No evidence for cerebral hypoperfusion during cerebral malaria.
OBJECTIVE
Among the mechanisms suggested for altered consciousness during cerebral malaria is the hypothesis of cerebral ischemia, which remains controversial, with little supportive O2 conflicting hemodynamic data. The purpose of this study was to test the hypothesis that cerebral ischemia is a main mechanism for altered consciousness during cerebral malaria.


METHODS
University hospital pediatric ward in a region with endemic cerebral malaria.


METHODS
Prospective evaluation of cerebral hemodynamics and cerebral oxygenation during cerebral malaria compared with severe malaria anemia without altered consciousness.


METHODS
During a 2-wk period, we evaluated all patients who were admitted for cerebral malaria (n = 5). Age-matched patients admitted for severe malaria anemia without altered consciousness (n = 3) and outpatients (n = 3) were investigated for comparison.


METHODS
All patients received the usual treatment according to their needs, which was determined by the physician in charge. Repeated neurologic evaluations were performed during the early management period in patients with cerebral malaria.


RESULTS
We repeatedly measured cerebral blood flow velocity (transcranial Doppler) and simultaneous systemic determinants of cerebral blood flow (arterial pressure, arterial oxygen saturation, PaCO2, rectal temperature, and hemoglobin concentration). The adequacy of cerebral blood flow to oxygen demands during cerebral malaria was assessed by continuous recording of jugular bulb venous oxygen saturation (using a fiberoptic device). Marked cerebral vasodilation was observed during cerebral malaria (systolic velocity, 1.45 +/- 0.09 m/s; diastolic velocity, 0.75 +/- 0.08 m/s; n = 4) and during severe malaria anemia (systolic velocity, 1.18 +/- 0.14 m/s; diastolic velocity, 0.55 +/- 0.05 m/s; n = 3) compared with control children (systolic velocity, 0.84 +/- 0.13 m/s; diastolic velocity, 0.35 +/- 0.06 m/s; n = 3; p < .05). During cerebral malaria, jugular bulb venous oxygen saturation remained stable, including during neurologic recovery, with initial values of 67.5 +/- 4.3%.


CONCLUSIONS
Because jugular bulb venous oxygen saturation remained within the normal range, cerebral hyperemia seems to be an adaptive response to altered systemic determinants, which argues against a hemodynamic mechanism for altered consciousness during cerebral malaria.
Clavier
N
N
Department of Anesthesiology and Critical Care Medicine, Lariboisiere University Hospital, Paris, France.
Rahimy
C
C
Falanga
P
P
Ayivi
B
B
Payen
D
D
D000740:Anemia / Q000209:etiology / Q000503:physiopathology*; D001783:Blood Flow Velocity; D001921:Brain / Q000098:blood supply*; D002545:Brain Ischemia / Q000209:etiology* / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D002675:Child, Preschool; D003243:Consciousness; D005260:Female; D015600:Glasgow Coma Scale; D006439:Hemodynamics; D006801:Humans; D007223:Infant; D016779:Malaria, Cerebral / Q000145:classification / Q000150:complications / Q000503:physiopathology*; D016778:Malaria, Falciparum / Q000150:complications*; D008297:Male; D011446:Prospective Studies; D017585:Ultrasonography, Doppler, Transcranial