Therapeutic Hypothermia
Also known as: Hypothermia after cardiac arrest, hypothermia after hypoxic-ischemic brain injury
Related conditions: Hypothermia for traumatic brain injury, intracranial pressure management, acute ischemic stroke
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1. Description of the problem
Therapeutic hypothermia is used as a neuroprotective measure following cardiac arrest. High-level evidence exists for this indication, and it is the standard of care at most tertiary medical centers worldwide. Its use is experimental/unproven in the management of traumatic brain injury, spinal cord injury, refractory status epilepticus, and ischemic stroke.
Therapeutic hypothermia is also a treatment option for refractory intracranial hypertension with good evidence for efficacy but few outcome data to support overall benefit vs. harm. Finally, it is used for neonatal hypoxic-ischemic brain injury, an indication beyond the current scope of discussion.
Patients who have suffered hypoxic-ischemic brain injury and remain comatose should be considered eligible recipients for therapeutic hypothermia. Comatose is generally defined as not able to be aroused to the point of following commands.
Hypothermia should be initiated immediately in patients with return of spontaneous circulation after cardiac arrest who have not awakened.
2. Emergency Management
Post-cardiac arrest with suspected hypoxic-ischemic brain injury:
Management points not to be missed
Successful cardiac resuscitation with return of spontaneous circulation (pressor support is OK)
Patient does NOT arouse; that is, CANNOT follow commands (Glasgow Coma Scale score ≤ 9)
Residual sedative/anesthetic effects, if any, considered unlikely by the treating physician
Hypoglycemia ruled out as a cause of coma
Emergently induce hypothermia with cold intravenous fluids (target temp 32-34° C)
Sedation and neuromuscular blockade (with endotracheal intubation)
Maintain hypothermia with surface cooling pads, cooling blankets, or endovascular device
Alpha-stat vs. pH-stat ABG management (no evidence to suggest one over the other)
Control hyperglycemia with insulin infusion
MAP > 80 to maintain cerebral perfusion
Maintain hypothermia for 24 hrs
Watch for hyperkalemia on rewarming
Low threshold for antibiotic therapy to cover aspiration pneumonia
Rewarm slowly after 24 hrs; usually 0.33-0.5 degrees Celsius per hour over 8-12 hrs
Avoid overshoot hyperthermia
Consider continuous EEG monitoring for subclinical seizures. Routine anti-epileptic drug therapy is not indicated.
3. Diagnosis
Considerations
A patient resuscitated after cardiac arrest, who remains comatose, does not mandate any specific neurologic testing prior to inducing hypothermia. In the real-world setting, patients are often ‘found down’ and a head CT is obtained to rule out intracranial hemorrhage (either as the primary event causing arrest or from cranial trauma due to falling, etc). Cervical spine plain films and/or CT are obtained to look for cervical injury. EKG and cardiac enzymes should be obtained immediately, as in any patient with suspected acute coronary syndrome.
Laboratory and toxicologic evaluation should also proceed as indicated by the clinical situation to evaluate for electrolyte abnormalities, hypoglycemia, and drug or alcohol intoxication. EEG monitoring, if available, can be used to monitor for seizures during the cooling phase of the hypothermia protocol and during rewarming. There is currently no indication for acute EEG monitoring in the initial phase of treatment (ambulance or emergency room).
Patients may still receive acute coronary interventions (angioplasty, stenting, thrombolysis, anticoagulants) while being treated with therapeutic hypothermia.
Prognostication hinges on neurologic examination after rewarming and in the days to follow. This should be guided by a neurologist. EEG monitoring is emerging as a useful prognostic tool. However, somatosensory evoked potentials are currently the only test with adequate predictive value to be relied upon in the clinical setting.
Special considerations for nursing and allied health professionals.
Hypothermia should be induced immediately in comatose survivors of cardiac arrest; all care providers should realize the urgency of delivering neuroprotective therapy as soon as possible. Positioning injuries and decubitus ulcers may be more likely in the hypothermic patient who is peripherally vasoconstricted. Frost-bite injuries can occur from surface cooling devices or ice packs. Finally, respiratory therapists should ask the physician whether to temperature-correct the arterial blood gas samples or not (i.e. pH-stat vs. alpha-stat management), since this will affect ventilatory management.
What's the evidence?
Bernard, SA. “Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia”. N Engl J Med. vol. 346. 2002. pp. 557-63.
“Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest”. N Engl J Med. vol. 346. 2002. pp. 549-56.
Peberdy, MA. “Part 9: post-cardiac arrest care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care”. Circulation. vol. 122. 2010. pp. S768-86.
Clifton, GL. “Very early hypothermia induction in patients with severe brain injury (the National Acute Brain Injury Study: Hypothermia II): a randomised trial”. Lancet Neurol. vol. 10. 2011. pp. 131-9.
Kwon, BK. “Emerging repair, regeneration, and translational research advances for spinal cord injury”. Spine. vol. 35. 2010. pp. S263-70.
Corry, JJ. “Hypothermia for refractory status epilepticus”. Neurocrit Care. vol. 9. 2008. pp. 189-97.
Hemmen, TM. “”. Stroke. vol. 41. 2010. pp. 2265-70.
Polderman, KH. “Induced hypothermia and fever control for prevention and treatment of neurological injuries”. Lancet. vol. 371. 2008. pp. 1955-1969.
Shankaran, S. “Whole-body hypothermia for neonates with hypoxic-ischemic encephalopathy”. N Engl J Med. vol. 353. 2005. pp. 1574-84.
Wijdicks, EF. “Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology”. Neurology. vol. 67. 2006. pp. 203-10.
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