Acute Care Handbook for Physical Therapists
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Acute Care Handbook for Physical Therapists
Acute Care Handbook for Physical Therapists Second Edition Jaime C. Paz, M.S., P.T. Assistant Clinical Specialist, Department of Physical Therapy, Northeastern University, Boston; Adjunct Faculty Member, Department of Physical Therapy, Simmons College, Boston; Adjunct Physical Therapist, Care Group Home Care, Belmont, Massachusetts
Michele P. West, M.S., P.T. Physical Therapist, Inpatient Rehabilitation, Rehabilita tion Services, Lahey Clinic, Burlington, Massachusetts
:
UTTERWORTH E I
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An Imprint of Elsevier
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Copyright © 2002 by Butterworth-Heinemann
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Every effort has been made to ensure that the drug dosage schedules within this text are accurate and conform to standards accepted at time of publication. However, as treatment recommendations vary in the light of continuing research and clillical experience, the reader is advised to verify drug dosage schedules herein with informa· tion found on product information shee[S. This is especially true in cases of new or infrequently used drugs. Recognizing the importance of preserving what has been written, Bunerworth Heinemann prints its books on acid-free paper whenever possible.
Library of Congress Cataloging-ill-Publication Data Paz, Jaime C., 1966Acute care handbook for physical therapists I Jaime c. Paz, Michele P. West.-2nd ed. p. ;cm. Includes bibliographical references and mdex. ISBN·13, 978·0·7506·7300·6 ISBN· 10, 0·7506·7300·1 I. Medicine-Handbooks, manuals, etc. 2. Hospital care-Handbooks, manuals, ere. I. West, Michele P., 1969-11. lide. [DNLM: I . Acute Discase-rherapy-Handbooks. 2.1mensive Care-Handbooks. WB 39 PJ48a 20021 RC55 .1'375 2001 6 I 6- 100 mm Hg ,,) O mm Hg
85-1 14
>150
mOl Hg mm Hg 60-90 mm Hg 90-100 mm Hg
58-88
Sources: Data from SL Woods, ES Sivarajian Froelicher, S Underhill-Moner (cds). Car diac Nursing (4th cd). Philadelphia: Lippincott, 2000; :md LS Bickley. Bate's Guide to Physical Examination and Hisrory Taking (7th cd). Philadelphia: Lippincon, 1999.
20
ActITE CARE HANDBOOK FOR PHYSICAL TIIERAPlm
venous fistula for hemodialysis, blood clots, scarring from brachial artery cutdowns, or lymphedema (i.e., status-post mastectomy). BP of the upper extremity should be measured ill the following manner: 1. Check for posted signs, if any, at the bedside that indicate which arm should be used ill taking BP. BP variations of 5- J 0 mm Hg between the right and lefr upper extremity are considered normal. Patients with arterial compression or obstruction may have differ ences of more than 10-15 mm Hg. 1 2 2. Use a properly fitting cuff. The inflatable bladder should have a width of approximately 40%, and length of approximately 80% of the upper arm circumference. 1 3
3.
Position the cuff 2.5 em above the antecubital crease.
4.
Rest the arm at the level of the heart.
To determine how high t o inflate the cuff, palpate the radial 5. pulse, inllate until no longer palpable, and nOte this cuff inflation value. Deflate the cuff. Note: With a patient who is in circulatory shock, auscultation may be too difficult. In these cases, this method can be used to measure the SBP and is recorded as systolic BPfP (i.e., "BP is 90 over palp"). 1 3 6.
Place the bell of the stethoscope gently over the brachial arrery.
7. Re-inflare rhe cuff to 30-40 mm Hg greater rhan the value in srep 5. Then slowly deflare rhe cuff. Cuff deflation should occur at approximately 2-3 mm Hg per second.1 3
8. Listen for the onset of tapping sounds, which represents blood flow returning to the brachial arrery. This is the systolic pressure. 9. As the pressure approaches diastolic pressure, the sounds will become muffled and in 5-10 mm Hg will be completely absent. These sounds are referred to as Korotkoff's sounds (Table 1_8). 12.1 3
Clinical Tip • Recording pre-, para-, and posrexerrion SP is important in identifying BP responses [0 activity. During recovery from exercise, blood vessels dilate to allow for greater blood flow to muscles. In cardiac-compromised or very
CARDIAC SYSTEM
21
Table 1-8. Kororkoff's Sounds Phase
Sound
Indicates Systolic pressure (blood stans to flow through compressed artery).
2
First sound heard, faint tapping sound with increasing intensity Start swishing sound
3
4
5
Sounds increase in inrensity with a distinct tapping Sounds become muf ned Disappearance
Because of the compressed artery, blood flow continues to be heard while the sounds change due to the changing compression on the anery.
Diasrolic pressure in children < 1 3 yrs old and in adults who are exercising, preg nanr, or hyperrhyroid (see phase 5). Diastolic pressure in adults-occurs 5-10 mm Hg below phase 4 i n normal adults. In states of increased rate of blood flow, it may be greater than 10 mm Hg below phase 4. In these cases, the phase 4 sound should be used as diasrolic pressure in adults.
Sources: Data from SL Woods, ES Sivarajian-Froelicher, S Underhill-Moner (eds). Car diac Nursing (4th ed). Philadelphia: Lippincott, 2000; and LS Bickley. Bate's Guide to Physical Examination and History Taking (7th ed). Philadelphia: Lippincott, 1 999.
decondirioned individuals, toral CO may nor be able to support this increased flow to the muscles and may lead to decreased Output to vital areas, such as the brain. • If unable to obtain BP on rhe arm, rhe thigh is an appro priate alternative, with auscultation at the popliteal artery. • Falsely high readings will occur if the cuff is too small or applied loosely, or if the brachial arrery is lower rhan rhe hearr level. • Evaluarion of BP and HR in differenr postures can be used to monitor orthostatic hypotension with repeat mea surements on the same arm 1-5 minutes after position changes. The symbols rhar represent parienr posirion are shown in Figure 1 -7.
22
AClJfE CARE HANDBOOK FOR PHYSICAL THERAPISTS
0-Supine
Sitting
Standing
Figure 1-7. Orthostatic blood pressure symbols.
• The same extremity should be used when serial BP recordings will be compared for an evaluation of hemody namic response. • A BP record is kept on the patient's vital sign flow sheet. This is a good place to check for BP trends throughout the day and, depending on your hospital's policy, to document BP changes during the therapy session. • An auscultatory gap is the disappearance of sounds between phase 1 and phase 2 and is common in patients with high BP, venous distention, and severe aortic stenosis. Its presence can create falsely low systolic pressures if the cuff is not inflated high enough (which can be prevented by palpating for the disappearance of the pulse prior to measurement), or falsely high diastolic pressures if the therapist stOps measurement during the gap (prevented by listening for the phase 3 to phase 5 transitions). 13
Auscultation Evaluation of heart sounds can yield information about the patient'S condition and tolerance to medical treatment and physical therapy through the evaluation of valvular function, rate, rhythm, valvular compliance, and ventricular compliance.4 To l isten to heart sounds, a stethoscope with both a bell and a diaphragm is necessary. For a review of normal and abnormal heart sounds, refer to Table 1-9. The examination should follow a systematic pattern using both the bell (for low-pitched sounds) and diaphragm ( for high-pitched sounds) and should cover all auscultatory areas, as illustrated in
CARDIAC SYSTEM
23
Table 1-9. Normal and Abnormal Heart Sounds Sound
Location
Description
5 1 (normal)
All areas
52 (normal)
All areas
53 (abnormal)
Best appreciated at apex
54 (abnormal)
Best appreciated at apex
Murmur (abnormal)
Over respective valves
Pericardia I friction rub (abnormal)
TIlird or fourth inrercostal space, anrerior axillary line
First heart sound, signifies closure of atrioventricular valves and corre sponds to onset of ventricular systole. Second heart sound, signifies closure of semilunar valves and corresponds with onset of ventricular diastole. Immediately following S2, occurs early in diastole and represents filling of the ventricle. In young healthy indi viduals, it is considered normal and called a physiologic third sound. In the presence of heart disease, it results from decreased ventricular compliance (a classic sign of conges tive heart failure). Immediately preceding S l , occurs late in ventricular diastole, associated with increased resistance to ventricu lar filling; common in patients with hypertensive heart disease, coronary heart disease, pulmonary disease, or myocardial infarction, or following coronary artery bypass grafts. Indicates regurgitation of blood through valves; can also be classified as sysrolic or diastolic ll1llfmurs. Common pathologies resulting in murmurs include mitral regurgita tion and aortic stenosis. Sign of pericardial innammation (peri carditis), associated with each beat of the hearr, sounds like a creak or leather being rubbed together.
Source: Data from LS Bickley. Bate's Guide to Physical Examination and Hisfory Taking 17th cd). Philadelphia: Lippincott, 1999.
24
AClITE CARE HANDnOOK FOR I)I·IYSICAL THERAPISTS
Pulmonic Area Aortic Area
Figure 1-8. Areas for heart sound auscultation. (Drawn by Barbara Cocanour. Ph.D., University of Massac/msetts, Loweff. Departmel1l of Physical Therapy.)
Figure 1-8. Abnormal sounds should be noted with a description of the conditions in which they were heard (e.g., after exercise or dur ing exercise).
Clinical Tip • Always ensure proper function of stethoscope by tapping the diaphragm before applying the stethoscope to the patient. • Rubbing the stethoscope on extraneous objects can add noise and detract from true examination. • Auscultation of heart sounds over clothing should be avoided, because it muffles the intensity of both normal and abnormal sounds. • If the patient has an irregular cardiac rhythm, HR should be determined through auscultation (apical HR). To save time, this can be done during a routine ausculta tOry examination with the stethoscope's bell or diaphragm in any location.
CARDIAC SYSTEM
25
Diagnostic and Laboratory Measures The diagnostic and laboratory measures discussed in this section pro vide information that is used to determine medical diagnosis, guide interventions, and assist with determining prognosis. The clinical rele vance of each test in serving this purpose varies according to the pathology. This section is organized across a spectrum of least inva sive to most invasive measures. When appropriate, the test results mOst pertinent to the physical therapist are highlighted. Information that bears a direct impact on physical therapy clinical decision mak ing usually includes that which helps the therapist identify indications for intervention, relative or absolute contraindications for interven tion, possible complications during activity progression, and indica tors of performance. Oximetry Oximetry (Sa0 ) is used to indirectly evaluate the oxygenation of a 2 patient and can be used to titrate supplemental oxygen. Refer to Chapter 2 for a further description of oximetry. Electrocardiogram ECC provides a graphic analysis of the heart's electrical activity. The ECC is commonly used to detect arrhythmias, heart blocks, and myocardial perfusion. It can also detect atrial or ventricular enlargement. ECC used for continuous monitoring of patients in the hospital typically involves a two- or three-lead system. A lead represents a particular portion or "view" of the heart. The patient'S rhythm is usually displayed in his or her room, in the hall, and at the nurses' station. Diagnostic ECC involves a 1 2-lead anal ysis, the description of which is beyond the scope of this book. For a review of basic ECC rate and rhythm analysis, refer to Table 1 -1 0 and Figure 1-3.
Holter Monitoring Holter monitoring is 24- or 48-hour ECC analysis. This is per formed to detect cardiac arrhythmias and corresponding symp toms during a patient'S daily activity. 12 Holter monitoring is different than telemetric monitoring because the ECC signal is recorded on a tape, and the subsequent analysis follows from this recording. Indications for Holter monitoring include the evaluation of syn cope, dizziness, shortness of breath with no other obvious cause, pal-
26
AClffE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Table 1 -10. Electrocardiograph Interpretation
Wave/Segment
Duration (sees)
Amplitude (mm)
Indicates
P wave PR interval
10 mm H8 He 1ta OropI >10 bpm Oiaphoralf" Pallor, Conlualon
I,;,a-eued R.f'E d�i'" no di.1Inpln vital ......
Cy;..-a
""ph-
Nasal Flaring 1ncrea.M'd UN of Aa:euory MWlCieoI 01 Respl�11on
�
rlcm 01 Stablt: va. U ta ble JUP01'M to Act1Vlf)' or iix...dae 10 blUed on mQnlloting �lvva"t �tit:fll variables during ExamlNotion or ln�ft\tlon and 1.5 maIm to the �&nl" ph)'lliul apKIty to pport die d�of thr aclivify.""" lnUNlty of 1M activity 15 alwa)'ll l'll'larive to ttw. patient'. a.p.dty,
-
...
...
..
Pump F.U rr. Congeo.UvO' Hun FaU.. ,..,.
-------
Stable RrIpo..... nuoy pl:'ell«ll as: · UnNr Inert In .fiR and Systolic 8P · · ·
.....
Un$UlblnK .... ,. p�1 as: · 0..- of I>!" lncrea$I:CI FlWluency of e, t Ventricular �(StopRJC If> IO/mIn..
....
with Inc:n!Uel ln activi ty 1ev..1. aI ted R8ponoes In HR and S)'IItoJk BP If on �'�'" al'd oome Calcium Channel 81oc:kfts Irw:reated RPE with �&Md worlmel; compromlMd) Unlfonl PVC'. become Mullifoo;al PVC. 0.-. of5lsn- 0'0-11' (Sft Table 1.17) Sy.tolk »Iood J>res.ure Dropf > 10 mm He DIutoIIc IItood f'TeM Incn-uea or Drcno >IO mm Ha
......
...
.....
Hea" RIlle 0I11pI >10 bpm Poor "",1M � « 10 mm Hgdllference bewft!n SyatOhc d DiaMoic l Blood .... � .. Diaphorftlt. Pallor. ConftWon In.cn&M:d IU'1i. deplte no o:hangn In vital "" bcNrnlc SyrnptOlN Sf �I Changes
In p.tlenr. � Invaalvely monltmM: 0 >10mm HglOCftUe In pulmofIaty .""ty ,,� 0 lncreue Or d� of '" mm Hg In CI!I'l�1 vena pns5UnI Cy'-
...
"'"ph .....
N.... I.. F\a.ri.na � U""(>f�tyM\OIIdft c>f Rapitiltion
Figure 1 - 1 0. Determination of stable liS. unstable responses to activity/exercise. rBP blood pressure; CHF congestive heart failure; HR heart rate; PVC premature ventricular contraction; RPE rating of perceived exertion; Rx Ireatmetlt.) =
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CARDIAC SYSTEM
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Table I·A.4. Electroc3rdlographic {EeGl Characteristics 3nd Causes of Arnovenrricul3r Blocks
N3me
ECG ChJracrcristics
Common Causes
PT Considerations
brst-degree AV block
Regular rhythm, rate nor· mal 60- 100, prolonged PR Interval >0.2 (con· stant).
Elderly wirh heart disease,
If chronic, need ro be more cmmous of u nderly ing he3rt disease; if new onset, mOOltOr c1osel)· for pro· gression to h igher level block.
Irregular rhythm, arrial rare > ventricular rate, usu311y both 60-100; PR Interval lengthens until P W3ve appears without 3 QRS complex.
Acute infection, acme �tI
Symproms are uncommon, as above.
Irregular rhythm, aerial rate > ventricular nne, PR interval may be normal or
Anterosepral MI
CHF
Second-degree AV block type I (Wenkebach, Mobltz I)
Second-degree AV block type II (Mobitz II)
prolonged bur is consr3nr for each conducted QRS. Regu la r rhythm, arrial rare >
Third-degree AV block (complete heart block)
AV = amoventricubr; ClIF
acute myocarditis, acute �1I
ventricular rarc.
=
congestive heart failure; MI
=
Ameroseprai MI, drug imoxi· c3rion, infections, electro· lyre imbal3nces, coronary artery disease, degenerative sclerotic process of AV can· duction system
IS commonj can have dizzl· ness, fainting, complete uneon· sciousnessj may need pacing and PT treatmem; should he held for medical management.
Severe CHFj patient will need med· ical management; a pacer (rem· porary or permanent depending on reversi hiliry of eriolob'Y) is
almosr always necessary.
myocardial infarction .
Sources: Data from B Aehlen. ACLS Quick Review Study Guide. St. Louis: Mosby, 1 994; and EK Chung. Manual of Cardiac Arrhythmias. 80s· tOn: Bunerwonh-Heinemann, 1 986.
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Appendix 1 -B
82
AClfrE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Figure 1-8.1. Paroxysmal supraventricular tachycardia. Note development from 110rmal sinus rhythm. (\Vith permission from M \'(/alsh, A Crumbie, S Reveley. Nurse Practitioners: Clinical Skills and Professional lssucs. Boston: Butterworth-HeiNematm, J 993;96.)
Figure 1-8.2. Atrial {lutter. Note regular rhythm (P waves) but vemriwfar rhythm depends on CONduction pattern. (\Vith permission fr011l M \Valsh, A Cmmbie, S RevelC),. Nurse PractitioNers: Clinical Skills and Professional Issues. Boston: Butterworth-Heinemann, 1 993;95.}
CARDIAC SYSTEM I\PPENDIX ] -B
83
Figure I-B.3. Atrial fibrillation. Note the irregular rhythm alld absence of normal P waves. (With permission from M Wafsh, A Crumbie, S Reveley. Nurse Practitioners: Clinical Skills and Pro(essional Issues. Boston: Butter worth-Heinemann, 1 993;95.)
Figure 1-8.4. Ventricular tachycardia. Rate 1 00-170 beats per minute. No P waves, broad electrocardiographic wave complexes. (Reprillted with pemlis sion (rom M Walsh, A Crumbie, S Reveley. Nurse Practitioners: Clinical Skills and 1)ro(essiollal ls5ues. BOSIOI1: Butterworth-Heinemann, 1 993;98.)
84
AClITE CARE HANDBOOK fOR I'HYSICAL THERAI'IS1S
p
p
p
Figure I-B.S. Ventricular ectopy with refractory period afterward. (\Vith per missioN from M \Valsh, A Crumbie, S Reveley. Nurse Praclltioners: Clinical Skills and Professional Issues. Boston: Butterworth-Hememallll, 1 993;97.)
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Whittle. Fractures of the Lower Extremity. In ST Canale (ed), Campbell's Operative Orrhopaedics. Vol. 3 (3rd ed). St. Louis: Mosby, 1998. =
=
=
=
Table 3-A.7. Managemenr and Physical Therapy Intervention for Patellar Fractures Physical Therapy Fracture Type
Management Options
Intervention
Nondisplaced
Closed reduction
Functional mobility
Long leg cast (or other immobilization
PWBor WBAT Avoid strong straight
brace) with full knee
leg raise and strong
extension
quadriceps contraction because it can stress the fracture site
Displaced (simple
ORIF with immobiliza-
See Nondisplaced, above
vertical or trnns-
rion of rhe knee at
verse fracture)
full extension
AAROM (per physician)
Continuous passive
after few days of immobilization
Illorion Comminuted
ORIF (with fragment removal, if applicable)
Functional mobility NWB, PWB, or WBAT
246
ACUTE CARE HANDBOOK FOR PHYSICAL THERAI%TS
Table 3-A.7.
Continued Physical Therapy
Fracture Type
Management Options
Intervention
Partial patellectomy
See Nondisplaced,
(when one large frag
above, in regard to
menr remains) or
quadriceps
total patellectomy (if no large fragments remain) and quadri ceps tendon repair Immobilization with long leg cast, long leg brace, or posterior splint at full k nee extension or slight flexion
AAROM = active-assisted range of motion; ORIF open-reduction internal fixation; NWB = non weight bearing; PWB parrial weight bearing; WBAT weight bearing as tolerated. Source: Data from AP Whittle. Fractures of Lower Extremity. In ST Canale (ed.) Camp· bell's Operative On:hopaedics, Vol. 3 (9th ed). Sr. Louis: Mosby, 1998. =
=
=
Table 3-A.S. Management and Physical Therapy Intervention for Tibial Plateau Fractures Physical Therapy Fracture Type
Management Options
Intervention
Nondisplaced
Closed reduction
Functional mobility
Cast-brace immobilization or postoperative knee brace Ligament repair (if appli cable)
TDWB or PWB AAROM exercise, continuous passive morion to knee joint, or both
MUSCULOSKELETAL SYSTEM APPENDIX J-A
247
Physical Therapy Fracture Type
Management Options
Imervention
Displaced; single
External fixation
Functional mobiliry
condylar or split compres sion fracrure
NWB ,mWB , or
ORIF Cast-brace application or posroperarive knee brace
PWB AAROM exercise, continuous passive morion to knee joint, or both
Sk eletal tractIOn and bed
Displaced; impacted, or
rest (5 I wk) to allow for
severely
soft tissue healing
comminuted bicondylar fracture
ORIF % bone graft Simultaneous ligamem or
Functional mobiliry NWB , TDWB ,orPWB Delayed knee NAAROM Positioning, breathing exercise, and uninvolved
meniscal repair, if appli-
extremity exercise if on
cable
bed rest
Immobilization brace
AiAAROM = aCflvelacllve-assisted range of motton; AAROM = active-assisted range of motion; NWB non weight bearing; ORIF = open-reduction internal fixation; PWB partial weight bearing; TOWS tOuch-down weight bearing. Source: Data from AP Whittle. Fractures of Lower Extremity. In ST Canale (cd), Camp bell's Operative Orthopaedics, Vol. 3 (9th ed). St. LoUIS: Mosby, 1998. =
=
=
248
ACUTE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Table 3-A.9. Medical-Surgical Management and Physical Therapy Intervention for Tibial Shaft Fractures Fracture Type
Management Options
Physical Therapy lntervenrion
Closed; minimally
Closed reduction
Functional mobility IDWB,
displaced
Long leg casr
PWB, or WBAT Quadriceps strengthening Edema management
Closed; moderately displaced
Open-reduction internal fixarion (ORIF) Short leg cast
Functional mobility N\VB, TDWS Knee ROM exercise Quadriceps strengthening Edema management
Closed; severely displaced, comminured, or borh
External fixation Temporary calcaneal traction [Q allow for soft tissue healing ORIF
Open
External fixation
Functional mobility N\VB Ankle;t; k nee ROM exercises Quadriceps strengthening Edema management See Closed; severely displaced,
comminuted,or both, above
with or without; NWB = non weight bearing; PWB = parrial weight bearing; ROM = range of motion; TOWB = touch-down weight bearing; WBAT weight bearing as tol erated.
�=
=
Table 3-A.I0. Medical-Surgical Managemenr andPhysical Therapy Intervention for Distal Tibial and Ankle Fractures Medic.al-Surgical
Physical Therapy
Fracture Type
Options
Intervention
Distal tibial;
Closed reduction
Functional mobility NWB
closed,mini mally displaced
Short leg cast
Knee ROM exercises Proximal joint strengthening Edema management
Distal tibial; closed,moder ately displaced
ORIF Short leg cast
See Distal tibial; closed,minimally displaced,above
MUSCULOSKE.LETAL SYSTEM APPENDIX J-A
249
Medical-Surgical
Physical Therapy
Fracture Type
Options
Intervention
Distal tibial;
Temporary calcaneal
Functional mobility NWB
closed, severely displaced
traction External fixation ORIF
Lower-extremity isomet riCS Neutral ankle positioning Proximal joinr strengthening Edema management
Distal tibial; open
External fixation
Functional mobility NWB Ankle ROM exercise Neutral ankle positioning Proximal joint strengthening Edema management
Ankle; closed, nondisplaced
Closed reduction Short leg cast or walk ing cast
Functional mobility NWB or PWB Edema management Proximal lower-extremity strengthening exercise
Closed reduction
Functional mobility NWB
placed, multi
ORIF
Edema management
fracture, or both
Cast application or
Proximal lower-extremity
Ankle; closed, dis
other immobilization
strengthening exercise
method dependenr on
Foot and ankle exercise as
degree of edema
per physician and type of immobilization device
Ankle; open
Irrigation and debride
See Ank le; closed, dis
menr with immediate
placed, multifracture,
or delayed wound
or both, above
closure Tracrion External fixation ORIF
NWB = non weight bearing; ORJF = open-reduction inrernal fixarion; PWB = p artia l weight bearing; ROM = range of morion. Source: Data from WB Geissler, AK Tsao, JL Hughes. Fracrures and Injuries of rhe Ankle. In CA Rockwood, Dr Green, RW Bucholz, JD Heckman (cds), Rockwood and Green's Ff3crurcs in Adults (4rh cd). Philadelphia: Lippincott-Raven, 1996.
250
AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Table 3-A.l1. Management and Physical Therapy lntervention for Calcaneal and Forefoot Fractures· Physical Therapy Fracture Type
Management Options
Intervention
Calcaneal; extra-
Closed reduction
Functional mobility
articular, minimally displaced
NWB
SLC
Proximal lower-extremity strengthening and ROM exercise Edema management Ank le/forefoot exercise as per physician and type of immobilization device
Calcaneal; avulsion
Closed reduction ORIF SLC
Calcaneal; intraarticular fracture involving the subtalar joint
Sk eletal traction Immediate or delayed SLC
See Calcaneal; extraarticular, minimally displaced, above See Calcaneal; extraarticular, minimally displaced, above
Closed reduction and percutaneous pinning ORfF Arthrodesis if fracture IS
Calcaneal; open
very severe
Irrigation and dehride-
See Calcaneal; exna-
menr with immedi-
articular, minimally
ate or deJayed
displaced, above
wound closure Skeletal traction External fixation
MUSCULOSKELETAL SYSTEM APPENDIX 3-A
251
Physical Therapy Fracrure Type
Management Options
lnrervention
Forefoot; minimally
Closed reduction
Functional mobility
displaced
Percutaneous pinning SLC or walking cast
NWB,PWB ,or WBAT, dependent on exact location and severity of frac ture Proximal lower extremity strength ening and ROM exercise Edema management
Forefoot; moderate or severe displacement, with fragmentation or angularion Forefoot; open
Sec Forefoot; minimally
ORJF Percutaneous pinning
displaced, above
SLC See Forefoot; minimally
See Calcaneal; open, above
displaced, above
ORIF
NWB = non weight bearing; ORIF open-reduction internal fixatioll; PWB = partial weight bearing; ROM range of motion; SLC short leg cast; WBAT weight bearing as tolerated. '"For calcaneal fractures, cast application may not be in the neutral ankle position to protect the fracture site from strong ankle muscle contractions. Source: Data from JD Heckman. Fractures and Dislocations of the Foot. In CA Rock wood, DP Green, RW Bucholz, JD Heckman (cds). Rockwood and Green's Fractures in Adults (4th cd). Philadelphia: Lippincon-Raven, 1996. =
=
=
=
252
AClITE CARE HANDBOOK FOR PHYSICAL TIIERAPISTS
Table 3-A.12. Management and Physical Therapy Imervention for Common Cervical Spine Fractures Physical Therapy Fracture Type
Management Options
Intervention
Hangman's fracture,
Cervical collar immo
Functional mobility with
or bilateral pedicle fracrure of axis IC I ) Type I-no angulation and 3 mm displacement of C2 on C3 Type !lA-minimal displacement and
possible) Posterior open reduc tion and halo vest or CT-3 fusion for type 11\
logroll precautions Posture and body mechanics training Therapeutic exercise and active-assisted/passive range of motion depcn dent on neurologic IIlJury Balance and scapular exercises for the patient in a halo vest
significant angu lation of C2 Type III-full uni or bilateral facet dislocation Odontoid process fracture Type l- �
D: Acalculia, agraphia, finger agnosia
�
Wernicke's area
Temporal lobe
NO: Ability to construct shapes, awareness of external environmenr, and body image 0: Sensory speech (auditory and written) comprehension center NO: Appreciation of content of emmional language (e.g., tone of voice)
NO: Constructional apraxia, geographic agnosia, dressing apraxia, anosognosia Wernicke's ( receptive) aphasia
Optic radiation GustatOry cortex
Visual tract Perception of taste
Lower homonymous quadrantanopia
Superior temporal gyrus (audicory cortex)
0: Appreciation of language
0: Decreased ability to hear NO: Decreased ability to appreciate music
NO: Appreciation of music, rhythm, and sound
Dysfunction is very uncommon
Middle and inferior tern poraI gyri
Learning and memory ceorers
Learning and memory deficits
Limbic lobe and olfaccory cortex
Affective and emotion center, including mood, primitive behavior, self preservation, shorr-term memory, visceral emotion processes, and interpretation of smell
Aggressive or antisocial behaviors Inability to establish new memories
See Parietal lobe, above
Wernicke's ( receptive) aphasia
Wernicke's area
z
i::
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> n
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'" �
0
'" � J: -< �
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r
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Pons
Middle cerebellar peduncles Respiratory center CNs V-VUI nuclei Forms anterior wall of fourth ventricle
Conduction pathway between higher and lower brain centers
See Midbrain. above
Medulla
Decussation of pyramidal tracts Inferior cerebellar peduncles Inferior olivary nuclei Nucleus cuneatus and gracilis CNs [x-Xil nuclei
Homeostatic center for cardiac, respiramry, vasomotor functions
See Midbrain, above
Anterior lobe
Medial portion Lateral portion
Sensory and motor input of trunk Sensory and motor input of extremities for coordination of gait
Ipsilateral ataxia and discoordination or tremor of extremities
Posterior lobe
Medial and lateral portions
Sensory and motor input for coordination of motor skills and postural tone
Ipsilateral ataxia and discoordination of the trunk
:erebellum
Z m '"
6
iii
�
N '" "
Table 4-2. Continued Brain Structure Flocculonodular
ADH
=
N a.. co
Substructure
Function
Dysfunction
Flocculus nodule
Sensory input from ears Sensory and motor input from eyes and head for coordina� rion of balance and eye and head movement
Ipsilateral facial sensory loss and Horner's syndrome. nys tagmus, visual overshooting Loss of balance
antidiuretic hormone; eN
=
cranial nerve; ICP
=
intracranial pressure.
Sources; Data from KW Lindsay, I Bone, R Callander (cds). Neurology and Neurosurgery Illustrated (2nd ed). Edinburgh, UK: Churchill Livingstone, 1991; S Gilman, SW Newman (cds). Manter and Gatz's Essentials of Clinical Neuroanaromy and Neurophysiology (7th ed), Philadelphia: FA Davis,
1989; JA Kiernan
(ed). Introduction to Human Neuroscience. Philadelphia: Lippincott, 1987; EN Marieb fed). Human
Anatomy and Physiology (5th ed). San Francisco: Benjamin-Cummings. 2001; and L Thelan, J Davie, M Lough reds). Critical Care Nursing: Diagnosis and Managemenr (2nd ed). St. Louis: Mosby.
1994.
8;;!
n > '" '"
:t >
15 1') o
"
Ci '" �
:t
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or :im
s:
�
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NERVOUS SYSTEM
269
Meninges The meninges are three layers of connective tissue that cover the brain and spinal cord. The dura marer, rhe outermost layer, lines the skull (periosteum) and has four major folds (Table 4-3). The arachnoid, the middle layer, loosely encloses the brain. The pia mater, the inner layer, covers the convolutions of the brain and forms a portion of the chor oid plexus in the ventricular system. The three layers create very important anatomic and potential spaces in the brain, as shown in Figure 4-2 and described in Table 4-4. Ventricular System The ventricular system nourishes the brain and acts as a cushion by increasing the buoyancy of the brain. It consists of four ventri cles and a series of foramen, through which cerebrospinal fluid (CSF) passes to surround rhe CNS. CSF i s a colorless, odorless solution produced by rhe choroid plexus of all ventricles. CSF cir culares in a pulse-like fashion through the ventricles and around the spinal cord with the beating of ependymal cilia rhar line the ventricles and intracranial blood volume changes that occur with breathing and cardiac systole] The flow of CSF under normal con ditions, as shown in Figure 4-3, is as follows4:
Table 4-3. Dural Folds Falx cerebri
Vertical fold that separates the two cerebral hemi· spheres ro prevent horizontal displacement of these structures
Falx cerebelli
Vertical fold that separates the two cerebellar hemispheres to prevent horizontal displacement of these structures
Tentorium cerebelli
Horizontal fold that separates occipital lobes from the cerebellum to prevent vertical displacement of these Structures
Diaphragm sellae
Horizontal fold that separates that subarachnoid space from the sella turcica and is perforated by the stalk of the pituitary gland
Source: Data from JL Wilkinson (ed). Neuroanatomy for Medical Srudents (3rd ed). Oxford, UK: Butterworth-Heinemann,
1998.
270
AClJTE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Figure 4-2. Coronal section o(cranial meninges showing a venous sinus and dural (old. ( With permission from PA Young, PH Young. Basic Clinical Nell roallatomy. Phi/adelphia: \Vil/iams & \Vi/kills, 1997;8.)
From the lateral ventricles via the interventricular foramen to the third ventricle
•
• From the third ventricle aqueduct
to
the fourth ventricle via the cerebral
• From the fourth ventricle to the cisterns, subarachnoid space, and spinal cord via the median and lateral apertures
Table 4-4. Dural Spaces Epidural (extradural) space
Potential space between the skull and outer dura mater.
Subdural space
Potential space between [he dura and [he arachnoid mater; a split in the dura con tains the venous sinus.
Subarachnoid space
Anaromic space between the arachnoid and pia ll1!lter containing cerebrospinal Auid and the vascular supply of the cortex.
NE.RVOUS SYSTE.M
271
Supenor saglnal Sinus Choroid plexus Cerebral aqueduct
Fourth veolflcle Foramen olluschka
•
Foramen 01 Magendle
Figure 4-3. The velltricular system of the brai". Arrows indicate the ciratla liol1 of cerebrospinal fluid from the site of formatioll in the choroid plexus to the site of absorptioll ill the villi of the sagittal 5;11115. (\Vith permission from J Bogouss/avsky, M Fisher /edsJ. Textbook of Neurology. Bostol1: Blitterworth Heillemallll, 1998;656.)
\Vhen ventricular pressure is greater than venous pressure, CSF is absorbed into the venous system via the arachnoid villi, capillary walls of the pia mater, and lymphatics of the subarachnoid space near the optic nerve. 2 Blood-Brain Barrier The blood-brain barrier is the physiologic mechanism responsible for keeping toxins, such as amino acids, hormones, ions, and urea, from altering neuronal firing of the brain. It readily allows water, oxygen, carbon dioxide, glucose, some amino acids, and substances thar are highly soluble in fat (e.g., alcohol, nicotine, and anesthetic agents) to pass across the barrier,s,· The barrier consists of fused endothelial cells on a basement membrane that is surrounded by astrocytic foot extensions.· Substances must therefore pass through, rather than
272
ACUTE CARE HANDBOOK FOR PHYSICAL THERAPISTS
around, these cells. The blood-brain barrier is absent ncar the hypo thalamus, pineal region, anterior third ventricle, and floor of the fourth ventricle.3
Central Brain Systems The central brain systems are the reticular activating systcm and the limbic system. The rcticular activating system is responsible for human consciousness level and integrates the functions of the brain stem with conical, cerebellar, thalamic, hypothalamic, and sensory receptor functions.s The limbic system is a complex interactive system, with primary connections berween the cortex, hypothalamus, and sensory recep tors.5 The limbic system is the emotional system, mediating cortical autonomic function of internal and external stimuli.
Circulation The brain reccives blood from the internal carotid and vertebral arter ies, which are linked together by the circle of Willis, as shown in Fig ure 4-4. Each vessel supplies blood to a certain part of the brain (Table 4-5). The circulation of the brain is discussed in tcrms of a sin-
Ant communicating att. AnI. cerebral art Middle cerebral att POSI. COmmunicating '".
---'tj:.-�-"'�''' rnlernal
carotid art
POSI cerebral art Greal cerebfal vein (Galen)
j
CIrcle 01 WilNs & associated veins
Figure 4-4. Schematic representation of the arterial circle of Willis and accompanying veins. (Ant. anterior; art. artery; Post. posterior.) (\Vith permission from £G Gonzalez, S) Meyers reds/. Downey and Darling's Phys iological Basis of Rehabilitation Medicine (Jrd ed/. Boston: Butterworth Heinemann, 2001 ;22.) =
=
=
NERVOUS SYSTEM
273
Table 4-5. Blood Supply of the Major Areas of the Brain Area of Perfusion
Artery Anterior circulation Internal carotid artery (ICA)
External carotid artery (ECA) Anterior cerebral artery (ACA)
Middle cerebral artery (MCA)
The dura, optic tract, basal ganglia, midbrain, uncus, lateral geniculate body, and tympanic cavity. Ophthalmic branch supplies the eyes and orbits. All structures external to the skull, the larynx, and the thyroid. Medial and superior surface of frontal and parietal lobes. Medial striate branch sup plies anterior portion of the internal capsule, optic chiasm and nerve, portions of the hypothalamus, and basal ganglia. Lateral surface of the frontal, parietal, and occipital lobes, including the superior and lareral surfaces of temporal lobes.
Posterior circulation Vertebral artery
Medulla, dura of the posterior fossa, including the falx cerebri and tentorium cerebelli. Pons and midbrain.
Basilar artery Posterior inferior cerebellar artery (PICA)
Posrerior and inferior surface of cerebellum.
Anterior inferior cerebellar artery (AICA)
Anterior surface of the cerebellum, flocculus, and inferior vermis.
Superior cerebellar artery (SCA)
Superior surface of cerebellum and vermis.
I)osterior cerebellar artery (PCA)
Occipital lobe and medial and lateral surfaces of the remporal lobes, thalamus, lareral gen iculate bodies, hippocampus, and choroid plexus of the third and lareral ventricles.
Sources: Data (rom CL Rumbaugh, A Wang, FY Tsai (cds). Cerebrovascular Disease Imaging and Interventional Tre:nment Oprions. New York: Igaku-Shoin Medical Pub lishers,
1995; and KL Moore (cd). Clinically Oriented Anaromy (2nd cd). Baltimore: 1985.
Williams & Wilkins,
gle vessel or by region (usually as the anterior or posterior circula tion). There are several anastomotic systems of the cerebral vascul ature that provide essential blood flow to the brain. Blood is drained from the brain through a series of venous sinuses. The superior sagit tal sinus, with its associated lacunae and villi, is the primary drainage
274
ACUTE CARE
HANDBOOK FOR
PHYSICAL THERAI)ISTS
site. The superior sagittal sinus and sinuses located in the dura and scalp then drain blood into the internal jugular vein for return to the heart. Spinal Cord The spinal cord lies within the spinal column and extends from the foramen magnum to the first lumbar vertebra, where ir forms the conus medullaris and the cauda equina and attaches to the coccyx via the filum terminale. Divided into the cervical, thoracic, and lumbar portions, it is prorected by mechanisms similar ro those supporting the brain. The spinal cord is composed of gray and white matter and provides the pathway for the ascending and descending tracts, as shown in cross section in Figure 4-5 and out lined in Table 4-6.
Peripheral Nervous System The peripheral nervous sysrem consists of rhe cranial and spinal nerves and the reflex system. The primary structures include peripheral nerves, associated ganglia, and sensory receptors. There are 12 pairs of CNs, each with a unique parhway and function (sensory, motor, mixed, or autonomic). Thirty-one pairs of spinal nerves (all mixed) exit the spinal cord to form distinct plexuses (excepr T2 rhrough T12). The peripheral nerves of rhe upper and lower extremities and thorax are listed in Tables 4-7 through 4-9, and the dermatomal system is shown in Figure 4-6. The reflex sys tem includes spinal, deep tendon, stretch, and superficial reflexes and protective responses.
Autonomic Nervous System The portion of the peripheral nervous system thar innervates glands and cardiac and smooth muscle is the autonomic nervous system. The parasympathetic division is activated in time of rest, whereas the sympathetic division is activated in times of work or "fight or flight" situations. The two divisions work closely togerher, wirh dual innervation of most organs, to ensure homeostasis.
Ulftlar i:!aCortiooSPlflai (l RubrOlf)lnal Tract An1
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AnI
Spmocerebellar Tracl
J AnI SPInothalamIC Tract
Ant. COrticospinal Tract DESCENDING PATHWAYS
ASCENDING PATHWAYS
Figure 4-5. Cross-section of the spinal cord. (Ant. :; anterior; Lat. :; lateral; Post. :; posterior.) ( With permission from RJ Love, we Webb ledsl. Neurology for the Speech·Language Pathologist 14th edl. Bosto", BuHerlVorth-Hei"ema"". 2001 ;44.)
z
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N .... v.
276
AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Table 4-6. Major Ascending and Descending White Maner Tracts"" Tract
Function
Fasciculus gracilis
Sensory pathway for lower-extremiry and lower-trunk joim proprioception, vibration, two-poim discrimination, graphesrhesia, and double simultaneous stimulation
Fasciculus cuneatus
Sensory pathway for upper-extremiry, upper-crunk, and neck joint proprioception, vibration, two-point dis crimination, graphesthesia, and double simulraneous stimulation
Laceral spinothalamic
Sensory pathway for pain, temperature, and light touch
Ventral spinocerebellar
Sensory pathway for ipsilateral subconscious proprioception
Dorsal spinocerebellar
Sensory pathway for ipsilateral and contralateral subcon scious proprioception
Lateral corticospinal (pyramidal)
Motor pathway for contralateral voluntary fine muscle movement
Anterior corticospinal (pyramidal)
Motor pathway for ipsilateral voluntary movement
Rubrospinal (extra pyramidal)
Motor pathway for gross postural tone
Tectospinal (extra pyramidal)
Mocor pathway for contralateral gross postural muscle cone associated with auditory and visual stimuli
Vestibulospinal (extra pyramidal)
Motor pathway for ipsilateral gross postural adiustments associated with head movemenrs
"Sensory tracts ascend from the spinal cord; motor tracts descend from (he brain
(0
the
spinal cord. Sources: Data from S Gilman, SW Newman (cds). Mamer and Gatt's Essenrials of Clin ical Neuroanatomy and Neurophysiology (7th ed). Philadelphia: FA Davis, 1989; and EN Marieb (cd). Human Anatomy and Physiology (5th cd). San Francisco: Benjamin Cummings, 2001.
NE.RVOUS SYSTEM
277
Table 4-7. Major Peripheral Nerves of the Upper Extremity Nerve
Spinal RoO[
Innervation
Dorsal scapular
C5
Levaror scapulae, rhomboid major and minor
Supmscapular
C5 and C6
Supraspinatus, infraspinatus
Lower subscapular
C5 and C6
Teres major
Axillary
C5 and C6
Teres minor, delraid
Radial
C5, C6, C7, and C8
Triceps, brachioradialis, anconeus, extensor carpi radialis longus and brevis, supinator, extensor carpi ulnaris, extensor digirorum, extensor digiti minimi, extensor indicis, exten sor pollicis longus and brevis, abduc ror pollieis brevis
Ulnar
C8 and T I
Flexor digitorum profundus, flexor carpi uln!lris, palmaris brevis, abduc ror digiti minimi, flexor digiti minimi brevis, opponens digiti minimi, pal mar and dorsal interossei, third and fourth lumbricals
Median
C6, C7, C8, and T l
Pronator teres, flexor carpi radialis, palmaris longus, flexor digirorum super ficialis and profundus, flexor pallicis longus, pronaror quadratus, abductor pollicis brevis, opponens pollieis, flexor pollicis brevis, first and second lumbricals
Musculo cutaneous
C5, C6, and C7
Coracobrachialis, brachialis, biceps
Source: Data from FH Nencr (cd). Arias of Human Anaromy. Summit Ciry, NJ: CIBA GEIGY Corporation, 1989.
Neurologic Examination The neurologic examination is initiated on hospital admission or in the field and is reassessed continuously, hourly or daily, as necessary. The neurologic examination consists of patient history; mental status examination; viral sign measurement; vision, motor, sensory, and coordination testing; and diagnostic resring.
278
AClITE CARE HANDBOOK FOR PHYSICAL Tt-IE.RAI)ISTS
Table 4-8. Major Peripheral Nerves of the Lower Extremiry Nerve
Spinal Root
Innervation
Femoral
L2, U, and L4
Iliacus Psoas major Sartorius Pecrinous Rectus femoris Vastus lateral is, intermedius, and medialis Articularis genu
Obturator
L2, L3, and L4
Obturator extern LIS Adductor brevis, longus, and magnus Gracilis
Sciatic
L4, LS, 5 1 , S2, and S3
Biceps femoris Adductor magnus Semitendinosus Semimembranosus
Tibial
L4, LS, S], 52, and S3
Gastrocnemius Soleus Flexor digitorum longus Tibialis posterior Flexor hallucis longus
Common peroneal
L4, LS, S l , and S2
Peroneus longus and brevis Tibialis amerior Extensor digitorum longus Extensor hallucis longus Extensor hallucis brevis Extensor digitorum brevis
Source: Dara from
FH Nener (cd). Arias of I-Iuman Anawmy. Summir Ciry, Nl: CI8A
GEIGY Corporarion, 1989.
Patietlt History A detailed h istory, initially taken by the physician, is often the most
helpful information used to delineate whether a patient presents with a true neurologic event or another process (usually cardiac or meta bolic in nature). The history may be presented by the patient or, more commonly, by a family member or person witnessing the acme or pro gressive event(s) responsible for hospital admission. One common
NERVOUS SYSTEM
279
Table 4-9. Major Peripheral Nerves of the Trunk Nerve
Spinal Root
Innervation Trapezius
Spinal accessory
C3 and C4
Phrenic
C3, C4, and C5
Diaphragm
Long thoracic
C5, C6, and C7
Serratus anterior
Medial pecroral
C6, C7, and C8
Pectoralis minor and major
Lateral pecroral
C7, C8, and T I
Pectoralis major
Thoracodorsal
C 7 and C8
Latissimus dorsi
Intercostal
Corresponds ro nerve root level
External intercostals Internal intercosrals Levatores costarum longi and brevis
Iliohypogastric and ilioinguinal
LI
Transversus abdominus Internal abdominal oblique
Inferior gluteal
L4, L5, 51, and 52
Gluteus maximus
Superior gluteal
L4, L5, and 5'1
Gluteus medius and minlmus Tensor fascia lame
Source: Data from FH Netter (cd). Arias of Human Anatomy. Summit City, NJ: eIBA GEIGY Corporation, 1989.
framework for organizing questions regarding each neurologic com plaint, sign, or symprom is presented here7,8: •
What is the patient feeling?
•
When did the problem initially occur and has it progressed?
•
What relieves or exacerbates the problem?
•
What is the onset, frequency, and duration of signs or symptoms?
In addition to the general medical record review (see Appendix 1A), questions relevant to a complete neurologic history include the following: •
Does the problem involve loss of consciousness?
•
Did a fall precede or follow the problem?
280
AClfrE CARE HANDBOOK FOR PHYSICAl H1FRAPISTS
Vlnuall)tlal UM of
limb
upper
Figure 4-6. Dermatome chart based 0" embryologic segments. (\vith permis sion from CD Maitland /ed/. Vertebral Manipulation /5th edt. Oxford, UK: Butterworth-Heinemallll, 1986;46.)
•
Is there headache, dizziness, or visual disturbance?
•
What are the functional deficits associated with the problem?
•
Is there an alteration of speech?
•
Does the patient demonstrate memory loss or altered cognition?
NERVOUS SYSTEM
•
281
Does the pariem have an altered sleep pattern?
• What is the handedness of the patient? (Handedness is a predic ror of brain [language] dominance.)
Observation Data that can be gathered from close or distant observation of the patient include the following: •
Level of alertness, arousal, distress, or the need for restraint
•
Body position
•
Head, trunk, and extremity posture, including movement patterns
•
Amount and quality of active movement
Amount and quality of interaction with the environment or family members •
•
Degree of ease or difficulty with activities of daily living
•
Presence of involuntary movements, such as tremor
•
Eye movement(s)
•
Presence of hemibody or hemispace neglect
•
Presence of muscle atrophy
•
Respiratory rate and pattern
Clinical Tip The therapist should correlate these observations with other information from the chart review and other health care team members ro determine (1) if the diagnosis is con sistent with the physical presentation, (2) what rypes of commands or tone of voice to use, ( 3 ) how much assis tance is needed, and (4) how to prioritize the portions of the physical therapy evaluation.
282
AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Mental Status Exam;natioll The mental status examination includes assessment of level of con sciousness, cognition, emotional state, and speech and language ability. Level of Consciousness COlIsc;ouslless consists of arousal and the awareness of self and environment, including the ability to interact appropriately in response to any normal stimulus' Coma is often considered the opposite of consciousness. Table 4- 1 0 describes the different States of consciousness. Evaluating a patient's level of consciollsness is important because it serves as a baseline ro monitor stability,
Table 4-10. Normal and Abnormal States of Consciousness Alerr
Completely awake. Aware of all stimuli. Able to interact meaningfully with clinician.
Lethargic or somnolent
Arousal with stimuli. Falls to sleep when nor stimulared. Decreased awareness. Loss of train of thought.
Obtundent
Difficult to arouse. Requires constant stimulation for all activities. Confused.
Stuporous
Arousal only with vigorous stimulation. Unable to complete mental Status examination because responses are usually incomprehensible words. Unarousable. Nonverbal.
Coma Delirium
State of disorientation marked by irritability or agitation, suspicion and fear, and misperception of stimuli. Patient demonstrates offensive, loud, and talkative behaviors.
Dementia
Alteration in mental processes secondary to organic disease that is nor accompanied by a change in arousal.
Sources: Data from RL Strub, FW Black (cds). Mcntal Status Examination in Neurolo!,'Y (2nd cd). Philadelphia: FA Davis, 1985; and F Plum, J Posner (cds). The Diagnosis of Scupor and Coma (3rd cd). Phil3delphia: FA Davis, 1980.
NERVOUS SYSTEM
283
improvement, or decline in the patient's condition. It also helps determine the severity and prognosis o f neurologic insult or dis ease state, thus directing the medical plan of care.
Clinical Tip • Level of consciousness is often vaguely described in medical charts; therefore, be specific when documenting a patient's mental status. Describe [he intensity of stim ulus needed to arouse the patient, the patient's best response, and the patient's response to the removal of the srimulus.9 • Changes in body position, especially the transition from a recumbent position to sitting upright, often stimulate increased alertness. Other stimuli to increase alertness include daylight, radio or television sound, or a cold cloth on the forehead. • Use a progressive intensity of stimuli to arouse a patient with decreased alertness or level of consciollsness. For example, call the patient's name in a normal tone of voice before using a loud tone of voice, or tap the patient'S shoulder before rubbing the shoulder. • Time of day, fatigue, and side effects of medication are factors that can calise variable levels of alertness or participation in physical therapy. The documentation of these factors is important for communication among the health care team and for the rehabilitation screening process. A & 0 x 3 is a common abbreviation for alert and • oriented to person, place, and time. The number may be modified to reflect the patient'S orientation (e.g., A & 0 x I [selfl).
G lasgow Coma Scale The Glasgow Coma Scale (GCS) is a widely accepted measure of level of consciousness and responsiveness and is described in Table 4-:1 1 . The GCS evaluates best eye opening (E), motor response (M), and verbal response (V). To determine a patient'S overal l GCS, add each
284
ActrrE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Table 4-11. The Glasgow Coma Scale Score
Response Eye opening (E) Spontaneous: eyes open without stimulation To speech: eyes open to voice
4
To pain: eyes open to noxious stimulus
2
3
Nil: eyes do nor open despite variery of stimuli Motor response (M) Obeys: follows commands Localizes: purposeful anemprs to move limb to sdmuJus Withdraws: flexor withdrawal without localizing
6 5 4
Abnormal flexion: decorticate posturing to stimulus
3
Extensor response: decerebrate posturing [Q stimulus
2
Nil: no motor movement Verbal response (V) Oriented: normal conversation
5
Confused conversation: vocalizes in sentences, incorrect context
4
Inappropriate words: vocalizes with comprehensible words
3
Incomprehensible words: vocalizes with sounds
2
Nil: no vocalization Source: Data from B jennen, G Teasdale (cds). Management of Head Injuries. Phibdel· phia: FA Davis,
198 I .
score (i.e., E + M signifies coma.10
+
V ) . Scores range from 3 to 15. A score o f 8 o r less
Clinical Tip Calculation of the GCS usually occurs at regular intervals. The GCS should be used to confirm the type and amount of cueing needed to communicate with a patient, deter mine what time of day a patient is most capable of partici pating in physical therapy, and delineate physical therapy goals.
NERVOUS SYSTEM
285
Cognition Cognitive testing includes the assessment of attention, orientation, memory, abstract thought, and the ability to perform calculations or conStruct figures. General intelligence and vocabulary are estimated with questions regarding history, geography, or current events. Table 4- 1 2 lists typical methods of testing the components of cognition.
Table 4-12. Tests of Cognitive Function Cognitive Function Attention
Definition
Task
Ability to artend to a specific stimulus or task
Repetition of a series of numbers or lerrers Spelling words forward and backward
Orientation
Ability to orient to person, place, and time
Identify name, age, current date and season, birth date, present location, rown, etc.
Memory
Immediate recall
Recount three words after a few seconds
Short-term memory
Recount words (after a few minutes) or recent events
Long-term memory
Recount past events
Calculation
Ability to perform verbal or written mathematical problems
Add, subtract, multiply, or divide whole numbers
Construction
Ability to construct a two- or three-dimen sional figure or shape
Draw a figure after a verbal command or reproduce a figure from a picture
Abstraction
Ability to reason in an abstract rather than a literal or concrete fashion
Inrerpret proverbs Discuss how two objects are similar or different
Judgment
Ability to reason (according to age and lifestyle)
Demonstrate common sense and safery
Source: Dam from LS Bickley, RA Hoekelman (cds). 8ate's Guide tion and History Taking {7th cd}. Philadelphia: Lippincott, 1999.
fO
Physical Examina
286
ACtITE CARE HANDBOOK fOR PHYSICAL THERAPISTS
Emotional State Emotional State assessment entails observation and direct question ing to ascertain a patient's mood, affect, perception, and thought process, as well as to evaluate for behavioral changes. Evaluation of emotion is not meant to be a full psychiatric examination; however, it provides insight as to how a patient may complete the cognitive portions of the mental status examination. I I
Clinical Tip It is important to note that a patient's culture may affect particular emotional responses.
Speech and Language Ability The physician should perform a speech and language assessment as soon as possible according to the patient'S level of conscious ness. The main goals of this assessment are to evaluate the patient'S ability to articulate and produce voice and the presence, extent, and severity of aphasi a . " These goals are achieved by test ing comprehension and repetition of spoken speech, naming, qual ity and quantity of conversational speech, and reading and writing abilities. 12 A speech-language pathologist is often consulted to perform a longer, more in-depth examination of cognition, speech, and swal low using standardized tests and skilled evaluation of articulation, phonation, hearing, and orofacial muscle strength testing.
Clinical Tip The physical therapist should be aware of and use, as appropriate, the speech-language pathologist's suggestions for types of commands, activity modification, and posi tioning as related to risk of aspiration. • The physical therapist is often the first clinician to notice the presence or extent of speech or language dys function during activity, especially during higher-level tasks or those activities that cause fatigue. The physical therapist should report these findings to other members of the health care team. •
NERVOUS SYSTEM
287
Vital Sig1ts The brain is the homeostatic center of the body; therefore, vital signs are an indirect measure of neurologic status and the body's ability to perform basic functions, such as respiration and tempera ture control. Blood pressure, heart rate, respiratory rate and panern (see Table 2-3), temperature, and other vital signs from invasive monitoring (see Appendix III-A) are assessed continuously or hourly to determine neurologic and hemodynamic stability.
Clinical Tip The therapist should be aware of blood pressure parameters determined by the physician for the patient with neurologic dysfunction. These parameters may be set greater than nor mal to maintain adequate perfusion to the brain or lower than normal to prevent further injury to the brain.
Cranial Neroes CN testing provides information about the general neurologic status of the patient and the function of the special senses. The results assist in the differential diagnosis of neurologic dysfunction and may help in determining the location of a lesion. CNs I through XII are tested on admission, daily in the hospital, or when there is a suspected change in neurologic function (Table 4 - 1 3 ) .
Vision Vision testing is an important portion of the neurologic examination, because alterations in vision can indicate neurologic lesions, as illus trated in Figure 4-7. In addition to the visual field, acuity, reflexive, and ophthalmoscopic testing performed by the physician during C N assessment, the pupils are further examined for the following: • Size and equality. Pupil size is normally 2--4 mm or 4--8 mm in diameter in the light and dark, respectively. 1 3 The pupils should be
Table 4-13. Origin, Purpose, and Testing of the Cranial Nerves
N 00 00
Nerve/Origin
Purpose
How to Test
SignslSymproms of impairment
Olfactory (CN III cerebral c ortex
Sense of smell
Anosmia
Optic (CN IIllthalamlls
Central and peripheral vision
Have the patiem close one nostril, and ask the patient to sniff a mildsmelling substance and idemify it. Acuity: Have the patient cover one eye, and ask patient to read a visual chart. Fields: Have the patient cover one eye, and hold an object (e.g., pen cap) at arm's length from the patient in his or her peripheral field. Hold the parient's head steady. Slowly move the object centrally, and ask the patiem to state when he or she first sees the object. Repeat the process in all quadrants.
,.
� \?
'" m J: ,. z "
Blindness
g'" " '" � :I:
�
!j r
J! !i!,.
�
Upward, inward, Jnd mferomedial cyc movemcllf
eNs III , IV, and VI are tcsted rogcther.
Eyelid eleva non
Pupd reaction [Q light: Shme a flashlight inro one eye and observe bilateral pupil reaction.
Pupil (onstricflon Visual focuslllg
Gaze: Hold oblect (e.g., pcn) at arm's length from the patient, and hold the patient'S head steady, Ask the patient to follow the object with a full honzon· tal, vertical, and diagonal gaze.
Loss of ipsilateral pupillary light and accommodation refle"(es
Trochlear (eN N)/I/I/dbra/ll
Inferolateral e}'c movement and proprioception
See Oculomotor (eN II I ), above.
Diplopia Head nit to unaffected side Weakncss in depression of ipsilateral adducted eye
Trigeminal (eN V)/pOIIS
Sensation of face
Conduct rouch, pam, and temperature sensory test· ing over the patiem's face. Observe for deviation of Jaw.
Loss of facial sensation
Oculomotor (CN lII)bmd.
hrdm
Mastication
Ophthalmoplegia with eye dcviation downward and outward ProSIS
z '"
"
i§ Ipsilateral deviation of opened Jaw
5i �
-
r
:i '" '"
> �
Rowland (ed). Merrirr's Neurology ( I Orh cd). Philadelphia: Lippin can,
Williams & Wilkins, 2000.
vertebral dislocation or fracture; (2) hyperextension, causing disconti nuity of the anrerior spinal ligaments, disc herniation, and vertebral dislocation or fracture; and (3) axial compression, rotation, contu sion, laceration, or transection. Penetrating forces, such as gunshot or stab wounds, may be ( 1 ) low velocity, in which the spinal cord and protective structures are injured directly, or (2) high velocity, in which a concussive force injures the spinal cord, and the protective struc tures remain intact. Seco/ldary SCI is a complex series of pathologic vascular and innammatory responses to primary SCI, which further compound the original injury over the course of several days. A summary of secondary SCI incl udes ( 1 ) vasospasm of superficial spinal vessels, intra parenchymal hemmorhage and disruption of the blood-brain and spinal cord barrier, complicated by neurogenic shock and loss of autoregulation, and (2) increased calcium levels, which stimu late frce radical production to cause further ischemia, the release of catecholamines and opioids, and the accumulation of activated microglia and macrophages.29,3o The severity of SCI is most commonly classified by the American Spinal Injury Association (ASIA) Impairment Scale.31 This scale clas sifies SCI acccording to motor and sensory funcrion32: A
=
Complete-No sensory or motor function is preserved in 54-5.
B Incomplete-The preservation of sensory function without motor function below the neurological level and includes 54-5. =
310
ACUTE CARE HANDBOOK fOR PHYSICAL THERAI'ISTS
C Incomplete-The preservation of motor function below the neurological level. Muscle function of more than half of key mus cles below this level is less than 3/5 . =
D Incomplete-The preservation of motor function below the neurological level. Muscle function of at least half of key muscles below this level is less than 3/5. =
E
=
Normal-Motor and sensory function are intact.
The most common types of incomplete SCI syndromes are described in Table 4-1 9. The immediate physiologic effect of SCI is spinal shock; the triad of hypotension, bradycardia, and hypother mia is secondary to altered sympathetic reflex activity." It is beyond the scope of this book to discuss in detail the physiologic sequelae of SCI. However, other major physiologic effecrs of SCI include auto nomic dysreflexia; orthostatic hypotension; impaired respiratory function; bladder, bowel, and sexual dysfunction; malnutrition; stress ulcer; diabetes insipidus; syndrome of inappropriate secretion of antidiuretic hormone; edema; and increased risk of deep venous rhrombosis.
Clinical Tip If, during physical therapy intervention, a patient • wirh SCI develops signs and symptoms associared wirh autonomic dysreflexia, return the patient to a reclined sitting position, and notify the nurse or physician immediarely. Signs and symptoms of autonomic dysre flexia include headache, bradycardia, hypertension, and diaphoresis ." • During rhe early mobilization of the patient with SCI into the sitting position, consider using compression stock ings or Ace wraps on the legs and an abdominal binder to prevent or minimize orthostatic hypotension. The management of SCI rypically includes medical srabilization with ventilatory support (if indicated); immobilization of the spine with a collar, orthosis, traction, halo vest, or surgical repair; methyl predisolone or other pharmacologic therapies; treatment of secondary injures; pain management; and psychosocial support.
Table 4- 1 9. Spinal Cord Injury Syndromes Syndrome
Mechanism of Injury
Description
Central cord
Hyperextension injury, or as a result of tumor, rheuma toid arthritis, or syringo myelia
Lesion of the central cord exerts pressure on anterior horn cells. Typically presents with bilateral motor paralysis of upper extremities greater than lower extremities, variable sensory deficits, and possible boweUbladder dysfunction.
Anterior cord
Hyperflexion injury. acute large disc herniation, or as a result of anterior spinal artery injury
Lesion of the amerior cord damages the anterolateral spinothalamic tract, cortical spinal tract, and anterior horn (gray marrer). Typically presents with bilateral loss of pain and temperature sensacion and motor func tion with rerained light touch, proprioception, and vibracion sense.
Brown-Sequard
Penetrating spinal trauma (e.g., stab wound), epidu ral hematoma. spinal arte riovenous malformation, cervical spondylosis, or unilateral articular process fracrure or dislocation
Lesion of one-half of the spinal cord; rypically presents with conrralateral loss of pain and temperature sensa tion; ipsilateral loss of rouch, proprioception, and vibration sensej and ipsilateral motOr paresis or paraly sis.
Sources: Data from DA Buckley, MM Guanci. Spinal cord trauma. Nurs Clin North Am of Neurological and Neurosurgical Nursing (4[h cd). Philadelphia: Lippincorr,
1997.
1 999;34(3); and ]V Hickey (ed). The Clinical Pracrice
z
� 8 :;;
� -
90 mm Hg to aid in cerebral perfusion, or anti hypertensives
Osmorherapy
Osmotic diuretic to minimize cerebral edema
Mechanical ventilation
Normocapnia· to maximize cerebral oxygen delivery by limiting cerebral ischemia from the vaso constrictive effects of decreased Paco2
Cerebrospinal fluid drainage
Ventriculostomy to remove cerebrospinal fluid
Sedation/paral ysis
Barbiturates to decrease cerebral blood flow or ocher medication to decrease the stress of noxious activities
Positioning
Head of the bed at 30-45 degrees to increase cerebral venous drainage Promote neutral cervical spine and head position
Environment
Dim lights, decreased noise, frequent rest periods to decrease external stimulation
Seizure control
Prophylactic anticonvulsant medication Normothermia or induced hypothermia to 32-35°C (e.g., cooling blanket or decreased room temperature) to decrease cerebral metabolism
Temperature control
· Routine aggressive hyperventilation is no longer used for the control of elevated ICP. Hyperventilarion can contribute to secondary brain injury because of a rebound increase in cerebral blood flow and volume in response to a decreased cerebrospinal fluid pH. Source: Data from
2000;20, 18-27.
F Wong. Prevemion of secondary brain injury. Crit Care Nurs
Midlille shift. The lateral displacement of the falx cerebri secondary to a space-occupying lesion Space-occupying lesion. A mass lesion, such as a rumor or hematoma, that displaces brain parenchyma and may result in the elevation of ICP and shifting of the brain Another primary goal of the team is to prevent further neurologic impairment. The main components of management of the patient with neurologic dysfunction in the acute care setting include pharmacologic therapy, surgical procedures, and physical therapy intervention.
NERVOUS SYSTEM
325
Phamtacologic Therapy A multitude of pharmacologic agents can be prescribed for the patient with neurologic dysfunction. These include anticonvulsant agents (see Appendix Table IV.5), osmotic diuretics (see Appendix Table lV.26), adrenocorricosteroids (see Appendix Table lV. I ), skeletal muscle relax ants (see Appendix Table lV.28), and anti parkinsonian agents (see Appendix Table IV.9). Additional pharmacologic agents for medical needs include antibiotics (e.g., for infection or after neurosurgery), anti hypertensives, thrombolytics, anticoagulants, chemotherapy and radia tion for CNS neoplasm, stress u lcer prophylaxis (e.g., after SCI), pain control, and neuromuscular blockade.
Neurosurgical Procedures The most common surgical and nonsurgical neurologic procedures arc described below (see Ta ble 3 - 8 for a description of surgical spine procedures and Appendix I II-A for a description of ICP mon itoring devices). Allellryslll clippillg. The obliteration of an aneutysm with a surgical clip placed at the stem of the aneurysm. Bllrr hole. A small hole made in the skull with a drill for access to the brain for the placement of ICP monitoring systems, hematoma evacuation, or stereotactic procedures; a series of burr holes is made before a craniotomy. Cralliectomy. The removal of incised bone, usually for brain (bone Aapl tissue decompression; the bone may be permanently removed or placed in the bone bank Or temporarily placed in the subcutane ous tissue of the abdomen (to maintain blood supply). Crallioplasty. The reconstruction of the skull with a bone graft or acrylic material to restore the protective properties of the scalp and for cosmesis. Cralliotomy. An incision through the skull for access to the brain for extensive intracranial neurosurgery, such as aneurysm or AVM repair or tumor removal; craniotomy is named according to the area of the bone affecred (e.g., frontal, bifrontal, frontotemporal [ pterional], temporal, occipital).
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ACUTE CARE HANDBOOK FOR PHYSICAl THERAPISTS
Embolization. The use of arrerial catheterization (entrance usually at the femoral artery) to place a material, such as a detachable coil, balloon, or sponge, to clot off an AVM or aneurysm. Evacuation. The removal of an epidural, subdural, or intraparenchy mal hematoma via burr hole or cranioromy. Shunt placement. The insertion of a shunt system that connects the ventricular system with the right atrium (VA shunt) or peritoneal caviry (VP shunt) to allow the drainage of CSF when ICP rises. Stereotaxis. The use of a stereotactic frame (a frame that temporarily attaches ro the patient's head) in conjunction with head CT results to specifically localize a pretargeted site, as in tumor biopsy; a burr hole is then made for access to the brain.
Clinical Tip • The physical therapist should be aware of the location of a craniectomy, because the patient should nOt have direct pressure applied to thar area. Look for signs posted at the patient's bedside that communicate positioning restrictions. • Pay close attention to head of bed positioning restric rions for the patient who has recently had neurosurgery. Often, the head of bed is at 30 degrees, or it may be flat for an initial 24 hours and then gradually elevated \ 5-30 degrees per day depending on the location of surgery ( supratenrorial or infratentorial, respectively)."
Physical Therapy Interoention Goals The primary physical therapy goals in treating patients with primary neurologic pathology in the acute care setting include maximizing independence and promoting safety with gross functional activiry. Another main goal is to assist in the prevention of the secondary man ifestations of neurologic dysfunction and immobility, such as pressure sores, joinr contracture, and the deleterious effects of bed rest (see Appendix I-B).
NERVOUS SYSTEM
327
Basic Concepts for the Treatment of Patients with Neurologic Dysfunction • A basic understanding of neurologic pathophysiology is neces sary to create appropriate functional goals for the parient. The therapist must appreciate the difference berween reversible and irreversible and between nonprogressive and progressive disease states. • There are a number of narural changes of the nervous system with aging, such as decreased coordination, reflexes, balance, and visual acuity. Be sure to accommodate for these normal changes in the examination of and interaction with the elderly patient. • Take extra time to observe and assess the patient with neuro logic dysfunction, as changes in neurologic status are often very subtle.
• A basic knowledge of the factors rhat a ffect ICP and the ability to modify treatment techniques or conditions during physical ther apy intervention for the patient wirh head rrauma, afrer intracra nial surgery, or other pathology interfering with intracranial dynamics is necessary for patient safety. • Patient and family or caregiver education is an important com ponent of physical rherapy. Incorporate informarion about risk fac tor reduction (e.g., stroke prevention) and reinforce health care team recommendations (e.g., swallowing strategies per the speech language pathologist). • There are a variety of therapeutic techniques and motOr control theories for the treatment of rhe patient with neurologic dysfunc tion. Do not hesitate to experiment with or combine techniques from different schools of thought. • Be persistent with patients who do nOt readily respond to typi cal treatment techniques, because these patients most likely present with perceptual impairments superimposed on mOtor and sensory deficits.
Recognize that it is rarely possible to address all of the patient'S impairments at once; therefore, prioritize the plan of care accord ing to present physiologic status and future functional outcome.
•
328
AClJIT CARE HANDBOOK !-"OR PHYSICAL THERAPISTS
References 1 . Marieb EN (ed). Human Anaromy and Physiology. Redwood Ciry, CA: Benjamin-Cummings, 1 989; 1 72. 2. Moore KL. The Head. In KL Moore (cd), Clinically Orienred Anaromy (2nd ed). Balrimore: Williams & Wilkins, 1 985;794. 3. Wesrmoreland BF, Benarroch EE, Daube JR, et al. (eds). Medical Neuro sciences: An Approach to Anatomy, Pathology, and Physiology by Sys rems and Levels (3rd ed). New York: Little, Brown, 1986; 1 07. 4. Young PA, Young PH (eds). Basic Clinical Neuroanatomy. Baltimore: Williams & Wilkins, 1 997;251-258. 5 . Marieb EN (ed). Human Anaromy and Physiology. Redwood Ciry, CA: Benjamin-Cummings, 1 989;375. 6. Wilkinson JL (ed). Neuroanatomy for Medical Srudents (3rd ed). Oxford, UK: Burterwonh-Heinemann, 1 998j 1 89-200. 7. Goldberg S (cd). The Four-Minute Neurological Exam. Miami: Med Masrer, 1 992;20. 8. Lindsay KW, Bone I, Callander R (cd). Neurology and Neurosurgery Illustrated (2nd cd). Edinburgh, UK: Churchill Livingstone, 1 99 1 . 9. Plum F, Posner J (cds). The Diagnosis of Srupor and Coma (3rd cd). Philadelphia: FA Davis, 1 980; 1 . 10. Jennett B, Teasdale G (eds). Management of Head Injuries. Philadelphia: FA Davis, 1 9 8 1 ;77. 1 1 . Strub RL, Black FW (eds). Mental Status Examination in Neurology (2nd ed). Philadelphia: FA Davis, 1 985;9. 1 2. Love RJ, Webb WG (eds). Neurology for rhe Speech-Language Patholo gist (4th ed). Boston: Butterwonh-Heinemann, 2001 ;205. 1 3 . Specrer "'VI. The Pupils. In HK Walker, WD Hall, JW Hursr (cds), Clin ical Methods: T�e History, Physical, and Laboratory Examinations (3rd ed). Boston: Butterworth, 1 990;300. '14. Hickey ]V. The Clinical Pracrice of Neurological and Neurosurgical Nursing (4th ed). Philadelphia: Lippincott-Raven Publishers, 1 997. 1 5 . Kisner C, Colby LA. Therapeutic Exercise Foundations and Techniques (3rd ed). Philadelphia: FA Davis, 1 996;57. 16. Katz RT, Dewald J, Schmir BD. Spasticity. In RL Braddon (ed). Physical Medicine and Rehabilitarion (2nd ed). Philadelphia: Saunders, 2000;592. 17. Victor M, Ropper AH. Moror Paralysis. In M Victor, AH Ropper (cds), Adam and Victor's Principles of Neurology. New York: McGraw-Hili, 200 I ;50-58. 1 8 . O'Sullivan SB. Motor Control Assessment. In SB O'Sullivan, TJ Schmitz (eds). Physical Rehabilirarion: Assessment and Trearment (3rd cd). Phil adelphia: FA Davis, 1 998; 1 1 5. 1 9 . Charness A. Gathering the Pieces: Evaluation. In A Charness (ed), SrrokelHead Injury: A Guide ro Functional Outcomes in Physical Ther apy Management. Rockville, MD: Aspen, 1 986; 1 . 20. Swartz MH. The Nervous System. In M H Swaru, W Schmitt (cds), Textbook of Physical Diagnosis History and Examinarion (3rd ed). Phil adelphia: Saunders, 1 998;529.
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2 1 . Gelh OJ. The Neurologic Examination. In OJ Ge1b (ed), Introducrion ro Clinical Neurology (2nd cd). Boston: Butterworth-Heinemann, 2000; 43-90. 22. Bickley LS, Hockclman RA. The Nervous System. In LS Bickley, B Bares, RA Hoekclman (cds), Bate's Guide ro Physical Examinacion and Hismry Taking (7rh cd). PhIladelphIa: LIppincott, 1 999;585. 23. Shpritz OW. Nellrodiagnostic studies. Nurs Clin North Am 1 999;34: 593. 24. Kelley RE, Gregor)' T. CT versus MRI: Which is better for diagnosing stroke? Patient Care. 1 999;33: 175- 1 78, 1 8 1 - 1 82 . 25. Delapaz R , Chan S . Computed Tomography and Magnetic Resonance Imaging. In LP Rowland (ed), Merritt's Neurology ( 1 0th ed). Philadel phia: LIPPJJ1COtt, W""ams & Wilkins, 2000;55-63. 26. MeN:lIf ND. Traumatic brain injury. Nurs eli" North Am 1999;34:637-659. 27. Wong E Prevenrion of secondary brain injury. eric Care Nurs 2000;20: 1 8-27. 28. Zank BJ. Traumatic brain injury ourcome: concepts for emergency care. Ann Emerg Med 200 I ;37:31 8-332. 29. DlIhcndorf P. Spmal cord inJury pathophysiology. Crit Care Nurs Q 1 999;22:3 1-3.1. 30. MaUlcs A, Weinzierl MR, Donovan F, Noble LJ. Vascular evenrs after spinal cord II1IUf)': conrributlon to secondary pathogenesis. Phys Ther 2000;80:673-687. 3 1 . Mitcho K, Yanko JR. Acute care managemenr of spinal cord injuries. Cm Care Nurs Q 1 999;22:60-79. 32. Selzer ME, Tessler AR. Plasticiry and Regeneration in the Injured Spinal Cord. In EG Gonzalez, SJ Myers (cds), Downey and Darling's Physio logical Basis of Rehabilirarion Medicine (3rd ed). Boston: Butterworrh Heinemann, 200 I ;629-632. 33. Buckley DA, Gu:: mci MM. Spinal cord trauma. Nurs Clin North Am 1 999;34:661-687. 34. Bradle)' WG, Daroff RB, Fel1lchel GM, Marsden CD (eds). Pocket Com panIon ro Neurology in Clinical Practice (3rd ed). Boston: Burterworrh Heinemann, 2000. 3.\. Ingall TJ. Preventing ischemic Stroke. Postgrad Med 2000 ; 1 07:34-50. 36. Meschia JE Managemenr of acute ischemic stroke. Posrgrad Med 2000;1 07:85-93. 37. Blank .. Keyes M. Thrombolytic therapy for patients with acute stroke In rhe ED setting. J Emerg Nurs 2000;26:24-30. 38. Hock NH. Brain attack: rhe stroke continuum. Nurs Clin North Am 1999;34:689-724. 39. Fieml1llllg KD, Brown RD. Cerebral infarction and transient ischemic attacks. Postgrad Med 2000; 1 07:55-83. 40. Mower-Wade D, Cavanaugh MC, Bush D. Protecting a patienr with ruptured cerebral aneurysm. Nursing 100 1 ;3 1 :51-57. 4 I . Drury IJ, Gclb OJ. Seizures. In OJ Gelb (cd), Introduction to Clinical Neurology (2nd cd). Boston: Butterworth-Heinemann, 2000; 1 2 9- 1 5 1 . �
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42. Aminoff MJ. Nervous System. In LM Tierney, SJ McPhee, MA Papadakis (eds), Current Medical Diagnosis and Treatment 2001 (40th ed). New York: Lange Medical Books/McGraw-Hili, 200 I ;979-980, 983-986. 43. Cox MM, Kaplan D. Uncovering the Cause of Syncope. Patient Care 2000;34:39-48, 59. 44. Fuller KS. Degenerative Diseases of the Ceorral Nervous Sysrem. in CC Goodman, WG Boissonnaulr (cds). Pathology: Implications for rhe Physical Therapist. Philadelphia: Saunders, ·1 998;723. 45. Worsham TL. Easing the course of Guillain-Barre syndrome. RN 2000;63:46-50. 46. King BS, Gupta R, Narayan RJ. The early assessmenr and intensive care unit management of parienrs with severe traumatic brain and spinal cord injuries. Surg elin North Am 2000;80:855-870.
5 Oncology Susan Polich
Introduction
Callcer is a term that applies to a group of diseases characterized by the abnormal growth of cells. The physical therapist requires an understanding of underlying cancer pathology, as well as the side cffects, considerations, and precautions related to cancer care to enhance clinical decision making to safely and effectively trear the patient with cancer. This knowledge will also assist the physical theta pist with the early detection of previously undiagnosed cancer. The objectives for this chapter are to provide the following: I. An understanding of the medical assessment and diagnosis of a patienr with cancer, including staging and classification 2. An understanding of the various medical and surgical methods of cancer management 3. A better understanding of a variery of the different body system cancers 4. Examination, evaluation, and intervention considerations for the physical therapist 331
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AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Definitions
The terms neoplasm, tumor, and cancer are currently used inter changeably. Neoplasm means "new growth" and applies to any abnormal mass of tissue which exceeds the growth of normal tissue, grows at the expense of itS host, and persists even after the stimulus to grow is removed. The term /1I1110r originally applied to the swelling caused by inf1�mmation but now refers only to a new growth. Cancer is the layperson's term for all malignant neoplasms.'''' Normal cells change in size, shape, and type, known collectively as dysplasia, if the proper stimulus is provided. Hyperplasia refers to an increase in cell number. Metaplasia is the change of one cell type to another. Hyperplasia and metaplasia can be reversible and normal or persistent and abnormaI.1,2,4 Neoplasms, or persistent, abnormal dysplastic cell growth, are classified by cell type, growth pattern, anatomic location, degree of dysplasia, tissue of origin, and their ability to spread or remain in the original location. Two general classifications for neoplasm are benign and malignant. Bellign tumors are usually considered harmless and slow growing and have cells that closely resemble normal cells of adjacent cissue. However, chese benign tumors may occasionally become large enough to encroach on surrounding tissues and impair their function. Malignant neoplasms, or malignant tumors, grow uncontrollably, invading normal tissues and causing destruction to surrounding tissues and organs. Malignant neoplasms may spread, or metastasize, to other areas of the body through the cardiovascular or lymphatic system. '-5 Tumors may also be classified as primary or secondary. Primary rumors are the original tumors in the original location. Secondary tumors are those metaStases that have moved from the primary site.4
Nomenclature
Benign and malignant tumors are named by their cell of origin (Table 5- J). Benign tumors are cusromarily named by attaching -oma to the cell of origin. Malignant tumors are usually named by adding carcinoma ro the cell of origin if they originate from epithe lium and sarcoma if they originate in mesenchymal tissuc.I-J Varia tions to this naming exist, such as melanoma and leukemia.
ONCOLOGY
333
Table 5-1. Cbssific3rion of Benign and Malignanr Tumors Tissue of Origin
Benign
Malignant
Surface epithelium
Papilloma
Carcinoma
Epithelial lining of gland or ducts
Adenoma
Adenocarcinoma
Epithelium
Connective tissue and muscle Fibrous tissue
Fibroma
Fibrosarcoma
Cartilage
Chondroma
Chondrosarcoma
Bone
Osteoma
Osteosarcoma
Smooth muscle
Leiomyoma
Leiomyosarcoma
Striated muscle
Rhabdomyoma
Rhabdomyosarcoma
Nerve tissue Glioma
Glial Meninges
Meningioma
Meningeal sarcoma
Retina
Retinoblasroma
Lymphoid tissue
Lymphoma! lymphosarcoma
Bone marrow White blood cells
Leukemias
Plasma cells
Multiple myeloma
Source: With permission from S Baird (ed). A Cancer Source Book for Nurses (6th cd).
Adama: American Cancer Society, 1991 ;28.
Etiology and Risk Factors
The causes, or etiologies, of neoplasm are often divided into two cate gories, external or environmental and generic. There are risk factOrs that are thought ro predispose a person ro cancer. Most cancers proba bly develop from a combination of facrors. The most common etiolo gies can be found in Table 5-2. Risk facrors can be found in Table 5-3.
Signs and Symptoms
Signs and symptOms of cancer are most often due to rhe tumor's growth and invasion of surrounding tissues. The American Cancer Society has the acronym CAUTI ON for several common signs of cance�:
334
ACUTE CARE HANDBOOK FOR PHYSICAl nI FRAI'IST')
Table 5-2. Cancer Etiologies Viruses Human papilloma virus Epstem-Barr virus Chemical agents Tar Soor Dyes Polycyclic hy drocarbons Nickel Arsenic Excessive ethanol ingestion Vinyl chloride Benzene Physical agents Ionizing radiation Ultraviolet light Asbestos Wood duse Drugs Some chemotherapeutic agents Hormones Estrogen Source: Adapted from LM Tierney, S1 McI>hee, �IA Papadakis (cds). Current �Icdl(;.ll Diagnosis and Treatment. Stamford, CT: Applcton & Lange.
1999.
• C; Change in bowel or bladder habits • A ; A sore that does nOt heal • U ; Unusual bleeding or discharge •
T; Thickening or lump in the breast or elsewhere
•
I ; Indigestion or difficulty in swallowing
• 0;
Obvious change in a wart or mole
• N; Nagging cough or hoarseness Additional signs and symptOms that may IIldicate cancer include fever, unexplained weight loss of more than 10 Ib, undue f,lIigue, unexplained pain, anorexia, anemia, and weakness.l
ONCOLOGY
335
Table 5-3. Risk Factors for Selected Cancer Sites Cancer Sire Lung
High-Risk Factors Heavy smoker, older than age 40 yrs Smoked one pack per day for 20 yrs Started smoking at age 15 or before Smoker working with or near asbestos
Breast
Lump in breast Nipple discharge History of breast cancer Filmily history of breast cancer Benign breast disease High-far diet Nulliparous or first child after age 30 yrs Early menarche or menopause
Colon/rectum
Hiscocy of rectal polyps or colonic adenomatosis Family histOry of rectal polyps Ulcerative colitis or Crohn's disease Obesity Increasing age
Uterine
Unusual vaginal blood or discharge History of menstrual irregularity Late menopause Nullipariry Infertility through anovulation Diabetes, hypertension, and obesity Age 50-64 yrs
Skin
Excessive exposure to the Slin Fair complexion that burns easily Presence of congenital moles or hisCOfY of dysplastic nevi or cutaneous melanoma Family history of melanoma
Oral
Heavy smoker and alcohol drinker Poor oral hygiene Long-term exposure to rhe sun, particularly to the lips
Ovary
Hiscocy of ovarian cancer among close relatives Nulliparity or delayed age at first pregnancy Age 50-59 yrs
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ACUTE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Table 5-3.
Continued
Cancer Sire Prosrare
High-Risk Factors Increasing age Occuparions relaring to the use of cadmium Family hisrory
Sromach
Hisrory of sromach cancer among close relarives Dier heavy in smoked, pickled,
or
salred foods
Source: Wirh permission from S Baird (ed). A Cancer Source Book for Nurses (6rh ed). Arbma: American Cancer Society, 1991 ;32.
Paraneoplastic syndromes are symptoms that cannot be related directly to the cancer's growth and invasion of tissues. They are thought to be due to abnormal hormonal secretions by the tumor. The syndromes are present in approximately 15% of persons diagnosed with cancer and often are the first sign of malignancy. Clinical find ings are similar to endocrinopathies (Cushing's syndrome, hypo glycemia), nerve and muscle syndromes (myasthenia), dermatologic disorders (dermatomyositis), vascular and hematologic disorders (venous thrombosis, anemia), and others,l.7
Diagnosis
After obtaining a medical history and performing a physical examina tion, the physician uses specific medical tests to diagnose cancer. These teStS may include medical imaging, blood tests for cancer mark ers, and several types of biopsy. Biopsy, or removal and examination of tissue, is the definitive test for cancer identification. Table 5-4 lists common medical tests used to diagnose cancer.
Staging and Grading
After the diagnosis of cancer is established, staging is performed to describe the location and size of the primary site of the rumor, the extent of lymph node involvement, and the presence or absence of metastasis. Staging helps to determine treatment options, predict life expectancy, and determine prognosis for complete resolurion.
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Table 5-4. Diagnostic Tests for Cancer Test
Description
Biopsy
Tissue is taken via incision, needle, aspirarion proce dures. A pathologist examines the tissue (Q identify the presence or absence of cancer cells; if cancer is presem, the rUlllor is determined to be benign or malignanr. The cell or tissue of origin, staging, and grading arc also performed.
Blood rests
Blood can be assessed for the presence or absence of rumor markers:
Marker
Cancer
Prostate surface amigen
Prostate disease
Carcinocmbryonic
Colon cancer
antigen Prostaric-acid
Prosrate cancer
phosphatase
Srool guaiac
Alpha-fcroprorein
Liver cell cancer
CAI2S
Ovarian cancer
CA19-9
Colon cancer
CAU-3
Stool guaiac
Detecrs small quantities of blood in srool.
Sigmoidoscopy
The sigmoid colon is examined with a sigmoidoscope.
Colonoscop}'
The upper porrion of the rectum is examined wirh a
Mammography
A radiographic method is used to look for a mass or
Radiography
X-ray is used ro detect a mass.
Magnetic resonance
These noninvasive imaging techniques are used to
colonoscope. calcification in breast tissue.
imaging and
assess lesions suspected of being cancerous.
computerized axial romography Bone scan
Radionuclide imaging used to detect rhe presence,
Pap smear
A type of biopsy in which cells from the cervix are
Sputum cytology
A sputum specimen is inspected for cancerous cells.
Bronchoscopy
A tissue or sputum sample can be taken by rigid or
amOunt of metastatic disease, or both in bones. removed and examined.
flexible bronchoscopy. CA
=
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ACUTE CARE HANDBOOK FOR PHYSICAL THERAPISTS
The mostly commonly used method to stage cancer is the TNM system. Tumors are classified according to the American Joint Com mittee on Cancer using this system based on the size of the primary tumor (T), presence or absence of tumor in local lymph nodes (N), and presence or absence of metastasis (M) (Table 5-5).' Grading reports the degree of dysplasia, or differentiation, from the original cell type. The higher the grade, the greater the differentiation, or appearance, from the original cell. In some cases, tumor cells may look so unlike any normal cell that no cell of origin can be determined. Higher degree of differentiation is linked to aggressive, fatal tU1110rs (Table 5-6).'
Management
Not all cancers are curable. Physicians may therefore foclls treatment on quality of life with palliative therapies rather than on curative therapies. Four major treatment options include: •
Surgical removal of the tumor
•
Radiation to destroy or shrink the tumor
•
Chemotherapy
• Biotherapy (including immunotherapy, hormonal therapy, bone marrow transplantation, and monoclonal antibodies)
Table 5-5. TNM System T: Primary rumor TX: Primary tumor cannot be assessed.
TO: No evidence of primary rumor. Tis: Carcinoma in situ (site of origin). Tt. TI, T3, T4: Progressive increase in
tlllllor
size and local involvcmcnr.
N: Regional lymph node involvemcnr NX: Nodes cannor be assessed. NO: No metastasis to local lymph nodes. N l , N2, N3: Progressive involvement of local lymph nodes. M: Distant metastasis MX: Presence of distam metastasis cannot be assessed. MO: No disrant metastasis. M1: Presence of distanr merastasis.
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Table 5-6. Grading of Neoplasms Grade I
Tumor cells closely resemble original tissue.
Grades II and III
Tumor cells arc inrermediate in appearance,
Grade IV
Tumor cells are so poorly differentiated (anaplas
moderately differentiated. tic) that the cell of origin is difficult or impos sible to determine.
Additional treatments may include physical therapy, nutritional sup port, acupuncture, chiropractic treatment, alternative medicine, and hospice care. Treatment protocols differ from physician to physician and from cancer to cancer. Standard treatment includes some combination of surgery, radiation, and chemotherapy.
Surgery Surgical intervention is determined by the size, location, and type of cancer, as well as the patient's age, general health, and functional sta tus. The following are the types of general surgical procedures for resecting or excising a neoplasm: • Exploratory surgery is the removal of regions of the tumor to explore for staging or discover the extent or invasion of the rumor. • Excisiolla/ surgery is the removal of cancerous cells and the sur rounding margin of normal tissue. Tissue cells are sent to pathol ogy to determine the type of cancer cell and to determine whether the entire growth was removed. • Debit/king is an incomplete resection used to reduce the size of a large tumor to make the patient more comfortable or prevent the tumor from impinging vital tissue. This surgery is usually used when the cancer is considered "incurable." • Mohs' surgery is a microscopically controlled surgery in which layers of the tumor are removed and inspected microscopically until all layers have been removed.s • Lymph node dissection involves rhe removal or resection of malignant lymph nodes to help control the spread of cancer.
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AClJrE CARE. HANDBOOK FOR PHYSICAl. TlI£RAI'ISTS
• Skin grafting may be indicated in large resections of tumors to replace areas of skin removed during resection of a neoplasm with donor skin (see Chaprer 7) . • Reconstructive surgery is the surgical repair of a region with a flap of skin, fascia, muscle, and vessels. It aids in a more cosmetic and funcrional resulr of surgical repair and prorects the underlying resected area.
Clinical Tip • Special care must be taken with skin grafts. Patients usually remain on bed resr to allow the graft to begin to adhere. (Lengrh of bed reSt is dependent on physician's protocol, ranging from 0 to 36 days.9-1l) During bed rest, therapeutic exercise may be performed with extremities not involving the skin graft sire. • Muscle contraction in newly constructed muscle flaps should be minimized or avoided.
Radiation High-ionizing radiation is used to destroy or prevent cancer cells from growing furrher, while minimizing the damage to surrounding healthy tissues. Radiation therapy reduces the size of a tumor to allow for resection surgically, to relieve compression on structures surrounding the tumor, and to relieve pain (by relieving compression on pain-sensi tive structures). Reducing the size of a tumor with radiation therapy may also help to reduce the need for a large resecrion, amputation, or complete mastectomy.7 Radiarion may be delivered via supervolrage radiotherapy (tele therapy) or by planting radioactive marerial near the rumor (seeding or brachytherapy). Radiation destroys cells in its path; therefore, spe cial consideration is given to irradiating as little normal tissue as pos sible. Teletherapy uses variolls methods, such as linear acceleration and modifying-beam wedges, to permit greater localization.' Seeding may destroy all surrounding tissues, including healthy tissue. Radio active seeds are implanted for several days, then removed.
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Common side effects of radiation therapy include skin reac tions, slow healing of wounds, limb edema, conrracrures, fibrosis, alopecia, neuropathy, headaches, cerebral edema, seizures, visual disturbances, bone marrow suppression, cough, pneumonitis, fibrosis, esophagitis, nausea, vomiting, diarrhea, cystitis, and U[I nary frequency.6·7
Clinical Tip • Physical therapy should be deferred while the person has implanted radioactive seeds. • Massage and heating modalities should be withheld for 1 year in an irradiated area. • Persons undergoing irradiation by beam (teletherapy) will have blue markings where the radiation is being deliv ered. Caution should be taken with the skin and underly ing tissues in that area, because it will be very fragile. Persons who have received the maximum allowable radia tion in an area will have that area outlined in black. Spe cial care should be taken with the skin and other tissues in that area, because it will be very fragile. • A patient may be prescribed antiemetics (see Appendix IV, Table TV-6) after radiation treatment to control nausea and vomiting. Notify the physician if antiemetic therapy is insufficient ro comrol the patient'S nausea or vomiting during physical therapy sessions.
Chemotherapy The overall purpose of chemotherapy is to treat or prevent meta sratic disease and reduce the size of the tumor for surgical resection or palliative care. Patients may receive single agents or a combina tion of agents. Chemotherapy can be performed preoperatively and postoperatively. Chemotherapy is usually delivered systemically, via intravenous or cenrral lines, bll[ may be directly injected in or near a tumor. Patients may receive a single or multiple rounds of chemo therapy over time to treat their cancer and to possibly minimize side effects. Side effects of chemotherapy include nausea, vomiting,
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ACtrrE CARE HANDBOOK FOR I'HYSICAL THERAI'ISTS
"cancer pain," and loss of hair and other fast-growing cells, includ ing platelets and red and white blood cells. Different types of chemotherapeutic agents have different mechanisms of action. Alkylating agents and nitrosoureas inhibit cell growth and divi sion by reacting with DNA. Antimetabolites prevent cell growth by com peting with metabolites in production of nucleic acid. Plant alkaloids prevent cellular reproduction by disrupting cell mitosis.12 Chemotherapeuric agents are listed in Appendix IV, Tables rV-IS.A-H.
Clinical Tip • Some chemotherapeuric agents are so toxic to humans that patients may have to remain in their rooms while the agents are being delivered to avoid risk to other patients and health care workers. Physical therapists should check with the patient'S physician if unsure. • Nausea and vomiting after chemotherapy vary on a patient-to-patient basis. The severity of these side effects may be due to the disease stage, chemotherapeutic dose, or number of rounds. Some side effects may be so severe as to limit physical therapy, whereas others can tolerate activity. Rehabilitation should be delayed or modified until the side effects from chemotherapy are minimized or alleviated. • Patients may be taking antiemetics, which help to control nausea and vomiting after chemotherapy. The physical thera pisr should alert the physician when nausea and vomiting limit the patient'S ability to participate in physical therapy so that the antiemetic regimen may be modified or enhanced. Antiemetics are listed in Appendix lV, Table lV-6. • Chemotherapy agents affect the patient's apperite and ability to consume and absorb nutrients. This decline in nutritional status can inhibit the patient's progression in strength and conditioning programs. Proper nutritional support should be provided and directed by a nutritionist. Consulting with the nutritionist may be beneficial when planning the appropriate activity level that is based on a patient's caloric intake. • Patients should be aware of the possible side effects and understand the need for modification or delay of rehabilitation effortS. Patients should be given emotional
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343
supporr and encouragement when rhey are unable to achieve the goals that they have initially set. Intervention may be coordinated around rhe patient's medication schedule. • Vital signs should always be monitored, especially when patients are taking the more toxic chemotherapy agents that affect the hearr, lungs, and central nervous system. • Platelet and red and white blood cell counts should be monitored with a patient on chemotherapy. The Bone Marrow Transplant section in Chapter 12 suggests thera pelitic activities with altered blood cell counts. • Patients receiving chemotherapy can become neutropenic. They can be at risk for infections and sepsis.' (A neutrophil is a type of leukocyte or white blood cell that is often the first immunologic cell at the site of infection; neutropenia is an abnormally low neutrophil count. Refer to Bone Marrow Transplantation in Chapter L2 for reference value of neurro penia.) Therefore, patients undergoing chemotherapy may be on neutropenic precautions, stich as being in isolation. Fol low the institution's guidelines for precautions when treating these patients to help reduce the risk of infections. Examples of these guidelines can be found in the Bone Marrow Trans plantation section of Chapter 12.
Biotherapy Hormonal therapy and immunotherapy also play an important role in managing cancer. Hormonal therapy includes medically or surgically eliminating the hormonal source of cancer (e.g., orchiectomy, oophorectomy, or adrenalectomy) or pharmacologically changing hormone levels.'·' Immunotherapy includes enhancing the patient'S immune system and changing the immune system's response to the cancer, most commonly with recombinant growth factors, such as interferon-alpha or interleukin. Hormonal therapy is most commonly used to treat breast and prostate cancer. Some breast tumor cells contain estrogen in their cytoplasm (estrogen-receptor positive). Use of antiestrogens, such as tamoxifen, may keep the tumor from enlarging or metastasizing.
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AClffE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Elimination of the source of androgens in prostate cancer via orchiec tomy may also reduce the cancer's spread. Colony-stimulating factors may be used to sustain the patient with low blood counts during cancer treatment. Colony-stimulating factors, such as erythropoietin, may be given to reduce anemia.7 MO/lOclona/ alltibodies are antibodies of a single type produced by a single line of B lymphocytes. The antibodies are produced specifically to attach themselves to specific types of tumor cells. These antibodies can be used alone to anack cancer cells or may have radioactive mate rial bound to them.
Cancers in the Body Systems
Cancers can invade or affect any organ or tissue in the body. The fol lowing is a description of various cancers in each body system.
Pulmonary Cancers
Cancer can affect any structure of the pulmonaty sysrem. The cOlTlmon types of lung cancer are squamous cell carcinoma, adenocarci1loma, small cell carcinoma, and large cell carcinoma.6.7 Symptoms associated with these include chronic cough, dyspnea, adventitious breath sounds (e.g., wheezing, crackles), chest pain, and hemoptysis.' Nonsurgical techniques, such as x-ray, computerized axial romography, and positron emission tomography, can be lIsed to stage lung cancer." Table 5-7 describes pulmonary cancer sites and
Table 5-7. Surgical lmerventions for Pulmonary Cancers Area Involved
Surgical Procedure
Pleura
Pleurecromy
Portion of pleura
Rib
Rib resection
Portion of rib
Trachea n.nd
Tracheal repair and
Trachea
bronchi
reconstcuction
Lung
Excision of
Sleeve resection
Portion of main stem bronchus
Pneumonectomy
Entire single lung
lobec(Qmy
Single oc mulriple lobes of the lung
Wedge cesection
\Vedge-shaped segmenr of lung
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345
surgical procedures used in their management. Recent surgical advances include the use of video-assisted, non-rib spreading lobec tOmy ro remove rumor and the lise of an intraoperative ultrasound probe to aid in tumor localization. 14•IS
Clinical Tip • Thoracic surgery may involve a large incision on the tho racic wall. Surgical incisions into the pleural space will cause deflation of the lung. Deep-breathing exercises, along with mucus clearance techniques with incisional splinting and range-of-motion exercises of [he upper extremity on the side of the incision, are important to prevent postoperative pulmo nary complications and restore shoulder and trunk mobility. • Patients may have chest rubes in place immediately afrer surgery (see Appendix III-A). • Oxygen supplementation may be required in post-tho racic surgical patients. Oxyhemoglobin saturation (Sao,) should be monitored to ensure adequate oxygenation, especially when increasing activity levels. • Caution must be taken when positioning patients after pneumonectomy. Placing patients with the existing lung in the dependent position may adversely affect ventilation, per fusion, and, ultimately, oxygenation. Positioning guidelines should be clarified with the surgeon, if not already stated.16
Musculoskeletal Cancers Tumors of bone are most commonly discovered after an injury or fracture or during a medical work-up for pain. Some tumors in the bone or muscle may arise from other primary sites. Common primary tumors that metastasize to bone include breast, lung, prostate, kidney, and thyroid tumors.17 Treatment of musculoskeletal tumors can include radiation, chemotherapy, amputation, arthroplasty (joint replacement), and reconstruction using an allograft (cadaver bone). Types of primary orthopedic cancers are described in Table 5-8. Although not all metastases to bone cause pathologic fractures, surgical intervention can be used for a patient with a bone metastasis because of the risk of pathologic fracture. These procedures may
346
AClJTE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Table 5-8. Orthopedic Cancers
Type of Tumor
Common Age Group
Osteosarcoma
Young children and young adults
Chondrosarcoma Fibrosarcoma Rhabdomyosarcoma (Ewing's sarcoma)
Adul" Adul" Children and adolescents
Common Site of Tumors Distal femur, proximal tibia Commonly metastasize to lung Pelvis or femur Femur or tibia Trunk. pelvis, and long bones
include the use of intramedullary rods, plates, and prosthetic devices (e.g., total joint arthroplasty) and are described in hapter 3 under Fracture Management, Appendix, and Total Joint Arthroplasty sec tions, respectively.
Clinical Tip • A patient with bone metastases must receive clearance from the physician before mobility, along with clarifying the patient's weight-bearing status. • Patients commonly experience fractures owing to meta static disease in the vertebrae, proximal humerus, and femur.'s Therefore, patients should be instructed in safety management to avoid falls or trauma to involved areas. • Check the weight-bearing status of patients after bone grafting, as weight bearing may be restricted.
Breast Cancer Breast cancer, although more prevalent in women, is also diagnosed in men to a lesser extent. It may be discovered during routine breast examinations or mammography. Common surgical procedures for the treatment of breast cancer are listed in Table 5-9.
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347
Table 5-9. Surgical Inrcrvcnrions for Breasr Cancer Surgical lnrcrvenrion
Tissues Involved
Radical l11
tion of dorsalis pedis or posterior tibialis pulses. The higher of the lower extremity pressures is rhen divided by the higher of rhe upper-extremity pres sures (e.g., an ankle pressure of
70 mm Hg and a brachial pressure of 140 mm
Hg will yield an AB) of 0.5). Normal ASI for foO[ arteries is 0.95-1.20. with indexes below 0.95 indicating arterial obstruction. Exercise testing
Exercise testing is performed to assess the nature of claudication by measuring ankle pressures and PVRs after exercise. A drop in ankle pressures can occur with arterial disease. This type of testing provides a controlled method to document onset. severity, and location of claudication. Screening for cardiorespiratory disease can also be performed, as patients with peripheral vascular disease often have concurrent cardiac or pulmonary disor ders (see Chapter I).
Computed tomography
(CT)
CT is used ro provide visualization of the arterial wall and its Structures. Indications for CT include diagnosis of abdominal aortic aneurysms and pOSt operative complications of graft infections, occlusions, hemorrhage, and abscess.
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Magnetic resonance imaging (MRI)
MRI has multiple uses in evaluating the vascular system and is now morc com monly used to visualize the arterial system than arteriograms. Specific uses for MRI include detection of deep venous thrombosis and evaluation of cerebral edema. Serial MRls can also be used to help detemline me optimal operative time for patients with cerebrovascular accidents by monitoring their progression.
Magnetic resonance angiography (MRA)
MRA uses blood as a physiologic contrast medium to examine the structure and location of major blood vessels and the flow of blood through these ves sels. The direction and rate of flow can also be quantified. MRA minimizes complications that may be associated with contrast medium injection.
Sources: Data from JM Black, E l\tatassarin-Jacobs (cds). Luckmann and Sorensen's Medical-Surgical Nursing: A PsychophYSiOlogic Approach (4th cd). Philadelphia: Saunders, 1993; P Lanzer,J Rosch (cds). Vascular Diagnostics: Noninvasive and Invasive Techniques, Peri-Interventional Evaluations. Berlin: Springer-Verlag, 1994; KL McCance,SE Huether (cds). Pathophysiology: The Biological Basis for Disease in Adults and Children (2nd ed). St. Louis: Mosby, 1994; JL Kee (cd). Laboratory and Diagnostic Tests with Nursing Impli cations (5th cd). Stamford: Appleton & Lange, 1999,606; VA Fahey (cd). Vascular Nursing (3rd ed). Philadelphia: Saunders, 1999j76, 86; and LM Malarkey, ME Morrow (cds). Nurses Manual of Laboratory Tests and Diagnostic Procedures (2nd ed). Philadelphia: Saun den. 2000;359.
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Acme CARE HANDBOOK FOR PHYSICAL THERAJlISTS
Frequent vital sign monitoring with pulse assessments.
• If a patient has been on heparin before angiography, the drug is not resumed for a minimum of 4 hours.s
The following are complications associated with angiography,·s.6: •
Allergic reactions to contrast dye
•
Thrombi formation
•
Vessel perforation with or without pseudoaneurysm formation
•
Hematoma formation
•
Hemorrhage
•
Infections at the injection site
•
Neurologic deficits from emboli dislodgment
•
Contrast-induced renal failure (refer
to
Chapter 9)
Hematologic Evaluation The medical work-up of the patient with a suspected hematologic abnormality emphasizes the patient history and laboratory studies, in addition to the patient's clinical presentation. History In addition to the general charr review (see Appendix I-A), the follow ing questions are especially relevant in the evaluation of the patient with a suspected hematologic disorder7-': •
What are the presenting symptoms?
• Was the onset of symptoms gradual, rapid, or associated with trauma or other disease? • Is the patient unable to complete daily activities secondary fatigue?
to
• Is there a patient or family history of anemia or other blood dis orders, cancer, hemorrhage, or systemic infection? •
Is there a history of blood transfusion?
VASCULAR SYSTEM AND HEMATOLOGY
377
• Is there a history of chemotherapy, radiation therapy, or other drug therapy? • Has there been an environmental or occupational exposure to toxins? •
Have there been night sweats, chills, or fever?
•
Is the patient easily bruised?
•
Is wound healing delayed?
• Is there excessive bleeding or menses? Other relevant data include rhe patient's diet (for the evaluation of vitamin- or mineral-deficiency anemia), history of weight loss (as a warning sign of cancer or altered metabolism), whether the patient abuses alcohol (a cause of anemia with chronic use), and race (some hematologic conditions have a higher incidence in certain races)_ Inspection During the hematologic evaluation, the patient is observed for the following7: •
General appearance (for lethargy, malaise, or apathy)
• Degree of pallor or flushing of the skin, mucous membranes, nail beds, and palmar creases
• Presence of petechiae (purplish, round, pinpoint, nonraised spotS caused by intradermal or subcuraneous hemorrhage)'o or ecchymosis (bruising) •
Respiratory rate
Palpation The examination performed by rhe physician includes palpation of lymph nodes, liver, and spleen as parr of a general physical examination. For specific complaints, the patient may receive more in-deprh examinarion of a body system. Table 6-6 summa rizes rhe abnormal hematologic findings by body system on physi cal examinarion. The physical rherapist may specifically examine the following :
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AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Table 6-6. Signs and Symproms of Hematologic Disorders by Body System Body System
Sign/Symptom
Associated Condition
Cardiac
Tachycardia Palpitations Murmur Angina. Dyspnea Orthopnea Back pain Bone pain Joint pain Sternal tenderness Headache
Anemia, hypovolemia Anemia, hypovolemia. Anemia, hypovolemia Anemia, hypovolemia Anemia, hypovolemia Anemia, hypovolemia Hemolysis Leukemia Hemophilia Leukemia, sickle-cell disease Severe anemia, polycythemia, metastatic tumor Severe anemia, polycythemia Severe anemia Vitamin BI1 anemia, malignancy Severe anemia, malignancy, infection Anemia, polycythemia Thrombocytopenia, anemia Iron-deficiency anemia Lymphoma, hemolysis, sickle-cell disease Hemolytic anemia
Respirarory Musculoskeletal
Nervous
Syncope Vertigo, tinnitus Paresthesia Confusion Visual Gastrointestinal, urinary, and reproductive
Visual disturbances Blindness Dysphagia Abdominal pain Spleno- or hepatomegaly Hematemesis, melena
Integumentary
Hematuria Menorrhagia Petechiae Ecchymosis Flushing Jaundice Pallor
Thrombocytopenia and clotting disorders Hemolysis and clotting disorders Iron-deficiency anemia Iron-deficiency anemia Hemolytic, pernicious anemia Iron-deficiency anemia Hemolytic anemia Conditions with low hemoglobin
Source: Data from JM Bbck, E Matassarin-Jacobs (eds). Medical-Surgical Nursing Clinical Management for Conrinuity of Care (5th cd). Philadelphia: Saunders, 1997.
VASCULAR SYSTEM AND HEMATOLOGY
379
• The presence, location, and severity of bone or joint pain using an appropriate pain scale (See Appendix V I.) • Joint range of motion and integrity, including the presence of effusion or bony abnormality • Presence, location, and intensity of parasthesia • Blood pressure and heart rate for signs of hypovolemia (See Pal pation in the Vascular Evaluation section for a description of viral sign changes with hypovolemia.) Laboratory Studies In addition to the history and physical examination, the clinical diagno sis of hematologic disorders is based primarily on laboratory studies. Complete Blood Cell COLlllt
The standard complete blood cell (CBC) count consists of a red blood cell (RBC) count, WBC count, WBC differential, hematocrit (Hct) measurement, hemoglobin (Hgb) measurement, and platelet (Pit) count. Table 6-7 summarizes the CBC. Figure 6-'1 illustrates a com mon method used by physicians to document portions of the CBC in daily progress notes. If a value is abnormal, it is usually circled within this "sawhorse" figure.
Clinical Tip • Hct is accurate in relation to fluid status; therefore, Hct may be falsely high if the patient is dehydrated and falsely low if the patient is fluid overloaded. • Hct is approximately three times the Hgb value. • A low Hct may cause the patient to experience weak ness, dyspnea, chills, or decreased activity tolerance, or it may exacerbate angina. • The term pancytopenia refers to a significant decrease in RBCs, all types of WBCs, and Pits.
Erythrocyte Indices
RBC, Hct, and Hgb values are used to calculate three erythrocyte indices: ( I ) mean corpuscular volume (MCV), (2) mean corpuscular Hgb, and (3) mean corpuscular Hgb concentration. At mOst institu-
Table 6-7. Complete Blood Cell Count: Values and Interpretation-
w 00 o
Test
Description
Value
Indication/Inrerpreration
Red blood cell (RBC)
Number of RBCs per �I
Female: 3.8-5.1 million/�I
To assess blood loss, anemia, polycythemia.
Male: 4.3-5.7 million/�I
Elevated RBC count may increase risk of
coum
of blood
venous stasis or thrombi formation. Increased: pol)'cythemia vera, dehydration, severe chronic obstructive pulmonary dis ease, acute poisoning. Decreased: anemia, leukemia, fluid overload, recent hemorrhage.
White blood cell (WBC) count
Number of WBCs per �I of blood
4.5-11.0xlOJ (4,500-11,000)
To assess the presence of infection, inflamma tion, allergens, bone marrow integrity. Monitors response to radiation or chemotherapy. Increased: leukemia, infection. tissue necrosis. Decreased: bone marrow suppression.
WBC differential
Proportion (%) of the different types of WBCs (out of 100 cells)
Neucrophils 54-62 % Lymphocytes 23-33% Monocytes 3-7% Eosinophils 1-3% Basophils 0-0.75%
To determine the presence of infectious states. Detect and classify leukemia.
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Hematocrit (Het)
Percentage of RBCs in whole blood
Female: 35-40%
To assess blood loss and fluid balance.
Male: 39-49%
Increased: Polycythemia, dehydration. Decreased: anemia1 acute blood loss,
Female: 12-16 gllOO ml
To assess anemia, blood loss, bone marrow
hemodilution. Hemoglobin (Hgb)
Amount of hemoglobin in 100 ml of blood
Male: 13.5-17.5
gllOO 1111
suppression. Increased: polycythemia, dehydration. Decreased: anemia, recent hemorrhage, fluid
Platelets (Pit)
Number of platelets in �I of blood
150-450
X
10'
150,000-450,000 �I
overload. To assess thrombocytopenia. Increased: polycythemia vera, splenectomy, malignancy. Decreased: anemia, hemolysis, DIC, ITP, viral infections, AlDS, splenomegaly, with radiation or chemotherapy.
·Lab values vary among laboratories. RBC, hemoglobin, and platelet values vary with age and gender. AIDS acquired immunodeficiency syndrome; DIC disseminated intravascular coaguloparhy; ITP idioparhic thrombocytopenic purpura. Sources: Adapted from RJ Etin. Laboratory Reference Inrervals and Values. In L Goldman, JC Bennett (cds), Cecil Textbook of Medi cine, Vol. 2 (21 Sf cd). Philadelphia: Saunders, 2000;2305; and E Marassarin-Jacobs. Assessment of Clienrs with Hemarologic Disorders. In JM Black, E Matassarin-Jacobs, M,edical-Surgical Nursing Clinical Management for Continuity of Care (5rh ed). Philadelphia: Saun ders, 1997;1465. =
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AClJTE CARE HANDBOOK FOR I)HVSICAL THERAPISTS
WBC Count
Hgb Hct
Pit Count
Figure 6-1. Illustration of portions of the complete blood cell count in short
hand format. (Hcl ::: hematocrit; Hgb
=
hemoglobin; Pit
=
platelet; \lIBe
=
white blood cell.)
tions, these indices are included in the CSc. Table 6-8 summari1.es these indices.
Erythrocyte Sedimelltatio/1 Rate The erythrocyte sedimentation rate, often referred to as the sed rate, is a measurement of how fast RSCs fall in a sample of anticoagulated blood. Normal values vary widely according to laboratory method. The normal value is 1-20 mm per hour for men and 1-15 mm per hour for women. The sedimentation rate is a nonspecific screening tool used to determine the presence or stage of inflammation, or the need for further medical testing, or it is used in correlation with the clinical course of such diseases as rheumatoid arthritis or temporal arteritis. II It may be elevated in systemic infection, collagen vascular disease, and human immunodeficiency virus. Erythrocyte sedimenta tion rate may be decreased in the presence of sickle-cell disease, poly cythemia, or liver disease or carcinoma.
Peripheral Blood Smear A blood sample may be examined microscopically for alterations in size and shape of the RSCs, WBCs, and Pits. RBCs are examined for size, shape, and Hgb distribution. WBCs are examined for proportion and the presence of immature cells. Finally, Pits are examined for number and shape." Peripheral blood smear results are correlated with the other laboratory tests to diagnose hematologic disease.
Coagulation Profile Coagulation tests assess the blood's ability to clot. The tests used to determine c10rting are prothrombin time (PT) and partial thrombo plastin time (PTT). An adjunct to the measurement of PT is the Inter national Normalized Ratio (INR). The INR was created to ensure reliable and consistent measurement of coagulation levels among all
Table 6-8. Erythrocyte Indices: V:t1ues and inrerpretation· Test
Description
Value
Interpretation
Mean corpuscular volume (MCV) (Het x 101RBC)
Mean size of a single RBC in a pi of blood
80-100 pgJ
Mean corpuscular hemoglobin (MCH) (Hgb x 101RBC)
Amount of Hgb in one RBC
26-34 pglcell
Increased by macrocytic, folic acid, or vitamin BI2 deficiency anemias; liver disease; and recent alcohol use. Decreased by microcytic, iron-deficiency, and hypochromic anemias; thalassemia; and lead pOisoning. Increased by macrocytic anemia. Decreased by microcytic anemia. Low mean corpuscular hemoglobin indicates Hgb deficiency. Increased by spherocytosis (small round RBC). Decreased by microcytic, hypochromic, and iron-deficiency anemias and thalassemia.
Mean corpuscular hemoglobin concentration (MCHC) (HgblHet x 100)
Proportion of eaeh RBC occupied by Hgb
3 1-37 gldl
Het hematocrit; Hgb hemoglobin; RBC red blood cell. "'Lab values vary among laboratories. Sources: Adapted from RJ Elin. LaboratOry Reference Intervals and Values. In L Goldman, JC Bennett (cds). Cecil Textbook of Medicine, Vol. 2 (21 st cd). Philadelphia: Saunders, 2000;2305j and E Matassarin-Jacobs. Assessment of Clients with Hemarologic Disorders. In JM Black. E Marassarin·Jacobs (eds),Medical-Surgical Nursing Clinical Management for Continuity of Care (5th cd). Philadelphia: Saun ders, 1997;1466. =
=
=
0 0
Rapid reversal of warfarin therapy. Albumin cells
� J: >z " =
lopathy. Factor Xl deficiency.
Albumin
>n
See Albumin, above.
"" J: m '" >�
"i
�
Cryoprecipitate
Factors VIII and XlII, von WiUe brand's factOr, and fibrinogen in plasma
Her = hematocrit, Hgb
=
Rcplacemenr of these factor deficiencies. Replacement of fibrinogen when an increase in volume would not be toler
Correction of these faeror or fibrinogen deficiencies. Cessation of bleeding in uremic patients.
ared with FFP. Bleeding associated with uremia.
hemoglobin.
Sources: Data from National Blood Resource Education Programs Transfusion Therapy Guidelines for Nurses. US Depanmem of Health and Human Services, National Institutes of Health, September 1990; and adapted from WH Churchill. Transfusion Therapy. New York: Sciemific American Medicine, 2001 ;4.
;; §
ollom)
I
+
_ blood viscosity
IJecf8ased ln1mascutar volume
+
IJecf8ased urine output (hypowlemla) Myogloblnll1a (muscle damage)
Increased peripheral resistance
+
IJecf8ased canliac output
+
Ilecreased 0, dotNery to vital orvans and tissues In the setting of decroased body temperature and Increased heart mt. The physiologic sequelae of major burn injury. (BUN blood urea nitrogen; Ct- chlorine; Hct hematocrit; K+ potassium; Na· sodium; 0, oxyge/l; RBC red blood cell; IVBC while blood cell.) (Mod ified from J Maruin. Therma/lnjuries. In VD Caradona. PD Hum, PJ Baslna gel Mason, et al. {eds}, Trauma Nursing from Resuscitation through Rehab ilitation [2nd ed]. Philadelphia: Saunders, 1994;740; and RH Demling, C LaLonde. Bum Trauma. New York: Thieme, 1989;99.) Figure 7-3.
=
=
=
=
=
=
=
=
BURNS AND WOUNDS
441
Table 7·2. Systemic Complications of Burn Injury Body System
Complications
Respiratory
Inhalation injury, restrictive pulmonar y pattern (which may OCCur with a burn on the trunk), atelectasis, pneumonia, microthrombi, and adult respiratory distress syndrome
Cardiovascular
Hypovolemiaihypotension, pulmonary hypertension, subendocardial ischemia, anemia, and disseminated intravascular coagulopathy
GastroinrestinaV genitourinary Renal
Stress ulceration, hemorrhage, ileus, ischemic co\iris, cholesrasis, liver failure, and urinary rract infection Edema, hemorrhage, acute tubular necrosis, acure renal failure
Source: Data from HA Linares. The Burn Problem: A Parhologist's Perspective. In DN Herdon (ed), Total Burn Care. London: Saunders, 1996.
summary of the most common complications of burns is listed In Table 7-2.
Types of 8ums Thermal Burns Thermal burns can be the result of conduction or convection, as in contact with a hot object, hot liquid, chemicals, flame, or steam. In order of frequency, the most common 'Ypes of thermal burns are scalds, flame burns, flash burns, and cOntact burns (Table 7-3)4 The severity of burn depends on the location of the burn, the temperature of the burn source, and the duration of contact.s Electrical Burns An electrical burn is caused by exposure to a low- or high-voltage current and results in superficial burns, as well as less-visible but massive damage of muscle, nerves, and bone. Tissue necrosis of these deeper structures occurs from the high heat intensity of the current and the electrical disruption of cell membranes.' Tissue damage occurs along the path of the current, with smaller distal areas of the body damaged most severely. This pattern of tissue
442
AClITE CARE HANDBOOK FOR PHYSICAL nIERAPISTS
Table 7-3. Thermal Burns: Types and Characteristics Burn Type
Description
Characterisrics
Scald burn
Spill of or immer
Often causes deep partial- or full
sion in a hot liquid, such as boiling water, grease, or tar
thickness burns. Exposure ro thicker liquids or immersion causes a deeper burn from increased contact time. Immersion burns commonly cover a larger total body surface area than do spills.
Flame burn
Flame exposure from fire or flammable liquids, or
Often causes superficial and deep partial-thickness burns. Associated with carbon monoxide poisoning.
ignition of ciorhing Flash burn
Explosion of flammable liquid, such as gasoline or propane
Often causes partial-thickness burns. Burns may be distribured over all exposed skin. Associated with upper airway thermal damage. Most common in the summer and associated with [he consumption of alcohol.
Contact burn
Exposure to hot objects, such as glass, plastic, mecal, or coal
Often causes deep partial- or full thickness burns. Associated with crushing injuries, such as moror vehicle accidents. Most common cause of serious burns in the elderly.
Sources: Data from GO Warden, OM Heimbach. Burns. In SI Schwartz (ed), Principles of Surgery, Vol. 1 (7th ed). New York : McGraw-Hili, 1999; and RF Edlich, JC Moghra der. Thermal Burns. In P Rosen (cd), Emergency Medicine Concepts and Clinical Prac tice, Vol. I (4th cd). Sr. Louis: Mosby, 1998.
damage accounts for the high incidence of amputation associated with electrical injury.'" The severity of an electrical burn depends primarily on the duration of contact with the source, as well as the voltage of the source, rhe type and parhway of currenr, and the amperage and resistance through the body tissues·
BURNS AND WOUNDS
443
Electrical burns are characterized by deep entrance and exit wounds or arc wounds. The entrance wound is usually an obvious necrotic and depressed area, whereas the exit wound varies in pre sentation. The exit wOllnd can be a single wound or multiple wounds located where the patient was grounded during injury.7 An arc wOllnd is caused by the passage of current directly between joints in close opposition. For example, if the elbow is fully flexed and an electrical current passes through the arm, burns may be located at the volar aspect of the wrist, antecubital space, and axilla.' Complications specific to electrical injury include the following"s: • Cardiovascular: Cardiac arrest (ventricular fibrillation for elec tric current or asystolic for lightning), arrhythmia (usually sinus tachycardia or nonspecific ST changes) secondary to alterations in electrical conductivity of the heart, myocardial contusion or infarc tion, or heart wall or papillary muscle rupture • Neurologic: Headache, seizure, brief loss of consciousness or coma, peripheral nerve injury (resulting from ischemia), spinal cord paralysis (from demyelination), herniated nucleus pulposus, or decreased attention and concentration • Orthopedic: Dislocations or fractures secondary to sustained muscular contraction or from a fall during the burn injury
• Other: Visceral perforation or necrosis, cataracts, tympanic membrane rupture, anxiety, depression, or post-traumatic stress disorder
Lightning Lightning, considered a form of very high electrical current, causes injury via four mechanisms9:
1.
Direct strike, in which the person is the grounding site
2. Flash discharge, in which an object deviates the course of the lightning current before striking the person 3. Ground current, in which lightning strikes the ground and a person within the grounding area creates a pathway for the current
444
AClITE CARE HANDBOOK FOR PHYSICAL n-iERAI}ISTS
4. Shock wave, in which lightning travels outside the person and static electricity vaporizes moisture in the skin Chemical Burns Chemical burns can be the result of reduction, oxidation, corrosion, or desecration of body tissue with or without an associated thermal injury.lo The severity of burn depends on the type of chemical and its concentra tion, duration of contact, and mechanism of action. Unlike thermal burns, chemical burns significantly alter systemic tissue pH and metabo lism. These changes can cause serious pulmonary complications (e. g. , air way obstruction from bronchospasm, edema, or epithelial sloughing) and metabolic complications (e. g., liver necrosis or renal dysfunction from prolonged chemical exposure). Ultraviolet and Ionizing Radiation Burns A sunbun1 is a superficial partial-thickness burn from the overexposure of the skin to UV radjation. Ionizing radiation burns with or without thermal burn occur when electromagnetic or particulate radiation energy is transferred [Q body tissues, resulting in the formation of chemical free radicals. I I Ionizing radiation burns usually occur in laboratory or indus trial settings. The severity of the ionizing radiation burn depends on the dose, dose ra te, and the tissue sensitivity of exposed cells. Often referred to as acute radiation syndrome, complications of ionizing radiation burns include the following I L • Gastrointestinal: Cramps, nausea, vomiting, diarrhea, and bowel i chemia • Hematologic: Pancytopenia (decreased number of red blood cells, white blood cells, and platelets), granulocytopenia (decreased number of granular leukocytes), thrombocytopenia (decreased number of platelets), and hemorrhage
•
Vascular: Endothelium destruction
Burn Assessment and Acute Care Management of Burn lnjury
Classificatioll of a Bllm The extent and depth of the burn determine its severity and dictate acute care treatment.
BURNS AND WOUNDS
445
Assessing the Extent of a Burn The accurate assessment of the extent of a burn is necessary to calculate fluid volume therapy and is a predictor of morbidity.12 The extent of a burn injury is referred to as total body sur(ace area (TBSA) and can be calculated by the rule of nines or the Lund and Browder formula.
Rille o( Nilles The rule of nines divides the body into sections, seven of which are assigned 9% of TBSA. The anterior and posterior trunk are each assigned 18%, and the genitalia is assigned 1% (Figure 7-4). This
,
\
Front 18% ! \ Back 18% :
18%
18%
The rule of nines method of assessing the extent of a bum injury. (\vith permission (rom M \Valsh led!, Nurse Practitioners: Clinical Skills and Pro(essionallssltes. Oxford, UK: Butterworth-Heinemann, 1999;32.)
Figure 7-4.
446
AClJT£ CARE HANDBOOK FOR PHYSICAL THERAPISTS
formula is quick and easy to use, especially when a rapid initial esti mation of TBSA is needed in the field or the emergency room. To use the rule of nines, the area of burn is filled in on the diagram, and the percentages are added for a TBSA. Modifications can be made if an entire body section is not burned. For example, if only the posterior left arm is burned, the TBSA is 4.5%.
Lund and Browder Formllia Table 7-4 describes the Lund and Browder formula. The body is divided into 19 sections, and each is assigned a different percent age of TBSA. These percentages vary with age from infant to adult to accommodate for relative changes in TBSA with normal growth. The Lund and Browder formula is a more accurate predictor of TBSA than the rule of nines because of the inclusion of a greater number of body divisions along with the adjustments for age and normal growth.
Estimating the Extent of Irreglliarly Shaped Bllms It is important to note that using the rule of nines or the Lund and Browder formula may not be accurate for irregularly shaped burns. To estimate TBSA with irregularly shaped burns, the patient's palm is used to measure the shape of the burn. The palm represents 1 % TBSA.'2 Assessing the Depth of a Burn The depth of a burn can be described as superficial, moderate partial thickness, deep partial thickness, or full thickness (Figure 7-5). Each type has its own appearance, sensation, healing time, and level of pain, as described in Table 7-5. The assessment of burn depth allows an estimation of the proper type of burn care or surgery and the expected functional outcome and cosmesis." Although clinical observation remains the standard for burn depth estimation, there is often error or underestimation. Experimental technologies for morc precise burn depth estimation include cell biopsy, vital dyes, fluores cein fluorometry, laser Doppler flowmetry, thermography, ultra sound, and nuclear magnetic rcsonance.4 A burn wound is considered to be a dynamic wound in that it can normally change in appearance, especially during the first few days. A partial-thickness burn can convert to a full-thickness burn from infec tion, inadequate fluid resuscitation, or excessive pressure from dress ings or spiints,I4
BURNS AND WOUNDS
447
Table 7-4. Lund and Browder Method of Assessing the Extenr of Burns'" '1-4
5-9
10-14
15
Birth
yrs
yrs
yrs
yrs
Head
19
17
13
1I
9
Neck
2
2
2
2
2
2
Anrerior trunk
13
13
13
13
'13
13
Posterior trunk
13
13
13
13
13
13
Adult
Head and trunk 7
Left butrock
2.5
2.5
2.5
2.5
2.5
2.5
Right burrock
2.5
2.5
2.5
2.5
2.5
2.5
Left upper arm
4
4
4
4
4
4
Right upper arm
4
4
4
4
4
4
Left forearm
3
3
3
3
3
3
Right forearm
3
3
3
3
3
3
Lef, hand
2.5
2.5
2.5
2.5
2.5
2.5
Righ' hand
2.5
2.5
2.5
2.5
2.5
2.5
Left thigh
5.5
6.5
8
8.5
9
9.5
Right thigh
5.5
6.5
8
8.5
9
9.5
5
5
5.5
6
6.5
7
5
5
5.5
6
6.5
7
Lef, foo,
3.5
3.5
3.5
3.5
3.5
3.5
Right foot
3.5
3.5
3.5
3.5
3.5
3.5
Genitalia Upper extremity
Lower extremity
Left lower leg Right lower leg
·Values represent percentage of rotaI body surface area. Sources: Adapted from WF McManus, BA Pmin. Thermal Injuries. In DV Feliciano, EE Moore, KL Matrox (cds), Trauma. Stamford, Cf: Appleton & Lange, 1996;941; and CC Lund, NC Browder. The estimation of areas of bums. Surg Gynecol Obstct 1944;79:355.
Act/Ie Care Ma/wgemenl of Bt/rn In;t/ry This scction discusses the admission guidelines and resuscitative and reparative phases of burn carc. Admission Guidelines In addition to the burn's extent and depth, the presence of associated pulmonary, orthopedic, or visual injuries determines what level of
Partial
/'
Hair shaft
Epldennl.-{ qL,.,.....;r..,...
Denn�-{
eous ����o�o�o�auou� ·���& SU.. bcut� ��o...o�V..:b�X,...,!-v
tissue
Muscle
r ' �; � �\.l"o'!.uO&OOOq,
Sweat gland
dODo
0
Bone (a) Superflcial bum
Deep
partiel{
thickness bum
(e)
Deep partial thickness bum
(b) Partial thickness bum
() C; ;;: () > " m ;:
Z 0 � 0 0 r. � 0
"
�
J: -
Z o
� )1 o " Of i r
:ji '" 5: �
�
BURNS AND WOUNDS
459
mal' be present postoperatively. The therapist should become familiar with the surgeon's procedures and proto cols and alter positioning, range of motion (ROM), thera peutic exercise, and functional mobility accordingly. •
The therapist should check with the physician to deter
mine whether the graft crosses a joint and how close the graft borders the joint. •
If possible, observe the graft during dressing changes to get
a visual understanding of the exact location of the graft. • The autograft site or donor site is often more painful than the burn itself. •
Donor sites are oriented longitudinally and are com
monly located on the thigh, low back, or outer arm and may be reharvested in approximately 2 weeks.
Nonsurgical Procedures Burn cleansing and debridement may be performed many times a day to minimize infection and promote tissue healing. These procedures, as described in Wound Cleansing and Debridement, may be per formed by a physician, nurse, or physical therapist depending on the hospital's or burn unit's protocol. Table 7-8 lists the topical agents used specifically for the treatment of burns.
Physical Therapy Examination in Burn Care Physical therapy intervention for the patient with a burn Injury
IS
often initiated within 48 hours of hospital admission.
History In addition to the general chart review (see Appendix I-A), the follow ing information is especially relevant in the evaluarion, treatment planning, and understanding of the physiological status of a patient with a burn. •
How, when, where, and why did the burn occur?
•
Did the patient get thrown (as in an explosion) or fall during the
burn incident?
Table 7-8. Topical Agents Commonly Used for the Treatment of Burns
...
:;
Agent
Description
Advantages (A)lDisadvantages (0)
Silver sulfadiazine (Silvadene)
Antimicrobial cream for use with parcial- and full-thickness burns Applied with or without a dressing
A D
Mafenide acetate (Sulfamylon)
Actico3r (Wcstaim Biomedical, Exeter, NH) silver dressing
Silver nitrate
Antimicrobial cream for use with partial- and full-thickness burns Applied with a dressing Can be applied directly to burns of the car Three-ply gauze dressing consisting of an absorbent rayon/polyester core and upper and lower layers of silver-coated, high densiry polyethylene mesh For use with partial- and full-thickness burns and meshed autografts Ami-microbial solucion or cream applied as a wct dressing Used for partial- and full-thickness burns
Painless application, wide spectrum coverage Poor eschar peneuation, may cause macer ation and epithelial retardation, associated with leukopenia, costly A Penetrates eschar well, effective against =
=
=
Pseudomonas
D
Painful, nor for use on large areas, can cause acidemia A Abrasion resistant, nonadherent, flexible D Cannot visualize the wound =
=
=
§
&? '" m :t > Z c
8
"
o '" � :t
�
�
r
J! ;:: > A D
Wide spectrum coverage, painless Poor eschar penetration, frequent reapplication, stains the patient's skin and the environment, can cause electrolyte imbalance =
=
�
�
Bacitracin
Nystatin
Collagenase
Ointment effecrJve against gram-positive organisms Used fot superficial and partial-thickness burns as well as dOllor sites Cream or powder mixed to solution and applied with a dressing Used on superficial, partial- or full-thickness burns Enzyme derived from Clostridium histolyticwn Digests collagen in necrotic tissue Applied as an ointment with a dressing over it Used on deep partial- and full-thickness burns
A:;::: Minimal systemic absorption, painless, can be used on the face o ::: Nephrotoxic in large amounts, no eschar penetration, frequenr reapplication A ::: Effective fungicide against Candida, painless D ::: Frequent reapplication, no eschar penetration
A:;::: Penerrates eschar, does nor affect healthy tissue D::: Painful, no antimicrobial properties
Sources: Data from ET Kaye, KM Kaye. Topical antibacterial agents. Infect Dis Clin North Am 1995;9:547-559; JO Kucan, EC Smoot. Five percent mafenide acetate solution in the treatmem of thermal injuries. J Burn Care Rehabil 1993;14: 158-163; RS Ward, JR Saffle. Topical agents in burn and wound care. Phys Ther 1995j75:526-538; and HS Soroff, DH Sasvary. Collagenase oinonent and polymyxin B sulfare!bac itracin versus silver sulfadiazine cream in partial thickness burns: a pilot srudy. J Burn Care Rehabil 1994;15:13-17.
� 0;:
�
,.
§ " o
2
� ... '" ....
462
ACUTE CARE HANDBOOK FOR PHYSICAL THERAPISTS
•
Is there an inhalation injury or CO poisoning?
•
\Vhat are the secondary injuries?
•
What is the extent, depth, and location of the burn?
•
Does the patient have a condition(s) that might impait tissue
healing? •
Was the burn self-inflicted? If so, is there a history of self-injury
or suicide? •
Were friends or family members also injured?
Inspection alld Palpatioll To assist with treatment planning, pertinent dara that can be gath ered from the direct observation of a patient or palpation include the following: •
Level of consciousness
•
Presence of agitation, pain, and srress
• Location of the burn or graft, including the proximity of the burn to a joint •
Presence and location of dressings, splints, or pressure garments
•
Presence of lines, tubes, or other equipment
•
Presence and location of edema
•
Posture
•
Position of head, trunk, and extremities
•
Heart rate and blood pressure, respiratory rate and partern, and
oxygen sarurarion
Clinical Tip •
Avoid popping any blisters on the skin during palpation
or with manual contacts. • Do not place a blood pressure cuff over a burn or graft sire or area of edema.
BURNS AND WOUNDS
463
Pain Assessment Good pain control increases patient participation and activity tol erance; therefore, pain assessment occurs daily. For the conscious patient, the physical therapist should nOte the presence, quality, and grade of (I) resting pain; (2) pain with passive, active assisted, or active ROM; (3) pain at the burn site versus the donor site; and
(4)
pain before, during, and after physical ther
apy intervention.
Clinical Tip •
The physical therapist should become familiar with the
patient's pain medication schedule and arrange for physi cal therapy treatment when pain medication is most effec tive and when the patient is as comfortable as possible. •
Restlessness and vital sign monitoring (i.e., heart rate,
blood pressure, and respiratory rate increases) may be the best indicators of pain in sedated or unconscious patients who cannot verbally report pain.
Rfl1lge of Motio1l ROM of the involved joints typically requires goniometric measure ments. Exact goniometric values can be difficult to measure when the patient has bulky dressings; therefore, some estimation of ROM may be necessary. The uninvolved joints or extremities can be grossly addressed actively or passively, depending on the patient's level of alertness or level of participation.
Clinical Tip •
The physical therapist should be aware of the presence
of tendon damage before ROM assessment. ROM should not be performed on joints with exposed tendons. • The physical therapist should always have a good view of the extremity during ROM exercise to observe for banding or areas of tissue that appear white when stretched.
464
AClffE CARE HANDBOOK FOR PHYSICAL THERAPISTS
• The physical therapist should pay attention to the posi tion of adjacent joints when measuring ROM to account
for any length-tension deficits of healing skin or muscle. •
The physical therapist should appreciate the fact that a
major burn injury is usually characterized by burns of dif ferent depths and types. The physical therapist must be aware of the various qualities of combination burns when performing ROM or functional activities. •
ROM may be decreased by the presence of bulky dress
ings. Try to evaluate or perform ROM when the dressings are temporarily off or down.
Strength Strength on an uninvolved extremity is usually assessed grossly by function. More formal strength testing, such as resisted isometrics or manual muscle testing, is indicated on either the involved or unin volved side if there is severe edema, electrical injury, or secondary injury.30
Ftmctional Mobility Functional mobility may be limited depending on state of illness, medication, need for warm or sterile environment, and pain. The physical therapist should evaluate functional mobility, as much as possible, according to medical stability and precautions.
Clinical Tip The skin at grafted areas, as well as at donor site areas, is more fragile than normal skin. These areas should be ace wrapped figure-of-eight style to provide support against venous pooling when the patient is being mobilized Ollt of bed. Without this extra support, the skin is more prone to shearing at graft sites and subcutaneous bleeding.
BURNS AND WOUNDS
465
Physical Therapy Intervention Goals The primary goal of physical therapy intervention for patients with burn injuries is to maximize function with ROM exercise, stretching, positioning, strengthening, and functional activity. General consider ations for physical therapy intervention by impairment are listed in Table 7-9.
Basic COllcepts for the Treat",ellt of Patie"ts with Btlnt Injtlry •
The patienr with a burn can have multisystem organ involve
ment and a hypermetabolic state; thus, the physical thetapist needs to be aware of cardiac, respirarory, and neurologic status, as well as musculoskeletal and integumentary issues. •
Fluid resuscitation and pain medications can affect blood pres
sure, heart rate, and respiratory pattern and rate, as well as level of alertness. MonitOring these variables will help the therapist gauge pain level and determine how aggressively to intervene during the therapy session. •
The parienr with a burn requires more frequent re-evaluations
than other patient populations, because the patienr's starus and therapy intervention can change dramatically as swelling decreases, wound debridement and closure occur, hemodynamic and respira tory stabiliry are achieved, and mental status improves. The goals and plan of care need to be updated throughout the patient'S admission, as activity may be temporarily restricted after surgical grafting. •
A porrio,1(s) of the plan of care is often held for
4-7
days after
skin grafting to prevent shearing forces on the new graft. Shearing can disrupt the circulation to the graft and cause it to fail. Grafts over joints or areas with bony prominences, as well as grafts on the posterior surfaces of the body, are at greater risk for shear injury. •
Time frames for physical therapy goals vary widely and are
based heavily on TBSA, the location of the burn, age, and pre existing functional starus.
466
AClffE CARE HANDBOOK FOR PHYSICAL THERAJ'ISTS
Table 7-9. Physical Therapy Considerations for Burn Injury Variable
Considerations
Decreased ROM and alrered limb position
Mosr patients have full ROM on admission bur may readily begin to exhibit decreased ROM due [0 edema, pain, and immobilization.
Decreased strength
Decreased endurance and funcrional mobiliry
Risk for scar development
Patienrlfamily knowledge deficit related to burns and physical therapy ROlvl
=
ROM of uninvolved joints may also be decreased secondary to the process of rota I body edema. Devices rhar can help to properly position rhe patient include splints, abduction pillows, arm boards attached to the bcd, pillows, and blanket rolls. Incorporate the use of a modality (i.e., pulley) in[O stretching activities. Active exercise is preferred unless sedation or rhe patient's level of consciousness prevents it. Active exercise (i.e., proprioceptive neuromuscular facilitation) provides muscle conditioning, increased blood flow, edema reduction, and contraction prevention and helps reduce hyperrrophic scar formation. Prolonged bed rest (sec Appendix I-B) may be necessar)' for weeks or months secondary to medical status or to accommodate grafting, especially of the lower extremity. The use of a tilt table for progressive mobilization from bed rest rna)' be necessary if orthostatic hypotension or decreased lower-extremity ROM exists. Assistive devices may need adaptations (i.e., platform walker) CO accommodate for ROM and strength deficits or weight-bearing restrictions. Consider the use of active exercise (i.e., resroraror) thar addresses cardiovascular conditioning while increasing ROM and strength. Healing of deeper burns and skin-grafted burns is accompanied by some scarring. H)'perrrophic scarring can be decreased by the use of pressure garments, silicone gel sheets, ROM, and massage. Parienrlfamily educarion emphasizes information about the role of physical therapy, exercise, positioning, pain and edema control, and skin care. Education before discharge is of the utmost importance to improve compliance, confidence, and independence.
range of mOlion.
BURN\ AND WOUNDS
•
467
The joints at risk for contracture formation need to be properly
positioned (Table 7-10). The positioning needs to be consistently carried out by all caregivers and documented in the patient care plan. Proper positioning will decrease edema and prevent contrac ture formation to facilitate the best recovery. •
The rherapist should be creative in treating rhe patient with a
burn. Traditional exercise works well; however, incorporating rec reational acriviries and other modalities into the plan of care can ofren increase functional gains and compliance with less pain. •
The plan of care must be comprehensive and address all areas
with burns. For example, burns of the face, neck, and trunk require intervention specifically directed to these areas. •
The therapist should attend bedside rounds with the burn team
to be Involved in multidisciplinary planning and to inform the
team of therapy progression.
Table 7-10. Preferred 11osltlOm. for P:mcnts with Burn Injury Area of Bod)
I)osition
Neck Shoulder
ExtenSion, no rotation Abduction (90 degrees) External rotation Horizontal flexion ( 10 degrees) Extension With supll13tion Neutral or slight extension Functional position (dorsal burn) Finger and thumb extension (palmar burn) Straight postural alignment Neutral extension/flexion Neutral rotation Slight abduction Extension Neutral or slight dorsiflexion No IIlversion Neutral roe extcnsion/flexion
Elbow and forearm \Vrist Hand Trunk �hp
Knee Ankle
Sourcc: With permission from RS Ward. Splinting. Orthotics. :lOd Prosthetics In the Management of Burns. In M�l Lusardi, CC Nielson (eds), Orthotics and Prosthetics in Rehahllitatlon. Boston: BUiterworth-Heinemann. 2000;315.
468
AClITE CARE HANDBOOK FOR I'HYSICAL TIIERAI'ISTS
Pathophysiology of Wounds The different types of wounds, their etiologies, and the facrors that contribute ro or delay wound healing are discussed in the following sections.
Types of Wounds Trauma Wounds A trauma
wound
is an injury caused by an external force, such as a
laceration from broken glass, a cut from a knife, or penetration from a buller. Surgical Wounds A surgical wound is the residual skin defect after a surgical incision. For individuals who do not have problems healing, these wounds are sutured or stapled, and they heal without special intervention. As the benefits of moist wound healing become more widely accepted, gels and ointments are now more frequently applied to surgical wounds. W hen complications, such as infection, arterial insufficiency, diabetes, or venous insufficiency, are present, surgical wound healing can be delayed and tequire additional care. Arterial Insufficiency Wounds A wound resulting from arterial insufficiency occurs secondary to ischemia of the tissue, frequenrly caused by atherosclerosis, which can cause irreversible damage. Arterial insufficiency wounds, described in Table
7-11, occur most
commonly in the distal lower leg because of a
lack of collateral circulation ro this area. Clinically, arterial ulcers fre quently occur in the pretibial areas and the dorsum of the toes and feet, but they may be present proximally if the ulcers were initially caused by trauma.31-JJ They show minimal signs of healing and are often gangrenous. Venous Insufficiency Wounds A wound resulting from venous insufficiency is caused by the improper functioning of the venous system that leads to poor nutri tion to the tissues. This lack of nutrition causes tissue damage, and ultimately tissue death, resulting in ulceration. The exact mechanism by which this occurs has not been established, although some theories do exist. One theory is that venous hypertension is transmitted ro the
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Table 7-11. Clinical Indicators of Vascular Insufficiency Wounds and Diabctic Ulcers Wound Etiology
Clinical Indicators
Arterial insuffi· ciency
Intermirtent claudication Extreme pain, decreased with rest and increased with clevmion Decreased or absent pedal pulses Decreased temperaturc of the distal limb Distinct, well-defined wound edges Deep wound bed Cyanosis Localized limb pain, decreased with elevation and increased with srandmg Pam with deep pressure or palpation Pedal pulses present Increased temperature around the wound Indistinct, Irregular edges Edema Mound the wound Shallow wound bed Suhsranrial drainage Painless ulcer; however, general lower-limb pain is present Absent pedal pulses Decreased temperature in the distal limb Deep wound bed frequently located at pressure points (e.g., metatarsal heads) Shin}- skill on dlsral limb
Venous Insufficiency
Diabetic ulcer
Sources: D.t l .1 Kloth. KH M111er (cds), Wound Ilc:lhnlt: Alternatives in Management. Ph1ladelphia: FA Da\·is, 1995; RG Sihbald. An approach to leg and foot ulcers:
a bnef overv1ew. Ostomy
Wound MJnage 1998;44:29; RG �Ibbald. Venou!t leg ulcers. Osromy Wound Manage 1998;44:53; P Lamg. DI;Ibcrif.: foot ukcrs. AmJ Surg 1994;167(IA):31; and ML Levin,
LW O'Ncill, JII Bowker (cd�). Thc D1abetlc Foot (5th cd). St. loUIS: Mosby, 1993.
superficial veins in the subcutaneous tissue and [he overlying skin, which causes widening of the capillary pores.J4.JS Clinically, this would result In the first sign of venous disease, which is the presence of a dilated long saphenous vein on the medial aspect of the calf. This dIlation allows the escape of large macromolecules, including fibrino gen, into the interstitial space. This results in the development of edema toward the end of the day because of the pooling of fluid in the
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AClITE CARE HANDBOOK FOR PHYSICAL TIIE.RAI'ISTS
dermis. In long-standing venous disease, fibrin accumulates in the der mis, creating a fibrin cuff that presents as hard, non pitting edema, and the surface skin is rigid and fixed. The theory states that this fibrin cuff forms a mechanical barrier to the transfer of oxygen and other nutrients, which progressively leads to cellular dysfunction, cell death and skin ulceration.H." Another hypothesis is called the white blood cell-trappil1g hypothe sis. This theory states that transient elevations in venous pressures decrease capillary blood flow, resulting in trapping of white blood cells at the capillary level, which in turn plugs capillary loops, resulting in areas of localized ischemia." These white blood cells may also become activated at this level, causing the release of various proteolytic enzymes, superoxide free radicals, and chemotactic substances, which can also lead to direct tissue damage, death, and ulceration." Venous stasis ulcers, described in Table 7-11, are frequently present on the medial malleolus, where the long saphenous vein is most superficial and has its greatest curvature. Venous ulcers may be present on the foot or above the midcalf but are more likely to have another primary etiology, such as trauma or infection. The leakage of red blood cells over time results in the deposit of hemosiderin and stimulated melanin, causing the characteristic hyperpigmenration around the medial ankle. Other characteristics include a thin skin sur face with a loss of hair follicles and sweat glands]4 Pressure Wounds A pressure ulcer, sometimes referred to as a decubitus ulcer, is caused by ischemia that develops as a result of sustained pressure in excess of cap illary pressure on the tissue. The pressure usually originates from pro longed weight bearing on a bony prominence, causing internal ischemia at the point of contact. This initial point of pressure is where tissue death first occurs. The tissue continues ro necrotize externally until a wound is created at the skin surface. By this time, there is significant internal tissue damage. Superficial tissue ulceration can be caused by the effect of mechanical forces acting on localized areas of skin and subcutaneous tissue, whether the forces are of low intensity over long periods or are higher forces applied intennittently.J6. J7 The relation ships between the amount of force applied, the duration of force, and the direction of the force contribute to the occurrence and severity of a pressure ulcer. Not only can direct pressure create tissue ischemia, but friction and shearing forces contribute as weI1.36-J8.40.41 Refer to Wound Staging and Classification for the pressure ulcer grading system.
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471
All bed- or chair-bound individuals or any individuals who have an impaired abiliry ro reposition themselves or weighr shifr are ar risk of developing pressure ulcers. Common pressure ulcer sires include rhe back of rhe head, rhe scapular spines, spinous processes, elbows, sacrum, and heels when a parient is laying in supine. While side-lying, a patient may experience increased pressure at the ear, acromion pro cess, rib, iliac crest, greater trochanter, medial and lateral condyles, and rhe malleoli.38•39 A person's body weighr also plays a role in pres sure ulcer development. A person who is tOO thin has more prominent bony prominences, whereas a person who is overweight has increased pressure on weight-bearing surfaces.J9-41 Neuropathic or Neurotropic Ulcers A /lel/ropathic or /lel/rotropic ulcer (see Table 7-11) is a secondary complication that occurs from a triad of disorders, including periph eral vascular disease, peripheral neuropathy, and infection.42 Neuro pathic ulcers are most commonly associated with diabetes. The development of ulcers and foot injuries are the leading causes of lower-extremity amputation in people with diabetes·3 Additionally, there is an increased incidence of atherosclerosis, which appears ear lier and progresses more rapidly than in patients without diabetes. However, many people with diaberes who develop foot ulcers have palpable pulses and adequate peripheral blood flow." Individuals with diabetes may also have changes in the mechanical properties of the skin. Insulin is essential for fibroblastic and collagen synthesis. A lack of insulin in type 1 diabetes can lead ro diminished collagen synthesis that can cause stiffness and poor tensile strength of tissue, both of which increase the suscepribility of wound develop ment and decrease healing potential.'s The peripheral and central nervous systems can be adversely affected in diabetes. Peripheral neuropathy is common, and sensation and strength can be impaired. Diminished light rouch, propriocep· tion, and temperarure and pain perception decrease the ability of the person with diabetes ro identify areas that are being subjecred ro trauma, shearing forces, excessive pressure, and warm temperatures, all of which can cause ulcers.'.....• Structural deformities can occur as the result of the neuropathies that may be present secondary to diabetes. Any structural deformi ties, sllch as "hammer toes" or excessive pronation or supination, can create pressure points that lead to ischemia and a subsequent ulcer.46-48
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AClfTE CARE. HANDBOOK FOR PHYSICAL THERAPISTS
Excessive plantar callus formation may form at the sites of increased pressure and in itself can increase the pressure to the affected area.44 The minor repetitive ischemia that occurs every time the person bears weight on the pressure points in the tissue underlying the callus can eventually cause the tissue to fail, and ulceration occurs.48 Peripheral mOtor neuropathy contributes to the development of an equinus contracture at the ankle as stronger plantarflexors overcome the weaker dorsiAexors. Weakness of the small intrinsic muscles of the foot causes clawing of the toes. These foot deformities lead to increased weight distribution through the forefoot and increased pres sure under the metatarsal heads. The abnormal mechanical forces and intermittent forces can stimulate callus formation.44 A neuropathy of the autonomic nervous system is present in the majority of individuals with diabetes and neuropathic ulcers. The autonomic nervous system regulates skin perspiration and blood flow to the microvascular system. Lack of sweat production contrib utes to the development of a callus. Altered cross-linkage between collagen and keratin results in predisposal to hyperkeratosis and cal lus formation. Beneath the callus, a cavity often forms as a response to the increased pressure and shear forces and fills with serous Auid, causing a seroma. If the deep skin fissure comes in contact with an underlying seroma, it can become colonized with bacteria and result in ulcer formation.44 The immune system is also affected by elevated glucose levels and their resultant problems. Edematous tissues and decreased vascularity, which contribute to lack of blood Aow, decrease the body's abiliry to fight infection because of its inability to deliver oxygen, nutrients, and antibiotics to the area.49-SS Although neuropathic ulcers are most often associated with diabe tes, they may also occur in individuals with spina bifida, neurologic diseases, muscular degenerative disease, alcoholism, and tertiary syphilis because of similar risk factors in these populations.JJ
Process of Wound Healing
Epidermal wounds heal by re-epithelialization. Within 24-48 hours after an injury, new epithelial cells proliferate and mature. Deeper wounds, which involve the dermal tissues and even muscle, go through a rather complex and lengthy sequence of (1) an inAammatory response, (2) a fibroplastic phase, and (3) a remodeling phasc.J7-41
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In the inflammatory phase, platelets aggregate and clOts form. leu kocytes, followed by macrophages, migrate to the area, and phagocy tosis begins. Macrophages also provide amino acids and sugars that are needed for wound repair. In preparing the wound for healing, they stimulate the fibroplastic phase. During the fibroplastic phase, granu lation begins. Granulation is indicative of capillary buds, growing into the wound bed. Concurrently, fibrocytes and other undifferenti ated cells multiply and migrate to the area. These cells network to transform into fibroblasts, which begin to secrete strands of collagen, forming immature pink scar tissue. In the remodeling phase, scar tis sue marures. New scar rissue is characterized by its pink color, as ir is composed of white collagen fibers and a large number of capillaries. The amount of time the entire healing process takes depends on the size and type of wound. It may take from 3 days to several months or more for complete closure to occur,49-5S
Factors That Can Delay Wound Healing
In addition to the problems indigenous to the wound, many other fac tors can delay wound healing. Age, lifestyle, nutrition, cognitive and self-care ability, vascular Status, medical complications, and medica tions all can affect wound healing. These factors may also be risk fac tors for the development of new wounds. These factors should therefore be included in the physical therapy assessment and consid ered when determining goals, intervenrions, and time frames.
Age Skin, just like other tissues and organs, changes with age. Decreased cellular activity during the aging process leads to decreased collagen production thar results in less collagen organization in older individu als. Reduced collagen organization resulrs in decreased tensile strength of the skin that could result in greater damage after trauma in the older individual. Other examples of skin changes with age include delayed wound contraction, decreased epithelialization, and delayed cellular migration and proliferation.56 Other comorbidities that delay wound healing, such as diabetes, peripheral neuropathies, and related vascular problems, occur with greater frequency in older individuals.
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AClJTE CARE HANDBOOK fOR PHYSICAL TIIERAIIISTS
Lifestyle A patient's lifestyle can have a great impact on the prognosis for healing, decision-making regarding wound management, and pre ventive care. For example, occupations and hobbies that require prolonged standing may predispose some individuals to varicosities and other venous problems. Individuals exposed to traumatic situa tions, such as construction workers, are also more likely to reinjure healing wounds. Behaviors such as cigarette smoking can impede wound healing significantly because of the vasoconstriction that nic otine creates.
Nutrition Good nutrition is necessary for the growth and maintenance of all body tissues. Macronutrients, such as carbohydrates, fats, and pro teins, and micronutrients, such as vitamins, are necessary for cell metabolism, division, and growth. Therefore, nutrition is closely linked with all phases of healing.57 Generally, poor nutrition decreases the body's ability to heal. Additionally, patients with burns, wounds, or infection who are adequately nourished at the time of their injury or the development of their wound may also develop pro tein-calorie malnutrition. There are major metabolic abnormalities associated with injury that can deplete nutritional stOres, including increased output of catabolic hormones, decreased Output of anabolic hormones, a marked increase in metabolic rate, a sustained increase in body tem perature, marked increase in glucose demands, rapid skeletal muscle breakdown with amino acids used as an energy source, lack of ketO sis, and unresponsiveness to catabolism to nutrient intake.-�8 Pro tein-calorie malnutrition can delay wound healing and cause seriou health consequences in patients with wounds, especially if infection exists. Poor nutritional status, whether due to decreased intake or the stress response, can set off a series of metabolic events leading to weight loss, deterioration of lean tissues, increased risk of infection, edema, and breathing difficulty.58 These events can lead to severe debilitation and even death. Inade quate diet control in patients with diabetes exacerbates all symptOms of diabetes, including impaired circulation, sensation, altered meta bolic processes, and delayed healing. A nutritional assessment by a
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registered dietitian, nutritional supplements, and careful monitoring of the patient's nurritional status and weight are important compo nents of a comprehensive assessment and treatment program for the patient with a wound. In addition, therapists should work with other health care profes sionals to curb the systemic stress response. Removing necrotic tis sues, treating infections, and ensuring adequate hydration and blood fluid volumes will help to limit physiologic stressors. Premed ication before painful procedures and avoiding extreme tempera tures help minimize stress. Exercise serves as an anabolic stimulus for muscle, facilitating a reduction of the catabolic state,58
Cognition and Self-Care Ability There is an increased risk of infection and other wound healing complications if neither the patient nor the caregiver has the cogni tive or physical ability, or both, to properly care for a wound, including wound cleansing and dressing removal and application. The patient'S or caregiver'S abilities, or both, have a great influence in the choice of dressing(s) and on discharge planning. Certain dressings require more skill than others to maintain. Complex wound care can justify a stay at a rehabilitation hospital or skilled nursing facility.
Vascular Statlls Any compromised vascular status may contribute to the development of delayed wound healing owing to a lack of oxygenation and nutri tion to the tissues.
Medical Status Generally, compromised health causes a decrease in the body's ability to progress through the healing process. Pre-existing infection or a history of cancer, chemotherapy, radiation, acquired immunodefi ciency syndrome, or other immunodeficiency disorders can decrease the patient's ability to heal. Congestive heart failure, hypertension, and renal dysfunction can also slow wound healing.
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ACUTE CARE HANDBOOK FOR I)HYSICAL THERAPISTS
Medications Steroids, antihistamines, nonsteroidal anti-inflammatory drugs, and oral contraceptives may delay wound healing, as can chemotherapy and radiation. These medications can decrease the tensile strength of connective tissue, reduce blood supply, inhibit collagen synthesis, and increase the susceptibility to infection.59 Amicoagulants thin the blood and decrease its ability to clot; therefore, the healthcare pro vider needs to diligently monitor bleeding during dressing removal and consider debridement methods that will not cause bleeding.
Chronic Wounds In healthy individuals without comorbidities, an acute wound should heal within 3 to 6 weeks, with remodeling occurring over the next year. If a wound remains in one of the stages of healing without pro gression, it becomes a chronic wound.6o Chronic wounds are defined as wounds that have "failed to proceed through an orderly and timely process to produce anaromic and functional integrity, or proceeded through the repair process without establishing a sustained anatomic and functional result. "61 The acute care therapist should be inclined to search for underlying causes of delayed wound healing, especially when treating a wound thar has not healed in more than 6 weeks.
Wound Assessment and Acute Care Management of Wounds
The evaluation of a patient with a skin wound includes a general his tory (identification of factors that can delay healing), performing a physical examination (sensation, pain, ROM, strength, and func tional mobiliry) and a specific examination of the wound itself.
History In addition to the general chart and medical history review (see Appendix I-A), the following information is especially relevant for determining wound etiology and risk facrors, an intervention plan, and potential outcomes:
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Wound History •
How and when did the wound occur?
• What interventions have been administered to the wound thus far? What were the results? • Is there a previous history of wounds? If so, what were the etiol ogy, intervention, and time frame of healing?
Risk Factors •
Howald is the patient?
•
Is the patient cognitively intact?
• Where and for how long is the patient weight bearing on areas involving the wound site? • What is the patient's occupation or hobby? How many hours does the patient spend on his or her feet per day? What positions and postures is the patient in throughout the day? •
Does the patient smoke?
• Is the patient generally well nourished? Is the patient taking any supplements? •
Has the patient experienced any weight loss or gain lately?
•
If the patient has diabetes, is it well controlled?
• Does the patient have an immunodeficiency disorder or a medi cal condition that increases his or her risk of infection? • Does the patient have a medical condition that causes altered sensation? • What medications (including anticoagulants) is the patient tak ing? What are their effects on wound healing?
Psychosocial Factors • Does the patient have a good support system, including physical assistance if necessary? •
What are the patient's mobility needs?
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A review of vascular tests, radiographic studies, and tissue biopsy results also lends valuable information about the integrity of the vas cular and orthopedic systems and the presence of underlying disease.
Physical Exami1!atio1! Sensation Sensation to light touch, pressure, pinprick, temperature, and kines thesia or proprioception, or both, should be examined. Impaired or absent sensation should be addressed through instruction in the appropriate prevention techniques, as well as modifications to shoes, weight bearing, and water temperatures in bathing. Pain The evaluation of pain in the patient with a wound is not unlike the evaluation of pain in any other type of patient. The therapist should evaluate the nature of the pain, including the location, onset, severity (using a pain-rating scale), duration, aggravating and alleviating fac rors, and the impact on activities of daily living. Understanding the nature of the pain will ultimately allow the physical therapist to pro vide or recommend the appropriate intervention. The pain experience associated with wounds has been described as having one of three components: a noncyclic acute component, a cyclic acute component, or a chronic wound pain component. Noncyclic acute Waf/lid paill is a single episode of acute pain that is likely ro occur with treatment (e.g., the pain felt during sharp debride ment). Cyclic acute pain is wound pain that recurs throughout the day because of repeated treatments. For example, a patient may expe rience pain after several days of dressing changes, which creates repet itive trauma to the wound. Chronic wound pain is persistent wound pain that occurs intrinsically, nOt as a result of external intervention (e.g., a patient with a neuropathic ulcer who has a constant, dull ache in the foot).62 Range of Motion Specific measurement of ROM may not be necessary in a patient with a wound. However, specific goniometric measurements are necessary if a wound crosses a joint line, if edema is present at a joint, or if decreased ROM inhibits mobility. Decreased ROM that inhibits mobility or increases weight bearing, pressure, or both may conrrib-
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ute to wound development. Therefore, passive or active ROM exer cise, or both, should be included, as necessary, in the treatment plan. Strength Strength should be evaluated for its impact on the patient's function. The therapist should keep in mind that the patient may have different functional demands secondary to the wound. For example, a patient who needs ro be non weight bearing because of a wound on his or her foot requires sufficient upper-extremity strength to use an assistive device to maintain this precaution while ambulating. if the parienr does not have adequate upper-extremity strength, then he or she may be nonambularory until the weight-bearing Status is changed. Functional Mobility Functional mobility, including bed mobility, transfers, and ambula tion or wheelchair mobility, should be evaluated. The therapist should consider that the patient's function may have changed simply because of the consequences of the pre ence of the wound. For example, bal ance may be compromised if the patienr requires orthotics or shoe modifications because of a wound. Gait training with an assistive device is often necessary to decrease weight bearing on an affected lower extremity. Edema and Circulation The evaluation of edema is important because it is frequently an indi caror of an underlying pathology. Edema is also a critical factor in lowering tissue perfusion of oxygen and increasing susceptibility to infection. In fact, edema is almost equivalent ro insufficient blood supply in lowering the oxygen tension in the area of the wound. Ulti mately, the presence of edema must be addressed to heal the wound. Refer ro Table I -6 for the scale on how to grade (pitting) edema. Therapists should also consider that lymphedema and chronic wounds can be closely linked. Lymphedema is commonly associated in individuals who aTC status post mastectomy; however, it can also occur after other surgeries and traumas. Cellulitis may actually be due ro a compromised lymphatic system that creates small, weeping blis ters from fluids being literally pushed through the skin. In addition, edema secondary ro chronic venous insufficiency frequently also has a lymphatic component. Circulation can be grossly evaluated and monitored by examining skin temperature, distal limb color, and the presence of pulses. Refer
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AClJTE CARE HANDBOOK FOR PHYSICAL THERAI'ISTS
to Vascular Evaluation in Chapter 6 for more information on the evaluation of circulation. The therapist should notify the physician when any significant changes in these indicators occur. The therapist should be aware of any arterial compromise before using compression bandages.
WOUlld Illspectioll alld EvalllatiOlI Wound observation and measurements create an objective record of the baseline status of a wound and can help to determine the best intervention to facilitate wound healing. Location, Orientation, Size, and Depth The location of the wound should be documented in relation to ana tOmic landmarks. The orientation of a wound; its length, width, and depth; or the presence of undermining (tumleling); or a combination of these factors, are essential measurements in wound assessment. The orientation of the wound must be determined to ensure consis tent length and width measurements, parricularly for a wound with an abstract shape or odd location. One method of determining wound orientation is to consider the wound in terms of a clock, with the patient'S head being 12 o'clock. When documenting length, the measurement is the distance of the wound (measured in the direction from the patient'S head to toe), and the width is the horizontal measurement. There are a variety of meth ods for measuring wounds. Tape measurements are one method, bur a calibrated grid on an acetate sheet on which the wound can be traced is optimal, especially for irregularly shaped wounds. Polaroid photo graphs on grid film can also be used.
Clinical Tip •
When taking a photOgraph of a wound, create or fol
low a consistent procedure for taking photOgraphs, as changes in the distance of the camera from the wound, as well as the position of the patient, can affect the appear ance of the wound. •
Also, to ensure consistency and accuracy in wound
assessments, a consistent unit of measure should be llsed among all individuals measuring the wound. Cen-
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timeters, rather than inches, are morc universally used in the literature. •
Multiple wounds can be documented relative to each
other if the wounds are numbered-for example, "Wound #1: left lower extremity,
3 cm proximal to the medial mal
leolus. Wound #2: 2 cm proximal to wound #1."
Depth can be measured by placing a sterile cotton-tip applicator perpendicular to the wound bed. The applicator is then grasped or marked at the point of the wound edge and measured. If the wound has varying depths, this measurement is repeated.
Undermining or tunneling describes a continuation of the wound underneath intact skin and is evaluated by taking a sterile cotton-tip applicator and placing it underneath the skin parallel to the wound bed and grasping or marking the applicator at the point of the wound edge. Assessment of undermining should be done all around the wound. It can be documented using the clock orientation (e.g., "Undermining: 2 cm at 12 o'clock, 5 cm at 4 o'clock"). Color The color of the wound should be documented, because it is an indi cator of the general condition and vascularity of the wound. Pink indicates recently epithelized tissue. Red indicates healing, possibly granulating tissue. Yellow indicates infection, necrotic material being sloughed off from the wound, or both. Black indicates eschar. It is important to doclimem the percentage of each color in the wound bed-an increase in the amount of pink and red tissue, a decrease in the amoum of yellow and black tissue, or both are indica tive of progress. An increase in the amount of black (necrotic) ti sue is indicative of regression. Drainage Wound drainage is described by type, amount, and odor. Drainage can be (I) serous (clear, thin; this drainage may be present in a healthy, healing wound), (2) serosanguineous (containing blood; this drainage may also be present in a healthy, healing wound), (3) puru lent (thick, white, pus-like; this drainage may be indicative of infec tion and should be cultured), or (4) green (usually indicative of Pseudomollas infection and should also be cultured). The amount of drainage is generally documented as absent, scant, minimal, moder-
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AClITE CARE HANDBOOK FOR PHYSICAL TI-IERAPISTS
ate, large, or copious. (Note: there is no consistent objective measure ment that correlates to these descriptions.) A large amount of drainage can indicate infection, whereas a reduction in the amount of drainage can indicate that an infection is resolving. The presence and degree of odor can be documented as absent, mild, or foul. Foul odors can be indicative of an infection.
Wound Culture A wound culture is a sampling of micro-organisms from the wound bed that is subsequently grown in a nurrient medium for the purpose of identifying the type and number of organisms present. A wound culture is indicated if there are clinical signs of infection, such as purulent drainage, large amounts of drainage, increased local or sys temic temperature, inflammation, abnormal granulation tissue, local erythema, edema, cellulitis, increased pain, foul odor, and delayed healing.o, Results of aerobic and nonaerobic cultures can determine whether antibiotic therapy is indicatedo,
Methods of culturing
include tissue biopsy, needle aspiration, and swab cultures. Physical therapists may administer swab cultures. Otherwise, wound cultures arc performed by the nurse or physician, depending on the protocol of the institution. All wounds are contaminated, which does not necessarily mean they are infected. Contamination is the presence of bacteria on the wound surface. Colonization is the presence and multiplication of surface microbes without infection. Infectioll is the invasion and mul tiplication of micro-organisms in body tissues, resulting in local cellu lar injury.63.65.66
Clinical Tip Unless specifically prescribed otherwise, cultures should be taken after debridement of thick eschar and necrotic mate rial and wound cleansing; otherwise, the culture will reAect the growth of the micro-organisms of the external wound environment rather than the internal environment.
Surrounding Areas The area surrounding the wound should also be evaluated and compared to noninvolved areas. Skin color, the absence of hair, shiny or Aaky skin, the presence of reddened or darkened areas, edema, or changes in the nailbeds should all be examined and documented accordingly.
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Clinical Tip Increased localized temperature can indicate local infec tion; decreased temperature can indicate decreased blood supply.
WOImd Stagillg alld Classification Superficial wOllllds involve only the epidermis. Partial-thicklless woullds further involve the superficial layers of the dermis; full-thick ness wounds continue through to muscle and potentially to bone. This terminology should be used to describe and classify wounds that are not pressure ulcers. Pressure ulcers have their own classification system because of their unique characteristic of developing from the "inside out." Pressure ulcers are traditionally described by a four stage system, presented in Table 7-12.
Woulld Clea1lsing a1ld Debride",e1lt It is beyond the scope of this chapter co discuss in derail the methods of wound cleansing and debridement. Instead, general descriptions and indications of each are provided. Wound cleansing and debride ment can be performed by physical therapists, nurses, or physicians,
Table Stage
7-12.
Four-Stage Pressure Ulcer Classification
Description Reddened area on the skin with an intact epidermis
((
\'(found similar to a blister or abrasion on which the dermis is
JIJ
Wound that exposes subcutaneous tissue down to, bur nor through,
IV
Wound that exposes muscle, bone, or other supporting structures,
exposed underlying fascia such as tendon or joint capsule Source: Dam from The National Pressure Ulcer Advisory Panel's Summary of [he AHCPR Clinical Practice Guideline. Prcssure Ulcers in Adults: Prediction and Preven [ion. (AHCPR Publication No. 92-0047). Rockville, MD. May 1992.
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AClJfE CARE HANDBOOK FOR PHYSICAL THFRAPISTS
depending on the policy of an individual facility. Physical therapists should also verify state practice acts regarding their ability to perform sharp debridement. Specific management considerations for physical therapists who work with patients who have wounds are described at the end of this chapter. Wound Cleansing
Wound cleansing is not synonymous with wound debridement or wound decontamination. The purpose of cleansing a wound is to remove loosely attached cellular debris and bacteria from the wound bed. In most cases, the use of sterile saline is effective and safe for cleansing the wound surface.67,68 Many studies indicate that using unsterile tap water does not increase the rate of infection and is appro priate to use to cleanse wounds.67 There are many commercial wound deansers that contain surfacranes. Surfactants help to break the bonds between coneaminants, debris, and the surface of the wound.67 The use of antiseptics is appropriate in the early management of acute trau matic wounds bllt is of little benefit in chronic wounds. They may be cytotoxic to living tissues and can delay healing.67.69.7o The most nelltral solution that will meet the needs of the patient should be used. Aggressive agents should be used only when indi cated. For example, a bleaching agent may help to dry a heavily exu dating wound. Cleansing should be discontinued when the majority of a wound bed is granulating or when re-epithelialization is occur ring to avoid damaging new tissue.
Clinical Tip •
If the water source is known or suspected to be contam
inated, it should nOt be used for wound deansing.67 If the physical therapist is unsure, the water can be culrured in the hospital laboratory. •
Sterile saline expires 24 hOllrs after opening the bottle
and must be discarded. A saline solution can be made by adding 2 tablespoons of salt to
1
quart of boiling
water.67,69 This recipe may be an inexpensive alternative to purchasing saline for the patient who will be deansing wounds at home. •
It is best to use cleansing materials at body temperature.
The application of a cold solution will reduce the tempera ture of the wound and may affect blood Aow.70
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485
Whirlpool, although commonly and perhaps habitually
used, does not cleanse the wound. The use of whirlpool jets is actually mechanical debridement and therefore should be used only if mechanical debridement is indicated.
Clean versus Sterile Technique Although clean versus sterile technique remains somewhat controver sial, clean technique is sufficient for local wound care to chronic wounds and is generally accepted in the medical community, because the chronic wound is already contaminated and far from sterile. Ster ile technique is typically reserved for surgical and acute traumatic wounds.71 Sterile technique, which includes the use of sterile instruments and sterile gloves, should always be used when invading the blood stream, as with sharp debridement. Otherwise, the use of clean gloves is suffi cient. Additionally, originally sterile dressings, once opened, can still be used as long as they are kept in a clean, controlled area.'! Wound Debridement Debridement has three primary purposes. The first is to remove necrotic tissue or foreign matter from the wound bed, optimizing healing potential. The presence of devitalized tissue prevents re-epi thelialization and can splint the wound open, preventing contraction and closure. The second purpose is to prevent infection. The necrotic tissue itself can be the source of the pathogenic organisms. The debride ment of the slough and eschar also increases the effectiveness of topi cal agents. The third purpose is to correct abnormal wound repair. Debridement is generally indicated for any necrotic tissue present in a wound, although occasionally it is advantageous to leave eschar in place. For example, eschar on heel ulcers that is firmly adherent to surrounding tissue without inflammation of surrounding tissue and without drainage and tenderness on palpation may not need to be removed.72 There are two types of debridement: selective and nonselective. Selective debridement removes nonviable tissue only and is indicated for wounds with necrotic tissue adjacent to viable tissue. Methods of selective debridement include sharp, autolytic, and enzymatic debride menr. NOllselective debridement removes both viable and nonvia ble tissues. It is indicated in necrotic wounds with minimal to no healthy tissue. Mechanical debridement is a method of nonselective debridcment.7l,73
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ACUTE CARE HANDBOOK FOR I'HYSICAL TIIl:.RAIJI5T5
Selective Debridemelll Sharp Debridement Sharp debridement involves the use of scalpels, scissors, and forceps ro remove necrotic tissue. It is a highly skilled technique best per formed by or under the direct supervision of an experienced clinician. (Note: Nor all states and facilities allow physical therapists to per form sharp debridement. ) Because rhe true selectiviry of sharp debride ment depends on the skill of the clinician, sharp debridement can also result in damage to healthy tissues that can cause bleeding and a risk of infecrion. Sharp debridement is especially expedient in the removal of large amounts of thick, leathery eschar. Removal of eschar is important in the patient who is immunocompromised, because rhe underside of eschar can provide a medium for bacterial growth. Sharp debridement has been shown to increase the degree of wound healing when combined with the usc of a topical growth factor." Sharp debridement can be painful; it is therefore recommended that pain medications or topical analgesics be administered before treatment. When debriding, the clinician should spare as much tissue as possible and be careful to have the technique remain selective by not removing viable tissue. Because of the potential for excessive bleeding, extra care should be taken with patients who are taking anticoagulants. Autolytic Debridement Alltolytic debridemellt is the natural and most selective form of debride ment. The body uses its own enzymes to lyse necrotic tissue and this is a normal process that occurs in any wound. It is painless and does not harm healthy tissues. Moist dressings facilitate autolytic debridement, as do films, hydrocolloids, and calcium alginates, which keep the wounds moist with the exudate from the wound.72•74 When using aurolytic debridement, it is important to cleanse the wound to remove partially degraded tissue.74 Because it takes time for autolytic debride ment to occur, sharp debridement of eschar is recommended before autolytic debridement to expedite the removal of the necrotic tissue. Owing to the risk of infection, autolytic debridement is contraindicated as the primary method of debridement in patients who are immunosup pressed or otherwise require quick elimination of necrotic material. NOllselective Debridemellt Mechanical Debridement Mechal1ical debridement removes dead tissue by agitating the necrotic tissue of the wound or adhering it to a dressing and removing it. Dry
BURNS AND WOUNDS
487
gauze dressings, scrubbing, whirlpool, and pulsed lavage or irriga tion, or both, are all examples of mechanical debridement. Wet-to-dry dress ings mechanically debride the wound by removing the dressing along with the necrotic tissue embedded in it. If mechanical debridement is indicated, and gauze is used, the sponge or gauze with the largest pores is the most effective for debridement." This technique involves applying a saline-moistened gauze dressing to the wound, allowing it to dry, followed by removal of the dressing. The dressing will also adhere to any growing tissue in the wound bed and may inad
vertently remove itn Wet-to-dry dressings, therefore, should not be used on clean, granulating wound beds. If s aline gauze dressings are used on a clean wound bed, they must continually be kept moist. Whirlpool may be used to debride loosely adherent tissue and exu date and deodorize the wound. It may also help to prepare a wound for sharp debridement by softening necrotic tissue and s eparating des iccated tissues from the wound bed. Or it can be used to soak off adhered dressings. If the intention of the therapist is to use a wet-to dry technique for mechanical debridement, the dressings should not be soaked off, as necrotic tissue will not be removed.41, There are many precautions and Contraindications for the therapist to consider before using whirlpool. For example, it may be inappro priate to place the lower extremity of a patient with venous insuffi ciency in a dependent pos ition with warm water, or perhaps the treatment may need to be modified by decreasing the temperature or length of a treatment. As with wound cleansing, the therapist should carefully weigh the benefits of antibacterial agents that can be added to the whirlpool versus their cytotoxic effects and use a s olution that is most neutral and least damaging ro viable tissue. Infected wounds that have foul odors, copious amounts of drainage, and a great deal of exudate and necrotic tissue require more aggressive additives. Whirlpool should be limited to stage III or IV wounds with greater than 50% of necrotic tissue, because, as with gauze debridement, granulating tissue may be damaged. Whirlpool should be discontin ued once the objectives of the whirlpool have been achieved41, Pulsed lavage is now a viable treatment option for wound manage ment, and systems s pecifically designed for wound care are currently available. Pulsed lavage uses a press urized, pulsed solution (usually saline) to irrigate and debride wounds of necrotic tissue. Suction may also be used to remove wound debris and the irrigation s olution.76 The pulsatile action is thought to facilitate growth of granulation tis sue because of its effective debridement, and the negative pressure cre ated by the s uction may also stimulate granulationn Pulsed lavage
488
AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
may be a more appropriate option than whirlpool for patients who are incominent, have venous insufficiency, should not be in a depen dem posicion, have an intravenous line, or are mechanically venri lated. Pulsed lavage may access narrow wound tunnels that may not be reached with whirlpool. Enzymatic Debridement
Enzymatic debridement is achieved through the topical application of enzymes that lyse collagen, fibrin, and elastin. The type of enzyme chosen depends on the type of necrotic tissue in the wound. Enzymes are categorized as proteolytics, fibrinolytics, and collagenases.72 Dif ferent enzymatic debriding agents are effective with each of these tis sues. Wounds with heavy black eschar are best debrided
by
proteinases and fibrolytic enzymes. Collagenases are used when necrotic collagen, which generally appears yellowish, is present. Enzy matic debridement agents are available only by prescription. Enzy matic debridement is indicated on stage III and IV wounds with yellow necrotic material bur should be discontinued as soon as the wound is clean. Sharp debridement of the wound can be performed before the use of enzymes to facilitate tissue healing.
Clinical Tip When applying an enzymatic debriding agent to eschar and it cannot be debrided, crosshatch the eschar and pull in the edges to allow the enzymes to penetrate the eschar.
Dressings and Topical Agents When applying dressings, the therapist should always follow universal precautions and use a clean technique to prevem cross contamination. When choosing a dressing for a wound, four factors related to the wound itself should be considered: (1) the color of the wound, amount of drainage, (3) the wound depth, and
(4)
(2)
the
the surrounding
skin. Other significant factors include the patient's cognitive and physi cal abiliry to apply the dressing and the accessibility of physical therapy or nursing services to the patient. Cost is also a consideration. A large number of wound care products are available, and it is vir tually impossible to be aware of the purpose and application instruc-
BURNS AND WOUNDS
489
tions of every available dressing. It is the responsibility of the therapist to read manufacturer's instructions for application, to know the purpose of the dressing, and to make educated decisions when choosing the appropriate dressing for a given wound at each stage of the healing process. Clinicians should not rely on manufacturer's claims of efficacy to justify a dressing's effectiveness. Although it is not possible to identify every dressing, it is possible to catalog most dressings into some basic categories: gauze, nonadherem dressings, hydrocolloids, semipermeable films, hydrogels, foams, and calcium alginates. Table 7-13 is a summary of the indications, advantages, and disadvantages of different dressings.77-8o Other Dressings The V.A.C. (Vacuum Assisted Closure) (Kinetic Concepts, Inc., San Antonio, TX) device assists in wound closure by applying localized negative pressure to a special porous dressing positioned in or over the wound. The porous dressing distributes negative pressure to the wound and helps remove interstitial fluids. The negative pressure applies noncompressive mechanical forces to the wound site and draws the tissue inward, subjecting it to subatmospheric pressure. The distortion causes epithelial cells to multiply rapidly and form granulation tissue. The stretching also increases cell proliferation by activating ion channels within the cells and releasing biochemical mediators from the plasma membrane. It is also thought to Stimulate the growth of new blood vessels. This device is worn continuously 24 hours a day. Dressings for noninfected wounds can be changed every
2-3 days or changed daily for infected wounds. Indications for this therapy include diabetic ulcers, pressure ulcers, traumatic wounds, meshed grafts, and flaps. Contraindications include fistulas, necrotic tissue or eschar, untreated osteomyelitis, malignancy in wound, and exposed arteries or veins.81.82 Cadexomer-iodine is an iodine-based wound filler (e.g., lodoflex, iodoform) and is indicated in highly exudating wounds. It is highly absorbent, provides a moist healing environment, and lowers the pH of the wound. The iodine is slowly released, so it is not cytotoxic to good tissue, but the bacteriostatic and bactericidal effects of iodine remain. Skin Substitutes and Biologicals Although these will not be a first line of defense, therapists in the acute care setting should be aware of other agents that may be used to
Table 7-13. Indications and Uses of Basic Types of Dressings
.. '" 0
Type of Dressing
Indication
Description
Advantages
Disadvantages
Gauze
May be used for any type of wound if properly applied and removed (although other dressings may be more effective)
Highly porous. Applied dry, wet-todry (i.e., the dressing is put on wet but will dry before removal), or wet-to-wet (i.e., the dressing is pur on wet and removed when wet). Nonimpregnated or impregnated (nonadherent substance integrated into dressing) dressings comprised of inert materials that conform to the wound surface.
Readily available Inexpensive
May require frequenr changes Can cause skin macerarion Permeable to bacteria Removal can be painful
Nonadherenr dressings
Wounds with low-tomoderate drainage, for minor lacerations or abrasions, or as a secondary dressing for deep fullthickness wounds
,. ()
'i '" ()
�
:t
� 0
� 0 0
" �
0
'" �
Generally nonirritating and nonroxic Less likely to adhere to wound, causing less tissue disruption Relatively inexpensive
May still adhere if allowed to get too dry before remOVing
:t -< �
!:?
r
5! '"
'" ,. �
�
Hydrocolloids
Semipermeable films
Hydrogels
Parrial- or fullrhickness wounds with low-tomoderate drainage, including partially necrotic wounds Provide a moist wound environmem and promotes autolysis Promote a moist wound environment for wounds wirh minimal drainage
Partial-thickness wounds with minimal drainage, or as a secondary dressing on a fullthickness wound
Dressings that contain absorptive particles that interact with moisture to form a gelatinous mass. Cause the pH of the wound surface ro decrease, thereby inhibiting bacterial growth. Transparent polyurethane with a water-resistant adhesive on one side. Semipermeable ro water and oxygen but impermeable to bacteria. Gel composed of 96% water or glycerin.
Prevent secondary wound infection Impermeable to water, oxygen, and bacteria Available in many forms (pastes, powders, and sheers) Changed infrequently Conforms well Allow for visual wound monitoring
Not for use with anaerobic wound infeccions Removal may cause skin rears on fragile surrounding skin
Highly adhesive, can be difficult to apply Can cause skin rears, especially on fragile skin
.. c
Highly conformable Safe for fragile skin Available in many forms
Do not absorb much
'" Z
�
,.
Z c " 0 c Z c
�
... '" ....
Table
7-13. Continued
... '" N
Type of Oressing
Indication
Description
Advantages
Disadvantages
Foams
Partial- or full-thick ness wounds with minimal-ro-moder ate drainage
Polyurethane foam with twO surfaces: a hydrophilic inner surface and a hydrophobic outef surface.
Nonadherenr to skin surface Highly absorbable and conformable Permeable to oxygen (reduce risk of anaerobic infection) Highly conformable
Expensive
Calcium alginates
Partial- and full thickness wounds with large amounts of drainage, infected or noninfected wounds Provide a moist wound environment and facilitate autolysis
Fibrous sheets and rope derived from brown seaweed. The main component, alginic acid, is converted to calcium and sodium salts, which in turn convert to a viscous gel after contact with wound exudates.
>
�
� " m J:
� 1)
o
o
"
Require a secondary dressing to keep from drying out
Sources: With permission from J Cuzell, D Krasner. Wound Dressings. In PP Gogia (ed). Clinical Wound Management. Thorofare, NJ: Slack, 1995;)5 Feedar. Clinical Managemenr of Chronic Wounds. In LC Kloth, KH Miller (eds). Wound Healing: Alrernatives in Managemenr. Phila delphia: FA Davis. 1995; ML Levin, LW O'Neal, JH Bower (cds), The Diabetic Foot (4th ed). St. Louis: Mosby. 1993; JC Lawrence. Dressings and wound infection. Am J Surg 1994; 167( I A):21 j and CT Hess. When to usc hydrocolloid dressings. Adv Skin Wound Care 2000;13:63.
o " � J: -< �
� r :;!
m
s:
�
BURNS AND WOUNDS
493
treat the chronic, nonhealing ulcer. Frequently a patient may have been receiving treatment for a wound before hospitalization for an acute medical condition and the therapist may be continuing or may need to
recommend alternative healing agents. Platelet-derived
growth {actor promotes cellular migration of leukocytes and mac rophages and stimulates fibroblasts to produce collagen. An example of platelet-derived growth factor is Regranex gel (becaplermin).83 Another possible solution is skill substitutes (e.g., Dermagraft), which consist of fibroblasts from a newborn foreskin donor, placed on a polygalactic acid mesh. The fibroblasts multiply, attach to the mesh, and release growth factors,S! Living skin equivalent (e.g., graftskin IApligrafJ) consists of bovine type I collagen that is acid dis sociated and added to a culture system. Human fibroblasts are then added.B' These are typically fairly expensive treatments and are reserved for nonhealing foot ulcers that have not responded to other topical agents and treatments.
Physical Therapy Intervention in Wound Care The responsibility and autonomy of the physical therapist in the treat ment of wounds vary greatly among facilities. The physical therapist can and should play a key role in the patient'S clinical course of pre venting a wound, initiating wound carc, or both. The physical thera pist in the acute care setting can also be responsible for making recommendations abour wound care on discharge from the hospital. Unless the wound is superficial and caused by trauma, wound closure is not likely to occur during the acute care phase. Therefore, the ulti mate long-term goal of complete wound closure, which may occur over many months, occurs at a different level of care, usually outpa tient or home care.
The following are the primary goals of p hy sica l therapy for wound treatment in the acute care scrring: •
To promote wound healing through wound assessment, dressing
choice and application, wound cleansing, and debridement •
To educate patienrs and families about wound care and preven
tion of furrher breakdown and future wounds
494
AC1JTE CARE HANDBOOK FOR PHYSICAL THERAI)ISTS
Table
7-14.
Physical Therapy Considerations for Wound Care
Physical Therapy lnrervention Pain manage ment
Range of morion, strength, and functional mobility
Edema managemenr
Prevention
•
Consideration Coordinate physical therapy session with pain premedi cation to reduce acute cyclic and noncyclic pain. Consider the use of positioning, relaxation techniques, deep breathing, exercise, or modalities to relieve pain. Modify wound treatmenr techniques as able to eliminate the source of pain. Adequate range of motion is necessary for proper positioning and minimizing the risk of pressure ulcer formation. Care should be taken with manual contacts with fragile skin, and care should be taken not to disturb dressings during exercise. Adequate strength is necessary for weight shifting and functional mobility with the maintenance of weight bearing precautions. Depending on the etiology, exercise, compression therapy, lymphatic drainage. limb elevation (used with caution in the patient with cardiac dysfunction), or a combination of these can be used to manage edema. Education (e.g. , dressing application. infection control, wound inspection, the etiology of wounds) Positioning (e.g., splines, turning schedule) Skin care and hygiene (e.g., dressing removal) Pressure reduction surfaces (e.g., air mattress, wheelchair cushion) Footwear adaptations (e.g., orthotics, inserts, extra depth shoes)
To maximize patient mobility and function while accommodat
ing needs for wound healing (e.g., maintaining non-weight-bcaring status) •
To minimize pain
•
To provide recommendations for interdisciplinary acute care
•
To provide recommendations and referrals for follow u p care -
BURNS AND WOUNDS
495
To fulfill these respons ibilities, the therapist must consider all information gathered during the evaluation process and establish appropriate goals and time frames. The etiology of the wound, risk factors, and other data guide the therapist toward the proper inter vention. Objective, measurable, and functional goals are as important in wound care as in any other aspect of physical therapy. Patients with wounds typically have many other medical complica tions and needs that a physical therapist cannot address alone. To provide optimal care, the physical therapist s hould function as a part of an interdisciplinary team that may include a physician, nurse, spe cialized skin and wound care nurse (referred to as an ellterostomai therapist), dietitian, and others. The physical therapist should be aware of and make proper recommendations to the appropriate per s onnel for all of the patient's needs for healing. Specific considerations for physical therapy intervention with a patient who has a wound include pain management, ROM, strength ening, functional mobility, edema management, and wound preven tion. Table 7-14 describes these considerations.
References 1. Williams WG, Phillips LG. Pathophysiology of the Burn Wound. In DN Herndon (ed), Total Burn Care. London: Saunders, 1996;63. 2. Falke! jE. Anatomy and Physiology of the Skin. [n RI Richard, Mj Sta ley (eds), Burn Care Rehabilitation Principles and Practice. Philadelphia: FA Davis, 1994; I O. 3. Totora Gj, Grabowski SR (eds). Principles of Anatomy and Physiology (7th ed). New York: Harper-Collins College, 1989;126. 4. \Varden GD, Heimback DM. Burns. In 51 Schwartz (cd), Principles of Surgery, Vol. I (7th cd). New York: McGraw-Hili, 1999;223-262. 5. johnson C. Pathologic Manifestations of Burn Injury. In RI Richard, Mj Staley (eds), Burn Care and Rehabilitation Principles and Practice. Phila delphia: FA Davis, 1994;29. 6. Rai J. Jeschke MG, Barrow RE, Herndon DN. Electrical injuries: a 30year review. j Trauma 1999;46(5):933-936. 7. High-Tension Electrical Burns. In RH Oemling, C laLonde (cds), Burn Trauma. New York: Thieme, J989j223. 8. Winfree J, Barillo OJ. Burn management. Nomhermal injuries. Nurs Clin North Am [997;32(2):275-296. 9. Lightning. In RH Oemling, C LaLonde (eds), Burn Trauma. New York: Thieme, 1989;242. 10. Milner SM, Rylah LTA, Nguyen IT, et.1. Chemical Injury. In DN Hern don (cd), Total Burn Care. London: Saunders, ] 996;424.
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AClTfE CARE HANDBOOK FOR PHYSICAL TIiE-RAPISTS
11. Milner SM, Nguyen IT, Herndon ON, Rylah LTA. Radiation injuries and Mass Casualties. in ON Herndon (ed). Total Burn Care. London: Saunders, 1996;425. 12. McManus WF, Pruin BA. Thermal Injuries. in OV F eliciano, EE Moore, KL Martox (eds), Trauma. Stamford, CE Appleton & Lange, 1996;937. 13. Marvin J. Thermal Injuries. in VO Cardona, PO Hum, PJ Bastnagel Mason, et al. (cds), Trauma Nursing: from Resuscitation through Reha biliration (2nd ed). Philadelphia: Saunders, 1994;736. 14. Richard R. Assessment and diagnosis of burn wounds. Adv \Vound Care 1999;12(9):468-4 71. 15. American Burn Association. Hospital and prehospital resources for opti mal care of patients with burn injury: guidelines for development and operarion of burn centers. J Burn Care Rehabil 1990;11(2):98-104. 16. Gordon M, Goodwin CWo Burn management. initial assessment, man agement, and srabilization. Nurs Clin North Am 1997;32(2):237-249. 17. Kao CC, Garner WL. Acure burns. Plasr Reconsrr Surg 2000;101(7): 2482-2493. 18. Schiller WR. Burn Care and Inhalarion Injury. In A Grenvik (cd), Texr book of Critical Care (4rh ed). Philadelphia: Saunders, 2000;365-377. 19. Desai MH, Herndon ON. Bums. In DO Trunkey, FR Lewis, BC Decker (cds), Current Therapy of Trauma (3rd ed). Philadelphia: Mosby, 1991;315. 20. Abraham E. Toxic Gas and inhalation Injury. In BE Brenner (cd). Com prehensive Management of Respiratory Emergencies. Rockville, MO: Aspen Publications, 1995;241. 21. Traber DL, Herndon ON. Parhophysiology of Smoke Inhalarion. In EF Haponik, AM Munster (cds), Respiratory Injury: Smoke Inhalation and Burns. New York: McGraw-Hili, 1990;61. 22. Crapo RO. Causes of Respiratory Injury. In EF Haponik, AM Munster (cds), Respiratory Injury: Smoke Inhalation and Burns. New York: McGraw-Hili, 1990;47. 23. Ahrns KS, Harkins DR. Initial resuscitation after burn injury: therapies, strategies, and controversies. MCN Clin Issues 1999;10:46-60. 24. Edlich RF, Moghrader JC. Thermal Burns. In P Rosen (ed), Emergency Medicine Concepts and Clinical Practice, Vol. 1 (4th ed). St. Louis: Mosby, 1998;941-953. 25. Jordan BS, Harrington DT. Management of the burn wound. Nurs Clin North Am 1997;32(2):251-271. 26. Linares HA. Pathophysiology of Burn Scar. In ON Herndon (ed), Toral Burn Care. London: Saunders. 1996;383. 27. Wild B, Kemp H. Skin cultures in burns care nursing. Nurs Times 1999;95(36):46-49. 28. Miller SF, Sraley MJ, Richard RL. Surgical Management of rhe Burn Parient. In RL Richard, MJ Sraley (eds), Burn Care and Rehabilirarion Principles and Practice. Philadelphia: F A Davis, 1994;177. 29. Kagan RJ. Skin substitutes: implications for burns and chronic wounds. Adv Wound Care 1999;12(2):94-95. 30. Richard RL, Staley MJ. Burn Patient Evaluation and Treatmcnc Plan ning. In RL Richard, MJ Staley (cds), Burn Care and Rehabilitation Principles and Practice. Philadelphia: F A Davis, 1994;20 1.
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3 J. Micheletti G. Ulcers of the Lower Extremity. In PP Gogia. Clinical Wound Management. Thorofare, N]: Slack, 1995;105-106. 32. McCulloch]M. EvaluatIOn of Patients with Open Wounds In LC Kloth, KH Miller. Wound Healing: Alternatives in Management. Philadelphia: FA Davis, 1995;I 18. 33. Sibbald RG. An approach co leg and foot ulcers: a brief overview. Ostomy Wound Manage 1998;44(9):28-32, 34-35. 34. Sibbald RG. Venous Leg Ulcers. Ostomy Wound Manage 1998;44(9): 52-64. 35. Donayre CEo Diagnosis and Management of Vascular Ulcers. In C Suss man, B Bates-Jensen. Wound Care: A Collaborative Practice Manual for Physical Therapists and Nurses. Gaithersburg, MD: Aspen Publishers, 1998;310. 36. Kosiak M. Etiology and pathology of ischemic ulcers. Arch Phys Med Rehah,l 1959;40:62-69. 37. Feedar JA. Prevemion and Management of Pressure Ulcers. In LC Kloth, KII Miller, Wound Healmg: Alternatives in Management. Philadelphia: FA Davis, 1995; 187-193. 38. Leigh lH. Pressure ulcers: prevalence, etiology, and treatmenr modali ties. A review. Am] Surg 1994;167(l A):25S-30S. 39. Bolander VP (ed). Sorensen and Luckmnl1l1's Basic Nursing. Philadel phia: Saunders, 1994;742. 40. Feedar JA. Prevention and Managemenr of Pressure Ulcers. In LC Kloth, KII Miller, Wound Henling: Alternatives in Management. Philadelphia: FA Dav,s, 1995; 193-195. 41. The National Pressure Ulcer Advisory Panel's Summary of the AHCPR Clinical Practice Guideline. Pressure Ulcers in Adults: Prediaion and Pre vention (AI ICPR Publication No. 92-0047). Rockville, MD. May 1992. 42. Brown AC, Sibbald RG. The diabetic neuroparhic ulcer: an overview. Ostomy Wound Manage 1999;45(Suppl I A):6. 43. Levin ME. Preventing amputation in the patient with diabetes. Diabetes Care 1995;18(10);1383-1394. 44. D.lI1iels TH.. Diaberic Foot Ulcerations: An Overview. Ostomy Wound Manage 1999;44(9):77. 45. Weiss EL Connective Tissue in Wound Healing. In LC Kloth, KH Miller, Wound Healing: Alternatives in Management. Philadelphia: FA Davis, 1995;26. 46. L,mg P. Diabetic foot ulcers. Am] Surg 1994,167(IA):31. 47. Levin ML, O'Neal LW, Bowker ]H. The Diabetic Foot (5th ed). St. LoUIS: Mosby, 1993. 48. Catanzanti AR, Haverstock BD, Grossman JP, Mendicino RW. Off loading techniques in the treatment of diabetic plantar neuropathic foot ulceration. Adv Wound Care 1999;12(9):452. 49. Kloth LC, McCulloch]M. The InAammatory Response to Wounding. In LC Kloth, KH M,lIer (cds), Wound Healing: Alternatives in Manage ment. Ph.Iadclphia: FA Davis, 1995;3-15. 50. Weiss EL. Connective Tissue in Wound Healing. In LC Kloth, KH Miller (cds), Wound Healing: Alternatives in Management. Philadelphia: FA Davis, 1995; I 6-31.
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51. Daly TJ. Contraction and Re-Epithelialization. In LC Kloth, KH Miller (cds), Wound Healing: Alternatives in Management. Philadelphia: FA Davis, 1995;32-46. 52. Gogia PP. Physiology of Wound Healing. In PP Gogia (ed), linical Wound Man3gement. Thorofare, NJ: Slack, 1995; 1-12. 53. Sussman C. Wound Healing Biology and Chronic Wound Healing. In C Sussman, B Bates·Jensen (cds), Wound Care: A Collaborative Practice Manual for Physical Therapists and Nurses. Gaithersburg, MD: Aspen Publishers, 1998;31-47. 54. Keast DH, Orsted H. The basic principles of wound care. Ostomy Wound Manage 1998;44(8):24-31. 55. Kernstein MD. The scientific basis of healing. Adv Wound Care 1997;10(3);30-36. 56. Mulder GD, Brazinsky BA, Seeley JE. Factors Complicating Wound Repair. In LC Kloth, KH Miller (cds), Wound Healing: Alternatives in Management. Philadelphia: FA Davis, 1995;48-49. 57. Bahl SM. Nutritional Considerations in Wound Management. In PP Gogia (ed), Clinical Wound Managcment. Thorofarc, NJ: Slack, 1995;73. 58. DeSanti L. Involuntary Weight Loss and the Nonhealing Wound. Adv Skin Wound Care 2000;13(Supp l 1):"11-20. 59. Mulder GD, Brazinsky BA, Seeley JE. Facrors Complicating Wound Repair. In LC Kloth, KH Miller (eds), Wound Healing: Alternatives in Management. Philadelphia: FA Davis, 1995;50-51. 60. Keast DH, Orsted H. The Basic Principles of \Xlound are. Ostomy Wound Manage 1998;44(8):28. 61. Lazarus G, Cooper DM, Knighton DR, et 31. Definitions 3nd guidelines for assessment of wounds and evaluation of healing. Arch Dermatol 1994;"130:489-493. 62. Gallagher SM. Ethical dilemmas in pain management. Ostomy \Vound Manage 1998;44(9):20. 63. Thomson PD, Smith DJ. What is infection? Am J Surg 1994;167(IA): 75-1 IS. 64. Fowler E. Wound infection: a nurse's perspective. Ostomy Wound Man· age 1998;44(8):45. 65. Icrow S. Infection Control Perspectives. In D Krasner, 0 Kan (eds), Chronic Wound Care: A Clinical Source Book for Healthcare Profes· sionals. \Xlayne, PA: Health Management Publications, 1997;90-96. 66. Thomson PD, Smith DJ. What is infection? Am J Surg 1994; 167(IA):75-11S. 67. Fowler E. Wound infection: a nursc's perspective. Ostomy Wound Man age J998;44(8):47. 68. Gilchrist B. Infection and Culturing. In 0 Krasner, 0 Kane (eds), Chronic \Vound Care: A Clinical Source Book for Healthcarc Profes sionals (2nd ed). \'V'ayne, PA: Health Management Publications, 1997;109-114. 69. Rodheaver GT. Wound Cleansing, Wound Irrigation and \Vound Disin fection. In D Krasner, D Kane (cds), Chronic \'V'ollild Care: A Clinical
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Source Book for Healthcare Professionals (2nd cd). Wayne, PA: Health Managemcnr Publications, 1997;97-106. 70. Sussman G. Management of the \Vound Environment. In C Sussman, B Bates-Jensen (cds), \'Vound Care: A Collaborative Practice Manual for Physical Therapists and Nurses. Gaithersburg, MD: Aspen Publishers, 1998;212. 71.
72. 73.
74.
75. 76.
Fowler E. Wound infection: a nurse's perspective. Ostomy W'ound Man age 1998;44(9): 19. Sieggreen MY, Maklebust JM. Debridement: choices and challenges. Adv Wound Care 1997; I 0(2):32-37. Feedar )S. Clinical Managemenr of Chronic Wounds. In LC Kloth, KH Miller (cds), Wound Healing: Alternatives in Management. Philadel phia, PA: FA Davis, 1995;151-156. Rodeheaver GT. Pressure ulcer debridement and cleansing: a review of current literature. Ostomy Wound Manage 1999;45( 1 A Suppl):80S87S. SCOtt RG, Loehne HB. Five questions-and answers-about pulsed lav age. Adv Skin Wound Care 2000;13(3):133-134. Loehne HB. Pulsatile Lavage with Concurrent Suction. In C Sussman, B Bates-Jensen (cds), Wound Care: A Collaborative Practice Manual for Physical Therapists and Nurses. Gaithersburg, MD: Aspen Publishers,
1998;389-403. 77. Sussman C. Whirlpool. In C Sussman, B Bates-Jensen (cds), \'Vound
78. 79.
80. 81.
82. 83. 84.
Care: A Collaborative Practice Manual for Physical Therapists and Nurses. Gaithersburg, MD: Aspen Publishers, 1998;447-454. Cuzell J, Krasner D. \'Vound Dressings. In PP Gogia. Clinical Wound Management. Thorofare, N): Slack, 1995:131-144. Feedar )S. Clinical Management of Chronic Wounds. In LC Kloth, KH Miller (eds), Wound Healing: Alternatives in Management. Philadel phia: FA Davis, 1995;156-169. Levin ML, O'Neal LW, Bower )H. The Diabetic Foot (4th ed.) St. Louis: Mosby, 1993. Philbeck TE, Whittington KT, Millsap MH, et al. The clinical and COst effectiveness of externally applied negative pressure wound therapy in rhe treatment of wounds in home healthcare medicare patients. Ostomy Wound Manage 1999;45( II ):41-50. Mendez-Eastman S. When wounds won't heal. RN 1998;61:20-23. Sibbald RG. An approach to leg and foot ulcers. Ostomy Wound Manage 1998;44(9):30. Sibbald RG. Venous leg uicers. Ostomy Wound Manage 1998;44(9):63.
8 Gastrointestinal System
Jaime C. Paz
lntroduction Disorders of the gastrointestinal (GI) system can have numerous effects on the body, such as decreased ourridon, anemia, and fluid imbalances. These consequences may, in turn, affect the activity toler ance of a patient, which will ultimately influence many physical ther apy interventions. In addition, physical therapists must be aware of pain referral patterns from the GI system that may mimic musculo skeletal symptoms (Table 8-1). The objectives of this chapter are to provide the following: I. A basic understanding of the structure and function of the G1 system
2. Information on the clinical evaluation of [he GI system, including physical examination and diagnostic studies 3. A basic understanding of the various diseases and disorders of the GI system
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AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Table 8-1. Gastroinrestinal System Pain Referral Patterns
Structure
Segmenral Innervation
Areas of Pain Referral
Esophagus
T'Hi
Substernal region
Sromach
T6-IO
Small inrestine
T7-IO
Middle thoracic spine
Pancreas
T6-IO
Upper abdomen
Gallbladder
T7-9
Upper abdomen Upper abdomen Middle and lower thoracic spine
Upper and lower thoracic spine Right upper abdomen Right, middle, and lower thoracic spine Liver
T7-9
Common bile duct
T6-10
Upper abdomen
Large intestine
T1 1 -L1
Middle lumbar spine Lower abdomen
Sigmoid colon
TII-12
Right, middle, and lower thoracic spine Right cervical spine
Middle lumbar spine Upper sacral region Suprapubic region Lefr lower quadrant of abdomen Source: With permission from we Soissonault. C Bass. Pathological origins of trunk
and neck pain: part I. Pelvic and abdominal visceral disorders. J On hop Sports Phys
Thcr 1990;12,194.
4. Information on the management of GI disorders, including pharmacologic therapy and surgical procedures 5. Guidelines for physical therapy intervention with GI diseases and disorders
In
patients
Structure and Function The basic strucrure of the GI system is shown in Figure 8-1, with the primary and accessory organs of digestion and their respective func tions described in Tables 8-2 and 8-3.
GASTROINffiSTINAL
Figure
SYSTEM
503
8�1 . Schematic representation of the ga.strointestinal system. (Original Wu.)
artwork by Peter
Clinical Evaluation Evaluation of the GI system involves combining information gathered through physical examination and diagnostic studies.
Physical Examillatioll Physical examination of the abdomen consists of inspection, allsculta� tion, percussion, and palpation. Physicians and nurses usually per form this examination on a daily basis in the acute care setting; however, physical therapists can also petform this examination to help delineate between systemic and musculoskeletal pain.
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ACUTF CARE IiANDBOOK FOR I'HYMCAI 11IERAI'ISTS
Table 8-2. Structure and Function of the Primary Organs of Digestion Structure
Function
Oral cavity
Entrance to the gastrointestln31 system, mecham cal and chemical digestion begins here
Pharynx
Involved in swallowing and mechanical movemcnr of food to esophagus
Esophagus
Connects mouth to the srom3ch, transports and disperses food
Stomach (cardia, fundus, body, pylorus)
Mechanical (unctIons: storage, mixing, and
grinding of food and regulation of outflow to small intestine EXOCrine f,mctiorls: secretion of hydrochloric acid, intrinsic factOr, pepsinogen, and mucus necessary for digestion Endocrine fu'''tiotls: secretion of hormones that
trigger the release of digestive enzymes from the pancreas, liver, and gallbladder IOto the duodenum Small inrestine (duodenum, jejunum) ileum)
Duodenum: neutralizes acid in food transported
from the stOmach and mixes pancreatic :lnd biliary secretions with food Jejullum: absorbs nutrients, W:lter, and
electrolytes Ileum: absorbs bile acids and intrinsic factors to
be recycled In the body-necessary to prevent Vitamin BIZ deficiency Large inrestine (cecumj appendix; ascending, transverse, descend· lng, and sigmoid coJonj rectumj 3nus)
Absorbs water and electrolytes Stores and eliminates mdigestible matenal as feces
Sources: Data from JC Scanlon, T Sanders (eds). Essentials of AnafOl11Y and Physiulogy (2nd ed). Philadelphia: FA Davis. 1993;362; :ll1d AC Guyron, JE Hall (eds). Textbook of Medicall)hysiology (9th ed). Philadelphia: Saunders, 1996;803-844.
GASTROINTESTINAl SYSTEM
Table
505
8-3. Structure and Function of the Accessory Organs of Digestion
Srructure
Function
Teeth
Break down food {Q combine with saliva. Provides taste sensations by cranial nerve VII (taste).
Tongue
Keeps the food between the teeth {Q maintain efficient chewing action for food
{Q
mix with saliva.
S.lhvary glands
Produce saliva, which is necessary to dissolve food for
Llvcr
Regulates serum levels of fats. proteins, and carbohydrates.
tasting and moistens food for swallowing. Bile I� produced in the liver and is necessary for the �lbsorption of lipids and lipid-soluble substances. The liver also assists with drug metabolism and red blood cell and vltamm K production. G..lllhiadder
Stores and releases bile IIltO the duodenum via the hepatic
Pancreas
Exocrme portion secretes bicarbonate and digestive
duct when food enters the stomach. cl11.ymes into duodenum. Endocrine portion secretes insulin, glucagons, and numerous other hormones IO{Q th e bloodstream, all of which are essential in regulating blood glucose levels. Spleen·
Filters out foreign substances and degenerates blood cells from the bloodstream. Also stores lymphocytes.
·Thc '>pleen
.\
not part 01 rhe ga�trolllre!lrmal system bur l!i localed ncar orher gas
rrolllre�rinal component!.
111
Ihe .lbdonunal caviry.
Source�: Data from JC Scanlon, T Sanders. Essentials of Anatomy and Physiology (2nd ed). PhLl.1delphta: rA DaVIS, 1993; and AC Guyron, JE Ilall. Texrbook of Medical Phys Iology (9th cd). Philadelphia: S"unders, 1996;803-844.
History Before performing the physical examination, the presence or absence of Items related to GI pathology is ascertained through patient inter view, questionnaire completion, or chart review. For a list of these items, see Table 8-4. Appendix I-A also describes the general medical record review. Inspection Figure 8-2 demonstrates the abdominal regions associated with organ location. DUring inspection, the physical therapist should notc asymmetries in size and shape in each quadrant, umbilicus
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AClJfE CARE HANDBOOK FOR PHYSICAL TI-lERAI'ISTS
Table
8-4. Items Associated with Gastrointestinal Pathology Stool and Urine
Signs and Symptoms
Characteristics
Associated Disorders
Nausea and vomiting
Change In stool color
History of hernia
Hemoptysis
Change in urine color
History of hepatitis
Constipation
Hematochezia (bright
Drug and alcohol
Diarrhea
red blood in srool)
Jaundice
Melena (black, tarry
Heartburn
abuse Fatty food inrolerance
stools)
Abdominal pain Sources: Data from MB Koopmeiners. Screening for Gastrointestinal System Disease. In WG Boisonnauh (cd), Exammation In PhYSical Therapy Practice. New York: Churchill LivingstOne, 1991; 1 13; and CC Goodman. The Gastrointestinal System. In
CC Goodman, WG Boisonnault (eds), Pathology: Implications for the Physical Thera pist. Philadelphia: Saunders, J 998;456-460.
appearance, and presence of abdominal scars indicative of previ ous abdominal procedures or trauma. The presence of incisions, tubes, and drains should also be noted during inspection, because these may require particular handling or placement during mobil ity exercises. I
Righi upper
lefl�r
""" GaI_
s_
"""'"' Colon (hegebc llexure and lransverse) Pancntes KlOOey and adrenal gland Kd1ey and adrenal gland DuOCl8nt.m with head of pancreas Colon (spleric t\eJcUfe and IransvetSeJ Smallnlestlne SmaI in186lnt (jejl.R.lm) Right lower t..fllower
Smallnleslne
Figure
8-2. The four abdominal quadrants. shOlv'''g the vIscera found III
each. (With permission from N Pa/astanga, D Field, R Soames. Anatomy and Human Movement: Structure and Function {2nd ed}. Oxford, UK: B"tter� worth-Heinemann,
1989;783.)
GASTROINTESTINAL SYSTEM
507
Clinical Tip Changes in abdominal girth, especially enlargement, should be documented by the physical therapist. In addi tion, the nurses and physicians should be notified. Abdom inal enlargement may hinder the patient's respiratory and mobility status.
Auscultation The abdomen is auscultated for the presence or absence of bowel sounds and bruits (murmurs) to help evaluate gastric motility and vascular flow, respectively. Bowel sounds can be altered postopera tively, as well as in cases of diarrhea, intestinal obstruction, paralytic ileus, and peritonitis. The presence of bruits may be indicative of renal artery stenosis. I Percussion Mediate percussion is used to evaluate liver and spleen size and bor ders, as well as ro identify ascitic fluid, solid- or fluid-filled masses, and air in the stomach and boweL' The technique for mediate percus sion is described in the physical examination section of Chapter 2. Palpation Light palpation and deep palpation are used to identify abdominal tenderness, muscular resistance, and superficial organs and masses. The presence of rebound tenderness (i.e., abdominal pain worsened by a quick release of palpatory pressure) is an indication of peritoneal irritation from possible abdominal hemorrhage and requires immedi ate medical attention. Muscle guarding during palpation may also indicate a protective mechanism for underlying visceral pathology.'
Diagnostic Stlldies Discussion of the diagnostic evaluation for the GI system will be divided into ( I ) the examination of the GI tract and (2) the examina tion of the hepatic, biliary, pancreatic, and splenic systems. Examina tion of the GI tract includes the esophagus, sromach, and the intestines (small and large). Table 8-5 summarizes the laboratory tests
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Table 8-5. Laboratory Tests for the Gastroimestinal System-
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Test
Descripcion
Ca,rcinoembryonic amigen (CEA) Reference value: Adul, nonsmoker 4.5 gl5 hrs Whole blood Adul, (25-g dose) >25 gl2 hrs
Purpose: investigate the cause of steatorrhea, to diagnose mal absorption syndrome, and to evaluate digestive ability of duodenum and jejunum. A 25-g dose of D-Xylose (carbohydrate) mixed in 250 ml of water is ingested by the patient. Blood samples are drawn periodically in the next 2 hrs. All urine samples for the next 5 rus are also measured. Decreased levels of D-Xylose recovered in the blood or urine during those time periods could indicate malabsorption. Purpose: to evaluate the ability of the stomach to produce acid secretions in a resting state and after maximal stimulation. Stomach acids are aspirated by a nasogasrric rube during rest ing states (basal output) and after injection of pentagastrin to stimulate gastric acid stimulation (peak output). Increased values can occur with duodenal ulcers and Zollinger Ellison syndrome. Decreased values can occur with gastric ulcers or cancer:
Gastric stimulation test (tube gastric analysis, pemagastrin stimulation test, gastric acid srimulacion test) Reference value: gastric pH 1.5-3.5 Basal acid output: Male, 0-10.5 mEqlhr; female, 0-5.6 mEq/hr Peak acid Output: Male, 12-60 mEq/hr; female, 8-40 mEqlhr
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Gastrin Reference value: 25-90 pg/ml
Helicobacter pylori tests
Serologic test Reference value: immunoglobulin G negative Urea breath test
Purpose: used to confirm the diagnosis of Zollinger-Ellison syn drome. Elevated levels of gastrin in venous blood occurs with Zollinger-Ellison syndrome. Purpose: to confirm the diagnosis of H. pylori infection, which is the cause of most peptic ulcers and is a proven carcinogen for gastric carcinoma. Purpose: identifies the presence of immunoglobulin G antibody [0 H. pylori in the blood. Purpose: identifies the presence of H. pylori in the stomach.
Reference value: negative Tissue biopsy Reference value: negative for H. pylori 5-Hydroxyindoleacetic acid (5-HlAA) Reference value: 1-9 mg/24 hrs
Lactose tolerance test (oral lactose tolerance test) Reference value: Blood glucose >30 mg/dl Urine lactose 12-40 mg/dl in 24 hrs
Purpose: to visualize the H. pylori bacteria. A tissue biopsy is obtained during an endoscopy procedure and microscopically examined. Purpose: used to diagnose carcinoid tumor and provide ongo ing evaluation oJ tumor stabiliry. 5-HlAA is a urinary metabolite of serotonin and is produced by most carcinoid tumors. Purpose: to identify lactose intolerance-lactase deficiency as a cause of abdominal cramps and diarrhea, as well as to help identify the cause of malabsorption syndrome. An oral dose of lactose is provided to a fasting patient, and serial blood and urine samples are measured. Minimal rise in blood glucose or urine lactose levels indicates lactose intolerance-lactase deficiency.
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Test
Description
Occult blood (fecal occult blood test, FOBT, FOB) Reference value: negative
Purpose: used as a screening tool for early diagnosis of bowel cancer. Three stool specimens are collected and examined for the pres ence of occult (nonvisible) blood in the feces, which can be indicative of adenocarcinoma and premalignanr polyps in the colon. Purpose: used to derect carcinoid rumor. Venous blood levels of serotonin 3re measured, as carcinoid rumors secrete excess amouncs of serotonin.
Serotonin (5-hyclroxytryptamine) Reference value, 50-200 ng/ml
·Text or abbreviations in parentheses signify synonyms to the test names. Source: Data from LM Malarkey, ME McMorrow. Nurse's Manual of Laboratory Tests and Diagnostic Procedures. Philadelphia: Saunders, 2000,412-431.
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511
used to measure functional aspects of secretion, digestion, absorption, and elimination within the GI tract.' Table 8-6 summarizes diagnostic procedures used to visualize the GI tract. Examination of the hepatic (liver), biliary (gallbladder and cystic ducts), pancreatic, and splenic systems involves numerous laboratory tests and diagnostic procedures, which are often performed concur rently to fully delineate the etiology of a patient'S clinical presenta tion. Because of the common location of these organs and shared access to the biliary tree, di ease or dysfunction in one organ can often extend into the other organs.)
Clinical Tip Laboratory tests used to examine the liver are frequently referred to as liver (llllction tests or LFTs.
Hepatocellular injury results in cellular damage in the liver, which causes increased levels of the following enzymes: aspartate ami notransferase (previously called serum glutamic-oxaloacetic transami nase), alanine aminotransferase (previollsly called serum glutamate pyruvate transamhlose), and lactate dehydrogenase.4 Hepatocellular dysfunction can be identified when bilirubin levels are elevated or when clotting times are increased (denoted by an increased prothrombin time). The liver produces clotting facrors and, therefore, an increased prothrombin time implicates impaired produc tion of coagulation facrors. Cholestasis is the impairment of bile flow from the liver to the duodenum and results in elevarions of the following serum enzymes: alkaline phosphatase, aspartate transaminase (previously known as )' glutamille-oxaloacetic transaminase or y-glutamyl trallspeptidase), and S!-nucleoridase.4 Table 8-7 summarizes the laboratory tests performed ro measure hepatic, biliary, and pancreatic function, whereas Table 8-8 sum marizes the diagnostic procedures performed to visllalize these organs. Additional diagnostic procedures used ro evaluate the GI system are laparoscopy, magnetic resonance imaging (MRI), and positron emission tomography (PET) scans. These methods are described in the following sections.
Table 8-6. Diagnostic Procedures for the Gastroinrestinal (GI) System" Test
Description
Barium enema (BE) Reference value: No lesions, deficits, or abnormalities of the colon are noted.
Purpose: To investigate and identify pathologic conditions that change the structure or function of the colon (large bowel). The colon is emptied of feces, and contrast medium (barium) is instilled rec tally. Fluoroscopic and x-ray images are then taken to idemify the presence of any structural anomalies. Purpose: To idenrify pathologic conditions that change the structure or function of the esophagus. The patient takes repeated swallows of barium liquid while x-ray and fluoroscopic images are taken in vertical, semivertical, and horizontal positions to examine the passage of contrasr medium during swallowing and peristaltic movement of the esophagus.
Barium swallow (esophagography) Reference value: No structural or functional abnormalities are visualjzed.
Colonoscopy (lower panendoscopy) Reference value: No abnormalities of struc ture or mucosal surface are visualized in the colon or terminal ileum.
Computed romography of the GI rraer (ef scan, computerized axial romography [CATJ)
Purpose: To perform routine screening of the colon for the presence of polyps or rumors and to investigate the cause of chronic diarrhea or other undiagnosed Gl complaints. Patients are sedated, and an endoscope is inserted inro the rectum and passed through the various parts of the colon. Tissue biopsy may be performed during this procedure. Purpose: Used to detect intra-abdominal abscesses, rumors, infarctions, perforation, obstruction, inflammation, and diverticulitis. Metastases ro the abdominal cavity can also be detected. lntravenous or oral contrast may be used during the procedure.
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Roentgenography of the abdomen (abdominal flat plate) Reference value: No abnormalities visual ized. Sigmoidoscopy and anoscopy Reference value: No tissue abnormalities are visualized in the sigmoid colon, rectum, or anus. Upper GI series and small bowel series (small bowel follow-through) Reference value: No structural or functional abnormalities are found.
·Text or abbreviations
in parentheses signify synonyms
Purpose: To provide information about rumors, swelling of the mucosa, abscess farmarion, fluid in the intestinal lumen, intestinal obstruction, and calcifications in the GI tract. Plain x-ray is taken of the abdomen. Purpose: Sigmoidoscopy is used as a screening tool for colon cancer and to investigate rhe cause of rectal bleeding or monitor inflammatory bowel disease. Anoscopy is used to investigate bleeding, pain, discomfort, or prolapse in the anus. Purpose: Detects disorders of strucrure or function of the esophagus, stomach and duodenum, and jejunum and ileum (the latter two are for the small bowel series). Imaging studies of all these areas are performed while the patient drinks a barium solution. Passage of the barium through these structures can range from 30 mins ro 6 hrs. (0
rhe tesr names.
Source: Data from LM Malarkey, .ME McMorrow (eds). Nurse's Manual of Laboratory Tests and Diagnosric Procedures. Philadelphia: Saun ders, 2000;432-468.
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Table 8-7. Laboratory Tests for the Hepatic, Biliary. and Pancreatic Systems'"
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Test
Involved Systems
Purpose
Alanine aminotransferase (ALT, glutamicpyruvic transaminase ICPTI, SG� transaminase) Reference value: 10-35 IU/liter
Hepatic
Used to detect hepatocellular injury. Very specific in detecting acute hepatitis from viral, [Oxic, or drug-induced causes.
Alkaline phosphatase (ALP, total alkaline phosphatase IT-ALPll Reference value: 4.5-13.0 King-Armstrong unitsldl
Hepatic, biliary
Alkaline phosphatase isoenzymes (I-ALP) Reference value: liver isoenzymes 50-70%
Hepatic, biliary
Used to distinguish between liver and bone pathology when total serum ALP is elevated. T here are ALP isoenzymes for both liver and bone.
Alpha l -fetoprotein (AFP1) Reference value: Z "
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GENITOURINARY SYSTEM
595
Clinical Tip • Pulmonary hygiene treatments can be performed during dialysis; however, this depends on the hemodynamic sta bility of the patient and is at the discretion of the nurse or physician. Extreme caution should be taken with the access site to prevent accidental disruption. • The dialysis nurse is generally nearby to monitor the procedure and is a valuable source of information regard ing the patient's hemodynamic stability. • Activity tolerance can be altered when fluid and electrolyte levels are unbalanced. Patients will demonstrate variable levels of fatigue; some are more fatigued before a dialysis session, whereas others are more fatigued after a dialysis session. • Fluid and electrolyte imbalance can also alter the hemo dynamic responses to activity; therefore, careful vital sign and symptom monitoring should always be performed.
Surgical Interventions Surgical interventions for genitourinary system disorders can be cate gorized broadly as procedures that remove diseased portions of the genitourinary tract or procedures that restore urinary flow. These interventions are briefly discussed in the following sections. Refer to Appendix V for general postoperative considerations. Nephrectomy There are three types of nephrectomy. The primary indications for removing a part or all of the kidney include renal tumor, polycystic kid ney disease, severe traumatic injury to the kidney, and organ donation, as well as removing a failing transplanted organ.47•48 Nephrectomy can be performed as an open or laparoscopic procedure. Open nephrectomy is the conventional method that requires an incision of approximately 7 in. Laparoscopic nephrectomy involves five access sites, ranging from less than 0.5 in. to 3 in. Laparoscopic nephrectomy is gaining acceptance as a viable alternative to open nephrectomy, as there have been fewer postop erative complications associated with the procedure.47-s o The types of nephrectomy and their definitions follow:
Radical nephrectomy-removal of the entire kidney, a section of the ureter, the adrenal gland, and the fatty tissue surrounding the kidney.
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AClTrE CARE HANDBOOK FOR I)HYSICAL TIIERAPISTS
Simple nephrectomy removal of rhe entire kidney wirh a secrion of the ureter. Generally performed when harvesting donor organs for kidney transplantation. Partial Ilephrectomy-only the infected or diseased portion of the kidney is removed. -
Open Prostatectomy Open prostatectomy is the surgical removal of a prostate gland with or without irs capsule and is primarily indicated for parienrs with prostare cancer. Five types of surgical approaches can be used: ( 1) transcoccygeal, (2) perineal, (3) retropubic, (4) transvesical, and (5) suprapubic. This procedure is contraindicated if the prostate is small and fibrou . The suprapubic and retropubic approaches of this procedure are contraindicated in the presence of cancer.42
Transurethral Resection Transurethral resectioll refers to the surgica I approach performed when managing bladder tumors, bladder neck fibrosis, and pros tatic hyperplasia. The most common type of transurethral resec tion is a TURP, which this section focuses on. TURP is indicated for obstructive BPH. Involved tissues arc resected with a resecto scope that is inserted through the urethra. Excision and coagulation of tissue are accompanied by continuous irrigation. Conrra-indica tions for TURP include the presence of urinary tract infection and a prostate gland weighing more than 40 g. TURP is also contrain dicated with conditions that interfere with operative positioning for the procedure, such as irreversible scrotal hernia or ankylosis of the hip."
Percutaneous Ncph.roscopic Stone Removal Percutaneous nephroscopic stone removal involvcs rhe removal of stones formed in the urinary tract with a perclltaneous nephrostomy tube that is placed under fluoroscopic monitoring. Depending on the size of the stone, stones may need to be broken up, thcn removed with a basket. Small fragments can be flushed through the system mechan ically or physiologically. Considerations for this procedure include controlling septicemia before removal of the stones.42 Open Urologic Surgery Open urologic surgery is a large category of surgical procedures that is beyond the scope of this chapter but includes the following"; •
Nephrolithotomy (renal incisions for kidney stone removal)
GENrrQURINARY SYSTEM
•
597
Pyelolithotomy (removal of the kidney stone from the pelvis of the
kidney) •
Ureterolithotomy (removal of a urinary srone from the ureter)
•
Cystectomy (bladder removal)
Bladder Neck Suspension Bladder neck suspension is a procedure used in women ro help resrore urinary continence by suturing the urethra to the pubic bones, which increases urethral resistance. It is indicated for women with stress incontinence as a result of pelvic relaxation. This procedure may also be called the Marshall-Marchetti-Krantz procedure or retropubic 5115pension. Bladder neck suspension is contraindicated in cases of ure thral sphincter damage leading to stress inconrinence.42,51.52 Urinary Diversion Obstructed urinary flow can be resolved by diverting urine with any of rhcse four procedures: (I) supravesical diversion, (2) incontinent urinary diversion, (3) continent urinary diversion and, (4) orthotopic bladder substitution"'" 5upravesical Diversion
A supravesical diversion is one in which the urine is diverted at the level of the kidney by nephrostomy. Nephrostomy involves placing a catheter through the renal pelvis and into the renal calyces to temporarily drain urine into an external collection device (Figure 9-7). Complications, such as stone formation, infection, hemorrhage, and hematuria, can be associ ated with long-term ncphrostomy tube placement."'" Incontinent Urinary Diversion Incontinent urinary diversion involves diverting urine flow to the skin through a stoma, which rhen requires an external appliance to collect urine. Segments of the ileum or colon are generally used as a conduit to bridge the gap from the ureter to the skin when the bladder must be removed or bypassed (see Figure 9-7). Once the diversion is com plete, urine drains from the Stoma into the collecting device every few seconds. These segments of intestine become totally isolated from the gastrointestinal rracr.3.47 Bladder carcinoma and severe neuropathic bladder dysfunction are common indications for this procedure. Continent Urinary Diversion COlltillent urinary diversions are internal urine reservoirs that are sur gically constructed from segments of the ileum, ileocecal segment, or colon. The internal reservoirs eliminate the need for external appli-
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AClITE CARE HANDBOOK FOR I'HYSICAL THERAPISTS
Isolated ileal segment with ureters implanted in posterior portion of segment
Protruding abdominal
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A
B
Ileal segment anastomosed to sigmoid colon Left ureter anostomosed to right ureter
C
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Cutaneous ureterostomy on abdomen
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Isolated ileal segment with ureters implanted in posterior portion of �menl Stab woond on skin _ISTS
to work and may need assistance at home from family members or even require transfer to a rehabilitation faciliry. Whether the patient is pre- or post-transplantation, physical thera pists focus on recondirioning patients to their maximum functional level and should have a basic knowledge of the patient's end-stage organ disease. The objectives for this chapter are to provide informa tion on the following: 1. The transplantation process, including criteria for transplantation, organ donation, and postOperative care 2. Complications rejection and infection 3.
after
organ
transplantation,
including
The various types of organ transplantation procedures
4. Guidelines for physical therapy intervention with the transplant recipient
Types of Organ Transplants
The kidney, liver, pancreas, heart, and lung are organs that are pro cured for transplantation. The most frequent of those are the kidney, liver, and heart.2 Double transplants, such as liver-kidney, kidney pancreas, and heart-lung, are performed if the patient has multiorgan failure. Although bone marrow is not an organ, bone marrow trans plantation (BMT) is a common type of tissue transplant that will be discussed.
Criteria for Transplantation
Transplantation is offered to patients who have end-stage organ dis ease for which alternative medical or surgical management has failed. The patient typically has a life expectancy of less than 1-3 years.J-5 Criteria for organ recipients vary, depending on the type of organ transplant needed and the transplant facility. The basic criteria for transplantation include the following': • The presence of end-stage disease in a transplantable organ
The failure of conventional therapy to treat the condition successfuII y
•
ORGAN TRANSPLANTATION
699
• The absence of unrrearable malignancy or irreversible infection • The absence of disease that would attack the ttansplanted organ
or tissue In addition ro these criteria, transplant candidates muSt demon Strate emotional and psychological stability, have an adequate support system, and be willing to comply with lifelong immuno suppressive drug therapy. Other criteria, such as age limits and absence of drug or alcohol abuse, are specific to rhe transplant facility. To determine whether transplantation is the best treatment option for the individual, all transplant candidates are evaluated by a team of health care professionals consisting of a transplant surgeon, transplant nurse coordinator, infectious disease physi cian, psychiatrist, social worker, and nutritionist. The patient undergoes many laboratory and diagnostic studies during the eval uation process. Acceptable candidates for organ transplantation are placed on a waiting list. Waiting times for an organ may range between 1 and 4 years. 37 • organ to become available.
Transplant Donation
Cadaveric Oa./Ors Cadaveric donors are brain-dead individuals who have had severe neurologic trauma, such as from head or spinal cord injury, cerebral hemorrhage, or anoxia.8 Death must occur at a location where car diopulmonary support is immediately available to maintain the potential organ donor on mechanical ventilation, cardiopulmonary bypass, or both; preserve organ viability; and prevent ischemic dam age ro viral organs." The cadaveric donor must have no evidence of malignancy, sepsis, or communicable diseases, such as hepatitis B or human immunodeficiency virlls. 6.9, I O
Living DOllors Because there are nOt enough cadaveric organs donated to meet the needs of all potential recipients, living donor transplantation offers an alternative means of organ donation. Living donors are always used
700
ACUTE CARE HANDBOOK FOR PHYSICAL THI:.RAI'ISl'S
for bone marrow transplants, often used for kidney transplants, and sometimes used for liver, lung, and pancreas transplantation. They may be genetically or emotionally related to the recipient-that is, they are a blood relative (e.g., sister) or non-genetically related indi vidual (e.g., spouse or close friend). Living donors also are evaluated by the transplant team to determine medical suitability. The age of a potential donor can r.nge from a term newborn to 65 years, depending on the organ considered for donation and the recipi ent. Donors do not have a history of drug or alcohol abuse, chronic disease, malignancy, syphilis, tuberculosis, hepatitis B, or human immunodeficiency virus infection. Ideally, the donor's height and weight approximate those of the recipient for the best "fit."
Donor Matching
The matching of a cadaveric or living donor with a recipient depends on the following factors: • ABO blood typing •
Histocompatibility typing
•
Size
The donor and recipient muSt be ABO blood type identical or com patible." The process of finding compatible donors and recipients is called tisslle typing or histocompatibility typing. Histocompatibility typing attempts to match the human leukocyte antigens (HLAs), which are the antigens that cause graft rejection. It is performed sero logically by adding a standard panel of typing antisera, complement, and ttyphan blue stain to purified lymphocytes and then observing the lymphocytotoxicity. 12 The better the histocompatibility match and degree of genetic similarity between the donor and the recipient, the less severe is the rejection response. In living related donors, an identical match is ideal; however, a half match is acceptable. 9 Also, a white cell crossmateh is performed in which the lymphocytes from the donor are mixed with the serum from the recipient and then observed for immune responses. A negative crossmatch indicates no antibody reaction and that the recipient's antibodies are compatible with the donor. A negative crossm.tch is required for successful kidney and kidney-pancreas transplants.7
ORGAN TRANSPLANTATION
701
Although pretransplant tissue typing is ideal, it is not always per formed. Somerimes, there is insufficient time to perform HLA ryping between donor and recipient because of the short cold ischemic times for different organs. '2 Owing to the shorr ischemic time of less than 6 hours for orthotopic cardiac transplants, ABO blood type compatibil ity, body weight, and accrued waiting time are used for allocation of the donor heart.!·'o A lung transplant recipient is matched on the basis of ABO blood rype and size, because the ischemic time is less than 4 hours. s A size match is based on the donor's height, weight, and thoracic dimensions as determined by chest radiograph.13 In the United States, organ procurement and distribution for trans plantation are administered by the United Network for Organ Shar ing (UNOS). UNOS sets the standards for ttansplant centers, transplant physicians, tissue ryping laboratories, and organ procure ment organizations. UNOS distributes organs based on the severity of the recipient's illness, blood type, donor-recipient weight match, and length of recipient waiting time. 14
General Post-Transplantation Care and Complications
Postoperative Care for Livittg Dottors PostOperative care for living donors is similar to that of any patient who has undergone major abdominal or cardiothoracic surgery. These patients are taken off mechanical ventilation in the recovery room and transferred to the general surgery or transplant ward. Vital signs and blood countS are monitored closely for possible postopera tive bleeding. Patients are usually out of bed and ambulating on post operative day 1 . On average, the duration of donor hospitalization may range from 3 days for a kidney donor to 8 days for a simulta neous pancreas-kidney (SPK) donor. ',1S
Postoperative Care for Tra1lsp[atlt Recipiettts Once an organ is transplanted, the postOperative care focuses on the monitoring and treatment of the following" : •
Allograft function
•
Rejection
702
AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
•
Infection
•
Adverse effects of immunosuppressive drugs
General postoperative care for rransplant recipients is also similar to the care patients receive after major abdominal or cardiothoracic surgery. Except for kidney transplant recipients, who are normally extubated before leaving the operating room, most patients are trans ferred from the operating room to the surgical intensive care unit, where they are weaned from mechanical ventilation within 24 to 48 hours.",I6,1 7 Once extubated and hemodynamically stable, recipients are transferred to specialized transplant floors. Nursing staff monitors the recipient closely for signs and symptoms of infection and rejec tion, which are the leading causes of morbidity and mortality in the first year after transplantation. Complications from postoperative transplantation may contribute to an increased length of hospital stay or hospital readmissions. They can be grouped to include the following types: •
Surgical
•
Medical
•
Rejection
•
Infection
Surgical complications include vascular problems, such as thr ombo sis, stenosis, leakage at anastomotic sites, and postoperative bleeding. Medical complications may include fluid overload or dehydration, elec trolyte imbalance, or hypertension.
Rejection The major problem in organ transplantation is nOt the technical diffi culties of surgery, but rather organ rejection, or the tendency of the recipient's body to immediately reject anything that is "nonself. " Graft rejection is actually a normal immune response to invasion of foreign matter, the transplanted organ or tissue. Some degree of rejec tion is normal; however, if the patient is not treated with immunosup pressive drugs, the donor organ would be completely rejected and cease to be viable in 10 days. IS Transplant recipients must receive
ORGAN TRAN5I'I.ANTAT10N
703
immunosuppressive drugs for the rest of their lives to suppress or minimize rejection of their transplanted organs. The pharmacologic agents most often used to prevent organ rejection include a double or triple drug therapy, consisting of a combination of tacrolimus or cyclosporine with methylprednisolone, and azathioprine or mycophe nolate mofetil." See Table 12-1 for common immunosuppressive medications used in organ transplantation. These immunosuppressive drugs decrease the body's ability to fight infection. A delicate balance must be reached between sup pressing rejection and avoiding infection. Insufficient immunosup pression may result in rejection that threatens the allograft and patie nt survival, whereas excessive immunosuppression increases the risk of infection and malignancy. 14 If detected early, rejection can be minimized or reversed with an increase in daily doses of immunosuppressive drugs. When treating postoperative transplant recipients, it is important to monitOr for adverse side effects of the immunosuppressive drugs. Immunosuppression protocols now promote the rapid tapering of ste roids post transplantation, which diminishes the harsh side effects of the drug. zo
Types of Graft Rejectioll There arc three types of graft rejection: hyperacute, acute, and chronic. I. Hyperacute rejection is characterized by ischemia and necrosis of the graft that occurs from the time of transplant to 48 hours after transplant· It is believed to be caused by ABO incompatibility and by cytotox ic antibodies present in the recipient that respond to tissue antigens on the donor organ. The manifestations of hyperacute rejection include general malaise and high fever. Rejection occurs before vascularization of the graft takes place. Hyperacute rejection is unresponsive to treannenr and removal of the rejected organ is the only way to stOp the reaction. Therefore, the recipient will need immediate retransplantation to survive.6,12,21
ACllte rejection is a treatable and reversible form of rejec2. tion that occurs within the fi rst year after transplantation. Almost every patient has some degree of acute rejection after transplanta tion. T lymphocytes detect foreign antigens from the graft, become
Table 12-1. Immunosuppressive Drugs Used in Organ Transplanrarion
C! ...
immunosuppressive Drug
Action
Possible Adverse Effects
>
Corticosteroids (methyl
inhibit gene transcription for
Muscle loss and weakness, hypertension, hyperglycemia,
�
prednisolone [Solu
cytokines, which affect all
delayed wound healing, osteoporosis, weight gain, peptic
Medral], prednisone)
immune responses
ulcers, cataracts, hypokalemia, mood swings, congestive
Inhibit T-cell activation
heart failure
Used to reverse early rejection Cydosporine (Neoral, Sandimmune)
Inhibits immune responses by inhibiting T-ceil lymphokinc
Hypertension, elevated cholesterol, renal dysfunction, [remOl; sodium retention, hyperkalemia, hyperglycemia, pares
production and cell-mediated
thesias, hepatic dysfunction, seizures, hirsmism, gum
immunity by blocking
hyperplasia, malignancy; long-term side effects: diabetic
transcription of early
neurotoxicity, decreased bone density
activation genes reverse, acme rejection Prograf)
Inhibits T-Iymphocyte activation Used to prevent acute rejection
Tremors, headache, hepatotoxicity, hypertension, hyperglycemia, hyperkalemia, constipation, diarrhea, nausea, vomiting, renal dysfunction, mental status changes
Azathioprine Omuran)
Inhibits lymphocyte proliferation Inhibits DNA and RNA synthesis Blocks antibody production Suppresses emire immune system
'" r >
6
g'" " "
:t i2i
n > ,...
Used to prevent, rather than Tacrolimus (FK506,
� '"
Bone marrow suppression, heparotoxicity, pancreatitis, cholestasis
::l � > �
�
Mycophenolare mofetil (CelICepr)
Inhibits T· and B-Iymphocyte proliferarion
Nausea, vomiting, diarrhea, leukopenia, neutropenia, sepsis, abdominal pain
Suppresses anribody formation Inhibits de novo parhway for purine synthesis Muromonab-CD3 (Orrhodone OKT3)
Inhibits T-cell function and proliferation Used only for acute rejection that
Chest pain, fever, nausea, vomiting, diarrhea, pulmonary edema, dyspnea, malignant lymphoma, rigors, malaise, meningitis
is refractory to other agents Sources: Adapted from JM Black, E Marassarin-Jacobs (eds). Medical-Surgical Nursing: Clinical Management for Continuity of Care (5rh ed). Philadelphia: Saunders, 1997;644-645; L Bucher, S Melander. Crirical Care Nursing. Philadelphia: Saunders, 1999;343; and data from E Winkel, VJ DiSesa, MR Costanzo. Advances in heart rransplantarion. Dis Man 1999;45(3):77-79.
o ,.
C) ,.
Z
� � !;:
�
o z
Cl
�
APPENDIX 1-8: AClITE CARE SETIlNG
757
wake cycles and partial or complete hypothalamic and autonomic brain stem functions but a lack of cerebral cortical function for longer than I momh afrer acute traumatic or nontraumatic brain injury or metabolic or degenerative disorders.s The initial clinical criteria for brain death include coma and unresponsiveness, absence of brain stem reflexes, and cerebral motor responses to pain in all extremities, apnea, and hypothermia.' Brain death is usually confirmed by cerebral angiog raphy, evoked potential testing, electroencephalography, or transcranial Doppler sonography.' Refer to Chapter 4 for more information on these neurologic diagnostic tests.
Intensive Care Unit Setting The ICU, as its name suggests, is a place of intensive medical-surgical care for those patients who require continuous monitoring, usually in conjunction with thcrapies such as vasoactive medications, sedation, cir culatory assist devices, and mechanical ventilation. ICUs may be named according to the specialized care that they provide, such as the coronary care unit (CCU) or surgical ICU. The patient in the ICU requires a high acuity of care; thus, the nurse to patient racio is onc to one or one to two.
Com mOil Patiellt and Family Respo1tses to the /lIte1tsiue Care Ullit • Behavioral changes or disturbances can occur in the patient who is critically ill as a result of distress caused by physically or psycho logically invasive, communication-impairing, or movement-restrict ing procedures.'o When combined with the environmental and psychological reactions to the ICU, mental status and personality can be altered. Environmental stresses can include crowding, bright overhead lighting, strong odors, noise, and touch associated with procedures or from those the patient cannot see.IO Psychological stresses can include diminished dignity and self-esteem, powerless ness, vulnerability, fear, an.xiety, isolation, and spiritual distress. 10 • ICU psychosis is a state of delirium that occurs between the third and seventh day in the ICU and is described as a "fluctuating state of consciousness characterized by features such as fatigue, confusion, distraction, anxiety, and hallucinations." II Delirium in the leU, which is reversible, is thought to be caused by pain, the side effects of drugs, and the ICU environment." Precipitants to delirium
758
ACtJrE CARE HANDBOOK FOR PHYSICAL TI-IERAI'ISTS
include a history of dementia, Alzheimer's disease, substance abuse, and chronic illness as well as advanced age, severe infection, fluid and electrolyte imbalance, hypoxia, and metabolic disorders." Treatment for delirium consists of antipsychotic medications (e.g., haloperidol), the discontinuation of nonessential medications, proper oxygenation and hydration, and the company of family or others. 13 The patient'S family is usually overwhelmed by the ICU. Family members may experience fear, shock, anxiety, helplessness, anger, hostility, guilt, withdrawal, or disruptive behaviors.!O Like the patient, the family may be overwhelmed by the timuli and tech nology of the ICU, as well as the Stress of a loved one's facing a critical or life-threatening illness . •
• The transfer of a patient from the ICU to a general floor can also be a stress to the patient and family. Referred to as transfer anxiety, the patient and family may voice concerns of leaving staff that they have come to recognize and know by name; they may have to learn to truSt new staff,!O or fear that the level of care is inferior to that in the leu. To minimize this anxiety, the physical therapist may continue to treat the patient (if Staffing allows), slowly transition care to another therapist, or reinforce with the patient and family that the general goals of physical therapy are unchanged.
CriricalIllness PolyneuropatlJY Critical illness polyneuropathy is the acute or subacute onset of wide spread symmetric weakness in the patient with critical illness, most commonly with sepsis or multisyStem organ failure, or both.!' The patient presents with distal extremity weakness, wasting, and sen ory loss, as well as parasthesia and decreased or absent deep tendon reflexes.15 The clinical features that distinguish it from other neuro muscular disorders (e.g., Guillain-Barre syndrome) are a lack of oph thalmoplegia, dysauronomia, and cranial nerve involvement and normal cerebrospinal fluid analysis,'4.'5 Nerve conduction studies show decreased motor and sensory action potentials.!S The specific pathophysiology of critical illness polyneuropathy is unknown; how ever, it is hypothesized to be related to drug, nutritional, metabolic,
APPENDIX I-B: AClITE CARE SE"lNG
759
and toxic factors, as well as prolonged leu stay, the number of inva sive procedures, increased glucose level, decreased albumin level' and the severity of multisystem organ failure. IS
eriticalllllless Myopathy Critical illness myopathy, otherwise known as acule quadriplegic myopathy or aClile steroid n1)'opathy, is the acute or subacute onset of
diffuse quadriparesis, respiratory muscle weakness, and decreased deep tendon reflexes IS in the serring of exposure to short- or long term high-dose corticosteroids and simultaneous neuromuscular blockade. I. It is postulated that neuromuscular blockade causes a functional denervation that renders muscle fibers vulnerable to the catabolic effects of steroids. I. Diagnostic tests demonstrate elevated serum creatine kinase levels at the onset of the myopathy, and, if severe, myoglobinuria or renal failure can ensue; a myopathic pattern with muscle fibrillation on electromyography; and a necrosis with dramatic loss of myosin (thick) filaments on muscle biopsy. I.
Sleep Pattern Disturbance The interruption or deprivation of the quality or hours of sleep or rest can interfere with a patienr's energy level, personality, and ability to heal and perform tasks. The defining characteristics of sleep pattern dis/llrbollce are difficulry falling or remaining asleep, with or without fatigue on awakening, dozing during rhe day, and mood alterations.17 In the acute care setting, sleep disturbance may be related to fre quent awakenings related to a medical process (e.g., nocturia or pain) or the need for nursing intervention (e.g., vital sign monitor ing), an inability to assume normal sleeping position, and excessive daytime sleeping related to medication side effects, stress, or environ mental changes." The physical therapist should be aware of rhe patient who has altered sleep patterns or difficulty sleeping, as lack of sleep can impact a patient'S ability to participate during a therapy session. The patient may have rrouble concentrating and performing higher-level cognitive tasks. The pain threshold may be decreased, and the patient may also exhibit decreased emotional control.17
760
AClITE CARE HANDBOOK FOR PHYSICAL TIIERAIIISTS
Confusion Confusion may be acute or chronic (e.g., related to a neurodegenera tive process). Acute confusion frequently occurs in the acute care set ting, especially in the elderly. AClIle cotlf"siotl is defined as "the state in which there is abrupt onset of a cluster of global, Auctuating distur bances in consciousness, attention, perception, memory, orientation, thinking, sleep-wake cycle, and psychomotor behavior. n18 Risk fac tors for confusion related to medications include the use of analgesics, polypharmacy, noncompliance, and inappropriate self-medicating." Other risk factors include dehydration, electrolyte imbalance, hyp oxia, infection, and poor nutrition. Acute or acute on chronic disease states can result in confusion, especially if metabolic in nature. Additionally, a change in environment can exacerbate medical risks for confusion. This includes unfamiliar surroundings, noises, procedures, and staff or a change in daily routine, activiry level, diet, and sleep.
Substance Abuse and Withdrawal The casual or habitual abuse of alcohol, drugs (e.g., cocaine), or med ications (e.g., opioids) is a known contributor of acute and chronic ill ness, traumatic accidents, drowning, burn injury, and suicide.20 The patient in the acute care setting rnay present with acute intoxication or drug overdose or with a known (i.e., documented) or unknown substance abuse problem. The physical therapist is not initially involved in the care of the patient with acute intoxication or overdose until the patient is medi cally stable. However, the physical therapist may become secondarily involved when the patient presents with impaired strength, balance, coordination, and functional mobility as a result of chemical toxicity. It is the patient with unknown substance abuse who is hospitalized for days to weeks who is a challenge to the hospital staff when with drawal (commonly referred to as the DTs, for delirillm Iremetls) occurs. It is beyond the scope of this text to list the symptoms of with drawal of the many different types of drugs. For the purposes of this text, alcohol withdrawal will be discussed because of its relatively high occurrence. Alcohol withdrawal sY/ldrome is the group of signs and symptoms that occur when a heavy or prolonged u er of alcohol (ethanol or ethyl alcohol) reduces alcohol consumption." The signs and symp-
APPENDIX 1-8: AClITE CARE Sl:.TT1NG
761
tolllS of alcohol withdrawal are the resllit of a hyperadrenergic state from increased central nervous system neuronal activity that attempts to compensate for the inhibition of neurotransmitters with chronic alcohol lIse.20 The signs and symptoms of alcohol withdrawal syn drome, which begin 5-10 hours after alcohol use is decreased, are21 •
Tachycardia and hypertension
•
Nausea and vomiting
•
Low-grade feve r
•
Hand tremor
•
Anxiety, insomnia, agitation, or hallucinations
•
Grand mal seizure or delirium (if severe)
Interventions to prevent or minimize alcohol withdrawal syndrome include hydration, adequate nutrition, reality orientation, thiamine, and the prophylactic lise of bcnzodiazepines.
References I. Carpenito Lj. Latex Allergy Response. In Nursing Diagnosis: Applica tion to Clinical Practice (8th cd). Philadelphia: Lippincott, 2000;553557. 2. Smith SF, Duell DJ, Martin BC (cds). Restraints. Clinical Nursing Skills: Basic to Advanced Skills (5th ed). Upper Saddle River, NJ: Prentice Hall Health, 2000;139-146. 3. Downey RJ, Weissman C. Physiological Changes Associated with Bed Rest and Major Body Injury. In EG Gonzalez, SJ Myers, JE Edelstein, er al. (cds), Downey and Darling's Physiological Basis of Rehabiliration Medicine (3rd ed). Boston: Bunerworth-Heinemann, 2001;449. 4. Buschbacher RM, Porter CD. Decondirioning, Conditioning, and the Benefits of Exercise. In RL Braddol11 (cd). Physical Medicine and Reha bilitation (2nd ed). Philadelphia: Saunders, 2000;716. 5. American Association of Critical-Care Nurses. Position Statement on Withholding and/or Withdrawing Life-Sustaining Treatment. In M R Kinney, SB Dunbar, J Brooks-Brunn, et al. (eds), AACN's Clinical Refer ence for Critical Care Nursing (4th ed). St. Louis: Mosby, I 998;12531254. 6. DeVita MA, Grenvik A. Forgoing Life-Sustaining Therapy in Intensive Care. In A Grenvick (ed), Textbook of Critical Care (4th ed). Philadel phia: Saunders, 2000;2110-2 I 13. 7. Schnell S5. Nursing Care of Comatose or Confused Clients. In JM Black, E Matassarin-Jacobs (cds), Medical-Surgical Nursing: Clinical
762
8.
9. 10.
11.
"12.
13.
14.
15. 16.
17.
18. 19.
20.
21.
AClJTE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Management for Continuity of Care (5th ed). Philadelphia: Saunders, 1997;743. Thelan LA, Urden LD, Lough ME, Stacy KM (eds). Neurologic Disor ders. In Critical Care Nursing: Diagnosis and Management (3rd ed). St. Louis: Mosby, 1998;795-798. Sullivan J, Seem DL, Chabalewski F. Determining brain death. Critical Care Nurse 1999;19:37-46. Urban N. Patient and Family Responses to the Critical Care Environ ment. In MR Kinney, 5B Dunbar, J Brooks-Brunn, et al. (cds), AACN's Clinical Reference for Critical Care Nursing (4th ed). Sr. Louis: Mosby, 1998;145-162. Hennemann AE. Preventing Complications in the Intensive Care Unit. In A Grenvick (ed), Textbook of Critical Care (4th ed). Philadelphia: Saunders, 2000;2035-2037. Roberts BL. Managing delirium in adult intensive care patients. Critical Care Nurse 2001 ;21 :48-55. Wise MG, Cassem NH. Behavioral Disturbances. In JM Civetta, RW Taylor, RR Kirby (eds), Critical Care_ Philadelphia: Lippincott-Raven, 1997;2022-2024. Victor M, Ropper AH (cds). Diseases of [he Peripheral Nerves. In Adams and Victor's Principles of Neurology (7th ed). New York: McGraw-Hili, 2001;1388. Juel VC, Bleck PI'. In Grenvik A (ed), Textbook of Crirical Care (4th ed). Philadelphia: Saunders, 2001;1891-1892_ Vicror M, Ropper AH (eds). The Metabolic and Toxic Myopathies. In Adams and Victor's Principles of Neurology (7th ed). New York: McGraw-Hili, 2001;1522. Carpeniro LJ. Sleep Parrern Disturbance. In Nursing Diagnosis: Applica tion ro Clinical Pracrice (8rh ed). Philadelphia: Lippincott, 2000;858865. Carpenito LJ. Confusion. In Nursing Diagnosis: Application to Clinical Pracrice (8rh ed). Philadelphia: Lippincott, 2000;230-239. Prevost 55. Elder Responses. In MR Kinney, 5B Dunbar, J Brooks Brunn, et 31. (eds), AACN's Clinical Reference for Critical Care Nursing (4rh ed). St. Louis: Mosby, 1998;169-172_ Shaffer J. Substance Abuse and Withdrawal: Alcohol, Cocaine, and Cpi oids. In JM Civetta, RW Taylor, RR Kirby (eds). Crirical Care. Philadel phia: Lippincott-Raven, 1997;1511-1514. Greicus L. Alcohol Wirhdrawal. In HM Schell, KA Puntillo. Critical Care Nursing Secrers. Philadelphia: Hanley & Belfus, Inc_, 2001;362-367.
II Fluid and Electrolyte Imbalances Susan Polich and Jaime C. Paz
Many causes and factors can alter a patient's fluid and electrolyte balance. These imbalance
can result in a multitude of clinical
manifestations, which in turn can affect a patient's functional mobility and activity tolerance. Recognizing the signs and symp roms of electrolyte imbalance is, therefore, an important aspect of physical therapy. Additionally, the physical therapist must be aware of which patients are at risk for these imbalances, as well as the concurrent pathogenesis, diagnosis, and medical management of these imbalances. Maintaining homeostasis between intracellular fluid, extracellular fluid, and electrolytes is necessary to allow proper cell function. Proper homeostasis depends on the following factors: •
Concentration of intracellular and extracellular fluids
•
Type and concentration of electrolytes
•
Permeability of cell membranes
•
Kidney function
763
764
AClTfE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Fluid Imbalance Fluid imbalance occurs when fluids are lost, either by loss of body water or failure to intake, or gained, either by fluid shift from the vasculature to the cell space or excessive intake without proper e1imination.I-3 Loss of bodily fluid (hypovolemia) can occur from loss of blood (hemorrhage), loss of plasma (burns), or loss of body water (vom iting, diarrhea). Any of these situations can result in dehydration, hypovolemia, or shock in extreme cases. Clinical manifestations include decreased blood pressure, increased heart rate, changes in mental status, thirst, dizziness, hypernatremia, increased core body temperature, weakness, poor skin turgor, altered respira tions, and orthostatic hypotension.l-4 Clinical manifestations in children also include poor capillary refill, absent tears, and dry mucous membranes,s Excessive bodily fluid (hypervolemia) can occur when there is a shift of water from the vascular system to the intracellular space. This can result from excessive pressure in the vasculature (venrricular fail ure), loss of serum albumin (liver failure), or fluid overload (excessive rehydration during surgery). Clinical manifestations of fluid over load include weight gain, pulmonary edema, peripheral edema, and bounding pulse. Clinical manifestations of this fluid shift may also resemble those of dehydration, as there is a resultant decrease in the intravascular fluid volume.I-3 Table II-I provides an overview of hypovolemia and hypervolemia.
Clinical Tip During casual conversation among physicians and nurses, patients who are hypovolemic are often referred to as being dry, whereas patients who are hypervolemic are referred to as being wet.
Electrolyte 1mbalance Fluid imbalances are often accompanied by changes in electrolytes. Loss or gain of body water is usually accompanied by a loss or gain of electrolytes. Similarly, a change in electrolyte balance often
Table 11-1. Fluid and Electrolyte Imbalances Imbalance
Definition
Contributing Factors
Clinical Manifestations
Diagnostic Test Findings
Hypovolemia
Fluid volume
Vomiting, diarrhea, fever,
Weak. rapid pulse; decreased BP; dizziness;
Increased hematocrit, BUN,
blood loss, and uncontrolled diabetes mellitus
thirst; confusion; and
deficit
serum sodium levels
muscle cramps Hypervolemia
Fluid volume excess
Renal failure. congestive
Shorrness of breath,
Decreased hematocrit,
heart failure. blood
increased BP. bounding
BUN, and serum sodium
> � � '"
transfusions, and
pulse, and presence of
levels
"
prolonged corticosteroid
cough
Hypernatremia
Sodium deficit
Diuretic therapy, renal
�
Lethargy, nausea, apathy,
(serum
disease, excessive
muscle cramps, muscular
sodium level
sweating, hyperglycemia,
twitching, and confusion
of z " '" r
�
Increased serum sodium
'" r
0
(serum
hyperventilation, and
lethargy or restlessness;
and decreased urine
sodium level
excessive corricosteroid,
thirst; dry, flushed skin;
sodium levels
01>145
sodium bicarbonate, or
weakness; irritability;
mEqniter)
sodium chloride
tachycardia; hyper- or
� >
administration
hypotension; oliguria;
z
and pulmonary edema
::j '" f< � n
lii
" '" Vo
Table 0-1.
Continued
�
'"
Imbalance
Definition
Conrribudng Factors
Clinical Manifestations
Diagnostic Test Findings
>
Ilypokalemia
Potassium defi-
Diarrhea, vomiting, chronic
Fatigue; muscle weakness;
ST depression or pro·
§
cit (serum
renal disease, gastric sue-
slow, weak pulse; ven-
longed PR interval on
potassium
tion, polyuria, corrico-
[Ticular fibrillation; par-
ECG
level of d.5
steroid therapy, and
esrhesias; leg cramps;
mEqniter)
digoxin therapy
and decreased blood
Potassium
Renal failure. Addison's dis-
Vague muscle weakness,
ST depression; rail, rented
excess (serum
ease, burns, use of potas-
nausea, initial tachycardia
T waves; or absent P
potassium
sium-conserving diuretics,
followed by bradycardIa,
waves on ECG
level of >5
and chronic heparin ther-
dysrhythmia, flaccid
mEqniter)
apy
paralysis, paresthesia, irritability, and anxiety
BP
=
blood pressure; BUN
=
blood urea nurogel1; ECG
=
elearocardiogram; NPQ
=
nothmg by mouth; SIADH
m J: >
S
pressure Hyperkalemia
� '"
=
syndrome of mappropriate
amidluretlc hormone secretion. Sources: Data from M Mulvey. Fluid and Electrolytes: Balance and Disorders. In SC Smeltzer, BG Bare (cds), Srunner and Suddanh's Textbook of �1edical·Surgical Nursing (8th cd), Philadelphia: Lippincott, 1996;231; CC Goodman, TE Kelly Snyder. Problems Affecting Multiple Sys· terns. In CC Goodman, WG Boissonnauh. Pathology: Implications for the PhYSical Therapist. Philadelphia: Saunders, 1998;72-82; and PJ Fall. Hyponatremia and hypernatremia: a systemarit: approach to causes and their correction. Posrgrad l\ted 2000; I 07(5):75-82,
8 " �
o '"
Of V\ n � :i ...,
� �
�
APPENDIX II: FLUID AND ELEcrROLYTE IMBALANCES
767
affects fluid balance. Cellular functions that are reliant on proper electrolyte balance include neuromuscular excitability, secretory activity, and membrane permeabiliry.6 Clinical manifestations will vary depending on the severity of the imbalance and can include those noted in Fluid Imbalance. In extreme cases, muscle tetany and coma can also occur. Common electrolyte imbalances are further summarized in Table II-I.
Clinical Tip Electrolyte levels are generally represented schematically in the medical record in a sawhorse figure, as shown in Figure II-I.
Medical management includes diagnosing and monitoring elec rrolyte imbalances via blood and urine tests. These tests include measuring levels of sodium, potassium, chloride, and calcium in blood and urine; arterial blood gases; and serum and urine osmolal ity. Treatment involves managing the primary cause of the imbal ance(s), along with providing supportive care with intravenous or oral fluids, electrolyte supplementation, and diet modifications.
Na
BUN
Cl
BS K
Cr
Figure 11-1. Scbematic representation of electrolyte levels. nitrogen; BS
=
blood sugar; CI
ate; K= potassium; Na
=
=
chloride; Cr
sodium.)
=
(8 UN
=
creatinine; HCOl
blood urea =
bicarbon
768
ACtrrE CARE HANDBOOK "'OR PHYSICAL THERAPISTS
Clinical Tip •
Review the medical record closely for any fluid
restrictions that may be ordered for a patient with hyper volemia. These restrictions may also be posted at the patient'S bedside. •
Conversely, ensure proper fluid intake before, during,
and after physical therapy intervention with patients who are hypovolemic. •
Slight potassium imbalances can have significant effects
on cardiac rhythms; therefore, carefully monitor the patient'S cardiac rhythm before, during, and after physical therapy intervention. If the patient is nOt on a cardiac monitor, then consult with the nurse or physician regard ing the appropriateness of physical therapy intervention with a patient who has potassium imbalance. •
Refer to Chapter 1 for more information on cardiac
arrhythmias. •
Refer to Chapter 9 for more information on fluid and
electrolyte imbalances caused by renal dysfunction. •
Refer to Chapter 11 for more information on fluid and
electrolyte imbalances caused by endocrine dysfunction.
References I. Rose BD (ed). Clinical Physiology of Acid-Base and Elecrrolyre Disor
ders (2nd cd). New York: McGraw-Hill, 1984. 2. Corran RS, Kumar V, Robbins S, Schoes Fj (cds). Robbins Parhologic Basis of Disease. Philadelphia: Saunders, 1994. 3. Kokko j, Tannen R (cds). Fluids and Elecrrolyres (2nd ed). Philadelphia: Saunders, 1990. 4. McGee S, Abernethy WB III, Simei DL. Is rhis parienr hypovolemic? JAMA 1999;281 (11):1022-1029. 5. Gorelick MH, Shaw KN, Murphy KO. Validiry and rcliabiliry of clinical signs in rhe diagnosis of dehydrarion in children. Pediarrics 1997;99(5): E6. 6. Marieb EN (ed). Human Anaromy and Physiology (2nd cd). Redwood City, CA: Benjamin Cummings, 1992;911.
III-A Medical-Surgical Equipment in the Acute Care Setting Eileen F. Lang
Introduction The purpose of this appendix is to (1) describe the vatious types of medi cal-surgical equipment commonly used in the acute care sening, inc1lld ing oxygen (02) therapy and noninvasive and invasive monitoring and management devices, and (2) provide a framework for the safe use of such equipment during physical therapy intervention. Some equipment is used in all areas of the hospital, whereas other type of equipment are u ed only in specialty areas, such as the inten sive care unit (leU). The ICU is defined as "a place for the monitor ing and care of patient with potentially severe physiological insrabiliry requiring technical andlor artificial life support." I The presence of certain types of equipment in a patient's room can provide the physical therapisr with a preliminary idea of the patient's general medical condition and the appropriateness of therapeutic or prophy lactic physical therapy intervention, or borh. The physical rherapist may initially be intimidated by rhe abundance of medical-surgical equipment (especially in the ICU); however, a proper orientation to sllch equipment allows the physical therapist to appropriately inter vene wirh safety and confidence. 769
770
AClITE CARE HANDBOOK FOR PIIYSICAL TIIERAI'ISTS
Oxygen Therapy The general indication for 0, therapy is hypoxemia. Hypoxemia is considered to be present when the arterial oxyhemoglobin saturation (Sao,) is less than 90%, corresponding to an arterial blood 0, partial pressure (Pao,) of less than 60 mm Hg.' Refer to Table 2-4 for the rela tion between 0, saturation as measured by pulse oximetry (Spo,) and Pao, and to Figure 2-7 for the oxyhemoglobin dissociation curve. The goal of 0, therapy is to treat and prevent hypoxemia, excessive work of breathing, and excessive myocardial work by increasing the Pao,.3 0, moves across the alveolar-capillary membrane by diffus ioll, the physiologic mechanism by which gas moves across a mem brane from a region of higher to lower pressure and is driven by the partial pressure gradient of 0, between alveolar air (Pao,) and pulmonary capillary blood. To improve diffusion, a rise in I'ao, can be attained by increasing the fraction of inspired 0, IFio,) with supplemental 0,' Supplemental 0, is delivered by variable performance ITable lIl A.l) or fixed performance (Table IlI-A.2) systems. Each cannula or mask is designed to provide a range of Fio,. A variable performance system should not be used if a specific Fio, is required. Variable per formance systems are nOt intended to meet the total inspiratory requirements of the patient. The actual Fioz for a given flow rate in a variable system is dependent on a patient's tidal volume and respira tory rate, and the type, fit, and placement of the cannula or mask. If a specific Fio, is required, then a fixed performance system is indicated. Fixed performance systems deliver a specific Fio, despite the patient's respiratory rate and pattern.4 0, delivery devices with masks or reservoirs allow 0, to collect about the nose and mouth during exhalation, which increases the avail ability of 0, during inhalation. As the storage capacity of the mask or reservoir is increased, the Fioz for a given flow rate is also increased.s The supplemental 02 requirements of a patient may fluctuate with activity. Monitoring Sao, with pulse oximetry (identified as Spo,) and subsequent titration (weaning) of 0, may be indicated during exer cise. The physician may order parameters for resting and exercise Spo, if a patient has a low activity tolerance or an abnormally low Spo, at baseline. A patient with chronic obstructive pulmonary disease who has chronic carbon dioxide retention may become desensitized to the respiratory stimulant effects of carbon dioxide. In these patients, ventilation is driven by means of a reflex ventilatory response ro a
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Table lIJ-A.l. Variable Performance Oxygen Delivery""
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DeviceIFio1
Description
Clinical Implications
Nasal cannula RA::::: 21 % Fio1, 1 Ipm::::: 24% Fio2, 2 Ipm ::::: 28% Fio" 3 Ipm::::: 32% Fio;, 4 Ipm 36% Fio" 5 Ipm::::: 40% Fio2, 6 Ipm ::::: 44% Fiol
Purpose: delivers supplemental 02 mixed with RA, usually 1-6 Ipm. The maxi mum is 8 lpm. Consists of: prongs, which are attached ro an 0, source via small-bore plastic tubing and are positioned in the patient's nose. The tubing is secured by placing it behind the patient's ears and under the patient's chin (Figure
•
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•
•
W.A.l). •
•
The rule of thumb for the cannula system is that Fio., is increased by 3-4% for each Iprn of °2, Mouth breathing does not necessarily indicate that a patient is nO[ receiving supplemental 0" If nasal passages are obstructed, 0., is able to colleer in the oral and nasal cavities and is d ;awn in on inspiration. Flow rates of greater than 8 Jpm are unlikely [0 increase delivered 02 further and may prove uncomfortable and lead to mucosa desiccation. Provide mobile patienrs with adequate lengths of extension tubing or a portable 01 rank to enable functional mobility. Patients should be instructed to avoid tripping over or becoming tangled in the tubing. The tubing may lead CO irritation or skin breakdown behind the ears of some patients. Sofr gauze padding may be placed around the rubing to protect the patient's skin.
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Device/Fio2
Description
Clinical Implications
Nasopharyngeal catheter Fio23S Nasal cal1nula, above RA 21 % Fio21 1 Ipm ... 24% Fio2! 2 Jpm "" 28% Fio" 3 Ipm ... 32% Fio ! 4 Ipm ... 36% Fio2,
Purpose: delivers supplemencal 02 inco the patient's oropharynx, which acts as an anatOmiC reservoir. This method is sometimes used with pediatric patients, who may dislodge a nasal cannula. Consists of: a soft tube with several distal holes, lubricated and inserted through a nare until its distal tip is visible juSt below the uvula. It is attached to an 0, source via small-bore tubing and held in place with tape.
•
Purpose: provides humidified, supplemental 0, mixed with RA. Consists of: a mas k with straps under the chin, contacts the cheeks, and is open over the patient's nose. It is secured with an elastic str:lP around the patient'S head. Ie connects to a humidified 02 source with large-bore tubing (Figure 111-A.2).
•
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5 Jpm ... 40% Fio2,
6 Ipm ... 44% Fio2
Open face mask/tent Fio, 35-50% �
The catheter is ch anged daily.
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A significant amount of mixmg with RA occurs,
although the capaciry of the mask allows 02 to colleer about the nose and mouth. It may be more comfortable than a closed face mask for claustrophobic patients. ,\101srure may collect m the tubmg and should be drained before moving the pmiem. The aerosol system is more cumbersome and may make mobilization of the patient more difficult than with nasal prongs. Collaborate with nursing to determme whether nasal prongs or a cl osed face mask can be used when mobilizing the patient. Titrate 02 appropriately to maintain 02 saturation as indicated.
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Closed face mask S-61pm �40% Fioz' 6-7 Ipm "" 50% Fio" 7-8 ' Ipm ",. 60% Fioz
Purpose: delivers supplemental 02 mixed
•
The closed face mask imerferes with coughing, talking, eating, and drinking and may be very drying and
with RA. The mask has a small
capacity but does allow for the
uncomfortable. Patients often remove the mask for
collecrion of 02 about the nose and
these reasons. Educate the patient on the importance of
mouth.
keeping [he mask in place.
Consists of: a dome�shaped mask
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elastic strap around the patient's head
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secures it in place. Ir is connected to an 02 source via small-bore tubing
2
(Figure 1Tl-A.3). Purpose: used for long�term 02 therapy.
2 Ipm "" 36% 3 Ipm 44% 4 Ipm "" 52% 5 Ipm 60% 6 Ipm "" 68% =
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Patients with severe bronchospasm, uncompensated respiratory acidosis (pH
BP cuff (sphygmomanometer)
P urpose: indirectly measures arterial
•
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Normal adult values: systolic
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100-J 40mm Hg, diastOlic � 60-90mm Hg
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Do not use a BP cuff on an extremiry with an
arterial line, lymphedema, AV fistula or graft,
blood pressure.
or blood clot, or in an extremity ipsilateral
Consists of: an inflatable cuff, usually
CO
placed 2.5 em proximal to the
mastectomy. Try to avoid measuring SP in an
a
antecubital space, attached to a
extremiry with a peripheral or central intra
pressure monitoring device.
venous line. Look for signs posted at the
Auscultate for Kororkoff's sounds
patient's bedside stating whether the use of a BP
(refer to Table 1-8) with a
cuff on a particular extremity is contrindicated.
stethoscope over an artery, usually
•
Use an appropriately sized cuff. The cuff bladder should be no less than 80% of limb
the brachial artery.
circumference. A cuff that is roo small •
overestimates SP. The cuff may be placed on the upper extremity distal to the elbow with auscultation of the
•
radial artery. Alternative sites for measurement in the lower extremiry are proximal to the popliteal space with auscultation of the popliteal artery or proximal to the ankle with auscultation of the
•
posterior tibial artery. Avoid contact between stethoscope tubing and the cuff robing to minimize extraneous sounds.
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Purpose: continuous monitoring of heart rare and rhythm and
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respiratory rate (see Table 1 - 1 0). Consists of: three to five color-coded electrodes placed on the chest. either
Notify the nurse before physical therapy intervention, as many activities may alter the rate or rhythm or cause artifact (e.g
•
.•
chest
percussion). If an electrode(s) becomes dislodged, reconnect it.
hard wired to a monitor in a
One way to remember electrode placemenr is
patient's room or monitored at a
white is right (white electrode is placed on the
distant site (telemetry). Twelve
right side of the chest superior and lateral to the
electrodes are used for a formal
right nipple), snow over grass (the green electrode
ECC.
is placed below the white electrode on the
anterolateral lower right rib cage). smoke over fire (the black electrode is placed on the upper left rib
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usually placed more cenrraIJy. Patients on telemetry should be instructed to stay in the area monitored by telemetry •
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red electrode is placed below the black one on the anterolateral left rib cage). The brown electrode is •
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antennas. Collaborate with the nurse to determine whether patienrs who are "hard wired" to monitors in their room may be temporarily transferred to telemetry for ambulation activities or whether the monitor may be temporarily disconnected.
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Device
Description
Clinical lmplic3tions
Pulse oximeter Normal Spo, (at sea level) " 93-94%
Purpose: a noninvasive method of mea suring the percentage of hemoglobin saturated with 02 in aneriaJ blood. Consists of: a probe with an electro optical sensor placed on a finger, roe, earlobe, or nose. The pulse oximeter emits two wavelengths of light to differentiate oxygenated from deox ygenated hemoglobin.
•
•
•
•
•
•
Sp02 S;88% indicates the need for supplemental oxygen. The waveform or pulse rate reading should match the ECG or palpated pulse. Monitor changes in pulse oximetry during exercise and position changes. Peripheral vascular disease, sunshine, or nail polish may lead to a false reading. In low-perfusion states, such as hypothermia, hypotension, or vasoconstriction, pulse oximetry may understate oxygen saturation. Small changes in the percentage of hemoglobin sites chemically combined (saturated) with oxygen (Sa02) can correspond to large changes in the partial pressure of oxygen. Refer to Table 2-4 and Figure 2-7.
AV arteriovenous; BP blood pressure; ECG electrocardiography; Sa02 arterial oxyhemoglobin saturation; Spo! measurement of Sa02 with pulse oximetry. Sources: Data from RR Kirby, RW Taylor, JM Civetta (cds). Handbook of Crincal Care (2nd cd). Philadelphia: lippincott-Raven, 1997;jM Rothstein (cd). The Rehabilitalion Specialist'S Handbook (2nd ed). Philadelphia: FA Davis, 1998; and MR Kinney, 58 Dunbar, JM Vitello Cicciu, et al. (cds). AACN's Clinical Reference for Critical Care Nursing (4th ed). St. louis: Mosby, 1998. =
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Table Ill-A.4. Invasive Medical Monitoring Device!Normal Values
Description
Clinical Implicacions
Arterial line (A-line) Normal values: systolic, 100-140 mm Hg; diastolic, 60-90 mm Hg; MAP, 70-105 mm Hg
Purpose: to directly and continuously record arterial blood pressure, to obtain repeated anerial blood samples, or to deliver medi cations. Consists of: an arcerial catheter. It is placed in the brachial, radial, or femoral arcery. The catheter is usually connected to a transducer that converts a physiologic pressure into an electrical signal that is visible on a monitor.
•
•
•
•
•
If the A-line is displaced, the parient can lose a significant amount of blood ar rhe insertion sire. If bleeding occurs from the line, immediately apply direct pressure to the sire while calling for assistance. The normal A-line waveform is a biphasic sinusoidal curve with a sharp rise and a gradual decline (Figure Ill-A.8). A damped (flattened) waveform may indicate hypotension, or it may be due ro pressure on the line. A patient with a femoral A-line is usually seen bedside. Hip flexion past 60-80 degrees is avoided. After femoral A-line removal, me patient is usually on strict bed rest for 60-90 mins, with a sandbag placed over the site. Upper-extremity insertion sires are usually splinted with an arm board to stabilize the catheter. The patient with a radial or brachial A-line can usually be mobilized out of bed, although the length of the line lirnirs mobility to a few feet. The transducer may be taped to the patient's hospital gown at the level of the phlebosratic axis (see Figure ill-A.7) during mobilization.
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Descri prion
Pacemaker (temporary)
Purpose: co provide temporary cardiac pacing postoperatively, status pOSt myocardial infarction, or before permanent pacemaker placement. Refer to Management in Chapter 1 for morc information on pacemakers. Consiscs of: pacing wires that connect to an external generator. There are three basic rypes. Epicardial-the wires are placed after heart surgery on the epicardium and exit through a mediastinal incision. Transvenous-the wires 3rc placed in the right ventricle via a central line. Transcutaneous-large elecrrodes 3rc placed on the skin over the anterior and posterior chese. Purpose: to dirocdy or indirocdy measure PAP, PAWP, LAP, RAP, CYP, core body temperarure, CI, and CO in cases of hemodynamic instabiliry, hean: failure, or cardiogenic shock. Provides access to mixed venous blood samples. Consists of: a multilumen catheter inserred through an introducing sheath into a large vein, usually the subclavian, or the
Pulmonary artery catheterization (PA line, Swan-Ganz) Normal values: PAP (mean), 10-20 mm Hg; PAWl' (mean), 6-12 mm Hg; RAP, 0-8 mm Hg; core temperature, 98.2°100.z°F (36.8°-37.9°C);
Clinicailmplic3rions •
The presence of a temporary pacemaker does not, in and of itself, limit functional mobility. However, the underlying indication for the pacemaker may limit the patient's activiry level. Check for mobility restrictions. Temporary pacing wires should be kept dry. • • Be aware of the location of the generator and wires at all times, especially during mobility activities. • If a temporary pacemaker is placed after a coronary an:ery bypass graft (CABG), the wires art' usually removed 1-3 days after surgery. The patient is usually placed on bed rest for 1 hr after pacing wire removal, with vital sign monitoring every 1 5 mins. •
•
• • • •
The patient with a PA line is usually on bed rest. Avoid head and neck (for subclavian access) or extremity movements that could disrupt the PA line at the insen:ion site, including the line dressing. PA\'(fP is an indirect measure of LAJ). PAP is equal to right ventricle pressure. RAP is equal to CVP. CO equals stroke volume (SV) x hean: rate (HR).
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brachial, femoral. or inrernal jugular vein (Figure III-A.9). The carherer is direcred by blood flow into various locations of the heart and pulmonary artery, with proper placement confirmed by x-ray. The catheter is connected to 3 transducer ro allow for continuous monitoring. The proximal lumen opens into the right atrium to measure RAP and CO, and for the delivery of fluids or medications. The distal lumen opens into the pulmonary artery to measure PAP and PAWP. To obtain a PAWP measurement, a balloon at the end of the distal lumen is temporarily inflated. h follows the blood flow from the right ventricle into rhe pulmonary artery ro a distal branch of the pulmonary artery, where it is "wedged" for a short time (up to 15 sees).
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A�line arterial line; CI cardiac index; CO cardiac Output; CVP central venous pressure; LAP left atrial pressure; Jpm li ters per minute; MAP mean arterial pressure; PAP pulmonary arrery pressure; PAWP pulmonary artery wedge pressure; RAP right atrial pressure. Sources: Data from RR Kirby, RW Taylor, JM Civetta (cds). Handbook of Critical Care (2nd cd). Philadelphia: Lippincott-Raven, 1 997; MR Kin� ney, SB Dunbar, J M Virello-Cicciu, et al. (cds). AACN's Clinical Reference for Critical Care Nursing (4rh cd). Sr. Louis: Mosby, 1998; EK Daily,JP Schroeder. Clinical Management Based on Hemodynamic Parameters. In FJ( Daily, JP Schroeder (eds), Techniques in Bedside Hemodynamic Mon itoring (5th ed). Sf. Louis: Mosby, 1994; and EJ Bridges. Moniroring pulmonary artery pressures: JUSt the facts. Crit Care Nurse 2000;2 1 (16):67. =
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AClITE. CARE HANDBOOK FOR PHYSICAL THERAPISTS
PHLEBOSTATIC AX'S
4ICS I
--
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Mid-Point A-P Chest Wall Figure m-A.7. The phlebostatic axis at the intersection of the fourth intercos
tal space (lCS) and the midpoint of the anterior (A) and posterior (P) chest wall. (Reprinted with permission from Edwards Lifesciences LLC.)
Aorta
Radial artery
Dorsalis pedis artery lime
Figure ID-A.8. Arteria/line tracing from different sites. (Repri"ted with per mission from SM Yent;s, NP Hirsh, GB Smith leds/, Anaesthesia and Inten sive Care A-Z. An Encyclopedia of Principles and Practice 12nd edJ. Oxford, UK: Butterworth-Heinemann, 2000;45.)
APPENDIX III-A: MEDICAL-SURCICAL EQUIPMENT
fN THE AClITE
CARE SITTING
791
Figure IU-A.9. Pulmonary artery {PAl catheter (four lumen model) in a branch of a PA with the bal/oon inflated; the pulmonary capillary wedge pres· SlIre (peWP) ref/ects left atrial pressllre (LAP). (LA left atrillm; LV left ventricle; RV= right vemricle.) (Reprinted with permission from LD Kersten led/. Comprehensive Respiratory Nursing: A Decision·Making Approach. Philadelphia: Sallllders, 1989;758.) =
=
lotracranial Pressure Monitoring Intracranial pressure (ICP) and cerebral perfusion pressure may be measured in a variety of ways, depending on how urgently ICP values are needed and the patient's neurologic or hemodynamic stability. Refer to Intracranial and Cerebral Perfusion Pressure in Chapter 4 for a description of these terms, Table 4-20 for a description of the early and late signs of increased ICP, and Table 4-21 for a list of treatment options to decrease ICP. Table lll-A.S describes the different types of ICP monitors. For some lCP monitors, such as the inrravenrricuJar catheter, the sensor and the transducer must be level. Often, the zero point for the transducer is at the traglls, or the top of the ear. A normal ICP waveform has a triphasic sinu soidal waveform and should correspond to heart rate.
General Physical Therapy Considerations with Intracranial Pressure Monitoring • As with hemodynamic monitoring, be aware of the lCP value and the corresponding waveform on the monitor. The waveform may change shape (plateau wave) if cerebral hypoxia or ischemia occurs.1J
Table OJ-A.S. Intracranial Pressure (ICP) Monirors
..... '" N
Device
Description
Clinical Implications
Epidural sensor
Purpose: to monitor fCP. Consists of: a fiberoptic sensor. It is placed in the epidural space (i.e., superficial ro the dura) and connects to a transducer and monitor.
•
Purpose: ro directly monitor ICP and provide access for CSF sampling. Consists of: a bolt or screw placed in the subarachnoid or subdural space through a burr hole.
•
Subarachnoidl subdural bol,
•
•
•
Intraventricular catheter (ventriculosromy)
Purpose: to directly monitor ICi> and provide access for the sampling and drainage of CSF. Occasionally used to administer medications. Consists of: a small catheter that is placed in the anterior horn of the lateral ventricle through a burr hole. The catheter connects to a transducer and to a drainage bag, where CSF collects.
•
•
•
•
The transducer does not need [Q be adjusted (releveled) with position changes. Fair reliability.
The physician will determine the level to which the transducer should be positioned. This is documented in the chart and posted at me bedside. The transducer must be repositioned to the appropriate level with position changes. Poor reliability. The nondominant hemisphere is the preferable insertion site. There are twO different types of drainage systems: intermittent and continuous. The intermittent system allows the nurse to drain CSF for 30-120 secs by momentarily opening a stopcock when the lCP exceeds the parameters set by 'he physician. A continuous system allows the drainage of CSF to occur against a pressure gradient when the collection bag is positioned (leveled) above [he foramen of Monro. This is usually 15 cm above the external auditory meatus.
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ACtJrE CARE HANDBOOK FOR PHYSICAL THERAPISTS
• Momentary elevations in ICP will normally occur. It is a sus tained elevation in ICP that is of concern and should be reported to the nurse. • Patients with elevated ICP are often positioned with the head of the bed at 30 degrees, which maximizes venous blood flow from the brain to help decrease ICP.'4 Therefore, be aware that lowering the head of the bed may increase ICP. Other positions that increase ICP are the Trendelenburg position, lateral neck flexion, and extreme hip flexion. • Additional conditions that increase ICP are the Valsalva maneu ver, noxious stimuli, pain, and coughing.
Medical-Surgical Management Devices Different lines, tubes, catheters, and access devices comprise the wide variety of medical-surgical equipment used in the acute care setting. In general, these devices may be peripheral or central, for shorr- or long-term use, and inserted or applied at the bedside in a special pro cedure (e.g., under fluoroscopic guidance) or in the operating room. Table LII-A.6 describes the medical-surgical management devices most commonly encountered in the acute care setting.
General Physical Therapy Considerations with Medical-Surgical Management Devices The following clinical tips apply to medical-surgical equipment, as well as to the 02 therapy and noninvasive, invasive, and ICP moniror ing equipment previously discussed.
Clinical Tip • Before entering a patient's room, review the medical record, particularly new orders, recent progress notes, and test results. Review graphic sheets for vital signs, noting trends or variations from the norms. • Note whether any particular precautions protecting the patient or the caregiver from specific pathogens are in
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Table UJ-A.6. Medical Management Devices·
"l
m
Device
Description
Clinical Implications
AntithromboIytic
Purpose: provides intermittent pressure to ehe lower extremi
•
Usually worn when the patient is in
boots (pneumatic
eies to promote venous return and prevent deep vein ehrom
bed, but can be worn when sitring
compression stock
bosis secondary to prolonged or postoperative bed rest.
in a chair.
ings/Venodyne
Consists of: inflatable sleeves, applied to the lower legs, which interminenrly inflate and deflate. In some cases, the
boots)
•
Reapply when patient returns to bed.
•
Discontinued when the parient is
sleeve is applied to the leg from the ankle to midthigh. AV graft or AV fistula
Purpose: provides access for hemodialysis.
Consists of: The graft is an artificial blood vessel, usually
ambuJating on a regular basis. •
made of Gore-Tex or Dacron. used to join an artery and vein when a patient's own vessels are not viable for an AV fistula. The
{istula is ehe surgical
•
joining of an artery and
vein, allowing arrerial blood to flow directly to a vein. Usually located in the forearm.
Elevate and avoid weight bearing on
•
Normal value, CVP
=
0-8 mOl Hg
repeated blood sampling, or administration of drugs or fluid. May measure CVP (see Pulmonary artery catheterization in Table m-A.4), May be used to place a temporary pacemaker or a vena cava filter or for hemodialysis. Consists of: a single- or multiple-lumen intravenous line placed in the subclavian, basilic, jugular, or femoral vein, terminaeing in the right atrium.
•
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Device
Description
Clinical l mplications
Chest tube
Purpose: removes and prevents the re-entry of air (pneumo�
•
Chest rubes may cause discomfort,
thorax) or fluid (hemothorax, pleural effusion, empyema, or
which may inhibit a cough, deep
chylorhorax) from the pleural space or mernasrmai space and
breath, or mobility. •
provides negative intrapleural pressure. Consists of: rube(s) placed in the pleural or mediastinal space that exit the chest and are usually connected
(0
The patient may benefit from pre medication for pain before treat
a drainage
ment.
system (Figure III-A.IO). The placement of [he tubes is determined by indication. Mediasrinal chest tubes, placed
•
to drain the pericardium after surgery, exit the chest
•
directly below the sternum. Apical chest tubes drain air,
The drainage system should be below
side of the bed or raped to the floor to If the reservoir is overturned, return
PostOperatively, rubes often exit the chest through the
the drainage container [Q the upright
surgical incision. If chest rubes are placed in a nonsurgical
position and notify the nurse. If the chest tube itself becomes dislodged, StOp activiry and notify the
system with three compartments: the drainage coUection
nurse immediately. If possible, place
chamber, the water seal chamber with a one-way valve that prevents air or fluid from re-entering the drainage
the patient in an upright sitting
collection chamber, and the suction chamber, which
breath sounds, viral signs, and
position, and monitor the patient'S
decreases excess pressure in the pleural space. Tubes may be connected ro a small one-way valve (Heimlich valve) that allows air or fluid to escape from the pleural space while preventing re-entry.
respiratOry rate and pattern for possible signs of tension •
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prevent tipping.
•
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Fluid tends to collect near the basesj in these cases, tubes are placed more inferiorly near the fluid collection.
situation, they are often placed along the midaxillary line at
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Avoid tipping the collection reservoir.
which typically collects in the apices of the pleural spaces.
the appropriate level. Tubes usually connect to a drainage
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the level of chest rube insenion. The reservoir may be hung &om rhe
•
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pneumothorax. Prevent kinks in the line.
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The presence of a chest tube should nor, in and of itself, limit activity. Position changes and mobility can
•
facilitate drainage. Ask the nurse or doctor whether the chest rube may be temporarily disconnected from suction during mobiury activities. If the suction must
remain connected, additional lengths
of tubing may be added, or a portable suction device may be used during mobility activities. •
The occlusive dressing, usually a petrolatum gauze dressing to prevent the influx of air, should remain imact. Do not apply pressure over the insertion site.
Esophagogastric tamponade rube (Blakemore tube, Sengstaken
Purpose: to compress hemorrhaging esophageal varices. The tube, which is passed by moU[h through the esophagus into the stomach, has a proximal (esophageal ) cuff, which compresses esophageal varices, and a distal (gastric) cuff,
Blakemore tube,
which compresses gastric varices. Channels allow
Minnesota tube)
aspiration of gastric contents. The balloons typically remain in place for up to 24-72 hrs, as longer duration may cause tissue necrosis or ulceration.
•
Patiems with this device are typical1y very ilJ and unable to participate in mobility activities.
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Device
Description
Clinical Implications
Lumbar drainage
Purpose: continuous drainage of CSF from the subarachnoid
•
device (LDD)
The position of the pacicot, the
space in the lumbar spine. For the treatment of CSF leaks
position of the transducer (if any),
or shunt infections or to reduce intracranial pressure.
and the position of the collection bag
Consists of: a spinal catheter inserted in
3rc determined by the rationale for
L4-5 subarachnoid
the LDD intervention.
space, advanced ro an appropriate level, and connected to 3 sterile closed CSF collection system.
•
Changes in me patient's position, in the level of the collection bag, or in the intrathecal pressure impact the amount and fate of drainage.
•
Note any restrictions in the medical record or posted in the patient'S room.
•
Patienrs are usually on bed rest whiJe the drain is in place.
•
Patients are often instructed to avoid
coughing while practicing post
operative deep breathing exercises. •
Over-drainage or under-drainage complications include tension pneumocranium, central herniation of the brain, compression of the brain stem. and subdural hematoma .
•
Monitor the patient for any changes in neurologic status. Notify nursing inunediately if any changes arc noted.
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This small-diameter rube can clog easily; some facilities require thar feeding rubes be flushed with water when placed on hold for > 1 5 mins to minimize the risk of dogging.
Percutaneous sheath introducer (Cordis)
Purpose: dilates a vein to provide a channel for introduction
•
of pulmonary catheter. Consists of: a Teflon sheath that often has a port for
The patient may be mobilized with the sheath in place once the
I.V.
pulmonary cameter has been
access.
Purpose: provides temporary access for delivery of medi
•
cations, fluids or blood transfusions. Cannot be used to draw blood. Consists of: a short catheter, 0.75-1.00 in. long, inserted into a small peripheral vein.
Avoid using blood pressure cuff on Watch i.v. rubing for kinks or occlusions.
•
Position the patient to avoid occluding flow.
•
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A secure dressing should cover the
can allow air into the venous system Peripheral intravenous
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if signs are present.
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lli-A.6.
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Continued
Device
Description
Clinical Implications
Peripherally inserted
Purpose: provides long-term administration of TPN,
•
central venous catheter
(Plcq
medications or fluid.
mobilizing the patient to confirm
Consists of: a catheter placed via the cephalic or basilic veins, terminating in the superior vena cava. This is the only central line placed by a nurse.
Wait for x-ray results before proper placement of the line.
•
Improper placement can break the line; cause a hematomaj pierce the lung, causing a pneumothorax; or terminate in a vessel other than the vena cava.
•
Do not usc a blood pressure cuff on the involved extremity.
•
Encourage range of motion of the involved extremity.
•
Use of axillary crutches may be contraindicated.
Rectal pouch/tube
Purpose: temporarily collects bowel drainage and protects fragile skin from contact with feces.
•
Both arc easily dislodged.
•
Use a draw sheet when moving the
Consists of: a pouch placed externally or a tube placed internally in the rectum. Suprapubic catheter
Purpose: drains the bladder temporarily after some bla.dder surgeries , or permanently in cases of blocked urethra due to a tumor, periurethral abscess , or a severe voiding
• • •
surgical incision in the lower abdominal wall.
Keep the collection bag below [he level of insertion. Keep the collection bag below the level of the bladder. The collection tubing may be taped ro the patient's thigh.
dysfunction. Consists of: a catheter pla.ced in the bladder through a
patient in bed.
•
Avoid pressure over the insertion site.
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Surgical drain
Texas catheter
Purpose: removes blood or fluid from a surgical site that would otherwise collect internally. Surgical drains are of two basic rypes: passive or active. Pas· s;ve drainage is accomplished by gravity or capillary action. Drainage is further facilitated by rransient increases in intra·abdominal pressure, as with coughing. Passive sur gical drains include Penrose, Foley, Malecot, and Word catheters. Active drainage is accomplished by suction from a simple bulb device or a suction pump. These systems may be closed, like the Hemovac and Jackson·Pratf (JP) drains. Purpose: noninvasively drains and collects urine from the penis. Consins of: a condom·like flexible shearh that fits over the penis ro drain urine into a collection bag. This noninvasive method of collecting urine has a much lower risk of infection and irritarion than does an indwelling catheter and is often the preferred method of managing male urinary incontinence.
•
•
•
Be aware of the location of the drain when moving the patient. The rubing may be taped or pinned to the patient's skin or clothing to prevent tugging. Check with the nurse before disconnecting a drain from suction.
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•
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It is easily dislodged. It may be held in place with a Velcro strap. The drainage bag should always be below [he level of the bladder to allow drainage by graviry. Keep the collccrion bag off the Ooor. Secure the collection bag or catheter rubing to patient's leg, clothing, or assistive device to prevent the patient from tripping or becoming tangled in the tubing during mobiliry activities.
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Table lli-A.6. Continued Device
Description
Clinical Implications
Totally implantable intravascular device (Port-A-Cath, MediPort)
Purpose: surgically implanted catheter used for long�term chemotherapy, TPN, or other long�teIm infusion therapy. Consists of: a completely implanted catheter, usually placed in the subclavian or jugular vein, terminating in the superior vena cava. Access to the catheter is obtained through a tunneled portion attached to a poct that is implanted in a subcutaneous pocket in the chest wall, usually below the clavicle. The subcutaneous titanium, plastic, or stainless steel port has a reservoir with a self sealing septum that is accessed by a special noncoring needle through imact skin. The tunneled ponion is anchored to a muscle or subcutaneous tissue with sutures.
•
Tunneled central venous catheter (Hickman, Broviac, Groshong, Silasric, and Quinton catheters)
Purpose: surgically implamed cameter used for long-term chemotherapy. TPN. or other long-term infusion therapy. May be used for months to years. Very similar to the totally implamable intravascular device (previously described); however, access is obtained through a "tailed" portion, which exits the skin from the amerior chest wall superior to the nipple. A Dacron cuff surrounds the tunneled portion just inside the exit site. The cuff causes a subcutaneous inflammatory reaction to occur aher insertion, which , when healed, provides fixation and a barrier to infection within 1 to 2 wks of implamation.
•
Once healed, physical activity is not limited. Patients can usuaUy swim or bathe without limitation.
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The tailed portion should be taped down to prevent dislodging. Do not perform manual techniques directly over the tail. Patients are allowed to shower once the insertion site is healed; howevex; tub bathing and swimming are usually limited.
i
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Urinary catheter (Foley carherer)
Purpose: temporarily drams and collects unne from bladder. It allows accurate measuremenr of urine output. Consists of: a tube mserted through the urethra inro the blad der that drams inro a collection bag. It is held in place inrernally by an mflated cuff.
•
•
•
•
Yen tricul0periton eal shunr (VP) Ventriculoatrial shunt (VA)
Purpose: drains excess CSF from the brain inro the abdominal cavity or heart. Consists of: a shunr, tunneled under the skin, from the cerebral venrricles to the collection cavity.
•
•
•
Yankauer suction
Purpose: clears secretions from the oral cavity or the oropharynx. Consists of: a hand-held clear rigid tube attached ro wall suction via tubing. The suction pressure is usually 1 20150 mm Hg.
•
•
Be aware of the poSition of the catheter. The collection bag should always be below rhe level of rhe bladder ro allow drainage by gravity. Secure the collection bag or tubing to the patient's leg, clothing, or assistive device to prevenr the paoent from tripping or becoming [angJed in the tubing during mobility activiries. The collection bag should be kepr off rhe floor. The parient may be on bed rest for 24 hrs after placement. The shunt can often be palpated under the skin. Avoid excess pressure over the shunt. Some patients use this independendy; if so, place within the patient's reach. Patients with a decreased cough reflex or dysphagia or on ventilator support may collect secretions in the mouth or in the back of the throat. Gentle Yankauer suctioning before rolling or other mobility may prevent aspiration of the collected secretions.
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� Description
Clinical Implications Yankauer suctioning may stimulate a cough and help clear secretions in patients who are unable to dear secretions independendy. • If a patient bites down on the Yankauer, do not anempt to pull on the device. Wait for the patiem to relax, then gendy slide the Yankauer from the patiem's mouth. •
AV arteriovenous; CSF cerebrospinal fluid; CVP central venous pressure; TPN total parenteral nutrition. Listed in alphabetical order. Sources; Data from RR Kirby, RW Taylor, J M Civena (cds). Handbook of Critical Care (2nd cd). Philadelphia: Lippincorr-Raven, 1 997; F Hal derman. Selecting a vascular access device. Nursing 2000; 1 1 :59-61; DF Colixxa. Actionstat: dislodged chest rube. Nursing 1 995;25-33; I-IJ Thompson. Managing patients with lumbar drainage devices. Crit Care Nurse 2000;20:60-68; and Guidelines for intensive care unit admission, discharge, and triage. Task Force of the American College of Critical Care Medicine, Society of Critical Care Medicine. Crit Care Med 1999;27: 633--638. =
•
=
=
=
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APPENDIX III-A: MEDICAL-SURGICAL EQUIPMENT IN 11-IE ACllfE CARE SETTING
807
Figure [[I-A. I O. A chest drainage system has three mai" compartments from left to right: ( 1) the suction control. (2) the water seal. (3) the collection chamber. (Reprinted with permission from Genzyme Biosurgery.)
place (e.g., conract precautions) . Refer to Table 10-4 for a summary of infection prevention precautions. • Practice universal precautions. The likelihood of encountering bodily fluids is increased in the aCllte care serring, especially in rhe ICU. • Discuss your planned intervention with the nurse. Scheduled procedures may rake precedence over rhis inter vention, or it may coordinate well with another planned procedure. • On entering the patient's room, take inventory. Observe rhe parient's appearance and posirion. Systemarically observe rhe parient and verify rhe presence of all docu menred lines. Develop a consistent method of surveying rhe room: lefr to righr, or rop of bed ro bottom of bed, ro ensure rhar all lines and equipmenr are observed and con-
808
ACUTI CARE HANDBOOK FOR PHYSICAL THERAPISTS
side red in your treatment plan. Take note of all readings on the monitors before intervention. • Anticipate how your intervention may change the patient's vital signs and how this will likely appear on the monitors. Be aware of which readings may change artifi cially owing to relative position change. • Using appropriate precautions, gently trace each line from the patient to its source. Ask for assistance, if needed, to untangle any lines or to free any lines that might be under the patient. • Ensure that there is no tension on each line before attempting to move the patient. • Never arrempt to free a line that cannot be completely visualized! • Discuss with the nurse whether any lines can be removed or temporarily disconnected from the patient before your treatment. • Ask for appropriate assistance when mobilizing the patient. • Most invasive monitoring systems have two alarm con trols: one to silence or discontinue the alarm for a few minutes, and another to disable or turn off the alarm. Do not silence or disable an alarm without permission from the nurse! • On completion of your tteatment, ensure that all appro priate alarms are turned on and that the patient is posi tioned with the appropriate safety and communication measures in place. Notify the nurse of any change in the patient'S status.
References 1 . Anonymous. Guidelines for intensive care unit admissions, discharge, and triage. Task Force of the American College of Critical Care Medicine, Society of Critical Care Medicine. Crit are Med 1 999;27(3),633--j)38. 2. Kirby RR, Taylor RW. Oxygen Therapy. In RR Kirby, RW Taylor, JM Civetta (cds), Handbook of Critical Care (2nd cd). I'hiladelphi., Lippin con-Raven, 1 997;254,260.
AI'PINJ)[X III-A: \H[)[C\[ -SURL[CA[ FQUIPMENT IN mE AClITE CARE'. SETnNG
809
.1 . Kacmarek RM. Oxygen Therapy. In RM Kacmarek, CW Mack, S
4.
5.
6.
7.
8.
9.
10.
II.
12.
13.
1 4.
Dimas (cds), The Essentials of Respiratory Care (3rd ed). St. Louis: Mosh), 1 990;408. Scanlan el, Heur A. Medical Gas Therapy. In DF Egan, CL Scanlan (eds), Egan's Fundamentals of Respiratory Care (7th ed). St. Louis, Mosby, 1 999;738,748. Ryerson EF, Block AJ. Oxygen as a Drug' Clinical Properties, Benefits, Modes and Hazards of Adminisrrarion. In GG Burron, JE Hodgkin (cds), Respiratory Care, A Guide to Clinical Practice (3rd ed). Philadel phi., Lippincott, 1 99 1 ;325-326. Kacmarek RM. Neurologic Control of Ventilation. In RM Kacmarek, CW Mack, S Dimas (eds), The Essentials of Respiratory Care (3rd ed). St. LoUIS, Mosby, 1 990;80. Dally FK, Schroeder JP. Clmical Management Based on Hemodynamic Parameters. In FK Dady, JP Schroeder (cds), Techniques in Bedside Hemodynamic Monironng (5rh cd). Sr. lOUIS: Mosby, 1994;235. Whalen DA, Kelleher RM. Cardiovascular Parient Assessmenr. In MR Kmney, SB Dunbar, JM Vitello-CiCClu, et al (eds), AACN's Clinical Ref erence for Crincal Care Nursing (4rh ed). Sr. louis: Mosby, 1 998j303. Smith RN. Conceprs of Monitoring and Surveillance. In MR Kinney, S8 Dunbar, JM Vircllo-Cicciu, er 31 (cds), AACN's Clinical Reference for Cntlcal Care Nurs11lg (4th ed). St. Louis: Mosby, 1 998;1 9. Bridges Ej. tvloniroring pulmonary ,urery pressures: jusr rhe facts. erir Care Nurse 2000;20,67. Daily EK, Schroeder JP. Principles and Hazards of MOnlroring Equip ment. In EK Dally, JP Schroeder (cds), Techniques in Bedside Hemody namic Moniroring (5th ed). St. louis: Mosby, 1 994;37. Bridges El. \Voods SL. Pulmonary artery pressure measurement: state of the art. Heart Lung 1 993;22,99. Hickey jV. Theory and Management of Increased Intracranial Pressure. In JV I hckey (cd), The Chnical Practice of Neurological and Neurosur gical NUr<mg (4th cd). Philadelphi" Lippincott, 1997;3 1 6 . Boss Bj. Nursing Management of Adults wirh Common Neurologic I'rohlems. In PG Beare, JL Myers (eds), Adult Health Nursmg (3rd ed). St. LouI" Mosby, 1 998;9 I 7-924.
III-B Mechanical Ventilation Sean M. Collins
Mechanical ventilatory support provides positive pressure to inAare the lungs. Patients with acme illness, serious trauma, exacerbation of chronic illness, or progression of chronic illness may require mechani cal ventilation.1 The following are physiologic objectives of mechanical ventilation': •
Support or manipulate pulmonary gas exchange
•
Increase lung volume
•
Reduce or manipulate the work of breathing
The following are clinical objectives of mechanical ventilation': •
Reverse hypoxemia and acme respiratory acidosis
•
Relieve respiratory distress
•
Reverse ventilatory muscle fatigue
•
Permit sedation, neuromuscular blockade, or both
811
812
AClITE CARE HANDBOOK FOR PHYSICAl THFRAI'ISTS
• Decrease systemic or myocardial oxygen consumption and intracranial pressure •
Stabilize the chest wall
•
Provide access to tracheal-bronchial tree for pulmonary hygiene
• Provide access for delivery of an anesthetic, analgesic, or seda tive medication
2 The following are indications for mechanical ventilation ; Partial pressure of arterial oxygen of less than 50 mm Hg with supplemental oxygen
•
•
Respiratory rate of more than 30 breaths per minute
•
Vital capacity less than 10 liters per minute
•
Negative inspiratory force of less than 25 em H20
•
Protection of airway from aspiration of gastric contents
•
Reversal of respiratory muscle fatigue3
Process of Mechanical Ventilation [lltubatioll [lltubatioll is the passage of an artificial airway (tube) into the patient'S trachea (Figure III-B. 1), generally through the mouth (elldo tracheal tube intubation) or occasionally through the nose (Ilasotra cheal intubation). Intubation is considered for four reasons: (1) the presence of upper airway obstruction, (2) inability to protect the lower airways from aspiration, (3) inability to clear pulmonary secre tions, and (4) the need for positive pressure ventilation.' The process of removing the artificial airway is called extllbatioll. When patients require ventilatory suppOrt for a prolonged time period, a tracheostomy is considered. According to one author, it is best to allow 1 week of endotracheal intubation; then, if extubation seems unlikely during the next week, tracheostomy should be consid ered.1 However, a patient can a)so be intubated for many weeks without tracheostomy, depending on the clinical situation. A trache-
,\PPENDIX III-B: MECHANICAL VENTILATION
813
Figure ill-B. I. A typical endotracheal tube.
ostomy tube is inserted directly into the anterior trachea below the vocal cords, generally performed in the operating room. Benefits of tracheostomy include (I) reduced laryngeal injury, (2) improved oral comfort, (3) decreased airflow resistance, (4) increased effectiveness of airway care, and (5) feasibility of oral feeding and vocalization.· If the patient is able to be weaned from ventilatory support, humidified oxygen can be delivered through a tracheostomy mask (Table IU-A.l).
814
AClffE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Cuff Approximately 0.5 in. from the end of an endotracheal or tracheal tube is a cuff (balloon). The cuff is inflated to (1) ensure rhar all of rhe supplemenral oxygen being delivered by rhe venrilator via the artifi cial airway enters the lungs and (2) help hold the artificial airway in place. Cuff inflation pressure should be adequate to ensure that no air is leaking around the tube; however, cuff pressures should not exceed 20 mm Hg. High cuff pressures have been linked to tracheal damage and scarring, which can cause tracheal stenosis.
Clinical Tip • A cuff leak should be suspected if the patienr is able to phonate or audible sounds come from his or her mouth. • Cuff leaks can occur if the endotracheal tube is shifted (positional leak) or if the pressure changes in the cuff. • If a cuff leak is suspected, then the respiratory therapist or nurse should be notified. (Physical therapists who spe cialize in critical or cardiopulmonary care may be able to add air to the cuff according to the facility's guidelines.)
Positive Pressure Ventilators Positive pressure ventilators are classified based on the method used to stop the inspiratory phase and allow expiration (cycling method) to occur.' There are three basic cycling methods: (1) pressure cycled, (2) volume cycled, and (3) time cycled. Pressure-cycled ventilators Stop inspiration at a preset pressure, volume-cycled ventilators stOp inspiration at a preset volume, and time-cycled ventilators stop inspiration at a preset time interval. Although these methods allow for increased conrrol of certain vari ables during inspiration, holding only one variable constant for the termination of positive pressure inhalation allows other factors to affect inspiration and potentially cause barotrauma or reduced inspiratory volumes. These factors include position changes and man ual techniques. For example, with a volume-cycled ventilator, a preset volume will be delivered regardless of the patienr's position, and reductions in chest wall expansion owing to a patienr's position (e.g., side lying)
APPENDIX 111-8: MECHANICAL VENTILAT10N
815
may increase the pressure placed on the dependent lung tissue and result in barotrauma. Conversely, in the same scenario, if a patient is on a pressure-cycled ventilator, then pressure will be delivered to the predetermined level, but because the patient's position may hinder chest expansion, a resultant lower volume of inspired air may be delivered, because the preset pressure limit was reached. Many newer ventilators provide the clinician with more than one cycling option, and certain modes of ventilation allow for more than one parameter ro derermine the inspirarory phase (as discussed throughout this appendix).
Clinical Tip • Being aware of the cycling method, the therapist can pay attention to changes in the pressure or tidal volume (VT) associated with his or her interventions. • Wide bore plastic tubing is used to create the mechani cal ventilator's circuit. The terminal end of this circuit directly connects ro an endotracheal or tracheal tube or, less commonly, to a face mask.4 Some ventilator circuits have an extra parr at their terminal end for an "in-line" suction catheter, which allows for suctioning without the removal of the ventilator circuit from the patient.4
Modes of Ventilation
Modes of ventilation can range from providing rotal support (no work performed by the patient) to minimal support (near-total work performed by the patient). Modes of ventilation are geared toward allowing the patient to do as much of the work of breath ing as is physiologically possible, while meeting the intended objectives of ventilatory support. Even short periods (11 days) of complete dependence on positive pressure ventilation can lead to respiratory muscle atrophy and concomitant reductions in dia phragm strength (25%) and endurance (36%).5 Figure III-B.2 pro vides a schematic of the conventional modes of ventilation based on the amount of support they provide. Characteristics of conven tional and alternative modes of ventilation are presented in Tables III-B. I and III-B.2, respectively.
00
�
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Sp«trum ofPatienl Participation
,.
No Spontaneous Breathing -
Some Spontnneous Breathing: RR < 10
Dependence
effons:
Total Ventilator
Weak. inspiratory VT 10 But inspiratory effort still
weak:
NlF < 10 em H10
ventilation and
Good EfTon:
able to
NIF> 20 em H:O
suppor t self
VT> 10 m.Vkg
Vt < 10 mllkg
lndependent with
physiologically
�
4 Synchronous
lntennittem
Mandatory
Ventilation
p"""", Support
Ventilation
Continuous Positive
[E,"�d�
Airway
p..,....
Figure ill-B.2. Schematic of mechanical ventilator modes: the ability of patients to participate in the process of ventilation and oxygenation in part determines the mode of ventilation. Parameters used to determine the patient's ventilatory effort include the presence of spontaneous breaths, the number of breaths per minute he or she initiates (respiratory rate [RR)). the volume of those breaths per breath (tidal volume /VT}). and the negative inspiratory force (NIF) generated with those breaths. The values indicated above are examples 0/ patient characteristics along the spectrum (rom complete ventilatory dependence to indepen dence. The effectiveness of the patient's efforts needs to be assessed based not only 011 the above parameters. but on "outcon-te" variables, such as oxygenation (Pao'}! oxygen saturation as measured by pulse oximetry). ventilation (Paco2), and overall status (hemodynamic stability. symptonts).
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APPENDIX III-B: MECHANICAL VENTILATION
817
Table HI-B.l. Conventional Modes of Ventilation Modes
Characteristics
CV
Toral control of the parient's ventilation: preset rate; Fiol; VT; flow rate; I:E ratio. Patients may be sedated or pharmacologically paralyzed. No active respirarory muscle activity is necessary. Patient controls cespirarory parrern and rare; breath initiated by patient creares negative airway pressure in circuit; once initiated, the volume is delivered with eirher a preset volume or pressure and flow ratc; respiratory muscles are still working. Patient can trigger RRs that are roo high, leading ro respirarory alkalosis or auto PEEP (see text). Combination of CV and AV; delivers breath of predetermined tidal volume with the patient'S inspiratory effort. If the patient does not initiate a breath within a specified time period, the ventilator will deliver a breath ro maintain preset RR. Delivers breaths intermittently at preset time intervals with a preset RR, VT,and flow rare. Patient is allowed to breathe spontaneously through a separate circuit between machine-delivered breaths. Different from AV in that attempts ro breathe by the patient are not assisted by the ventilaror. Patient may "fight" the ventilator if patient tries [0 exhale during the mechanical inspiratory phase, leading to dyssynchrony; this mode has largely been abandoned replaced by SIMY. Similar to IMV: Mandarory breaths are delivered with a preset RR, Vpand flow; however, like AV, it will assist a patient-initiated breath. Mandarory breaths are only delivered when the patient is nor initiating enough breaths ro allow a preset minute venrilation. Patient-initiated breaths are augmented wirh a preset flow of gas from the ventilator to maintain consrant inspirarory pressurej when the inspirarory flow drops to a preset value, the flow of gas terminates. Patient controls RR, inspiratory time, and flow; patient and ventilator determine VT and minute ventilation. The VT received from the machine is relared nor only to the patient's effort but also to the amounr of pressure provided by the ventilator.
AV
A ssist! control ventilation
IMV
SIMV
Pressure supponed ventilation
818
ACUTE CARE HANDBOOK FOR PHYSICAL THERAI'ISTS
Table m-B.1. Continued Modes
Characteristics
Continuous positive airway pressure
Intended to decrease work of breaching by reducing the airway pressure necessary to generate inspiration throughout the respiratory cycle while the patient is spontaneously breathing. Positive pressure is constantly maintained above atmo spheric pressure. Most commonly used during weaning from the mechani cal ventilator or in an artempt to postpone intubation (can be delivered via an endotracheal tube or a specially designed face mask, respectively). Commonly used at night for the treatment of sleep apnea.
AV
=
assisted venrilation; CV
gen; l:E rat io
=
=
conrrolled venrilation; FlO:
=
inspiratory rime to expiratory rime ratio; IMV
ventilation; PEEP
=
positive end-expiratory pressure; RR
=
fraction of inspired oxy =
Intermittent mandatory
respiratory rate; SIMV
=
synchronous IMV; VT = tidal volume. Sources: Dara from P Marino. The ICU Book (2nd cd), Philadelphia: Lea & Febiger,
1998; AS Slutsky. Mechanical ventilation. American College of Chest Physicians' Con
sensus Conference Isee comments). Chest 1993; 104: 1833; and SF !-lowman. Mechani cal ve'nrilation: a review and update for clinicians. Hospital Physician 1999;December:
26-36.
Ventilatory Settings
Ventilatory settings are parametets established ro provide the neces sary support to meet the patient'S individual ventilarory and oxygen ation needs."· Establishment of the ventilatory serrings is dependent on the patient'S (1) atrerial blood gas levels, (2) vital signs, (3) airway ptessures, (4) lung volumes, and (5) pathophysiologic condition, including the patient'S ability to spontaneously breathe."· Ventilator serrings, subdivided into those that influence oxygenation and those that influence ventilation, are presented in Table III-B.3.
Complications of Mechanical Ventilation
Auto Positive End-Expiratory Pressure
Auto positive end-expirarory pressure (PEEP) occurs when lung vol umes fail to return ro functional residual capacity before the onset of the next inspiration. The process leading ro auro PEEP is referred ro
API'ENDIX [II-B: MECHANICAL VfNIlLATION
819
Table III-B.2. Alternative Modes of Ventilation Mode
Characteristics
Pressure control ventilation
Delivers a preset airway pressure for a predetermined inspiratory time interval. Inspiratory time is usually prolonged, and patients are generally sedated because of discomfort due CO the prolonged mechanical inspiration. VT is determined by lung compliance; useful in cases in which barotrauma is thought to exacerbate the acute lung injury (ARDS); now also available in ACV or SIMV modes. A relatively rare technique of ventilation that is administered with frequencies of 100-3,000 breaths per minute and consequently small tidal volumes of 1-3 ml/kg. Primary advantage is dramatic reduction of airway pressure and has shown beneficial results in neonates and adults with ARDS. A rarely used technique involving the use of an inspiratory to expirarory ratio of morc than 1 ro 1; can be delivered as a pressure-controlled or volume cycled mode. The proposed benefit is the recruitment of a greatcr number of lung units during the respiratory pause and longer inspiration. Potential risk of generating autO PEEP and dynamic hyperinnation (see text). Only set parameter is the minute ventilation; if spontaneous, unassisted breaths do not meet that minute ventilation, the venrilator makes up the difference by supplying mechanical breaths. Delivery of ACV, SIMV, and PSV modes of ventilation via a nose or face mask to reduce the need for intubation. Shown to be useful in reducing in-hospital mortality in CO PO patients and long-term use in patients with neuromuscular diseases. Exposes the chest wall to subatmospheric pressure during inspiration ro reduce intrapleural pressure, thereby allowing air ro emer the lungs. Efficacy has not been demonstrated in patients with COPD and is unproven for acute respiratory failure.
High-frequency oscilla.rion ventilation
Inverse rario ventilation
Mandatory minute ventilation
Noninvasive positive pressure ventilators (NIPPV)
Negative pressure ventilators
820
AClITE. CARE HANDBOOK FOR PHYSICAL THERAI'ISTS
Table ill-B.2. Corltj,med Mode
Characteristics
Airway pressure release ventilation
Lungs are kept inflated with a preset airway pres sure, and exhalation occurs during cyclic reduc tions in pressure. Advocated for protecting thc lung from high peak airway pressures, although no benefit ha been demonstrated over conventional methods.
(APRV)
High-frequency jct ventilation
Uses a nozzle and injector to deliver jets of gas directly into the lung at high rates. Attempts to reduce mean airway pressurc; howcver, no benefits have been identified.
Partial liquid ventilation
Uses perfluorocarbon liquids (docs not mix with surfacranr and has a high solubility for 02 and CO2). Lungs are filled with the liquid to approximately functional residual capacity; then, standard mechanical ventilation is attempted. Has nor demonstrated benefits above conventional ventilator modes.
ACV =
=
assist/comrol ventilation; AROS
=
adult respiratOry distress syndrome; COPO
chronic obstructive pulmonary disease; I:E rario
ratio; PEEP
=
=
positive end-expiratory pressure; PSV
inspiratOry lime 10 expIratory time =
pressure supported ventilation;
synchronous intcrmittcnr mandatory ventilation; VT = tidal volume. Sources: Data from P Marino. The ICU Book (2nd cd). Philadelphia: Lea & Fcbiger,
SIMV
=
1998; AS Slutsky. Mechanical ventilation. American College of Chest Physicians' Con
sensus Conference Isee commentsj. Chest 1993; I 04: 1833; and SF Howman. Mechani
cal ventilarion: a review and updare for clinicians. Hospital Physician I 999;Oecember: 26-36.
as dynamic hyperinf/atioll.2•J The primary consequence of dynamic hyperinflation is increased air trapping, which results in physiologic dead space due to pulmonary shunting (perfusion is delivered to alve olar units that are not receiving fresh ventilation), which decreases gas exchange. Ultimately, this leads to an increased work of breathing owing to higher respiratory demand, as well as altered length-tension relationships of the inspiratory muscles. Auto PEEP and concomitant air trapping can occur when the minute ventilation or respiratory rate is too high, the inspiratory-expiratory ratios are not large enough, or the endotracheal tube is tOO narrow or kinked, when there is excess water condensation in the tubing, or in patients with obstructive lung disease. A combination of the aforementioned factors can increase the likelihood of auto PEEP. In patients with chronic obstructive pulmo-
Table lli-B.3. Ventilator Serrings Purpose
Setting
Characteristic
Oxygen
Fraction of
The percentage of inspired air that is oxygen; at normal respiratory rare (RR), tidal volume
ation
inspired oxy gen
(FIO,)
(VT), and flow rates, an FlO! of 21% (ambient air) yields a normal oxygen partial pressure of 95-100 mm Hg; an increase in the percentage of oxygen delivered to the alveoli results in a
greater Paol and therefore a greater driving force for the diffusion of oxygen 1Oto the blood. of 60% has been set as the threshold ....alue ro aVOid toxiclry with prolonged use.
Positive end expiratory pressure (PEEP)
FIOZ
The pressure maintained by the mechanical ventilator in (he air""ays at (he end of expiration; normal physiologic PEEP (maintained by sufficient sutfactant levels) is considered to be 5
em H 1 0. Semngs are adjusted as needed to maintain functional residual capaclry above closing capacity to avoid closure of alveoli. Closure of alveoli can result in shunting of blood past the alveoli without gas exchange, which results in decreased oxygenation.
Ventilation
RR
Set according to the amount of spontaneous ventilatory efforts by the patient; different
ventilatory modes, described in Table IlI-S.I, are prescribed according to the patient's needs; patients who are unable to generate any spontaneous breaths are fully ventilated at respiracory rates of
12-20 breaths per minute.
This rate is decreased accordingly for those who are able to generate spontaneous breaths. The amount of volume delivered with each breath is adjusted with respiracory rate to control partial pressure of arterial carbon dioxide (Pacoz)' VT
Excessive volume leads to increased airway pressures, and therefore pressures are routinely monitored to pre....ent barotrauma. At times, hypercapnia is allowed to prevent high lung pressures due to the delivered volume and noncompliance of lung tissue, termed permissive hypercapnia.
>
:g Z " X �
.. ?: l:
::; S; z
�
r
=
pressure·supponed ventilarion.
Sources: Data from P Marino. The lCU Book (2nd ed). Philadelphia: Lea & Febiger, 1998; AS Slutsky. �lech3nical ventilation. American Col·
lege of Chest Physicians' Consensus Conference Is� comments). Chest 1993; 1 04: 1833; and SF Howman. Mechanical ventilation: a review 3nd update for clinicians. Hospital Physician 1999;December:26-36.
� \? � �
Z o
g ,.,
o '"
�
-< �
� r
:i! '" '" >
"
� �
APPENDIX 111-8: MECHANICAL VENTILATION
823
nary disease who are on ventilator modes that allow them ro initiate ventilaror-assisted breaths (assisted ventilation, assist/control ventila tion, synchronous intermittent mandatory ventilation [SLMV], pressure supported ventilation [PSV]), the therapist should realize that activity could increase the patient-generated respiratory rate. Some modes will then, given the initiation of a breath, provide a set volume of air (assisted ventilation, assistlcontrol ventilation, SIMV) that could increase the likelihood of hyperinflation owing to autO PEEP. This can also happen in modes that do nOt deliver a set volume of air (PSV), because inspiration is assisted with positive pressure.
Barotrauma Barotrauma refers to damage ro the lungs caused by excessive airway
pressure. Many of the alternative modes of ventilation are geared toward reducing this complication (see Table III-B.2). In the normal lung, spontaneous inhalation without ventilatory suppOrt takes place because of negative pressure. The volume of inhaled air is limited by the return of intrapulmonary pressure back to atmospheric pressure in the lungs during inhalation. Because mechanical ventilation is pre dominantly delivered with positive inspiratory pressure, these normal physiologic mechanisms for preventing such trauma are bypassed, and pressures in the lung exceed normal pressures. Another consider ation is that many of the lung conditions requiring mechanical venti lation do not uniformly affect the lungs (adult respiratory distress syndrome, pneumonia). Inhalation volumes are delivered to those areas that are still normal, which can overdistend (causing high pres sure) as a result. This can produce stress fractures in the walls of the alveoli, thus exacerbating the acute lung condition.7,. Infants who are mechanically ventilated are five times more likely to develop bron chopulmonary dysplasia than are infants who are not mechanically ventilared.' It is thoughr thar batorrauma exacerbates the acute lung injury associated with adult respiratory distress syndrome.' Other complications associated with barotrauma include pneumothorax and subcutaneous emphysema.j The following are other possible complications of mechanical ventilation2,J.6: Improper intubation can result in esophageal or tracheal tears. If the artificial airway is mistakenly placed in the esophagus and is
•
824
ACUTE CARE HANDBOOK FOR PHYSICAL TIIERAI)ISTS
not detected, gastric distention can occur with the initiation of pos itive pressure. • Oxygen toxiciry: Oxygen levels rhar are roo high and maintained for a prolonged rime can resulr in (1) subsrernal chesr pain rhar is exacerbared by deep brearhing, (2) dry cough, (3) rracheal irrirarion, (4) pleuriric pain wirh inspirarion, (5) dyspnea, (6) nasal sriffness and congesrion, (7) sore rhroar, and (8) eye and ear discomfort.
Cardiovascular: High positive pressures can result in decreased car diac ourput from compression of great vessels by over-inflated lungs.
•
Weaning from Mechanical Ventilarion
The process of decreasing or discontinuing mechanical ventilation in a patient is referred to as the weaning process.6 A contributing factor to a successful wean from ventilatory support is the resolution or stability of rhe condirion rhar led to rhe need for venrilarory supporr. The parient cri teria for an attempt at weaning from mechanical ventilation include •
Spontaneous breathing
• Fracrion of inspired oxygen 20 em H20
•
Respiracory rate , 295-296
components of, 606, 608r
Hypertrophy of pro!>tate. benign. S84-
factors affectmg, 606, 609t in re,ectlon of organ transplantation,
586, 196
702-707
Hypcrvcnlilanon, lOOt H)·pcrvolenua. 764, 76S(
Immunocompronllsed patients, 607r
I lypodcrmis, 4,�8t
ImmunodefiCiency virus infection, human, 631-634. See also
11)'I>oglo!>sal nervc. 2921 llypoglyccnlla
III
HIV mfection and AIDS
diabetes melhrus, 677,
Immunoglobulm IgA nephropathy, 574-
685 Ilypoglycenlic agent!!. oral.
III
575
diabetes
mellnu!>. 678
II ypokalem l a, 766t
Immunosuppression, 607, 111
transplantation procedures, 703
Hyponatremia. 76.5t
and acutc relcction, 706
Hypoparathyroldl!im, 688-689
In bone marrow transplantation, 734
HYPOpituitarism, 666-667 Hypotension. orthostatic in heart transplantallOn, 726
111 IIlfectlon!!, 639-640 l lypOlh.ll.1nlll!o
and chrolllc relectlon, 706-707 drugs used 111, 704t-705t infections m, 707-708 Immunotherapy in cancer, 343, 344
and pituitary flillCtlOn, 660, 663
Impedance plethysmography, 373t
strULture and function of, 265t
Incontinence
Ilypothyroidlsm, 658-660
fecal,
Ilyporomclt)" of muscles, 295-296
urmary, 562, 584, 585(
Hypoventllalion, lOOt Hypovolemia, 764, 765t
III
cancer, 349
bladder neck suspension procedure in, 597
950
AClITE CARE HANDBOOK FOR PHYSICAL ll-iERAPISTS
Inconrinence--cotztitzlled In cancer, 348, 349
prostatitis in, 586 pyelonephritis In, 572-574
physical therapy in, 600
respiratory. 6 1 8-624
types of, 585t
sepsis in, 637-638
Infarction
of skin, 630
cerebral, 3 1 3
sputum analysis in, 109, 1 1 9
myocardial, 39-43. See also Myocar·
subclinical, 607t
dium, ischemia and infarction
terminology related (0, 606, 607t
of
roxoplasmosls, 637
Infections, 605-640 in arthroplasty, 207
in transplant recipients, 707-708 In bone marrow transplantation,
resection procedure in, 207-209 bacterial. See Bacterial infections
735-736 in lung transplantation, 730
in burns, 452-453
viral. See Viral infections
cardiac, 624-625
of wounds, 482
carrier in, 607t
Inflammatory demyelinating polyradicu
cerebrospinal fluid analysis in, 303 in chemotherapy and neutro�nia,
lopathy, acute, 320 Inflammatory phase of wound heahng,
343
472-473
communicable, 607t
Infl uenL1 , 6 1 9-620
in diabetes mellitus, 6 8 1
Inhalation IIljury in burns, 450-451
disseminated, 607t
Inotropic drugs in heart failure, 59, 867t
drug therapy in, 638, 848t-850t
Inspection. See Observation and inspcc·
sensitivity and resistance to, 6 1 2 , 6 1 5� 1 8, 623 evaluation of, 606-6 1 3
tion Inspir�Uion, 92-94 auscultation In, 1 0 1 , 103
history taking in, 606
capacity in. l 22f, 1 27t
laborarory studies in, 6 1 0-613
flow rale
physical examination in, 607-609 fungal
ratio
histoplasmosis in, 623-624, 635t in rml1splanr recipients, 707, 708 gastrointestinal, 630-63 I glomerulonephritis in, 575-576 host in, 607t immune system in, 606, 608t, 609t musculoskeletal, 629-630 neurologic, 625-629 nosocomial, 607t, 6 1 4
III
mechanical venrilation,
8221 to
expiration in mechanical ven tilation, 822t
reserve volume in, 1 22f, 126t Insulin in dLabetes mellitus, 674, 676t, 677 and hypoglycemia, 685 type 2, 678 Integumentary system, 436(, 436-437, 438t. See also Skin Intensive care
UI1I1,
757-759
antibiotic·resistant, 6 1 5-6 1 8
anxiery in transfer from, 758
prevention of, 6 1 4 , 6 1 5t. 639, 750
equipment in, 769
opportunistic, 607t in HIV infection and AIDS, 633634
patienr and family responses ro, 757758 Intercosral nerve, 279t
pathogen In, 607r
Interferons, 8591
physical therapy in, 639-640
Interleukin IL-2, 860t
in antibiotic-resistant infections, 6 1 7� 1 8 i n HIV infection, 634 in osteomyelitis, 630 in respiratory infections, 6 1 9 prevention of, 6 1 4, 615t, 639
Imental capsule, 260, 26 1 f, 2661 International normalized ratio, 28, 382384, 3851 abnormal, physical therapy guide· lines in, 429-430 in anticoagui:mt therapy, 4 15
INDEX
Interstitial cell stimulating hormone, 66 1 t Intervertebral disc disorders, 210-
Jackson-Prarr drams, 803t in liver transplantation, 7 1 5 Jejunostomy, percutaneous endoscopic, 800t-802t
213 artificial disc implantation in, 2 1 2213 indications for surgery in, 21 1 t intestines. See Gastroimesnnal system
Jejunum, 504t Jewen brace, 226t Joints arthroplasty of, 190-209. See also Arthroplasty
Intra-aortic balloon pump, 829-832, 830f-83 I f Intracranial pressure increase, 315, 321324
contracture in amputation, 895t dislocations of. See Dislocations Jugular vein distension pressure, 1 5- 1 6, 16f
brain herniation in, 321, 322f, 323 burr hole placement m, 325
951
Junctional arrhythmias, 78t
dlureflcs in, osmotic, 867t dramage m, 324t, 798t
KapoSI'S sarcoma in HIV infection and
mass effect in, 323
AJDS, 635t
midline shift m, 324
Ketoacidosis, diabetic, 680-68)
monitoring in, 791 -794
Ketonuria, 565t
equipment in, 792t-793r patient positioning in, 794 physical therapy in, 327, 791-794
Kidneys disorders of, 570-582 acure failure, 570-571
shunt procedures in, 326, 805t
in burns, 441t, 452
signs and symptoms in, 32 1 , 323t
calculi, 566, 579-580
treatment options m, 32 1-323, 324t Intubation, 794-808
surgery in, 596-597 chronic failure, 57 1-572, 600
m end-of-life care, deCISions on, 755
diabetes insipidus in, 667, 668
m mechanical ventilation, 812-813,
in diabetes mellirus, 572, 580-58 t I
8 1 3f
600
complications of, 823-824
end stage disease in, 5 7 1
cuff in, 8 1 4
glomerulonephritis, 574-577
and extubation, 8 1 2
in hypertension, 394t, 572
phYSical therapy in, 794, 807-808 T tubes for oxygen delivery m, 777t, 825 Iodine, radioactive, thyrOid uptake of, 655t Iron deficiency anemia, 405, 416, 866t
hypertension in, 395t interstitial nephritis, 578-579 nephrotic syndrome, 577-578 pathophysiology in, 570-582 postope:rative, 874 pyelonephritis, 566, 572-574
Irritable bowel syndrome, 534-535
referred pain in, 558(, 600
Ischemia
replacemenr therapy in, 587-595
cerebral, 312, 313 transient auack. 312 m vasospasm, 315 mtesrmal, 533-534 myocardial, 39-43. See also Myocar
surgery in, 595-596 vascular, 581-582 evaluation of, 561-570 angiography in, 567 biOpsy m, 569
dIUm, ischemia and mfarction
computed tomography in, 569
of
physical examination in, 563
pressure wounds in, 470 Ischium, fractures of, 174 Isoenzymes in cardiac evaluation, 2930, 30t hchmg In casts, 224
postoperative, in transplantation, 710 radiographic examination in, 566 radionuclide scans in, 568 ultrasonography in, 569
952
AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Kidneys--couti" lled
Lamineclomy, 2 1 0, 2 1 1 t
Structure and function of, 558-56 1 , 560f
Languagc. See Spt.."'tCh and languagc
rransplamation of, 708-7 1 2
Laparoscopy, 522, 523r
donors in, 700, 709
Large imestine
funerion rests in� 7 1 0
cecum in, 5041
mdications for, 708-7 1 2
colon Ln. See Colon
with pancreas transplantation, 720-
disorders of, 530-.540
nl
referred paLn
physical therapy in, 7 1 1-712 postoperative care and complications
Ill,
502r
funerion of, 504t Laryngectomy, I S I Laryngoscop� l S I
in.7!()-7 1 1
L.. .. l.rynx
rejection 10, 707, 71 t vascul;\( supply of
procedures Ulvolving, 1 5 1 struCture and function of, 9 1 t
angiography of, 567
Laser techniqucs III coronary angioplasty.
disorders of, 58 1-582
51
Knee amputation at level of, 891 r
L1tex allergy, 7S1
arthroplasty of, 1 96-20 t
Latissimus dorsi muscle in dynamic car
complications in, 199, 1 99t IIldicatlons for, 196 Infecnon and resection
diomyoplasry, 57 Lavage
Ill,
207, 209
physical therapy in, 1 99-20 1
gastric, 6 t 3 pulsed, in wound debridement, 487-
rricompanmental or fOtal, 1 97199, .l98f uOicompartmenral, 196-1 97, 197f
488 Laxatives, 864c Legionellosis. 624
arthroscopy of, 2 1 5-2 1 6 , 2 1 7t-2 1 8t
Leptrudin, 844t
cartilage transplantation procedure,
Leucine amillopepudase levels, 5 1 91
2 1 9-220, l l l f i n femoral fractures, distal, 179, 244r-245 r immobilizer device for, 227t in hip arthroplasty, 195 III
Leukemia, 332, 3331, 3 5 1 -352 rrealmCIll and prognosis In, 3B types of, 352, 3521 Leukocytes, 366r count of
in knee :lrthroplasty, 200, 20 I, 209
in cardiac evaluanon, 28
patellar fractures, 179-180, 245(-
differential, 379, 3801, 6 1 0
246,
i n hemarologlc disorders, 379,
range of morion in, 1 66t In arthroplasry, t 99, 200, 20 I , 209 in arthroscopy, 2 J 7t, 2 1 8t
in tibial plateau fractures, 180, 246t247, Kororko(f's sounds, 20, 2 I t Kussmaul's respiration, lOOt Kyphoscoliosis, respiratOry disorders in, ISO
380l, 38lf III
infections, 6 1 0
III
polycythemia vera, 409
trapping
III
venous insufficiency,
470 Leukoencephaloparhy, progressive mul ufocal, in HIV infcCtlon and AIDS, 635, Leukoplakia. oral hairy, in I-IlV mfcction and AIDS, 635r
Laceration, cerebral, 307t Lactase deficiency, 509t Lactate dehydrogenase
Lifestyle factors affecting wound heallng, 474 Light response of pupils, 293-294
in cardiac evaluation, 30r, 3 1
Lighrning injuries, 443-444
in liver disorders, 5 1 J I 5 1 8t
Limb posilion, observation of, 162
Lactogenic hormone, 661 r
Limbic system, 272
Lactose tolerance test, 509t
Lipase lc"cls, 5 1 9r
INDEX
Lipids
953
levels of, 890f
fecal,5 1 8t serum levels of in atherosclerosis,28-29, 387
treatment suggestions in,895t, 896t types of, 891 r-892t braces,splints,and orthoses for, 226t-
in cardiac evaluation, 28-29 drug therapy lowering, 61, 865t Lipoproteins high-density, 28-29, 387
227t casts for,222t coordination tests of, 300t fractures of,174-182,238t-251 t
low-density,28, 29, 387
leg length discrepancy in, 209
serum levels of
musculoskeletal examination of,163,
in :nherosclerosis, 28-29, 387 in cardiac evaluation, 28-29 drug therapy lowering, 61, 865t Lithiasis. See Calculi Liver
165t range of 1110tion in,166t peripheral nerves of,274,278t tendon reflexes of, 296t traction applied to, 231 r
cancer of, 350t, 350-35 I diagnostic tests in, 337t,5 16t, 5191 surgery in,350r cirrhosIs of, 542-543
ulcerations of in arterial insufficiency,468 in diabetes mellitus, 469f,471-472 neuropathic or neurOtropic,471-
encephalopathy and coma in diseases of, 543-544 evaluation of, 511, 516t-522t function rests in,511, 516t-520t, 715
472 in venous insufficiency, 468-470 Lumbar drainage device,798t Lumbar puncture,303 Lumbar spine fractures, 182, 184f
imagmg procedures in, 521t-522t
Lumpectomy in breast cancer, 347t
postoperative, in transplantation,
Lund and Browder formula on burns,
715 failure of, 713, 714t postoperative,111 transpl:lI1tarion, 716 function of, 505r labor:uory tests on, 511,516t-520t postoperative, In transplantation, 715 hepatitis of, 540-542 referred pain from. 502t regeneration of,542 transplalllarion of,712-717 domino procedure, 713 donors in,700,713 funenoll tests in,715 indicanons for,712 orthotopic, 713 posroperative care and complica tions in,7 J 5-716 rejection in. 707, 716 split liver procedure,713 veno-occlusive disease of, in bone marrow transplantation, 736 Lomusrine,855t Lower extremir)' amputation in, 887-888
446, 447t Lungs air trapping in,130 auscultation of,99-105 landmarks for,10 I , 1 0 1f barotrauma in mechanical ventilation, 823-824 in burns and inhalation injuries,451 cancer of, 344r. 344-345 diagnostic tests in, 337t risk factors in,335t conrusion of, 140t,144 in rib fractures,144,149 embolism in, 140t, 143-144. See also Embolism,pulmonary function rests of,121-124,122f-125f capacity measurements in, 121, 122f, 126t-l27t description and significance of, 126t-129t flow-volume loops in, 1 2 1 , 125f, 129t in obstructive disorders,121,123f, 125f postoperative, in lung transplanta tion, 729,730
ACI.1T1:. CARE HANDBOOK FOR PHYSICAl nl�RAPI\l\
954
I n neurologIC evaluatton, .10 1
Lungs-colltl1J11ed III
restrictive disordcrs, 1 2 1 , 124f.
m
vascular dIsorders. 37,�,
Malab�orpllon syndromes, 51.5-536.
125r
.1 5 1
volume measuremcnts in, 1 2 1 , 122f, 126" 1 27,
MalformatIon!., vascular
gas exchange In, 94-96
arteriovenous, 3 1 3-314. 403
hypermfbnon of, 1 3 0
congennJI, 403-404
dynamIc. t n postUve end-explratory pressure, 8 1 8. 820, 823
Malgalgne fractures. 175f Mammography. 337t
Interstitial dIsease of. 144
Manometry, esophageal. 5 t 3r
motions m respiranon. 92-94. 95f
Marshall·Man.:hetil-Kranrl procedure.
pneumonectOmy of, 1 5 1 . 345
197
scgmclltocromy of, 1 5 1
Masre((omy
structure and function of, 91t. 93f-
Mechanical venlllauon, 8 1 1-826. Su
94r
III
hreast cancer• .147,
a/so Ventilatory �upport
transplantatIon or, 727-732
M«hanor�eptof'j:. 1 1- 1 2
donors tn. 700, 701. 729
Mechlorethamine. 8.5.�r
double lung or bIlateral, 728, 7 3 1
MedIan nerve. 277t
functIon tests tn, postoptratlve,
Mediasuno!.Cop)'. IS I Mediastmum. 2
729, 730 with heart tr.msplamanon, 732-733
endoscopic examinarion of, 1 5 1
indications for, 727-728
MedIcal rC�()fd!.. 745-748
physical therapy
MedICal-surgICal eqUIpment. 769-808
m,
729-730, 731-
732 postoperative care and complica· nons in. 729-731
Medulla ohlong.1t.l. 267r MelanoC)'te-"llmulattng hormone, 661 r Melanoma. 332, .157
relectton in. 707, 730-73 1
Melena. $17
stngle lung, 728, 73 1
�Ielphalan. 8551
volume reductIon surgery, 1 5 1
Memory tests, 285 (
wedge resection of, 152
�tenmges
LuteinIZIng honnone, 661 t
tnflammatton nt. 626-627, 6J5t
Lymph node mvolvement in cancer. 336
structure .1nd jUllctlon of. 269, 269t. 270r
in lymphoma, 352-353. 3S3t stagmg of. 338, 338t surgery In, 339
�temnglus. 626-627 III
HIV IIlfec:uon and AIDS. 635t
Lymphatic system, 364
�lenlllgoenccphalltls. amebIC. 628
Lymphedema In breast cancer, 347,
Memsc«tomy. arthroscopIC. 216, 2 1 7,
348 Lymphoma, .l33" 352" 352-353, 353, Burkltt·s. 352 characteristics of, 352, 352, U1
HIV mfection and AIDS, 635t
Hodgkin's, 352, 352, stJging of. 353, 353,
Mental �tatu.. III
acute carc senlng. 757-758. 760
and cognitIve funetton, 285. 28St. See
a/so Cogmuve funetton examtnatton of. 282-286 COIl$CI(}u!.ness levels m, 282t. 282281 emouonal assessment
MacrolIde anllblotics, 849t Mafentde acelate tn burns, 460t Magnetic resonance imaging in cancer diagnosis, 337t
m.
286
Glasgow Coma Scale tn. 283-284. 284, spe«h and language ahlllt'Y
m,
286
m Ll1tr.lt:ramal pressure II1cre3!.C, 3231
tn gasrrolntestmal evaluation. 522
Mercapropunne. 8H(
m genttourmary evaluation, 569
Metabolic eqUIvalent) m exerCISC, 3.5t,
tn musculoskeletal examUlatJon, 1 6 8
49, 62
INDEX
Metabolism
in hip arthroplasty, 1 94, 196
in burns, 439
patient education on, 1 95, 196
disorders of
in resection procedure,208
acid-base balance in, 1 13, I 14, 115t, 1 1 6
weight bearing in, 192 in knee arthroplasty, '1 99, 200
bone disease in,689-692
patiem education on, 199, 200
screening for,651-652
weight bearing in, 199
tests in evaluation of, 67 I
in musculoskeletal examination, 165167
Metacarpal fracrures,189-190 Metaplasia,332 Metastasis, 332
955
in spinal surgery, 213,2 1 4 i n wounds,479, 494t
to bone,345-346
Mobirz type atrioventricular blocks, 79t
physical therapy in, 358-359
Mohs surgery,339
staging of, 338, 338t
Monoclonal amibodies in cancer ther-
Metatarsal fractures, 182 Methicillin-resistant staphylococcal infections. 615-616, 617 Methotrexate, 857t Microalbuminuria in diabetic nephropa thy, 580 Microbiology studies in infections,6 1 1 612 Microdisctctomy, 210,2 1 1t Micturition patterns
apy, 344 Mononucleosis, 634--6 36 Mosquito-borne viral encephalitis, 628 Motiliry disorders of esophagus, 525 of intestines, 532, 534 of stomach, 529 Motor function evaluation of, 294-297, 901-918 Berg balance [eS[ in, 902, 903f-
in acute renal failure, 570-57 1 history of, 5 6 1 -562 in prostatic hy pemophy, benign, 584585 urodynamic studies of,568
907£, 9071 cranial nerve tests in,289t-292t in Glasgow Coma Scale, 283, 284r muscle tone in, 295-296 reach rest in, 909-9 1 1, 9 1 0t
Midbrain, 266t
reflex testing in, 296-297
Midline catheters, 799r
six-minute walk rest in, 915-918, 9 17t
Mineralocorticoids,668,670-671 target sites and actions of,669t Minnesora rube,797t
strength testing in, 294-295 rimed get up and go test in, 902,
Miromycin,856t Mitoxantrone, 856t
908t, 908-909 Tinetti assessment in, 91 1 - 9 15,
Mitral valve anatomy and function of, 4t
9121-9 1 5!,9161 lnd gastrointestinal motility disor
disorders of, 45t replacement surgery in, 57
dets, 525,529, 532, 534 in intracranial pressure increase,
Mobility
323!
in amputation,895r-896t in ankle arthroplasty,206 in burns, 464,466t in claudication, intermirrent, 388 evaluation of
mobility in, See Mobiliry Momh cancer of, 354,355 risk factors in,335t,355 funcrion in gastrointestinal system,
six-minute walk test in,9 1 5-9 18, 9 1 7t timed get up and go test in, 902, 908!, 908-909 Tinetti assessment in, 911-915, 9 1 21-915t, 9 1 6t
504! Mucolytics,865t Multiple sclerosis,320-321 j\1urmurs cardiac,23t, 68 genitourinary, 563
956
ACt.rrE CARE HANDBOOK FOR PHYSICAL THERAI'I')TS
Muromonab-CD3 in organ rransplama rion,705t, 706 Muscle relaxants, 868r Muscles 111
respiratory muscles in, 92. 92t strucrure and fUllcrion of, 1 60 Mycob3cterial mfections in HIV mfection and AIDS, 635r,
critical illness myopathy,759
electromyography of,304 respiratory, 92, 92t strength testing of, 294-295 In burns, 464, 466[ in wounds, 479, 494t structure and funcrion of, 1 60
636r tuberculosis in,62 1 ,622, 636r tuberculosis in. 6 1 3, 620-623, 636l Mycophenolate mofetil in organ rrans plantarion. 70Sr Myelogcaphy, 1 68-1 69,304-305 prCC3utions after,305
tone of, 295-296
Myeloma, multiple. 333[, 354
tumors of, 333r
Myocardium
Musculocutaneous nerve,277t
anatomy and function of, 4t
Musculoskeletal system, 1 59-258
diseases of, 44,46r
disorders of, 1 69-232 anhroplasry in, 1 90-209 arthroscopy in, 2 1 5-2 1 7 braces and splints in,225-229 cancer,345-346, 346t
biochemical markers
111,
chest pain
Ill,
39-40, 92 1 , 923
cholestcrol levcls
rypes of, 3331, 345, 346r
complication!' in, 40, 4 1 t
casts in,220-224 cmical illness myopathy, 759
29-3 1 ,
301
diagnostic rests in, 337t
chest pain in, 922r III
classification of, 46r ischemia and inf3rcrion of, 39-43
111,
29
coronary arrcry byp3SS graft in, 52-53 drug therapy Ill, 59
in electrical burns,443
p-adrcnergic blockers in,853t
external fix3ror devices in, 229-
calcium channel blockers In,
230 fractures, 1 69-190, 237-258. See also Fractures
854, nitrates
Ill .
866t
lhrombolyti�, 50
Infections,629--630
electrocardiography in, 43
mecabolic, 689-692
hean ratc vari3bility in,26-27
osteomyelitis,629-630
management of, 50-53
physic3l therapy in, 237-258, 630
pathophysiology 111. 39-43
111
prolonged bed rest, 754t
soft tissue surgery in,2 1 4-220 experimental, 2 1 9-220 spine surgery in, 2 1 0-214 tmcrion in,230-232 exanllnnrion of, 1 60 - 1 6 9 diagnostic tests in, 1 67- 169 functional mobility and safety
physical therapy in, 3 1 revasculari7.3UOn procedures
111.
50-52 oxygen demand
III
exercise,67
Myoglobin in cardiac evaluation, 30t, 3 1 Myopathy in cmical illness, 759 Myotomes in musculoskelctal cX3rnin3uon, 1 63, 1 64t, 165t
issues in, 1 65- 1 67 history taking in, 1 60- 1 6 1 i n pain, 1 6 1
Nasal cannula for oxygen delivery, 7711 with humidificarion, 778f
physical examination in, 1 6 1 - 1 65
Nasoenteric feeding rubes,799t-800t
radionuclide scans in. 1 68, 337t
Nasogastrlc tubes, 8001
r3nge of morion in, 163, 1 65, 1 66t
Naso-pharyngeal c:lthClCr for oxygen
upper and lower-quarter screens in, 1 63-165, 1 641,1 65r in hem3tologic disorders, 378t, 379
deliver)" 772r-773r Nasotracheal tntubation in mechanical ventilation,8 1 2
INDEX
Nausea and vomiting antiemetic agents in, 34 1 , 342, 846t8471
957
anriparkinsonian, 321, 85 I t diuretic, 867t muscle relaxant, 868t
in chemotherapy, 34 1 , 342
in electrical burns, 443
hematemesis in, 527
in HIV infection and AJDS, 635t,
in radiation therapy, 3 4 1
6361
Nebulizers, 800t
infections, 625-629
Neck
in intracranial pressure increase,
cancer of, 354-355
3 2 1 -324
collar support for� 225t
neurosurgery in, 325-326
fractures of, 182, 183f, 1 84, 252t-
pathophysiology in, 305-321
2531 traction applied (0, 2 3 1 t
physical therapy in, 326-327, 356 postoperative, 872, 873
Neoplasms, 33 1-359. See also Tumors
in prolonged bed rest, 754r
Nephrectomy, 595-596
seizures, 3 1 6- 3 1 8 , 324t, 845t
Nephritis, interstitial, 578-579
in spine fractures, 1 82
Nephrolithiasis, 566, 579-580
syncope in, 3 1 9
surgery in, 596-597 Nephrolithotomy, 596
traumatic, 305-310 ulceration in, 4 7 1-472
Nephrons, 558
ventricular, 3 1 5-3 1 6
Nephropathy
i n viramin 812 deficiency, 406
in diabetes mellitus, 580-581 immunoglobulin (gA, 574-575 Nephros(Omy
evaluation of, 277-305 in coma, vegetative state, and brain death, 756f, 757
percutaneous stone removal in, 596
coordination tests in, 299
urinary diversion in, 597, 598f
cranial nerve tests in, 287, 288t-
Nephrotic syndrome, 577-578
2921
Nerve conduction velocity studies, 304
diagnostic procedures in, 299-305
Nervous system, 259-327
history taking in, 278-2 8 1
anesthesia affecting, 872 autonomic. See Au(Onomic nervous system
mental status examination in, 282286 mOtor function in, 294-297
and cardiovascular function, 1 0
observation
central. See Central nervous system
sensory function in, 298-299
conduction velocity in, 304
vision tests in, 287, 293-294
disorders of, 305-327
in,
281
vital signs in, 287
bladder dysfunction in, 584
in hematologic disorders, 378t
in cancer, 333t, 356
peripheral. See Peripheral nervous sys
cerebrovascular, 3 1 2-3 1 5 claudication in, 388 in compression from cast, 223 in critical illness polyneuropathy, 758-759 degenerative, 3 1 9-321 in diabetes mellitus, 47 1-472, 681684 signs and symptoms of, 683t6841 types of, 683r-684t drug therapy in, 325 anticonvulsant, 845t
tem and respiratory function, 90, 92t structure and function of, 260-277 Neuropathy in critical illness, 758-759 in diabetes mellinls, 471-472, 681-684 signs and symptoms of, 683t-684t types of, 683t-684t familial amyloidotic polyneuropathy, liver transplantation in, 7 1 3 i n HlV infection and AIDS, 635t, 6361 ulceration in, 4 7 1-472
958
AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Neurosurgery, 325-326
in musculoskeletal evaluarion, 1 61162
Neutropenia in chemotherapy, 343 Neutrophil coum in chemotherapy, 343 in infections,610
in neurologic evaluation,281 in respiratOry evaluation,98-99 in extrapleural disorders, 1 45(147t
Nitrate preparations, 866t Nocturia,561
111
134t
Non-rebreather masks for oxygen deliv ery,775t, 781 f partial,774t
obstructive disorders, t 3 1 t-
physical therapy based on, 1 54t in restrictive disorders, 138t-140t
Norepmephrlne,668, 671
in ruberculosis therapy,623
cardiac effects of,11 r
in vascular evaluatIon,367-368
target sites and actions of. 669t urine levels of, 671
Occipital lobc, 264t
Nose,91t Nosocomial infections, 607t,614 amibiotic-resistam,6 1 5-618 prevenuon of, 614, 615t, 639, 750 Nucleoside analogs in HIV infection and AIDS, 633 5'-Nucleotidase levels,5 1 9t
OculomotOr nerve,289t Odomoid process fracture,2521 Olecranon fractures, 186,188f,257t Olfactory nerve,2881 Oliguria, 561 in acute renal failure,570 Oncology,331-359. See also Tumors
Nutrition in anemia, 4 1 6, S66t in chemotherapy, 342 in
in wounds,480-482 Obturator nerve, 278t
Opioid therapy, 879, 8 8 1 t-882t epidural,882t
diabetes mellitus, 674,677
implanted pump for, 884t
and hypogl)'cemia, 685
in panem-controlled analgesia, 883t
in gastrointestinal disorders,550551
OpportulllstlC infections,607r in IfIV mfcct10n and AIDS, 633-634
dysphagia affecting, 524-525
Optic nerve,288t
and malabsorption syndromes,
Oral cavlry
535-536, 551 gastrostOmy/jejunostomy rubes in, percutaneous endoscopic,
cancer of,354, 355 risk factors in, 335t, 355 (unction in gastrolOtestinal system, 504t
800t-801t in hypoparathyroidism,689 nasoentcric feeding rubes in, 799t800t nasogastric rubes in, SOOt and wound healing, 474-475
Orders on comfort measures,755 do not resuscitate/do not intubate, 755 medIcal records on,746
Nystatin in burns, 461 t
Orientation to person,place,and time,
Obesity, respiratory disorders in, 150
Orthopnea, l OOt
Observation and inspection in burns, 462 in cardiac evaluation, 1 5-16 in gastrointestinal evaluation, 505507,506f abdominal quadrants in, 505, 50M in genitourinary evaluation, 562-563
assessment of,283, 285r Orthoses,225-229 Osmosis, 587 Osmotherapy in intracranial pressure increase,324t Osmotic diurencs, 867t Osteomalacia, 69 1 OsteomyelItIS,629-630
in hematologic evaluation,377
Osteoporosis. 689-690
in infections, 607-608
Osteosarcoma, 333t,3461
INDEX
Otorrhea, 316
959
Oxytocin, 661 t
Ovarian cancer, .148, 349r Pacemakers, cardl3c, 54-56, SSt
diagnosnc t�rs In, J37t risk buors
111,
temporary, 788t
.l3Sr
Paget's disease of bone, 691-692
surgery m, 3491
Pain, 877-884
Overflow Int:ontlllence, S85t
in arterial and venous disorders, 386t
OXlIlletry. 786t III cardiac evaluation, 2S 111
111
back, indications for spinal surgery
III
burns, 453, 465
III
chest. See Chest pam
III
compartment syndrome, 399
in,210
respiratory ev:tluarion, 109-1 1 1
Oxygen
assessment of, 463
akcolar partial pressure, 770 arterial partial pressure, 770 III
cardiac evaluation, 31
evaluation of, 877-879
normal values for, 112 III
respiratory evalu:ttion, 1 10,
III
I I Or, 1111, 112
burns, 463
physical therapy considerations In,
arterial satur:ttion
879 scales used
In cardiac evaluation, 25 III
hypoxemia. 770
III
oxygen therapy, 770
III respiratory evaluuion, 109-111,
Ill,
878t
111
sensory teSting, 298t
111
wounds, 478
In gastrointestinal disorders, 525, 921, 9221
I l or. 1111. 112
esophageal, 525
hypoxemia. 130, 770 indicanons for oxygen therap)" in. 770 l>igns and symptoms of. 11 I t
III
physical therapy
10,
551-552
referral parrerns
10,
50 I , 502t
genitourinary disorders
hypoxia, 113. 1 3 0
history of, 561
inspired fr:tCtlon. 770, 783
III
III
management of. 879-884
7761-7771, 770 In mcchalllc:tl vemilanon, 821t III
variable performance delivery, 7711-7751, 770
musculoskeletal, 161 In pancreatitis, 546. 547 III
therapy. 770-783 fixed performance system
Ill.
770,
phamom 11mb, 894r
III
reflex sympathetIC dystrophy, 398
10
wounds c\lalu3tion of. 478
7761-7771 humidification
nephroluhlaSlS, 579
referral parrerns in, 557, 558t, 600
fixed performance delivery,
Ill.
physical therapy in, 494, 494t
778f, 783, 813
IIldicatlons for, 770
Pallor in elevation test, 371t
III lung cancer. postoperative,
Palpation in burns, 462
]45 physIcal therapy
111,
778-782
tOXICity In, 824 variable performance SyStem
Ill,
770, 7711-7751 Ir.lnspon of, 96-97 Oxygenation, exrral:orporeal membrane, 836-837
III
cardiac evaluation, 16-17
III
gastroinre5[inal evaluation, 507
in genitourinary evaluation, 563 In hematologiC evaluation, 377-379 in infections, 608 In musculoskeletal evaluation, 163 or pulse, 16-17, 368-370 sires of, 18f, 369
Oxyhemoglobin saturation, 1 09-111, I l or. I I I I
III
respiratory evaluation, 105-107, 106£
111 hypoxemia. 770 monnoring of. 786r
III
extrapleural disorders, 145t-147t
960
ACUTE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Palpation-continued in obstructive disorders, 1 3 1 t-134t physical therapy based on, 154r in restrictive disorders, 1 3 8t-HOt in vascular evaluation, 368-370 Pancreas, 545-547 disorders of
Parietal lobe, 262t-263t Parkinson's disease, 321 drug theraPY
Ill,
32 1 , 85 1 t
Patella fractures of, 179-1 80, 245t-246r III
knee arthroplasty, 1 97- t 99
Pecwrai nerves, 279t
cancer, 350t, 35 1
Pectonloquy, whispered, 104
diabetes mellitus in, 673-685
Pelvis
pancreatitis, 545-547
ampUlation at level of, 892t
referred pain in, 502t
fracrures of, 1 74-175, 175f
scrccning for, 652
man 1 4-3 I .�
10,
Subdural space, 270t
S02t
in Zollinger·Ellison syndrome, 529
Sun exposure burn� In. 444 skin cancer in, .1)6-1)7
function of, S04t
Suprascapular nerve. 277t
gastrectomy of, 549
Supravemflcular tachycardia. 74t
lavage procedure, 6 t 3
paroxysmal, 82f
Stool analysis
Swallowing difficulty, S24t, 524-.525.
In cancer diagnosis. 337t fat In, S 1 8 t
126• .\ 5 1 Sweat glands. I n IIltegume1Hary system.
occult blood in, 5 1 Or
416.417
Stratum
Sweat rest
111
cystic fibrosis. J 19t
basale, 438r
Syme's amputation. 8 9 1 t
corneum, 438t
Sympathetic nervous system, 274
granulosum. 438t
of heart. 1 0
spmosum, 438t
III reflex sympathetic dystrophy, 398
Strength testing, 294-29S in burns, 464, 466r
Symphysis pubiS disruption. 1 7Sf. 2381
in wounds, 479, 494t
Syncope. 3 1 8-3 I 9
Strcngthenlng exercises III
Synovial fluid an.llysls. 6 1 2-6U
hip arthroplasty, 1 95
in knee arthroplasty, 199, 200 10
SympathomlmetlCs. 8671
Systole. 6 blood prl:�ure In. 1 9, 19t. 391t. 7841,
resection procedure, 209
7871
Streptococcal infections glomerulonephrins
In,
57S-S76
rheumatic fever 10, 624-625 of skin, 630 Streptokinase. 868t
T tubes for oxygen dehvery. 777t 111
wealllng from mechanical ventil., tion, 825
T.1chycardm
Streptozocin, 855t
Junctional, 78t
Stress, In intensive care unit sening,
supraventricular, 74t
757-758 Stress incontinence, 585t Stress testing, 33-36. 374t
paroxysmal. 82C ventricular, 76t. 83f· Tachypnea, 1 0 1 1
dobutamine In, 32, 33
Tacrolimlls In organ transpbnt:mon, 7041
echocardiography in, 32, 33
Takayasu'l. arteritis• .397
exercise 10, 32, 33-36
Tamponade
indICations for, 33-34
pericardia I, 47t
thallium in, 36
In variceal hemorrhage. esophagogas·
Stridor, 1 0 3
Inc lube in. 797t
Stroke, 3 12-3 1 3
TaMc sense. testing of, 290t, 2 9 1 1
Stroke volume, and cardiac output, 7
TectOspiTl.ll traCI, 276t
Stupor, 2S2r
Teeth. S05t
Subacromial decompression, arthro·
Telemetric monitoring in electrocardio
SCOpIC, 2 1 6, 2 1 7, 2 1 9t Subarachnoid space, 270t
graphy. 27. 78.\1 cellular phone Interference in. 27
INDEX
Teletherapy, 340, 34 t
969
venous, 400-40 I
Temperature
in hip arthroplasty, 195
In burns, 453
I-Iomans' sign in, 372t, 40 I
in infections, 609
pneumatic compression stockings in, 795t
integumentary system in regulation
pulmonary embolism in, 143-144,
of,437 in IIltracr:mial pressure IIlcrease man
400, 401-402 renal vein, 582
agement, 324t testing of sensanon of, 298t Temporal arteritis, 397 Temporal lobe, 26 ..[
Thyrocalcitonin, 653t Thyroid gland, 6 5 1 , 653-660 disorders of, 656-660
Teniposide, 859t
exercise in, 655-656, 660
Tentoriulll cerebelli, 269t
hyperthyroidism, 656-658, 657t, 660
Tesllcular cancer, 348, 349t
hypothYTOidism, 658-660
Tetracyclines, 850t
screening for, 65 1
Texas catheters, 803t Thalamus, 265t
function of, 653, 653r and pituitary function, 660
Thalassemia, 4 1 2 Thallium
III
stress resnng. 36
tests in evaluation of, 653-656, 654r, 6551
with dipyridamole, 36 Thioguanine, 857t
Thyroid stimulating hormone, 653, 6541, 660
Thiotepa, 855t Thoracentesis, 1 5 1 , 6 12 Thoracic nerve, long, 279t
target sites and actions of. 66 1 t Thyroiditis, 657t
Thoracodorsal nerve, 279t
Thyrotoxicosis, 656-658, 657t, 660
Thoracolumbar spine fractures, 182,
Thyrotropin, 653, 654t, 660
2531-2541 Thoracolumbosacral orthosis, molded, 2261 Thoracoscopy, 1 5 2 Thromboangiitis obliterans, 396-397
target sites and actions of, 66lt Thyrotropin-releasing hormone, 654t Thyroxine, 653 serum levels of, 654, 654[, 655 target sites and actions of, 653t
Thrombocyres, 366t
Thyroxine-binding globulin, 654
Thrombocytopenia, 4 1 2-414
'Tibia
In bone marrow transplantation, 736
in ankle arthroplasty, 206
In heparin therapy, 4 1 3-4 14
fractures of, 180-182, 246t-249t
physical therapy in, 429 and thrombotic purpura, 4 1 4 Thrombolytic therapy, 868t in myocardial infarction, 50 transcatheter, 423 Thromboplastin time, partial, 382, 384, 3851 in anticoagulant therapy, 4 1 5 111
cardiaC evaluation, 28
Thrombosis arterial, 392 in thromboangiitis obliterans, 396397 111
disseminated intravascular coagula tion, 4 10
In thrombocytopenic purpura, 4 1 4
diSl.I, 180-182, 2481-2491 in plateau, 1 80, 1 8 1 f, 246t-247t Schatzker classification of, I SO, l S I r in shaft, 1 80, 24St in knee arthroplasrr, 1 96-201 Tibial artery, in femoral-posterior tibial bypass graft. 424f Tibial nerve, 278t liclopidine hydrochloride, 8 5 1 r Tidal volume, 122£, 126t in mechanical ventilation, 821 t Tineni performance oriented mobility asscssmem, 9 1 1-915, 9 1 2t9 1 51, 9 1 61 Tirofiban, 8 5 1 t Tissue plasminogen acrivarors, 312
970
AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
TNM staging system, 338,338t
in bone marrow transplantation,
Tobacco use, 355. See also Smoking Tone of muscles, 295-296 Tongue, 505r
735-736 in lung transplantation, 730 of kidney, 708-7 1 2 . See also Kidneys,
Torsades de poi nrc,76t Touch sensation, testing of, 298t
transplantation of
of liver, 712-717. See also Liver,
Toxicity
transplantation of
of carbon monoxide, 451
of lung, 727-732. See also Lungs,
of digitalis,59,60t, 867t Toxoplasmosis,637
transplant:nion of organ procurement and distribution
cerebral, in HIV infection and AIDS, 635r
system in, 701 of pancreas,717-721. See also Pan
Trachea
creas, transplantation of
auscultation of breath sounds in,102
physical therapy In, 737-741
cancer of,344t
activity progression in, 740
inrubation in mechanical ventilation,
basic concepts in, 738-740
8 1 2-8 1 3, 8 I3f
in bone marrow rransplam::aion,
complications of, 823-824 cuff in, 8 1 4
735,736, 737 education of patients in, 740-741
resection and reconstruction of, 1 5 2
goals of,738
StruCture a n d function of, 91t
in heart transplantation, 725-727
and transtracheal catheter for oxygen
in kidney rransplanration, 711-7 1 2
delivery, 773t Tracheostomy, 152, 812-8 1 3
in liver rransplamarion, 717 in lung transplant:uion,729-730,
and mask o r collar for oxygen deliv ery, 774r, 780f, 8 1 3 and rube for mechanical venrilation, 812-813
731-732 in pancreas transplanration, 720 postoperative care in,701-702 rejection in, 702-707. See also Rejec
Traction, 230-232 complications of, 230-231 , 232 rypes of, 230, 231r
tion in organ transplantation types of procedures, 698 Transtracheal catheter for oxygen deliv
Transfer anxiety, 758 Transfusions, 416-422
cry, 773r Trauma
adverse reactions to, 4 J 6, 420t-4 2 1 t
axonal injury in, diffuse, 307r
indications for, 417t-419t
barotrauma in mechanical ventilation,
and physical therapy,416, 422 products used in, 4 1 7t-4 19t
823-824 of b,,;n, 305-306, 307r-309r
Transient ischemic attack,3 1 2
in burns, 439-467. See also Burns
Transplam:uion,697-741
compartment syndrome in, 399
of bone marrow, 343, 353, 733-737.
See also Bone marrow, trans plantation of of cartilage, autologous, 21 9-220, 221f donors in. See Donors in transplanta tion procedures gastrointestinal procedures, 549 of heart,58, 7 2 1 -727. See also Heart, transplantation of indications for,698-699 infections in,707-708
equipment in manag�ment of, 220232 flail chest in, 149 fractures in. See Fractures lung contusion in, l t,Or, 144, 1 49 pneumothorax in, 148 reflex sympathetic dystrophy in,398 of spinal cord, 306-3 10,3 1 1 t in fractures o f spine. 1 82 wounds in,468 Trendelcnburg position in postural drainage, 897, 899
INDEX
Trendelcnburg rcst, 371 t
971
staging in, 338, 338t
Tricuspid valve. 41
myeloma, 333[, 354
Trigeminal nerve, 289r-290r
of nervous system, 356
Triglyceride levels, 29
of pancreas, 350t, 3 5 1
Triiodothyronine, 653
para neoplastic syndromes in. 336t
resin uptake, 6! 5t serum levels of, 654, 654t, 655 target sites and actions of, 653t
of parathyroid gland, 687 pheochromocytoma, 395t, 672-673 physical therapy in, 358-359
Trochlear nerve, 289t
of pituitary, 664, 667
Troponins in cardiac evaluation, 30t,
of prostate. See Prostate, cancer of
30-3 I
radiation therapy in, 338, 340--3 4 1
Trypsinogen immunoreactive assay, 520t
renin-secreting, hypertension in, 395t
Tuberculosis, 620-623
risk facrors for, 333, 335t-336t
classification of, 621
signs and symptoms in, 333-336
disseminated or miliary, 622
of skin, 356-358
gastric lavage in, 6 1 3
staging of, 336-338, 338r
i n I-IIV infection and AIDS, 62 1 . 622, 636r multidrug-resistanr, 623 Tumors, 3 3 1 -359
in lymphoma, 353, 353r surgery in, 338, 339-340 of thyroid gland, 657t Tunica
of biliary fraCI, 350
adventitia, 364t
biothcrapy in, 338, 343-344
intima, 364t
of bone, 333t, 345-346, 346t bone marrow transplantation in, 343,
media, 364t Tuttle test, 5 1 3t
353 of breast, 335[, 337r, 343, 346-348 chemotherapy in, 341-343, 854t860t. See also Chemotherapy
Ulceration in arterial insufficiency, 468, 469t in diabetes mellitus, 469t, 4 7 1 -472
classification of, 332, 333t
neuropathic or neurotropic, 471-472
definitions of terms related [C, 332
in peptic ulcer disease
diagnosis of, 336, 337t
drug therapy in, 862r-863r
etiologies of, 333, 334t
duodenal ulcer in, 528-529
gastrointestinal, 348-349, 349t, 539,
gastric ulcer in, 528
540 diagnostic tests in, 337r of esophagus, 526 risk factors in, 335t, 336t of stomach, 348, 3491, 529 genitourinary, 335t, 337t, 348-349
in pressure wounds, 162, 163, 470-471 staging and c1assificarion of, 483. 483r in venous insufficiency, 402, 403, 468-470, 469, Ulna, fractures of
grading of, 338, 339t
in olecranon, 1 86, 1 88(, 25h
of head, neck, and face, 354-355
in shaft or distal, 1 8 9, 258t
hematologic, 35 1-354
Ulnar artery, Allen's test of, 372t
hyperthyroidism in, 657t
Ulnar nerve, 277c
leukemia, 332, 333t, 351-352, 353
Ultrafiltration, 587
of liver, 337r, 350-351, 5 1 6t, 5 1 9 t
Ultrasonography
of lungs, 335t, 3371, 344-345
in gastrointestinal evaluation, 522t
lymphoma, 352-353. See also Lym-
in genitourinary evaluation, 569
phoma metastasis of, 332 to bone, 345-346 physical therapy in, 358-359
in neurologic evaluation, 301-302 of thyroid gland, 655t in vascular evaluation, 373t Ultravioler radiation burns, 444
ACUTE CARE HANDBOOK FOR PHYSICAL THERA1)ISTS
972
Up and go test, rimed, 902, 908[, 908-909 Upper extremity amputation in, 888 levels of, 889f
poliovirus, 626 Vacuum Assisted Closure device, 489 Vagus nerve, 291 t Valvular heart disease
treatment suggestions in, 8951
pathophysiology in, 44
types of, 892t-893,
replacement surgery in, 5 7
casts for, 222t-223t coordination tests of, 300t
signs and symptoms m , 45t Vancomycin-resistant enterococcal infec tions, 6 16-61 7
fractures of, 1 85-190, 254t-258t musculoskeletal examination of, 1 63, 164t range of morion in, 166r peripheral nerves of, 274, 277t slings and splints for, 22St tendon reflexes of, 2961 traction applied to, 2 3 1 r Uracil mustard, 855r Urea nitrogen in blood, 565-566 after angiography, 370 Ureterolithotomy, 597 Ureters
Vanil1ylmandelic acid, urinary, 671 VariCOSIty esophagea l, 526 esophagogastric tamponade tube in, 797t positioning precautions in, 5 5 1 venous, 399�00 Trendelenburg's test in, 37 1 t Vascular resistance, systemic, 1 2 , 1 9 Vascular system, 363�30. See also Blood vessels VasculitIS, 395-397
calculi in, 597
Vasodilators, 869t
pain referred from, 558r
Vasopressin. See Antidiuretic hormone
radiographic examination of, 566
Vasospasm
Urethra biopsy of, 570 endoscopy of, 568
of cerebral artenes, 3 1 5 o f coronary artery, myocardial ischemia in, 40
Urge incontinence, 585t
Vegetative scate, persistent, 755-757, 756r
Urinalysis, 563-564, 565r
Veins, 364
etiology of abnormalities in, 565t
characteristics of, 365{
specimen collection in, 564
disorders of, 399-403
Urinary system. See Genitourinary system
chrOniC insufficiency, 402--403
Urine
clinical lindings in, 386t
analysis of, 563-564, 565t diversion procedures, 597-599, 598f specimen collection, 564 Urobilinogen, 520t Urodynamic srudies, 568
skin dIsorders
Ill,
thrombosis. Sce Thrombosis, venous varicose, 37lt, 399�OO
Uroflowmetry, 568
Vena cava, Sf
Urography
Venodyne boots, 795t
excretory, 566-567 retrograde, 567
Veno-occlusive dlse3se of liver, in bone marrow transplantation, 736
Urokinase, 868t
Venti mask, 776t
Urolithiasis, 583-584
Ventilation, 92
Uterus, cancer of, 348, 349t
402, 403. 468-
470, 469t
airway pressure rtlease, 820t
diagnostic tests in, 3371
alveolar. 127t
risk factors in, 335t
assist/control, 8 1 7t, 813
surgery in, 349t
ventilator settings in, 822t assisted, 8 1 7t, 823
Vaccination influenza, 620
controlled, 8 1 7t definition of, 89
INDEX
high-frequency jet, 820t
increase in, 315, 32 1 -324
high-frequency oscillation, 819t
normal range in, 3 2 1
and hyperventilation, lOOt
973
Ventricles o f hean
and hypoventibtion, lOOt
anatomy of, 4t
intermittent mandatory, 8 1 7t
arrhythmias of, 76t-77t, 83f-86f
synchronous, 8 1 7e, 823
ablation procedures in, 53
in weaning from mechanical venti-
automatic implantable defibrillator
lation, 824
in, 56
inverse ratio, 8 1 9t
in ectopic foci, 44, 77t, 84f
maximum voluntary, 129t
in premature contractions, 44, 77t,
minute volume in, 127t, 8 1 9t negative pressure, 8 1 9t partial ltquid, S20t and perfusion ratio, 96 mismatch in, 96, 97f in radionudide scan, 120- 1 2 1 positive pressure, 8 14-8 1 5, 8 1 9r noninvasive, 8 1 9r pressure control, S I 9t pressure suppaned, 8 1 7t, 823 ventilator settings in, 822t in weaning from mechanical venti lation, 825 Ventilatory support, 8 1 1-826
85£ assist devices for, 832-836, 838 external, 833, 834£, 835r internal, 833, 833f, 835t physical therapy in, 835-836 weaning from, 834 in Batista procedure, 58 diastole of, 6, 1 9 , 1 9 t and end diastolic pressure, 6 ejection fraction of, 6 function of, 4t factors affecting, 7, 8f systole of, 6, 1 9, 19t Venrriculectomy of heart, partiaJ Jeft, 58
bronchopulmonary hygiene in, 826
Venrriculoatrial shunt, 326, 805t
complications in, 8 1 8-824
Ventriculography, 38
cuff in, 8 14
Ventriculoperironeal shunt, 326, 805t
extubation in, 8 1 2
Ventriculostomy
indications for, 8 1 2 i n intracranial pressure increase, 324t intubation in, 8 1 2- 8 1 3 , 8 1 3f complications of, 823-824 modes of, 8 1 5 , 8 1 6f
drainage of cerebrospinal fluid in, 324t monitoring of intracranial pressure in, 792t Venturi mask, 776f, 782f
alternative, 8 1 9t-820t
Vertebral arteries, 272, 273t
conventional, 8 1 7t-81 8t
Vertebral column. See Spine
negative pressure, 819t
Vesicular breach sounds, '102
objectives of, 8 1 1 - 8 1 2
Vestibulocochlear nerve, 290[-291 t
physical therapy i n , 8 1 4, 826-827
Vestibulospinal cract, 276r
positive pressure, 8 1 4-8 1 5 , 8 1 9t
Vibration sense, testing of, 298t
noninvasive, 8 1 9f
Vinblastine, 859r
pressure-cycled. 8 14, 8 1 5
Vincristine, 859c
time-cycled, 8 1 4
Viral infections
volume-cycled, 814-8 1 5
cancer related to, 334t
ventilator settings in, 8 1 8, 821 t-822t
cytomegalovirus, 635f, 636-637
weaning from, 824-826
encephalitis in, 627-629
physical therapy in, 826-827 Ventricles of brain, 269-271 circulation of cerebrospinal fluid in, 269-271 , 271£
gastroenteritis in, 630 HIV infection and AIDS in, 63 1 -634.
See also HJV infection and AIDS
dysfunction of, 3 1 5-3 1 6
influenza in, 6 1 9-620
pressure of cerebrospinal fluid in, 321
meningiris in, 627
974
AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Viral infections-co1ltinued
ascendtng and descending tracts in, 274, 276t
mononucleosis in, 634-636 poliomyelitis in, 625-626
Whooping cough, 620
rhinitis in, 6 1 8
Willis arterial circle, 272, 272f
i n transplant recipients, 707, 708
Withdrawal syndrome in alcohol abuse, 760-76 1
Vision cranial nerve functions in, 288t, 289t
Withholding and Withdrawing medICal therapy, 755
in hematologic disorders, 378t hypertension affecting, 394t in intracranial pressure increaSt, l2lt resting of, 287, 293f, 293-294
Wounds, 435-436, 468-495 in arterial insufficiency, 468, 4691 assessment of. 476-483
Visual field deficit, 287, 293f
in burns. See Burns
Vital capacity, J 22f, 126t
chronic, 476
forced, 1 2 1 , 124, 128t
cleansing and debridement of, 483--488 sterile technique in, 485
Vital signs in chemotherapy, 343
culrure of, 482
in infections, 609
in decubtrus ulcers, 162, 163, 470-
in intracranial pressure incre3St, 323t
471 stagmg and classification of. 483,
in neurologic evalu3tion, 287
483t
Vitamin B I 2 deficiency, 405-406, 4 1 6, 866t
in dia betes mellitus. 469t, 471-472
Vitamin 0, 437
drainage from. 4 8 1 -482
in liver failure, 7 1 4 1
dressings in, 487, 488-489, 490t492t
in osteomalacia, 6 9 1
Voice sounds in respir:ltory evaluation, 104-105
healing of, 472-476 management of, 483-495
Vomiting. See Nausea and vomiting
III
von Willebrand's discase, 4 1 1
phYSical therapy in. 493-495. 494l
neuroparhles, 471-472
prevention of. 494t Warfarin therapy, 4 1 5, 845t
staging and classification of, 483.
Water deprivation test, 662r-663r
483t
Water loading test, 663t
surgical, 468
Weaning
in trauma, 468
from intra-aortic balloon pump, 832
in venous IIlsufficiency, 402. 403,
from ventilatory suppOrt, 824-826 physical therapy in, 826-827 from ventricular assIst device. 834
468-470, 469t Wrist
Wegener's granulomatOSIs, 396
amputanon at level of, 892t I n carpal (racfures. 1 89
Weight-bearing
range of motion in, 1 66t
in casts, 224 in hip arthroplasty, 192
Xylose absorption test, 508t
in knee arthroplasty, 199 in resc