Much attention was drawn to the randomized trials conducted by Bernard and colleagues and by the Hypothermia After Cardiac Arrest Study Group, of mild hypothermia applied to unconscious patients immediately after cardiac arrest. They reduced the core temperature to 33çC (91çF) within 2 h of the arrest and sustained this level for 12 h in the first trial, and between 32çC and 34çC for 24 h in the second study. Both trials demonstrated improved survival and better cognitive outcome in survivors, compared to leaving the patient in a normothermic state; this led to the development of guidelines and a change in clinical practice in the United States and elsewhere after 2002. The outcomes were evaluated by coarse measures of neurologic function. Implementing and sustaining hypothermia is done either by external cooling, infusion of cooled normal saline, or intravenous cooling devices, and the iatrogenic problems of hypotension, bleeding, ventricular ectopy and infection have sometimes arisen, although this mild degree of temperature reduction is usually well tolerated. A third larger trial conducted by Nielsen and colleagues compared temperature maintenance after cardiac arrest at 33çC to maintenance of 36çC and found no difference in the rate of death or in neurological outcome. Whether these results should be interpreted as demonstrating that hypothermic treatment is ineffective or if, more likely, it is the avoidance of hyperthermia that creates an advantage is still under discussion.
A meta-analysis of trial data and observational studies by Schenone and colleagues concluded that therapeutic hypothermia after cardiac arrest was associated with benefit for survival and neurologic outcome (return to work or moderate disability), even when patients are included with asystole or pulseless electrical activity (PEA), prolonged duration of arrest, and those with persistent shock. Another systematic review by Arrich and colleagues also found that induced mild hypothermia improved neurological outcome after cardiac arrest, but found insufficient evidence to support therapeutic hypothermia in participants with in-hospital cardiac arrest, asystole, or noncardiac causes of arrest. It is difficult to gauge how many individuals were changed from the category of dying to one of vegetative or severely disabled state. Given a lack of other proven neuroprotective interventions, we generally favor initiation of induced hypothermia after cardiac arrest unless there are strong clinical contraindications.
Vasodilator drugs, glutamate blockers, opiate antagonists, and calcium channel blockers have been of no proven benefit despite their theoretical appeal and some experimental successes. Corticosteroids ostensibly help to allay brain (possibly cellular) swelling, but, again, their therapeutic benefit has not been evident in clinical trials.
Seizures should be controlled by the methods indicated in Chap. 15. If convulsions are severe, continuous, and unresponsive to the usual medications, infusion of a drug such as midazolam or propofol, and eventually the suppression of convulsions with neuromuscular blocking agents may be required. Often the seizures cease after a few hours and are replaced by polymyoclonus. For the latter, clonazepam, 8 to 12 mg daily in divided doses may be useful but the commonly used antiepileptic drugs have little effect. A state of spontaneous and stimulus-sensitive myoclonus as well as persistent limb posturing usually presages a poor outcome. The striking disorder of delayed movement-induced myoclonus and ataxic tremor that appear after the patient awakens from an anoxic episode (Lance-Adams myoclonus) is a special issue, which is discussed in Chap. 4. Its treatment usually requires the use of multiple medications. Fever is treated with antipyretics or a cooling blanket combined with neuromuscular paralyzing agents.