Different Responses to MODS

Vascular Response

In an uncontrolled inflammatory response, activation of inflammatory cells, release of mediators, damage to endothelium, and hypermetabolism occur.
Vasodilatation becomes excessive and leads to decreased SVR, hypotension, and an increase in vascular permeability allowing mediators and protein to leak out of the endothelium into the interstitial space.
Hypotension and decreased SVR causes compromised organ perfusion and microemboli.

Respiratory Problems

In MODS, the respiratory system is often the first system to show signs of dysfunction.
Inflammatory mediators and endothelial damage cause an increase in capillary permeability and movement of proteinaceous fluids into pulmonary interstitial spaces.
These fluids then move into the alveoli, causing edema and a decrease in surfactant production and alveolar collapse.
Ultimately the result is ARDS.

The Cardiac Response

Myocardial depression, massive vasodialation, decreased SVR, and decreased BP are factors that decrease the CO.
The baroreceptor reflex causes the release of inotropic and chronotropic factors and an increase in HR are factors that attempt to compensate for the low CO.
Capillary permeability causes a shift of albumin and fluid out of the vascular space, eventually leading to poor organ tissue perfusion from low CO.

Neurologic Response

Neurologic dysfunction is caused by hypoxia

Renal Problems

Acute renal failure is caused by hypoperfusion, and the effects of the mediators.
Decreased perfusion activates the renin angiotensin system, causing systemic vasoconstriction, release of aldosterone, and water resorbtion.

GI Dysfunction

Early in MODS blood is shuted away fro the GI tract making it susceptible to ischemic injury.
Decreased perfusion leads to the breakdown of the protective mucosal barrier leading to the risk of ulceration and GI bleeding.
Bacteremia can result from can translocate from the gut to the blood with the breakdown of the mucosal layer.

Liver Dysfunction

Hypermetabolism results in liver dysfunction.
Protein synthesis is impaired
Synthesis of albumin is impaired leading to decreased oncotic pressure of the plasma and fluid and protein leakage into the interstitial space.
Administration of albumin does not normalize oncotic pressure in these patients.

Electrolyte Imbalances

Electrolyte imbalances are common and are related to fluid shifts as well as metabolic and hormonal changes.
Decreased renal perfusion results in ADH and aldosterone release, resulting in Na and water retention, potassium loss, and metabolic acidosis
Hypocalcemia, hypomagnesemia, and hypophosphatemia are common

(Lewis, et. al 2007 pg 1794-1795)