Critical illness can be viewed as consisting of 4 distinct stages: (1) acute critical illness (ACI), (2) prolonged acute critical illness, (3) chronic critical illness, and (4) recovery. ACI represents the evolutionarily programmed response to a stressor. In ACI, substrate is shunted away from anabolism and toward vital organ support and inflammatory proteins. Nutrition support in this stage is unproven and may ultimately prove detrimental. As critical illness progresses, there is no evolutionary precedent, and man owes his life to modern critical care medicine. It is at this point that nutrition and metabolic support become integral to the care of the patient. This paper (1) delineates and develops the 4 stages of critical illness using current evidence, clinical experience, and new hypotheses; (2) defines the chronic critical illness syndrome (CCIS); and (3) details an approach to the metabolic and nutrition support of the chronically critically ill patient using the metabolic model of critical illness as a guide. It is our hope that this clinical model can generate testable hypotheses that can improve the outcome of this unique population of patients.

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Metabolic bone disease in the ICU is potentially a devastating consequence of critical illness. Screening with biochemical markers of bone turnover may allow identification of those most likely to have fracture after ICU discharge. Intravenous bisphosphonates are safe and very effective at preventing osteoporotic fracture in other populations. There is likely a subset of individuals who remain critically ill for a prolonged period of time that may benefit from an intravenous infusion of a potent aminobisphosphonate.

A single dose of intravenous ibandronate causes a significant but transient reduction in osteoclast activity in patients with CCI, which persists over a 6-day period.

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