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Burns Treatment

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

Figure 1 I Systemic response to larger burns
Large burns affect both the respiratory system, the cardiovascular system, metabolic rate, and the immunological 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 shifts the body into a general catabolic state with a greater risk of developing infections with fatal outcome (2). Sepsis is the leading cause of death among patients with large burns (3,4). The damages leads to severe capillary leakage and accentuates to a state of shock. The immune response is activated, which increases the production of nitric oxide synthase (NOS), vasodilatation and capillary leakage, leading to hypovolemia and hypoperfusion (Stage 1 shock) (5).

 Systemic Responses to large burns
  Cardiovascular changesIncreased 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 changesInflammatory mediators cause bronchoconstriction and in severe burns and/or combined with inhalation injury can lead to acute respiratory distress syndrome (ARDS).   
Metabolic changesThe 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 changesNon-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 can last years after initial trauma. 
Table 1 | Systemic responses to burns

Local response

Figure 2 | The local pathophysiological changes of burns, consist of three zones, described by Jackson in 1947.

The zone of coagulation

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

Is the peripheral to 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 acute treatment with the cooling of the burn, fluid resuscitation and the importance of 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

Is the peripheral to the zone of stasis that 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, lower legs can compromise the perfusion.

  • Change of color towards more pale and bluish.
  • Decreased movement/mobility and sensibility 
  • Pain that worsens with movement 
  • Clinical examination: Assessment of skin color and temperature, measuring the saturation in fingers and palpating pulse. 
  • Treatment: Surgical fasciotomy by incision, which will release the skin contraction.

References

  1. Freiburg C, Igneri P, Sartorelli K, Rogers F. Effects of Differences in Percent Total Body Surface Area Estimation on Fluid Resuscitation of Transferred Burn Patients. J Burn Care Res [Internet]. 2007 Jan [cited 2018 Mar 25];28(1):42–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17211199
  2. Church D, Elsayed S, Reid O, Winston B, Lindsay R. Burn wound infections. Clin Microbiol Rev [Internet]. American Society for Microbiology (ASM); 2006 Apr [cited 2018 Mar 25];19(2):403–34. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16614255
  3. Nunez Lopez O, Cambiaso-Daniel J, Branski LK, Norbury WB, Herndon DN. Predicting and managing sepsis in burn patients: current perspectives. Ther Clin Risk Manag [Internet]. Dove Press; 2017 [cited 2018 Mar 25];13:1107–17. Available from: http://www.ncbi.nlm.nih.gov/pubmed/28894374
  4. Greenhalgh DG. Sepsis in the burn patient: a different problem than sepsis in the general population. Burn trauma [Internet]. BioMed Central; 2017 [cited 2018 Mar 25];5:23. Available from: http://www.ncbi.nlm.nih.gov/pubmed/28795054
  5. Nielson CB, Duethman NC, Howard JM, Moncure M, Wood JG. Burns: Pathophysiology of Systemic Complications and Current Management. J Burn Care Res [Internet]. Wolters Kluwer Health; 2017 [cited 2018 Mar 25];38(1):e469–81. Available from: http://www.ncbi.nlm.nih.gov/pubmed/27183443
  6. JACKSON DM. [The diagnosis of the depth of burning]. Br J Surg [Internet]. 1953 May [cited 2018 Mar 25];40(164):588–96. Available from: http://www.ncbi.nlm.nih.gov/pubmed/13059343
  7. Hettiaratchy S, Dziewulski P. ABC of burns: pathophysiology and types of burns. BMJ [Internet]. BMJ Publishing Group; 2004 Jun 12 [cited 2018 Mar 25];328(7453):1427–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15191982

Acknowledgements

Illustrations: Caroline Lilja, med.stud.

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