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Objective: In patients with traumatic or ischemic brain injury, hyperthermia is thought to worsen the neurological injury. We studied fever in the neurosurgical intensive care unit (ICU) population using a definition common to surgical practice (rectal temperature >38.5 degrees C). We sought to determine fever incidence, fever duration, and peak temperature and to quantify the use of antipyretic therapy. We also attempted to determine the patient subgroups that are at highest risk for development of fever., Methods: In a retrospective chart review of a 6-month period, all febrile episodes that occurred in a consecutive series of neurosurgical ICU patients in a university hospital setting were studied. A febrile episode was defined as a rectal temperature of at least 38.5 degrees C; an episode lasted until the temperature fell below this threshold., Results: The 428 patients studied had 946 febrile episodes. Fever occurred in 47% of patients, with a mean of 4.7 febrile episodes in each febrile patient. Fevers occurred in more than 50% of patients who were admitted to the ICU for subarachnoid hemorrhage, a central nervous system infection, seizure control, or hemorrhagic stroke, but they occurred in only 27% of patients admitted for spinal disorders. Fevers occurred in 15% of the patients who stayed in the ICU less than 24 hours, but in 93% of those who remained longer than 14 days. Despite the use of antipyretic therapy for 86% of the febrile episodes, 57% lasted longer than 4 hours and 5% lasted longer than 12 hours., Conclusion: Fever is common in critically ill neurosurgical patients, especially those with a prolonged length of stay in the ICU or a cranial disease. If hyperthermia worsens the functional outcome after a primary ischemic or traumatic injury, as has been suggested by several studies of stroke patients, treatment of fever is a clinical issue that requires better management.

Objective: The purpose of this study was to compare brain temperature (Tbr) with conventional indicators of core body temperature (i.e., rectal temperature [Tre] and bladder temperature [Tbl]), in adults with severe head injury., Methods: The relationships between Tbr and Tbl and between Tbr and Tre are described in terms of differences in temperature in eight patients with severe head injury., Instrumentation: Brain tissue temperature was measured every minute, with a thermocouple embedded 2 cm from the tip of a ventriculostomy catheter used to measure intracranial pressure. Tbl was measured with a thermistor embedded in a bladder catheter, and Tre was measured with a thermistor in a rectal probe., Results: Tbr was usually greater than Tbl and Tre. The average difference between Tbr and Tbl for each patient ranged from 0.32 to 1.9 degrees C, with standard deviations of the difference ranging from 0.30 to 0.80 degrees C. The average difference between Tbr and Tre for each patient ranged from 0.1 to 2.0 degrees C, with standard deviations of the difference ranging from 0.32 to 1.08 degrees C. In the majority of patients, the differences (Tbr - Tbl and Tbr - Tre) were greater at temperatures outside of the normal temperature range (Tbr < or =36 degrees C and >38 degrees C)., Conclusion: Tbl and Tre often underrepresent Tbr after traumatic brain injury, particularly when the patient is hypo- or hyperthermic.

Objective: Uncoupling of cerebral blood flow (CBF) and oxidative metabolism is observed after severe head injury in comatose patients; however, the mechanism(s) involved remain undefined. Adenosine can produce cerebral vasodilation and reduce neuronal activity and is a possible mediator of uncoupling. We hypothesized that cerebrospinal fluid (CSF) adenosine concentrations would be increased during uncoupling of CBF and oxidative metabolism, defined as a narrow arterio-jugular venous oxygen difference [D(a-v)O2 4 vol%] after head injury., Methods: Adenosine concentrations were measured using fluorescent-based high-pressure liquid chromatography in 67 CSF samples obtained from 13 comatose (Glasgow Coma Scale score 7) adult patients who sustained a severe closed head injury. At the time each sample was obtained, CBF was measured by the xenon-133 method, and blood samples were obtained for determination of D(a-v)O2., Results: CSF adenosine concentration was negatively associated with D(a-v)O2 (P < 0.05, generalized multivariate linear regression model). In addition, CSF adenosine concentration was increased when D(a-v)O2 was 4 versus > 4 vol% (38.5 [3.2-306.3] versus 14.0 [2.7-795.5] nmol/L, respectively, median [range]; P < 0.025) and in patients who died versus survivors (40.1 [6.9-306.3] versus 12.9 [2.7-795.5] nmol/L, respectively, median [range]; P < 0.001)., Conclusion: The association between increased CSF adenosine concentration and a reduction in global cross-brain extraction of oxygen supports a regulatory role for adenosine in the complex balance between CBF and oxidative and nonoxidative metabolism severe head injury in humans.

Objective: Basilar cranial fractures have been associated with injury to the carotid artery. We sought to determine whether fracture through the carotid canal was a significant risk factor for carotid injury., Methods: A retrospective chart review was performed, and 230 patients with basilar cranial fractures were identified. Fifty-five of the 230 patients had visible fractures that extended through one or both carotid canals (CC fx group). Evidence for vascular injury, based on medical records, angiography, magnetic resonance imaging, and other studies, was compiled. The anatomic characteristics of the fractures were also noted and recorded., Results: Ten patients in the CC fx group suffered vascular complications; for six of them, the complications were directly related to the intracranial carotid artery. This compares to four patients in the non-CC fx group with vascular complications (P < 0.005), only one of which was carotid-specific (P < 0.005). The most common site of fracture through the canal was at the junction of the lacerum and cavernous portions of the canal (the spheno-occipital suture) (62% of all carotid canal fractures occurred at that site); however, vascular injury was seen most often in patients who sustained fractures through the petrous segment (67% of carotid canal-specific injuries occurred in that group, and 25% of patients with petrous canal fractures suffered carotid injury, [P = not significant]). The mean Glasgow Coma Scale score and the mean age were both lower (P < 0.05) in the CC fx group., Conclusion: Vascular complications are more frequently observed after basilar cranial fractures when there is involvement of the carotid canal. The lacerum-cavernous junction, which is partly formed by the spheno-occipital suture, is the most frequently fractured segment of the carotid canal. Fracture through the petrous segment of the carotid canal is associated with a relatively high incidence of carotid injury. Fracture through the carotid canal may serve as an index of injury severity, because patients with these fractures suffered more severe head injuries.

Hypothermia has been shown to cause coagulation abnormalities, primarily related to platelet dysfunction. We reviewed coagulation function and the incidence of delayed traumatic intracerebral hemorrhage in a series of 36 patients with severe head injuries (Glasgow Coma Scale 3-7) enrolled in a prospective, randomized, clinical trial of therapeutic moderate hypothermia. Patients were randomized to a normothermic group (n = 16) or to a group cooled to 32 to 33 degrees C within 6 hours of injury (n = 20). Prothrombin times, partial thromboplastin times, and platelet counts were obtained in the emergency room and then again within 24 hours of randomization. Delayed traumatic intracerebral hemorrhage occurred in 6 of 20 (30%) hypothermic patients and 5 of 16 (31%) normothermic patients. In the hypothermic group, 9 of 17 patients had an increased prothrombin time during hypothermic therapy, as opposed to 11 of 16 in the normothermic group during the corresponding time period. The partial thromboplastin time was prolonged in 2 of 17 hypothermic patients and 2 of 16 normothermic patients. Three patients in the hypothermic group and one in the normothermic group developed thrombocytopenia (a platelet count of less than 100,000). There were no significant differences between the two groups in the incidence of delayed traumatic intracerebral hemorrhage, in measured coagulopathy, or in the mean values of measured coagulation parameters. Although the possibility of a hypothermia-induced coagulopathy has not yet been excluded, the short-term use of hypothermia does not appear to increase the risk for intracranial hemorrhagic complications in head injuries.

Previous studies using the xenon-133 cerebral blood flow (CBF) method have documented the impairment of CO2 vasoresponsivity after a severe head injury, but only global values can be obtained reliably with this technique. We studied CO2 vasoresponsivity using the stable xenon-enhanced computed tomographic CBF method, which provided information about well-defined cortical regions and deep brain structures not available with the xenon-133 method. In 17 patients with admission Glasgow Coma Scale scores of 8 or less, hemispheric CO2 vasoresponsivity ranged from 1.3 to 8.5% per mm Hg change in partial CO2 pressure. Lobar, cerebellar, basal ganglia, and brain stem CO2 vasoresponsivity frequently varied from the mean global value by more than 25%. In all but one patient, local CO2 vasoresponsivity in one or more of these areas differed from the mean global value by more than 50%. The greatest variability occurred in patients with acute subdural hematomas and diffuse (bihemispheric) injuries. This variability in CO2 vasoresponsivity has important implications for the effective and safe management of intracranial hypertension that frequently accompanies severe head injury.

Complications associated with the use of perioperative steroids in elective craniotomies were evaluated in a single-blind prospective study of 222 consecutive microvascular decompression operations. Patients were randomized into one of three groups: Group A received steroids preoperatively and for 4 days postoperatively, Group B received steroids pre- and postoperatively for 1 day, and Group C received no steroids. There were 17 complications in Group A; 12 of these were wound-related. There were significantly fewer complications in Groups B and C (P less than 0.01). Group B had 3 complications, Group C had 4, and there was only 1 wound-related complication in Group C. There were no deaths, deep wound infections, or life-threatening complications. Severe postoperative headaches, a symptom that steroids were intended to minimize, occurred in 38% of patients in Group A, 42% of patients in Group B, and 25% of patients in Group C. The use of perioperative steroids did not reduce the length of postoperative hospitalization. Duration of the operation had no significant effect on the incidence of postoperative complications or the length of postoperative hospitalization. We conclude that there is no indication for the routine perioperative use of steroids with microvascular decompression operations of the posterior fossa cranial nerves and that such use leads to a higher incidence of postoperative complications.

Hyperventilation is used routinely to reduce intracranial pressure in victims of severe head injury. In the clinical setting, the effects of hyperventilation on regional cerebral blood flow usually are not known. We describe a case in which hyperventilation resulted in local, paradoxic increases in cerebral blood flow (i.e., "inverse steal") associated with a reduction in intracranial pressure. Although the reduced intracranial pressure was thought to be beneficial, serial computed tomographic scans suggested that the inverse steal response could have promoted cerebral edema, resulting in secondary brain injury.

Electrocardiographic abnormalities, both morphological and rhythmic, are frequently seen in association with spontaneous subarachnoid hemorrhage. These changes, which often reflect subendocardial damage, seem to be caused by hypothalamic stimulation leading to an acute increase in sympathetic tone. As a result, potentially life-threatening ventricular arrhythmias may develop in subarachnoid hemorrhage patients. These arrhythmias have responded to sympathetic blocking agents, which may also have a protective effect on subendocardial tissue in this setting. There is no evidence that the prophylactic administration of propranolol or other autonomic blockers significantly alters outcome in these patients. Ultimate morbidity and mortality are clearly related to the degree of intracerebral-intraventricular hemorrhage and vasospasm. This article reviews experimental and clinical evidence regarding the causes of cardiac abnormalities after subarachnoid hemorrhage, the types of abnormalities most frequently seen, their relationship with subendocardial lesions, and the role of autonomic blockers.