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BURNS

A Concise Textbook of Surgery - Chapter 6

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DEFINITION

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TYPES OF BURNS

1. Ordinary Burns

2. Scalds

3. Electric Burns

• Low-voltage: Direct injury at the point of contact; skin and subcutaneous tissue most commonly involved.
• High-voltage: Causes direct injury at the contact point AND damages all tissues conducting the electricity through the body. Electrical energy converts to thermal energy, producing a thermal burn.
• Skin is an effective insulator, but at high voltage its resistance is overcome and current flows through deep tissues - muscle, nerve, and blood vessels suffer maximum damage as they offer least resistance.
• The skin is involved at 2 points: the entry point (contact with electrical source) and the exit point (where patient is grounded).
• Electrical resistance of skin is reduced by moisture, so ulcers are more often seen in the axilla and antecubital fossa.
• "Port-wine coloured urine" is not unusual following major electrical injury due to haemochromogens released from injured muscle.

4. Chemical Burns

• Concentration of the chemical
• Amount of agent
• Duration of contact
• These burns tend to be deeper than externally assessed.

5. Radiation Burns

• Acute radiodermatitis: Erythema, oedema, exfoliation (develops around the 5th day); excessive doses may cause necrosis with slough formation leaving deep indolent ulcers.
• Chronic radiodermatitis: From repeated small doses or as a legacy of acute radiodermatitis; features include irregular pigmentation, telangiectasias, small indolent ulcers, atrophy of epidermis, and sclerotic dermis. The most important feature is its liability to undergo malignant transformation.

6. Cold Burns

• Frostbite: Actual freezing of tissues, formation of ice crystals, affects skin and subcutaneous tissues of hands, feet, ears, nose. Necrosis is related to ice crystal mechanical effects, cellular dehydration, and microvascular occlusion.
  • 1st degree: Hyperaemia and oedema, no necrosis
  • 2nd degree: Hyperaemia, vesicle formation, partial thickness necrosis
  • 3rd degree: Necrosis of entire skin thickness
  • 4th degree: Necrosis of full thickness skin + subcutaneous tissue + muscle + bone → gangrene
• Chilblain: Localized painful erythema of fingers, toes, or ears from cold damp weather.
• Trench foot: Soldiers; prolonged exposure to extreme cold water + circulatory disturbances.
• Immersion foot: Shipwrecked persons in waterlogged boats.

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PATHOLOGY OF BURNS

I. LOCAL CHANGES

1. Severity (Depth Classification)

• Partial thickness burn: Epidermis and superficial dermis destroyed but epithelial cells around hair follicles/sweat glands remain → spontaneous regeneration possible; no skin graft needed.
• Full thickness burn: Entire epidermis and full dermis destroyed; no regeneration possible → scar and contractures inevitable without grafting. Sensation is lost (pin prick test is NEGATIVE).

2. Extent of Burn - Rule of Nines

Note: The rule of nines applies to adults only. In a 1-year-old child, the head is ~19% (vs. 7% in adults), and each lower extremity represents only 13% of total body surface.

3. Vascular Changes

• Dilatation of small vessels due to direct injury and liberation of histamine → increased blood flow.
• Greatly increased capillary permeability → protein-rich plasma pours out continuously → collects as blisters or dries to form a protective brown crust (separates in 1-2 weeks for superficial burns; longer for deep burns).

4. Infection

• At the moment of burning, skin is sterilized.
• In 1st degree burns, intact epidermis acts as a barrier.
• In deep burns, if the protective crust is broken, virulent organisms can enter.
• Infection is aggravated by general malnutrition, plasma and blood volume loss, and anaemia.
• Bacteraemia and bacteraemic shock are the second most common cause of death after oligaemic shock (usually occurs between 2nd and 3rd weeks).

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II. SYSTEMIC CHANGES

1. Shock

• Heat and vasoactive materials from the injury increase capillary permeability → fluid and protein lost from intravascular to extravascular compartment.
• Volume shifts are proportional to burn extent → oedema and blebs.
• Blood becomes haemoconcentrated; haemoglobin rises markedly.
• Sodium chloride falls (lost in exudate); potassium rises (cell destruction releases intracellular K+).
• Sludging of blood occurs - intravascular agglutination of RBCs.
• Haemolysis can be massive → haemoglobinuria.
• Ischaemia of liver and kidney → acidosis and uraemia.

2. Biochemical Changes

• Low sodium and chloride; high potassium
• Hypoproteinaemia (excessive plasma protein loss)
• Hyperglycaemia often develops
• Rise in blood urea, NPN, and creatinine (kidney damage)

3. Changes in Blood

• Haemoconcentration (Hb may rise to 150% in severe burns)
• Apparent increase in RBC count (plasma loss)
• Blood sludging
• Abrupt fall in eosinophil count in first 12 hours - very characteristic; persistent eosinopenia = bad prognosis
• Biphasic coagulation alteration: early depletion of platelets and fibrinogen, increase in fibrin split products, rise in factors V and VIII; intravascular coagulation may occur with infection

4. Systemic Lesions

• Liver: Focal necrosis with Councilman bodies (similar to yellow fever); found in majority of burn deaths.
• Kidney: Low perfusion + blood pigment deposition from haemolysis → haemoglobinuria → oliguria → anuria → uraemia.
• Adrenals: Enlarged, congested; decreased cholesterol and lipid; in severe burns petechial haemorrhages and focal necrosis; bilateral cortical necrosis can occur.
• Gastrointestinal tract: Gastric and duodenal mucosal ischaemia within 3-5 hours; Curling's ulcers (acute gastroduodenal ulcers, first described 1842, in ~25% of hospitalised burn cases); colonic ulceration in severe burns.
• Lungs: Pulmonary vascular resistance increases; hyperventilation; pulmonary insufficiency may require mechanical ventilation.
• Endocrine: Elevated glucagon, cortisol, catecholamines; depressed insulin and T3 → increased metabolic rate, negative nitrogen balance.
• Neurological: Delirium and disorientation from low cerebral blood flow and electrolyte imbalance; specific neurologic changes mostly in high-voltage electrical burns.
• Immunological: Impairment in burns over 50% of body surface; depressed immunoglobulins; depressed lymphocytes (relative decrease in T cells, increase in B cells); impaired neutrophil function.

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TREATMENT

I. Treatment of Shock

• Start immediately; adults with ≥15% burns; children with ≥10% burns.
• Blood transfusion required when burns involve >20% full thickness or >40% partial thickness.
• Key fluid formulas:

• Urine output monitored: target 75-100 ml/hr. Diuretic (mannitol 12.5g per litre of IV fluid) used in 4 categories: high-voltage electrical burns, associated soft tissue injury, deep burns involving muscles, extensive burns remaining oliguric.

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II. General Treatment

• Circumferential full-thickness burns form an unyielding eschar (crust) → compresses vessels → diminished peripheral pulses, cyanosis, paresthesia.
• Chest wall escharotomy if ventilation is impaired.
• Escharotomy: incised on midlateral or midmedial line, no anaesthesia needed (eschar is insensitive), controlled by electrocoagulation.
• If escharotomy fails → fasciotomy under general anaesthesia (releases fascia of all compartments).

• Prophylactic penicillin on 1st or 2nd day (gram-positive cover), before burn becomes avascular (~48 hours).
• After 48 hours, systemic antibiotics cannot penetrate the avascular eschar effectively.
• Gram-positive organisms colonize first; by late 1960s, Pseudomonas became dominant gram-negative organism.
• For bronchopneumonia: aminoglycoside + semisynthetic penicillin (Pseudomonas commonly implicated).
• Avoid prophylactic antibiotics beyond the initial period; treat based on culture and sensitivity.

• Resting metabolic rate ~2x normal in burns >50% body surface.
• ~2000 calories/m² body surface/day for burns >40%.
• Enteral route preferred (nasogastric tube feeding, 24h continuous pump delivery).
• If ileus or diarrhoea: parenteral nutrition via central vein (amino acids + hypertonic glucose).
• 500-1000 ml fat emulsion given twice weekly to prevent essential fatty acid deficiency.
• Sudden glucose intolerance = early sign of sepsis.

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III. Local Treatment

• Cleanse with surgical detergent; trim loose nonviable skin.
• Puncture blisters of 2nd degree burns and remove overlying dead skin.
• Topical agents:
  • Silver nitrate (0.5%): Applied early; drawback - electrolyte imbalances.
  • Mafenide acetate (Sulfamylon): Penetrates eschar; effective against Pseudomonas and clostridia; drawback - hyperchloraemia and respiratory alkalosis.
  • Silver sulphadiazine (Silvadene): Same spectrum as Sulfamylon.
  • Betadine (Povidone-iodine): Wide gram-positive and gram-negative spectrum; also some antifungal activity.

• Exposure method: Burn left uncovered; topical agent applied every 12 hours; a crust forms and protects the area. Suitable for head, face, neck.
• Closed method: 3-layer dressing - (i) inner non-adherent antiseptic layer (oily tulles or water-based cream with chlorhexidine/soframycin), (ii) sterile cotton gauze, (iii) cotton bandage.

• Indicated when the wound has red finely granular granulation tissue, bacterial count <10⁵/cm², no residual nonviable tissue.
• Split thickness autograft is standard.
• Mesh grafts: Used when donor sites are limited; parallel incisions allow expansion up to 6x; do NOT use on face, hands, feet, or flexion creases.
• Biologic dressings (homograft/heterograft): Temporary cover while waiting for the wound to be ready for autograft; advantages include infection prevention, pain reduction (covering sensory nerves), protection of neurovasular tissue, decreased water loss.
• Tangential excision: Successive thin layers removed until uniform capillary bleeding; closed by autograft immediately.

• Starts immediately on admission.
• Progressive range-of-motion exercises in direction opposite to anticipated deformity.
• Avoid prolonged immobilization.
• Splints to maintain anticontracture positions during sleep.
• Upper extremities are more susceptible to contracture than lower extremities.

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COMPLICATIONS

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SPECIAL TYPES - TREATMENT SUMMARY

Electrical Injury

1. Stop the current first (first aid).
2. CPR if cardiac arrest.
3. Fluid: Ringer's lactate to maintain urine output 50-75 ml/hr (increase to 100 ml/hr if myoglobinuria visible); add mannitol 12.5g per litre.
4. Mafenide acetate preferred (penetrates injured tissue, anticlostridial spectrum).
5. Stony hard muscle compartment oedema or absent peripheral pulses → immediate surgical exploration.
6. Meticulous debridement of all necrosed tissue; wounds packed loosely and left open.
7. Late complication: delayed haemorrhage from blood vessels due to electrical "arteritis."

Chemical Burns

1. Copious water irrigation immediately (EXCEPT phenol burns - water accelerates absorption; use polyethylene glycol).
2. Remove all contaminated clothing.
3. Irrigate for at least 30 minutes (sometimes continuous shower for 24 hours).
4. Hydrofluoric acid burns: irrigation with benzalkonium chloride + excise necrotic tissue.
5. Phenol burns: wash with polyethylene glycol or glycerol.
6. Early excision + skin grafting for extensive chemical burns.

Cold Injuries

• Frostbite: Managed conservatively by rapid warming in warm water; surgery rarely required unless depth properly assessed.
• Industrial cold injury (liquid nitrogen): Skin/dermis destruction; human tissue is more resistant to cold injury than heat injury; surgery rarely required.

Ionizing Radiation Injury

• Localized: Conservative management until true extent is assessed; if ulceration → excision + coverage with vascularized skin.
• Whole body: Potentially lethal; causes immune dysfunction and gut mucosal damage; management is mainly supportive.

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