Does a bolus of mannitol initially aggravate intracranial hypertension? A study at various PaCO2 tensions in dogs

In two groups of anaesthetized dogs, with (n = 28) or without (n = 28) induced intracranial hypertension, we compared the effects on intracranial pressure (ICP) of the rapid administration of mannitol 2 g kg-1 i.v. at PaCO2 2.7, 4.0, 5.3, and 6.7 kPa (n = 7). In dogs with no induced intracranial hypertension, ICP increased during the administration of mannitol, reached a peak at 2 min after infusion, and then gradually decreased (P less than 0.05). More marked changes in ICP were observed in response to higher values of PaCO2 (P less than 0.05). In dogs with induced intracranial hypertension, the rapid infusion of mannitol caused an exponential decrease in ICP, without initial increase, which was significantly steeper at higher values of PaCO2 (P less than 0.05). This was followed by a more gradual decrease which achieved pre-balloon inflation values 10 min after infusion. We postulate that the absence of the initial increase in ICP is the result of a concomitant decrease in arterial pressure, a reduction in the volume-pressure response of the brain, the failure of mannitol to dilate further the cerebral arterial vascular bed and a hitherto unnoticed early water-drawing effect. Our study confirmed the safety of rapidly expanding the circulating blood volume with mannitol in circumstances of increased ICP in dogs

Circulatory and Respiratory Effects of Ketamine in Horses Anesthetized with Halothane

Ketamine (0.3 mg/kg) administered intravenously to 12 halothane anesthetized horses caused a significant respiratory depression during ten minutes when respiration was spontaneous. Significant hemodynamic effects were not observed except for cardiac index. Clinical application was also discussed

Changes in CSF pressure after mannitol in patients with and without elevated CSF pressure

In view of the current concern that rapid infusion of mannitol might initially aggravate intracranial hypertension, the effects of a mannitol infusion on lumbar cerebrospinal fluid pressure (CSFP) were investigated in 49 patients. The studies were performed when the patients were under general anesthesia prior to elective craniotomy for tumor resection or intracerebral aneurysm clipping. The patients were divided into two groups: 24 patients with normal CSFP (Group I, mean CSFP 10.5 mm Hg) and 25 with raised CSFP (Group II, mean CSFP 20.8 mm Hg). Measurements of CSFP, mean arterial blood pressure (MABP), and central venous pressure (CVP) were made serially during and after the infusion of 20% mannitol (1 gm.kg-1 infused over a 10-minute interval). In both groups, mannitol infusion provoked a fall in MABP and an increase in CVP. An immediate decrease [corrected] in CSFP was observed in Group II, whereas CSFP increased transiently but significantly in Group I. Analysis of the arterial and venous driving pressures which contribute to CSFP suggests that the transient increase in CSFP after mannitol in Group I was partly due to the increase in CVP. The presence of intracranial hypertension may thus alter the CSFP response to arterial and venous pressure changes. Cerebral blood volume (CBV) was measured in dogs in a separate study analogous to the human protocol. The CBV increased approximately 25% over control values after mannitol infusion both in the normal animals and in those with CSFP raised by an epidural balloon. The response of the CSFP to mannitol infusion differed between both groups in a fashion similar to that observed in the human subjects. Thus, differences in CBV changes after mannitol do not account for the difference in CSFP response between normal subjects and those with raised CSFP