What is MODS?

“Multi-Organ Dysfunction Syndrome” is the internationally recognized term to describe loss of physiologic reserve and progressive organ injury through failure associated with critical illness.

A colleague of mine, in the early 1990s, once commented to me: “the difference between intensive care now and ten years ago, is that we can keep seriously ill patients alive for longer, but they still die”. He was, of course referring to the condition to which I have alluded in the preceding discussion – Multi-Organ Dysfunction Syndrome. Many patients now survive the initial injury for which they were admitted to the ICU, only to succumb to progressive organ damage, apparently caused by “malignant” inflammation, or “autodestruction”. 

Before there was intensive care, MODS did not exist: critically ill patients died. We know that certain patients are “primed” towards MODS – the elderly, patients with chronic disease, alcoholism and malnutrition (depleted physiologic reserve). The picture of disease is remarkably constant – the patient has an initial injury, this either causes a direct cascade of sequential injuries or causes massive release of inflammatory cytokines, which causes collateral damage. The result is widespread microvascular injury, organ dysfunction and failure. The prototype cause is systemic sepsis, with corresponding loss of capillary endothelial integrity, vasodilatory shock and activation of coagulation cascades. The propensity to develop this type of malignant inflammation appears to be genetically programmed (36).

Several systems have been directly implicated in the amplification of the systemic inflammatory response: e.g. 1) the lungs – ventilator induced lung injury contributes to mortality, probably due to cytokine release from injured tissue, 2) the gut – loss of gut mucosal integrity may lead to bacterial or toxin translocation into the portal system and into the liver (the gut origin theory). Moreover, inadequate control allows the source of sepsis (undrained abscess, infected intravenous catheter) to act like a cytokine factory, with consequent injury at distant organs.

Organ dysfunction occurs when the organs reserve runs out: the organ malfunctions but dose not necessarily fail. Individual organ dysfunction, such as acute renal failure following an aortic cross clamp, is usually associated with a good prognosis. When several organs begin to misbehave simultaneously, the likelihood of survival diminishes geometrically. Therefore, the objective of critical care is to prevent MODS, not to treat it.

High quality critical care can influence outcomes, by vigilant screening for iatrogenic injuries, rapid source control and protocol driven strategies for finding and treating nosocomial infections, ventilator and feeding strategies. Inflammation modulating therapies are beginning to emerge, with Activated Protein C a harbinger. A new model of intensive care is emerging, with less aggressive interventions, less number counting and correcting. “Physiologic replacement” has become a cat call – note the emergence of vasopressin as a physiologic vasoconstrictor (19). Conservative management strategies are beginning to dominate: abscesses are more likely to be drained by interventional radiology than laparotomy, pulmonary artery catheterization is gradually falling from favor, parenteral nutrition is preserved for patients with non functioning bowels. We have learned that many of the interventions which were considered dogma when I was a medical student – hyperventilating head injuries, avoiding oxygen in COPD, renal dose dopamine to save the kidneys, large tidal volume ventilation – either don’t work or harm the patient. Evidence based medicine is becoming pre-eminent.

Pre-emptive strategies may influence outcome in certain patient populations. For example, there is now compelling evidence that peri-operative beta blockade lowers mortality in patients undergoing major vascular surgery (24;28) .

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