Burn Injury

Date the injury before you plan anything - The early phase is hypovolemia, low cardiac output and high systemic vascular resistance. It converts into a hyperdynamic, hypermetabolic phase lasting months. Fluid strategy, hemodynamic targets and drug requirements all differ between the two, so establish how many hours or days out you are before you draw anything up.

The succinylcholine window - Succinylcholine is acceptable within 24 hours of the burn. Beyond 24 hours, and for at least 18 months after the injury, avoid it: the burned patient's response to it is a hyperkalemic one severe enough to arrest the heart. Use rocuronium when you need a rapid sequence in that window.

Expect to fight the nondepolarizers - During the hyperdynamic phase both the dose and the dosing frequency of nondepolarizing relaxants go up, on the order of two- to fivefold. Dose against measured neuromuscular function rather than against a weight-based number, and plan to redose sooner than habit suggests.

Take the airway early - Airway obstruction and edema, pulmonary edema and carbon monoxide poisoning all belong to the burn airway, and inhalation injury may not be clinically evident at first. Build the airway assessment from what the burn team already documents: percentage TBSA burned, burn depth and distribution, whether inhalation injury is present, whether the patient is already intubated and, if so, the ventilator mode and settings. If the face and airway are burned and the airway is not yet secured, secure it before edema removes the option.

Fluid resuscitation cuts both ways - Crystalloid is the mainstay during the early phase, with colloid considered after the first 24 hours. Resuscitation across the first 48 hours drives survival, but excessive fluid is its own injury. Titrate to endpoints rather than running a formula to completion.

Volatiles as a component, not the whole anesthetic - Dose-dependent vasodilation and cardiac depression limit volatile agents as sole agents in a patient who is already hypovolemic with a low cardiac output, so use them inside a balanced technique. They do earn a place in inhalation injury for their bronchodilating effect.

Access is one of the hard parts - Direct trauma to skin and soft tissue makes vascular access difficult, and you will often be siting lines through or near burned tissue. Get large-bore access in before you need it, plan for central access rather than converting to it under pressure, and secure everything mechanically - suture or wrap - because tape has nothing intact to hold.

Warm from the start - Plan active warming before the drapes go on: warm the room, warm every fluid and blood product, cover whatever intact skin you can with forced air, and run a continuous core temperature for the whole case rather than a spot check at the end.

Follow the kidney - The early phase brings a falling glomerular filtration rate and myoglobinuria. Follow hourly urine output, and send a creatinine and a potassium rather than working from the admission labs.

Check the blood before excision - Hemoconcentration early, then hemolysis and thrombocytopenia. Excision and grafting are bleeding operations. Send a current hematocrit and platelet count, have blood available in the room, and know where the next units are.

The operation is not elective - Wound excision and closure are critical to survival and must not be delayed. These patients come to you less optimized than you would normally accept and they come back repeatedly. Negotiate the margins of the plan, not whether the case happens.

Pain is a long-term problem, not a case-day one - Excision, grafting and dressing changes recur over months. Build a multimodal plan and document what worked, because the next provider is starting from your record and the requirement moves between visits.

Past about 20% total body surface area in an adult, a burn stops being a skin problem. Large-scale destruction of tissue sets off a profound inflammatory response and massive fluid shifts, and the early burn shock phase follows: hypovolemia with falling cardiac output and rising systemic vascular resistance, hemoconcentration, hemolysis and thrombocytopenia, a falling glomerular filtration rate with myoglobinuria, gut hypoperfusion with mucosal damage, reduced hepatic perfusion and cerebral edema.

Patients who get through that convert into a hyperdynamic, hypermetabolic phase that runs for months. The two phases want opposite things from you, so the date of the injury is a clinical variable. Running alongside both is the airway: obstruction and edema, pulmonary edema and carbon monoxide poisoning, with inhalation injury that may not be clinically evident when you first meet the patient.