Felis ISSN 2398-2950

Multiple organ dysfunction syndrome (MODS)

Synonym(s): MODS, Multiple organ failure, Multiorgan failure, Multiorgan dysfunction

Contributor(s): Graham Bilbrough, Elisa Mazzaferro

Introduction

Pathogenesis

Etiology

  • A variety of inciting causes, including viral, fungal, and bacterial infections, envenomation, and inflammatory conditions can all lead to activation of the immune system and the release of proinflammatory cytokines and oxygen-derived free radical species.
  • This can be a protective mechanism by which the body overcomes and treats the inciting cause, or the result can be overwhelming inflammation and activation of the coagulation cascade to such an extent that Disseminated Intravascular Coagulation (DIC) Disseminated intravascular coagulation, Acute Respiratory Distress Syndrome (ARDS) Acute Respiratory Distress Syndrome (ARDS), and end-organ damage occurs to the neurologic, hepatic, coagulation, cardiopulmonary, gastrointestinal, and vascular endothelial systems.

Predisposing factors

General

Pathophysiology

  • MODS is the end result of systemic inflammation, caused by a variety of conditions.
  • Any predisposing factor that can cause systemic inflammation, disseminated intravascular coagulation can ultimately lead to MODS.
  • Bacterial endotoxin, severe trauma or tissue injury, and any condition that causes hypotension can cause activation of neutrophils, macrophages and complement.
  • The recruitment and activation of neutrophils and macrophages results in the production of pro- and anti-inflammatory cytokines, including interleukin-10 (IL-10), IL-1, Tumor necrosis factor (TNF-a), IL-6, Interferons, Prostaglandins, Leukotrienes, and Platelet activating factor (PAF). The proinflammatory cytokines can perpetuate the inflammatory cascade, and also target end organs including the vascular endothelium, pulmonary vasculature and myocardium, leading to vascular injury, vascular leakiness, and myocardial depression. Additionally, upregulation of inducible nitric oxide synthetase (iNOS), can lead to the production of nitric oxide, a potent vasodilator agent, leading to areas of vasodilation, while other vascular areas become inappropriately vasoconstricted. Activation of neutrophils and complement also can trigger the production of oxygen-derived free radical species that damage the vascular endothelium. Activation of the coagulation cascade, either by tissue factor or complement activation leads to the consumption of platelets and multiple microthrombi forming globally, leading to end-organ thrombosis. The result of hypotension, decreased myocardial contractility, decreased oxygen delivery to tissues, and vascular endothelial damage ultimately leads to tissue hypoxia and end-organ damage that can lead to failure if left untreated.

Timecourse

  • The progression of organ failure in patients with MODS usually occurs as follows:
    • Lungs: 24-72 hours.
    • Liver and gastrointestinal tract: 48-72 hours.
    • Acute renal failure:  48-72 hours.
    • Cardiac and brain dysfunction usually >72 hours.

Diagnosis

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Treatment

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Prevention

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Outcomes

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Bellhorn T & Macintire D K (2004) Bacterial Translocation. Compend Contin Educ Pract Vet 26 (3), 229-236 VetMedResource.
  • Brady C A & Otto C M (2001) Systemic inflammatory response syndrome, sepsis, and multiple organ dysfunction. Vet Clin North Am Small Anim Pract 31 (6), 1147-1162 PubMed.
  • Deitch E A (1992) Multiple organ failure. Pathophysiology and potential future therapy. Ann Surg 216 (2), 117-134 PubMed.


ADDED