Etiology and Pathogenesis of MODS
The pathophysiology of MODS is not very well understood although various hypotheses on the …show more content…
events leading to MODS have been documented. Elliott, Aitken, and Chaboyer (2011) observed that the development of MODS is associated with multiple causative factors namely: direct cytotoxicity, parenchymal and endothelia cells injury, immunosuppression, apoptosis, and coagulopathy. A number of theories have been used to explain MODS’s chains of events.
Hypoxia: This connotes a condition in which there is inadequate supply of oxygen to the body tissue—the cells are deprived of oxygen due to some pathological condition.
Prolonged tissue hypoxia causes depletion of Adenosine Triphosphate (ATP) which is an energy storage molecule. Consequently, cells disintegrate –typical of necrosis—as energy fall below critical levels for organ function. Inadequate oxygenation is quite common in patients with acute lung injury and sepsis (Baue, Faist, & Fry, 2012). Another example is cardiac arrest and hemorrhagic shock which are easily managed, for example, with red blood cells transfusion and resuscitation for cardiac arrest. While many randomized control studies have supported systemic and tissue hypoxia as an important factor in MODS pathophysiology, it is not the only variable since some patients may develop MODS without necessarily experiencing decreased oxygen
supply.
Infection: This hypothesis argues that systemic attack by pathogens could result in MODS. Baue (2012) observed that MODS is in most cases, associated with infection or sepsis at the time a patient is admitted to ICU. Bacterial infection stimulates release of kinins by activating the compliment and plasmin complex. This further activates macrophages and cytokines which when combined with kinins, cause granulocytes adherence to the endothelial layer of the capillaries. This culminates in an increase in permeability of the capillaries, interstitial edema, and decline in uptake of oxygen by tissues, and eventually, organ dysfunction.
Systemic Inflammatory response syndrome: while infection and hypoxia are known precipitating factors for MODS, systemic inflammatory response syndrome especially in AIDS patients my cause organ dysfunction especially that associated with iatrogenic causes (Elliott, Aitken, & Chaboyer, 2011)
Clinical Manifestations and Complications
A MODS is manifested through derangement of main organ systems: circulatory system, pulmonary dysfunction, gastrointestinal system, liver dysfunction, renal dysfunction, and derangement of the central nervous system. The circulatory system dysfunction is typical case of sepsis—which causes systemic vasodilatation. The endothelial injury and septic shock worsen gastrointestinal dysfunction. Liver dysfunction on the other hand, contributes to initiation of sepsis and its progression. Total liver failure is manifested by elevated bilirubin and liver enzymes, defects in coagulation, and poor excretion of toxins which further exacerbates encephalopathy. Renal system derangement is a manifestation of acute kidney injury which is closely associated with sepsis. The central nervous system dysfunction is a manifestation of systemic hypotension, peripheral neuropathy, and encephalopathy which too, are linked to sepsis. Brain hypoperfusion is a common complication.