Multiple organ dysfunction syndrome

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: Multiorgan failure; multiorgan system failure; multisystem failure; MODS; multiple organ failure; MOF; systemic inflammatory response syndrome; SIRS

Overview[edit | edit source]

Multiple organ dysfunction syndrome is defined as altered organ function in an acutely ill patient requiring medical intervention to perform homeostasis. The use of "multiple organ failure" should be avoided since that term was based upon physiologic parameters to determine whether or not a particular organ was failing.^[1] Multiple organ dysfunction syndrome is the presence of altered organ function in acutely ill patients such that homeostasis cannot be maintained without intervention. It usually involves two or more organ systems.^[1]

Historical Perspective[edit | edit source]

Originally patients were classified as having sepsis or the sepsis syndrome. This resulted in two concepts: the systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS).^[1]

Pathophysiology[edit | edit source]

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 after the original insult. Following this one might see hepatic failure (5-7 days), gastrointestinal bleeding (10-15 days), and renal failure (11-17 days)^[1]

Gut hypothesis[edit | edit source]

The most popular theory to explain MODS 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. Hepatic dysfunction leads to toxins escaping into the systemic circulation and activating an immune response. This results in tissue injury and organ dysfunction.^[1]

Endotoxin macrophage theory[edit | edit source]

Gram-negative infections in MODS 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.^[1]

Tissue hypoxia-microvascular hypothesis[edit | edit source]

As a result of macro- and microvascular changes insufficient supply of oxygen occurs. Hypoxemia causes organ dysfuntion and cell death.^[1]

Integrated hypothesis[edit | edit source]

Since in most cases no primary cause is found, the condition could be part of a compromised homeostasis involving the previous mechanisms.^[1]

Causes[edit | edit source]

The primary cause triggers an uncontrolled inflammatory response. In the absence of infection a sepsis-like disorder is termed systemic inflammatory response syndrome (SIRS). Both SIRS and sepsis could ultimately progress to multiple organ dysfunction syndrome. However, in one-third of the patients no primary focus can be found.^[1] Underlying causes or triggers include:

• Hypermetabolism
• Hypoperfusion
• Sepsis, septic shock or infection
• Trauma (accident, surgery)

Natural History, Complications, Prognosis[edit | edit source]

Mortality varies from 30% to 100% where the chance of survival is diminished as the number of organs involved increases. Since the 1980s the mortality rate has not changed.

Diagnosis[edit | edit source]

The European Society of Intensive Care organized a consensus meeting in 1994 to create the "Sepsis-Related Organ Failure Assessment (SOFA)" score to describe and quantitate the degree of organ dysfunction in six organ systems. Using similar physiologic variables the Multiple Organ Dysfunction Score was developed.^[1]

Four clinical phases have been suggested:

• Stage 1 the patient has increased volume requirements and mild respiratory alkalosis which is accompanied by oliguria, hyperglycemia and increased insulin requirements.
• Stage 2 the patient is tachypneic, hypocapnic and hypoxemic. Moderate liver dysfunction and possible hematologic abnormalities.
• Stage 3 the patient develops shock with azotemia and acid-base disturbances. Significant coagulation abnormalities.
• Stage 4 the patient is vasopressor dependent and oliguric or anuric. Ischemic colitis and lactic acidosis follow.

Treatment[edit | edit source]

At present there is no agent that can reverse the established organ failure. Therapy therefore is limited to supportive care, i.e. safeguarding hemodynamics, and respiration. Maintaining adequate tissue oxygenation is a principal target. Starting enteral nutrition within 36 hours of admission to an Intensive care unit has reduced infectious complications. ^[1]

See also[edit | edit source]

• Acute renal failure
• Acute respiratory distress syndrome
• Heart failure
• Intensive care
• Liver failure
• Respiratory insufficiency
• Shock
• systemic inflammatory response syndrome

References[edit | edit source]

de:Multiorganversagen

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