SIRS, MODS, and Burns: Module 20 Discussion

Abstract

Burns are one of the most severe insults to the body. Such a severe reaction is likely to induce distributive shock, which involves the incorrect distribution of blood flow necessary for proper physiological function. The shifts in fluid overload from vascular areas to interstitial spaces as a result of increased permeability of cellular structures and capillaries can result in extensive damage to the body beyond the affected area. When the body fails to achieve homeostasis, it can result in systemic inflammatory response syndrome (SIRS) which can lead to a variety of complications including Multiple organ dysfunction syndrome (MODS) and death. The patient scenario involves a male who receives second and third-degree burns on his face, neck, and arms from a campfire. The patient enters hypovolemic shock as a result of the effective loss of < 2000 ml of blood.

SIRS, MODS, and Burns

Shock is a broad term used to describe various states in which the body and mind stop functioning regularly, usually induced by sudden trauma, of a physiological or psychological nature. According to Cheatham and Block (2008), “Shock is currently best defined as a multifactorial syndrome resulting in inadequate tissue perfusion and cellular oxygenation affecting multiple organ systems” (p. 1). Since the definition of shock is so broad, it can result in a variety of symptoms including, discoloration of the lips and extremities, confusion, slurred speech, dizziness, nausea, and vomiting. In 1972 Hinshaw and Cox proposed a system of classification of the types of shock that is still widely used. Hypovolemic shock is the most common shock state and is the result of decreased blood volume. Obstructive shock is the result of an actual obstruction to normal blood flow such as a puncture wound. This shock state results in cardiac tamponade. Cardiogenic Shock is the result of the ventricles of the heart failing to function effectively. This results in insufficient oxygenation of cells due to inadequate blood flow. Distributive shock involves a region of the body receiving and inadequate oxygen supply. Anaphylactic shock and septic shock are two examples of distributive shock. The final shock state is Endocrine shock, which is difficult to distinguish from the other states of shock, as Endocrine shock is frequently induced by one of the other forms. A good question surrounding these different shock states is how can you quickly determine what sort of shock a patient is undergoing in order to attempt to treat the condition effectively. These various shock states are important to understand when dealing with burns, especially given the severity of SIRS.

The body frequently uses heavily controlled localized inflammation to deal with various problems. Systemic Inflammatory Response Syndrome, however, is the loss of the body’s ability to control this mechanism resulting in widespread inflammation leading to Multiple Organ Dysfunction Syndrome as a result of this systemic inflammation. Meeran and Messent (2001) present an explanation for the relationship between SIRS and MODS called the “Two hit theory” which suggests that an initial insult triggers the inflammatory response, while subsequent sepsis and infection trigger the uncontrollable response that leads to more serious complications (p. 94). SIRS is a delicate condition at best, “MODS, however, is constituted not only by the sum of all failing organs, but also by a severe impairment of inter-organ communication” (Werdan, Schmidt, and Elbet, 2013, p. 274). In the case of burns, the body is unable to properly regulate the massive damage it undergoes, which can result in SIRS.

During the early phases of an acute burn injury, the cell walls become extremely permeable. Rapid shifts in fluid from vascular areas to interstitial spaces result in severe dehydration of otherwise healthy tissue. The infected tissue is initially depleted of H20 and sodium, but depending on the severity of the burn other substances can be depleted as well. Patients will begin to exhibit signs of shock, including increased BP, and increased pulse. Hemolysis of RBC resulting from a circulating factor released when the body is burned will impair the circulatory status. This impairment of the circulatory status will cause coagulation necrosis and thrombosis. The immune system will become impaired. Due to the destruction of the skin barrier, bone marrow depression occurs along with decreased circulating levels of immunoglobulins. Hypovolemic shock can lead to renal failure.

Case Scenario

A patient who has been severely burned on multiple regions of the body as a result of falling into a campfire has 2nd and 3rd degree burns on the chest, neck, and arms. Due to the loss of fluids involved in the fluid shift phase of the burn, the patient enters hypovolemic shock. The patient is exhibiting incredible anxiety, rapid breathing, pale skin coloration, and other signs of shock. Triage shows low BP. Blood loss is determined to be <2000 ml, the resultant loss of systolic pressure invalidates BP as the primary determinant factor for assessing shock level. Reduced intravascular volume adversely affects preload. Cardiac output falls as preload is one of the main determinants of stroke volume. Fluid loss activates the compensatory mechanism under neuroendocrine control, which maintains central perfusion despite the fall in cardiac output.

References

Cheatham, M. L., Block, E. F., Promes, J., Smith, H., Dent, D. L., & Mueller, D. L. (2008). Shock: an overview. Irwin R.S., Rippe J.M. (eds)“ Intensive care medicine”. Lippincott Williams & Wilkins, Philadelphia, 1831-1842.

Meeran, H., & Messent, M. (2001). The systemic inflammatory response syndrome. Trauma, 3, 89-100.

Werdan, K., Schmidt, H., Ebelt, H., Zorn-Pauly, K., Koidl, B., Hoke, R. S., ... & Müller-Werdan, U. (2009). Impaired regulation of cardiac function in sepsis, SIRS, and MODS This article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 2 of a 2-part Special Issue). Canadian Journal of Physiology and Pharmacology, 87(4), 266-274.