What is included in supportive therapy during targeted temperature management (TTM)?

Answer

Note the following:

A mean arterial pressure (MAP) goal of more than 80 mm Hg is preferred from a cerebral perfusion standpoint. Hypertension is potentially additive to the neuroprotection of hypothermia. Norepinephrine can be used, beginning at 0.01 mcg/kg/min and titrated to a MAP greater than 80 mm Hg. The treating team should determine the MAP goal, balancing the cardiac safety with the theoretical advantage of higher cerebral perfusion pressures. Often, blood pressure remains elevated during hypothermia as a result of peripheral vasoconstriction. Hypotension is a concern during the warming phase.
Practice standard neuroprotective strategies such as placing the head of the bed at 30º.^[5]
Monitor the patient for dysrhythmia (most commonly bradycardia) associated with hypothermia. If life-threatening dysrhythmia arises and persists, or hemodynamic instability or bleeding develops, then active cooling should be discontinued and the patient rewarmed. An electrographic (ECG) Osbourne or camel wave may be present when cooling. Heart rate less than 40 bpm is frequent and is not a cause for concern in the absence of other evidence of hemodynamic instability.
Hematologic testing recommendations include a complete blood cell (CBC) count, chemistry panel, troponin level, arterial blood gas (ABG) level, and partial thromboplastin time (PTT) at 0 hours. Hypothermia commonly causes hypokalemia, which may be exacerbated by insulin administration. Conversely, when patients are rewarmed, potassium exits cells, and hyperkalemia may occur. Repeat measurements of glucose, potassium, and ABG are needed every 6 hours. Unexplained increases in serum amylase and lipase levels have been observed during hypothermic therapy and appear to have limited clinical significance.
Potassium values less than 3.5 mEq/L should be treated while the patient is being cooled. Potassium administration should be stopped once rewarming begins.
Elevated serum glucose level is deleterious to the injured brain. Tight glycemic control should be maintained, although a specific range is not recommended by the American Heart Association (AHA).^[2]
Normocarbia is advised, with the partial pressure of carbon dioxide (PaCO₂) and end-tidal carbon dioxide (CO₂) in the reference range (35-45 mm Hg for PaCO₂; 30-40 mm Hg for end tidal CO₂).
Avoid fever following targeted temperature management (TTM), as any elevated temperature is associated with worse neurologic outcome.
Avoid hypoxia, with administration of oxygen saturation above 94%. However, hyperoxia is also harmful.
Skin care should be checked every 2-6 hours for thermal injury caused by cold blankets.
Regularly check the patient’s temperature with a secondary temperature monitoring device when cooling.
Do not provide nutrition to the patient during the initiation, maintenance, or rewarming phases of the therapy.

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Media Gallery

Targeted temperature management (therapeutic hypothermia). This is the Alsius CoolGard 3000. It is used in conjunction with the endovascular cooling catheter shown in the next image.
Targeted temperature management (therapeutic hypothermia). This is the Alsius Fortius 9.3 Fr endovascular cooling catheter.
Targeted temperature management (therapeutic hypothermia). This is the Arctic Sun heat-exchange device. It is used with the cooling pads as depicted in the next image.
Targeted temperature management (therapeutic hypothermia). Cooling pads.
Targeted temperature management (therapeutic hypothermia). Overview of neuronal apoptosis and approaches to inhibit this cell death cascade. Caspases play an important role as signal transducers (caspases 8, 9, 10) and as terminal executioners (caspases 3, 6, 7) in apoptosis. More recent neuroprotective therapeutic strategies involve enhanced activation of survival receptors (eg, via erythropoietin [EPO]). P = phosphate group, ROS = reactive oxygen species. Image and caption courtesy of Dr. Bernd Böttiger, Professor and Chairman of the Department of Anaesthesiology and Postoperative Intensive Care Medicine, University of Cologne.

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Author

Alex Koyfman, MD Assistant Professor, Department of Emergency Medicine, University of Texas Southwestern Medical Center, Parkland Memorial Hospital

Alex Koyfman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Brit J Long, MD Assistant Professor, Department of Military and Emergency Medicine, Uniformed Services University of the Health Sciences; Staff Physician, Department of Emergency Medicine, Associate Program Director - Research, San Antonio Uniformed Services Health Education Consortium

Brit J Long, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Department of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, National Association of EMS Physicians

Disclosure: Medical Director for: SironaHealth.

Chief Editor

Karlheinz Peter, MD, PhD Professor of Medicine, Monash University; Head of Centre of Thrombosis and Myocardial Infarction, Head of Division of Atherothrombosis and Vascular Biology, Associate Director, Baker Heart Research Institute; Interventional Cardiologist, The Alfred Hospital, Australia

Karlheinz Peter, MD, PhD is a member of the following medical societies: American Heart Association, German Cardiac Society, Cardiac Society of Australia and New Zealand

Disclosure: Nothing to disclose.

Additional Contributors

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Jonathan Adler, MD, MS Instructor, Department of Emergency Medicine, Harvard Medical School, Massachusetts General Hospital

Jonathan Adler, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Acknowledgements

The author would like to acknowledge the contributions of Dr. Imre Rainey, Mount Auburn Hospital Cambridge, Massachusetts, and Harvard Medical School, in the review and editing of this manuscript.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Mark E Brauner, DO, and Michael R Sayre, MD, to the development and writing of this article.

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