Current strategies for cerebral protection during planned cerebral ischemia include hypothermia, colloidal volume expansion, induced hypertension, and barbiturate coma. Hypothermia between 34-35°C is an effective cerebral protector. Colloidal volume expanders are preferable to crystalloids. Induced hypertension can be achieved short-term with phenylephrine or long-term with dopamine. Barbiturate coma decreases cerebral metabolism and intracranial pressure, but carries risks of hemodynamic and respiratory depression that require intensive monitoring. The goal is to maintain intracranial pressure below 20mmHg and cerebral perfusion pressure above 70mmHg.

1. Current Strategies for Planned
Cerebral Ischemia
(Cerebral Protection)
R2 정태석

2. Cerebral Protection
• Commonly used techniques include
– Hypothermia
– Colloidal volume expansion
– Induced hypertension
– Barbiturate coma

3. Hypothermia
• Recent laboratory research
– hypothermia (34 to 35°C)
– powerful cerebral protector
– not necessary to cool the patient to the level of 30°C
when cardiac arrhythmias may occur
– keeping the room cool
– using a cooling blanket

4. Colloidal volume expansion
• Important first step to cerebral protection
• Colloid agent
– more useful than crystalloids as volume expanders
– blood, blood products
– recommended limit for hetastarch in 24hr
• 1,200 mL

5. Induced Hypertension
• Short term therapy
– phenylephrine
– easily titrated, its effect is rapidly terminated
– most vascular beds are constricted except for coronary and cerebral
vasculature
• Longer therapy
– dopamine
– minimal effect on the renal vasculature
• Mean arterial blood pressure
– 20 to 30 mmHg above the patient’s normal mean BP

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

7. Barbiturate Coma
• Benefits
1. Decrease in cerebral metabolic rate (CMRO2), caused by de
crease in synaptic transmission, presumably by affecting GAB
A transmission
2. 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 is
oelectric EEG
3. Promote or induce hypothermia
4. Increase in IC glucose, glucagon, and phosphocreatine en
ergy store

8. Barbiturate Coma
5. Decrease in nitrogen excretion following acute head injury
6. Shunt blood from regions of normal perfusion to those of redu
ced CBF due to vasoconstriction
7. Anticonvulsant prophylaxis
8. Stabilization of lysosomal membranes
9. Decrease in excitatory neurotransmitters and IC calcium
10. Free radical scavenging ( thiopental only)

9. Barbiturate Coma
• Risks
1. Direct myocardial depressant
2. Increase in venous capacitance, due to central and peripheral s
ympatholytic action
3. Impaired gastrointestinal motility Increased hepatic micr
osomal activity
4. Direct CNS depressant, resulting in unreliable neurological ex
amination
5. Possible allergic reaction Impaired lymphocyte immune res
ponse and function

10. Barbiturate Coma
• Goals
1. Maintenance ICP < 20 mmHG
2. Therapeutic EEG response: burst suppression or c
ortical electrical silence (with preservation of SSEP a
nd BAEF)

11. Barbiturate Coma
• Dosing Regimens
– Thiopental
 Loading: 3-5 mg/Kg bolus IV over 10 minutes
 Maintenance: 3-5 mg/Kg/hr for 24 hours
 Therapeutic serum level: 6-8.5 mg/dl
 Weaning: dosage is halved q 12 hr.

12. Barbiturate Coma
• Monitoring
– Cardiovascular
1. A-line: arterial BP, blood gases
2. PA catheter: CO, CI, SV, SVR, PVR, right heart filling pres.,
PCWP
3. Bladder catheter: urine output

13. Barbiturate Coma
• Monitoring
– Cerebrovascular and neurophysiological
1. ICP: maintain < 25 mmHg, preferably less
2. CPP: maintain > 70 mmHg
3. EEG: burst suppression, or cortical electrical silence op
tional
4. Brain temperature
5. Jugular bulb O2 monitor/ oxymeter catheter
6. Somatosensory or brainstem auditory evoked potentials (S
SEP, BAEF)

14. Barbiturate Coma
• Monitoring
– Other monitoring
1. Core body temperature: NP, TM, E: 32 to 35 degrees C is acc
eptable
2. Serum barbiturate levels
3. nasogastric catheter: pH and output
4. intake and output
• Therapy may be required for 7-14 days or longer, may
be weaned after 3-6 days

15. Barbiturate Coma
• Therapeutic end points
– Success
 ICP < 20 mmHg for at least 48 hours, at a minimum
 Resolution of intracranial mass effects or midline shift, pre
ferably
 ICP must remain controlled with conventional therapies

16. Barbiturate Coma
• Therapeutic end points
– Failure
 Diagnosed brain death
 Uncontrollable ICP despite adequate serum levels, EE
G burst
 Suppression, or electrical silence
 Intolerable side effects;
Hypotention not responsive to cardiac inotropes, perip
heral 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

17. • Reference
– J. Greenberg; Handbook of Head and Spine Trauma,
1993. pp230-233