Burns

A) Classification
i) first degree: only involves epithelial layer. Often very painful but resolves with no residual scarring. Skin is red and painful but blisters are not present - second degree: involves epithelium and part of dermis. Pain and scarring vary according to depth of burn. ii) superficial second-degree burns damage is limited to epidermis and uppermost part of dermis. iii) Deep second-degree burns spare only the deepest portion of dermis iv) third degree: full thickness. Usually painless due to destruction of cutaneous innervation. Leads to scarring. Usually dry and have milky white or tanned leather appearance
Burn depth Superficial 2nd degree Clinical features Blisters, erythema, capillary refill, intact pain sensation Treatment Tetanus prophylaxis. Cleaning (eg with chlorhexidine), topical agent (eg silver sulphadiazine), sterile gauze dressing, physio, splints as necessary. # As above. Early surgical excision and skin grafting an option Usual result

Epithelialization in 7-21 d rare, return of full functio

Deep 2nd degree

Blisters, pale white or yellow colour, no capillary refill, absent pain sensation Blisters may be absent. Leathery, inelastic, wrinkled appearance over bony prominences. No capillary refill. Thrombosed subcutaneous vessels may be visible. Absent pain sensation.

Epithelialization in 21-60 Hypertrophic scar commo function with surgical the

3rd degree

As for superficial partial thickness burns. Wound excision and grafting at earliest feasible time. For 25% burns should be enough donor site to close all wounds at the same operation. For more extensive burns: staged excision and closure or complete excision and temporary skin substitute to cover areas remaining after all available autologous skin has been harvested and grafted

Functional limitation mor scar mainly at graft margi

# Can also be treated effectively by covering the denuded wound with skin allograft or xenograft or a commercially available synthetic membrane. If adherent these reduce pain and eliminate the need for dressing changes.

B) Pathophysiology
- may be inflicted by heat, chemicals, electricity or radiation - human skin can tolerate temperatures up to 40C but cellular injury follows exposure to temperatures >45C - skin & deeper tissues injured by direct cellular injury and delayed progressive ischaemia - 3 zones of injury:

central zone of coagulation zone of stasis extending from centre; viable tissue will undergo ischaemic necrosis if resuscitation inadequate distant zone of hyperaemia which will recover

- oedema formation:

maximal within 24 h due to fluid and protein shifts due to increased vascular permeability, low intravascular oncotic pressure and increased interstitial osmotic pressure. Latter due sodium binding to damaged collagen generalized in burns >20-30% BSA. Due to a decrease in cell transmembrane potential of non-burn tissue resulting in a shift of ECF sodium and water into ICF

- SIRS precipitated by inflammatory mediators (eg leukotrienes, prostaglandins, oxygen radicals and histamine)

Cardiovascular and circulatory effects

- significant changes likely in first 48h in burns >20% BSA - cardiac output decreased due to decreased preload and myocardial depression (? due to cytokines)

Respiratory effects
- major cause of mortality and morbidity - thermal injury in a closed environment may cause pulmonary inhalation injury and intoxication from combustion products. Of these most important are carbon monoxide and cyanide Airway injury - upper airway damage is due to heat - upper and middle airway damage due to inhalation of hot particles or noxious chemicals or direct flame injury

- maximal oedema formation at about 24h but depends on a variety of factors including adequacy of resuscitation Lung injury - pathophysiology of parenchymal lung damage not known. ? due to direct thermal injury and chemical injury. ? due to indirect effects such as fluid overload, secondary infection, ARDS, PE - steam is only agent that results in immediate injury to lung parenchyma - impairment of gas exchange due to V:Q mismatch due to airway injury rather than alveolar injury - lung complications can occur following major burns without inhalation injury - increased airway resistance and decreased lung compliance increase work of breathing - changes most marked during 10-14 days following burns - respiratory acidosis due to inhalation of smoke Cellular injury - inhalation of CO, cyanide and other noxious gases affect respiration at cellular level - CO and cyanide have synergistic toxic effects

Metabolic effects
- increased catabolism: greater than after any other form of trauma - proportionate increase in oxygen consumption - stress response is manifested as: persistent hyperpyrexia, tachycardia. hyperventilation, hyperglycaemia - plasma insulin low immediately after thermal injury but is usually followed by a prolonged "insulin resistance" phase - hypermetabolism increases with cooling, pain and sepsis: hence try to increase environmental temperature, cover burn areas with heterograft to reduce evaporative loss and give analgesia - acidosis develops within hours after > 30% burns. Has both metabolic and respiratory components. Former due to products of heat-damaged tissues and relative hypoxia - some evidence to suggest that stress response can be modulated and reduced if enteral feeding is started in first 24 h

Immunological changes
- immune and inflammatory response depressed in severe burn injuries - sepsis accounts for >50% of mortality in burns

Haematological
- red cell loss due to haemolysis and intravascular coagulation likely in patients with >20% burns. May be as high as 1% of red cell mass per % of full thickness burn. Red cell extravasation also occurs - increase in red cell destruction thought to be due to some factor in plasma which makes red cells more liable to destruction - coagulopathy may occur during resuscitation phase due to dilution and consumption - DIC common in extensive burns - hypercoagulable state may develop 2-4 weeks post burn

Others
- oliguric/non-oliguric renal failure may occur due to renal hypoperfusion, haemoglobinuria, myoglobinuria or sepsis. Associated with high mortality even with dialysis - stress ulceration in 11% of burn patients

C) Management
- calculate area of burn: in adults each arm 9%, each leg 18%, each side of trunk 18%, head 9% and perineum 1%. Age adjusted approximations available for assessing burn size in children

Fluid resuscitation
- IV fluids if burn >20% or 15% with inhalation injury - disagreement regarding quantity and choice of fluids - larger volumes should be given in first 8-12 h when fluid loss is greatest with gradual reduction over next 16h. Patients with inhalational injuries frequently require up to 50% more fluid to be resuscitated adequately during the first 24 h. (NB amount of lung water appears to be higher in patients who are underresuscitated than those who are fully resuscitated) - Parkland formula: 4 ml/kg/% burn of Ringer's solution during first 24 h with one half given in first 8 h - sodium requirement 0.5 mmol/kg/% burn - recommended regimes should be titrated to individual requirements. Frequent monitoring of patient response and biochemical investigations are necessary to adjust fluid regime. Aim for urine output >0.5 ml/kg in adults and > 1 ml/kg in children <25 kg in the absence of rhabdomyolysis. Fluid regimes which result in appreciably higher urine outputs increase wound oedema and may necessitate otherwise unneeded escharotomies - blood transfusion indicated in patients with massive haemolysis or blood loss - mannitol to maintain urine output of 1-2 ml/kg/hr if haemolysis or muscle

damage significant to prevent renal failure secondary to haem proteins or rhabdomyolysis - use of colloid for resuscitation has decreased mainly because controlled trials have shown no clear advantage to its use and one showed potentially harmful effects: increased accumulation of water in lungs and an increased rate of clinical pulmonary complications associated with use of albumin - beyond 24 h: increased permeability to protein (but not Na) has largely returned to normal and thus thought that colloid should be used for resuscitation. However this practice may be harmful: administration of albumin to patients in stable condition after 24 h of clinically satisfactory crystalloid resuscitation led to a significant decrease in GFR below the normal range despite an increase in plasma volume. Also important to give water (dextrose) due to high evaporative loss from skin. High K requirement due to shift of K from ECF to ICF as injured cells recover

Respiration
- may be no respiratory symptoms in first 24h - careful assessment of airway with immediate intubation if any doubt with regard to patency exists. UAO may develop suddenly and catastrophically. - other indications for intubation:

stridor circumferential burns of neck facial burns full thickness burns of nose or lips oedema of pharynx or larynx unconsciousness loss of airway reflexes carbon monoxide or cyanide poisoning any signs of respiratory distress > 40% burns due to risk of laryngeal oedema as part of generalised oedema that occurs with large BSA burns. (May be necessary for 25-40% burns. Usually unnecessary < 25%)

- use largest ETT possible to facilitate lung toilet +/- bronchoscopy - humidification particularly important in those with lower airway burns - tracheostomy occasionally required on presentation because of facial and upper airway burns - avoid suxamethonium: may result in severe hyperkalaemia 2-60 days following burn - burn patients relatively insensitive to non-depolarizing drugs and may require large doses for paralysis - burn or soot around mouth or nose should increase suspicion of an inhalational burn. Any patient burned in a closed space where smoke can accumulate should be treated as having a smoke inhalation injury

- lungs particularly sensitive to barotrauma. HFV and permissive hypercapnia have been advocated to reduce complications - suspect carbon monoxide poisoning if patients show signs of mental disturbance - minority of patients will require bronchodilators for smoke-induced irritation of airways

Nutritional support
- commence when resuscitative phase is complete - enteral preferable - requirements of burn patients not significantly different from those of other trauma victims - additional protein may improve immune function and mortality - formulations with high protein, low fat and linoleic acid, but enriched vitamins A & C, zinc, histidine, cysteine, arginine and omega 3 fatty acids said to be superior to standard regimes

Sepsis
- skin and lungs are most common sources of infection - diagnosis of sepsis may be difficult - signs of burn wound sepsis:

focal or diffuse areas of discolouration (black, brown or violet) purulent fluid from eschar signs of cellulitis at unburned margins of burn wound too rapid eschar separation

- general signs of sepsis in burned patients include:

change in sensorium development of ileus development of glucose intolerance

Specific treatment of burn

- early excision and grafting minimizes infection, hastens wound healing, reduces blood loss and improves survival - only after fluid resuscitation and when patient's condition is stable, usually 2436 hrs post burn - mortality high in patients at extremes of age and with > 60% burns - best wound coverage is split thickness autografts but donor sites limited and there is associated morbidity - allogeneic skin grafts have problems of availability and disease transmission - topical antimicrobial therapy after wound cleaning and deroofing of blisters may lower infection rate but is not of itself the treatment of choice. Silver

sulphadiazine 1% is agent most commonly used. May cause dermal hypersensitivity reactions and transient leucopaenia in up to 5%. Latter is due, in part, to marrow toxicity. Nearly always resolves within a period of several days despite continuation of drug. - other agents include:

mafenide acetate 10%. Deep wound penetration but can produce pain and metabolic acidosis by carbonic anhydrase inhibition silver nitrate. Effective and safe in concentrations of up to 0.5%. Occasionally causes hyponatraemia and metbaemoglobinaemia chlorhexidine effective against many bacteria, yeasts and viruses povidine iodine. Wide range of bactericidal activity but may cause metabolic acidosis, renal dysfunction and ? thyroid abnormalities antibiotic solutions. Resistance, hypersensitivity, skin irritation and limited efficacy

- wound dressing changes can precipitate significant haemodynamic changes and careful monitoring important Grafting skin on established, granulating wounds from which the eschar has sloughed is the poorest surgical option but may be necessary in the presence of severe illnesses or systemic complications

Systemic antibiotics
- routine prophylactic antibiotics no longer recommended - when used to treat specific infection altered pharmacokinetics in burns patients should be taken into account

Others
+/- tetanus toxoid - analgesia +/- dialysis - haptoglobin to reduce myoglobin toxicity to renal tubules has been advocated Analgesia - pain in immediate post burn period can aggravate shock - immersion or showering with cool water reduces extent of thermal damage and provides analgesia - opioid infusions recommended - requirements increase with time

D) Prognosis

- > 20% burn and smoke inhalation associated with 50-80% mortality

E) Burns in pregnancy

maternal outcome unaffected by pregnancy fetal outcome o <20% BSA burn: no effect o >30% BSA burn: increased risk of preterm labour o >40% BSA burn: high risk of fetal death o >50% BSA burn: consider elective cesarean section if fetus is still viable initial resuscitation unchanged

Further reading
Freebairn RC & Oh TE. Burns. In Oh TE (ed), Intensive Care Manual, 4th Ed., Butterworth Heinemann, Oxford, 1997, pp 622-30 Deitch EA. Burn managment. Rippe JM, Irwin RS, Fink MP, Cerra FB (eds), Intensive Care Medicine, 3rd ed. Little Brown & Co., Boston, 1996, pp 1957-65 Monafo WW. Initial management of burns. NEJM, 1996; 335(21): 1581-1586