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).
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
- 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)
- 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.
Success
- 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
Failure
- 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.)