A definite explanation has not been found. Local and systemic responses are initiated by tissue damage. Respiratory failure is common in the first 72 hours. Subsequently, one might see liver failure (5–7 days), gastrointestinal bleeding (10–15 days) and kidney failure (11–17 days). Gut hypothesis The most popular hypothesis by Deitch to explain<unk>  in critically ill patients is the gut hypothesis. Due to splanchnic hypoperfusion and the subsequent mucosal ischaemia there are structural changes and alterations in cellular function. This results in increased gut permeability, changed immune function of the gut and increased translocation of bacteria. Liver<unk>  leads to toxins escaping into the systemic circulation and activating an immune response. This results in tissue injury and<unk><unk> . Endotoxin macrophage hypothesis Gram-negative infections in<unk>  patients are relatively common, hence endotoxins have been advanced as principal mediator in this disorder. It is thought that following the initial event cytokines are produced and released. The pro-inflammatory mediators are: tumor necrosis factor-alpha (TNF-α), interleukin-1, interleukin-6, thromboxane A2, prostacyclin, platelet activating factor, and nitric oxide. Tissue hypoxia-microvascular hypothesis As a result of macro- and microvascular changes insufficient supply of oxygen occurs. Hypoxemia causes cell death and<unk><unk> . Mitochondrial DNA hypothesis According to findings of Professor Zsolt Balogh and his team at the University of Newcastle (Australia), mitochondrial DNA is the leading cause of severe inflammation due to a massive amount of mitochondrial DNA that leaks into the bloodstream due to cell death of patients who survived major trauma. Mitochondrial DNA resembles bacterial DNA. If bacteria triggers leukocytes, mitochondrial DNA may do the same. When confronted with bacteria, white blood cells, or neutrophil granulocytes, behave like predatory spiders. They spit out a web, or net, to trap the invaders, then hit them with a deadly oxidative blast, forming neutrophil extracellular traps (NETs). This results in catastrophic immune response leading to<unk> . Integrated hypothesis Since in most cases no primary cause is found, the condition could be part of a compromised homeostasis involving the previous mechanisms.
Multiple organ dysfunction syndrome
Cytokine release syndrome
Tumor lysis syndrome
Systemic inflammatory response syndrome
Macrophage activation syndrome
Decompression sickness
Pulmonary-renal syndrome
Culture-bound syndrome