Pathophysiology

Authors: Rami Mossad Ibrahim, MD, Elisabeth Lauritzen, MD, Frederik Gulmark Hansen med.stud., Magnus Balslev Avnstorp, MD and Rikke Holmgaard, Consultant, Burns Specialist, MD, PhD

The damage of burns should be evaluated both systemic and locally.

Systemic response

The systemic response depends on the size of the burn and occurs when burned TBSA exceeds 20-25 % (1). The damage alters homeostasis, fluid balance, nutrient absorption and induces a hypermetabolic state with a humoral and cellular immunodeficiency (2).

These changes shift the body into a general catabolic state with a greater risk of developing infections with fatal outcome (2). Sepsis is one of the leading causes of death among patients with large burns (3,4). Larger burns lead to severe capillary leakage and can accentuates into a state of shock. The immune response is activated leading to increased production of nitric oxide synthase (NOS), vasodilatation and capillary leakage, resulting in hypovolemia and hypoperfusion (Stage 1 shock) (5).

	Systemic Responses to large burns
Cardiovascular changes	Increased capillary permeability leading to loss of intravascular proteins and fluids into the interstitial compartment, which results in loss of fluid from the capillary lumen. Peripheral and splanchnic vasoconstriction occurs. Myocardial contractility is decreased. These changes, combined with fluid loss from the burn wound, result in systemic hypotension and possibly organ hypoperfusion leading to organ dysfunction.
Respiratory changes	Inflammatory mediators cause bronchoconstriction. Severe burns combined with inhalation injury can lead to acute respiratory distress syndrome (ARDS).
Metabolic changes	The basal metabolic rate increases up to three times its original rate. This, combined with splanchnic hypoperfusion, necessitates early an aggressive fluid resuscitation and nutrients to decrease catabolism and maintain gut integrity.
Immunological changes	Non-specific down regulation of the immune response occurs affecting both cell- and humoral mediated pathways. This can lead to an increased rate of infections and may last years after initial trauma.

Local response

The zone of coagulation, Zone 1

Is a result of direct contact with the burning hot object, which results in local denaturation of proteins and necrosis of the tissue. Zone of coagulation is the point of maximum damage, with an irreversible tissue loss (6,7). 

The zone of stasis, Zone 2

Zone 2 sorrounds the zone of coagulation. The blood flow in this zone is decreased and the tissue has approximately 50% chance of survival. Tissue in this zone is potentially salvageable, depending on the acute treatment i.e. cooling of the burn and burn resuscitation leading to increased tissue perfusion. Additional damage — such as prolonged hypotension, infection or oedema, can convert this zone into an area of complete tissue loss(6,7).

The zone of hyperaemia, Zone 3

Is the peripheral to the zone of stasis (Zone 2). This zone maintains a normal blood flow. The tissue will recover unless severe sepsis or prolonged hypoperfusion occurs(6,7).

Symptoms of compromised perfusion (circular burns)

Circular burns on fingers, arms and/or lower legs can compromise the perfusion.

• Symptoms
  • Change of color towards a pale and bluish tone, distant of the burn
  • Decreased movement/mobility and sensibility 
  • Pain that worsens/increases with movement
• Clinical examination
  • Assessment of skin color and temperature, measuring oxygenation of the fingers and palpating the pulse. 
• Treatment
  • Surgical fasciotomy by incision, will result in release of the skin contraction.

Acknowledgements

Illustrations: Caroline Lilja, med.stud.