A Colour Atlas of Burn Injuries (Chapman & Hall Medical Atlas Series, 9)

Contents Preface

1 Classification of burns Introduction Partial thickness burns Full thickness burns Burn depth Area

2 Types of burn Scalds Flame Contact Friction Electrical Burns Chemical Burns

3 Early management

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1

2

4

5

6

7

9

11

13

14

16

16

21

25

Resuscitation Wound care Escharotomy Fixation of fractures

26

28

35

39

4 Complications

43

Inhalational injuries Tracheostomy Burn wound infection Trauma: Metabolic consequences of injury

5 Late management Anaesthesia Wound excision Wound closure Burn injuries of special areas Physiotherapy

6 Sequelae Scars Splints Heterotopic calcification Renal stones Pigmentation and malignant changes Neglected burn injuries Non-accidental injuries Pathology

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49

51

59

63

64

69

74

79

92

101

102

105

108

109

110

110

111

113

Further reading

115

Index

117

v

re face ~

.,.:-". are several excellent text-books on bums and their management, but few -.'. ",U illustrated and almost none in colour. Most of these texts are written ~ ;;pccialists, or those planning to become specialists, or cater for special - :~:-£>st groups. There is therefore an opportunity for a book that is written for - ~ ~ .: who may work in a burns centre, or for others who deal with bum :-':::;:::1(S and who need a broader view than the burns specialist. ~e s tudy of burns lends itself well to visual representation as the injuries ~~-: at least initially, in the skin and are therefore readily observable . This :: ~' __"ur Atlas is designed for those who wish to find out more about the - ;:,: ~e nt kinds of bum, how they are caused and how they can be managed. It ~ :,x' those who are seeking an introduction, whether nurses, physio­ ,- ,:.~a pi s ts, occupational therapists, dieticians, pharmacists, social workers or :-~:..::..l-to logists, for doctors in training, those preparing for higher exams, for C~~-:eri ologists and pathologists. ~e text is short and didactic, and is used to elaborate and explain the _...;,s rrations and their legends. I have deliberately avoided being controversiaL _ . _,.an ~' areas have been glossed over or ignored, but it was felt that it was better 0..:' ~1a \' e a short interesting text that could be quickly comprehended, rather :.:-..l.' an all-embracing text that would be too detailed and of less general ~:." ~eaL The reader is advised to go to the textbooks listed in the bibliography !,:, ~ :he arguments and further opinions and advice. There is a generous index .:.:-.j a specially selected list of excellent references which give a review of many : ~ ? :cs , and are themselves a source of further and specific references. The Colour Atlas is written and published as a mark of respect to the nurses .. the Bums Unit at Queen Mary's Hospital, Roehampton . I sincerely admire ,'-,eir care, concern and love. It is a privilege to work with them . The nursing of :~~ ents with burns remains one of the few areas in medicine where individual :-::.: ses can be o(profound and lasting influence. Their compassion and gentle­ :-."'5S, their concern and understanding, is remembered for ever by patients and ~neir relatives . Everi. when it is clear that one of their patients cannot survive an ,,:':envhelming injury, they are comforted and guarded, and treated with ~ .-?5pect and dignity . I honour all who work with burn patients . To Jonathan Chandy, who has written the section on anaesthesia, my s:.." cere thanks. Enormously kind and considerate to his patients, who have got : 0 know him well, he has been unstinting with his time and concern . He has :Yerseen aIr patients on ventilators and those critically ill, and has, together -·.i th Alain Landes, safely cared for those undergoing surgery and repeated "'::cessing changes. He has shared much of the burden of management of the 3..:-u te patients, and has been responsible for the training of many young i :-.aesthetists in burn care. ~ly gratitude is offered to all those who work in the Burns Unit at Roehamp­ :,'n . in particular Ruth Clarke and Debbie Steer, nursing sisters, Manu Perin­ ?anayagam and Mike Weinbren, microbiologists, and Duro Johnson, social '.\'orker, Muriel Gaul, dietician, Claire Clarke, physiotherapist, and Sarah '''"right, occupational therapist, and the many trainee plastic surgeons who . d\'e worked hard and long into the night. I am indebted to Bob Jankowski and Neil Maffre, and others in the Depart­ ~ ent of Medical Illustration at Roehampton for the photographs . These are ob\'iously the greatest strength and asset of an Atlas, and they have taken 0 eat pains and trouble to reflect the injuries as they really are. They have always been enthusiastic and very considerate to the patients, and without :hem the work could not exist . I am particularly grateful to my friends, Arieh Eldad, for the illustrations of phosphorous burns, and Ian Wilson, for the -~

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PREFACE

picture of mustard gas burns. All other illustrations are of patients from Roehampton, and my thanks go to them for allowing me to publish pictures of them when not looking their best. Finally, I should like to thank the publishers for their patience and under­ standing, and my wife and children who were less patient but very tolerant, yet perhaps more understanding. John Clarke Roehampton

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1 CLASSIFICATION OF BURNS

PARTIAL THICKNESS BURNS

Superficial dermal

Partial thickness burns can be subdivided into those involving the epidermis and superficial layers of the dermis (superficial dermal) and those reaching down into the deeper layers of the dermis (deep dermal) . In both cases, spontaneous healing can occur from un­ damaged epidermal appendages-hair follicles, and sweat and sebaceous glands; epithelium will regener­ ate and resurface the remaining dermis (Fig. 1.2).

Superficial dermal burns blister, exposing the pink­ coloured surface layers of the dermis which is sensi­ tive to pain (Fig. 1.3). There is considerable loss of protein-rich tissue fluid from the wound, which when left to dry for two or three days will form an adherent scab. Spontaneous healing can occur within 10 to 14 days.

Fig. 1.2 Deep dermal burns after treatment in dress­ ings for two weeks. White dermal net with a source of new epithelium from underlying hair follicles and sweat glands at the centre of each pink spot are seen .

Fig. 1.3 Superficial dermal burns. (a) Very superficial burn. There is little erythema and only superficial blis­ tering, as the burns were immediately cooled with run­ ning water.

(b) The blistered skin has been removed to expose a moist, pink base which is very sensitive to touch.

(c) The pink and red mottled dermal base has been exposed . Dessication following exposure to dry air pro­ motes scab formation with some deepening of the der­ mal damage.

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FULL THICKNESS BURNS

Full thickness burns do not blister as there are no patent capillaries remaining in the bed and coagula-

tion destroys the entire dermis together with all epi­ dermal cells. The surface of the burn is initially grey-white and leathery (Fig. 1.5), and is completely painless. If allowed to dry a transparent brown es­ char forms, revealing thrombosed vessels beneath (Fig. 1.6). With very deep burns, damage can extend to muscle and bone, thus adding a volume compon­ ent to the injury (i.e. not only depth but also volume of dead tissue). Only small, deep burns will heal spontaneously. The granulation tissue which eventually forms in the wound contracts (Fig. 1. 7), making it smaller, allow­ ing the surrounding undamaged epithelium to migrate onto the surface of the burn. In larger deep burns, healing is by secondary intention only and skin grafting is invariably required.

Fig. 1.4 Deep dermal burn. The dry white dermal bed is painful to pinprick, yet not entirely anaesthetic. Spon­ :a.neous healing may be slow and followed by hypertro­ ic scarring.

Fig. 1.5 Full thickness burn. There is a numb central leathery area, with white deep dermal damage around the periphery. The vascular flare is a zone of hyperaemia and indicates superficial damage.

Fig. 1.6 Deep burn. Some areas are leathery and dull, others parchment-like and transparent, revealing :-·om bosed vessels beneath.

Fig. 1.7 Deep flame burn. The dry and leathery eschar around the abdomen is impairing respiration. Flexures show cracking and splitting .

Deep dermal Deep dermal burns also blister but the base is crea­ -ny-white and not sensitive to pain as nerve endings ave been damaged (Fig. 1.4). Overt fluid loss is not 3S excessive and it is easy to confuse with a more superficial burn when the wound has been allowed to dry. Spontaneous healing may be delayed for three to ·our weeks and is frequently followed by the devel­ opment of a hypertrophic scar.

FULL THICKNESS BURNS

a.~:J

5

1 CLASSIFICATION OF BURNS

BURN DEPTH Assessment The depth of a burn can be suggested by the circums­ tances of the accident, such as the causative agent and the duration of contact. Scalds, which are inju­ ries caused by wet heat, tend to be superficial, al­ though they will be deeper where contact is prolonged (Fig. 1.8) . Flame burns are usually deep (Fig. 1.9), particularly where clothing has been ig­ nited . Flash burns can appear severe, but although

Fig. 1.8 Immersion scald. A deep dermal burn caused by prolonged contact with very hot water. The dry red base is stained by haemoglobin pigments.

the temperature involved may be high, it is applied for only a fraction of a second with the deeper dermis invariably unaffected . An enquiry into first aid measures taken immedi­ ately after the injury is essential. Rapid immersion in cold water cools tissues and limits or even reverses some of the cellular damage. It is necessary to estab­ lish the actual time of a burn injury, as the nature of the wound surface changes with time, thus altering the characteristic diagnostic appearances (Fig . 1.10).

Fig. 1.9 Mixed depth flame burn. Areas of erythema, superficial and deep dermal burns, together with smoke staining of the skin, indicate full thickness skin loss.

Fig. 1.10 Typical scald from hot water. The burn is 24 hours old, hence the surface is no longer moist and glistening . Because of delayed presentation , the level of injury is more difficult to assess.

6

AREA

_:-· ~ar ance

remarkably difficult to judge the depth of a .-\5sessment may be made on the presence or _. :e of blister formation and also on the colour of ·-:-·.md, although these are not necessarily defini­ _ 3:i.stering implies that fluid is formed through -:.:::ge :0 the capillaries. However, absence of blis­ -; 5'-1ggests that the underlying capillaries have _t~ :.:"rombosed and that the damage is more sev­ _. -oh·ing the full thickness of the dermis. These -, -5 are summarized in Table 1.l. := .: : -: ,0:"\

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Pinprick test Light pressure with a sterile needle will establish the degree of sensitivity. This test requires co-operation from the patient and is thus of limited value in uncon­ scious patients or small children. Inability to perceive pain indicates that nerve end­ ings have been destroyed and that the burn is likely to be deep , whereas sharp appreciation of pain sug­ gests that the wound is superficial. Dullness to pain but awareness of touch is the most reliable objective test of a deep dermal injury.

"" . . f A Table 1.1 Classification of burns -­ -­ ? t assessment of an area of burn is essential, as _ -~ of an extent greater than 10 per cent in children - .: ~: per cent in adults warrant an immediate intra:::;- ,-':':~ infusion. The Wallace Rule of Nine is con­ ~ :-~"':' t when estimating a burn area in adults (Fig. ~ = but it is less applicable in young children due -) I:.:i:rent proportions of head to trunk (i.e. larger -'==. ': . ::ompared with trunk area) . For children, the __- ::i and Browder chart is more relevant (Fig. 1.11b­ .:"5 a general guideline, the area of the patient's , :: .:._~ . is equal to 1 per cent of body surface area. . ~ skin thickness varies in different parts of the _.:>0..:.: . :: is important to have a good working know­ -.:g-= oi these variations to assess a particular burn ' - ~ .: \ !ortality from a burn is related to the patient's the surface area involved, and a reasonably ~~:_ ;ate estimation of the chances of survival can be :-;..::i:-,ed from the Bull and Fisher mortality tables :: ;::

Type of burn Blistering

Appearance

Pinprick test

Superficial dermal

Bright red

Sensitive to pain

Deep dermal Blisters Creamy are broken coloured/ mottled

Dullness to pain, sensitive to touch

Full thickness

Present

Absent

Grey/white or brown

No sensation

~ .1 2).

7

..­ 1 CLASSIFICATION OF BURNS

36%

~

32%

/

17%

Fig. 1.11 Estimation of burn area. (a) Wallace rule of nine.

(b) Lund and Browder modification of (c) Modification for children of up to area in children of five to ten years of four years of age . age.

Body area burned

% 93 + 88-92 83-87 78--82 73-77 *72 63-67 58--{l2 53-57 48-52 43-47 38-42 3~37

28-32 23-27 18-22 13-17 8-12 3-7 0-2

Age (year) 0-4 5-9 10-14 15-1920-24 25-2930-34 35-3940-44 45-49 50-54 55-5960-64 65-69 70-74 75-79 80 +.

0.9 10.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.2 0.1 0.1 0 0 0 0 0 0 0

1 0.9 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.2 0.1 0.1 0 0 0 0 0 0 0

1 0.9 0.9 0.8 0.8 0.7 0.6 0.4 0.3 0.3 0.2 0.1 0.1 0 0 0 0 0 0 0

1 0.9 0.9 0.8 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0.1 0 0 0 0 0 0 0

1 0.9 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.2 0.1 0.1 0 0 0 0 0 0

1 0.9 0.9 0.8 0.8 0.7 0.6 0.5 0.3 0.3 0.2 0.1 0.1 0 0 0 0 0 0

1 1 0.9 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.2 0.1

1 1 0.9 0.9 0.8 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0.1 0.1 0 0 0 0

1 1 0.9 0.9 0.8 0.7 0.7 0.6 0.4 0.3 0.3 0.2 0.1 0.1 0 0 0 0

1 1 0.9 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.2 0.1 0.1 0 0 0

1 1 1 1 1 0.9 0.9 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0.1 0.1 0 0

Fig. 1.12 Bull and Fisher mortality tables. This chart shows the relat ionshi p between mortality, age of the patient and total area of the body burned. 1 = 100% mortality; 0.1 = 10% mortality (from Bull, 1971).

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1 1 1 1 0.9 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0.1 0 0

1 1 1

I

1 1 0.9 0.8 0.8 0.7 0.6 0.4 0.3 0.2 0.1 0.1 0

1 1 1 0.9 0.7 0.5 0.4 0.2

UJnq /0 sadli~ Z

g- 2.1 Typical scalds from boiling water. (a) A -.::' :::.: :er Si C distribu tion was caused on the face, neck, ~ - '=-0 : ;:C;J arr'l from boiling water, The bright red base, ~ """O, SI and shining immediately after injury, sug­ ;;=' 5' s ' ''at :, e injury is supe rficial.

Fig_ 2.2 Deep immersion scalds through prolonged contact with hot water. (a) The deep red base is anaes­ thetic and analgesic, sugge sti ve of a deep burn.

3 ) :" ,ery superiicial scald, This was seen very soon after '- ~ ~ , ury , There is little evidence of any serious exudate ,,' ' - s stage,

(b) Haemoglobin pigment is trapped within the lissues giving this typical dull, deep red appearance.

-=' .:, more extensive scald . The burn has all the charac­ of a superficial injury, but because of its extent - ' -e. enous resuscitation would be required.

' '0' SlI CS

(c) The toenails have come away with the blisters, which usually indicates coagulation of the digital vessels and will result in loss of the loes.

11

2 TYPES OF BURN

Fig. 2.3 Scald from boiling water. The white base is apparent immediately after injury and indicates a deep dermal or full thickness burn. Unfortunately, first aid measures of dousing with cold water were delayed and the burn needed skin grafting .

Fig. 2.4 Other agents causing scalding. (a) B "" milk. The blistering is patchy and care should be ta' e - :: ensure that the un blistered areas are not deep , by t8 oo: - ; sensation. Healing should be uneventful.

(b) Hot oil. The nC'ticeable red margin with paler dermal base is characteristic of a deep dermal burn, and the distribution corresponds to the pattern of clothing. First aid measures were delayed.

(c) Hot fat. The base is pale and mottled , witr :=:::­ areas of numbness . The burns were dressed ana ::2 '? : spontaneously.

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FLAME

FL~\fE

:r,i'se injuries result from the direct effect of burning ~ase5 on the skin . The temperatures involved are ·- c~" high and coagulation of protein is greater than in :: .:alds. Such burns are deep (Fig. 2.5), often with :!:":'1oke staining of the skin (Fig. 2.6); a dry e ~char

Fig. 2.5 Deep flame burns. (a) caused by ignition of hair. =:-'se::> bu rn s of forehead and scalp :;:-:;- ~ee n with oedema of the eyes :=.-: -'ose. Hair should be shaved, : _~ :3arJy surgery is often :: sB:)ooin ting.

=- _'-"

develops through which thrombosed vessels are seen (Fig. 2.7). Prognosis is dependent on the extent of area burned (Fig. 2.8). Flame bums may often pre­ sent with inhalational injuries (Fig. 2.9); early surgery may be contraindicated in the presence of significant pulmonary complications.

(b) Deep burn caused by ignition of alcohol. With such a burn over the neck early excision and grafting is important to protect access to airways.

Fig. 2.6 Deep charring burns. Very deep circumferential ;:: _--5 ); the leg . With this type of injury, underlying mus·

:c '= ::allage may be anticipated, and immediate surgical ,:::: x ""1p ression including fasciotomy is required.

(c) Patchy blistering indicates that there is little capillary function remaining in the skin, and the anaesthetic white base is revealed in places. Local oedema is typical and the hourly output of urine is monitored. Micturition is not impaired by penile oedema, which is usually confined to the foreskin only.

Fig. 2.7 Full thickness skin loss. The transparent es­ char, 24 hours after admission, reveals thrombosed veins beneath, which is a typical characteristic. Sharp excision and skin grafting should be performed without delay.

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2 TYPES OF BURN

Fig. 2.8 Massive flame burn. Treatment is by exposure , An escharotomy on the leg is dressed with a strip of nitrofurazone, and the wound surface is clean and dry Over 80 per cent of the body surface is deeply burned and prognosis is very poor indeed ,

Fig. 2.9 Mixed depth burns with inhalational injuries. The cream coloured areas are deep and require gra ': - ;! Oedema of the lips , together with a stridor, indica 'e ::­ upper airways obstruction, and early endotracheal r:_­ bat ion is prudent. In this case, injuries were caused t . :: gas explosion in a confined area

CONTACT

cally trapped (Fig 2.12), damage will extend m u ~ more deeply, often reaching bone (Fig. 2.13). Cont c burns from molten bitumen, or tar often cause dee~ burns and physical removal of the agent may v'orse:-. injuries (Fig. 2.14), Solvents are themselves irritar.: and should be avoided . A frequently applied tla ma:­ zine dressing allows the bitumen to separate spor.­ taneously.

Contact burns follow the direct conduction of heat from a hot surface to the body . This contact is usually short lived, with rapid reflex withdrawal. In circums­ tances where such protective mechanisms are not working, such as the patient suffering a blackout (Fig. 2.10), cases of alcoholism, epilepsy (Fig. 2.11) and drug addiction, or where the hand is mechani-

Fig. 2.10 Full thickness contact burns, sustained when protective mechanisms were not functioning. (a) Although water temperature in radiator pipes may not be very hi9h , prolonged contact at temperatures above 45°C combined with the effects of local pressure cause full th ickness burns of this type,

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(b) Burns are deep due to prolonged contact , b narrow extent allows conservative treatment.

CONTACT

Fig. 2.12 Full thickness contact burns. Both hands had been momentarily trapped within a hot press.' Although this burn is not particularly severe, prolonged contact at very high temperatures will cause devastating injuries.

Fig. 2.11 Mixed flame burns with a deeper central area from prolonged contact with fire. The patient had an ep ileptic fit whilst ironing in front of an open fire.

Fig. 2.13 Contact burn from a hot water pipe. These are typically deep burns which may extend down to zygoma, requiring flap cover .

....

Fig. 2.14 Contact burns from clten bitumen, tar and metal. 2. Ylolten bitumen burns.

(b) Tar burns . Typical splashes on the face . Immediate first aid measures should be taken by thorough irrigation with water.

(c) Full thickness burn from molten metal. The hot metal melted the shoe in this instance. The injury will require skin grafting.

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2 TYPES OF BURN

FRICTION

ELECTRICAL BURNS

Friction burns often involve large areas of abrasion with some thermal damage caused by generated heat. Genuine friction burns are seen where the body is in contact with a rapidly moving mechanism such as a tyre or belt drive. These burns are deep and may expose fat, tendon or bone. Early primary excision may be necessary (Fig. 2.15).

In electrical burns, the severity of damage depends upon the resistance of tissues (high resistance in bone and skin), the voltage and amperage (Fig. 2.16). This electrical energy is transformed to thermal energy, often with explosive force (Fig. 2.17).

~..... :.~~~

Fig. 2.15 Extensive friction bu rns. (a) Full thickness skin loss of the back, caused by the patient being dragged along a road for some distance.

(b) Deeply ingrained road dirt which cannot be excised by shaving with a skin graft knife, as the grit quickly causes the blade to blunten. Removal is best performed with a wire dermabrasion brush.

Fig. 2.16 Deep burns to the hands. Caused by contact with a cable carrying 660 volts. Damage is more exten­ sive than with ordinary domestic voltage. The metacarpo­ phalangeal joint will need cover with a local flap.

16

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(c) Six days post-injury, followi g abrasion and thin skin grafting.

Fig. 2.17 Electrical injury with explosive force. 8 2.'s bone without periosteum is exposed but the hand "- ' though insensate, still retains an adequate circ u la: ~ ­ Late thrombosis can be anticipated and the arm '­ :­ ~ case was amputated.

ELECTRICAL BURNS

_.:.. : ordinary domestic voltages the size of a cutaneous ·:ru.rn may appear small but is always deep, with a surprisingly large volume of tissue damaged (Fig. : .18) . Small punctate burns (Fig. 2.19) often mask :~u ombosed vessels and devascularized fat (Fig. ::' 20). The body becomes part of an electrical circuit, "nd it is at the point of entry of the current that the ;·:ound is most severe (Fig. 2.21) . Current passing

across the heart can induce fatal ventricular fibrilla ­ tion or cardiac arrhythmias_ Similarly, flow across flexural surfaces can cause arcing; tetanic spasms may prevent the victim from releasing contact and may even be strong enough to rupture muscles (Fig . 2.22). Tetanic spasm of respiratory muscle may cause res­ pira tory failure.

Fig. 2_18 Very deep electrical burns. (a) This injury involves nerves, blood . essels, tendons and bone and will require wide excision and flap cover. (b) -- e iingers have been mummified and dessicated . Both middle and ring , - ;Jers will require amputation .

g. 2.19 Electrical contact burn. This injury , sustained ·- -:_ gh wearing a wedding ring, is fortunately minor; in .- -:: "",atori ty of cases the underlying neurovascular pedi­ S :'lrombosed with eventual loss of the finger.

:=

Fig. 2.20 Small punctate burns. (a) The peripheral blis­ ters have been removed, revealing the full thickness central loss. These burns were treated with zinc oxide tape, allowing almost full return of function.

17

2 TYPES OF BURN

Injuries occurring in infants caused by chewing or sucking on live leads or plugs, where moist tissues decrease resistance to the passage of current, are

(b) The central area shows charring. These injuries may be treated conservatively.

always extensive (Fig. 2.23). Secondary haemorrhage from the labial artery can be dramatic.

.­

Fig. 2.21 Entry and exit burns. (a) The exit burns on the abdomen were superficial and irregular.

(b) The entry burn in the neck was deep , and a muscle flap was required to cover the exposed inominate vessels . These injuries were caused by a fall onto an electrified railway line.

Fig. 2.22 Electrical injury. The biceps tendon has been ruptured following tetanic contracture. Note slight bruis­ ing of the antecubital fossa and contracted muscle belly in the upper part of the arm .

Fig. 2.23 Deep burns of lips and tongue. (a) Injuries were caused by sucking on a live plug.

(b) Two weeks later, after conservative treatment. Heal­ ing is almost complete.

(c) This injury was caused by chewing an electric caD e There has been local arcing with extensive tissue loss Secondary haemorrhage from the labial artery is a risk

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ELECTRICAL BURNS

In the case of flash burns from arcing, where tem­ poeratures may exceed 4000°C for a fraction of a sec­ ~~:td J no current flows through the body but the ::::tpact may throw the patient several feet. Damage to ::,e tissues is therefore superficial (Fig. 2.24) unless othing has been ignited. However, damage to the 2:.-es, when the blink reflex is too slow, may be more ~e\-ere (Fig. 2.25), albeit very unusual. High tension injuries of greater than 1000 volts ~e" ult in massive muscle damage and charring,

thrombosis of vessels and often fractures caused by the fall (Fig. 2.26). The volume of tissue damaged is always extensive (Fig. 2.27), and the temperature of these tissues may take hours to return to normal. Surgical decompression with excision of coagulated muscle, as well as wide fasciotomies and escharoto­ mies should be undertaken urgently and the wound inspected repeatedly. Late thrombosis occurs with the apparent extension of the area devitalized, and secondary haemorrhage is common.

Fig. 2.24 Burn from high energy arc. Tiny punctate due to vaporized metal, sustained when the patient -- revv a metal chain across electrified rails_

Fig. 2.25 High energy flash burn. There is spotting of the skin from vaporized metal. Early conjunctival oedema and an apparently serious burning to the cornea which will, however heal rapidly_ The blink reflex is sometimes too slow to protect the cornea in electrical flash injuries_

Fig. 2.26 A high tension electrical injury. (a) Circulation - ~ '1 e arm has been interrupted by thrombosis of the : 'anchial vessels.

(b) An incision made through the biceps muscle at the time of amputation shows complete thrombosis of the vessels and coagulation of the muscle.

~..eas

19

2 TYPES OF BURN

In thermoelectric bums tetanic spasms prolong these instances a fern-like pattern can be seen in the skin, which fades within hours . Cutaneous burns are contact with the source . In the common case of elec­ tric bar fires, massive damage to the palmar surface of usually small and neurological signs can be transi­ the hand results in destruction of skin, tendons, tory. Paralytic ileus is seen, and cataracts may nerves, vessels and even bone (Fig. 2.28). Skin graft­ develop many years after the accident. Instant car­ diac arrest is the usual cause of death although many ing and flap cover is often necessary. In lightning injuries, the current from a lightning cases of complete recovery have been recorded where strike can flow through the body but more commonly cardiac massage and mouth to mouth resuscitation it flows across its surface, stripping off clothing. In . was persisted with for 30 minutes.

Fig. 2.27 Very deep electrical burn. This was caused by a fall onto a railway line. There is a very deep burn over the sternum, with loss of pectoralis major muscle and part of the sternum, thrombosis of the internal mammary vessels, and deep involvement of the pericardium . An omental flap was used to cover the exposed heart.

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Fig. 2.28 Thermoelectric burns. The hand has been held in prolonged contact with a heated electrical ele­ ment by a tetanic spasm. The tissue damage is always very extensive; all structures are involved and growth of the bones is invariably arrested.

CHEMICAL BURNS

CHEMICAL BURNS :\cid -:-he extent of injuries depends on the concentration

.:i the acid, duration of contact and first aid measures :aken. Acids cause a coagulative necrosis of tissues ~n d with few exceptions (i.e. hydrofluoric acid; Fig. : 29) do not penetrate deeply (Fig. 2.30). The acids "-re consumed and neutralized by the proteins them­ :;elves, and the burns tend to be deep and leathery, ·.·.; th a characteristic appearance (Fig. 2.31). First aid :.s by thorough irrigation with running water, al­ ::-'ough in acid burns to the eye blepharospasm, swel­ ing and oedema may make adequate irrigation difficult (Fig. 2.32).

Fig. 2.29 Hydrofluoric acid burns. These are very cor­ rosive and penetrating. Extensive irrigation should be carried out as soon as possible after contact. Calcium gluconate gel is widely used in limiting symptoms, but intradermal injection of calcium gluconate can cause extensive tissue necrosis.

Fig. 2.30 Hydrochloric acid burns. There is coagulative - -= ~ro sis with little penetration of deeper tissues. These :: _ ' p s are usually deep but do not worsen with time. The ; -e,' appearance is typical.

Fig. 2.31 Typical acid burns. (a) Sulphuric acid burn. Brown discoloration is typical. The coagulative necrosis limits penetration. This type of injury should be treated by irrigation with water.

itric acid burn. This was irrigated copiously for an , and healed spontaneously, albeit with subsequent -. ;:::e rtrophic scarring ..

Fig. 2.32 Acid burn to eye. Corneal clouding in the lower half with some conjunctival irritation. Intense blepharos­ pasm may prevent adequate irrigation.

21

2 TYPES OF BURN

Alkali Alkali burns are usually more severe as they pene­ trate more deeply (Fig. 2.33). The colliquative necro­ sis does not isolate the chemical reaction and the alkali continues to penetrate (Fig. 2.34). First aid and initial therapy involve thorough irrigation, which should be prolonged for at least several hours. At­ tempts at chemical neutralization are also to be avoided as the exothermic reaction adds a thermal element to the injury. Cement burns are seen fre­ quently; they usually present late and are common around knees and ankles (Fig. 2.35) .

Fig. 2.33 Deep burn from oven cleaner. One week after the accident. There is obvious full thickness loss, and instant excision and grafting are indicated.

Fig. 2.34 Caustic soda burns. (a) These are very deep and penetrating . In this case, first aid measures were delayed . Early excision and grafting are warranted .

(b) The black and brown areas are deep and will heal slowly, leaving bad scars .

Fig. 2.35 Cement burns. (a) At the time of injury there is little pain experienced thus patients often preseht late. Management is by early shaving with delayed split skin grafting.

(b) This burn has been dressed with a simple greasy dressing for two weeks . The deeper layers of the dermis are exposed and there is obvious full thickness loss centrally.

22

CHEMICAL BURNS

Other chemicals _.iany different chemicals can cause tissue damage :'ut the principles of treatment are the same: tho­ : \.~ ugh irrigation (Fig. 2.36), physical removal of the .:ausative agent (Fig. 2.37), and prevention of infec­

tion with early excision and grafting if the lesions are insensitive to pinprick. Systemic absorption or inhalation of the chemical can cause serious metabolic ...:r toxic problems (Fig. 2.38) and advice must be ~ 'Jtained from a toxicologist as early as possible after oresentation.

Fig. 2.36 Chemical burn from prolonged contact with petrol. These are usually superficial provided thorough irrigation and washing with soap and water are prompt.

Fig. 2.37 Phosphorus burns. (a) Weak copper sulphate . solution has been used to stain the particles black, to enable physical removal. Phosphorus continues to burn if exposed to air, therefore burns should be kept moist or wet dressings applied before the phosphorus particles are removed . (b) Appearance some weeks later,

23

2 TYPES OF BURN

Fig. 2.38 Burns caused by toxic chemicals. (a) Phenol burns. Although locally toxic to the skin, phenol rarely causes full thickness injuries. This patient suffered renal failure and needed haemodialysis for six weeks to restore renal function.

(b) Mustard gas burns. Vesiculation with erythema and scattered deep dermal loss. Most of these burns healed spontaneously, albeit slowly. Grafting is rarely required, but changes in pigmentation are frequent. The inhalatio­ nal component is much more important clinically .

1-UalUa~VUVlU

IiZJv'J f

3 EARLY MANAGEMENT

Pathophysiology Heat can cause complete destruction and necrosis of Hu e _ the dermis. Protein is coagulated and vasoactive sub­ "'~I stances are liberated into the local tissues, increasing / the permeability of capillaries. This results in rapid loss of fluid and protein elements from the circulating blood into the interstitial tissues. Consequently the burn wound becomes swollen and oedematous. The volume of fluid and protein loss from the blood becomes maximal at about eight hours after the incident. Fluid loss will continue for about 48 hours, by which time the capillary per­ meability has reverted to normal and extravasated water returns to circulation. Swelling is reduced and '-..--' "­ the wet, oozing surface becomes dry and leathery; an Pelvis eschar will develop if no dressing is applied. 1-21 Femur ____ Over the next three to four days, there is a gradual 1-11121 increase in local circulation. With the ingrowth of capillaries into the boundary between dead and dam­ aged tissues, the process of repair begins . At the same time, the undamaged peripheral tissues start to regenerate, with an increase in the rate of mitosis in epidermal cells and fibroblasts of the dermis. The process of repair, with the formation of granu­ lating tissue, fibrosis and scar, is concurrent with the process of regeneration and reconstruction of dam­ aged tissues. Repair and regeneration can be affected by bacterial infection . Non-virulent or contaminant Fig. 3.1 Anticipated blood loss associated with fra c­ organisms delay the ability of the body to regenerate tures in different areas of the body. tissues. Virulent organisms damage the capability for regeneration and encourage the pathological pro­ cesses of repair. The two processes of regeneration of body surface area in children, or 15 per cen~ :....-. and repair are thus competing, i.e. the ability to heal adults, are likely to need intravenous fluid the!'d F'.­ with little destruction of the tissues, or the develop­ Those with smaller burns should only require \. _ water and sodium, although in infants care mll:;: b.: ment of scars and contractures. In the superficial wound, epithelial regeneration taken to avoid giving large amounts of electr In e­ proceeds provided there is no contamination by viru­ free water as hyponatraemia and water intoxica:·L :-. lent organisms. In the deeper wound, where the can result. Preparations used in the treatrnen (:'

-.:.

•

..: f·

t., /'

~t..J .

~~

.

· . >~ ~t

:,:. :=.""" -~.

:?~'a\,..:., --.

'::.: ~1 '~

....:'" '

"

'

.

,,' ",

4'.1"

,~~~~:';: .~

.~ :' r\. ·t~ , .' - ,~

",4'

",

.'.\ ,

~

t1':'", ....,••: .

l.

1.­

II: Fig. 6.33 Congested kidneys with vascular stasis in the renal medulla. Terminal renal failure followed uncon­ trolled sepsis,

Fig. 6.34 Congested, soft and heavy spleen. The pa­ tient died from sepsis,

Fig. 6.35 Heavy consolidation of the lungs following inhalational injury. The lungs are filled with protein-rich oedema fluid and are relatively stiff and inelastic. PEEP is needed to inflate such lungs,

thorough notes and colour photography are taken by the medical attendants, to be used as subsequent evidence.

PATHOLOGY It is remarkable how unusual it is to ascertain the exact cause of death at post-mortem examination in the majority of those patients dying from burns , Even those who have slowly fallen into uncontrolled sepsis and multiple organ failure rarely show more than congestion of most of the organs (Fig. 6,33), with enlargement and friability of the spleen (Fig. 6.34) and pulmonary consolidation (Fig. 6.35). Tissue auto-

lysis occurs quickly and little help is available from histological examination. Death occurs at the bioche­ mical level and gross derangements are often observed during the days preceding the patient' s death. Examination of the respiratory tract and lungs will pinpoint the focal damage following inhalational in­ juries (Fig. 6.36), but the changes due to the injury itself are obscured by the effects of secondary infec­ tion (Fig. 6.37), Ante-mortem histological examination of the bum wound can be very useful in determining the pres­ ence of invasive burn wound sepsis, particularl~­ those due to yeasts and fungi.

IE

6SEOUELAE

Fig. 6.37 Damage to the major bronchi following inha­ lational injury and secondary infection.

Fig. 6.36 Appearance of larynx and upper trachea from a case of inhalational injury. This shows smoke damage and early ulceration.

114

Further reading

Strasser, E.J. (1977) Lightning injuries. 315-19.

J.

Trauma , 17,

GENERAL

CHAPTER 3 RESUSCITATION

Muir, LF.K. , Barclay, T.L. and Settle, J.A.D. (1987) Burns and their management, 3rd edition, Butterworth Heinemann, Oxford. Wachtel, T.L. and Frank, D.H. (1984) Burns of the head and neck, W.P. Saunders, Philadelphia . Hummel, R.P. (1982) Clinical burn therapy, John Wright, Boston. Ruberg, R.L. (1986) Advances in burn care. Clinics Plastic Surgery, 13.1, W.B. Saunders, Philadelphia. Cason, J.S. (1981) Treatment of Burns,. Chapman & Hall, London. Carvajal, H.F. and Parks, D.H. (1988) Burns in children, Year Book Medical Publishers, Chicago.

Demling, R.H. (1987) Fluid replacement in burned patients.

Surg. Clin. North. Am., 67, 15-22.

Settle, J.A.D. (1974) Urine output following severe burns .

Burns, 1, 23-42.

Carvajal, H .F. (1980) A physiological approach to fluid

therapy in severely burned children . Surg. Gynecol. Obstet.,

150,379-84.

CHAPTER 2 CHEMICAL BURNS

Luterman, A., Dasco, e.e. and Curreri, P.W. (1986) Infec­

tion in burn patients. Am. f. Med., 81 (1 A), 45.

Lawrence, J. e. (1985) The bacteriology of bums. f. Hosp.

Infect., 6 (8), 3--17.

Winkelstein, A. (1989) What are the immunological altera­

tions induced by burn injury? J. Trauma, 22, 72-80.

Cole, R.P. and Shakespeare, P.G. (1990) Toxic shock syn­

drome in scalded children. Burns, 16, 221-24.

CHAPTER 4 INHALATIONAL INJURY

Kinsella, J. (1988) Smoke inhalation. Burns, 14, 269-79 .

Herndon, D.N., Barrow, R.E., Linares, H .A. et al. (1988)

Inhalational injury in burned patients: effects and treat­

ment. Burns, 14, 349-56.

Boutros, A.R., Hoyt, J.L., Boyd, W.e. and Hartford, C.E.

CHAPTER 1 PATHO-PHYSIOLOGY (1977) Algorithm for management of pulmonary complica­

Arturson, G. (1980) Pathophysiology of the burn wound. tions in burn patients. Crit. Care Med., 5, 89-92 .

Ann. Chir . Gynaecol., 69, 178-83.

Hunt, T.K. (1990) Basic principles of wound healing. f.

Metabolism Trauma, 30, (Suppl. )122-8.

Moritz, A.R. and Henriques, F.e. (1947) Studies of thermal

injury: the relative importance of the time and surface Henley, M. (1989) Feed that burn . Burns, 15,351-61.

temperatures in the causation of cutaneous burns. Am. J. Wilmore, D.W. (1974) Nutrition and metabolism following

Pathol. 23, 695-720 .

thermal injury . Clin. Plast. Surg. , 1, 603--19.

Curreri, P.W. (1975) Metabolic and nutritional aspects of

thermal injury . Burns, 2, 16-21.

Area, Depth Sutherland, A.B. (1976) Nitrogen balance and nutritional

Jackson, D.M. (1953) The diagnosis of the depth of burn­ requirements in the burn patient: a reappraisal. Burns, 2,

238-44.

ing. Br . f. Surg., 40, 588-96.

Lund, e.L. and Browder, N .L. (1944) The estimation of

areas of burns . Surg. Gynecol. Obstet., 79, 352-4.

Infection

Saydjari, R., Abston, S., Desai, M.H. and Herndon, D.N .

(1986) Chemical burns. f. Burn Care Rehabil. 7, 404-8.

Rozenbaum, D. and Baruchin, A.M . (1991) Chemical burns

of the eye with special reference to alkali burns. Burns, 17,

136-40.

James, N .K. and Moss, A.L.H. (1990) Review of burns

caused by bitumen and the problem of its removal. Burns,

16,214-16.

Hunter, G.A. (1968) Chemical burns after contact with

petrol. Br. f. Plast. Surg., 21, 337-41.

Wilson, G.R . and Davidson, P.M. (1985) Full thickness

burns from ready mixed cement. Burns, 12, 139-45.

Electrical burns, lightning Bingham, H. (1986) Electrical Burns. Clin. Plast. Surg ., 13,

75-85.

Hunt, J.L. , Mason, A.D., Masterson, T.S. et al. (1976) The

pathophysiology of acute electrical injuries. f. Trauma, 16,

335-40.

CHAPTER 5 ANAESTHESIA Park, R.E. (1982) Anaesthesia in the bum patient, in Clinical

Burn Therapy (ed. P .D. Hummel), John Wright, Boston.

De Camp, T., Aldrete, J.A. (1981) The anaesthetic manage­

ment of the severely burned patient. Intens. Care Med., 7,

55-62.

Wound excision and closure Janzekovic, Z. (1970) A new concept in the excision and immediate grafting of burns. f. Trauma , 10, 1103--8. Hunt, J.L., Sato, R. and Baxter, e.R. (1979) Early tangential

115

FURTHER READING

excision and immediate mesh autografting of deep dermal

hand burns . Ann. Surg. , 189, 147-51.

Sykes, P.J. and Bailey, B.N . 1975) Treatment of hand burns

with occlusive bags. Burns, 2, 162-6.

Alexander, J.W., Macmillan, B.W., Law, E. and Kittur,

D.S. (1981) Treatment of severe burns with widely ex­

panded meshed skin autograft and meshed skin allograft

overlay.]. Trauma , 21, 433-41.

McMillan, B.G. (1978) Closing the burn wound. Surg. Clin.

North Am. , 58,1205-31.

Burke, J.F., Bondoc, e.e. and Quinby, W.e. (1974) Pri­

mary burn excision and immediate grafting. ]. Trauma , 14,

389-95.

Deitch, E.A . and Staats, M. (1982) Child abuse through

burning. J. Burn Care Rehabi!. , 3, 89-94.

Prasad, J.K., Thomson, P.D. and Feller, 1. (1987) Gastro­

intestinal haemorrhage in burn patients. Burns, 13, 194-7.

PhYSiotherapy Parks, D.H., Evans, E.B. and Larson, D.L. (1978) Pre­

vention and correction of deformity after severe burns.

Surg. Clin. North Am. , 58, 1279-89.

Ward, RS. (1991) Pressure therapy for the control of hyper­

trophic scar formation after burn injury: a history and re­

view.]. Burn Care Rehabi!., 12, 257-62.

Edlich, RF., Horowitz, J.H., Rheuban, K.S. et a!. (1985)

Heterotopic calcification and ossification in the burn pa­

tient. J. Burn Care Rehabi!., 6, 363-71.

CHAPTER 6 MALIGNANT CHANGE Bartle, E.J., Sun, J.H . and Wang, X.W. (1990) Cancers arising from burn scars. ]. Burn Care Rehabi!. , 11, 46--9. Fishman, l .R.A. and Parker, M.G . (1991) Malignancy and chronic wounds. J. Burn Care Rehabil. , 12, 218--23. Non accidental injury Deitch, F.A. and Staats, M. (1982) Child abuse through burning. J. Burn Care Rehabi!. , 3, 89-94. Lenoski, E.F. and Hunter, K.A. (1977) Specific patterns of inflicted burn injuries. J. Trauma , 17, 842-6

116

121

INDEX

Index

References in bold are to figures and references in italic are to tables. Acid burns 21,2.29-32 Acinetobacter 51

AIDS in allograft skin 77

Airway patency maintenance 64, 5.1

Airway problems 64-6

Alcoholism, and contact burns 14

Alkali burns, 22, 2.33-35

of face and eyes 84, 5.35

Allografts 77-8,5.23

Aminoglycoside absorption 57

Amputation

in diabetes 91, 93, 5.54

of fingers 81-2,5.30

Anaesthesia 64-9

corneal protection 88, 5.45

for eye irrigation 86

Analgesia, self-administered 68-9,5.7

Ankle, splinting 97, 5.61

Antibacterial dressings 27,3.1

Antibacterial prophylaxis, topical 54

Antibacterials, topical 57

Antibiotics

choice 57,4.3

prophylactic 55

resistance 56,4.28

systemic 57,4.3

Antihistamines for irritation 104

Aponeurosis 88, 90, 5.49

Arm, escharotomy and fasciotomy 36,

3.18b

Arterial blood gas estimation 45

Aseptic measures 52

At risk register, non-accidental burns

110

Atelectasis 44

Axilla, difficulties, 96, 5.60b

Bacteria, plate surveillance 56, 4.28

Bacterial colonization 33, 81, 85, 5.37

Bacterial cultures, surveillance 55-6

Bacterial flora, mixed 51

Bactroban 27, 3.1,57

Basal metabolic rate 59

Betadine 30

Bipolar coagulator 35,3.23

Bitumen and contact burns 14-15,

2.14a

Bjork flap tracheostomy 49

Bleeding control 73

Blistering 7, 1.1

and neurovascular bundle thrombosis 81-2, 5.30

Blood loss in fractures 26,3.1

Blood pressure, monitoring 67

Blood transfusion, massive, problems 66

Blood transfusions 56

Boiling water scalds 11-12, 2.1,2.3

Bone, radiologically immature 108,

6.18

Bones and joints, burn injuries 91 , 94,

5.56

Bronchodilators 48

Bronchoscopy 48

Bronchospasm 44

Bull and Fisher mortality tables 7-8,

1.12 Burns

appearance 7, 1.1

area 7-8,1.11

chronic non-healing 60, 4.33

classification 2

'closed method' excision 70-1,5.11

depth assessment 6-7

early care 94-6

ears 85-6, 5.39-41

exposed, excision 69-72, 5.9-10

exposure treatment 53

late treatment and rehabilitation

97- 9

metabolic considerations 59

neglected 110-11, 6.24

non-accidental 110, 112-13, 6.27-32

pathology 113-14

pathophysiological changes 2-3,

1.1

pathophysiology 26

physiotherapy 92-9

self-inflicted 110, 112, 6.32

surface, surveillance of bacteria 55,

4.27 wound

colonization 51

early surgery 55

infection 51-8,4.29

Buttock, as donor site 74-5, 5.17c

non-accidental burns 110, 112,

6.28-9

Calcium 67

Caloric requirement estimation 59

Cannula, large intravenous 73, 5.16

Capillary permeability, increased 26

Capnometer 67

Carbon monoxide exposure 44-5

Carbon stained pharyngeal aspirate

47,4.7 Carboxy haemoglobin, increasing level effects 45, 4.1

Caustic soda burn 22, 2.34

Cellulitis 53, 4.23, 58

streptococcal 104, 6.8b Cement burns 22, 2.35

Chemical burns 21-3

to eyes 86-7, 5.42

Chemosis 87, 5.44b

Chest, escharotomy 38,3.23

Chest wall, ventilatory limitation 35,

3.16

Chloramphenical eye ointment 86-8,

5.45

Chlorhexidine 27,3.1 , 54

Cigarette burns 110, 112, 6.30

Circumferential burns, contracture 35,

3.15

Cold water immersion 6

Colloids 27

adult formulae 31 , 3.2 Contact bums 14-15

electrical 17, 2.19

full thickness 14,2.10

Contamination

avoidance 52-3

prevention 29, 3.5

Cornea, protection 86-8, 5.44-5 Cricothyroid membrane for tube introduction 64, 5.2a

Croup tent use 45,4.3

Crusts removal 81

Crystalloids 27

adult formulae 31 , 3.2 Curreri and Sutherland estimations of caloric requirements 59, 4.4

Deep burns 5, 1.6

reaching bone 94,5.56

scalp 88, 90, 5.49-50

to neck 106, 6.12a

Deep charring burns 13, 2.6, 85, 5.36 escharotomy 36, 3.18 Deep contact burns, of hand 83, 5.31 Deep dermal burns 4-5, 1.2, 1.4 exposure treatment 29, 3.4

hypopigmentation 110, 6.23

Deep flame burns 5, 1.7, 13,2.5

with complications 54,4.26

escharotomy 35,3.16

facial 81, 84, 5.34

hand, excision to fascia 71 , 5.12

leg, excision to fat 72,5.14

tangential excision 68, 5.8

Dextran 27

Digital vessel coagulation 11, 2.2c

Disablement, burn treatment, 91, 93,

5.55 Donor sites 74-5,5.17 dressing 75,5.18 infection 54, 4.26c Drips for excision and grafting 64

Drug addiction and contact burns 14

Drugs, response in burns 66-7

117

INDEX

Ears

burns 85-6, 5.39-41

cartilage swelling 86, 5.39

ECG electrodes, standard 67, 5.5

ECG monitoring 67

Ecthema gangrenosum 52, 4.20b

Ectropion

of lower lid 89, 5.47

correction 90, 5.48

of upper lid 89, 5.46

Elastic bandage 97

Elasticface mask 105, 108, 6.15

Elastic gloves for hand skin grafts

96--7,5.62 Elastic net dressing 31,3.8£ Elastic pressure garments 97--8, 5.62 Elasticated pressure garment 107,6.15 Elastomer 99,5.66 Elbow, calcification 108--9, 6.19 Electric bar fire deep contact burns of hand 83, 5.31 hand damage 20,2.28 Electrical arc flash burn, corneal damage 86--7, 5.44 Electrical burns 16--19, 2.16-28 very deep 17,2.18

Electrical injury 17-18, 2.22

Endotracheal intubation 14,2.9

advantages and hazards 48, 4.2 via nasal route 48,4.9 via oral route 48, 4.10 Endotracheal tube insertion 50, 4.16 introduction with restricted mouth opening 64, 5.2 withdrawal 50, 4.15

Enflurane 66

Enteral feeding 61

Entry and exit burns 18, 2.21

Epilepsy

and contact burns 14-15, 2.11 and deep charring burns 85, 5.36

Epithelial regeneration 26

Epithelium, cultured, applica tion

78--9, 5.25 Eschar

dry exposed 53,4.22

with partial infection 53,4.24

separation 33, 3.12, 35

Escharotomy 35--8 inadequate 37,3.19 indication 35,3.15 Exercise program 97, 5.63

External fi xation for fractures 39,

3.24-5

Eye

acid burn 21 , 2.32

alkali burns 84, 5.35

burn injuries 86--8

damage in flash bums 19

118

Eyelid

damage 86, 88, 5.44e

eversion 87-9, 5.44b, 5.46-47a

lower

ectropion 89, 5.47 ectropion correction 90, 5.48 skin grafting 88--9,5.46 upper, ectropion 89, 5.46 Face

alkali burns 84, 5.35

burn injuries 81-5

humidified oxygen mask 48,4.8 spontaneous healing 83, 5.33

deep charring burns 85, 5.36

elastic mask 105, 108, 6.15

flexible plastic mask 105, 108, 6.16

reconstruction 81 , 84-5,5.35--6

Fascia, excision to 71, 5.12 Fasciotomy 35, 3.18,72,5.13 for fracture fixation 39

Fat, excision to 72, 5.14

Fat scald 12, 2.4c

Featherstone gag use 65, 5.4

Feeding, postoperative 69

Femora, external fixation 39, 3.24

Fetal membranes 78,5.24

Fibreoptic laryngoscopy 49

Fingernail loss in hand burn 81

Fingers

amputation 81-2, 5.30

escharotomy 35-6,38,3.17,3.22

webbing 104

Flamazine

for bitumen burns 14

for hand burns 34,3.13

Flamazine dressing 30,3.8 Flame burns 6, 13

with compound fracture 41,3.25

massive 14, 2.8

Flap cover 80-1 , 5.29

Flash burns of face 81, 83, 5.33

Fluid loss,

initial 26--8

measurement 66

Fluorescein eye staining in acid burns

86

Foot, burns, 91, 93--4, 5.53-5

Fractures

and burn injuries 27-8

fixation 39--41

Friction burns 16, 2.15

Full thickness burns 5, 1.5

Fungal infection 113

Furacin 54

Genitalia burns, 91-2, 5.51

Gentamicin resistance 56, 4.28e

Graft dressing 77

Grafting

early 55

inadequate 111, 6.26

late, scarring difficulties 66, 5.2-4

special techniques 77-8

for tracheostomy 50,4.17

Grafts

applied to infected area 57, 4.31

taking of 76, 5.21

Granulation, over-, chronic 110-11,

6.25

Groin, electrical burn, fasciotomy 72,

5.13

Haematocrit 27

Haemoglobinometer 28, 3.2b

Haemolytic streptococcal infection 51,

4.19

Halothane 66

Hand

burn injuries 79--83 burns, childhood, oyster shell principle 105, 107, 6.14

burns treatment 34, 3.13

deep flame burns, excision to fascia

71,5.12 early grafting 79-80,5.28 elevation 94, 5.57 escharotomy 35-6,3.17,38,3.22 immobilization 107, 6.14 long-term function 97--8, 5.64 palmar burn 80,5.29 physiotherapy, 95-6, 5.58-9 plastic bag with silver sulphadiazine cream 79,5.26 skin flaps 79-81, 5.29 thermoelectric burns 20, 2.28 Heat and inhalational injury 44

Heat loss counteraction 66

Hepatitis B in allograft skin 77

Heterotopic calcification 108--9

at surgical neck of humerus 108--9, 6.20 deposition 108, 6.17

Hibiscrub 30

High energy arc burn 19, 2.24, 83, 5.33

High energy flash burn 19,2.25

High tension electrical injury 19, 2.26

HIV-positive patients 53

Hot press contact burns 14, 2.12

Hot water pipe contact burn 14-15,

2.13

Hot water scald 6, 1.10

Hydrochloric acid burns 21, 2.30

Hydrocortisone ointment 110

Hydrofluoric acid burns 21 , 2.29

Hyperalimentation 59

Hyperbaric chamber 45

INDEX

H'. ~ertrophi c

scarring 98, 5.65 e\'elopment 102, 6.2 mature 102-3, 6.4 in pigmented skin 104, 6.7 reticular pattern 102, 6.1 spontaneous healing 102-3, 6.3 see also Scar tissue Hypopigmentation 110, 6.23

Hypotension, induced 67

Hypoxia 27

and inhalational injury 44

Immersion scalds 6, 1.8, 11, 2.2

Immunosuppression 51

Infections

prevention 30,3.6

secondary 113-14, 6.36

surgical excision 57

treatment 57-8

Inhalational injuries 14, 2.9, 44-8,

4.5-6

anaesthesia 66

bronchial damage 114, 6.37

diagnosis 47-8

lung congestion 113, 6.35

muscle wasting 96

pathology 47

smoke damage 114, 6.36

treatment 48

Intermittent positive pressure ventilation 69

Intravenous fluid therapy 26

Irrigation for chemical burns 23, 2.36

Jobst mask 107, 6.15b Joints, skin grafts 96,5.60 Keloid scars 104

Keratinocytes, cultured 78--9,5.25

Keratoacanthoma 109-10, 6.22

Lancefield group A beta haemolytic streptococci, appearance 56, 4.28a Leg, deep flame bums, excision to fat 72,5.14 Lightning injuries 20 Lips, electrical burns 18, 2.23 Lower leg, escharotomy 37,3.20 Lund and Browder chart 7, 1.11b-c Lungs chronic disease 46

consolidation 113, 6.35

function deterioration 44,4.1

necrotizing damage 46

secondary changes 44

Macmillan model of allograft 77, 5.23a Mafenide 27, 3.1,54

Meshed skin grafts 75-6, 5.19 cosmetic appearance 76,5 .20

Metabolic acidosis 48

Metacarpophalangeal jOints,

hyperextension 79-80, 5.27

Milk nutrition 59

Milk scald 12, 2.4a

Mini-centrifuge 28, 3.2a

Mixed depth burns

with inhalational injuries 14,2.9 treatment 33,3.11

Mixed depth flame burn 6,1.9

Mobility encouragement 96

Molten metal contact burn 15, 2.14c

Monitoring instruments 28,3.2

Mouth, burns 85-6, 5.38

Mupirocin 27, 3.1 , 57

Muscle damage in high tension

injuries 19, 2.26

Muscle flap for joint burns 91

Muscle strength restoration 97, 5.63

Mustard gas burns 24, 2.38b

Nasogastric intubation nutrition 56

Nasogastric tube fine bore 61 , 4.34 in lungs 61, 4.34b Neck

deep burns 49

marked contracture 65,5.3

splinting 105-6,6.11-12

Needle electrodes 67,5.6

Neomycin 57

Neurovascular bundles damage and

amputation 81-2, 5.30

Night-splint 98, 5.64

Nitric acid burn 21, 2.31b

Nitrofurazone 27, 3.1,54,57

Nitrofurazone, for flame burns 14

Non-accidental burns 110, 112-13,

6.27-32

Non-polarizing muscle relaxants 66

Nutrition 56

inadequate 59, 4.32 Oedema, of hand 96

Opiates 67

Oven cleaner burn 22, 2.33

Oxygen, humidified, administration

45,4.2

Oxygen saturation 45

Oyster shell principle for hand burns

in children 105, 107,6.14 Paraffin gauze 75, 5.18b

Parenteral nutrition 61

Partial thickness burns 4--5

Pathology 113-14

PEEP 48

Penicillin resistance 56, 4.28d

Penis

scald 92, 5.51

very deep burn 92, 5.52

Perichondri tis, end-stage 87, 5.41 suppurative 86, 5.40 Perineum, burns 91-2,5.51

Peripheral circulation 27

Petrol, contact burn 23, 2.36

Phenol burns 24, 2.38a

Phosphorus burns 23, 2.37

Physiological support 58

PhYSiotherapy 48, 92-9

Pinprick test 7, 1.1

Plasma, adult dosage 31, 3.2

Plaster slab immobilization of hand 83,

5.32

Plastic bag for hand burn 34,3.13, 79,

5.26

physiotherapy 95, 5.58

Plastic face mask 105, 108, 6.16

Positioning of burn injuries 94--6, 5.57

Post grafting 96-7, 5.62-3

Postoperative anaesthetic care 69

Postural drainage 48

Povidone iodine 27, 3.1 , 54

Pressure garments 97-8, 5.61, 5.64

Pressure relief 94

Protein loss 26

Proteus infections 51,4.21

Pseudomonas contamination 58, 4.31a

drug resistance 57

sensitivity plate 56, 4.28e

septicaemia 54, 4.26b

Pseudomonas aeruginosa 51,4.20 ear infection 86, 5.40 growth 56, 4.28c Psychogeriatric unit, scald injuries 110, 112, 6.31

Psychological consideration 69

Pulmonary oedema 44,46,4.4

Pulse oximetry 67

Pump-action delivery feed 61, 4.34a

Punctate bums 16-17, 2.20

Pyocyanin 56, 4.28c

Regeneration 26

Rehabilitation 97-9

Renal failure 113, 6.33

Renal stones 109

Respiratory failure 46,4.5

in electrical burns 17

Resuscitation 26-8

formulae for adults 31,3.2

Ribbon gauze for escharotomy 38,

3.23c

119