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Nutrition Support Blog: Nutrition and the Extended ICU Admission

Posted by SF8N at Dec 19, 2011 03:55 PM |
December 19, 2011
Nutrition Support Blog: Nutrition and the Extended ICU Admission

by Joe Krenitsky, MS, RD

It is a difficult experience to see an ICU patient who survives the initial insult that brought them into the hospital, and then “fail to launch” and end up with an extended admission.  Patients may have an unexpected and unavoidable event(s) such as a code, nosocomial infection, drug reaction or it may be that the ravages of time or multiple medical conditions have resulted in several organs or organ systems that were marginally compensated before the illness, and now the limitations of cardiac, respiratory, renal and/or hepatic function are fully realized. 

We know that malnutrition never helps these patients, but sometimes it seems a cruel trick of fate that these very same patients that end up with a complicated or extended admission end up being the very same that have too many interruptions in their nutrition provision.  Interruptions in nutrition from clogged or “displaced” enteral access, multiple essential procedures, and even the dread “feeding intolerance,” as well as a myriad of other factors can lead to an accrued nutrition deficit exacerbating the loss of lean muscle mass, and ultimately, can prevent the body from rebounding from the insults.  The loss of lean muscle mass and accelerated skin breakdown that patients experience is compounded by immobility and the lack of exercise, or even normal activity to stimulate muscle protein synthesis.  Add in episodes of hyperglycemia, catabolic medications such as corticosteroids and protein breakdown that occurs during repeated infectious insults and you have a picture of a deep metabolic hole that is difficult for many patients to climb out of.

Older patients are at a particular disadvantage because they are “anabolically challenged” due to increased insulin resistance, decreased growth hormone, IGF-1, testosterone as well as other hormone levels.  Furthermore, they have a decreased responsiveness to the protein synthesis stimulating effects of dietary protein itself. 

It would seem obvious that agents that increase protein synthesis or decrease catabolism would be beneficial for patients with extended hospitalizations, prolonged rehabilitation, wounds or skin breakdown.  However, the attempts to reverse catabolism associated with critical illness such as intensive insulin, anticytokines, or β-blockade have largely been a dismal failure.  The studies of the most potent agents to stimulate protein synthesis such as human growth hormone or anabolic steroids have actually demonstrated net harmful effects.1,2 

Nutritional approaches that optimize protein synthetic capacity or decrease catabolism would be extremely desirable.  Arginine, branched-chain amino acids (or leucine alone), HMB (β –hydroxy methylbutyrate), glutamine or combinations of these nutrients have all been proposed to be potential aids to prevent muscle loss or enhance rehab and healing.  The animal studies and small trials of surrogate markers in humans such as nitrogen balance or collagen deposition are promising.  Unfortunately, to date there is insufficient human research that looks at outcomes that matter such as survival, time in the hospital, frequency or rate of wound healing, to justify routine supplementation in our patients with these nutrients.  We simply have no way to know if supplementation of our patients with these nutrients would result in positive, negative or neutral overall effects.  Certainly the results of research with arginine in sepsis, vitamin E in heart disease, β-carotene in cancer, vitamin A and long bone fracture, calcium supplements in cardiovascular disease, zinc and increased UTI’s, etc. has taught us that it is simply not acceptable to treat nutritional supplements as “might help, won’t hurt” type of interventions based on early data.  Interestingly, some experts have theorized that over suppression of catabolism in critically ill patients can have negative effects as well by impairing removal of damaged proteins and mitochondria, which in theory could impair recovery from organ failure.  What is clear is that the topic of anabolism and catabolism in critical care and recovery is complicated and we have a lot to learn about the most effective ways to help our patients recover.

In the meantime, we do know that our patients frequently accrue large nutritional deficits during their hospitalization, and attention from nutrition support experts can help reduce this deficit.  Additionally, one of the most effective ways to stimulate protein synthesis – mobilization/exercise, is often not implemented as aggressively as it could be in our ICUs (or anywhere else in the hospital for that matter).  It seems to me that we still have a lot of mileage to be gained from attention to the most basic aspects of care while the experts study what other interventions might be useful.


1.    Bulger EM, et a.l  Oxandrolone does not improve outcome of ventilator dependent surgical patients.  Ann Surg. 2004 Sep;240(3):472-478.

2.    Takala J, et al.  Increased mortality associated with growth hormone treatment in critically ill adults.  N Engl J Med. 1999 Sep 9;341(11):785-792.


“Research at its best is elegant, clean, provocative, and enlightening, but for the most part, it is messy, chaotic, and contradictory. The truth may be out there, but it is rarely easy to find. We engage in research because we question the status quo, knowing that tomorrow must be better than the present.”

          - Alan Fein, MD , MPH

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