Hypertensive Hypervolemic Therapy Research Articles

Visual deterioration after endonasal endoscopic skull base surgery: causes, treatments, and outcomes.

Visual deterioration after endoscopic endonasal transsphenoidal surgery (EETS) for sellar and parasellar masses is a rare but serious complication caused by either compressive or ischemic mechanisms. Timely diagnosis and intervention may restore vision if instituted appropriately. The associated risk factors and their relation to the success of intervention are not well understood. The authors examined a series of 1200 consecutive EETS cases performed by the senior author at Weill Cornell/NewYork-Presbyterian Hospital from 2010 to 2020. Cases with postoperative visual deterioration were identified. Pre- and postoperative clinical data, mechanism of visual decline, latency to intervention, and long-term visual outcome were retrospectively collected and analyzed with appropriate statistical methods. Twenty-one patients (1.75%) complained of early postoperative visual deterioration. The most common pathology associated with postoperative visual loss was craniopharyngioma (7.69%), followed by meningioma (5.43%) and then pituitary adenoma (1.94%). Timely intervention restored vision in 81% of patients for a 0.33% rate of permanent visual deterioration. Average time to visual deterioration was 28.8 hours, and over 70% of patients experienced vision loss within the first 13 hours. Compressive etiology (n = 11), consisting of either hematoma (n = 8) or graft displacement (n = 3), occurred 7.3 hours and 70.3 hours after surgery, respectively, and was more common in adenomas. Acute postoperative visual deterioration was more common in firm closures (4.78%) compared with soft closures (1.03%; p = 0.0006). Ischemic etiology (n = 10) occurred 10.3 hours after surgery and was more common with craniopharyngiomas and meningiomas (p = 0.08). Sixteen patients (76.2%) underwent early reoperation to explore and decompress the optic apparatus. Vision was restored to baseline after reoperation in all 11 compressive cases, whereas 6/10 ischemic cases improved with supplemental oxygen and hypervolemic hypertensive therapy (p = 0.02). Fluid expansion from 8 to 16 hours (p = 0.034) and systolic blood pressure elevation from 32 to 48 hours (p = 0.05) after surgery were significantly higher in those ischemic patients who recovered some vision compared with those with persistent visual deficits. Visual deterioration after EETS is a rare event but can be effectively treated if acted upon appropriately and in a timely fashion. Compressive etiology is reversible with early reoperation. Ischemic etiology can be successfully treated in roughly half of cases with supplemental oxygen and hypertensive hypervolemic therapy but may result in permanent visual deterioration if not instituted appropriately or if delayed with unnecessary exploratory surgery.

Continuous intra-arterial nimodipine infusion as rescue treatment of severe refractory cerebral vasospasm after aneurysmal subarachnoid hemorrhage

Severe refractory cerebral vasospasm (CV) is a major cause of disability and death in patients with aneurysmal subarachnoid hemorrhage (SAH). One rescue therapy in selected patients is intra-arterial nimodipine, either given as a single shot or as continuous infusion. To evaluate treatment efficacy, we analyzed outcome factors such as the incidence of craniectomy, ventriculo-peritonial (VP) shunting, and tracheotomy after intra-arterial nimodipine infusion. We retrospectively analyzed the rates of cerebral infarction, decompressive craniectomy, VP shunting, and tracheotomy in patients with severe CV after SAH. Three different patient groups were compared: group 1 had only been treated with oral nimodipine and hypervolemic hypertensive therapy (HHT) (2006–2010), group 2 with a single shot of intra-arterial nimodipine (SSN) in addition to oral conservative treatment (2006–2010), and group 3 with continuous intra-arterial nimodipine (CIAN) (2011–2017). The incidence of cerebral infarction was significantly lower in CIAN group (p = 0.005) than in conservative and SSN group. The indication for consecutive decompressive craniectomy was significantly lower in CIAN group in comparison with the conservative group (p = 0.018). The rates of VP shunting and tracheotomy were significantly higher in the CIAN group than in the conservative group (p = 0.028 for VP, and p = 0.003 for tracheotomy). The significantly lower rate of craniectomy in the CIAN group was most probably attributable to the significantly lower rate of CV-induced infarction. The higher rate of tracheotomy reflects more extensive sedation and the need of longer stays on the intensive care unit. Thus, the effect on long-term neurological outcome and quality of life has to be evaluated separately.

Continuous intra-arterial nimodipine infusion in patients with severe refractory cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a feasibility study and outcome results.

Severe cerebral vasospasm is a major cause of death and disability in patients with aneurysmal subarachnoid hemorrhage. No causative treatment is yet available and hypertensive hypervolemic therapy (HHT) is often insufficient to avoid delayed cerebral ischemia and neurological deficits. We compared patients receiving continuous intra-arterial infusion of the calcium-antagonist nimodipine with a historical group treated with HHT and oral nimodipine alone. Between 0.5 and 1.2 mg/h of nimodipine were continuously administered by intra-arterial infusion via microcatheters either into the internal carotid or vertebral artery or both, depending on the areas of vasospasm. The effect was controlled via multimodal neuromonitoring and transcranial Doppler sonography. Outcome was determined by means of the Glasgow Outcome Scale at discharge and 6 months after the hemorrhage and compared to a historical control group. Twenty-one patients received 28 intra-arterial nimodipine infusions. Six months after discharge, the occurrence of cerebral infarctions was significantly lower (42.6 %) in the nimodipine group than in the control group (75.0 %). This result was reflected by a significantly higher proportion (76.0 %) of patients with good outcome in the nimodipine-treated group, when compared to 10.0 % good outcome in the control group. Median GOS was 4 in the nimodipine group and 2 in the control group (p = 0.001). Continuous intra-arterial nimodipine infusion is an effective treatment for patients with severe cerebral vasospasm who fail to respond to HHT and oral nimodipine alone. Key to the effective administration of continuous intra-arterial nimodipine is multimodal neuromonitoring and the individual adaptation of dosage and time of infusion for each patient.

Can Quantitative EEG Reliably Predict Deterioration from Delayed Cerebral Ischemia Secondary to Vasospasm?

Functional outcome after subarachnoid hemorrhage (SAH) has significantly improved over the past decades but secondary complications such as delayed cerebral ischemia (DCI) continue to take their toll [1]. In fact secondary complications are major determinants of outcome in neurocritical care [2]. Improving the detection of DCI has a high yield since it is frequent (approximately 25–40% of patients with SAH), has a significant impact on outcome, and is potentially treatable when diagnosed in a timely fashion [3–6]. Treatment includes hypertensive hypervolemic therapy, nimodepine per mouth, intraarterial or intrathecal calcium channel blockers, and angioplasty. Most crucial for the effectiveness of these interventions is the timing of starting them. To this date diagnosis of DCI at most institutions relies primarily on changes in the clinical examination and TCD, both of which are clearly limited and inadequate in a large portion of patients. Symptoms from DCI are extremely variable depending on the affected brain tissue and particularly in patients with high Hunt Hess grade, and therefore a poor baseline neurological exam, clinical changes may be extremely difficult to detect [3]. TCD, which are usually only obtained once a day, have been shown to have poor specificity and sensitivity for DCI [7–12]. This has led to the development of a number of ancillary diagnostic tests primarily to increase the sensitivity to detect DCI prompting angiographic confirmation. Most of these tests, such as CT angiography, MRI, or conventional angiography, have a poor temporal resolution or in other words cannot be obtained continuously. The ideal diagnostic test would have a very high sensitivity with reasonable specificity. It should be continuous and automatically alert physicians to initiate the appropriate next steps: first confirm the suspicion with a test that has a high specificity, and second initiate appropriate treatment if DCI secondary to vasospasm is confirmed. Quantitative analysis of continuously recorded digital EEG data has the potential to offer many of these requirements. Prior studies have demonstrated that EEG changes can be seen with brain that is underperfused [13–15]. Actually, with decreasing perfusion sequential EEG changes are observed while brain tissue initially is in a state of reversible and then later irreversible brain injury [16]. A number of quantitative EEG parameters have been shown to correlate with DCI and vasospasm after SAH [17, 18] and may indicate this secondary complication up to 2 days prior to other tests [17]. However, all of these prior studies were conducted in an artificial study setting, which is one of the reasons that this technique is not widely used. What remains to be solved is a practical way to integrate this test into daily clinical practice. Rathakrishnan and colleagues report in this issue of Neurocritical Care on a first attempt to integrate qEEG into the daily clinical routine of managing SAH patients in the Neuro ICU. They studied of a subgroup of 12 SAH patients deemed at high risk for DCI and found increasing accuracy when comparing predictions for clinical deterioration made purely on clinical data versus clinical data together with qEEG findings. Prediction of clinical deterioration improved from 40 to 67% with the use of qEEG data and clinical improvement from 8 to 50%. In a small subset of J. M. Schmidt J. Claassen Division of Critical Care Neurology, Department of Neurology, Columbia University Medical Center, New York, NY 10032, USA

Intra-Aortic Balloon Pump Counterpulsation in the Setting of Subarachnoid Hemorrhage, Cerebral Vasospasm, and Neurogenic Stress Cardiomyopathy. Case Report and Review of the Literature

The management of symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH) can be often complicated by the presence of stunned myocardium and left ventricular failure. Vasopressors and inotropes are commonly used to optimize mean arterial pressure (MAP) and cerebral perfusion pressure (CPP). Intra-aortic balloon counterpulsation pump (IABP) may be indicated in the management of these patients. We report the case of a 55-year-old patient who suffered an aSAH complicated by severe left ventricular failure, who subsequently developed symptomatic cerebral vasospasm. Left ventricular failure precluded traditional hemodynamic augmentation, and IABP was successfully used instead, which allowed for reinstitution of hypertensive hypervolemic therapy and prevented delayed cerebral ischemia. A review of the literature conducted on symptomatic cerebral vasospasm after aSAH and severe left ventricular failure revealed seven publications describing 14 patients with aSAH treated with an IABP during the period of vasospasm. Intra-aortic balloon counterpulsation pump (IABP) is used for hemodynamic support of patients in cardiogenic shock and its use in the setting of aSAH, cardiomyopathy, and cerebral vasospasm can be beneficial in preventing delayed ischemic deficits.

Clinical Response to Hypertensive Hypervolemic Therapy and Outcome After Subarachnoid Hemorrhage

Hypertensive hypervolemic therapy is widely used to treat symptomatic vasospasm after subarachnoid hemorrhage. Few data exist to support a relationship between early clinical response and mortality or functional outcome. In a prospective cohort of 580 subarachnoid hemorrhage patients, we studied 95 patients with acute symptomatic vasospasm who received stepwise volume expansion with crystalloid and/or 5% albumin solution followed by intravenous pressors to maintain systolic blood pressure between 180 and 220 mm Hg. We separately assessed the effects of volume expansion and induced hypertension on the neurological examination during the first 2 hours of each intervention. We used multivariate logistic regression analysis to calculate adjusted odds ratios assessing the relationship between clinical response to hypertensive hypervolemic therapy and 3-month outcome, as measured by the modified Rankin Scale. Of 95 patients with symptomatic vasospasm, volume expansion was used in 94% (n = 89), of whom 43% had a clinical response; 85% of the patients (n = 81) received pressors, of whom 68% responded. Early clinical improvement attributable to either volume expansion or pressors was not related to the development of infarction on computed tomography, but response to either modality within 2 hours was independently protective against death (adjusted odds ratio, 0.03; P < 0.05) and death-or-severe-disability (modified Rankin Scale score, 4-6; adjusted odds ratio, 0.1; P < 0.05) after adjusting for age, Hunt-Hess grade, angioplasty, and aneurysm size. Subarachnoid hemorrhage patients with symptomatic vasospasm who fail to demonstrate early clinical improvement in response to volume or pressor therapy are at high risk for death or disability. Urgent endovascular intervention in this high-risk patient cohort may be justified.

Hemodynamic Monitoring in the Care of the Critically Ill Neuroscience Patient

Hemodynamic monitoring in the care of the critically ill neuroscience patient provides information that assists the clinician in minimizing secondary neuronal injury. Whereas no technology replaces the critical care nurse's physical assessment, hemodynamic and neurological monitoring provides additional data beyond what is possible with the clinical examination alone. If neurological technology, such as intracranial pressure monitoring, is not available, hemodynamic monitoring along with the neurological examination provides limited but useful information essential to minimizing secondary neuronal injury. The use of hemodynamic monitoring in critically ill neuroscience patients is best exemplified in the management of cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Although improved outcomes have not been scientifically substantiated, multimodality monitoring of intracranial dynamics and systemic hemodynamics and manipulation of these parameters during hypertensive hypervolemic hemodilution therapy may lessen the incidence of cerebral infarction secondary to vasospasm. Monitoring systemic hemodynamics and intracranial dynamics simultaneously assists in prevention, prompt recognition, and effective treatment of neurological deterioration.

Cerebral vasospasm after subarachnoid hemorrhage.

To summarize new pathophysiologic insights and recent advances in the diagnosis and treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Important, newly recognized mediators of cerebral arterial spasm after subarachnoid hemorrhage include superoxide free radicals, ferrous hemoglobin (which acts as a nitric oxide scavenger), endothelins, protein kinase C, and rho kinase. Microvascular dysfunction and autoregulatory failure also has been an area of increasing research focus in recent years. New diagnostic modalities include measures of cerebral blood flow such as single-photon emission computed tomography and perfusion computed tomography, magnetic resonance imaging, intracranial brain oxygen tension probes, and jugular venous oxygen saturation monitors. Proton magnetic resonance spectroscopy and microdialysis can detect tissue biochemical abnormalities, but these techniques have not found their way into routine clinical practice as of yet. In addition to nimodipine and hypertensive hypervolemic therapy, promising new treatments for vasospasm or its ischemic complications include magnesium sulfate, fasudil hydrochloride, tirilazad mesylate, erythropoietin, and induced hypothermia. Balloon angioplasty has emerged as the primary weapon for treating medically refractory ischemia from vasospasm and in many centers is being used as a first-line treatment or even prophylactically. The neurointensive care management of vasospasm after subarachnoid hemorrhage has evolved significantly over the past 10 years, with many new diagnostic modalities and promising treatments now available. Clinical trials are needed to evaluate the efficacy of these new techniques and to further define the optimal management of this often devastating complication.

Risk of hemorrhage from unsecured, unruptured aneurysms during and after hypertensive hypervolemic therapy.

Hypertensive hypervolemic therapy for vasospasm is widely practiced. It is not clear, however, whether the use of hypertension and hypervolemia as a treatment for vasospasm risks hemorrhage from an unsecured, unruptured aneurysm. From 1991 to 2000, the neurovascular unit at the Massachusetts General Hospital treated 1908 aneurysms, of which 966 were ruptured. Forty patients with ruptured aneurysms had unsecured, unruptured aneurysms and underwent hypertensive hypervolemic therapy for vasospasm. Hypertension was induced by intravenously administered phenylephrine, norepinephrine, and/or dopamine, and hypervolemia was achieved by intravenously administered crystalloid and colloid solutions. The 24-hour mean arterial systolic blood pressure (SBP) and the 24-hour mean central venous pressure were calculated on the basis of hourly measurements during hypertensive hypervolemic treatment. The 40 study patients harbored 124 aneurysms, of which 51 aneurysms were treated (clipping, 37; coiling, 14) by the time hypertensive hypervolemic therapy began, leaving 73 unsecured aneurysms at risk. The mean size of the unsecured aneurysms was 4.45 mm. Nineteen patients were treated with mild hypertension (SBP, 140-180 mmHg), 12 patients were treated with moderate hypertension (SBP, 180-200 mmHg), and 9 patients were treated with severe hypertension (SBP, >200 mmHg). The 24-hour mean SBP readings were 166.81 +/- 8.19, 187.57 +/- 5.79, and 204.01 +/- 3.75 mmHg for the mild, moderate, and severe hypertension groups, respectively. The mean central venous pressure was 10.43 +/- 3.89 mmHg. The mean course of hypertensive hypervolemic therapy was 7.25 days, and therapy began on mean post-subarachnoid hemorrhage Day 6.73. Twenty-eight aneurysms were eventually treated in later procedures (clipping, 25; coiling, 3). The mean interval to treatment was 6.93 months. In a treatment and follow-up period of 121.75 aneurysm-years of risk, there was no instance of hemorrhage. Hypertension and hypervolemia do not seem to increase the risk of hemorrhage from unsecured, unruptured aneurysms in the acute setting or in their short-term natural history.

Risk of Hemorrhage from Unsecured, Unruptured Aneurysms during and after Hypertensive Hypervolemic Therapy

Risk of Hemorrhage from Unsecured, Unruptured Aneurysms during and after Hypertensive Hypervolemic Therapy

Therapeutic aspects of brain tissue pO2 monitoring after subarachnoid hemorrhage.

Prolonged phases of brain tissue hypoxia (ptiO2 < 10 mmHg) lead to cerebral infarction. Therefore, the present study investigates the role of ptiO2--monitoring to guide hypervolemic hypertensive therapy in patients suffering from severe subarachnoid hemorrhage (SAH). Besides transcranial doppler, neuromonitoring of ICP/CPP was supplemented by ptiO2 monitoring. The ptiO2 catheter was inserted into viable tissue in the vascular territory with the highest risk for vasospasm. Patients were divided in an infarction (n = 21) and a non-infarction group (n = 11). Critical CPP (< 70 mmHg) as well as hypoxic ptiO2 (< 10 mmHg) was significantly more frequent in the infarction group (CPP: 25 vs 13%, p < 0.001; ptiO2: 16 vs 7%, p < 0.001). In both groups, over 25% of the critical ptiO2 values occurred at a CPP > 90 mmHg. In the infarction group, 13 patients showed transient phases of hypoxia which normalized under induced hypervolemic hypertension and 5 patients developed persistent hypoxia. In the non-infarction group 6 patients showed transient hypoxia and in 5 patients no hypoxic values could be found. In conclusion, monitoring of ptiO2 provides an additional independent parameter to detect hypoxic events and to guide therapy.

702 Risk of Hemorrhage from Unsecured Unruptured Aneurysms during and after Hypertensive Hypervolemic Therapy

702 Risk of Hemorrhage from Unsecured Unruptured Aneurysms during and after Hypertensive Hypervolemic Therapy

702 Risk of Hemorrhage from Unsecured Unruptured Aneurysms during and after Hypertensive Hypervolemic Therapy

702 Risk of Hemorrhage from Unsecured Unruptured Aneurysms during and after Hypertensive Hypervolemic Therapy

Current intensive care management proposals after aneurysmal subarachnoid hemorrhage

Aneurysmal subarachnoid (SAH) is a serious disease associated with considerable mortality and morbidity: it accounts for 6–10% of all strokes and 22–25% of cerebrovascular deaths (46). The most common causes of death or disability include direct effect of initial bleed and rebleeding (5). Subsequent causes of death include vasospasm (43), hydrocephalus, and surgical and medical complications of SAH treatment. After surgery patients remain at risk of developing secondary neurologic deficits and medical complications for at least 2 to 3 weeks. During this period patients are closely monitored for early detection of onset of delayed ischemic symptoms. As no good evidence exists to support hypertensive and hemodilution therapy to prevent vasospasm, the initial goal should be oriented to maintain euvolemia, considering that patients potentially have pronounced negative fluid balance and then considerable maintenance fluids and sodium must be substituted. However, if symptoms of delayed cerebral ischemia appear, the goals of treatment are immediately converted to hypertensive hypervolemic and hemodilution therapy. Oral, when possible, otherwise intravenous Nimodipine is recommended, its dosage must be adapted to maintain the desired blood pressure.

Complications Associated with Intraarteriul Administration of Papaverine for Vasospusm Following Subarachnoid Hemorrhage. Two Case Reports.

Complications associated with intraarterial papaverine infusion occurred in two patients treated for vasospasm due to subarachnoid hemorrhage (SAH). A 42-year-old male with an anterior communicating artery aneurysm underwent craniotomy and aneurysm clipping. Five days after the SAH occurred, angiography demonstrated moderate vasospasm in spite of hypervolemic-hypertensive therapy. During papaverine infusion into the carotid artery, he suffered loss of consciousness due to a seizure for a few minutes. A 61-year-old female with a right internal carotid-posterior communicating artery aneurysm underwent clipping. Six days after the SAH occurred, angiography demonstrated severe vasospasm in spite of hypervolemic-hypertensive therapy. Angiography performed immediately after papaverine infusion into the carotid artery revealed exacerbation of the vasospasm. Finally she suffered cerebral infarction and died. Complications of intraarterial papaverine infusion are potentially dangerous. We recommend trial administration of papaverine with angiography and neurological examination before full dose infusion to avoid complications.

Should endovascular therapy for cerebral vasospasm coincide with hypervolemic-hypertensive therapy (HT) in aneurysmal subarachnoid hemorrhage (SAH)?

In patients suffering from SAH, cerebral vasospasm is a major cause of morbidity and mortality from multifocal cerebral infaretion. Hypervolemic-hypertensive therapy is considered the cornerstone of the medical management and generally the first line approach. The therapeutic role of intra-arterial infusion of papaverine and balloon angioplasty has been established as an alternative therapy. The timing of neuroradiological intervention is unknown.

Severe thrombocytopenia following intraarterial papaverine administration for the treatment of vasospasm

Selective intraarterial infusion of papaverine is used in the treatment of symptomatic cerebral vasospasm. The authors report two episodes of severe thrombocytopenia in a patient that were related to intraarterial administration of papaverine. A 70-year-old man with a right internal carotid artery aneurysm underwent craniotomy and aneurysm clipping. He became lethargic 8 days after the hemorrhage occurred. Cerebral angiography revealed moderate vasospasm. In addition to hypervolemic-hypertensive therapy, the patient was treated on two occasions with intraarterial administration of papaverine. Within 24 hours of both treatments he developed severe thrombocytopenia. On one occasion epistaxis requiring transfusion of blood products occurred. Laboratory data support the diagnosis of immune-mediated papaverine-induced thrombocytopenia. The authors conclude that intraarterial administration of papaverine for treatment of vasospasm can be associated with severe, rapidly reversible thrombocytopenia.

Medical complications of aneurysmal subarachnoid hemorrhage

This report examines the frequency, type, and prognostic factors of medical (nonneurologic) complications after subarachnoid hemorrhage in a large, prospective study. The influences of contemporary neurosurgical, neurological, and critical care practice on mortality and morbidity rates after aneurysmal subarachnoid hemorrhage are evaluated. A study of medical complications observed in the placebo limb of a large, randomized, controlled trial of the calcium antagonist, nicardipine, after subarachnoid hemorrhage. Patients were recruited from 50 hospitals in 41 neurosurgical centers in the United States and Canada. A total of 457 patients with subarachnoid hemorrhage, > or = 18 yrs of age, were randomly assigned to the placebo group. All patients arrived at the participating center within 7 days (mean 1.0 +/- 1.8 [SD] days) of rupture of an angiographically documented saccular aneurysm. The frequency rates of symptomatic vasospasm, rebleeding, and total mortality rate after subarachnoid hemorrhage at 3-month follow-up were 46%, 7%, and 19%, respectively. The frequency of having at least one severe (life-threatening) medical complication was 40%. The proportion of deaths from medical complications was 23%. This value was comparable with the proportion of deaths attributed to the direct effects of the initial hemorrhage (19%), rebleeding (22%), and vasospasm (23%) after aneurysmal rupture. The frequency of life-threatening cardiac arrhythmias was 5%; less ominous rhythm disturbances occurred in 30% of the patients. There was an increased frequency of cardiac arrhythmias on the day of, or day after, aneurysm surgery. Pulmonary edema occurred in 23% of the patients, with a 6% occurrence rate incidence of severe pulmonary edema. There was a wide variation from center to center, with the greatest frequency on days 3 through 7. There was a nonsignificant association of pulmonary edema with the use of hypertensive hypervolemic therapy (p = .10), and a significant association with the timing of surgery (p < .05). Some degree of hepatic dysfunction was noted in 24% of patients, the majority with only mild abnormalities of hepatic enzymes with no clinical accompaniment (4% frequency of severe hepatic dysfunction). Thrombocytopenia occurred in 4% of patients, usually in the setting of sepsis. Renal dysfunction was reported in 7% of the patients, with 15% of that figure deemed to be of life-threatening severity. There was an association (p = .001) with antibiotic therapy. Potentially preventable medical complications after ruptured cerebral aneurysm add to the total mortality rate of patients, and may increase length of hospital stay in the critical care setting. The proportion of deaths after subarachnoid hemorrhage from medical complications equals those deaths from either direct effects, rebleeding, or vasospasm individually. Pulmonary complications are the most common nonneurologic cause of death. Cardiac arrhythmia, although frequent, was not associated with significant mortality. The frequency of cardiac arrhythmia and pulmonary edema increased on the day of, or day after, aneurysm surgery. Renal and hepatic dysfunction, and blood dyscrasias, were also observed, underscoring the need for meticulous monitoring for metabolic and hematologic derangements.

Angioplasty for the treatment of symptomatic vasospasm following subarachnoid hemorrhage

Angioplasty of narrowed cerebral arteries was performed in 10 patients who became symptomatic from vasospasm following subarachnoid hemorrhage. This procedure was accomplished with a microballoon catheter via percutaneous transfemoral insertion. Patients were selected for treatment if they had delayed neurological deficits due to vasospasm which were not responsive to hypervolemic hypertensive therapy. Eight patients (80%) showed sustained improvement in neurological function following the procedure. In two patients transcranial Doppler ultrasound recordings were obtained which revealed decreased mean blood flow velocities following angioplasty. Two patients died, one from an aneurysmal rebleed, and one secondary to diffuse vasospasm. There was one case of delayed stroke 6 weeks following the procedure. The overall results of this series indicate that in selected cases percutaneous balloon angioplasty can offer marked improvement to patients with ischemic deficits due to vasospasm following subarachnoid hemorrhage.

Early aneurysm surgery and prophylactic hypervolemic hypertensive therapy for the treatment of aneurysmal subarachnoid hemorrhage.

The prevailing sentiment of North American neurosurgeons is that there is no significant difference in overall morbidity between patients who are treated with early aneurysm surgery and those who are treated with delayed aneurysm surgery. This concept is based primarily on the high incidence of ischemic events after early intervention. Recent experience, however, indicates that prophylactic hypervolemic hypertensive therapy may be beneficial in reducing delayed ischemia after early aneurysm surgery. During the preceding 21 months, we have performed 125 operations for intracranial aneurysms. Fifty-six patients in this group presented less than 7 days after subarachnoid hemorrhage (SAH) (47 within 3 days) and were treated by a prospective protocol of urgent aneurysm surgery performed within 24 hours after presentation. In all cases, the aneurysm was clipped with the use of mannitol and spinal drainage for brain relaxation. All patients were then treated with prophylactic volume expansion therapy and induced hypertension with a central venous pressure or a Swan-Ganz catheter until the 14th day after SAH. Preoperatively, 17 patients were Hunt and Hess Grade I, 9 were Grade II, 28 were Grade III, and 2 were Grade IV. In this group of 56 patients at risk for delayed ischemia from vasospasm, 5 patients had significant intraoperative complications. Ten patients (18%) had delayed cerebral ischemia, totally reversible in 6 cases, with small infarcts in 3 cases, and with 1 death (2% mortality from delayed ischemia), there were 5 cases of shunted hydrocephalus, and 3 deaths from other complications. Overall, 41 patients (73%) returned to their premorbid occupations without neurological deficit.(ABSTRACT TRUNCATED AT 250 WORDS)