Effect of Hypothermia on Serum Electrolyte, Inflammation, Coagulation, and Nutritional Parameters in Patients With Severe Traumatic Brain Injury

Tokutomi, Takashi; Miyagi, Tomoya; Morimoto, Kazushige; Karukaya, Takashi; Shigemori, Minoru

doi:10.1385/ncc:1:2:171

Cited by 37 publications

(39 citation statements)

References 30 publications

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“…However, there were no significant differences in blood glucose level or insulin requirements in patients subjected to hypothermia (Clark et al, 2009;Tokutomi et al, 2004). Diuresis during hypothermia is due to increased venous return caused by vasoconstriction, leading to atrial natriuretic peptide activation and a decrease in the level of antidiuretic hormone (Giraud et al, 2013).…”

Section: Other Complicationsmentioning

confidence: 92%

“…Given that saline at higher temperatures can cause damage to red blood cells or coagulation factors, the saline-to-blood temperature gradient was significantly lower during rewarming than cooling (13°C vs. 31°C) (Dae et al, 2003). Slow rewarming is also advised because potassium levels decline during cooling, and the reverse can occur if rewarming occurs too rapidly (Tokutomi et al, 2004).…”

Section: Rewarming Speedmentioning

confidence: 99%

“…Electrolyte disorders are common during cooling, especially in the induction phase during which magnesium and potassium levels are reduced (Polderman, 2009;Tokutomi et al, 2004), although no change have been reported for serum sodium concentrations (Yanamoto et al, 1999). Hypokalemia is associated with the development of polymorphic ventricular tachycardia (Mirzoyev et al, 2010), while low magnesium can aggravate brain injury (Polderman, 2009).…”

Section: Other Complicationsmentioning

confidence: 99%

“…Hypokalemia is associated with the development of polymorphic ventricular tachycardia (Mirzoyev et al, 2010), while low magnesium can aggravate brain injury (Polderman, 2009). Myocardial sensitivity to potassium is increased by hypothermia, which can offset the effects of hypokalemia and have an overall protective role (Tokutomi et al, 2004). Although maintaining normal electrolyte levels through supplementation is both safe and effective, caution must be applied since rebound hyperkalemia has been reported in patients who undergo rapid rewarming (Mirzoyev et al, 2010;Tokutomi et al, 2004).…”

Section: Other Complicationsmentioning

confidence: 99%

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Therapeutic hypothermia for stroke: Where to go?

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Section: Other Complicationsmentioning

confidence: 92%

Section: Rewarming Speedmentioning

confidence: 99%

Section: Other Complicationsmentioning

confidence: 99%

Section: Other Complicationsmentioning

confidence: 99%

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“…However, therapeutic hypothermia does not appear to affect serum sodium levels (Tokutomi and Miyagi, 2004).…”

Section: Why Do Electrolytes Shift During the Induction Of Hypothermia?mentioning

confidence: 95%

Clinical Q & A: Translating Therapeutic Temperature Management from Theory to Practice

Bader¹

2012

Therapeutic Hypothermia and Temperature Management

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Edited by Mary Kay Bader, R.N., M.S.N., CCNS We were wondering if anyone has had experience with transcutaneous pacing or transvenously pacing patients who are in their goal of 32-34°C. Do you have any problems with capture and so on?Therapeutic hypothermia (TH), now referred to as targeted temperature management (TTM), is endorsed by the American Heart Association and International Liaison Committee on Resuscitation (ILCOR; Neumar et al., 2010). This is the standard of practice for post resuscitation care of patients whose initial pulseless rhythm is identified as ventricular fibrillation (VF) or ventricular tachycardia (VT). As with many medical therapies, risks as well as therapeutic benefit are associated with TTM (Polderman, 2009).Cardiac arrhythmias and ECG changes are common in TH, with the incidence increasing as core body temperature decreases. One potential side effect of TH in post cardiac arrest patients is bradycardia. A thorough review of the TTM literature reveals minimal publications documenting the need for temporary cardiac pacing. In 2006, the University of Minnesota published a case report of two patients requiring temporary cardiac pacing (in the form of transcutaneous pacing) for hemodynamic stability (Ho et al., 2007). Ho and others did not report any difficulties with the ability to acquire capture and maintain adequate transcutaneous pacing. Several animal studies have demonstrated improved cardiac function and hemodynamic stability post rewarming after undergoing severe hypothermia (24°C) and being treated with temporary pacing. The main outcome of these studies was to show a more rapid rate of rewarming when temporary pacing was utilized. (Dixon et al., 1997). Neither human retrospective studies nor prospective randomized controlled trials have been published demonstrating the benefit of temporary cardiac pacing in patients undergoing mild or moderate therapeutic hypothermia.Our experience at Harborview Medical Center in Seattle, Washington, is that temporary cardiac pacing is not typically warranted for patients experiencing mild ( > 34°C) or moderate (30-34°C) hypothermia. In 2009, we published one of the largest single center retrospective studies, n = 204 (Don et al., 2009). No clinical conditions warranted temporary cardiac pacing in any of the 132 out of 204 patients who achieved the goal temperature of 33°C. No evidence exists to suggest that temporary cardiac pacing (transcutaneous or transvenous) is not safe or reliable in the hypothermic patient. In the setting of hypothermia and hemodynamic instability, if temporary cardiac pacing is indicated, then it should be cautiously considered along with other chronotropic and inotropic medications to improve cerebral blood flow, restore end-organ perfusion, and prevent further cardiovascular collapse. The mode of temporary pacing (transcutaneous vs. transvenous) should also be carefully evaluated prior to use. ReferencesDixon RG, Dougherty JM, White LJ, et al. Transcutaneous pacing in a hypothermic dog model. Ann Emerg Med 1997;32:602...

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Hypothermie nach Herz-Kreislaufstillstand

Heer

2007

Intensivmed

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Effect of Hypothermia on Serum Electrolyte, Inflammation, Coagulation, and Nutritional Parameters in Patients With Severe Traumatic Brain Injury

Abstract: Hypothermia of 33 degrees for 48-72 hours does not appear to increase the risk for coagulopathy and infections, although hypothermic patients exhibited significant increments in inflammatory markers such as C-reactive protein and white blood counts after rewarming.

Cited by 37 publications

References 30 publications

Therapeutic hypothermia for stroke: Where to go?

Therapeutic hypothermia for stroke: Where to go?

Clinical Q & A: Translating Therapeutic Temperature Management from Theory to Practice

Hypothermie nach Herz-Kreislaufstillstand

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