Ketamine is all the rage these days (in the ED, I mean, not just with teens). Its use is expanding from the traditional indication as a procedural sedation medication and occasional RSI agent. Now it is being used for analgesia in the complex trauma patient, for managing complex regional pain syndrome, and for refractory status epilepticus.
It can also help children relax during noninvasive positive-pressure ventilation. We recently saved a 5-year-old in severe respiratory distress from going into cardiac arrest because it bought us time for preoxygenation before intubating. It also works for patient takedown in agitated delirium; I am a huge fan.
Head trauma was removed as a relative contraindication to ketamine in ACEP's Clinical Practice Guidelines 2011 Update. Despite this, controversy often arises with ketamine and the concern of increasing ICP in the head-injured patient. Ketamine will often facilitate the CT scan and expedite care in a young child with a potential intracranial injury. This article evaluates the literature behind the medical myth that ketamine cannot be used in the head-injured patient.
The Effect of Ketamine on Intracranial and Cerebral Perfusion Pressure and Health Outcomes: A Systematic Review
Cohen L, Athaide V, Wickham ME, et al.
Ann Emerg Med
2014 July 16 (Epub ahead of print)
The available evidence is synthesized on the effect of ketamine on intracranial and cerebral perfusion pressures, neurologic outcomes, ICU length of stay, and mortality. This article is a systematic review of 10 trials that included 953 adults. The studies were randomized and nonrandomized prospective studies that compared the effect of ketamine with another intravenous sedative in intubated patients and reported at least one outcome of interest. A big limitation of the data collected was that the studies were heterogeneous in design, patient population, reported outcome, and follow-up period. Their primary objective was to measure the effect of ketamine on intracranial pressure and cerebral perfusion pressure. The secondary objective was to evaluate the effect of ketamine on neurological outcome, ICU length of stay, and mortality.
The studies found mixed effect on intracranial pressure (all changes mild) and no adverse effect on cerebral perfusion pressure or neurologic outcomes. The authors concluded that the use of ketamine in critically ill patients does not appear to affect patient outcomes adversely.
The data suggesting ketamine causes a clinically significant increase in intracranial pressure is remarkably weaker than the evidence showing that it does not.
Ketamine is simply a great drug. It is a rapidly acting dissociative agent that provides analgesia, sedation, and amnesia with stable hemodynamic properties and limited suppression of ventilatory drive. The uses are multiple in the ED and its indications are expanding. Initial reports suggesting that ketamine increases ICP were from observations of patients with pre-existing intracranial pathology (intracranial lesions and obstructive hydrocephalus) that were published more than 40 years ago.
These reports were extrapolated to ketamine in the acute head-injured patient because of fear of increasing ICP, worsening the intracranial injury, or even causing patient demise. Unfortunately, this has resulted in physicians avoiding ketamine and using inferior medications that likely are far more hazardous to critical and hemodynamically unstable patients. Surprisingly, as pointed out in ACEP's Clinical Guidelines, no evidence suggests that ketamine presents a danger to the acutely traumatized brain. There remains, however, caution against using ketamine in patients with structural barriers to normal cerebrospinal fluid flow.
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