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Nutrition Support Blog: Therapeutic Hypothermia and Nutrition Support

Posted by SF8N at Feb 13, 2015 09:00 AM |
February 13, 2015
Nutrition Support Blog: Therapeutic Hypothermia and Nutrition Support

by Joe Krenitsky, MS, RDN

Therapeutic hypothermia (TH), also called targeted temperature management, is a medical intervention to cool the body to 33-34°C (91.4 – 93.2°F) to provide neuroprotection after cardiac arrest or hypoxic/ischemic insult (other temperature goals continue to be investigated).1  Cold intravenous fluids, ice packs/bags, cooling blankets or garments, and in some cases peritoneal lavage, endovascular or intranasal cooling devices are used to reach and maintain target temperature for 24 hours, then slow rewarming is initiated.

In the past, considering the limited research, we did not initiate enteral nutrition (EN) during TH because hypothermia was utilized for a short duration, hemodynamic stability was still a “work in progress” and metabolic demands were decreased during the cooling process.  However, recently we have received requests to begin EN during the temperature management process.  On one hand there is a real celebration for physicians who are in favor of nutrition, but on the other, we realize that there is a dearth of controlled studies, with some conceivable negative consequences.

One potential mechanism for the beneficial effects of therapeutic hypothermia is the decreased metabolic rate from cooling allows less oxygen and energy consumption, with a resultant decrease in carbon dioxide production, which may prevent secondary injury when oxygen supply or perfusion is suboptimal.2  Providing nutrition can create diet-induced thermogenesis, increasing oxygen consumption and carbon dioxide production at a time when the goals of TH include reduced metabolic activity.  Enteral nutrition will increase oxygen consumption of enterocytes at a time when hemodynamic stability may be marginal.

Mild hypothermia creates an intracellular shift of electrolytes, with resultant potential for hypokalemia, hypocalcemia, hypomagnesemia, and hypophosphatemia. During rewarming, there is potential for elevated serum levels of these same electrolytes, especially after generous electrolyte replacement during the cooling phase.3,4  Providing nutrition during the TH, especially to those admitted with malnutrition, may add refeeding associated electrolyte shifts to those caused by cooling.

Therapeutic hypothermia also decreases insulin sensitivity, which may require increased insulin doses during the cooling phase.2, 5  Insulin sensitivity is increased during the warming phase which can increase the risk of hypoglycemia and the potential for increased glucose variability.2, 5  One study demonstrated that more than 40% of patients undergoing TH required an insulin infusion to prevent hyperglycemia.5  However, patients who received the insulin infusion during TH also had a significantly increased risk of hypoglycemic events, and mortality. 5 Providing nutrition will increase insulin requirements raising the possibility of hypoglycemic events or glucose variability, especially during the rewarming phase as insulin sensitivity improves.

Obviously, issues related to glucose control and electrolyte management during nutrition support are dealt with on a daily basis in the ICU, and they should not normally be a reason not to feed.  However, given the lack of data during TH – we need to be vigilant in case we need tighter monitoring or alternate protocols during TH and the warming phase.  Two observational studies have documented apparent tolerance to enteral nutrition during TH.6,7 However, considering that there are no randomized studies during TH that have investigated the effects of nutrition on patient outcome, it is clear that we need more data.  Delving into the literature on TH, it is also clear that this is a “big” topic, with a lot of unknowns that are still being actively investigated. Perhaps the most important nutrition questions are: does providing nutrition support diminish the benefits of TH, or compromise outcome in some way that we cannot yet anticipate?

It is possible that providing nutrition during TH may have beneficial effects. In an animal model of TH it was reported that metabolic acidosis induced by rewarming was prevented by administration of the glycolytic intermediate fructose 1,6-biphosphate.8  (My sincere apologies for bringing up glycolysis if you found Nutritional Biochemistry mildly traumatizing).  Fructose 1,6-biphosphate also protected against the oxidative stress induced after rewarming.8  Although it is way premature to assume that carbohydrate provision will have the same effects as fructose 1,6-biphosphate, or that these basic science animal-model results will transfer directly to critically ill humans, it is still possible that nutritional support during TH may have beneficial effects.  As I mentioned, it is clear we need more data.  My conclusions are that:

(1) Anyone suggesting that we know for sure that EN is safe (or dangerous) during TH is expressing more hubris than contemplation.

(2) We have an obligation to remember that until we have evidence of benefit, we have an obligation to first, do no harm.

 

“Ignorance is a steep hill with perilous rocks at the bottom.”

        -The Wind and The Lion, John Milius, Columbia Pictures, 1975

References

1.   Bro-Jeppesen J, Annborn M, Hassager C, et al.  Hemodynamics and Vasopressor Support During Targeted Temperature Management at 33°C Versus 36°C After Out-of-Hospital Cardiac Arrest: A Post Hoc Study of the Target Temperature Management Trial*.  Crit Care Med. 2015 Feb;43(2):318-327

2.   Polderman K.H.: Mechanisms of action, physiological effects, and complications of hypothermia. Crit Care Med 2009; 37:S186-S202.

3.   Nielsen N., Sunde K., Hovdenes J., et al: Adverse events and their relation to mortality in out-of-hospital cardiac arrest patients treated with therapeutic hypothermia. Crit Care Med 2011; 39:57-64.

4.   Polderman KH, Peerdeman SM, Girbes AR: Hypophosphatemia and hypomagnesemia induced by cooling in patients with severe head injury. J Neurosurg 2001, 94:697-705.

5.   Forni AA, Rocchio MA, Szumita PM, et al.  Evaluation of glucose management during therapeutic hypothermia at a Tertiary Academic Medical Center. Resuscitation. 2015 Jan 17;89C:64-69.

6.   Smith C, Nolan J, Williams M.  Enteral feed absorption during therapeutic hypothermia following out-of-hospital cardiac arrest. Crit Care. 2011; 15(Suppl 1):P377.

7.   Williams ML, Nolan JP.  Is enteral feeding tolerated during therapeutic hypothermia? Resuscitation. 2014 Nov;85(11):1469-1472.

8.   Alva N, Carbonell T, Roig T, et al. Fructose 1,6 biphosphate administration to rats prevents metabolic acidosis and oxidative stress induced by deep hypothermia and rewarming.  Eur J Pharmacol 2011 659:259-264.

 

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