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BarbComa AKA Barbiturate Coma - Important Details

Brain damage resulting from head injury is the leading cause of death among individuals younger than 24 years of age. The most hazardous is increased ICP. High-dose barbiturates are used to control intracranial hypertension in selected patients.

Dr. Bill Butcher
Nov 02, 2022212 Shares2830 Views
Brain damage resulting from head injuryis the leading cause of death among individuals younger than 24 years of age. The most hazardous is increased ICP.
High-dose barbiturates are used to control intracranial hypertension in selected patients. ICP is decreased due to a decrease in CBV due to vasoconstriction caused by an increase in cerebrovascular resistance.


  • Potentially survivable head injury.
  • No surgically treatable lesion accounting for intracranial hypertension (except when used for preparation for surgery).
  • Other conventional therapies for controlling ICP have failed (posture, hyperventilation, osmotic and tubular diuretics, corticosteroids).
  • ICP > 20 to 25 mmHg for more than 20 min, or >40 mmHg at any time.
  • Unilateral cerebral hemispheric edema with significant (>.7 mm) shift of midline structures shown on CT.
  • A low Glasgow Coma score.


  • Decrease in cerebral metabolic rate (CMRO2), caused by decrease in synaptic transmission, presumably by affecting GABA transmission.
  • Decrease in cerebral blood volume and ICP, due to increase in cerebrovascular resistance, due vasoconstriction - Both CMRO2 and CBF are decreased in a dose dependent fashion: About 50% decrease at a dose sufficient to produce isoelectric EEG.
  • Promote or induce hypothermia.
  • Increase in IC glucose, glucagon, and phosphocreatine energy store.
  • Decrease in nitrogen excretion following acute head injury.
  • Shunt blood from regions of normal perfusion to those of reduced CBF due to vasoconstriction.
  • Anticonvulsant prophylaxis.
  • Stabilization of lysosomal membranes.
  • Decrease in excitatory neurotransmitters and IC calcium.
  • Free radical scavenging ( thiopental only).


  • Direct myocardial depressant.
  • Increase in venous capacitance, due to central and peripheral sympatholytic action.
  • Impaired gastrointestinal motility Increased hepatic microsomal activity.
  • Direct CNS depressant, resulting in unreliable neurological examination.
  • Possible allergic reaction Impaired lymphocyte immune response and function.


  • Maintenance ICP < 20 mmHG.
  • Therapeutic EEG response: burst suppression or cortical electrical silence (with preservation of SSEP and BAEF).

Dosing Regimens


High dose:
  • Loading:30-40 mg/Kg over 4 hours (~2500mg/70Kg)
  • Maintenance: 1.8-3.3mg/Kg/hr (~175mg/70Kg)
Mid-level dose:
Loading: 10mg/Kg over 30min, 20-25mg/Kg over 4hr
Maintenance: 5mg/Kg/hr for 3hrs,then 2-2.5mg/Kg/ with 5mg/Kg bolus prn if serum level < 3mg/dl
Low dose:
  • Maintenance: .3-3mg/Kg/hr
  • Loading: 3-6mg/Kg over 30min
Therapeutic serum level:2.5-4 mg/dl (6 mg/dl may be needed)


  • Loading: 3mg/Kg bolus, followed by 10-20mg/Kg over 1 hr
  • Maintenance: 3-5 mg/Kg/hr
  • Therapeutic serum level: 6-8.5 mg/dl
  • Weaning: dosage is halved q 12 hr.



  • A-line: arterial BP, blood gases
  • PA catheter: CO, CI, SV, SVR, PVR, right heart filling pres., PCWP
  • Bladder catheter: urine output

Cerebrovascular And Neurophysiological

  • ICP: maintain < 25 mmHg, preferably less
  • CPP: maintain > 70 mmHg
  • EEG: burst suppression, or cortical electrical silence optional
  • Brain temperature
  • Jugular bulb O2 monitor/ oxymeter catheter
  • Somatosensory or brainstem auditory evoked potentials (SSEP, BAEF)

Other Monitoring

  • Core body temperature: NP, TM, E: 32 to 35 degrees C is acceptable
  • Serum barbiturate levels
  • nasogastric catheter: pH and output
  • intake and output
Therapy may be required for 7-14 days or longer, may be weaned after 3-6 days.

Therapeutic End Points

  • ICP < 20 mmHg for at least 48 hours, at a minimum
  • Resolution of intracranial mass effects or midline shift, preferably
  • ICP must remain controlled with conventional therapies
  • Diagnosed brain death
  • Uncontrollable ICP despite adequate serum levels, EEG burst-
  • Suppression, or electrical silence
  • Intolerable side effects; (Hypotention not responsive to cardiac inotropes, peripheral vaso-pressors, or intravenous fluid therapy (cardiac isotopes: dopamine, dobutamine, epinephrine) (peripheral vasopressors: ephedrine, phenylephrine); (IV fluids: packed RBCs, albumine, hetastarch, LR); Progressive pulmonary dysfunction; Sepsis.)
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