohol , d rugs, e.g . non-ste roi dal s, poi sons i nc l ud i ng corrosi v es. Di rec t d amage, es pec i al l y at the l ower oes ophagus, may oc cur from feed i ng t ube s. Muc osal d amag e (‘s tress ul cers’) may al so occ ur as a c ons equenc e of t i ss ue hyp ope rfusi on. Gas tri c hyp ers ecreti on i s unc omm on i n cri ti cal l y i l l p ati ent s; i nd eed , g ast ri c ac i d conte nt and sec re ti on i s ofte n reduced .

Prophylaxis Smal l -bore fe edi ng tub es Nasogas tri c ent eral nutri t i on (nasoj ejunal and p are nte ral fe edi ng has al so been shown to re duc e t he i nc i de nce of

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stress ul cer bl eed i ng) Ade quat e t i s sue pe rfusi on (fl ow and p res sure) The rol e of p rop hyl act i c drug the rap y i ncl udi ng H 2 antagoni st s, proton pump i nhi bi tors and sucralfate i s cont roversi a l . Evi dence sug ges ts that e nte ral nutri ti on al one i s as effect i ve and there are c l ai ms that l os s of t he aci d envi ronment i n t he s tomach predi sp ose s t he pat i ent t o nosoc omi al i nfec ti on. Pat i ents at hi g hes t ri s k are thos e requi ri ng prol onge d m echani cal ve nti l at i on or wi th a c onc urrent c oag ul opat hy.

Treatment of major haemorrhage Fl ui d res usc i tati on w i t h c ol l oi d and b l ood wi th bl ood products as ap propri ate to corre ct any coagul op athy. Mai ntai n haem ogl obi n b etw een 7–10g /dl and have ade quat e c ross-matc hed bl ood av ai l abl e s houl d further l arge haem orrhag es occ ur. If p oss i b l e, di sconti nue any on-goi ng anti coagul ati on, e. g. hepari n. Urg ent di agnost i c fi b reopti c e ndoscopy. Local i njec ti on of e pi nephri ne or a sc l e ros ant i nto (or therm al sealing of) a bl eed i ng pe pti c ul c er bas e m ay hal t furt her bl eed i ng . Li ke wi s e, bandi ng or s cl e ros ant i njec ti on may arrest bl e edi ng vari ce s. If oesophageal v ari ces are k nown or hi ghl y sus pec ted , c ons i de r v asopre ssi n or t erl i p res si n ± a Seng staken-ty pe tub e for s eve re hae morrhage, ei the r as a bri dg e t o endos cop y or i f b and i ng /i njec ti on i s uns ucc ess ful . R emem ber that s ources of bl eedi ng other than v ari ce s may b e p res ent , e .g. pe pti c ul ce r. For pep ti c ul ce rat i on and g eneral i se d i nfl amm ati on com mence an H 2 antag oni st or proton pump i nhi bi tor. Gi v e i nt rav enousl y t o ensure effe ct. Enteral ant aci d may al s o b e b ene fi c i al . Surgery i s rare l y nec ess ary but s houl d be consi dered i f b l e edi ng conti nues , e .g. >6–10 uni t t ransfusi on req ui reme nt. Inform a surge on p rom ptl y of any pat i ent w i th major bl eedi ng . P.345

See also: End otracheal i ntubat i on, p 36; Sengst ake n-t ype tub e, p72; Uppe r g ast roi nt est i nal e ndoscopy, p74; Coagul at i on moni tori ng, p156; Col l oi ds, p180; Bl ood transfusi on, p182; H 2 bl ocke rs and proton p ump i nhi b i t ors , p 218; Suc ral fat e, p220; Ant aci ds , p222; Coagul ant s and ant i fi bri nol yt i cs , p 254; Basi c re sus ci tat i on, p 270; Fl ui d challe nge , p 274; Vom i t i ng /gas tri c stasi s, p338; Bl eed i ng vari c es, p346; Bl e edi ng di s ord ers , p 396; Sy ste mi c i nfl ammati on/m ul t i organ fai l ure, p484 P.346

Bleeding varices Vari c es dev el op fol l owi ng a prol onge d p eri od of portal hy pertensi on, usual l y rel ate d t o l i ve r c i rrhosi s . Approxi mat el y one thi rd wi l l bl eed . T hey are commonl y found i n the l ower oe sop hag us but , occasi onal l y, i n the s tom ach or duodenum. Torre nti al hae morrhage may occ ur. Approxi mat el y 50% of pati e nts di e w i t hi n 6 week s of p res ent ati on of the i r fi rst bl eed ; e ach subse quent b l e ed c arri e s a 30% mortali ty.

Management 1. If airway and /or breat hi ng are com promi s ed, pe rform end otracheal i ntub ati on and i nsti tute mechani cal vent i l ati on. Thi s fac i l i tates Se ngs tak en-t ype tube pl a cem ent and e ndos copy b ut may be as soc i at ed wi t h s evere hypotensi on s econdary to cov ert hy pov ol a emi a. If p oss i b l e, ensure adequate i ntravas cul ar fi l l i ng be fore i nt ubati on. 2. Fl ui d res usc i tati on w i t h c ol l oi d and b l ood wi th bl ood products as ap propri ate to corre ct any coagul op athy. Ens ure good ve nous acce ss (at l e ast two 14G c annul a e). Group -sp eci fi c or O-neg ati ve bl ood may be nee ded for emergency use . M ai ntai n haem ogl obi n > 10g /dl and have at l east 4 uni t s of c ros s-m atc hed bl ood avail abl e for urg ent trans fus i on. T here i s a theoreti cal ri sk that over-transfusi on m ay p rec i p i tate furthe r b l ee di ng b y rai s i ng portal venous pres sure. Cardi a c outp ut moni tori ng s houl d be consi d ere d i f t he pat i ent remains haemodynami cal l y uns tab l e or the re i s a hi st ory of heart di sease. 3. If b l ee di ng i s torrenti a l , i nsert a Se ngs tak en-t ype tube and commence adm i ni st rat i on of IV vasopre ss i n/terl i p res si n (q. v.). 4. Gent l e pl ace ment of a l arge-bore nasogas tri c t ube i s a reasonabl y s afe proce dure t hat fac i l i tates drai nag e of bl ood, l es se ns the ri sk of aspi rati on and can be use d t o asse ss conti nui ng bl ood l os s. 5. Perform urgent fi breop ti c e ndoscopy t o e xcl ude ot her sourc es of bl e edi ng. Thi s al so p ermi t s v ari ceal b and i ng or l oc al i nj ect i on of a s cl erosi ng agent. Bl e edi ng i s arres ted i n up to 90% of cases . Endoscopy may be i mp oss i bl e i n the short te rm i f bl e edi ng i s too se vere. It may hav e t o be de l ay ed for 6–24h unti l a peri od of tamponade by the Sengst aken-ty pe tub e ± vas opress i n has enabl ed som e c ont rol of the b l ee di ng. 6. Ei t her oc tre oti de, vasop res si n or te rl i press i n can be ad mi ni s tered for sev ere bl eed i ng , or p rop hyl axi s agai ns t fres h b l e edi ng. Vasop res si n control s b l ee di ng i n approxi mat el y 60% of cases and i ts effi cacy and safet y ap pears to b e e nhance d b y c onc urrent GT N. The si de-effe ct profi l e of t erl i p res si n i s l ower as i t d oes not ap pear t o pre ci p i tate as muc h m ese nte ri c , c ard i ac or di gi tal i s chaemi a, Oct re oti de i s a s omat os tat i n analog ue b ut l onger-act i ng t han i t s p are nt com pound; l i ke s omatos tat i n, i t i s p rob abl y as e ffec ti ve as v asopre ss i n but wi thout

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the si de-e ffe cts . 7. If b l ee di ng c ont i nues aft er prol onge d b al l oon tamponade (2–3 days ) and rep eat ed endosc opy, consi der transj ugul ar i ntrahep ati c portos yst emi c s tented shunt (T IPSS). Thi s can be pe rforme d q ui c kl y and c arri es a rel ati vel y l ow mortal i ty compared to surge ry al t hough the ri sk of enc ephal opat hy i s i nc reased . 8. The tradi ti onal al ternat i ve to TIPSS i s oesop hag eal trans ec ti on (now performed wi th a s tap l e gun) wi th or wi t hout de vas cul ari sati on. Mortal i t y i n t he acut e s i t uat i on i s of the orde r of 30%. P.347

Drug dosages Octreotide

50µg bolus then 50µg/h infusion

Vasopressin

20 units over 20min then 0.4 units/min infusion Also give glyceryl trinitrate 2–20mg/h to counteract myocardial and mesenteric ischaemia

Terlipressin

2mg IV followed by 1–2mg IV 4–6-hrly until bleeding controlled for up to 72h

See also: End otracheal i ntubat i on, p 36; Sengst ake n-t ype tub e, p72; Uppe r g ast roi nt est i nal e ndoscopy, p74; Coagul at i on moni tori ng, p156; Col l oi ds, p180; Bl ood transfusi on, p182; Bas i c re sus ci tat i on, p 270; Fl ui d challe nge , p 274; Up per gas troi ntes ti nal hae morrhage, p344; Acute l i v er fai l ure, p360; Chroni c l i v er fai l ure, p364 P.348

Bowel perforation and obstruction Pat i ents wi t h b owe l p erforati on or obst ruc ti on may be adm i tt ed to the IC U after surg ery , for p re-ope rat i ve res us ci t ati on and cardi ore spi ratory opti mi s ati on, or for c ons erv ati ve manage ment . Al t hough rarel y oc curri ng de novo i n the IC U p ati ent , t hes e c ond i ti ons may b e d i ffi cul t to di a gnose bec aus e of se dat i on ± mus cl e re l ax ati on. Consi der whe n t here i s: Abd omi nal pain, te nde rne ss, pe ri t oni sm Abd omi nal di ste nsi on Agi tat i on Inc reased nas ogast ri c as pi rat es, vom i ti ng Inc reasi ng m etabol i c aci dos i s Si g ns of hypovol aem i a or sep si s A fi rm di ag nos i s i s oft en not mad e unti l l ap arotom y al though supi ne and ei t her erec t or l ate ral ab dom i nal X-ray m ay rev eal ei the r free gas i n t he peri toneum (perforati on) or di l at ed bowe l l oop s w i t h mul t i pl e fl ui d l eve l s (ob struc ti on). Ul t rasound i s usual l y unhe l pful though faecal fl ui d m ay occ asi onally be as pi rate d from the pe ri toneum fol l owi ng perforati on. It may be di ffi cul t t o d i st i ngui sh bow el obs tructi on from a paral yti c i l e us as (i ) bow el sounds may be prese nt or abs ent i n ei the r and (i i ) X-ray appe arance s m ay b e s i mi l a r.

Management 1. Correc t fl ui d and el e ctrol y te abnorm al i ti es. Res usc i t ati on shoul d be promp t and aggres si v e and usuall y c ons i st s of c ol l oi d repl ace ment p l us bl ood to mai nt ai n Hb >7g /dl . Inot rop es or vas opress ors may b e requi re d t o rest ore an adeq uat e c i rc ul ati on, parti cul arl y fol l ow i ng pe rforat i on. Earl y c ard i ac output m oni tori ng s houl d be consi d ere d i f t he ci rcul at ory st atus remains unst abl e or v asoact i ve drugs are requi re d. 2. The surgeon s houl d be i nform ed earl y. A conservat i ve ap proach may be ad opt ed, e. g. wi t h upper s mal l b owel perforati on; how eve r, surgery i s usuall y requi re d for l arge bowe l p erforati on. Sm al l or l a rge bowel ob struct i on may som eti mes be manage d c ons erv ati vel y as s pontaneous resol ut i on may occur, e.g . adhes i ons. Promp t expl orati on shoul d be enc ourage d i f t he pat i ent s how s s i gns of s yst emi c t oxi ci ty. 3. Bot h c ons erv ati ve and pos t-operati ve manage ment of pe rforat i on and obst ruc ti on usual l y requi re conti nuous nasogas tri c drainage to dec omp res s t he stomac h, ni l by mouth and parenteral nut ri ti on. 4. Pai n rel i ef shoul d not b e wi thhel d. 5. Broad spe ctrum ant i bi oti c the rap y s houl d be c omm enc ed for bowel perforati on aft er app rop ri ate sp eci mens have been taken for l aborat ory anal y si s . T herapy us ual l y com pri ses ae rob i c and anaerobi c Gram ne gat i ve cover (e. g. 2nd or 3rd ge nerati on cep hal os pori n, qui nol one or c arb ape nem , pl us met roni d azol e ± am i nogl ycos i d e).

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6. Post -op erati v e m anageme nt of bow el perforati on may i nv ol v e repe ate d l aparot omi es to exc l ud e c ol l ect i ons of p us and bow el i sc hae mi a /i nfarcti on; surge ry shoul d be ex ped i te d i f t he pat i ent's condi ti on det eri orates . Al t ernati vel y, reg ul ar i magi ng ± drai nage of col l ec ti ons may be ne ede d. P.349

See also: Parent eral nutri t i on, p 82; Fai l ure t o open bowel s , p 342; Abdomi nal sep si s, p350; Pancreat i ti s, p354; Met abol i c aci dos i s , p 434; Sy ste mi c i nfl a mmati on/m ul t i organ fail ure , p 484; Post -op erati v e i nte nsi ve care, p534 P.350

Lower intestinal bleeding and colitis Causes of lower gastrointestinal bleeding Bowe l i sc hae mi a /i nfarcti on Infl amm atory bow el di s eas e (ul c erati v e c ol i ti s, Crohn' s d i se ase ) Infe ct i on, e. g. Shige lla, Campy lob act er, am oeb i c dys ent ry Uppe r g ast roi nt est i nal s ource , e. g. pep ti c ul ce rat i on Ang i od ysp l as i a Neop l as m Al though re l at i ve l y rare, mas si v e l owe r g ast roi nte st i nal haemorrhag e c an b e l i fe -threateni ng .

Ischaemic/infarcted bowel Can oc cur fol l owi ng p rol ong ed hyp ope rfusi on or, occ asi onally , s econdary to a m esenteri c em bol us. It us ual l y pre sents wi t h s eve re abd omi nal pain, bl ood y d i arrhoea and si gns of sys te mi c toxi c i ty i ncl udi ng a rapi dl y i ncreasi ng met abol i c aci dos i s . Pl as ma p hos phate l ev el s may also be el evat ed. X-ray ap pearances of thi ck ene d, oede mat ous bowel l oops (‘t hum b p ri nti ng’ ) wi th an i ncre ase d d i st anc e b etw een bow el l oops are sugge sti ve. Treat ment i s b y rest orati on of ti ssue p erfusi on, bl ood trans fus i on to maint ai n haemog l obi n >7g /dl and, i f cl i ni cal fe atures fail to set tl e promp tl y, l ap arotom y w i th a vi e w to bowel ex ci s i on.

Inflammatory bowel disease Pre sents wi t h w ei g ht l os s, abd omi nal pain and di arrhoea w hi c h usuall y c ont ai ns b l ood. Comp l i cat i ons of ul ce rat i ve col i t i s i nc l ude p erforati on and tox i c meg acol on whi l e compl i c ati ons of Crohn' s d i s eas e i ncl ude fi stul ae , absc ess es and perforati ons . Manage ment i nvol ves : 1. Fl ui d and el e ct rol yte re pl a cem ent . 2. Bl ood transfusi on to mai ntain hae mogl ob i n >7g/dl . 3. Hi g h d ose st eroi ds IV and, i f di s tal bowel i nvol vem ent , b y enema. 4. Nut ri t i on (ofte n p are nte ral ). 5. Regul ar surg i cal revi ew. Surge ry may be i ndi c ate d i f s ymp tom s fail to se ttl e afte r 5–7 days , for tox i c meg acol on, perforati on, abs ce sse s or obst ruc ti on. 6. Ant i di arrhoeal drugs shoul d b e av oi d ed.

Angiodysplasia Usual l y p res ent s as fres h b l e edi ng per re ctum and t hi s m ay b e c ons i de rab l e . It i s d ue to an arte ri ovenous mal format i on and c omm oner i n t he e l d erl y. Loc al i sat i on and e mbol i s ati on by ang i og rap hy may be curat i ve duri ng act i ve bl eed i ng , Surgery m ay b e requi red i f b l ee di ng fai l s to set tl e on conse rvati v e manag eme nt and , oc casi onal l y, ‘bl i nd’ l ap aroscopi c em bol i s ati on of a me senteri c ves sel . Howe ver, l ocalis ati on of the l e si on m ay be d i ffi c ul t at l ap arotom y, nec ess i tati ng exte nsi ve bow el res ect i on. P.351

See also: Col l oi ds , p180; Bl ood trans fus i on, p 182; Coagul ants and ant i fi bri nol yt i c s, p254; Basi c resusci tat i on, p270; Fl ui d chall eng e, p 274; Bowe l p erforati on and obs tructi on, p348; Bl eed i ng di sorders, p396 P.352

Abdominal sepsis Thi s i s a c ommon b ut di ffi c ul t t o di ag nos e condi ti on i n i nt ens i ve care pat i ents. A proporti on of s uc h p ati ent s are adm i tt ed fol l ow i ng l a parotomy but ot hers m ay deve l op ab dom i nal s eps i s de nov o or as a se condary c omp l i c ati on fol l ow i ng ab dom i nal s urg ery, i n p arti c ul a r afte r b owe l rese cti on. Se psi s may ei t her be l ocal i s ed to an organ, e.g . chol ec yst i t i s, or the p eri toneal cavi t y (abs ces s); al ternat i ve l y, there may b e a generalis ed peri t oni ti s . N on-bow el

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i nfect i on or i nfl ammati on c an present i n a si mi l ar manne r, e.g . p anc reati t i s, chol ecys ti ti s , g ynaecol og i cal i nfect i on, pye l onephri t i s .

Clinical features Non-spe ci fi c si gns i ncl udi ng pyrexi a (e spe ci al l y s wi ngi ng), ne utrophi l i a, fal l i ng pl a tel et count, i ncreasi ng metabol i c ac i dosi s , c i rcul atory i ns tab i l i ty Abd omi nal di ste nsi on ± l ocalis ed di scomfort, peri t oni sm Abd omi nal mas s, e.g . g al l b l ad der, p seudoc yst , absc ess Fai l ure t o t ol e rat e enteral fee d/l arg e nasogas tri c asp i rates Pl eural e ffus i on (i f s ubd i ap hragmati c s eps i s) Di a rrhoea (i f pe l vi c sep si s )

Diagnosis Ul t ras ound CT s can Lap arotomy Gal l i um w hi t e c el l sc ans are occasi onal l y us eful for i de nti fi c ati on of abs ces ses . Sam pl e s s houl d be tak en for mi crobi ol og i c al anal ys i s from b l ood, uri ne, st ool , abdomi nal drain fl ui d and vagi nal di s charg e i f p res ent . A sampl e of pus i s pre ferred to a s wab . Hype ram yl a sae mi a may sugge st pancre ati ti s t hough amy l as e l eve l s can al so be el e vate d w i th ot her i ntra-ab dom i nal p athol ogi es.

Treatment Ant i bi oti c the rap y provi di ng Gram negati v e and anae rob i c cov er (e. g. 2nd or 3rd g enerat i on ce phalos pori n, qui nol one or carbapene m, pl us m etroni dazol e ± ami nog l yc osi de). T reatme nt can be ame nde d d epe ndi ng on cul ture resul t s and p ati ent resp ons e. Ul t ras oni c or C T-g ui d ed drainage of p us. Lap arotomy wi th rem oval of p us, peri t one al l av age , et c. A negati v e l aparot omy shoul d b e v i ewe d as a us eful m eans of ex cl udi ng i nt ra-abdomi nal sep si s rather than an unnece ssary proced ure. Laparot omy shoul d b e e ncouraged i f the p ati ent de teri orate s and a hi gh suspi ci on of abd omi nal pathol og y p ers i st s. Chol ec yst i t i s, wi th or wi t hout (acal cul ous) gal l st one s, may prese nt wi t h s i gns of i nfe cti on. There i s a charac teri s ti c ul t rasound appe arance of an enl arged organ wi t h a thi c kene d, oed ematous wall surround ed by fl ui d. Treat ment i s oft en conservat i ve wi th ant i bi oti cs (as ab ove ) and p erc ut aneous, ul trasound -gui de d drai nag e vi a a pi gtail cathe ter. Chol ec yst ect omy i s rarel y nece ssary i n the ac ute si tuati on unl ess the g al l bl add er has pe rforat ed, thoug h s ome aut hori t i es argue that thi s i s t he treatm ent of choi c e for acalcul ous c hol ecy st i ti s. P.353

See also: Parent eral nutri t i on, p 82; Bac teri ol og y, p158; Col l oi d s, p180; Inot rop es, p196; Vasop res sors, p200; Ant i mi crobi a l s , p260; Bas i c res us ci t ati on, p270; F lui d c hal l e nge, p274; Bowel pe rforat i on and ob st ruc ti on, p348; Panc reati t i s , p 354; Infect i on—di ag nos i s, p480; Infect i on—treat ment, p482; Syst emi c i nfl am mati on/mul ti org an fai l ure, p484; Sep si s and sep ti c s hoc k t reatment, p550; Pai n, p 532; Post -op erati v e i nte nsi ve care, p534 P.354

Pancreatitis Infl am mat i on of the p anc reas and s urroundi ng ret rop eri toneal t i ss ues . T he app earanc e of the p anc reas m ay range from m i l d l y oed ematous t o haemorrhagi c and nec roti s i ng . A ps eud ocy st may de vel op w hi c h c an bec ome i nfec ted and the bi l e duc t m ay be obs tructe d c aus i ng bi l i ary ob struct i on and j aundi c e. Though mortalit y i s quot ed at 5–10%, thi s i s muc h hi g her (ap prox. 40%) i n t hos e wi th sev ere pancreat i t i s req ui ri ng i nte nsi ve care.

Causes Al c ohol Gal l st one s Mi s cel l aneous, e.g . i schaem i a, traum a, vi ral , hy perl i p i d aemi a Part of the m ul t i pl e org an fai l ure s ynd rom e

Diagnosis

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Non-spe ci fi c features i ncl ude central, sev ere ab dom i nal p ai n, p yre xi a , haemodynami c i nst abi l i ty, vomi t i ng , i l e us. Di s col ourati on around the umbi l i cus (Cul l en' s s i gn) or fl anks (Grey T urner's si g n) i s rarel y s een. Pl as ma enz yme s—e l ev ate d l evel s of amyl ase (usually >1000IU/m l ) and pancreat i c l i pas e are s ug ges ti v e b ut non-spe ci fi c . Level s may be normal , e ven i n se vere pancreat i t i s. Ul t ras ound CT s can Lap arotomy

Complications Mul ti -org an dys func ti on syndrome Infe ct i on/abs ces s formati on Hypocal cae mi a Di a bet es mel l i t us Bl e edi ng

Management Gene ral me asures i ncl udi ng fl ui d re sus ci t ati on, maint ai ni ng Hb at 7–10g /dl , res pi ratory sup port, analge si a , and anti -em eti cs . Routi ne ant i b i ot i c the rap y i s of unprove d b enefi t . Ade quat e m oni tori ng s houl d be i ns ti t ut ed, i ncl udi ng c ard i ac output m oni tori ng i f c ard i oresp i ratory i ns tab i l i ty i s pre sent. The pat i ent i s convent i onal l y kept ni l by mout h w i th conti nuous NG drai nage , and nutri t i on and v i tami ns provi d ed IV. Howeve r, rec ent st udi es show s afe ty and effi c acy of di s tal nasoj ejunal —and e ven nasogas tri c— ent eral feed i ng . Gal l st one ob struct i on s houl d be rel i ev ed e i t her endos cop i cally or surgi cally . Hypocal cae mi a , i f s ymp tom ati c, shoul d be treat ed by i nt erm i t tent s l ow IV i njec ti on (or, oc cas i onal l y, i nfusi on) of 10% cal ci um c hl ori de. Hype rgl yc aemi a s houl d be control l ed by a conti nuous i nsul i n i nfusi on. No s pec i fi c tre atm ent i s routi nel y used . The rol e and ext ent of surge ry rem ai ns c ont rov ers i al ; Some ad voc ate percutaneous drai nag e of i nfec ted and/or necrot i c deb ri s whi l e surg ery frequent l y consi s ts of reg ul a r (oft en dai l y) l a parotomy w i th de bri dem ent of ne croti c ti s sue and p eri toneal l a vag e. Pseudoc yst s m ay res ol v e or requi re drai nag e ei ther percut ane ous l y or i nt o t he bowe l . P.355

Ranson's signs of severity in acute pancreatitis On hos pit al adm iss ion: Age >55 ye ars ol d Bl ood gl ucos e >11mm ol /l Serum l ac tat e d ehyd rogenase (LD H) >300U/l Serum asp art ate ami not ransferase (AST) > 250U/l Whi te bl ood c ount > 16× 10 9 /l At 48 h afte r admi ssi on: Haem atocri t fal l >10% Bl ood ure a ni troge n ri se >1mmol /l Serum cal ci um < 2mmol /l PaO 2 4mmol /l Est i mated fl ui d se que strati on >6000m l Pancre ati ti s s evere i f m ore than 2 c rit eri a m et wit hin 48h of ad mis si on

Imrie scoring system Whi te bl ood count >15 × 10 9 /l

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Bl ood gl ucose > 10m mol /l Bl ood urea ni t rog en > 16m mol /l LD H >600IU/l AST >200IU/l Al bum i n Tab le of Co n te n ts > H ep ati c D isor de r s

Hepatic Disorders Jaundice Jaundi ce i s a c l i ni c al di a gnosi s of ye l l ow p i gm ent ati on of s cl era and s ki n re sul ti ng from a rai sed pl asm a b i l i rubi n. It i s usual l y v i s i bl e w hen the pl as ma b i l i rubi n ex cee ds 30–40µ mol /l .

Commoner causes seen in the ICU Pre-hep ati c—i nt rav asc ul a r haem ol y si s (e .g. drugs , m al a ri a , haem ol y ti c uraem i c syndrome), Gi l bert 's sy ndrome . Hepatoc el l ul ar— cri ti cal i l l ness , v i ral (hep ati ti s A, B, C , Ep st ei n–Barr), alcohol , d rug s (e.g . p aracet amol , hal othane), t oxopl a smosi s , l ept osp i rosi s. Chol est ati c— cri ti cal i l l ness , i ntrahe pat i c causes (e .g. drugs such as chl orpromaz i ne , eryt hromyc i n and i s oni azi d, pri mary b i l i ary ci rrhos i s ), e xtrahe pat i c causes (e .g. bi l i ary obs truct i on by galls tones, ne opl asm , p anc reati t i s ).

Diagnosis Uri nal ysi s—unconjugat ed bi l i rubi n d oes not appear i n the uri ne . Meas ure ment of c onj ugat ed and unconjug ate d b i l i rubi n—conjugat ed bi l i rubi n p red omi nat es i n chol es tat i c jaundi c e, unc onj ugated bi l i rub i n i n pre -he pat i c jaundi ce, and a mi xed pi cture i s oft en see n i n hepat oce l l ul a r jaundi c e. Pl as ma al k al i ne phosphatase i s usual l y markedl y e l ev ate d i n obst ruc ti ve jaundi ce w hi l e p rothromb i n ti m es, aspart ate trans ami nas e and alani ne am i notrans ferase are el evated i n he pat oce l l ul ar jaund i c e. Ul t ras ound or CT sc an wi l l di a gnose extrahepat i c bi l i a ry obs truct i on.

Management 1. Identi fy and treat cause. Where possi bl e, d i s conti nue any drug that c oul d b e i mpl i cated . If e xtrahe pat i c, cons i d er percut ane ous trans hep ati c d rai nage, bi l e duc t s tenti ng or, rarel y, s urgery. 2. Li v er bi opsy i s rarel y nece ssary i n a j aundi c ed ICU pati e nt unl ess the d i ag nos i s i s unknow n and the pos si bi l i t y exi s ts of l i ver i nvol vem ent i n the underl y i ng pathol og y, e.g. mali gnancy. 3. Non-obs truct i ve jaundi ce us ual l y set tl e s w i th conse rvati v e m anageme nt as the pati e nt rec ove rs. 4. An ant i hi stami ne and top i cal c al a mi ne l oti on may provi de sym ptomat i c rel i ef for p ruri t us i f troubl esome. Chol est yrami ne 4g t ds PO may be hel pful i n obs tructi ve jaundi ce.

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P.359

See also: Li ver funct i on te sts , p 152; Ac ute l i ver failure, p360; C hroni c l i ver fail ure , p 364; Hae mol ysi s, p404; Infect i on control — general p ri nci pl e s, p476; Infec ti on—d i ag nos i s, p480; Infect i on—treat ment, p482; Sys temi c i nfl am mat i on/mul ti organ fai l ure, p484; HELLP s ynd rom e, p540 P.360

Acute liver failure Thi s c ond i t i on re sul ts from m ass i ve ne crosi s of l i ver c el l s l ead i ng to se vere l i ve r d ysfunc ti on and enc ephal opat hy. Survi val rates for l i ve r fai l ure wi th Grade 3 or 4 he pat i c enc ephal opat hy vary from 10–40% on med i c al the rap y alone, to 60–80% wi th ort hot opi c l i ve r t ransp l antat i on.

Major causes Al c ohol Drugs, parti cul arl y parace tam ol overdos e Vi ral hep ati ti s, parti c ul arl y hepat i t i s B, hep ati ti s C Poi s ons , e .g. carbon t etrac hl ori d e Acute dec ompe nsati on of c hroni c d i se ase , e. g. fol l ow i ng i nfec ti on

Diagnosis Shoul d be consi dered i n any pat i e nt pre senti ng w i th jaund i ce , g ene ral i se d b l ee di ng, enc ephal opat hy or marked hypogl y cae mi a . Abnorm al l i v er functi on tes ts , i n p art i cul ar, p rol onged PT or INR and hyperbi l i rub i naemi a. In seve re l i ver fai l ure, pl a sma enz yme l e vel s m ay not be el e vat ed.

Management Gene ral me asures i ncl ude fl ui d re sus ci tat i on and b l ood t ransfusi on t o k eep Hb 7–10g/dl . The c i rc ul ati on i s usual l y hyperdy nami c and di l at ed; vas opress ors may b e need ed t o m ai ntai n an adeq uat e BP. Correc ti on of coagul op athy i s ofte n w i thhel d as t hi s provi des a good g ui d e t o recovery or t he need for transp l antat i on. Use of fres h frozen pl asma i s rest ri c ted to pati e nts who are bl e edi ng or are ab out to und ergo an inv asi ve p roced ure . Ade quat e m oni tori ng s houl d be i ns ti t ut ed i f c ardi ores pi ratory i nstabi l i t y i s p res ent . Mechani cal ve nti l a ti on m ay b e nece ssary i f the ai rway i s unprote cte d or resp i ratory fai l ure d eve l op s. Lung s hunts are fre que ntl y p res ent , c aus i ng hypox aem i a. Infe ct i on i s commonpl ace and i s frequent l y ei the r Gram posi t i ve or fungal. Cl i ni c al si gns are often ab sent. Samp l e s of bl ood , s put um, uri ne, w ound s i te s, drain fl ui d , i ntravascul ar c atheter s i te s and asc i te s s houl d be sent for reg ul ar mi c rob i ol ogi cal s urv ei l l ance. Syst emi c anti mi c rob i al t herapy , wi th or wi t hout s el ect i ve gut decontami nati on, has b een shown to re duc e t he i nfe ct i on rate. Fungal i nfec ti ons are al so wel l rec ogni se d. Som e Li v er Uni ts gi v e p rop hyl act i c ant i fung al the rap y. Hypogl y cae mi a i s a com mon oc currence. It shoul d b e freq uentl y moni t ore d and tre ate d wi th ei the r e nte ral (or parent eral) nut ri t i on, or a 10–20% g l uc ose i nfus i on to maint ai n normogl y cae mi a . Renal fai l ure oc curs i n 30–70% of cas es and may ne ces si tat e renal repl ace ment t herapy . T he i nc i de nce may be red uce d by careful mai nte nance of i nt rav asc ul a r v ol ume. Vasop res si n/t erl i pres si n has also be en used suc ces sful l y for hepatorenal s ynd rom e. Uppe r g ast roi nt est i nal b l ee di ng i s more c ommon d ue to the ass oc i at ed coag ul opat hy. Prophyl a ct i c H 2 bl ock ers or proton pum p i nhi bi tors m ay be of b ene fi t . N-ac ety l c yst ei ne and/or e pop ros tenol i mp rov es O 2 consum pti on. Thoug h t i ss ue hyp oxi a m ay b e reduced by these drugs, parti cul arl y when vasop res sor drug s are need ed, outcome bene fi t remai ns unproved. Cort i c ost eroi ds , p ros tag l andi n E and charcoal haemoperfus i on have not bee n s how n t o have any outcome b ene fi t . P.361

See also: Venti l at ory support— ind i c ati ons , p 4; Li ver funct i on te sts , p 152; Coagul at i on moni t ori ng, p156; Hep ati c enc ephal opat hy, p362; Parace tam ol poi soni ng, p 456 P.362

Hepatic encephalopathy Grading

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1. Confuse d, al t ere d m ood 2. Inap propri at e, drowsy 3. Stuporose but rous abl e, very c onfused , agi t at ed 4. Coma, unre sponsi ve to pai nful s ti m ul i The ri sk of cerebral oed ema i s far hi gher at Grades 3 and 4 (50–85%) and i s the l e adi ng cause of d eat h. Sug ges ti v e si gns i ncl ude sys tem i c hyp ert ens i on, p rog re ssi ve heart rat e s l ow i ng and i ncreas i ng muscl e ri g i di ty. These oc cur at i nt racrani a l p res sures >30mmHg.

Management Correc t/av oi d potenti a l aggravati ng fact ors, e.g. gut haem orrhag e, ove r-s edat i on, hypoxi a , hypogl y cae mi a , i nfect i on, e l ec trol yt e i mbalance. Cons i de r e arl y i nt rac rani al pres sure (ICP) moni t ori ng. CT and c l i ni c al feat ures correl ate poorl y w i th IC P t hough no c ont rol l e d s tud i es have yet bee n p erform ed to show outcome benefi t from ICP moni t ori ng whi ch carri es i ts own com pl i cat i on rate (bl eed i ng , i nfe ct i on). Mai ntai n pat i ent i n s l i g ht head-up p osi ti on (20–30° ). Regul ar l act ul ose, e. g. 20–30ml qd s PO, to achi ev e 2–3 bowe l m oti ons /day. Di e tary rest ri cti on of p rotei n i s now not enc ourage d as t hi s promotes endog enous protei n uti l i s ati on. Hype rve nti l a ti on t o achi eve a PaCO 2 of 3. 5–4kPa i s often at tem pte d b ut i s fre que ntl y unsucce ssful i n achi e vi ng i mp rov ement. It may al so com promi s e c ere bral b l ood fl ow . Manni t ol (0.5–1m g/k g over 20–30m i n) i f se rum os mol al i ty 100s Or any three of the fol l owi ng: Age 40 y ears Aet i ol ogy i s he pat i ti s C , hal othane, or ot her drug reacti on Durati on of j aundi c e p re-enc ephal opat hy >2 d ays Prot hromb i n ti m e >50s Serum bi l i rubi n >225µ mol /l If p aracet amol -i nduced : pH < 7.3 or prothrom bi n ti me >100s and creat i ni ne >200µm ol /l p l us Grad e 3 or 4 e nce phalop athy. As onl y 50–85% of pat i ents i de nti fi e d as requi ri ng trans pl a ntati on w i l l s urv i ve l ong enough to re cei ve one, the Reg i onal Li v er Uni t s houl d be i nformed soon afte r d i ag nos i s of al l possi bl e c andi dates . P.363

See also: Venti l at ory support— ind i c ati ons , p 4; Intracrani al pre ssure moni tori ng, p134; Li ver funct i on te sts , p 152; Coagul ati on moni tori ng, p156; Sed ati ves , p 238; Jaund i ce , p 358; Chroni c l i ver failure , p364; Parace tam ol poi soni ng , p 456 P.364

Chronic liver failure Pat i ents adm i tt ed to i nt ens i v e c are wi t h c hroni c l i ve r fai l ure may d eve l op sp eci fi c as soc i at ed probl ems : Acute dec ompe nsati on— thi s m ay b e s econdary to i nfect i on, s edati on, hyp ovol ae mi a , hypot ens i on, d i uret i cs , gast roi nt est i nal haem orrhag e, exc ess di etary protei n and el e ctrol yte i m bal anc e. Infe ct i on—the p ati ent may trans mi t i nfe cti on, e. g. hep ati ti s A, B or C and, by bei ng i m munosuppress ed, i s al so more prone to ac qui ri ng i nfect i ons s uch as TB and fung i . Drug m etab ol i sm —as many d rug s are al l or p art -met abol i sed by the l i ver and/or e xcrete d i nto the b i l e, t he drug act i on may be prol onge d or s l ow ed depe ndi ng on whe the r t he met abol i t es are ac ti v e or not. Inparti c ul ar,

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sedati ves may have a great l y prol onged durat i on of ac ti on. Port al hyp ertensi on—resul ts i n as ci tes , v ari ces and s pl e nom egaly. As ci t es may produce di a phragm ati c s pl i nt i ng and i s at ri sk of b ecomi ng i nfe cte d. Drai nage may i ncur a consi d erabl e prot ei n l oss. Vari ces may bl eed whi l e spl enomegaly may re sul t i n t hrombocyt ope ni a . R enal fai l ure i s al so rec ogni s ed due to hi g h i nt ra-abdomi nal pre ssure. Bl e edi ng— an i nc reased ri sk i s prese nt due to dec reased product i on of cl ott i ng factors (II, VII, IX, X), vari c es and spl enomegaly rel at ed t hrombocyt ope ni a . Al c ohol —t he mos t freq uent c aus e of ci rrhos i s i n the we ste rn worl d; ac ute wi thd raw al may l ead t o d el i ri um tre mens wi th sev ere ag i tati on, hal l uci nati ons , s ei zures and cardi ovascul ar di st urb anc es. 2° hype ral doste roni sm —re sul ts i n ol i guri a, s al t and w ate r rete nti on. Inc reased te ndency to jaundi ce, es pec i al l y duri ng c ri t i c al i l l ne ss.

Management 1. Asc i te s T ake spe ci mens for m i crob i ol ogi cal anal y si s (i nc l ud i ng TB), protei n and cyt ol ogy. If WBC > 250 pe r hi gh p ower fi el d, g i v e Gram neg ati ve ant i bi ot i c cov er. If p res ent i n l a rge quant i ty , (i ) dec rease sod i um and water i ntak e, (i i ) c omm enc e sp i ronol ac tone PO (or p otassi um canrenoat e IV) ± furos emi de. Parac ent esi s ± col l oi d re pl a cem ent , or as ci ti c re i nfus i on (i f uni nfec ted /non-pancreat i t i c i n ori gi n) m ay be consi d ere d, parti c ul arl y i f d i ap hragmati c sp l i nti ng occ urs . 2. Coag ul opat hy: Vi tami n K 10m g/day s l ow IV bol us for 2–3 day s. Fres h froz en p l asma, pl at el e ts as nec ess ary . 3. Hypogl y cae mi a —shoul d b e p rev ent ed by adeq uat e nutri t i on or a 10% or 20% gl ucose i nfusi on. 4. Ade quat e nutri t i on and v i tami n suppl eme ntati on. 5. Acute dec ompe nsati on— avoi d any pre ci p i t ati ng causes , e .g. i nfec ti on, sed ati on, hy pov ol a emi a, e l ec trol y te i mb al a nce . 6. Drug admi ni s trati on— rev i ew typ e and dos e regul arl y. P.365

See also: Li ver funct i on te sts , p 152; Sed ati ves , p 238; Jaundi c e, p358; Acute l i v er fai l ure, p360


Ed itors:


Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Neu r ol ogi cal Di sor der s

Neurological Disorders Acute weakness Sev ere ac ute we akne ss may re qui re urg ent i ntubat i on and me chani c al venti l at i on i f the F VC < 1l or gas ex change det eri orate s ac ut el y .

Investigation Metabol i c myopat hi e s—e xcl ud e and t reat hypophosphataemi a, hypokal aem i a, hy poc al c aem i a and hypomag nes aem i a. Prol onged effect s of m usc l e rel axants —a prol onged effect of suxam ethoni um wi l l usuall y be cl i ni cally ob vi ous and shoul d promp t as se ssm ent of pse udochol i nes terase l e vel s. Sux amet honi um effec ts wi l l al s o b e prol ong ed i n myas the ni c s. Prol onge d effec ts of non-dep ol a ri si ng m usc l e rel axants are s ugg est ed by a resp ons e t o an anti chol i nes terase (neos ti g mi ne 0.5 mg by s l ow IV b ol us wi th an ant i c hol i ne rgi c). Thi s shoul d not be atte mpt ed i f p aral y si s i s compl ete . Pati ent s w i th my ast heni a gravi s wi l l al so res pond. Gui l l a i n–Barré sy ndrome —a l um bar punct ure shoul d b e p erform ed t o c onfi rm rai s ed CSF protei n wi t h norm al cel l s. If these features are not found b ut sus pi c i on i s s trong, ne rve conducti on studi es m ay dem ons trate segm ent al dem yel i nati on w i th sl ow conduc ti on v el oci ti e s. Myas the ni a gravi s— fati gueabl e w eak nes s or p tos i s sug ges ts myastheni a g rav i s ; re sponse to IV ed rop honi um

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(Tensi l on tes t) and a strong l y pos i t i ve ace tyl chol i ne rec ept or ant i body ti t re confi rm thi s d i ag nos i s. A myastheni c synd rome associ ated wi th mal i g nanc y (Eat on–Lam bert s ynd rom e) i nv ol v es pel vi c and t hi g h m usc l es pre domi nantl y, tendi ng t o s pare t he ocul ar muscl es. Other di a gnoses are made l argel y on t he bas i s of cl i ni cal suspi ci on and spe ci fi c sp eci al i sed te st s.

General management FVC shoul d be moni t ore d 2–4-hrl y and i nt ubati on and mec hani cal v ent i l a ti on s houl d fol l ow i f FVC < 1l . Ot her i nd i ce s of resp i ratory func ti on are l es s s ens i t i ve . In p art i cul a r, art eri al bl ood gas es may be mai ntained up t o t he poi nt of resp i ratory arrest . Weak re spi ratory musc l es l e ad to progre ssi ve bas al ate l ec tas i s and sp utum rete nti on. Chest i nfec ti on i s a si g ni fi cant ri sk; reg ul ar che st phy si othe rap y w i th i ntermi t te nt pos i ti ve pre ssure bre athi ng are requi red for pre vent i on where me chani c al venti l at i on i s not nece ssary. Pati ent s who are i m mob i l e are at ri sk of ve nous s tas i s and de ep v enous thromb osi s. Prophy l ax i s wi t h sub cut ane ous hep ari n i s reasonabl e. Imm obi l e pat i ents al s o requi re at tenti on t o p ost ure t o preve nt pre ss ure sores and contract ure s. Weak bul bar m usc l es may c omp rom i se sw al l owi ng wi t h c ons equent malnutri ti on or pul monary asp i rati on. Enteral nut ri t i onal sup port vi a a nasogas tri c tub e i s nece ssary. In c as es w i t h c oexi st ent aut onomi c ne uropat hy ent eral nutri t i on may b e i mpos si bl e , nece ssi tat i ng parenteral nut ri t i onal sup port. These pat i ents may al so suffer arrhy thm i as and hypotensi on requi ri ng ap propri ate support. P.369

Causes of severe weakness Common in ICU Met abol i c my opathi es Prol onged effec ts of m usc l e re l ax ant s Cri ti cal i l l ness ne uropat hy or m yop athy Gui l l ai n–Barré s ynd rom e Myastheni a g rav i s Ponti ne C VA Sub st anc e ab use (e spe ci a l l y be nze ne ri ng c omp ounds)

Uncommon in ICU Chroni c rel aps i ng pol yneuri ti s End ocri ne my opathi es Sarcoi d neurop athy Pol i om yel i t i s Di pht heri a Carci nomatous neuropathy Porphy ri a Bot ul i sm Fam i l i al peri odi c paral ysi s Mul ti pl e sc l erosi s Lead p oi s oni ng Organophosphorus p oi soni ng

See also: Venti l at ory support— ind i c ati ons , p 4; IPPV—ass ess ment of we ani ng, p18; Ent eral nutri t i on, p 80; Pare nte ral nutri ti on, p82; Pul m onary func ti on tes ts, p94; El ec trol y tes , p 146; Calc i um , m agne si um and phosphate , p 148; Musc l e rel axants , p 240; Re spi ratory fail ure , p 282; Gui l l ai n–Barr é syndrome, p384; Myastheni a g rav i s , p 386; ICU ne uromus cul ar di sorders, p388 P.370

Agitation/confusion In the IC U, agi tat i on and/or c onfusi on are predom i nant l y rel ate d t o s eps i s, ce reb ral hy pop erfusi on drugs or drug wi t hdrawal. ‘IC U p syc hos i s’ , w i t h l oss of day –ni ght rhyt hm and i nabi l i t y t o s l ee p, i s a c ommon occurrenc e i n t he pat i ent rec overi ng from sev ere i l l ness .

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Commoner ICU causes Infe ct i on—i ncl udi ng g ene ral i s ed sep si s , c hes t, cannul a s i t es, uri nary tract. Ce reb ral i nfec ti on suc h as me ni ngi ti s , ence phali ti s and m al a ri a are rel a ti v el y rare but shoul d always be consi d ere d. Drug-rel a ted —(i ) ad verse reacti on (parti cul arl y affect i ng the e l de rl y ), e.g . s edati v es, anal g esi cs, di ureti cs; (i i ) wi t hdrawal , e .g. se dat i ve s, analge si c s, et hanol ; (i i i ) abuse, e. g. opi ate s, amp het ami nes , al cohol , hal l uci nog ens . Metabol i c —e. g. hypo- or hype rgl ycaemi a, hyp o- or hype rnatraemi a, hyp erc al c aem i a, uraem i a, he pat i c ence phalop athy, hyp o- or hype rt hermi a , d ehyd rat i on. Resp i ratory— infect i on, hypoxaem i a, hy percap ni a . Neurol ogi cal —i nfec ti on (meni ng o-e nce phal i t i s, malari a ), p ost -he ad i nj ury , s pac e-oc cupyi ng l es i on (i ncl udi ng haem atoma), post-i c tal , p ost -cardi ac arrest . Card i ac —l ow outp ut st ate, hy pot ens i on, e ndocardi t i s . Pai n—ful l bl add er (bl ock ed F ol e y c athete r), ab domi nal p ai n. Psyc hos i s —‘ICU psy chosi s ’, other psy chi atri c st ate s.

Principles of management 1. Exam i ne for s i gns of (i ) i nfect i on (e. g. pyrexi a, purul ent sp utum, cat het er si t es, ne utrophi l i a, fal l i ng pl a tel et count, CXR , m eni ngi sm), (i i ) cardi ovascul ar i nst abi l i ty (hyp ote nsi on, i ncreas i ng met abol i c aci d osi s, ol i guri a , arrhyt hmi as), (i i i ) c overt pai n, parti c ul arl y abdom i nal and l ow er l i mbs (e. g. com partme nt syndrome, DVT), (i v) focal neurol ogi cal si gns (e .g. meni ngi s m, une qual p upi l s, he mi p are si s), (v) re spi rat ory failure (arteri a l b l ood gase s), (v i ) metabol i c de rangeme nt (bi ochemi cal s cre en). If any of t he abov e are found, treat as app rop ri ate . Psyc hos i s shoul d not be ass umed unti l t reatab l e causes are e xcl ude d. 2. Reas sure and cal m t he pat i ent. Mai ntain qui et atm osp here and red uce noi se l e vel s. Att emp t t o rest ore day–ni ght rhy thm , e. g. by changi ng amb i ent l i ghti ng and us e of oral hyp not i c age nts . 3. Cons i de r s tarti ng, chang i ng or i ncreas i ng dose of s edati v e or m ajor t ranqui l l i se r t o c ont rol the p ati ent . If hi ghl y agi tat ed and l i kel y t o endanger thems el v es, rapi d short t erm control can be achi e ved by a s l ow IV bol us of sedati ve. Consi d er propofol , a benzod i azepi ne, halop eri dol or chl orpromazi ne i n t he smalle st pos si bl e dos e t o achi eve the d esi red effec t; obs erv e for hypotensi on, res pi rat ory de pre ssi on, arrhy thm i as and e xtra-p yrami d al effe cts . Opi ates may b e neede d, esp eci al l y i f pai n or wi thdrawal i s a fact or. An e thanol i nfus i on can b e cons i d ere d for del i ri um tremens resul t i ng from al c ohol w i thdrawal . 4. Sed ati on can be mai ntaine d b y c ont i nuous i nfus i on or i nte rmi tte nt i nj ect i on, e i t her re gul arl y or as requi red. The l es s agi t ate d p ati ent may resp ond to IM i nj ect i ons of a major tranq ui l l i ser, t hough the se shoul d be avoi de d w i th conc urrent c oag ul opat hy. P.371

Drug dosages for severe agitation •Chlorpromazine—12.5 mg by slow IV bolus. Repeat, doubling dose, every 10–15 until effect. May need up to 100 mg. For regular prescription, give qds. •Haloperidol—2.5 mg by slow iIV bolus. Repeat, doubling dose, every 10–15 minutes until effect. For regular prescription, give qds. •Midazolam/diazepam—2–5 mg by slow IV bolus. •Propofol—30–100 mg by slow IV bolus. •Morphine—2.5–5 mg by slow IV bolus. NB beware excessive central and respiratory depression with the above agents

See also: IPPV—fai l ure t o t ol e rat e ve nti l a ti on, p12; Tox i col og y, p162; Sed ati ves , p 238; Acut e l i ve r fai l ure, p 360; Chroni c l i v er fai l ure, p364; Thyroi d em erg enc i e s, p446; Poi s oni ng—general p ri nci pl es, p452; Am phe tam i ne s i nc l ud i ng Ec stasy, p462; Coc ai ne, p 464; Infe cti on—di agnosi s, p480; Syst emi c i nfl amm ati on/mul ti org an fai l ure, p484; Head i njury (1), p504; Head i njury (2), p506; Py rex i a (1), p518; Py rex i a (2), p 520; Pai n, p 532 P.372

Generalised seizures Control of s ei z ure s i s nec ess ary to prevent i sc hae mi c brai n damag e, t o reduce cerebral oxy gen re qui rem ent s and to red uce i ntracrani al pre ss ure . W here poss i bl e c orrect the c aus e and gi v e s pec i fi c t reatme nt. A CT scan m ay b e nec ess ary to i d ent i fy st ructural cause s. Com mon causes i ncl ude : Hypoxae mi a

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Hypogl y cae mi a Hypocal cae mi a Space-occupyi ng l e si ons Metabol i c and toxi c di sorde rs Drug wi thdrawal , e .g. al cohol , benzod i azep i ne s, ant i convul sants Infe ct i on, es pec i a l l y me ni ngoe nce phalit i s Trauma Idi opathi c e pi l eps y Mos t s ei z ures are sel f-l i m i ti ng, re qui ri ng no more t han protec ti on from i njury (com a p osi ti on, protec t head and d o not force any thi ng i nt o t he mouth).

Specific treatment Hypoxae mi a shoul d b e c orrect ed wi t h oxyg en (FIO 2 0.6–1. 0). Int ubati on and v ent i l ati on i f the ai rway i s unprote cte d or SpO 2 30 mi n or there i s c yanosi s. A b enz odi aze pi ne (e .g. l orazepam, di a zep am) i s the usual fi rs t l i ne t reatment. Phenytoi n— a l oad i ng dose shoul d be gi ven i ntravenous l y i f the pati e nt has not p rev i ousl y re cei ved pheny toi n. Phenytoi n may not p rov i de i m medi at e c ont rol of sei zures wi thi n t he fi rst 24 h. If sei zures conti nue ap propri ate anti c onv ul s ant s i nc l ud e: Magnesi um sul phate. Cl onaze pam , w hi c h i s p art i c ul a rl y us eful for myocl oni c se i zure s. Thi opental or p rop ofol i nfusi on i n s eve re i nt rac tab l e epi l ep sy. Wi t h all anti c onv ul s ant s c are shoul d b e t ake n t o av oi d hy pov ent i l a ti on and res pi rat ory failure. Howeve r, mec hani c al venti l at i on wi l l certai nl y be re qui re d i f t hi opental i s us ed, and p rob abl y t o maintai n oxyge nat i on i n cases of conti nue d sei zures .

Other supportive treatment Mus cl e rel a xant s p re vent muscul a r c ont rac ti on d uri ng se i zures but w i l l not p rev ent conti nued s ei zures. They m ay be nec ess ary to faci l i t ate mec hani c al vent i l ati on but conti nuous EEG moni t ori ng shoul d b e used to jud ge sei zure c ont rol . Correc ti on of c i rcul atory di s turbance i s re qui red to maint ai n op ti m al cerebral bl ood fl ow. P.373

Drug dosages

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Lorazepam

4 mg IV.

Diazepam

Initially 2.5–5 mg IV or PR. Further increments as necessary to a maximum of 20 mg.

Midazolam

Initially 2.5–5 mg IV or PR. Further increments as necessary to a maximum of 20 mg.

Phenytoin

Loading dose 18 mg/kg IV at a rate 200/120 m mHg) and hypotensi on. Drug t herapy i ncl udi ng t hrombol ys i s and as pi ri n. T he evi dence for ant i c oag ul a ti on remains conte nti ous as there i s an i nc reased ri sk of bl e edi ng and no consi ste nt sub group benefi t has been shown. Earl y anti coagul ati on i s

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probabl y b ene fi c i a l for i nt rac rani al s tenosi s, a s troke-i n-evol ut i on, c ompl et e ve sse l occ l us i on wi th mi ni mal defi ci t and i n l ow ri sk pat i ents wi t h a hi gh probab i l i ty of rec urrence (sec ond ary preve nti on). For thromb ol y si s t he exte nt of rep erfusi on dep end s on t he aeti ol ogy wi t h b asi l a r > mi ddl e c ere bral arte ry > i nt ernal caroti d, and em bol i c > t hromboti c . Pool ed studi e s w i th rt -PA (0.9 mg/kg) gi v en wi t hi n 3 h of s troke onse t (and ti ght bl ood press ure c ont rol ) s howe d a favourabl e outc ome . Howe ver, t here was a 6-fol d i ncreas e i n haem orrhag e (to 5.9%), of whom 60% d i ed . T hi s was more com mon i n the e l de rl y , and wi t h m ore se vere st roke. Neuros urg i cal i nt erv ent i on may be consi dered for ce reb el l ar hae mat oma, c ere bel l ar i nfarct i on and the m al i gnant mi d dl e ce reb ral artery s ynd rom e (for mas si ve i nfarc ti on on t he non-dom i nant si d e). P.381

Key paper Hac ke W, et al . As soc i at i on of outcome wi t h earl y s troke tre atm ent : pool e d anal ysi s of ATLANT IS, EC ASS, and NIN DS rt -PA st rok e tri a l s. Lance t 2004; 363:768–74

See also: Venti l at ory support— ind i c ati ons , p 4; Bl ood press ure moni t ori ng , p 110; Neurop rot ect i ve ag ent s, p244; Basi c res us ci t ati on, p270; Hype rt ens i on, p 314; Ge neral i se d s ei z ure s, p372; Intracrani al hae morrhage, p376; Sub arachnoi d hae morrhage, p378; Rai sed i ntracrani al pre ss ure , p 382 P.382

Raised intracranial pressure Clinical features Head ache, vom i ti ng, di zz ine ss, vi sual d i st urbance Sei zures, focal ne urol og y, pap i l l oed ema Inc reasi ng b l ood p res sure, bradyc ard i a (l a te res ponses ) Agi tat i on, i ncreas i ng d row si ness , c oma Sl ow de ep bre aths, Che yne –St oke s b reathi ng, ap noea Ips i l a teral progress i ng to bi l at eral p upi l l ary di l at at i on Dec ort i cate progre ssi ng to dec erebrate pos turi ng

Diagnosis CT s can or MR I Int rac rani al pres sure (ICP) me asurem ent >20 mm Hg Lum bar punct ure s houl d be avoi ded be cause of t he ri sk of c oni ng . Nei the r C T s can nor abse nce of pap i l l oe dem a wi l l exc l ude a rai s ed ICP.

Causes Space-occupyi ng l e si on (e .g. ne opl asm , b l ood c l ot , absc ess ) Inc reased capi l l ary p erm eab i l i ty (e. g. trauma, i nfe cti on, encep hal opathy ) Cel l de ath (e .g. post-arrest hy pox i a) Obs tructi on (e. g. hyd roc ephal us)

Management 1. Bed re st, 20–308 head-up ti l t, se dat i on, q ui e t e nvi ronment, mi ni mal s uct i on and noi s e. Sed ati on i s oft en nece ss ary to ove rcome a hyperadrenerg i c state but se dat i ve -i nduc ed hyp ote nsi on shoul d be avoi de d. The tape tet heri ng the e ndot rache al tub e i n p l ac e s houl d not oc cl ude jug ul a r v enous drainage. 2. Venti l ate i f GC S ≤ 8, ai rway unp rot ec ted or exc ess i v el y agi tated . 3. Mai ntai n PaCO 2 at 4–4.5 kPa and av oi d rapi d ri ses . C SF bi c arb onate l ev el s re -eq ui l i b rat e wi thi n 4–6 h, neg ati ng any benefi t from hy pervent i l ati on. 4. If p oss i b l e, moni t or ICP. Ai m to mai ntain ICP 220–230 m mHg ). 5. Jugul ar bul b venous saturat i on (Sj O 2 ) and l act ate may be us eful m oni tori ng te chni ques though do not d ete ct reg i onal i sc hae mi a . 6. Gi v e manni tol 0.5 m g/k g over 15 mi n. R epe at 4-hrl y de pendi ng on CPP m eas ure ment s and/or cl i ni cal si gns of

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dete ri orati on. Stop w hen pl asm a os mol al i ty re aches 310–320 mOsm ol /k g. 7. Avoi d seve re al k al osi s as c ere bral v asc ul a r resi st anc e ri se s and cerebral i s chaemi a i ncreas es. 8. Cons i de r s pec i fi c tre atm ent , e .g. for me ni ngo-enc ephal i ti s, mal ari a, hep ati c e nce phalop athy, surgery. Som e neuros urg eons d ecom press the c rani um for g eneral i se d oedem a b y removi ng a skul l fl ap. Se ek l oc al advi ce . Dexamet has one 4–16 mg q ds IV i s be nefi ci al for oe dema surroundi ng a tumour or ab sc ess and for herp es si mpl ex ence phali ti s .

Acute deterioration/risk of imminent coning 1. Mechani cal l y venti l at e t o PaCO2 3. 0–3.5 kPa for 10–20 mi n. 2. Gi v e manni tol 0.5 g /kg IV ov er 15 mi n. R epeat 4-hrl y as nec ess ary whi l e pl asm a osmol al i ty 0. 4 g /l ). Ne rve conducti on studi es show sl ow c ond uct i on ve l oc i t i es wi th prol onged F w ave s. Other features i nc l ude m usc l e tendernes s and bac k p ai n. T he maj or contri but ors t o morb i di ty and mortalit y are res pi rat ory mus cl e we akness and autonomi c dys functi on (hy pot ens i on, hype rte nsi on, arrhy thm i as , i l e us and uri nary ret ent i on).

Differential diagnosis Other causes of ac ute we akne ss mus t b e e xcl ude d b efore a di agnosi s of Gui l l a i n–Barré sy ndrome can be made.

Specific treatment Int rav enous g amm agl obul i n (0.4 g/k g/day for 5 d ays ) or pl as ma e xchang e (fi ve 50 ml /kg exc hanges ov er 8–13 days ) i s e ffe cti ve i f starte d w i thi n 14 day s of onset of sy mpt oms . Ste roi ds hav e not b een shown to be benefi ci al .

Supportive treatment Respiratory care Reg ul a r c hes t p hys i ot herapy and s pi rome try are requi red. Mec hani c al vent i l ati on i s nee ded i f FVC 2, gi v e 4–6 uni ts FFP. If not b l ee di ng (or hi g h ri s k), gene ral l y onl y c orrec t i f INR >2.5–3. Re peat c l ot ti ng s creen 30–60 mi n after FF P i nfused . Gi ve more F FP i f bl e edi ng conti nues and/or INR > 3. 3. For bl e edi ng rel at ed t o t hrombol ys i s , (i ) s top t he d rug i nfusi on, (i i ) g i ve ei the r aproti ni n 500,000 uni t s over 10 mi n, t hen 200,000 uni t s over 4 h or t ranexami c ac i d 10 mg/kg rep eate d 6–8-hrl y (i i i ) g i ve 4 uni ts FFP. 4. Cryopre ci pi t ate i s rarel y need ed. Consi der when t he thromb i n ti me i s el e vat ed, e.g . w i th DIC. Si m i l arl y, fac tor VIII i s g ene ral l y use d for hae mop hi l i ac s onl y . 5. If aspi ri n has bee n t aken wi thi n t he pas t 1–2 wee ks, pl ate l et funct i on may be de ranged . Gi ve fresh pl ate l et s, even thoug h c ount m ay b e adeq uat e. 6. Fact or VIIa may be use ful for s evere, i ntractabl e bl eed i ng but m ore st udi es are ne ede d t o c onfi rm i t s e ffi cac y. P.397

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Management of major bleeding 1. If e xte rnal, di rec t occl usi on/dee p s uture. 2. Urg ent exp ert op i ni on—e.g . for surgery, end osc opy + i nj ect i on, e tc. 3. Correc t c oagul opat hy.

Management of vascular catheter or percutaneous drain site bleeding 1. Di rect press ure/oc cl usi ve dre ssi ng. 2. Correc t c oagul opat hy; consi d er us e of ap rot i ni n or t ranexami c ac i d . 3. Surgi c al i nterventi on i s rare l y nec ess ary al though pe rforat i on/l a cerat i on of l oc al artery/ve i n shoul d be cons i d ere d i f b l ee di ng fai l s t o s top or be com es si g ni fi cant.

See also: Coagul ati on moni tori ng, p156; Bl ood t ransfusi on, p182; Bl ood produc ts, p252; Coagul ant s and ant i fi bri nol yt i cs , p 254; Aprot i ni n, p256; Haemopty si s , p 304; Uppe r g ast roi nte st i nal haemorrhag e, p 344; Lower i ntes ti nal bl eedi ng and col i ti s , p348; Acute l i ver fai l ure, p360; Chroni c l i ver failure, p364; Pl a tel et di s ord ers , p 406; Syst emi c i nfl am mat i on/mul ti organ fai l ure, p484; Post -op erati v e i nte nsi ve care, p534 P.398

Clotting disorders Unc omm on as a se condary e vent i n c ri t i c al l y i l l pati e nts as they tend t o be auto-ant i coagul at ed. The ri sk of maj or venous throm bos i s i nc re ase s wi th l ong term i mmob i l i ty and p aralys i s, and i n s pec i fi c pro-throm bot i c condi t i ons s uc h as pre gnancy , t hromboti c thromboc ytopeni c purpura, SLE (l up us ant i coagul ant), si ckl e c el l c ri s i s , hype ros mol ar di a bet i c coma. Di sse mi nate d i ntravascul ar coagul at i on i s associ a ted wi th mi c rov asc ul a r c l otti ng, a consum pti on coagul opathy and i nc re ase d fi bri nol ys i s . Cl otti ng of ext rac orp ore al ci rcui ts , e .g. for renal repl ac ement t herapy , m ay be d ue to (i ) mec hani c al obs tructi on to fl ow, e.g . ki nk ed c athete r, (i i ) i nad equate anti c oag ul a ti on or (i i i ) i n sev ere i l l ne ss, a dec rease i n end oge nous ant i c oagul ants (e. g. ant i thrombi n III); thi s may re sul t i n ci rcui t bl ockage des pi t e a coe xi s ti ng thromb ocy top eni a and /or coagul op athy. Axi l l ary ve i n or sub cl a vi a n v ei n throm bos i s may re sul t from i ndwe l l i ng i ntravenous cathe ters.

Management If the pati e nt i s not auto-ant i coagul at ed, prophyl a cti c l ow mol ecul ar we i ght hepari n (5000 IU od SC ) s houl d be g i ve n for l ong term i mmobi l i t y/paral ys i s and to hi gh ri s k p ati ent s (e.g . p rev i ous D VT, fe moral fractures ). For pul monary e mbol i s m or d eep vei n t hrombosi s g i ve 200 IU/kg SC daily (or 100 IU/k g b d i f at ri sk of bl eed i ng ). Parti al thromb opl ast i n ti m es (PT T) s houl d be che cke d regul arl y i f gi vi ng unfract i onate d hepari n and m ai ntai ned at app rox i matel y 2–3 × norm al . Moni t ori ng i s not ne ces sary for LMW he pari n though anti -Fac tor Xa l e vel s c an be use d. Int ra-art eri al cl ot can be treat ed wi t h l ocal i nfusi on of t hrombol yt i c s, usual l y fol l owe d by he pari ni sati on. See k vas cul ar surgi cal ad vi c e. Axi l l ary ve i n or sub cl a vi a n v ei n throm bos i s shoul d be manag ed by e l ev ati on of the affect ed arm , e .g. i n a Bradford sl i ng , and hepari ni s ati on. Spe ci fi c condi ti ons may re qui re spe ci fi c therapi e s, e.g . p l as ma exchang e for SLE and T TP, whol e bl ood exc hange for si ckl e c el l cri s i s. Warfari ni sati on s houl d generally be av oi d ed unt i l shortl y b efore ICU di scharg e b ecause of the ri sk of conti nue d bl e edi ng fol l ow i ng rout i ne i nvas i ve proce dures suc h as c ent ral ve nous c athete ri s ati on. P.399

See also: Coagul ati on moni tori ng, p156; Ant i coagul ants, p248; Thromb ol y ti c s, p250; Bl ood produc ts, p252; Pul monary em bol us, p308 P.400

Anaemia Defi ne d as a l ow haemogl obi n due t o a dec re ase d red c el l m ass , i t m ay als o be ‘p hys i ol og i cal’ due to di l ut i on from an i nc re ase d pl as ma v ol ume, e. g. pre gnancy , vasod i l ate d s tat es.

Major causes in the ICU patient Bl ood l os s, e.g . haemorrhage , regul ar b l ood s ampl i ng Seve re i l l ne ss— analog ous to the ‘ anaemi a of chroni c di sease’ , t here i s d ecreas ed marrow producti on and ,

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poss i b l y, a dec reased l i fes pan

Rarer causes include: Mi c roc yti c anae mi a —predomi nant l y i ron d efi ci enc y Normocy ti c Chroni c d i se ase Bone marrow fai l ure (i di opat hi c, drugs, ne opl asm , radi ati on) Haem ol y si s Renal fai l ure Macroc yti c—v i tami n B 1 2 and fol a te defi ci enc y, al c ohol i sm, ci rrhosi s, si derobl ast i c anaemi a, hyp othyroi di sm Cong eni tal di se ases —s i ck l e cel l , thalas saemi a

Management 1. Tre atme nt of the cause whe re pos si bl e . 2. Bl ood transfusi on: T he i de al haem ogl obi n l eve l for opt i mal oxyg en carri a ge and vi scosi t y remains c ont ent i ous. A rece nt m ul t i ce ntre t ri al showed i m proved out com es i f a t ri g ger of 7 g/d l w as used . A hi gher transfusi on threshol d, e .g. 9–10 g /dl , m ay be need ed i n those wi t h c ard i ores pi ratory di s eas e. T ransfusi on i s usuall y gi ven as packe d c el l s w i th or wi thout a s mal l d ose of furos emi de to m ai ntai n fl ui d b al a nce . T hi s may ne ed to be gi v en rap i dl y d uri ng act i ve bl ood l oss, or sl owl y for corre cti on of a gradual l y fal l i ng haemogl obi n l e vel . Rarel y, pat i e nts ad mi t ted wi th a c hroni c al l y l ow hae mogl ob i n, e. g. < 4–5 g/dl , whi ch often fol l ows l ong t erm m al nutri ti on or vi tami n defi ci enc y, wi l l need a m uch sl owe r e l ev ati on i n hae mog l ob i n l ev el to avoi d p rec i pi tat i ng acut e heart fail ure . An i ni t i a l t arg et of 7–8 g/d l i s ofte n acce ptabl e . Obvi ous l y , t hi s may ne ed t o b e al tered i n the l i ght of any c onc urrent acut e i l l ness where el evati on of ox yge n d el i very i s d eem ed nece ssary. Eryt hropoe i ti n reduces t he need for b l ood t ransfusi on i n l ong -te rm ICU pati e nts and m ay b e useful i n those wi th mul ti pl e anti b odi es or dec l i ni ng t ransfusi on for rel i g i ous reas ons . P.401

Key trial Hebe rt PC, et al for t he T ransfusi on Requi rements i n Cri ti cal Care Inv est i gators, Canadi an Cri ti cal Care T ri al s G roup. A mul ti c ent er, randomi z ed, control l ed cl i ni cal t ri a l of t ransfusi on requi reme nts i n cri t i cal c are . N Engl J M ed 1999; 340:409–17

P.402

Sickle cell disease A c hroni c, heredi tary d i se ase al mos t e nti rel y c onfi ned t o t he bl a ck pop ul a ti on w here t he gene for Hb S i s i nhe ri t ed from e ach parent. The re d bl ood ce l l s l ack Hb A; whe n d epri ve d of oxyge n t hes e c el l s ass ume si ckl e and othe r b i z arre shapes re sul ti ng i n ery throst asi s, oc cl usi on of b l ood v ess el s , t hrombosi s and t i ss ue i nfarcti on. After st asi s, ce l l s rel eas ed bac k i nto the c i rcul ati on are more fragi l e and prone t o haem ol y si s . Occ asi onally , t here m ay b e b one marrow fai l ure.

Chronic features Pat i ents wi t h s i c kl e ce l l di s eas e are chroni cal l y anaemi c (7–8 g/dl ) wi th a hy perdynami c c i rcul ati on. Spl e nome gal y i s com mon i n youth but, wi t h p rog res si v e e pi s ode s of i nfarct i on, s pl e ni c at rophy occ urs l ead i ng to an i ncre ase d ri sk of i nfect i on, p arti c ul a rl y pneum ococcal. Chroni c feat ure s i nc l ud e s ki n ul cers, renal fai l ure, avascul a r b one nec ros i s (± sup erv eni ng ost eom yel i ti s, es pec i al l y Sal monell a), he pat omeg al y , j aundi c e and cardi omyopat hy. Sudde n c ard i ac de ath i s not uncommon, usuall y b efore t he age of 30.

Sickle cell crises Cri ses are p rec i p i tated by vari ous tri gge rs , e. g. hyp oxaemi a (air trave l , anae st hes i a, et c.), i nfec ti on, col d, dehydrati on and em oti onal s tre ss.

Thrombotic crisis Occ urs m ost frequent l y i n bones or joi nts but also affect s c hes t and abd ome n g i vi ng ri s e t o s eve re pai n. Neurol ogi cal sym ptoms (e. g. s ei zures, focal si gns ), hae mat uri a or p ri a pi s m m ay be pre sent. Pul monary cri se s are the commonest

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reason for ICU admi ss i on; s econdary c hes t i nfect i on or AR DS may supervene, w ors eni ng hyp oxaemi a and furt her exacerbat i ng the c ri si s .

Aplastic crisis Rel ate d t o p arv ovi rus i nfec ti on, i t i s sugge ste d b y worse ni ng anae mi a and a re duc ti on i n t he normal l y el e vat ed ret i c ul ocyt e c ount (10–20%).

Haemolytic crisis Int ravasc ul ar hae mol ysi s w i th haemog l ob i nuri a, jaundi ce and re nal fai l ure som eti mes oc curs.

Sequestration crisis Rap i d hep ati c and spl eni c e nl a rg ement d ue to red ce l l trappi ng wi th seve re anaemi a. Thi s c ond i ti on i s parti cul arl y seri ous.

Management Prophy l ax i s agains t c ri ses i ncl ude s av oi d anc e of hypoxaem i a and ot her known pre ci pi t ati ng fac tors, prophy l ac ti c peni ci l l i n and pneum ococcal v acc i ne , and exc hang e t ransfusi ons . 1. Pai nful c ri s es usual l y requi re p rom pt opi ate i nfus i ons. Al t hough psy chol og i c al dep end enc e i s hi gh, anal ges i a shoul d not be wi thhel d . 2. Gi v e ox yge n t o m ai ntai n SaO 2 at 100%. 3. Rehy drate wi t h i ntrave nous fl ui ds and ke ep warm. 4. If i nfe ct i on i s suspe cte d, ant i bi oti cs shoul d b e g i ve n as i ndi cat ed. 5. Transfuse bl ood i f hae mog l ob i n l ev el drops or central nervous s yst em or l ung c ompl i c ati ons prese nt. 6. Lowe r p rop orti on of si ck l e cel l s to 20 mmol/l 20 mmol/l

nephrotic syndrome, cirrhosis, heart failure

20 mmol/l

Causes of inappropriate ADH secretion Neop l as m, e.g . l ung , p anc reas, l ym phoma Most pul monary l esi ons Most ce ntral ne rvous sys tem l e si ons Surgi c al and em oti onal s tre ss Gl ucoc ort i c oi d and thyroi d defi c i ency Idi opathi c Drugs, e. g. chl orp rop ami de, carbamazepi ne, narcoti c s

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Enteral nut ri ti on, p80; Parent eral nut ri t i on, p 82; El e ct rol yte s , p 146; Uri nal y si s , p 166; Cryst al l oi ds, p176; Col l oi ds, p180; Di ure ti c s, p212; Acut e renal fai l ure—di ag nos i s, p332; Ac ute re nal fai l ure— managem ent , p 334; El ect rol yt e m anag eme nt, p414; Di abe ti c ke toaci d osi s, p442; Hyperos mol ar di a bet i c eme rge nci es , p 444 P.420

Hyperkalaemia Pl a sma potas si um d epe nds on the balance bet wee n i ntake, exc re ti on and t he di stri buti on of p otassi um across c el l mem branes . Excreti on i s normal l y control l ed by the ki dne ys.

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Causes Reduced re nal ex cre ti on (e.g . c hroni c re nal fail ure , ad re nal i nsuffi c i ency, di abe tes , p otassi um spari ng di uret i cs ) Int rac el l ul ar pot ass i um re l ease (e.g . aci d osi s, rapi d trans fus i on of ol d b l ood, cel l l ysi s i nc l ud i ng rhab domy ol y si s, haem ol y si s and t umour l ys i s , K + channel ope ners (ni c orandi l )) Potassi um poi soni ng

Clinical features Hyp erk al a emi a m ay c aus e d ang erous arrhyt hmi as i ncl udi ng c ard i ac arre st. Arrhythmi a s are more cl os el y re l at ed to the rate of ri s e of p otassi um than t he abs ol ute l ev el . Cl i ni cal fe atures such as paraes the si a e and are fl e xi c we akne ss are not c l earl y rel a ted to the de gre e of hyperkal aem i a but us ual l y occ ur aft er ECG chang es (tall ‘T’ waves , fl at ‘P’ wav es, prol onge d PR i nterval and w i de QR S).

Management Pot ass i um re st ri c ti on i s need ed for al l c ase s and hae modi afi l t rat i on or haemodi a l ys i s may be ne eded for resi st ant cas es.

Cardiac arrest associated with hyperkalaemia Sod i um bi carbonat e (8.4%) 50–100 m l s houl d be gi ven i n add i t i on to st and ard CPR and ot her t reatme nt det ai l ed bel ow.

Potassium >7 mmol/l Cal ci um c hl ori de (10%) 10 m l s houl d be gi v en urg ent l y i n add i ti on to tre atm ent de tai l ed be l ow . Al thoug h c al c i um chl ori de does not red uc e the p l as ma pot ass i um , i t s tabi l i se s t he myocardi um agai nst arrhythmi a s.

Clinical features of hyperkalaemia or potassium >6 mmol/l with ECG changes Gl ucose (50 ml 50%) and s ol ubl e i nsul i n (10 i u) shoul d be gi ven IV ove r 20 m i n. Bl ood gl uc ose shoul d b e moni t ored eve ry 15 mi n and more gl ucos e g i ve n i f nece ssary. In ad di t i on, c al ci um resoni um 15 g qd s PO or 30 g bd PR can be consi dered. P.421

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Enteral nut ri ti on, p80; Parent eral nut ri t i on, p 82; El e ct rol yte s , p 146; Uri nal y si s , p 166; Cryst al l oi ds, p176; Di ure ti c s, p212; Cardi ac arres t, p272; Brad yarrhy thm i as , p 318; Acut e renal fai l ure— di a gnosi s , p 332; Ac ut e renal fail ure —manage ment, p334; El ec trol y te managem ent , p 414; Rhabdomyol ys i s, p528 P.422

Hypokalaemia Pl a sma potas si um d epe nds on the balance bet wee n i ntake, exc re ti on and t he di stri buti on of p otassi um across c el l mem branes . Excreti on i s normal l y control l ed by the ki dne ys.

Causes Inad equate i ntak e Gas troi nt est i nal l os ses (e. g. vom i ti ng , di arrhoea, fi stul a l os ses ) Renal l oss es (e. g. di a bet i c ket oac i dosi s , C onn's syndrome, se condary hype ral dos teroni sm, Cushi ng' s s ynd rome, renal tub ul a r aci d osi s, met abol i c al kal os i s, hy pom agne sae mi a , d rug s i nc l ud i ng di ureti cs, st eroi ds , t heophy l l i ne s) Haem ofi l trat i on l osse s Potassi um trans fer i nto cel l s (e. g. acute al k al osi s , g l uc ose i nfus i on, i ns ul i n t reatme nt, fami l i al p eri odi c paral y si s )

Clinical features Arrhyt hmi as (SVT, VT and Torsades de Poi nt es) ECG change s (ST dep res si on, ‘T’ wave fl a tte ni ng, ‘U’ wav es) Metabol i c al kal osi s Cons ti pat i on Il e us Weak nes s

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Management Whereve r p oss i b l e, the c aus e of potas si um l oss s houl d be t re ated . Potassi um re pl a cem ent shoul d b e i ntrave nous wi th ECG moni t ori ng whe n t here i s a cl i ni cally si gni fi cant arrhyt hmi a (20 m mol ov er 30 mi n, repe ate d ac cordi ng to l ev el s ). Sl ower i ntravenous re pl a cem ent (20 mm ol ove r 1 h) shoul d be us ed whe re the re are cl i ni cal fe atures wi thout arrhyt hmi as. Oral s upp l em ent ati on (to a t otal i nt ake of 80–120 mm ol /d ay, i ncl udi ng nut ri t i onal i nput ) c an be g i ve n w here there are no cl i ni cal fe atures . P.423

See also: Ent eral nut ri t i on, p 80; Parent eral nutri ti on, p82; El e ctrol y tes , p 146; Uri nal y si s , p 166; Cryst al l oi ds, p176; Di ure ti c s, p212; Steroi d s, p262; C ard i ac arres t, p272; Tac hyarrhythmi as, p316; El e ctrol y te managem ent , p 414; M etabol i c al k al osi s , p 436; Di ab eti c k etoaci dos i s, p442; Pos t-operati ve i nt ens i ve care, p534 P.424

Hypomagnesaemia Causes Exce ss l oss, e. g. d i uret i cs , othe r c aus es of pol yuri a (i ncl udi ng poorl y control l ed di a bet es mel l i tus ), seve re di a rrhoea, p rol ong ed vomi ti ng, l a rge nasog ast ri c as pi rat es Inad equate i ntak e, e.g . s tarvat i on, p are nte ral nutri ti on, al cohol i sm, malab sorpt i on sy ndromes

Clinical features Mag nes i um i s pri m ari l y an i nt rac el l ul ar i on i nvol ved i n the p rod uct i on and uti l i s ati on of energy st ore s and i n t he med i at i on of ne rve trans mi s si on. Low pl asm a l eve l s, whi ch do not nece ssari l y refl ect ei ther i nt rac el l ul ar or whol e bod y s tores, may t hus be ass oc i at ed wi t h fe atures rel a ted to these functi ons: Confusi on, i rri tab i l i ty Sei zures Musc l e weakne ss, l e thargy Arrhyt hmi as Symp tom s rel ate d t o hy poc al c aem i a and hy pokalae mi a whi ch are resi st ant to calci um and potas si um sup pl e ment at i on re spe cti vel y Normal pl asm a l eve l s range from 0.7–1.0 mmol /l ; s eve re sym ptoms do not usual l y occ ur unt i l l ev el s drop bel ow 0.5 mmol /l .

Management Where p oss i b l e, i d ent i fy and t reat t he cause. For sev ere , s ymp tom ati c hypomagnesaemi a, 10 mmol of magne si um s ul p hat e c an be gi v en IV ove r 3–5 mi n. T hi s can be rep eat ed onc e or t wi c e as ne ces sary. In l es s acut e s i tuati ons or for asym ptomat i c hyp omag nes aem i a, 10–20 mm ol MgSO 4 s ol uti on can be gi v en ove r 1–2 h and rep eat ed as nec ess ary , or ac cordi ng to rep eat pl asm a l evel s. A c ont i nuous IV i nfus i on (e .g. 3–5 m mol MgSO 4 s ol uti on/h) c an be gi v en; how eve r, thi s i s usual l y rese rve d for therap eut i c i nd i cati ons whe re sup ranormal pl asm a l evel s (1.5–2 mmol /l ) of magne si um are sought , e .g. tre atm ent of sup rav ent ri cul ar and ve ntri cul ar arrhythmi a s, pre -ec l am psi a and ecl amp si a , b ronchospasm. Oral m agnesi um sul phate has a l axati ve e ffe ct and may cause se vere d i arrhoea. Hi g h p l as ma l eve l s of mag nes i um may de vel op i n renal fai l ure; cauti on s houl d be app l i ed w hen ad mi ni st eri ng IV magnesi um. P.425

See also: Ent eral nut ri t i on, p 80; Parent eral nutri ti on, p82; Cal c i um, m agnesi um and phosp hat e, p148; D i uret i cs , p 212; As thm a—ge neral manage ment, p296; T achyarrhythmi a s, p316; El ec trol yt e m anageme nt, p414; Ge neral i sed se i z ure s, p372; Pre -ec l am psi a and e cl amps i a , p 538 P.426

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Hypercalcaemia Causes Mal i gnanc y (e .g. my el oma, bony m etastati c di sease, hy pernep hroma) Hype rparat hyroi di s m Sarcoi dos i s Exce ss i ntak e of calci um, vi tam i n A or D Drugs, e. g. thi azi des , l i t hi um Immobi l i s ati on Rare l y, thyrotox i c osi s, Add i son's di se ase

Clinical features Usual l y b ecome app are nt when total (i oni sed and un-i oni sed ) p l as ma l ev el s >3.5 m mol /l (normal rang e 2.2–2.6 mmol /l ). Sym ptoms depe nd on the pati e nt' s age, the d urati on and rat e of i ncreas e of pl asm a c al c i um, and the pre sence of concurrent m edi cal c ondi ti ons . Naus ea, vomi t i ng , w ei g ht l os s, pruri tus Musc l e weakne ss, fati g ue, l e thargy Depres si on, mani a, ps ychosi s Drowsi nes s, com a Abd omi nal pain, const i pati on Acute pancre ati ti s Pept i c ul cerati on Pol y uri a, re nal calcul i , renal fail ure Arrhyt hmi as

Management 1. Identi fy and treat cause whe re pos si b l e. 2. Care ful l y moni tor haem ody nam i c vari ab l es , uri ne outp ut, and ECG morphol og y wi th frequent est i m ati ons of pl a sma Ca 2+ , PO 4 3- , Mg 2+ , Na + and K + . 3. Int rav asc ul a r v ol ume rep l et i on—thi s i nhi b i ts proxi mal t ubul ar re abs orp ti on of c al c i um and ofte n l owers the pl a sma cal ci um by 0.4–0.6 mm ol /l . It shoul d prec ede di ure ti c s or any other the rap y. Ei t her col l oi d or 0.9% sal i ne shoul d b e used , de pendi ng on t he pre sence of hypovol aem i a-rel ate d feat ure s. 4. Cal c i ures i s— aft er ade quate i nt rav asc ul a r v ol ume rep l et i on, a force d d i ures i s wi t h furosem i de pl us 0.9% s al i ne (6–8 l /day ) may b e atte mpt ed. An effect i s us ual l y se en w i t hi n 12 h. Loop d i uret i cs i nhi bi t calci um reabsorp ti on i n the asc end i ng l i mb of the l oop of Henl é. More aggres si v e furosemi de re gi m ens can be at tem pte d b ut can pote nti al l y res ul t i n c ompl i c ati ons . T hi a zi des shoul d not b e used as tubul ar reabsorp ti on m ay b e reduced and hype rc al c aemi a w ors ene d. 5. Di a l ys i s/hae mofi l t rat i on—may b e i ndi cat ed at an earl y stage i f the pat i e nt i s i n est abl i s hed ol i go-anuri c renal fai l ure ± fl ui d ove rl oade d. 6. Ste roi ds can be effect i v e for hype rcalc aemi a rel ated to haematol ogi cal cance rs (l y mphoma, m yel oma), v i tami n D overdos e and sarcoi dos i s . 7. Cal c i t oni n has the mos t rap i d ons et of acti on wi t h a nadi r often re ached wi t hi n 12–24 h. It s acti on i s us ual l y short-l i v ed and re bound hype rcalc aemi a m ay occ ur. It ge neral l y d oes not d rop the p l as ma l ev el more t han 0.5 mmol /l . 8. Bi p hos phonat es (e.g . p ami dronat e) and IV phosp hat e s houl d onl y b e gi ven after sp eci al i st ad vi c e i s t ake n i n vi ew of thei r toxi c i t y and p ote nti al com pl i cati ons. P.427

Drug dosage

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Diuretics

Furosemide 10–40 mg IV 2–4 h (may be increased to 80–100 mg IV every 1–2 h)

Steroids

Hydrocortisone 100 mg qds IV or prednisolone 40–60 mg PO for 3–5 days

Pamidronate

15–60 mg slow IV bolus

Calcitonin

3–4 U/kg IV followed by 4 U/kg SC bd

See also: Cal ci um, mag nes i um and p hos phate, p148; Di ure ti c s, p212; Steroi d s, p262; Acut e renal fai l ure—d i ag nos i s, p332; Ac ute re nal fai l ure— managem ent , p 334; Pancreat i t i s, p354; El e ctrol yte manage ment, p414; D i ab eti c ket oaci dosi s , p442; Thy roi d e mergenci e s, p446; Hypoadrenal c ri si s , p 448 P.428

Hypocalcaemia Causes Ass oci ate d w i th hy perphosphataemi a: Re nal fail ure Rhabd omy ol y si s H ypop arathyroi di sm (i ncl udi ng s urgery), ps eudohyp oparat hyroi d i s m Ass oci ate d w i th l ow/norm al phos phate: Cri t i cal i l l nes s i nc l ud i ng se psi s, burns Hypom agnesaemi a Panc reati t i s Oste omalac i a Over-hyd rati on Mass i v e bl ood trans fus i on (c i t rat e-b i nd i ng ) Hype rve nti l a ti on and the re sul ti ng resp i ratory al k al osi s may reducet he i oni se d p l as ma cal ci um frac ti on and i nd uce cl i ni cal fe atures of hy poc al c aem i a

Clinical features The se usual l y appe ar whe n t otal p l as ma c al ci um l eve l s 7.7). It s houl d be g i v en v i a a c ent ral ve i n i n a c onc ent rat i on of 1 mm ol HCl pe r m l w ate r at a rat e not exc eed i ng 1 mmol /kg /h. 4. Comp ens ati on for a l ong-s tandi ng resp i ratory aci dos i s, fol l owed by corre cti on of t hat ac i d osi s, e.g . wi th mechani cal ve nti l a ti on, wi l l l ead to an uncom pensat ed m etabol i c al kal osi s. Thi s usuall y c orrect s w i th ti me though treat ment s s uc h as ac etazol ami de can be consi dered. Me chani c al ‘hy pov ent i l ati on’ , i .e. mai nt ai ni ng hype rc apni a, can al so be consi d ered. P.437

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Bl ood gas anal ysi s, p100; Sod i um bi carbonate , p 178; Bl ood trans fus i on, p 182; Ac ute re nal failure—di agnosi s, p332; Ac ut e renal fail ure —manag ement, p334; Vom i t i ng /gas tri c stasi s, p338; Hyp okalae mi a , p 422; Gene ral ac i d–bas e m anagem ent , p432 P.438

Hypoglycaemia Causes Inad equate i ntak e of c arb ohy drate Exce ss i nsul i n or sul phonyl urea Li v er fai l ure w i th de pl e ti on of g l yc oge n s tores Al c ohol Hypoadrenali sm (i nc l udi ng Addi son's di sease), hy pop i tui t ari sm Qui ni ne, asp i ri n

Clincal features

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Naus ea, vomi t i ng Inc reased sy mpat het i c ac ti v i ty , e .g. sw eat i ng , t achycardi a Al t ere d b ehavi our and consc i ous l eve l Sei zures, focal ne urol og i cal s i g ns

Management 1. Moni tor c are ful l y wi t h regul ar be dsi de est i mati ons . T he freq uency shoul d be i ncrease d i n c ond i t i ons k nown to pre ci p i tate hyp ogl ycaemi a, e.g . i nsul i n i nfus i on, l i v er fai l ure, qui ni ne t re atme nt of mal ari a. 2. Adm i ni ste r 25 m l 50% gl ucos e s ol uti on i f t he bl ood gl ucos e i s: ≤ 3 m mol /l or ≤ 4 m mol /l and the p ati ent i s sy mpt omati c or W i thi n the normal rang e b ut the pati e nt i s sym ptomat i c (us ual l y l ong-s tandi ng p oorl y control l ed di a bet i cs ) Re peat as nece ssary eve ry few mi nute s unti l symp tom s abat e and the bl ood gl ucose l ev el has normal i s ed. 3. If t he bl ood gl ucos e i s 3–4 mmol /l and t he pat i ent i s non-sym ptomati c, ei the r reduce the rate of i ns ul i n i nfusi on (i f pre sent), or i ncreas e calori e i ntak e (e nte ral l y or parenteral l y). In i nsul i n dep end ent di abe tes me l l i tus, the i ns ul i n s houl d conti nue wi t h adeq uat e g l uc ose i ntak e. 4. A c ont i nuous parenteral i nfusi on of 10%, 20% or 50% gl ucos e s ol uti on v ary i ng from 10–100 ml /h may be req ui red, de pendi ng on t he d egree of conti nui ng hypogl y cae mi a and t he p ati ent's fl ui d balance/uri ne out put . 5% gl ucos e s ol uti on onl y contains 20Cal /100 ml and s houl d not be us ed to pre vent or t reat hypogl y cae mi a . 5. In t he rare i ns tance of no v enous acc ess , hypogl y cae mi a may be te mporari l y re versed by gl ucagon 1 mg g i v en ei t her IM or SC . 6. Cont i nui ng hypog l yc aem i a i n the face of adeq uat e t reatme nt and l a ck of s ymp tom s s houl d be confi rmed wi th a form al l ab oratory b l ood s ugar e st i mati on t o ex cl ude mal funct i oni ng of the be dsi de tes ti ng equi pm ent . P.439

See also: Nut ri ti on—use and i ndi c ati ons , p 78; Ent eral nutri t i on, p 80; Pare nte ral nutri ti on, p82; C rys tal l oi ds , p 176; Ac ute l i ver fai l ure, p360; Gene ral i s ed sei zures, p372; Hyp oadrenal c ri si s , p 448; Parac etamol poi soni ng, p456 P.440

Hyperglycaemia Causes A c ommon occurrenc e i n c ri t i c al l y i l l pat i e nts due t o a com bi nati on of i mp ai red gl ucos e t ol e rance, i nsul i n res i st anc e, hi g h c i rcul ati ng l ev el s of endog enous c at echol a mi nes and corti cos teroi d s, and re gul ar adm i ni st rat i on of s uch drugs whi c h antag oni se the effec t of i nsul i n Panc reati ti s re sul ti ng i n i sl et cel l dam age

Clinical features None i n t he short term, other than p ol y uri a from the osmoti c di ure si s. The pat i e nt may com pl a i n of thi rs t or s how si gns of hyp ovol ae mi a i f fl ui d balance i s al l owe d t o b ecom e t oo neg ati ve.

Metabolic effects Rel ati ve l ac k of i nsul i n preve nts ce l l ul a r g l uc ose up tak e and uti l i s at i on re sul ti ng i n: Inc reased l i pol ysi s Al t ere d c el l ul ar met abol i s m Inc reased ri sk of i nfect i on (d ecreas ed neut rophi l acti on)

Prognostic significance St ri c t m ai ntenanc e of g l yc aemi c control (app rox . 4–7 m mol /l ) re sul ted i n s i gni fi cant outc ome i m provem ent i n a surgi cal IC U p opul at i on. W het her thi s i s rel at ed t o p rev ent i on of hy pergl y cae mi a and/or an effec t rel a ted to ad di t i onal adm i ni st rat i on of i nsul i n rem ai ns unc ert ai n.

Management 1. Tre atme nt shoul d be gi ven i f bl ood gl ucose el e vat i ons p ers i s t (> 7–8 mm ol /l ). 2. A s hort-acti ng i ns ul i n i nfusi on (e. g. act rap i d) shoul d b e us ed and ti trate d t o maint ai n norm ogl ycaemi a (4–7

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mmol /l ). Usually 1–4Uni ts /h are re qui red thoug h m ay need to be much hi g her i n di abe ti cs who bec ome cri ti cally ill . R egul ar be dsi de moni tori ng of b l ood s ugar s houl d be performed ; thi s shoul d b e undertaken hourl y i f unst abl e. 3. Oral hypogl y cae mi c ag ent s s houl d be g ene ral l y avoi de d i n t he ICU pati e nt bec aus e of thei r p rol ong ed durati on of act i on and unpredi ctabl e ab sorpti on. P.441

Key trial Van den Be rg he G , e t al. Int ens i ve i nsul i n therapy i n cri ti cal l y i l l p ati ent s. N Engl J Med 2001; 345:1359–67

P.442

Diabetic ketoacidosis Thi s m ay occ ur de novo i n a previ ous l y und i ag nos ed d i abet i c or fol l ow an acute i ns ul t (e.g. i nfec ti on) i n a k now n di a bet i c pat i e nt.

Clinical features Exce ss fat me tab ol i sm to fat ty aci ds wi t h k etone produc ti on An osmoti c d i uresi s w i t h l arg e l oss es of fl ui d (up to 6–10l ), s odi um (400–800 mmol ), pot ass i um (250–800 mm ol ) and mag nes i um Sym ptoms res ul t from hyp ovol ae mi a , m etab ol i c aci dos i s and el ect rol yt e i mbal ance w i t h pol yuri a. Hyp erv ent i l a ti on i s a p rom i ne nt feature. Com a ne ed not ne ces sari l y be prese nt for l i fe to be threat ene d. Pl a sma am yl a se comm onl y e xce eds 1000U/l but doe s not i nd i c ate pancreat i ti s. If sus pec ted , p erform an ab dom i nal ul t rasound.

Monitoring Ade quate i nv asi ve moni tori ng i s ess ent i al , p art i c ul a rl y i f the p ati ent has c i rcul atory i ns tab i l i ty or cardi ac dys functi on. Uri ne out put , b l ood g ase s and pl a sma el ect rol yte s s houl d al s o b e m oni tored fre que ntl y.

Fluid and electrolyte management 1. Fl ui d and el e ct rol yte re pl e ti on s houl d be tai l ored to i nd i v i dual nee ds. Tradi ti onal re gi mens (e .g. 3–4 l wi thi n t he fi rst 3–4 h) i ncre ase the ri sk of ce reb ral oe dema, c ard i ac and/or renal fai l ure. 2. Col l oi d fl ui d c hal l enges shoul d b e g i ve n t o rest ore the c i rc ul ati ng bl ood vol ume i n ti ssue hypoperfus i on. 3. Fl ui d rep l ac eme nt wi t h 0.9% sal i ne s houl d be g i ve n at a rate of 200 ml /h unti l the sal t and wat er deb t has bee n rep l eni shed. 4. Hypotoni c (0. 45%) s al i ne res usc i t ati on may be app rop ri a te i n the non-s hoc ked pat i e nt i f the pl asm a s odi um i s ri s i ng rapi dl y (shi ft of water and p otassi um i nt o c el l s and sod i um out). 5. Sub sti tut e 5% g l uc ose sol ut i on (100–200 ml /h) aft er rep l aci ng t he sod i um de bt; usual l y when the b l ood s ugar fal l s to 48h.

Artemether

3.2mg/kg IM followed by 1.6mg/kg daily

Second line after asexual parasites eliminated Sulfadoxine 500mg/pyramethamine 25mg

3 tablets once

Doxycycline

200mg then 100mg daily for 7 days

See also: Hae mo(d i a)fi l trati on (1), p62; Haemo(di a )fi l trat i on (2), p 64; Bl ood transfusi on, p182; Fl ui d c hal l enge, p274; Ol i guri a, p330; Acute renal fai l ure— di a gnosi s , p 332; Ac ute re nal fai l ure—manage ment , p 334; Ge neral i se d s ei z ure s, p372; Jaundi ce, p358; Anaemi a, p400; Hae mol ysi s, p404; Pl a tel et di s ord ers , p 406; Infec ti on—di a gnosi s , p 480; Infect i on—t reatment, p482; Pyre xi a (1), p518;Pyre xi a (2), p 520 P.492

Rheumatic disorders

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Rheumatoid arthritis A d ebi l i tat i ng arthri t i s that m ay pre sent t o i nte nsi ve care t hrough pul monary i nvol ve ment or t hrough compl i cati ons of treatm ent (e .g. re nal failure, i m munosuppress i on, b l e edi ng di s ord ers ). Pl e uro-pul monary i nvol ve ment may p rec ede the arthri t i c sym ptoms and i s more com mon i n those wi t h acti ve rhe umatoi d d i s ease and m i dd l e age d m en. Care i s req ui red whe n i ntubat i ng p ati ent s w i th rheum atoi d art hri ti s s i nc e t he nec k j oi nts may subl ux.

Rheumatoid pleurisy Rhe umatoi d p l euri s y, oft en wi t h e ffus i on, i s mos t c ommon and i s usual l y asym ptomat i c. Howev er, effusi ons may b e rec urrent or c hroni c and m ay i mp ede res pi rat ory funct i on. T he effusi on i s an exud ate , l ow i n gl ucos e and oft en hi g h i n chol es te rol .

Rheumatoid lung Rhe umatoi d l ung i s a di ffus e i nte rst i t i al pneum oni ti s wi th bi -bas al fi b roti c chang es on the CXR . T he condi t i on may b e di ffi c ul t t o d i st i ng ui sh from i di opat hi c pul monary fi brosi s and produc es a rest ri cti ve pul monary de fec t. The mai ns tay of tre atm ent i s earl y sy ste mi c st eroi d therapy, al though chroni c cas es do not re spond.

Systemic lupus erythematosis (SLE) A non-org an spe ci fi c aut oi m mune d i se ase characte ri sed by ant i nucl ear anti b odi es wi t h hi gh ti tres of ant i doubl e-s trand ed D NA ant i b odi es. A vas cul i t i s i s promi nent , althoug h c utaneous and ce ntral nervous s yst em i nv ol v eme nt are not v asc ul i ti c. SLE may pres ent to i ntensi v e c are through pul monary , renal or c ent ral ne rvous sys tem i nvol vem ent .

Renal failure Renal fai l ure i s v asc ul i ti c i n ori gi n and may p rog res s t o e nd stage renal fai l ure requi ri ng l ong term d i al ysi s. Earl y treatm ent wi th sys tem i c st eroi ds and i mmunos upp res si v es may hal t di s eas e p rog res s.

Lupus pleurisy and pericarditis Unl i ke rheum atoi d pl e uri sy the p l eural i nvol vem ent i n SLE i s ofte n p ai nful and associ a ted wi th l arge pl e ural effusi ons .

Pulmonary haemorrhage Pul monary haemorrhage i s as soc i at ed wi t h renal fai l ure and m ay be l i fe t hre ate ni ng. Pl a sma exc hange may be hel pful .

Interstitial pneumonitis Int ersti ti a l p neumoni ti s i s unc omm on i n SLE. It i s m ore l i kel y t hat parenchy mal i nfi l trate s are i nfect i ve i n ori g i n sec ond ary to i m munosuppress i ve therapy.

Pulmonary thromboembolic disease Pat i ents typ i c al l y have a p rol ong ed act i vated parti al throm bop l as ti n ti me due to ci rcul a ti ng l upus anti coagul ant . b ut are more prone to thromb oti c e pi s ode s. Lup us ant i c oagul ant i s ass oci ate d w i th anti c ard i ol i p i n ant i bodi e s and a fal s e pos i t i ve VD RL. Rec urrent p ul m onary embol i may be as soc i at ed wi t h c hroni c p ul m onary hype rt ens i on. T reatment i s l ong t erm anti c oag ul ati on. P.493

See also: End otracheal i ntubat i on, p 36; Pl a sma exc hange, p68; Non-op i oi d anal ges i cs , p 236; Steroi d s, p262; Haem opt ysi s, p304; Acute renal fai l ure— di a gnosi s , p 332; Ac ute re nal fai l ure—manage ment , p 334; Up per gastroi nte sti nal hae morrhage, p344; Vascul i t i d es, p494 P.494

Vasculitides Vas cul i t i s shoul d b e susp ect ed i n any pat i ent w i th mul t i sy ste m d i se ase , e spe ci a l l y i nvol vi ng t he l ungs and ki dne ys.

Wegener's granulomatosis A s yst emi c vasc ul i ti s c harac teri se d b y necroti si ng granul omas of the uppe r and l ow er res pi ratory tract , gl omerul onep hri ti s and small ves sel vascul i ti s . W ege ner's granul omatos i s i s as soc i at ed wi t h p osi ti v e c ore ant i ne utrop hi l cy top l as mi c anti bodi es (c-ANC A), parti cul arl y granul ar wi t h c ent ral atte nuati on on i mm unofl uore sce nce . Inte nsi ve care admi ss i on i s us ual l y bec aus e of renal and/or p ul m onary i nv ol v eme nt.

Renal failure Foc al nec rot i s i ng gl ome rul one phri ti s l eads to progre ssi ve renal fai l ure. Treatm ent wi th ste roi ds and cyc l op hos phami d e m ay gi v e c ompl et e remi ssi on.

Upper airway disease Mos t p ati ent s w i l l have nas al sym ptoms i nc l udi ng e pi s tax i s, nasal di sc harge and sep tal pe rforat i on. Int ens i ve care adm i ss i on may b e requi re d rare l y for se vere e pi s tax i s. Ul cerat i ng l e si ons of the l a rynx and t rache a may c aus e

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sub gl ott i c ste nos i s. Thi s i s us ual l y i ns i d i ous b ut may present p robl e ms on atte mpt ed i nt ubati on.

Pulmonary involvement Usual l y associ ate d wi th hae mop tys i s, dy spnoea and c oug h wi th round ed opac i t i es on the CXR. The re may be cav i tati on. Nod ul es m ay be sol i tary. Al veol ar haemorrhage may b e l i fe threateni ng . T he mai nst ay of t reatme nt i s ste roi ds and c ycl ophosp hami de whi ch may produce com pl e te rem i ss i on. Pl as ma exc hange may be hel pful .

Polyarteritis nodosa (PAN) PAN i s a nec rot i s i ng vascul i t i s affect i ng s mal l and medi um si zed muscul ar arteri e s. Int ens i ve care admi ss i on may be provok ed by renal fai l ure, i sc hae mi c he art di sease, hy pertensi ve c ri si s and b ronchospasm, al though true pul monary i nv ol v eme nt i s unc omm on. Di agnosi s m ay be c onfi rmed by mes ent eri c angi ograp hy or renal b i opsy . Treat ment i nv ol v es renal rep l aceme nt the rap y, hi g h d ose st eroi d s and c ycl op hos pham i d e.

Goodpasture's syndrome Ant i g l om erul ar basem ent me mbrane (anti -GBM ) anti bod i es bi nd at the gl ome rul us and al veol us . Pati ent s p res ent wi th a p rol i fe rat i v e gl ome rul onephri t i s and haemopty si s . D i ag nos i s i s confi rme d b y p osi ti v e anti -GBM anti bod i es and renal bi opsy . T reatme nt i s wi t h i mmunos upp res si ve the rap y and p l as ma exc hange. P.495

See also: Pl a sma ex change , p68; Ai rway obst ruc ti on, p280; Ste roi ds, p262; Hae mop tys i s, p304; Ac ute re nal failure—di agnosi s, p332; Acute renal fai l ure— managem ent , p 334; Rheumati c d i sorde rs, p492 P.496

Anaphylactoid reactions Mi nor react i ons t o al l e rge ns (i t chi ng, urti cari a) are c omm on b efore a s evere reac ti on occ urs ; any s uc h hi st ory shoul d be tak en seri ousl y and p ote nti al al l ergens av oi d ed. Most reacti ons are acut e i n onse t and cl e arl y rel ated to the causat i ve al l erge n. Howe ver, s ome com pl ement-m edi ate d reac ti ons may take l ong er to dev el op.

Clinical features Resp i ratory— laryng eal oe dema, b ronchospasm, pul monary oede ma, pul monary hy pertensi on Card i ov asc ul ar— hyp ote nsi on, tachy cardi a , g ene ral i se d oede ma Other— urt i c ari a, ang i o-oede ma, ab domi nal c ram ps, ri gors

Management 1. Stop al l i nfusi ons and b l ood t ransfusi ons and wi thhol d any p ote nti al drug or food al l ergen. Bl ood and bl ood produc ts shoul d be re turned to the l aborat ory for anal ysi s. 2. Start oxy gen (FIO 2 0.6–1. 0). If there i s evi de nce of persi ste nt hyp oxae mi a consi der urgent i nt ubati on and mechani cal ve nti l a ti on. 3. If t here i s l aryng eal ob struct i on, b ronchosp asm or fac i al oe dem a g i ve IM or neb ul i se d e pi nephri ne and IV hydroc ort i sone. If there i s not rapi d rel i ef of ai rway ob struct i on, c ons i d er urg ent i ntub ati on or, i n ex tre mi s , emergency cri cothy roi dot omy or tracheos tom y. Pers i s tent b ronchospasm may re qui re an epi nep hri ne i nfusi on, ami nophyl l i ne i nfusi on or assi st ed e xpi rat i on (m anual che st com pre ssi on). 4. Hypotensi on s houl d be treate d w i th ep i ne phri ne IV/IM and rapi d c ol l oi d i nfusi on. Large vol ume s of c ol l oi d may b e req ui red to rep l ac e t he pl a sma vol ume de fi c i t i n se vere anaphyl a xi s . Seve re oede ma may coe xi s t w i t h hy pov ol a emi a. Pl as ma v ol ume has not b een ade quatel y repl ace d i f t he hae mog l ob i n i s hi g her than normal . Hetastarch i s the m ost ap propri ate fl ui d for c ol l oi d resusci tati on unl e ss the re act i on i s due t o a hydroxye thy l s tarch. 5. Pers i s tent hypotensi on s houl d be tre ate d wi th further epi nep hri ne, hy drocorti sone and c ol l oi d i nfusi on g ui d ed by cent ral v enous p re ssure ± c ard i ac output m oni tori ng . An e pi nephri ne i nfusi on may be req ui red to ove rcome myoc ard i al d epress i on. T he use of mi l i t ary anti s hoc k t rousers or nore pi nephri ne shoul d be consi dered to di v ert bl ood c ent rally and i ncreas e p eri phe ral resi stance . 6. Urt i cari a re qui re s c hl orphenami ne IV or PO d epe ndi ng on the sev eri ty of the re act i on. 7. Aft er control of t he anap hyl act oi d reac ti on, adv i ce shoul d b e s oug ht from the i mmunol ogy l a boratory and appropri a te sam pl e s t aken for c onfi rmati on. 8. Reac ti ons to l ong-acti ng drugs or fl ui d s w i l l requi re conti nue d s upp ort (p erhaps for m any hours). P.497

Drug dosages

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Laryngeal oedema and bronchospasm Initial dose

Continued treatment

Epinephrine

0.3–0.5mg IM or 0.5mg nebulised

Start at 0.05µg/kg/min

Hydrocortisone

200mg IV

Hypotension Initial dose

Continued treatment

Epinephrine

0.5–1.0mg IM or 0.05–0.2mg IV

Start at 0.05µg/kg/min

Hetastarch 6%

500ml

According to response

Hydrocortisone

200mg IV

200mg IV qds

Chlorphenamine

10mg IV tds

Urticaria Chlorphenamine

10mg IV tds or 4mg PO tds

Hydrocortisone

50–100mg IV tds

Prednisolone

20mg PO daily

See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; Col l oi ds , p180; Bl ood trans fus i on, p 182; Inotropes , p 196; Bl ood p rod uct s, p252; Ste roi ds, p262; Bas i c re sus ci t ati on, p270; F l ui d c hal l e nge , p274


Ed itors:


Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > Tr a u ma an d Bu r n s

Trauma and Burns Multiple trauma (1) Suc h p ati ents are adm i t ted ei the r afte r s urg ery or for c l os e obse rvati on and medi cal m anag eme nt. The p ri nci pl e s of manage ment are t o: Mai ntai n or qui ckl y rest ore ad equate ti ssue p erfusi on and gas e xchange Cont rol pain Sec ure haemos tas i s and c orrect any c oagul opat hy

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Prov i d e ad equate nutri ti on Moni tor c l os el y and d eal prompt l y wi th any com pl i cati ons

Circulatory management Pati ent s are oft en col d and vas oconst ri c te d on ad mi s si on. Thi s serves to camoufl ag e c onc urrent hypov ol a emi a and com promi s e t i s sue perfusi on. Ade quat e m oni tori ng m ust be i nsti tut ed at an earl y stage. Deve l op ment of a persi sti ng ti ssue oxyge n d ebt has b een shown to l ead t o s ubs equent mul ti pl e organ dysfunc ti on whi ch may not be com e c l i ni call y ap parent for 3–7 day s. The refore , adequate pe rfusi on m ust be res tored prompt l y by rep eat ed fl ui d challe nge s. Add i ti on of a v asodi l ati ng age nt, e. g. gl y ceryl tri ni trate, may b e bene fi c i a l . An i nc reasi ng m etabol i c aci dos i s shoul d p rom pt sus pi c i on of i nade quate res usc i t ati on, covert haemorrhag e or ti s sue ne crosi s . M yoc ard i al de press i on or fai l ure may al so b e i mpl i c ate d.

Respiratory management Cons i de r t he pos si bi l i t y of a fractured , unst abl e neck , e spe ci a l l y i n unconsc i ous p ati ent s. Thi s s houl d be excl ud ed b y appropri at e radi ol ogy and an ex pert opi ni on. Unti l t hen the neck shoul d b e i mmobi l i se d. If v ent i l ate d, e nsure hae mod ynami c st abi l i ty, re moval of any metabol i c ac i dosi s , adeq uat e rewarmi ng and sat i sfact ory gas e xchange be fore atte mpt i ng to wean. If the pati e nt rem ai ns unst abl e, i t i s ad vi s abl e t o d el a y extubat i on i n c ase urgent s urg ery i s re qui red . If s pontaneousl y breat hi ng, gi ve s upp l e ment al oxy gen to provi de adeq uat e arte ri al oxyg enati on, enc ourage de ep bre athi ng to prevent atel ec tas i s and se condary i nfe cti on, and ensure suffi c i ent anal ges i a, al bei t not too much to sup pre ss venti l atory dri ve.

Haematological management Mai ntai n haem ogl obi n > 7g/dl (hi ghe r w i th cardi oresp i ratory d i se ase ) t o as si st oxy gen trans port. Cross-mat che d bl ood s houl d be readi l y avai l ab l e for se condary haem orrhag e. Correc t any c oag ul opat hy wi t h fres h frozen pl a sma, ± pl atel et s, and , oc cas i onal l y, ot her bl ood products (e .g. cry opreci pi t ate ) or acti vat ed fac tor VII.

Peripheries Inj ury to the l i mb may resul t i n nerve i nj uri es , ob st ruc ti on of t he vas cul ar sup pl y , or m usc l e dam age whi ch may l e ad to com partme nt syndrome and rhabd omyol ys i s . A hi gh l ev el of s us pi c i on shoul d b e hel d and c orrect i ve surg ery und ert ake n p rom ptl y i f nece ssary. P.501

See also: Venti l at ory support— ind i c ati ons , p 4; Che st drai n i nserti on, p42; Nutri ti on—use and i ndi cat i ons, p78; Bl ood gas analys i s , p100; Bl ood press ure moni t ori ng, p110; Ful l b l ood c ount, p154; C oag ul a ti on m oni tori ng, p 156; Lact ate , p170; Cry stalloi ds , p 176; Col l oi d s, p180; Bl ood t ransfusi on, p182; C oag ul a nts and anti fi b ri nol yti cs, p254; Bas i c res us ci t ati on, p270; Fl ui d challe nge , p 274; Pneum othorax, p300; Hae mot horax, p302; Hyp ote nsi on, p312; Anaem i a, p400; General aci d –base managem ent , p 432; Metabol i c ac i dosi s , p 434; Infec ti on—d i ag nos i s , p 480; Infect i on—t reatment, p482; Mul ti p l e trauma (2), p 502; Head i njury (1), p504; Head i njury (2), p506; Rhabdomyol ys i s, p528 P.502

Multiple trauma (2) Analgesia Ade quat e anal ges i a i s i m perati ve to avoi d c i rcul atory i ns tabi l i ty and d ecreas ed che st wal l e xcursi on, es pec i al l y fol l owi ng chest , ab dom i nal or s pi nal traum a. Inc reased us e of re gi onal te chni q ues (de pendi ng on abse nce of i nfect i on and c oag ul opat hy) and pati ent-c ont rol l ed anal g esi a has fac i l i tat ed pai n rel i ef and we ani ng. Opi ate s are rec omme nde d for i ni ti al analge si a . N on-s te roi dal s are parti c ul arl y e ffec ti ve for bony p ai n thoug h may occ asi onall y prec i pi tat e c oag ul opat hi e s, stres s ul ce rat i on and renal fai l ure . Agi tat i on may b e due t o c aus es other than p ai n, e .g. i nfec ti on, i nt rac rani a l l esi on.

Nutrition Earl y nut ri ti on has bee n s hown to re duc e p ost -op erati v e c omp l i c ati ons . T hi s s houl d i de al l y b e e nte ral , an approac h

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whi ch has be en demonst rated to be safe, even after ab dom i nal l aparot omy for t rauma.

Infection Depe ndi ng on the si te of trauma, t he typ e of wound (op en/cl osed , c l ean/d i rt y), and t he need for s urg ery, prophyl ac ti c te tanus and anti b i ot i c cover varyi ng from 1 dos e t o 1–2 week s m ay b e need ed. The trauma pati e nt i s at hi gh ri s k of de vel opi ng sec ond ary i nfec ti on, i n parti cul ar chest , wound si tes , i nt rav asc ul a r c athete r i ns ert i on si tes , p ost -ab dom i nal t rauma, i ntra-ab dom i nal absc ess es. Preve nti ve measures and stri c t i nfe cti on control shoul d be undertak en. Int rav asc ul a r c athete rs i nserted duri ng e mergency res usc i t ati on und er non-ste ri l e condi t i ons s houl d be rep l ac ed.

Prophylaxis Att ent i on shoul d b e p ai d to press ure areas ; t hi s may i nvol ve the us e of s pec i al i s ed m att re sse s or s upp ort be ds. Cl ear i ns tructi ons s houl d be obtaine d from the s urg eon re gardi ng c are of the wound and d rai n s i t es. Esp eci al l y afte r orthopaedi c p roc edures on the p el v i s and l ower l i mb, or i f the p ati ent wi l l rem ai n i mmob i l i se d, hepari n p rop hyl axi s agai nst de ep venous thromb osi s shoul d be i nsti tut ed.

Review Regul ar revi ew of t he pat i ent i s nece ssary to ens ure compl i cati ons are de tec ted and d eal t w i th promp tl y . T hi s may req ui re repe at l ap arotom y, ul t ras ound or C T s canni ng. Lat er com pl i cat i ons i nc l ud e p anc reati t i s , ac al cul ous chol e cys ti t i s , and mul ti p l e org an dys functi on (i ncl udi ng ARD S). P.503

See also: Nut ri ti on—use and i ndi c ati ons , p 78; Spe ci a l s upp ort s urface s, p86; Opi oi d anal g esi cs , p 234; Non-op i oi d anal ges i cs , p236; Ant i c oagul ants , p 248; Anti m i crob i al s, p260; Acut e resp i ratory d i s tre ss syndrome (1), p292; Acute res pi ratory di s tress sy ndrome (2), p 294; Infe cti on—di a gnosi s , p 480; Infec ti on—tre atm ent , p 482; Mul ti pl e traum a (1), p500; Head i njury (1), p504; Head i nj ury (2), p506; Pai n, p532 P.504

Head injury (1) The he ad may be i nj ure d w i th or wi thout si g ni fi c ant traum a t o ot her part s of the b ody . Pri ori ty i n managem ent of the mul ti pl y i njured pat i ent m ust be pl ace d on s ecuri ng adeq uat e gas e xchang e and ci rcul at ory re sus ci t ati on, and d eal i ng wi t h any l i fe-t hre ate ni ng i njury, e. g. an art eri al i njury, b efore defi ni ti ve t re atme nt for he ad i nj ury . The pati e nt wi l l usual l y b e ad mi t te d t o the ICU aft er CT s canni ng has i d ent i fi ed the ext ent of i njury. The ne ck shoul d al s o b e i mag ed by C T, parti cul arl y i f t he pat i ent i s v ent i l ate d. It i s al s o l i ke l y that s urg ery wi l l have b een undertak en for any s i gni fi cant s pac e-occupyi ng l es i on or for e l ev ati on of a d epress ed fracture.

General management An uns tab l e nec k frac ture s houl d be ass umed unti l e xcl ude d b y an ex pert opi ni on and appropri at e i nve sti gati ons. Most he ad i nj ury pati e nts ad mi t ted to non-neurosurgi cal ICUs wi l l have di ffuse or l oc al brai n i njury for whi ch a non-ope rat i ve ap proach has b een adopte d. The Reg i onal Neuros urgery Ce ntre s houl d be contac ted i f rai s ed i nt rac rani al pres sure i s p res ent as l ocal pol i cy may enc ourage earl y bone fl ap de com pre ssi on or re ferral for i nv asi ve m oni tori ng (e.g. i ntracrani al press ure , j ugul ar ve nous bul b O 2 s aturat i on). If a basal sk ul l frac ture i s s usp ect ed (e. g. X-rays , rhi norrhoe a, otorrhoea), avoi d nasal i ns ert i on of fee di ng or endotracheal tubes . Det eri orati on i n c ons ci ous l e vel , d evel opi ng neurol og i cal d efi ci t s or focal s i g ns (e.g . uni l at eral p upi l l ary di l atati on) shoul d promp t urge nt rep eat CT sc anni ng for l ate compl i cati ons, e. g. sub dural hae mat oma.

Complications Act i ve l y manage rai se d i ntracrani al press ure . Act i ve l y tre at sei zures wi th ant i convul sants to preve nt furthe r hypoxaem i c ce reb ral damag e, reduce cerebral oxyg en req ui reme nts and ICP. The pati ent shoul d b e l oade d w i th IV pheny toi n as p rop hyl axi s agai nst furt her fi ts. Cons i de r addi ti onal c aus es suc h as hypogl y cae mi a , de vel opm ent of a new space-occ upy i ng l e si on, rec reati onal drugs and i nfec ti on. Di a bet es i ns i pi dus s ugg est s hypot hal ami c i nj ury and c arri es a poor p rog nos i s. De smopre ssi n 1–4µg IV shoul d be gi v en d ai l y t o m ai ntai n uri ne out put of 100–150ml /h. Act i ve l y manage hyp erp yre xi a . Some st udi es show l ong -te rm benefi t from i nduc ed hypothe rmi a b ut thi s nee ds to

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be aggress i v el y i nsti tut ed as earl y as pos si b l e aft er the i njury t o b e e ffec ti ve. Act i ve l y manage hyp erg l yc aem i a wi t h i ns ul i n, and avoi d hyp ogl ycaemi a. P.505

Key papers Rov l i a s A, K ots ou S. The i nfl uenc e of hy pergl yce mi a on neurol ogi cal outc ome i n pat i e nts wi th sev ere head i njury. Neuros urgery 2000; 46:335–42 Cl i fton GL, M i l l er ER, Choi SC et al . Lack of e ffe ct of i nd uct i on of hy pot hermi a aft er acute brain i njury. N Engl J M ed 2001; 344:556–63

See also: Ant i c onv ul s ant s, p242; Ne uroprote cti ve agents , p 244; Ge neral i sed se i zures , p 372; Intracrani al haem orrhage, p376; Rai sed i ntracrani al pre ssure, p832; M ul t i p l e trauma (1), p 500; Mul t i pl e t rauma (2), p520; He ad i nj ury (2), p 506; Spi nal c ord i njury, p508 P.506

Head injury (2) Analgesia Ade quat e anal ges i a (us ual l y opi ate s) mus t b e g i ve n t o t he head -i njured pat i ent as p ai n and agi t ati on wi l l i nc rease i nt rac rani a l p res sure, the reb y c aus i ng a sec ond ary i nsul t. Short-act i ng se dat i on shoul d b e used as thi s enabl e s rapi d asse ssm ent of the underl y i ng consc i ous l eve l and any focal neurol ogi cal de fi c i t.

Respiratory management Agg res si v e hype rve nti l at i on i s no l onge r rec omme nde d apart from short -te rm managem ent of raise d i ntrac rani al pre ssure. If venti l at ed, ai m t o maintai n t he PaCO 2 at 3.5–4kPa. Face or ne ck i nj uri es may have requi red emergency cri cothy roi dot omy or tracheos tom y t o ob tai n a patent ai rway. If orotracheal l y i ntub ate d, ens ure l ocal sw el l i ng has s ubs i d ed (nas end osc opy , air l eak around defl at ed cuff) b efore extubat i on. Seve re agi tat i on and c onfusi on may l a st for se veral week s; thi s w i l l ofte n de l ay we ani ng and ext ubati on. Judi ci ous se dat i on, e .g. wi t h c hl orp rom azi ne, may be ne ces sary.

Circulatory management Hypotensi on s houl d be avoi de d w i th ad equate fl ui d re sus ci t ati on ± v asopre ssor t herapy . El e vate d b l ood p res sures may be tol erate d unl e ss exc ess i ve . β-bl ock ers may b e useful i n red uci ng the my ocardi al effect s of ex ces si ve c at echol a mi ne l evel s.

Other drug therapy Ant i bi oti c prophy l ax i s i s not routi nel y rec omme nde d. Hi g h-dose ste roi d the rap y has not yet be en shown t o b e b ene fi c i al . Tri al s of ot her ne uroprotec ti v e agents, e. g. fre e radi cal sc ave nge rs, have als o fail ed t o s how be nefi t.

Indications for consideration of intracranial pressure monitoring Indications GCS ≤8 and any ab normal i t y on CT sc an GCS ≤8 and a normal CT scan b ut any tw o of the fol l owi ng: Age >40 ye ars Hypotensi on Dec ere brate pos turi ng GCS >8 but : Requi ri ng ge neral anae st hes i a for treat ment of ot her i njuri e s Requi ri ng treat ment l i ke l y to i nc rease ICP, e .g. hi gh l ev el s of PEEP

Contraindications

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Coag ul opat hy Infe ct i on? ICP moni t ori ng shoul d be conti nue d: As l ong as t he ICP i s el e vat ed Duri ng ac ti v e m anageme nt of ICP For up to 3 d ays i n the ab sence of si g ni fi c ant el evat i on P.507

See also: Venti l at ory support— ind i c ati ons , p 4; Endot rac heal i ntubat i on, p 36; Int racrani a l p res sure m oni tori ng, p134; Jug ul a r venous bul b sat urati on, p136; Hypotensi on, p312; Rai sed i ntracrani al pre ssure, p382; Pai n, p 532 P.508

Spinal cord injury Spi nal i njury, wi th or wi t hout d amag e t o t he cord, may be app are nt soon afte r admi ssi on to hos pi t al ; howeve r, det eri orati on may occ ur, requi ri ng a hi gh i ndex of suspi ci on and careful m oni tori ng.

Immobilisation The spi ne shoul d be i m mob i l i se d unti l a se ni or s urgi c al /ort hop aed i c opi ni on has confi rmed that no uns tab l e frac ture i s pre sent, bot h radi ol ogi cal l y and cl i ni cal l y . Pl ac e a hard cervi c al col l a r i f a ne ck fracture i s pos si b l e . Thi s does not st abi l i s e t he spi ne; ei the r s kul l t racti on or operati ve st abi l i s ati on wi l l be need ed for an unstabl e fract ure . Move the p ati ent by ‘l og-rol l i ng’ or st rai ght -l i fti ng , usi ng at l eas t four st aff mem bers. Exe rci se care w i t h ne ck mani pul at i on; i ntubat i on shoul d b e p erform ed b y an e xpe ri e nce d operator.

Circulatory instability So-c al l ed ‘s pi nal shock’ may oc cur w i th marke d hy pot ens i on due t o s ymp atheti c outfl ow di sturbance . Hypovol aem i a shoul d be exc l uded fi rst . C ons i de r d amage t o othe r organs/ves sel s, e.g . s pl e en, aorta. Vas opress or the rap y m ay b e nece ssary i f evi dence of t i s sue hy pop erfusi on persi s ts , e. g. ol i guri a , m etabol i c aci dos i s. Post ural hyp otensi on and ci rcul at ory i nst abi l i t y (i nc l udi ng s ymp tomati c b rad ycardi a) i s com monpl a ce for the fi rs t few week s. Aut onomi c dy sfunct i on affec ts 50% of ce rvi cal and hi gh thoraci c c ord i njuri es .

Respiratory management Hi g h c erv i cal c ord i njury abov e C5 resul ts i n l oss of di a phragm ati c func ti on, whe reas abov e C8 can resul t i n l oss of i nte rc ost al functi on. Thi s may compromi se or pre vent b reathi ng and weani ng from IPPV. When ab l e, the p ati ent shoul d b e m anaged i n an upri g ht pos ture. Ate l ec tas i s i s common and requi re s regul a r p hys i ot herapy . Earl y trache ost omy may faci l i t ate support and com fort.

General measures Care ful l y moni tor neurol ogi cal funct i on to enabl e e arl y d ete cti on of s pi nal cord com pre ssi on and re ferral for urg ent re medi al surge ry. Gi v e LMW hepari n SC for t hromboemb ol i sm prophy l ax i s . The i nc i d enc e of st re ss ul c erati on i s hi g h. Ide al l y, ent eral nutri t i on shoul d b e i nst i tuted at an earl y st age thoug h thi s m ay p rov e unsucce ss ful . D rug s (e.g . s ucral fate , H 2 bl ocke rs ) may b e neede d. Ent eral feedi ng may be di ffi cul t t o i ns ti t ute i ni t i al l y as gas tri c d i s tensi on and paral y ti c i l eus i s c omm on fol l owi ng spi nal cord i nj ury . A NG tube shoul d be i nserted for g ast ri c d ecompress i on. An e nte ros tom y m ay e ventually be need ed to enabl e l ong-t erm fe edi ng. Bowe l and bl a dde r func ti on m ay be derang ed. Long-t erm si l a sti c b l ad der cathe ters and reg ul ar l ax ati ve and enem a t herapy shoul d b e i nst i tuted at an earl y st age . Spe ci a l c are i s ne ede d t o p rev ent press ure sores . Ins ti t ute re gul ar exe rci se s t o p rev ent contract ure s. Psyc hol ogi cal s upp ort for p ati ent and fami l y i s cruci al , parti cul arl y i f l ong-t erm di sab i l i ty i s l i kel y.

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Hi g h-dose ste roi d the rap y may b e b enefi c i al i f st art ed wi t hi n 8h, t hough thi s sti l l re mai ns controversi a l . Hype rbari c oxyge n t herapy i s of unproved be nefi t. Aft er spi nal i njury, mus cl e rel a xant s m ay cause sev ere hyp erkal aemi a. Ste roi ds hav e b een shown to be useful but t hi s re mai ns controversi al . P.509

Key trial Brack en M B, et al . Ad mi ni s trati on of m ethyl p red ni s ol one for 24 or 48 hours or ti ri l az ad mes yl a te for 48 hours i n the treatm ent of ac ute sp i nal c ord i njury. Res ul t s of t he Thi rd Nat i onal Ac ute Sp i nal C ord Injury R and omi zed Control l ed Tri al . N ati onal Acut e Spi nal Cord Injury St udy . JAMA. 1997; 277:1597–604

See also: Spe ci al sup port s urface s, p86; Bl ood press ure moni t ori ng, p110; H 2 bl ocke rs and proton p ump i nhi b i tors, p218; Suc ralfate, p220; Ant i coagul ants , p248; St eroi ds , p 262; Fl ui d chal l eng e, p274; Hyp ote nsi on, p312; Ac ute weakne ss, p368; Met abol i c ac i dosi s , p 434; Mul t i pl e t rauma (1), p500; Mul ti pl e trauma (2), p502; Head i njury (1), p504; Head i nj ury (2), p506 P.510

Burns—fluid management Maj or the rmal i njuri es (i .e . > 20% bod y s urface area) are ad mi tte d t o an i ntensi ve c are uni t , usually sp eci al i si ng i n the manag ement of b urns, for me ti c ul ous att ent i on t o fl ui d resusci tat i on, pre vent i on of i nfec ti on, and the freq uent nee d for mec hani cal v ent i l a ti on.

Monitoring The fl ui d l oss from major burns requi re s c are ful as ses sme nt of i nt rav asc ul a r v ol ume status . T he tradi t i onal mark ers of fl ui d resusci tat i on i n burns of ce ntral venous press ure, uri ne out put and haematoc ri t are gene ral l y i nadequate . Ei t her i nvas i ve or non-i nvas i v e c ard i ac output m oni tori ng i s ne ede d for acc urate ti t rati on of fl ui d. Thi s i s parti c ul a rl y ap pl i cabl e i n the p res enc e of a hyp erd ynami c , v asodi l ate d c i rcul ati on whi ch oft en com menc es wi t hi n 1–2 day s. Al though i nfec ti on i s not nec ess ari l y present, vas opress or therapy m ay be need ed to mai ntain adeq uat e s yst emi c b l ood p res sures . Pul monary art ery and c ent ral ve nous c athete rs shoul d not b e i nse rt ed t hroug h affec ted sk i n are as i f at al l poss i b l e. Ins ert i on of i ntravas cul ar cat het ers, uri nary c athete rs and NG tubes shoul d b e c arri ed out s oon after ad mi s si on as rapi d ons et s wel l i ng wi t hi n a few hours may make t hes e p roc edures i mpos si bl e .

Fluid management The ext ent of i njury wi l l have been es ti mate d b y p l as ti c s urg eons who w i l l al so det ermi ne t he p roporti on of ful l thi ckness de rmal i njury to cal cul ate the approxi mat e fl ui d resusc i tati on requi red. Fl ui d res usc i tati on i n the UK oft en fol l ows t he M ount Vernon (al bum i n-bas ed) formul a w hi l e t he Parkl a nd (cryst al l oi d -based ) formul a i s oft en use d i n t he US. Col l oi ds may reduce oed ema at non-burn si t es and re store bl ood v ol ume fas ter than cry stall oi d s. Thes e form ul a e onl y provi de an approxi mat e g ui de and fre que ntl y unde res ti mate l oss es b oth i nto the i nte rst i ti al spac es and through the l ost ski n barri e r. Evaporati ve l os ses are approxi mat el y 2m l /k g/h. Water l oss es may be i nc reased i f wounds are not cov ere d. Los ses i ncreas e furt her wi th i nhal a ti on i njury. Overze al ous fl ui d i nfusi on shoul d be av oi d ed to m i ni mi se oed ema. The i nc re ase d pe rme abi l i ty and fl ui d l e ak phas e l as ts app rox i matel y 1–2 d ays . Afte r 2–5 day s, a d i ureti c phas e usual l y c omme nce s w hen ex ces s t i ss ue fl ui d i s l ost and the body swe l l i ng re duc es. El e ctrol y te l ev el s (e spe ci a l l y K + and Mg 2+ ) can fl uc tuate wi d el y i n both peri od s requi ri ng moni t ori ng and rep l ac ement as nece ssary. Though som e haemol ys i s may oc cur, bl ood t ransfusi on req ui reme nts are usuall y l ow, but de bri dem ent wi l l re sul t i n major b l ood l oss often re qui ri ng major t ransfusi on (>8–10 uni ts ). A coagul op athy w i l l often oc cur, i n p art d ue to a di l uti onal effect of the albumi n i nfus i on. P.511

Fluid resuscitation regimen (adapted from Mount Vernon formula) Not e: thi s regi men shoul d b e used as a g ui de onl y. 1. Di v i de fi rst 36h from the t i me of burn i nt o s i x consec uti ve peri od s of 4, 4, 4, 6, 6 and 12h. For eac h p eri od gi ve 0.5m l 4.5–5% al b umi n × body w t [kg] × %burn

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2. Gi v e bl ood as ne ces sary t o m ai ntai n haem ogl obi n > 10g /dl . 3. Comm enc e enteral nutri ti on as s oon as possi bl e 4. Gi v e 1. 5–2ml /kg/h 5% gl uc ose 5. Reas ses s c ard i ores pi ratory vari ab l es and uri ne outp ut at fre que nt i nt erval s t o d etermi ne whet her vol um e rep l ac ement i s i nadeq uat e or ex ces si ve. Ad jus t fl ui d i nput as nece ssary.

See also: Bl ood press ure moni t ori ng, p110; Cent ral ve nous c athete r—use, p114; Col l oi d osm oti c p res sure, p172; Crys tal l oi ds , p176; Col l oi ds, p180; Bas i c re sus ci t ati on, p270; F lui d c hal l e nge , p274; Hy pot ens i on, p 312; Ol i g uri a, p330; Burns —ge neral managem ent P.512

Burns—general management Surgery Esc harotomy m ay be need ed on hos pi t al adm i ss i on t o affec ted l i mbs , as w el l as to the neck and /or chest i f a ci rcum ferent i al burn i s prese nt. Debri d eme nt of necroti c ti s sue i s often be gun wi thi n t he fi rst few days as e arl y g rafti ng i s ass oci ate d w i th i mp rov ed outc ome . Cove rag e i s obtaine d usi ng e i ther spl i t sk i n grafts from the pati e nt' s own unaffec ted sk i n, donor sk i n grafts or even ex peri me ntal ‘ ski n’. Bl ood l os s m ay b e rapi d and mas si v e, e.g . 100m l p er 1% of b ody surface grafte d.

Wound care Earl y appl i c ati on of dre ssi ngs and F lam azi ne (si l ve r s ul p had i azine) c re am w hi c h has ant i -b act eri al prope rti es agai ns t G ram neg ati ve bac teri a may us eful l y preve nt sec ond ary i nfec ti on. Earl y grafti ng oft en t ake s p l ac e w i thi n the fi rs t 2–3 days t o provi de a s ki n prote ct i ve barri er.

Nutrition Ent eral nutri ti on shoul d b e comme nce d s oon aft er adm i s si on as s tud i es have s how n t hat earl y enteral nut ri ti on i mp rov es outc ome . Target i ntak e i s p rot ei n of 1g/kg + 2g/%b urn and a calori e i nt ake of 20Cal /kg + 50Cal /%b urn.

Infection Prop hyl ac ti c anti b i ot i c s are oft en not gi v en to burn p ati ent s. Bod y te mpe rat ure ri se s on d ay 1–2 as hi g h as 40°C , m ay p ers i s t for sev eral d ays and does not i ndi c at e sec ondary i nfect i on. Li k el y i nfec ti ng agents i nc l ude s trept ococci , s tap hyl ococci and Gram ne gat i ve bacte ri a such as Pseudom onas. App rop ri a te ant i bi ot i c tre atm ent shoul d b e g i ve n as i ndi cat ed.

Other considerations Any suspe cte d i nhalat i on i njury s houl d be di a gnosed and t reated . Ens ure ade quate analge si a (opi a tes ). Ketami ne i s a us eful anae stheti c as i t has analge si c prop ert i es i n ad di t i on. Tetanus toxoi d s houl d be gi v en soon after hosp i tal admi ssi on. Reduce heat and fl ui d l os ses by pl aci ng the pati e nt on a heate d air fl ui d i se d b ed and by earl y cov erage of b urnt ski n t hrough ap pl i cat i on of oc cl usi ve d res si ngs and p l ac ement of affe cte d l i mb s i n t ransparent p l asti c b ags . Stress ul cerat i on can us ual l y be avoi de d t hrough promp t resusc i tati on and earl y ent eral nutri t i on. Pres sure sores and contract ure s s houl d be pre vented by careful nursi ng and phy si othe rap y. Sux amet honi um shoul d b e avoi ded from 5–150 d ays ' p ost -burn bec aus e of t he ri s k of rapi d and s eve re hype rkalae mi a . Inc reasi ng resi st anc e t o non-d epol ari si ng mus cl e rel a xants may be see n. β-bl ock ade has b een ass oc i at ed wi t h outc ome i mp rov eme nt i n chi l d ren sustaini ng burn i nj ury . P.513

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See also: Ent eral nut ri t i on, p 80; Spe ci a l s upp ort surfaces , p 86; Opi oi d anal g esi cs , p 234; Non-opi oi d anal ges i cs , p 236; Muscl e rel axants , p 240; Anti mi crobi a l s, p260; Hyp erk al a emi a, p 420; Infe cti on control — gene ral p ri nci p l e s, p476; Infect i on—di ag nos i s, p480; Infect i on—treat ment, p482; Burns—fl ui d managem ent , p 510; Py rex i a (10; Pyre xi a (2), p520; Rhab dom yol ysi s, p528; Pai n, p532


Ed itors: Si nge r, M ervyn; We bb, An dre w R. Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > P h y sica l Diso r d er s

Physical Disorders Hypothermia Clinical features Above 33°C —shi ve ri ng i s usual l y m ark ed i n an att emp t t o c orrect body temp erature. Bel ow 33° C—ne urol og i c al si g ns of dys art hri a and sl owne ss app ear. Bel ow 31° C—hy pertoni c i ty and s l ug gi s h refl exe s w i th cardi ovascul a r d ysfunc ti on b ecome l i fe t hre ate ni ng. Bel ow 28° C—arteri a l p ul s es oft en bec ome i mp al pabl e. Hyp otherm i c ri gi d i t y i s d i ffi cul t to di s ti ngui sh from death. Prog nos i s de pend s on t he deg ree and d urati on of hy pot hermi a.

ECG changes Si nus brady cardi a i s fol l owed by at ri a l fl ut ter and fi bri l l at i on wi th ventri cul ar ec top i cs . T he PR i nt erv al , QR S c omp l ex and QT i nterval are p rol ong ed. At ri al act i vi ty eve ntual l y c eas es. The ‘ J’ wave i s most oft en see n 6.7 kPa. Any re spi rat ory effort negates the di agnosi s of b rai n s tem de ath. P.549

See also: Bl ood gas anal y si s , p 100; EEG/C FM moni tori ng, p138; Ure a and c reati ni ne, p144; El ec trol yt es , p 146; T oxi col ogy , p 162; Op i oi d anal ges i c s, p234; Non-opi oi d analge si c s, p236; Sed ati ves , p 238; Muscl e rel axants , p240; Cardi a c arre st, p272; Hyp ogl ycaemi a, p438; Hypothe rmi a, p516; Care of the p ote nti al org an donor, p552 P.550

Withdrawal and withholding treatment Thi s i s arg uab l y the mos t d i ffi c ul t and s tre ssful dec i s i on that has to be mad e for the cri ti cally i l l p ati ent. Wi t hdrawal inv ol v es red uct i on or c ess ati on of v asoact i ve drugs and/or resp i ratory sup port. In som e ICUs the pati e nt i s heavi l y sed ate d and di s connec ted from the venti l at or. Wi thhol d i ng i nvol ve s non-c omm enc eme nt or non-esc al a ti on of treatm ent , e .g. ap pl y i ng an up per thres hol d d ose for an i not rop e and/or not start i ng re nal re pl a cem ent therapy. Before ap proachi ng the p ati ent /fami l y, the re shoul d i d eal l y be a c ons ens us among m edi cal and nursi ng s taff t hat quanti ty and /or qual i ty of l i fe are si g ni fi c ant l y com promi s ed and unl i k el y to re cov er. Often, t he p ati ent 's vi ewpoi nt i s very w el l -de fi ned and the carers may rue the fact that the di scussi on was not i ni t i a ted earl i er. Ethni c, cul tural and re l i gi ous fac tors w i l l i nfl uence b oth doctor and pat i ent/fami l y i n the ti mi ng and fre que ncy of such dec i s i ons. In som e soci eti es doc tors have a m ore paternal i s ti c ap proach wi th l i t tl e i nvol ve ment of pati e nt and /or fam i l y i n the d eci si on-m aki ng proces s. Ot hers are overl y i ncl usi v e, som eti mes to the p oi nt of ex ces si vel y ac qui es ci ng to the fami l y's de mands des pi t e obvi ous futi l i t y i n c ont i nui ng care. Cl earl y, a bal anc e needs to be st ruc k t hat se rve s the be st i nt erest s of the p ati ent . Al t hough pot ent i al l y awk ward , t he mental l y com pet ent pati e nt shoul d be i nvol ved i n the most i mp ort ant de ci s i on affec ti ng t hei r l i fe. Thi s s houl d be done as c ons i de rat el y as possi bl e , avoi di ng unnece ssary di s tress . A se ri es of d i sc us si ons ove r s everal days m ay be need ed, al l ow i ng ti me to contem pl a te. Consensus i s re ached wi t h > 95% of pat i ents/fam i l i es by the thi rd d i sc uss i on. It shoul d be st re sse d t o t he p ati ent and fami l y that c are i s not be i ng wi thd raw n/wi thhel d b ut that p ai n re l i e f, com fort, hyd rat i on and g ene ral nursi ng care are to be conti nued . Li ke wi s e, no dec i si on i s bi ndi ng but can b e am end ed dep end i ng on the p ati ent 's progre ss , e. g. mov i ng from wi t hhol di ng to wi t hdrawal, or re-i ns ti tut i on of ful l tre atm ent . A ‘ne got i at ed set tl ement’ i s oft en a useful i nt eri m comp romi s e for fami l i es unabl e to acc ept a wi t hdrawal d eci si on, whe reb y l i mi tat i on of treat ment i s i ns ti t ute d and sub seq uentl y re vi e wed Rel ati ves can s ome ti m es be very di st raught and, occ asi onally , i rrati onal on d i sc uss i ng wi thdrawal /wi t hhol d i ng . F or many, thi s w i l l be thei r fi rs t e xpe ri e nce of the dy i ng proc ess i n a l ov ed fami l y mem ber. A numbe r of ot her factors i nc l udi ng g ui l t, ang er and wi thi n-fami l y di s agreem ent s m ay al s o s urface . It s houl d be stress ed that t he wi t hdraw/wi t hhol d dec i si on shoul d not b e l eft to the fami l y al one as t hi s i s an unfair burden for t hem to carry . Rat her, i t i s t hei r pas si v e agre ement w i t h a med i cal rec omme ndati on t hat i s be i ng sought. The em phasi s of the di s cussi on i s to i nform them of t he l i kel y outc ome and to se ek t hei r vi e w of what the pat i e nt woul d w ant . T hey ne ed to be dealt wi t h b oth se nsi ti v el y and hone stl y, and they s houl d not fe el pre ss ure d t o gi ve i nstant dec i si ons . Di scussi ons shoul d i nvol ve the p ati ent 's nurse and ot her i nvol ved carers as appropri a te. It shoul d b e accurat el y doc ume nte d i n t he cas e note s t o ensure g ood communi c ati on bet wee n c are gi v ers and act as source data s houl d sub seq uent c omp l ai nt s s urface . P.551

See also: Com muni cati on, p564 P.552

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Care of the potential organ donor Pat i ents wi t h s us pec ted brai n st em deat h s houl d be consi dered c and i d ate s for org an d onati on unl e ss there i s evi de nce of: Canc er (ex cep t p ri m ary ce ntral nervous s yst em) HIV or he pat i ti s s urface anti g en pos i t i ve Hi g h ri sk for HIV Uncontrol l ed se psi s Si g ni fi cant sys tem i c di sease Sl ow vi rus i nfe cti on The trans pl ant co-ord i nator s houl d be c ont ac ted earl y (be fore t he fami l y are ap proached) to confi rm l i k el y sui t abi l i t y. If the fami l y are amenabl e, the trans pl ant co-ord i nator wi l l then i ni ti ate organ donati on proced ures. Do not rejec t those brain dead p ote nti al donors who, for exampl e, hav e ful l y t reated i nfec ti ons or acute renal fai l ure w i thout consul tati on wi th the t ranspl ant co-ordi nator.

Management 1. Confi rm brai n s tem death wi t h appropri at e t est i ng. 2. Lab oratory t est s for bl ood group, HIV and hepati ti s st atus and el e ctrol yte s. 3. Confi rm organ donat i on i s pe rmi ss i bl e b y t he corone r (or e qui val ent ). 4. Mai ntai n opt i mal c ard i oresp i ratory status wi th fl ui d ± i not rop es, op ti m al venti l at i on and physi ot herapy. Di ab etes i ns i pi dus shoul d b e t reated wi th DDAVP. 5. Cont act surg i cal and anae st het i c teams.

Organ suitability Ki dneys —Age 4–70, acce ptabl e U&E and cre ati ni ne Heart— Age 0–50, acc ept abl e C XR and EC G Lungs— Age 0–50, ac cep tab l e CXR and bl ood gases Li v er— Age 0–55, no al cohol or drug abus e, acc ept abl e LFTs Corneas —Ag e 0–100, no pre vi ous i nt raocul ar surge ry The trans pl ant co-ord i nator wi l l ad vi s e on ot her organ and t i s sue sui tabi l i t y, e.g. pancreas , t rache a, b owe l , ski n. P.553

See also: Bl ood gas anal y si s , p 100; Urea and creat i ni ne , p144; El ect rol yte s , p 146; Col l oi d s, p180; Inot rop es, p196; Vasop res sors, p200; F lui d c hal l e nge , p 274; Hy pot ens i on, p 312


Ed itors:


Ti tle : O xf ord Ha ndbook of Cr itic al Car e, 2nd Ed ition Cop yri ght © 1997,2005 M. Si nge r and A. R. W ebb , 1997, 2005. Publ i shed i n the Uni te d Stat es by Oxford Uni ve rsi ty Press Inc > Tab le of Co n te n ts > I CU Or gan isa tio n a n d Ma n ag eme n t

ICU Organisation and Management ICU layout The i ntensi ve c are uni t shoul d b e easi l y acc ess i bl e b y d epartm ent s from whi ch pat i e nts are ad mi tte d and c l ose t o dep art ments whi ch share eng i ne eri ng servi ces . It i s d esi rabl e that cri ti cal l y i l l pati ent s are sep arated from t hos e req ui ri ng c oronary c are or hi gh dep end enc y c are whe re a q ui e ter envi ronm ent i s often ne ede d. It i s pos si b l e to provi d e i nt ens i ve care and hi g h d epe nde ncy care i n the same uni t s o l ong as pat i e nts can b e se parate d w i thi n the uni t. How eve r, the di ffe ri ng requi rements of the se pat i ents may l i mi t such fl e xi b i l i ty . T he fl oor si z es gi v en bel ow rep res ent a mi ni mum g ui d e.

Size Int ens i v e care bed re qui re ment s d epe nd on the ac ti v i ty of the hosp i tal w i th ad di t i onal bed s requi red for re gi onal

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spe ci al t i es such as cardi othorac i c surge ry or neuros urg ery. Very s mal l (< 6 b eds ) or v ery l a rge (>14 b eds ) uni t s m ay be di ffi c ul t t o manag e althoug h l arg er uni ts may be di vi d ed ope rat i onal l y and al l ow bet ter conce ntrati on of res ources .

Patient areas Pati ent areas must provi de unob struc ted passage around the be d w i th a fl oor space of 26m 2 per bed . C urt ai ns or screens are req ui red for pri vacy. Fl oors and ce i l i ng s m ust be const ruc ted to support heavy equi pm ent (some pi e ces may we i gh 1000k g). Doors mus t al l ow for p ass age of bul ky equi p ment as we l l as wi d e b eds . Every b ed shoul d have acc ess to a w ash hand bas i n. The spe ci fi c ati on shoul d i ncl ude 1 c ubi cl e p er 2 b eds wi t h 26m 2 fl oor area for i s ol ati on. Ai r c ond i t i oni ng shoul d al l ow for pos i t i ve and ne gat i ve press ure control i n cubi c l es and t emp erature and hum i di ty control . Servi c es mus t i ncl ud e ad equate el ect ri ci t y s upp l y (at l e ast 28 socket s per bed ) w i th em erg enc y b ack -up sup pl y. Oxyg en (4), me di c al ai r (2) and suc ti on (2) out l et s m ust be avail abl e for every b ed. The bed areas shoul d have nat ural dayl i g ht and pati e nts and s taff s houl d i de al l y have an out si d e v i ew . Comm uni cat i ons s yst ems i ncl ude an ade quate num ber of tel ep hone s t o avoi d all tel ephone s b ei ng i n use at onc e, i nt erc om sys tem s t o al l ow be d t o b ed com muni cati on and a s yst em t o c ont rol entry t o t he d epartm ent . Comp ute r netw ork s s houl d enabl e communi c ati on wi t h c ent ral hospi tal ad mi ni s trati on and l ab oratory s yst ems .

Other areas Other areas i ncl ude adeq uat e s torage sp ace , d i rty uti l i t y, cl ean uti l i ty, offi c es, l a boratory, se mi nar room, cl e ane rs' room, staff res t room , l ock er room, toi l et s, rel ati ves ' are a, b edroom and i nte rvi ew room. P.558

ICU staffing (medical) Int ens i v e care has ev ol v ed from t he e arl y s uc ces s i n s i mp l e mec hani cal v ent i l ati on of t he l ungs of pol i o vi c ti ms to t he pre sent d ay whe re pat i ents adm i tt ed to i nt ens i ve care wi l l usuall y have fai l ure or d ysfunc ti on of one or more organ sys tem s requi ri ng me chani c al sup port and moni tori ng. The i ntensi ve c are uni t shoul d have ded i c ated consul t ant ses si ons wi th addi ti onal allocat i on for m anagem ent , t eachi ng and audi t act i vi ti e s. The se ses si ons shoul d be di vi ded bet wee n s everal i ntensi v e c are sp eci al i st s. In add i ti on, the i nte nsi ve care s pec i al i s t s houl d be sup ported by juni or doc tors i n traini ng who can p rov i de 24h pe r d ay cov er on a rota whi ch provi des ade quate res t.

Required skills of intensive care medical staff Management Seni or i nte nsi ve care m edi cal st aff, assi ste d b y s eni or nursi ng and pharmacy col l eague s, com mand t he pri mary res ponsi bi l i t y for t he fi nanc i al manag eme nt of t he i nt ens i v e c are uni t. It i s through the i r ac ti ons that t reatme nt of t he cri ti cal l y i l l i s i ni ti a ted and p erp etuate d; t hey are ul ti mat el y resp ons i bl e for the ac ti v i ty of the uni t and pati ent out com e.

Decision making In the IC U m ost dec i s i ons are ul t i matel y m ade by te am c ons ens us. Cl i ni cal d eci si ons i n the i nte nsi ve care uni t can b e thought of unde r t hre e c ate gori es : (i ) d eci si ons re l at i ng t o common or rout i ne probl ems for w hi c h a uni t pol i c y exi sts ; (i i ) de ci s i ons rel ati ng to unc omm on p robl e ms req ui ri ng di sc uss i on wi th al l IC U and non-ICU st aff curre ntl y i nv ol v ed and (i i i ) de ci s i ons of an urge nt nat ure taken by i ntensi v e c are st aff wi t hout d el a y.

Practical skills Exp ert i s e i n t he m anagem ent of com pl e x e qui pme nt, moni t ori ng proced ures and performance of i nv asi ve proced ure s are re qui re d.

Clinical experience Med i cal s taff requi re ex peri ence i n the recog ni ti on, pre venti on and managem ent of cri ti cal i l l ness , i nfe ct i on control , anaest hes i a and organ support.

Technical knowledge The i ntensi ve c are sp eci al i st has an i mportant rol e i n t he choi ce of eq ui p ment used i n the i nte nsi ve care uni t .

Pharmacological knowledge Drug t herap y regi mens are c l e arl y open to the probl ems of drug i nt eract i ons and, i n add i t i on, p harmac oki net i cs are oft en sev ere l y al t ere d b y t he e ffe cts of major organ sys tem dy sfunct i on, p art i c ul a rl y i nvol vi ng the l i ver and ki dneys .

Teaching and training The modern i nte nsi ve care s pec i al i s t has acq ui red a numb er of s ki l l s that cannot be gai ne d outs i de the i nte nsi ve care uni t. It i s there fore nece ssary to be abl e to provi de thi s e duc ati on to juni or doct ors i n trai ni ng for i nt ens i ve care.

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P.559 P.560

ICU staffing (nursing) Cri ti cal l y i l l p ati ent s requi re cl os e nurs i ng supervi s i on. M any wi l l req ui re hi g h-i nte nsi ty nursi ng throug hout a 24h peri od whi l e ot hers are of a l ower d ependency and can s hare nurs es. In ad di t i on to the b eds i de nurse s, the dep art ment need s addi ti onal st aff to manage the d ay to day ope rat i on of the uni t , t o assi st i n l i fti ng and handl i ng of pat i ents , t o rel i eve bed si de nurses for rest pe ri ods and to col l e ct drugs and eq ui p ment. The se add i ti onal nurs es (or nurse ass i s tants) can b e te rme d t he ‘fi xed nursi ng est abl i s hme nt’ and t he nat ure of the i r duti e s i s s uch that the y w i l l usual l y b e hi gher grade nurse s. The bed si de nurses are a ‘vari abl e es tab l i shm ent ’ and the i r num bers are dep end ent on act i vi ty suc h t hat more pat i ents re qui re hi g her numbe rs. Most dep art ments fi x thei r vari a bl e es tab l i shm ent by ass umi ng an ave rag e ac ti vi t y.

Fixed establishment In the UK provi di ng 1 nurse pe r s hi ft c ont i nuous l y re qui res 5. 5 nurs es. In ad di t i on s taff handover, annual l eave, st udy l eave and si ckness are usually calcul a ted at 22% such that 1 ad di t i onal nurse i s re qui red . T hus , t he provi s i on of 1 nurse i n charg e of each shi ft and 1 nurse to sup port t he bed si d e nurs es req ui res 11 nurse s. In l arger uni ts t here may be a need for ad di t i onal support nurses .

Variable establishment The same pri nci pl es appl y for the provi si on of b eds i de nurs es. Thus, to provi de 1:1 nursi ng for a b ed req ui res 5.5 nurses and t o p rov i de 1:2 nurs i ng re qui re s 2.75 nurse s. The total number requi re d d epe nds on the oc cup anc y and the nurse to pat i ent rat i o for eac h occupi ed b ed. One of t he d i ffi c ul t i es i n s taffi ng an i ntensi ve c are uni t re l at es to the vari ab l e dep end enc y and occ upancy . An av erage dep end enc y we i ghted oc cup anc y (ave rag e oc cupanc y × av erage nurse to pat i ent rat i o) shoul d be us ed to set the e stabl i shm ent of be dsi de nurses wi th add i ti onal nurses be i ng draft ed i n from a bank or agency to cov er peak de mands.

Skill mix Nursi ng ski l l mi x i s t he s ubj ect of much controversy as the ne ed for econom y i s b al a nce d agai nst the need for qual i ty . As st ate d ab ove the fi xe d nurs i ng wi l l usual l y be of hi gher grade si nce the rol e i ncorporate s t he admi ni strati on of the uni t and sup erv i s ory nursi ng. The b eds i de nurse s w i l l be made up of t hos e w ho have re cei ved post-qualific ati on trai ni ng i n i ntensi ve c are and t hos e w ho have not. The rati o of trai ned to unt rai ned i ntensi v e c are nurse s s houl d be of the order of 3:1 t o faci l i t ate i n-se rvi ce teachi ng. P.561 P.562

Fire safety Fi res affect i ng the ICU are rare but are p art i cul arl y di ffi cul t i n t hat pati ent s are not eas i l y ev acuate d, yet thei r l i ves dep end on se rvi ces whi ch fi re may di srupt. Sm oke , w hi l e d ang erous to staff and the l e ss cri ti cal l y i l l p ati ent s w ho may be breat hi ng s pontaneous l y , i s l ess of a p robl e m t o those on me chani c al venti l ati on si nce thei r fresh gas s upp l y i s from outs i d e the affe cte d e nvi ronment. It the refore fol l ows t hat , i n the eve nt of fi re, the pri ori t y i s t o ensure safety and me ans of es cap e for t he st aff fi rst .

Control of smoke Smoke and toxi c gases are a com mon as soc i at i on wi th fi re and may , i n t hems el ves , be fl amm abl e, parti c ul arl y i n ass oci at i on wi th hi g h c onc ent rat i ons of oxyge n. The main tec hni que s for control of s mok e i ncl ude containm ent (e. g. fi re-resi st i ng walls , d oors and seals) and d i sp ers al (e. g. pos i ti ve pre ssure ai r c ond i ti oni ng), t he l at ter be i ng us ed i n pat i ent areas. The possi bi l i t y of fl amm abl e or t oxi c fume s s houl d be consi d ere d w hen equi p pi ng and furni s hi ng t he i nt ens i v e c are uni t.

Escape from fire Esc ape routes s houl d be w el l marke d and unobst ruc ted . The nat ure of cri t i cal i l l nes s i s s uch that not al l p ati ent s c an be evacuated . The staff shoul d es cap e fi rs t b y p roc eed i ng to the nearest ex i t away from the fi re. Pati ent s shoul d be evacuated i n the orde r of t he l east si c k fi rs t. Evac uat i on of pati e nts shoul d b e m anaged by som eone t rai ned i n the use of b reathi ng app aratus; i n m ost cases thi s w i l l be the fi re bri gade. If p ati ent s are to be evacuated they s houl d be mov ed to a pl ace of safet y on the s ame fl oor as the i nte nsi ve care uni t. Pat i ents shoul d not b e moved downs tai rs. In t he maj ori ty of fi res contai nme nt wi l l red uce the ne ed for ful l evacuati on.

Preventing fire Aut omat i c sm oke or heat alarms shoul d be provi ded i n al l areas. Cook i ng areas and l aborat ory areas mus t be s eparat ed from p ati ent areas by fi re doors.

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Fi re doors are p rov i d ed t o p rot ect s taff and p ati ent s and shoul d not b e we dge d open. If a cl ose d d oor woul d compromi se the care gi v en to p ati ents but i s es senti a l t o s eparat e fi re compartm ent s t hen an e l ec tro-me chani c al dev i c e shoul d hol d t he d oor op en and be di sab l ed by the fi re al a rm. Fi re ex ti ngui shers of the ap propri at e t ype s s houl d be readi l y avai l ab l e and st aff shoul d be prope rl y t rai ned i n thei r use . P.563 P.564

Communication Good c omm uni cat i on i s es senti al to the smooth runni ng of the IC U. Thi s i ncl ud es c omm uni cat i on b etwe en the IC U staff, pati e nts , v i si ti ng profes si onal s and rel ati ves .

Patient communication Cri ti cal l y i l l p ati ent s m ay s ti l l be abl e t o hear conversati on d esp i te se dat i on or ap parent unconsci ous nes s. Bed si de di s cussi ons shoul d t ake thi s i nt o account and all proced ures shoul d be exp l ai ned to the p ati ent i n si mp l e terms before start i ng . T he pat i ent who i s not com pet ent to conse nt to tre atm ent may ap pre ci ate verbal di sc uss i on or ex pl a nat i on.

Doctor–nurse communication It i s es senti a l t hat the m ul t i di sc i pl i nary app roach to i nt ens i v e c are i nvol ves med i c al and nursi ng staff i n dec i si on mak i ng . W ard round s are a forum for s uc h i nte rdi sci pl i nary com muni cati on and the consul tant l eadi ng t he round shoul d ensure t hat al l pre sent are trul y i nv ol v ed. The p l an for t he d ay can be se t on the w ard round but i s m ore l i kel y to suc cee d i f all invol ved i n effect i ng the p l an are i nvol ve d i n s ett i ng i t. Si m i l a rl y, al l chang es from t he p l an, w het her due to unforese en e mergenci es or d ue to fai l ure of t he pat i ent t o resp ond , s houl d be ful l y di s cus sed .

Communication with visiting teams The i ntensi ve c are st aff shoul d b e resp ons i bl e for the day t o d ay c are of cri t i cally i l l pat i ents, i ncl udi ng coordi nat i ng the i nput from vari ous non-ICU profes si onals i nv ol v ed i n the manage ment of p ati ent s and affe cti ng the treat ment pl a n. The ad mi t ti ng t eam shoul d b e i nvol ve d i n m ajor de ci si ons. Vi si ti ng m edi cal st aff shoul d not see pati e nts wi thout bei ng acc omp ani ed by a me mbe r of t he i nt ens i ve care med i cal s taff.

Communication with relatives Rel ati ves are ofte n ov erw hel med by the envi ronment of an i ntensi v e c are uni t, are w orri ed ab out the p ati ent and are eas i l y confused by the i nformati on t hey are gi ven ab out cri t i call y i l l pat i ents. Most com muni cati on s houl d be fac e t o fac e, avoi di ng l engthy d i sc uss i ons on t he tel ephone . W here s eve ral pe opl e are i mp art i ng i nformat i on, d i ffere nce s i n emp has i s or content d est roy any c hance of e ffe cti ve com muni cati on. It i s ess ent i a l t hat the b eds i de nurse i s prese nt whe n rel a ti v es are sp oke n t o s i nc e t here are ofte n q ues ti ons and conce rns whi c h c rop up l a ter and are d i rect ed to the nurse; i t i s wort h remem beri ng t hat the rel a ti v es have great er contac t w i t h t he nurses and often bui l d up a rel at i onshi p w i th them. Where adm i t ti ng t eam s need to com muni cate wi t h rel a ti ves about a s pec i fi c aspe ct of the i l l ne ss the be dsi de nurse and , i deally , a mem ber of the i nte nsi ve care m edi cal st aff, s houl d be pre sent. Mos t i nt ervi e ws w i t h rel a ti v es shoul d be away from the b eds i de al though i t i s often he l pful to i mp art si mpl e i nformati on at the be dsi de, parti cul arl y to dem ons trate parti c ul ar i ss ues . Agai n i t mus t b e remem bered that t he pat i ent m ay hear the conve rsati on. Whi l e i t i s he l pful to i nt erv i ew al l rel ati ves toget her thi s i s not al way s p rac ti c al , ei ther bec aus e the y c annot al l be prese nt at onc e or b ecause the y d o not rel ate to eac h othe r. Informati on oft en change s w hen del i ve red se cond hand so i t i s be tte r t o c omm uni cat e d i rect l y wi t h v ari ous re l at i ve s s eparat el y i n t hes e ci rcumst anc es. P.565 P.566

Medicolegal aspects The i ntensi ve c are uni t i s a s ource of many m edi col egal p rob l em s. Pat i ents are often not c ompe tent t o c ons ent to treatm ent . T hey may be ad mi t ted fol l owi ng t rauma, vi ol e nce or poi soni ng, al l of whi ch may i nvol ve a l egal p roc es s. Adm i s si on m ay als o fol l ow c omp l i c at i ons of treat ment or m edi cal mi shaps oc curri ng e l s ewhe re i n the hospi tal . T he nat ure of cri t i cal i l l nes s i s s uch that com pl i cat i ons are common and l i ti gati on m ay fol l ow.

Consent and agreement Many p roc edures i n i ntensi ve c are are i nvasi ve or i nvol ve si gni fi cant ri sk . T he pat i ent i s ofte n not com pet ent to consent for suc h t reatme nt and , i n m any count ri e s, surrogat e conse nt or ass ent cannot b e l egally gi ven by the nex t-of-ki n. It i s i m portant t hat the ri sk s and benefi ts of the proce dure are expl ai ned to the ne xt-of-k i n and that thi s di s cussi on i s doc ume nte d i n t he cas e records . F or major d eci si ons , p art i c ul a rl y those i nvol vi ng w i thdrawal or wi t hhol di ng of l i fe-p rol ong i ng t reatme nts , t he pat i ent s houl d i de al l y b e i nvol ve d i n d i sc uss i ons. If not fe asi bl e, rel at i ve s s houl d be aske d t o g i ve thei r vi ew of w hat the p ati ent woul d want i n thi s s i tuati on. Res earch pre sents consent p rob l em s i n t he cri ti cal l y i l l and req ui res cl ose et hi c al com mi t tee supervi s i on.

Note-keeping It i s i m pos si b l e to rec ord ev ery thi ng that happ ens i n i ntensi ve c are i n t he p ati ent 's notes . T he 24h obs erv ati on chart provi d es the most det ai l ed rec ord of what has hap pened but summary not es are es senti a l . Suc h note s m ust be factual wi t hout unsubst ant i a ted opi ni ons ab out the pati ent or about previ ous treat ment . Al l entri es mus t b e t i me d and

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si gned . R ecords of ward rounds must rec ord the name of the consul tant l eadi ng t he round. It must be rem emb ere d that t he not es may be use d l ate r i n l eg al procee di ngs. They m ay be use d ag ai nst you but, i f wel l k ept , w i l l us ual l y form t he bes t d efence. In the e vent of a med i cal m i s hap the ep i sode shoul d be cl earl y doc ume nte d afte r w i tness ed exp l anati on to rel ati ves .

Dealing with the police Mos t p ol i ce enq ui ri e s rel a te to pat i ents who are ad mi t te d after susp i ci ous ci rc ums tances . W hi l e t here i s a duty to pat i ent c onfi de nti al i ty i t may b e i n t he p ati ent's i nterest s t o i mpart i nformat i on ab out them. Thi s m ay be wi t h t he consent of t he pat i ent or t he next of ki n. Wri tt en statem ent s or ve rb al i nform ati on may be req ues ted . Any i nform ati on gi v en shoul d av oi d op i ni on and be st ri c tl y fact ual .

Dealing with the Coroner The Coroner mus t b e i nformed of any d eath where a deat h c erti fi cate cannot be i s sue d. Death certi fi c ate s c an b e i s sue d where the d eat h i s d ue to a natural cause and the p ati ent has b een se en p rofess i onal l y by the doc tor wi thi n 14 day s p ri or t o d eat h. The tabl e docum ent s t he condi t i ons requi ri ng the Coroner to be i nform ed. Where there i s any doubt the Coroner shoul d be i nformed . P.567

Deaths which must be informed to the Coroner Uni dent i fi ed body No d oct or att end i ng wi thi n pri or 14 day s Deat h w i thout recov ery from anaest hes i a Sud den or une xpl ai ned death Medi cal mi shap Ind ust ri a l acci de nt or di s eas e Vi ol ence, ac ci d ent or mi sad venture Sus pi c i ous c i rcum stance s Al c ohol i s m Poi s oni ng Deat h i n c us tod y P.568

Clinical governance Cl i ni cal governance i s a frame work t hrough whi ch he al t hcare org ani zat i ons are acc ountab l e for conti nuous l y i mp rov i ng t he q ual i t y of thei r s erv i ce s and safeguard i ng hi gh standards of care by c re ati ng an envi ronment i n whi ch exc el l enc e i n c l i ni c al care w i l l fl ouri s h. For the ICU c l i ni c al gov ernanc e requi res the cul ture, the s yst ems and t he sup port m echani sms t o ac hi eve good c l i ni c al performance and ens uri ng that qual i t y i mprove ment i s e mbed ded i nto the uni t' s routi ne. Thi s i ncl ud es act i on to ens ure ri sk s are managed , adve rse effec ts are rapi d l y det ect ed, op enl y i nv est i g ate d and l ess ons l earned , good practi ce i s rapi d l y di s se mi nate d and s yst ems are i n p l ac e t o e nsure conti nuous i mp rov ements i n cl i ni cal c are . There must be sys tem s t o e nsure al l cl i ni ci ans have the ri ght ed ucati on, trai ni ng , s ki l l s and compe tenci e s t o d el i ver t he c are ne ede d b y p ati ent s. The re mus t b e s yst ems i n pl ace to re cog ni s e and ac t on p oor performance.

Essential components of clinical governance Clear management arrangements Eve yone must know w ho t hey are account abl e t o, the l i mi t s of t hei r d eci si on maki ng and who m ust be i nformed i n the dec i s i on mak i ng proc ess .

Quality improvement Throug h t he proces s of c l i ni c al aud i t the st and ard of pract i ce i s moni t ored and change s e ffe cte d t o i mprove quali ty.

Clinical effectiveness Evi dence bas ed practi ce i s es senti a l w here ev i d enc e ex i st s to s up port c l i ni c al dec i si ons . Prot ocol s and gui de l i nes standardi se pract i ce .

Risk assessment and management A regi st er of cl i ni c al ri sks shoul d b e k ept , t o whi c h new ri s ks are app end ed as the y are ass ess ed. An ac ti on p l an shoul d be de vel ope d for m anagi ng e ach ri sk.

Staff and organisational development Inc l udi ng c ont i nued profes si onal ed ucati on, cl i ni cal supervi si on and p rofess i onal re gul ati on.

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Patient input Com pl a i nt s m oni tori ng s houl d be used to l e arn l ess ons and i mprove pract i ce wi thi n ICU. Pat i e nt and rel at i ve surve ys can be us ed to adap t q ual i t y i ni t i at i v es t o t he nee ds of pat i ents. P.569

See also: Aud i t , p 570 P.570

Audit Aud i t has b ecom e an e sse nti al part of m edi cal pract i c e. The mai n p urp ose i s t o i mprove quali ty of c are whi ch, i n t he i nt ens i v e c are uni t, must i nv ol v e al l memb ers of the m ul t i d i sc i pl i nary te am. Change i n pract i c e i n one d i sc i p l i ne w i l l i ne vi t abl y have a knoc k-on e ffec t i n others . Audi t m ay i nv ol v e a re vi e w of ac ti v i ty , p erform anc e agai nst pre det erm i ned i nd i cators or c ost -effec ti v ene ss. Audi t may focus on s pec i fi c t opi cs or may encom pas s t he p erformanc e of sev eral i nte nsi ve care uni t s. Succe ssful aud i t req ui res commi tme nt from se ni or staff t o e nsure pract i ce i s de fi ned, dat a are col l ec ted and c hange i s effect ed w here nece ssary. Where chang e i s s ugg est ed by aud i t a furt her re vi e w i s req ui red to ens ure t hat such change has oc curre d.

Data collection Ide al l y, a b asi c d ata se t s houl d be com mon to al l i nte nsi ve care uni t s nati onall y t o al l ow me ani ngful com pari sons to be mad e. T hi s requi re s t he dat a s et to be d etail ed enough to ans wer quest i ons p ose d b ut not so det ai l ed that col l e cti on bec omes unsustainabl e . R esourc es mus t b e provi de d i n t erm s of computer datab ase s and staff to c ol l ec t and anal y se dat a. T hos e c ol l ec ti ng t he dat a s houl d be p rovi d ed w i t h regul ar summary rev i ews t o ensure t hat ent hus i as m c ont i nues , and q ual i t y c ont rol i s maint ai ned. Me thods of dat a entry shoul d c ons i d er the ti me i nv ol v ed and the fact that m ost of those col l e cti ng dat a are not key board exp ert s. Typ ographi cal m i s take s d est roy the v al ue of col l e cte d d ata suc h t hat error t rap pi ng and dat a v al i dat i on must form p art of the house kee pi ng i n any dat abas e used . Som e audi t t opi cs re qui re dat a c ol l ect i on that i s not part of the basi c data set . C ol l ect i ng ap propri at e d ata req ui res cl ari ty i n set ti ng t he que sti on to be ans wered and care i n c hoosi ng dat a i tems t hat wi l l trul y ans wer the q ues ti on.

Audit meetings Reg ul a r audi t m eet i ng s s houl d fol l ow a pre defi ne d t i me tab l e. Thi s hel ps to ens ure maxi m um staff atte ndance and also set s t arget dat es for data col l ec ti on and analys i s . Audi t m eet i ng s s houl d be chaire d and hav e de fi ned ai m s. Di scussi on of the topi c be i ng audi t ed mus t l ead to re com mend ed change s i n p rac ti ce and the se mus t b e fol l owe d throug h afte r t he mee ti ng. It i s cl ear that al l st aff cannot at tend all mee ti ngs . D i ss emi nat i on of i nformat i on pri or t o i mp l em ent i ng prop osed chang es i s nec ess ary t o st and some chance of carry i ng them throug h. P.571

See also: Cl i ni cal governance, p568 P.572

ICU scoring systems Vari ous ICU sc ori ng sys tem s have evol ve d t o p rov i de : An i nd ex of d i se ase se veri ty , e .g. APACHE, SAPS. An i nd ex of w ork l oad and c ons ump ti on of resources , e. g. TISS. A me ans of compari s on for (i ) Aud i t i ng pe rformance —ei the r i n t he sam e ICU or b etw een ICUs. (i i ) Re search, e .g. ev al uati on of new produc ts or treatm ent re gi mens . Pati ent manag eme nt obje ct i ve s, e.g. se dat i on, p res sure are a c are . Other than t he Gl asg ow C oma Sc ore , t here i s no uni v ers al sys tem pract i s ed b y e very ICU. Whi l e APACHE i s t he pre dom i nant sys tem us ed i n the USA and UK for sc ori ng di s eas e s eve ri t y, SAPS i s more popul ar i n mai nl and Europ e. Int erpre tat i on of the same sys tem can also be hi ghl y v ari abl e.

TISS (Therapeutic Intervention Scoring System) Thi s s yst em att aches a sc ore t o proc edures and te chni q ues performed on an i ndi v i dual pat i e nt (e.g . use and numb er of vas oac ti v e d rug i nfus i ons, renal rep l aceme nt the rap y, adm i ni st rat i on of ent eral nut ri t i on). It has bee n used by some ICUs to de vel op a me ans of costi ng i nd i vi dual pat i ents by att achi ng a mone tary v al ue to e ach TISS poi nt sc ore d. It i s al s o used as an i ndex of workl oad act i vi ty. A d i sc harge TISS s core can be use d t o e sti mat e t he amount of nursi ng i nt erv ent i ons requi red for a p ati ent i n ste p-down fac i l i ti es (e.g . a hi gh dep end enc y uni t ) or on the g ene ral ward.

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TISS d oes not ac curat el y me asure nursi ng w ork l oad acti vi t y as i t fai l s t o c ate r for tas ks and duti e s s uc h as copi ng wi th the i rri t abl e or c onfuse d p ati ent , d eal i ng wi th gri ev i ng re l at i ve s, etc .

Glasgow Coma Scale Fi rst des cri be d b y T eas dal e and Jennett i n 1974, i t ut i l i se s e ye openi ng , b est motor re sponse and b est ve rbal res ponse to cat egori s e neurol ogi cal st atus. It i s the onl y sys tem us ed uni versal l y i n ICUs, though l i mi tat i ons e xi s t i n mec hani call y ve nti l a ted , s edat ed pat i ents . It c an be used for p rog nos ti cat i on and i s also frequent l y use d for the rap eut i c dec i s i on maki ng, e.g . el ec ti v e ve nti l a ti on i n p ati ent s p res ent i ng wi th a GCS

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