David J. Boarini

Overall management of ruptured aneurysm: comparison of early and late operation.

The overall management results with 61 consecutive patients admitted within 3 days of subarachnoid hemorrhage from a ruptured intracranial aneurysm were analyzed. During the course of this study, the preferred method of management shifted from late surgery (planned at least 7 days after the last hemorrhage) to early surgery (within 4 days of the last hemorrhage). Ten moribund patients were excluded from analysis, leaving 24 in the late group and 27 in the early group. Both groups had comparable patient demographic characteristics and neurological conditions, and their care was supervised by one neurosurgeon (N.F.K.). A microsurgical intracranial operation was performed on all patients who survived long enough to have surgery. The intraoperative conditions and complications were similar for the two groups. The average length of follow-up was 11 months in the late and 9 months in the early group. The overall management results for the late group showed a 42% favorable outcome, a 17% unfavorable outcome, and a 42% mortality. The early group had an 81% favorable outcome, a 7% unfavorable outcome, and an 11% mortality. Patients in both good and poor conditions fared better in the early group. Seven late group patients rebled, compared to none in the early group. The number of medical complications, the length of hospitalization, and the occurrence of symptomatic vasospasm were all greater in the late group. Vasospasm in the early group occurred only postoperatively and, with the aneurysms secured, was treated more aggressively and successfully with hypertensive/hypervolemic therapy than the predominantly operative vasospasm in the late group.

Intraluminal clot of the carotid artery. A clinical-angiographic correlation of nine patients and literature review

Between March 1980 and March 1985, intraluminal thrombi of the carotid artery were noted in 9 of 2250 patients undergoing arteriography for symptoms of cerebral ischemia. Five patients had transient ischemic attacks, and four had acute cerebral infarctions. Six patients had surgery, but a thrombus was only found in five. Two patients had new neurological deficits after surgery. Three patients received only medical therapy, and all remained stable. Intraluminal thrombus is an uncommon radiographic finding in patients with cerebral ischemia. Not all clots are confirmed at operation. The optimal treatment of this situation is not known. Both surgical and medical treatments deserve further investigation.

Postoperative prophylactic anticonvulsant therapy in cerebral gliomas

A retrospective study was performed to evaluate the efficacy of prophylactic anticonvulsants in preventing seizures in 68 patients with supratentorial astrocytomas who had been treated with operation and irradiation and who had no previous history of convulsions. Thirty-three patients received prophylactic anticonvulsants and 38 patients did not. The incidence of all types of seizures (generalized convulsions or partial) was lower in patients receiving anticonvulsants. No seizures with an impairment of consciousness occurred in the patients with documented therapeutic anticonvulsant blood levels. The overall incidence of seizures was 39% in untreated patients and 21% in treated patients. The incidence of major seizures including tonic/clonic or partial complex seizures with impairment of consciousness was zero in patients with therapeutic anticonvulsant levels and 18% in untreated patients. Regarding the overall incidence of seizures in both groups, there tend to be fewer seizures in older patients, females, patients with a higher grade of malignancy, and patients who had a more radical resection of the tumor. This study suggests that seizures are a frequent occurrence after operation and irradiation for supratentorial glioma and that anticonvulsants may be effective in reducing the incidence of those seizures.

Spontaneous subarachnoid hemorrhage in young adults.

We evaluated 95 hospitalized patients (50 women and 45 men) aged 15 to 45 who had nontraumatic subarachnoid hemorrhage (SAH). Aneurysmal SAH was identified in 75 patients. Other causes for SAH were ruptured arteriovenous malformations (2 cases), amphetamine arteritis (1 case), and leptomeningeal melanoma (1 case). The cause of SAH was undetermined in 16 (17%) patients. Thirteen patients had histories of hypertension, 5 used oral contraceptives, and 4 had consumed large quantities of alcohol during the day before SAH. Only 1 patient had Type I diabetes mellitus. Diagnosis was delayed in 21 patients. Operation was performed in 71 patients, with only 3 (4.2%) deaths. The overall mortality was 8.4% (8 of 95), with all deaths due to neurological causes. Our data suggest that the overall management and surgical results of treatment of ruptured aneurysms in young adults are excellent, diabetes is rare among young adults with SAH, recent alcohol consumption does not seem to be a major factor predisposing to SAH in young adults, and misinterpretation of the early symptoms of SAH continues to be a serious problem.

Unruptured fusiform aneurysms of the posterior circulation with thalamic infarction.

Three patients with unruptured fusiform aneurysms of the posterior circulation presented with nonhemorrhagic thalamic infarctions. All of the aneurysms were seen on enhanced computed tomographic (CT) scans preangiographically. Although unruptured fusiform aneurysms are probably a rare cause of nonhemorrhagic thalamic infarction, their importance lies in the therapeutic implications of this diagnosis. In patients with nonhemorrhagic thalamic infarction, we suggest careful scrutiny of the blood vessels on enhanced CT scans.

Comparison of nitroprusside, nitroglycerin, and deep isoflurane anesthesia for induced hypotension.

Three methods of inducing hypotension were studied for their effects on the cardiovascular system and intrapulmonary shunting. Thirty patients were anesthetized with isoflurane in 70% N2O to a total of 1.25 to 1.3 MAC. Patients were divided into three groups of 10 each on the basis of the drug used to induce hypotension; sodium nitroprusside (SNP), nitroglycerin (NTG), or deep isoflurane anesthesia (ISF). Cardiac index was significantly decreased by NTG and ISF at a mean arterial blood pressure of 40 mm Hg compared to SNP (P less than 0.05). Systemic vascular resistance was decreased in all groups. Mixed venous oxygen content was significantly decreased from control in the NTG and ISF groups. There was no difference between the groups in arterial and mixed venous O2 content. Intrapulmonary shunting decreased with induction and, in the NTG and SNP groups, increased slightly but not significantly with induction of hypotension. Our data do not show a clear superiority of any agent over the other to induce hypotension, although SNP and perhaps ISF appear to be better than NTG to induce hypotension.

Time-dependent Changes in Cerebral and Cardiovascular Parameters in Isoflurane-Nitrous Oxide-anesthetized Dogs

The purpose of this study was to examine the time-dependent effects of isoflurane-nitrous oxide anesthesia on cerebral blood flow and metabolism and on cardiovascular parameters. Eleven 15-kg mongrel dogs were anesthetized with 0.8% isoflurane (approximately 1.3 MAC (minimal anesthetic concentration], 70% nitrous oxide, and 30% O2 and were paralyzed with pancuronium. Blood flow (using the radioactive microsphere technique) and cerebrovascular and cardiovascular parameters were measured 6 times at 30-minute intervals beginning 2 hours after the induction of anesthesia. In this experiment, cerebral blood flow was markedly elevated at 2 hours after the induction of anesthesia, but then declined progressively by 40 to 50% over the 2 1/2-hour time period investigated, approaching values for normal awake dogs. The decline was accompanied by a progressive decrease in the cerebral metabolic rate of oxygen and a constant rise in cerebrovascular resistance. Blood flow to organs outside the central nervous system declined progressively, but with more variability between tissues. The mean arterial pressure increased slightly, and the peripheral vascular resistance almost doubled, but cardiac index, cardiac work, and stroke volume all decreased gradually. We conclude that isoflurane-nitrous oxide anesthesia produces significant cerebral vasodilatation in dogs, but that this effect diminishes over time. These time-dependent circulatory changes merit further investigation in humans.

Cerebrovascular Adaptation to Prolonged Halothane Anesthesia Is Not Related to Cerebrospinal Fluid pH

The purpose of this study was to evaluate the time-dependent effects of steady-state halothane anesthesia on cerebrovascular variables and their relationship to cerebrospinal fluid (CSF) pH. Eight mongrel dogs underwent a 7-h anesthetic, receiving halothane (1.0% end-tidal), O2 (50%), and balance N2. Cerebral blood flow (CBF) was measured by injection of radioactively labeled micro-spheres. CSF was sampled from the cisterna magna and cerebral venous blood from the superior sagittal sinus. Measurements were made at 2 h postinduction and hourly for 5 h thereafter. Total CBF at 2 h postinduction was 148 ± 36 ml·100 g−1·min−1 and showed a significant decay over the subsequent 5 h to 70 ± 3 ml·100 g−1·min−1. Regional variations were noted, those areas with highest initial flows showing both a greater relative and absolute reduction in flow. Cerebral vascular resistance increased significantly (39%), as did mean arterial pressure (15%). CSF pH values remained constant throughout the experiment. Arterial blood acid-base physiology was also unchanged. Sagittal sinus PCO2 increased significantly from 43 ± 4 to 49 ± 3 mmHg while sagittal sinus pH decreased from 7.31 ± 0.01 to 7.37 ± 0.02, consistent with the normalization of CBF. Cerebral metabolic oxygen consumption did not change significantly. The authors conclude that time-dependent changes in cerebrovascular parameters under prolonged steady-state halothane anesthesia are not due to changes in CSF pH and thus brain extracellular acid-base chemistry.

Effects of naloxone on cerebral blood flow and metabolism in isoflurane/nitrous oxide-anesthetized dogs.

The purpose of this study was to document the changes in the cerebral and systemic circulations that result from various doses of naloxone. Twenty-four dogs were anesthetized with 0.8% isoflurane and 70% nitrous oxide (1.3 minimal anesthetic concentration). Thirteen of the dogs received bolus injections of naloxone at logarithmically increasing doses 30 minutes apart. Blood flow to the brain and other organs was determined using the radioactive microsphere technique. Electrical activity was measured by electroencephalography (EEG). High dose naloxone increased both cerebral blood flow (CBF) and cerebral metabolism. The changes in CBF were most pronounced in structures containing a large amount of gray matter, particularly the cerebral cortex, brain stem, and cervical spinal cord. The increase in blood flow was proportionately greater than the increase in the cerebral metabolic rate of oxygen, and EEG activity was unchanged. Naloxone did not produce any significant cardiovascular changes or alterations in myocardial, renal, hepatic, stomach, jejunum, or temporalis and paraspinous muscle flow. Accordingly, it seems that naloxone may have direct cerebral vasodilator properties.

Effect of dimethyl sulfoxide on the cerebral and systemic circulations of the dog.

Dimethyl sulfoxide (DMSO) has a variety of properties suggesting that it may be a useful agent in the management of central nervous system trauma and stroke. The purpose of this investigation was to determine the systemic and cerebrovascular effects of varying doses of DMSO in a normal animal. Five mongrel dogs were subjected to a constant infusion of 100% DMSO at a rate of 4 g/kg/hour. Using the radioactive microsphere technique, we measured blood flow before giving DMSO and after 2, 4, 6, and 8 g of DMSO per kg had been infused. After 2 g/kg had been given, hemolysis was evident and the intravascular volume increased, resulting in a lowered hematocrit. The cerebral metabolic rate of oxygen remained stable throughout the study. The total cerebral blood flow increased over 20% after a cumulative dose of 6 g/kg. Blood flow to the cerebellum and brain stem was unchanged, while flow to the caudate nuclei and cerebral hemispheres increased. There was a reduction in flow to the corpus callosum and spinal cord. DMSO caused an increase in the cardiac index accompanied by a large increase in the right and left ventricular blood flows, but a reduction in kidney flow. The relationship of this redistribution of blood flow, especially within the cerebrospinal axis, to the therapeutic effects of DMSO bears further investigation.