Comparison of moderate hyperventilation and mannitol for control of intracranial pressure control in patients with severe traumatic brain injury--a study of cerebral blood flow and metabolism.
OBJECTIVE
To compare the respective effects of established measures used for management of traumatic brain injury (TBI) patients on cerebral blood flow (CBF) and cerebral metabolic rates of oxygen (CMRO2), glucose (CMRGlc) and lactate (CMRLct).


METHODS
Thirty-six patients suffering from severe traumatic brain injury (TBI) were prospectively evaluated. In all patients baseline assessments were compared with that following moderate hyperventilation (reducing PaCO2 from 36 +/- 4 to 32 +/- 4 mmHg) and with that produced by administration of 0.5 gr/kg mannitol 20% intravenously. Intracranial and cerebral perfusion pressure (ICP, CPP), CBF and arterial jugular differences in oxygen, glucose and lactate contents were measured for calculation of CMRO2, CMRGlc and CMRLct.


RESULTS
Following hyperventilation, CBF was significantly reduced (P < 0.0001). CBF remained most often above the ischemic range although values less than 30 ml x 100 gr(-1) x min(-1) were found in 27.8% of patients. CBF reduction was associated with concurrent decrease in CMRO2, anaerobic hyperglycolysis and subsequent lactate production. In contrast, mannitol resulted in significant albeit moderate improvement of cerebral perfusion. However, administration of mannitol had no ostensible effect either on oxidative or glucose metabolism and lactate balance remained mostly unaffected.


CONCLUSIONS
Moderate hyperventilation may exacerbate pre-existing impairment of cerebral blood flow and metabolism in TBI patients and should be therefore carefully used under appropriate monitoring. Our findings rather support the use of mannitol for ICP control.
Soustiel
J F
JF
Department of Neurosurgery, Rambam Medical Center, Haifa, Israel. j_soustiel@rambam.health.gov.il
Mahamid
E
E
Chistyakov
A
A
Shik
V
V
Benenson
R
R
Zaaroor
M
M
D000293:Adolescent; D000328:Adult; D000368:Aged; D001929:Brain Edema / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D001930:Brain Injuries / Q000150:complications*; D002545:Brain Ischemia / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004234:Diuretics, Osmotic / Q000627:therapeutic use; D005260:Female; D005947:Glucose / Q000378:metabolism; D006019:Glycolysis / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006985:Hyperventilation / Q000378:metabolism*; D019586:Intracranial Hypertension / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D008353:Mannitol / Q000627:therapeutic use*; D008875:Middle Aged; D010101:Oxygen Consumption / Q000187:drug effects; D011446:Prospective Studies; D012121:Respiration, Artificial / Q000009:adverse effects / Q000592:standards; D016896:Treatment Outcome
D004234:Diuretics, Osmotic; D019344:Lactic Acid; D008353:Mannitol; D005947:Glucose