Ketamine

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Red flags

• In the catecholamine-depleted heart (severe prolonged shock, chronic severe heart failure, late sepsis) the expected sympathomimetic pressor response fails and ketamine's DIRECT negative inotropic effect is unmasked, producing severe hypotension rather than the expected rise in blood pressure. The profoundly shocked patient still needs concurrent vasopressor support ready and running — ketamine is not a pressor in its own right.
• Ketamine historically carried a relative contraindication in raised intracranial pressure and traumatic brain injury, on the grounds that it increases cerebral blood flow, cerebral metabolic rate and intracranial pressure. The modern reassessment is more nuanced: with controlled normocapnic ventilation and a suppressed cough, ketamine does not adversely raise ICP and may preserve cerebral perfusion pressure through its sympathomimetic effect, and it is increasingly accepted for neurotrauma RSI.
• Ketamine increases the intraocular pressure and the extraocular muscle tone — caution in the open-eye or globe injury, where a sudden rise in intraocular pressure can extrude intraocular contents.
• Emergence phenomena — vivid hallucinations, nightmares and delirium on emergence — are common after a large bolus, especially in adults. Reduce them with benzodiazepine pretreatment or by using a low-dose infusion rather than a bolus; avoid ketamine where postoperative delirium is particularly undesirable.
• Hypersalivation is prominent, especially in children, and combined with preserved airway reflexes can precipitate laryngospasm — give an antisialagogue (glycopyrrolate or atropine).
• Ketamine preserves airway reflexes and the respiratory drive better than other induction agents BUT a large or rapid bolus still causes transient apnoea and airway loss — equipment for airway control and ventilation must always be immediately available; it is not a licence for unmonitored sedation.
• Ketamine is a drug of misuse and potential dependence. Repeated or prolonged administration in the chronic-pain and palliative populations can produce tolerance, dependence, and the hepatobiliary and lower-urinary-tract toxicity (ulcerative cystitis) of chronic use. Prescribing must follow institutional and regulatory controls.