Ultimately, all trauma leads to decreased organ perfusion, cellular ischemia, and a cascade of edema and inflammation. Once begun, inflammation becomes a disease process independent of its origin, and can lead to multiple organ failure and death even after a patient has been completely resuscitated.
The CNS response to trauma is predominantly neuroendocrine in nature, and acts to preserve the CNS, heart, and kidneys. It is enacted primarily by the kidneys and adrenal glands, which collectively produce renin, angiotensin, aldosterone, cortisol, erythropoietin, and catecholamines. The kidney is generally able to maintain GFR via vasoconstriction but loses its ability to concentrate urine (and preserve volume). In most patients, the heart is well-preserved until the late stages of shock, however in elderly patients (with a more fixed stroke volume) or those with cardiac disease, cardiac function may not be responsive to fluid resuscitation and decompensation may occur much earlier [Dark PM et al. Intensive Care Med 26: 173, 2000]. The lungs, which may act as a depository for the mediators of inflammation, are often the sentinel organs for multiple organ system failure (MOSF) in traumatic shock patients [Demling R et al. Curr Probl Surg 30: 345, 1993; Horovitz JH et al. Arch Surg 108: 349, 1974]. The GI tract vasoconstricts early in the trauma/shock process, exhibits “no-reflow” phenomena (where cellular edema after a hypotensive event prevents microcirculatory flow following restoration of blood pressure) [Reilly PM and Bulkley GB. Crit Care Med 21(2S): S55, 1993] and possibly being the initiating organ in multi-organ failure. The liver is notable for its susceptibility to reperfusion injury [Chun K et al. Shock 1: 3, 1994] – if recovery of synthetic function does not occur, death is almost always imminent.