Barbiturate-Induced Coma: Indications, Risks, and Modern Context

Barbiturates (e.g., pentobarbital, thiopental, phenobarbital) are potent GABA_A agonists that depress cerebral metabolism and reduce intracranial pressure (ICP). A barbiturate coma is a controlled, reversible state of profound CNS suppression used as a last-resort therapy for:

• Refractory intracranial hypertension (TBI, stroke, encephalitis) unresponsive to sedation, osmotherapy, hypothermia, hyperventilation.
• Refractory status epilepticus (RSE) failing first/second-line agents.

Protocol & Monitoring

• EEG-guided titration to burst-suppression pattern (typically 6–12 bursts/min).
• Continuous EEG, ICP monitor, hemodynamic support (vasopressors common), infection surveillance, nutritional support.
• Typical duration: 3–14 days; wean slowly guided by EEG and ICP.

Risks

• Hypotension (myocardial depression, vasodilation) → reduced CPP.
• Immune suppression → pneumonia, sepsis.
• Ileus, pancreatitis, skin breakdown.
• Prolonged recovery, cognitive sequelae.

Current Status

Use has declined with multimodal ICP management and newer antiseizure drugs. Guidelines (BTF, Neurocritical Care Society) reserve it for salvage therapy with clear goals and time limits. Propofol is preferred for RSE due to faster offset.

Barbiturate coma is a high-risk, resource-intensive intervention requiring neuro-ICU expertise and family goals-of-care alignment.