Functional outcome after repair of unruptured intracranial aneurysms.

OBJECT: Repair of unruptured aneurysms is a reasonable course of action if their expected natural history is worse than the predicted risks of treatment. The purpose of this study was to examine the presenting symptoms of unruptured aneurysms and to test the hypothesis that unruptured intracranial aneurysms can be repaired without significant functional worsening. A second hypothesis was also examined--that is, that the experience of the surgeon, the aneurysm size, and the patient age can be used to predict functional outcome. METHODS: Consecutive patients who underwent repair of an unruptured intracranial aneurysm at a single institution between 1980 and 1998 were studied. Clinical and radiographic data were collected in all patients. Their modified Rankin Scale (mRS) score was determined before treatment (baseline), at 6 weeks, and at 6 months. The primary endpoint for analysis was the mRS score. Four hundred forty-nine aneurysms were repaired in 366 patients by 10 surgeons. The mean size of the primary lesion repaired was 14.6 + 10.4 mm and 27% were judged to be symptomatic. Aneurysm treatment involved either microsurgical clipping (78%), wrapping (4%), trapping with or without bypass (5%), hunterian ligation with or without bypass (9%), or other methods (4%). The mRS scores at 6 weeks were worse than at baseline (p < 0.0001), but there was no significant difference between the baseline and 6-month mRS score. At 6 months, 94% of patients showed no significant functional worsening as a result of treatment. The number of aneurysms treated by a specific surgeon was a strong predictor of better functional outcome (r = 0.99, p = 0.05). Increasing patient age (r = 0.16, p = 0.003) and increasing aneurysm size (r = 0.15, p = 0.004) were predictors of worsened functional outcome. CONCLUSIONS: Many unruptured aneurysms produce symptoms. Unruptured intracranial aneurysms can be treated without significant permanent functional worsening. The surgeon's experience, aneurysm size, and patient age are predictors of functional outcome.

Nuances of middle cerebral artery aneurysm microsurgery.

Middle cerebral artery aneurysms, a common source of subarachnoid hemorrhage, occur predominantly at the main bifurcation of the middle cerebral artery. Microsurgical clipping is the most effective treatment of these aneurysms because of their peripheral location, wide necks, and straightforward surgical anatomy. Despite the moderate technical requirements of this type of surgery, patients with ruptured aneurysms often have poor outcomes because of the high incidence of intracerebral hematomas. Although several different surgical approaches can be used, we favor a lateral-to-medial transsylvian approach for most aneurysms. This description of our surgical technique stresses minimizing retraction to avoid injury to the brain and preparing broad-based middle cerebral artery aneurysms for clipping. Management of outcomes when using these techniques also is presented.

Inflammation and intracranial aneurysms.

OBJECTIVE: An intracranial aneurysm is an important acquired cerebrovascular disease that can cause a catastrophic subarachnoid hemorrhage. Despite modern therapy, most patients die or are left disabled as a direct result of a severe initial hemorrhage. The development of more effective treatment strategies depends on understanding the fundamental biology of cerebral aneurysms. The purpose of the present study is to determine whether inflammation or immunological reaction occurs in cerebral aneurysms. METHODS: Aneurysm tissue was collected at the time of microsurgical repair from 23 unruptured and 2 ruptured aneurysms (25 patients) and compared with 11 control basilar arteries harvested at autopsy. Immunohistochemistry was used to localize complement (C3c, C9), immunoglobulins (IgG, IgM), vascular cell adhesion molecule-1, macrophages and monocytes (CD68), T lymphocytes (CD3), and B lymphocytes (CD20). RESULTS: Complement (C3c, P < 0.0001; C9, P = 0.0017), immunoglobulin (IgG, P = 0.0013; IgM, P = 0.031), vascular cell adhesion molecule-1 (P = 0.0022), macrophages (CD68, P = 0.004), and T lymphocytes (CD3, P = 0.0004) were all frequently present in the wall of aneurysm tissue but were rarely identified in control basilar arteries. A few B lymphocytes (CD20, P = 0.41) were found in aneurysm tissue, but none were found in the basilar arteries. CONCLUSION: Extensive inflammatory and immunological reactions are common in unruptured intracranial aneurysms and may be related to aneurysm formation and rupture.

Detachable balloon embolization: concomitant use of a second safety balloon.

We describe a relatively unusual case of carotid cavernous fistula in association with a persistent trigeminal artery, presumably related to aneurysm rupture near the carotid origin of the vessel. We emphasize the use of a second, nondetachable balloon solely for the purpose of stabilizing placement of the first device at the time of detachment.

Cortical NOS inhibition raises the lower limit of cerebral blood flow-arterial pressure autoregulation.

The maintenance of constant cerebral blood flow (CBF) as arterial blood pressure is reduced, commonly referred to as CBF-pressure autoregulation, is typically characterized by a plateau until the vasodilatory capacity is exhausted at the lower limit, after which flow falls linearly with pressure. We investigated the effect of cortical, as opposed to systemic, nitric oxide synthase (NOS) inhibition on the lower limit of CBF-pressure autoregulation. Forty-four Sprague-Dawley rats were anesthetized with halothane and N2O in O2. With a closed cranial window placed the previous day in a ventilated and physiologically stable preparation, we determined the CBF using laser-Doppler flowmetry. Animals with low reactivity to inhaled CO2 and suffused ADP or ACh were excluded. Five arterial pressures from 100 to 40 mmHg were obtained with controlled hemorrhagic hypotension under cortical suffusion with artificial cerebrospinal fluid (aCSF) and then again after suffusion for 35 (n = 5) and 105 min (n = 10) with aCSF, 10(-3) M Nomega-nitro-L-arginine (L-NNA; n = 12), or 10(-3) M Nomega-nitro-D-arginine (D-NNA; n = 5). An additional group (n = 7) was studied after a 105-min suffusion of L-NNA followed by a single blood withdrawal procedure. The lower limit of autoregulation was identified visually by four blinded reviewers as a change in the slope of the five-point plot of CBF vs. mean arterial blood pressure. The lower limit of 90 +/- 4.3 mmHg after 105 min of 1 mM L-NNA suffusion was increased compared with the value in the time-control group of 75 +/- 5.3 mmHg (P < 0.01; ANOVA) and the initial value of 67 +/- 3.7 mmHg (P < 0.001). The lower limit of 84 +/- 5.9 mmHg in seven animals with 105 min of suffusion of 1 mM L-NNA without previous blood withdrawal was significantly increased (P < 0.01) in comparison with 70 +/- 1.9 mmHg from those with just aCSF suffusion (n = 37). No changes in lower limit for the other agents or conditions, including 105 or 35 min of aCSF or 35 min of L-NNA suffusion, were detected. The lack of effect on the lower limit with D-NNA suffusion suggests an enzymatic mechanism, and the lengthy L-NNA exposure of 105 min, but not 35 min, suggests inhibition of a diffusionally distant NOS source that mediates autoregulation. Thus cortical suffusion of L-NNA raises the lower limit of autoregulation, strongly suggesting that nitric oxide is at least one of the vasodilators active during hypotension as arterial pressure is reduced from normal.

The ciliospinal reflex in pentobarbital coma.

OBJECT: This study was conducted to delineate the ciliospinal reflex (CSR), which is defined as pupillary dilation caused by a noxious stimulus to the face or head. The authors anecdotally observed that patients in a pentobarbital coma have a CSR that can mimic pathological conditions. A pentobarbital coma obscures the results of the neurological examination in patients with potentially life-threatening cerebral edema; pupil size and reactivity are the only readily monitored signs. Any condition that incorrectly suggests evolving intracranial pathological processes can lead to unnecessary clinical actions. METHODS: The authors evaluated six consecutive patients in the neurointensive care unit in whom a pentobarbital coma had been induced, documenting the presence and duration of the CSR. The CSR was always bilateral and symmetrical, manifesting as enlarged (6-8 mm), seemingly nonreactive pupils continuing from 1 to 6 minutes and was usually seen after routine nursing maneuvers. The pupils appeared nonreactive to short flashes of direct light but did react if longer flashes were used. CONCLUSIONS: Recognition of the CSR can potentially lead to reduction of unnecessary transportation and complicating medical interventions in critically neurologically ill patients in whom a pentobarbital coma has been induced.

Vascular extracellular matrix remodeling in cerebral aneurysms.

OBJECT: The occurrence of cerebral aneurysms has been linked to alterations in the extracellular matrix and to matrix-degrading proteases. The purpose of the present study was to determine whether active extracellular matrix remodeling occurs within cerebral aneurysms. METHODS: Aneurysm tissue was collected from 23 patients (two of whom had a ruptured aneurysm and 21 of whom had an unruptured aneurysm) and compared with 11 control basilar arteries harvested at autopsy. Active proteinases capable of gelatin lysis were identified by performing in situ zymography in the presence and absence of a metalloproteinase inhibitor (ethylenediamine tetraacetic acid) and a serine proteinase inhibitor (phenylmethylsulfonyl fluoride). Immunohistochemical analysis was used to localize plasmin, tissue-type (t)-plasminogen activator (PA), urokinase-type (u)-PA, membranetype (MT1)-matrix metalloproteinase (MMP), MMP-2, MMP-9, and tenascin. Focal areas of gelatin lysis occurred in most cerebral aneurysm tissue samples (17 of 21), but rarely in control arteries (two of 11) (p = 0.002). Both serine proteinases and MMPs contributed to gelatin lysis; however, the MMPs were the predominant enzyme family. Plasmin (p = 0.04) and MT1-MMP (p = 0.04) were expressed in the aneurysm tissue but were unusual in control tissue. The MMP-2 was also expressed more commonly in aneurysm than in control tissue (p = 0.07). The MMP-9 and t-PA were expressed in both groups; however, different staining patterns were observed between aneurysm and control tissue. Tenascin staining was commonly present in both groups, whereas u-PA staining was rarely present. CONCLUSIONS: Aneurysm tissue demonstrates increased proteolytic activity capable of lysing gelatin and increased expression of plasmin, MT1-MMP, and MMP-2 when compared with normal cerebral arteries. This activity may contribute to focal degradation of the vascular extracellular matrix and may be related to aneurysm formation and growth.

Identification of a serum gelatinase associated with the occurrence of cerebral aneurysms as pro-matrix metalloproteinase-2.

BACKGROUND AND PURPOSE: Subarachnoid hemorrhage from intracranial aneurysm rupture produces a severe form of stroke. Extracellular matrix remodeling is associated with cerebral aneurysms and may play a role in the formation or rupture of these lesions. We previously reported a 3-fold increase in a 72-kDa serum gelatinase in a subgroup of aneurysm patients. The purpose of the present study was to further characterize and identify this gelatinase. METHODS: Serum samples were collected from surgical patients with intracranial aneurysms. The following series of experiments was designed to further characterize and identify the predominant serum gelatinase found in the subgroup of patients with increased gelatinase activity. Gelatin zymography was performed on native serum samples and compared with serum that had been pretreated with a known metalloproteinase activator (4-aminophenylmercuric acetate [APMA]). Gelatin zymography was repeated in the presence of a matrix metalloproteinase (MMP) inhibitor (EDTA) and a serine proteinase inhibitor (phenylmethylsulfonyl fluoride [PMSF]). Final identification was made by Western blotting with the use of monoclonal antibodies to MMP-2 and MMP-9. RESULTS: A consistent gelatinolytic band (72 kDa) was identified in all serum samples (n = 60). Pretreatment of the serum by APMA (n = 60) lowered the molecular weight of the band to 66 kDa. The band was inhibited by EDTA (n = 10) but not PMSF (n = 10), thus characterizing the circulating 72-kDa gelatinase as an inactive pro-MMP. Western blotting (n=20) identified the 72-kDa band as MMP-2. CONCLUSIONS: These findings confirm that the increased gelatinolytic activity observed in vitro in a subset of cerebral aneurysm patients is due to pro-MMP-2.

Increasing hospital admission rates for intracerebral hemorrhage during the last decade.

BACKGROUND: The incidence and mortality of all types of strokes, including intracerebral hemorrhages, declined during the 1970s. However, some evidence exists that these trends stabilized or reversed during the 1980s. In the present study, a large North American population was observed from 1981 to 1989 to assess changes in the annual hospital admission rates of intracerebral hemorrhage. METHOD: Data provided by the Connecticut Health Information Management and Exchange (CHIME, Wallingford, Connecticut), a state-wide clinical database of records submitted voluntarily by all of Connecticut's 36 acute care, nongovernment hospitals, was analyzed for all patients with primary diagnosis of intracerebral hemorrhage (ICD-9-CM=431) for the fiscal years 1981, 1983, 1985, 1987, 1988, and 1989. RESULTS: During the time periods studied, there were 3,277 hospitalizations with a primary diagnosis of intracerebral hemorrhage. There was an initial annual hospital admission rate of 12 per 100,000 in 1981. Rates steadily increased to nearly 20 per 10,000 in 1988 and 1989. This increase in hospital admission rates from intracerebral hemorrhage was statistically significant when the data were adjusted for gender, race, and age (P<.001). When admission rates for intracerebral hemorrhage were stratified by age, admission rates increased dramatically only in those 65 years and older (P<.001). The in-hospital death rate decreased during the study decade (P=.004); however, age-adjusted analysis indicated that in-hospital deaths increased significantly (P<.001) in patients 65 years and older. CONCLUSIONS: Hospital admission rates for intracerebral hemorrhage nearly doubled from 1981 to 1989. This change may be due to an actual increase in the annual incidence of intracerebral hemorrhage caused by mechanisms that are not yet fully understood.

Rare lesions of the posterior fossa with initial retrocochlear auditory and vestibular complaints.

OBJECTIVE: To catalog a series of rare lesions of the posterior fossa that appeared with unusual initial retrocochlear symptoms and signs and to make the reader more aware of these unusual lesions with a view to improving initial assessment and treatment planning. STUDY DESIGN: The study was a retrospective case review of seven patients. SETTING: Multidisciplinary team evaluation in a tertiary hospital referral center. PATIENTS: Patients with unusual lesions of the cerebellopontine angle and posterior fossa with initial retrocochlear symptoms and signs were included. INTERVENTIONS: Diagnostic and therapeutic. MAIN OUTCOME MEASURES: Hearing preservation and balance function. RESULTS: The rare lesions presented include two aneurysms of the anterior inferior cerebellar artery, one giant basilar artery aneurysm, and one each of the following neoplasms: endodermal cyst, choroid plexus papilloma, cavernous angioma, and ependymoma. CONCLUSIONS: A close working relationship among the otolaryngologist, neurotologist, neurosurgeon, and neuroradiologist is necessary to accurately evaluate these unusual cerebellopontine angle lesions and effect the best treatment outcome.

Gelatinase activity and the occurrence of cerebral aneurysms.

BACKGROUND AND PURPOSE: Cerebral aneurysms are associated with decreased arterial collagen content; however, whether this deficiency results from impaired collagen synthesis or enhanced collagen degradation is unknown. This study tested the hypothesis that enhanced collagen degradation, not impaired collagen synthesis, is associated with the occurrence of cerebral aneurysms. METHODS: Cultured skin fibroblasts and serum samples were studied in patients with angiographic evidence of aneurysm (n = 31) and control subjects (n = 14). Transcription of the type III collagen gene was assessed with the use of Northern blots prepared from RNA harvested from confluent cultured fibroblasts. Translation of type III collagen was assessed by Western blot analysis of proteins produced by cultured skin fibroblasts. Collagen metabolism was assessed by radioimmunoassay for type I (PICP) and type III (PIIINP) procollagen peptides in conditioned tissue culture media and serum. We assessed collagen degradation in serum and conditioned tissue culture media by evaluating gelatinase activity using quantitative zymography. RESULTS: Type III collagen synthesis was the same in aneurysm and control patients. Neither the molecular weight nor the relative amount of type III collagen mRNA differed between aneurysm and control patient fibroblasts. Western blot analysis revealed no difference in the relative amount or molecular weight of procollagen III synthesized by aneurysm and control cells. Aneurysm patients had a threefold increase in native serum gelatinase activity compared with control subjects (P = .004). This increase occurred along with serum evidence of increased collagen metabolism. Serum levels of PICP (P = .03) and PIIINP (P = .02) were decreased in aneurysm patients. Elevated serum gelatinase activity and altered collagen metabolism could not be explained by enhanced secretion of gelatinase by cultured fibroblasts or altered net collagen synthesis by fibroblasts. High serum gelatinase activity was more common in men than in women (P = .04). CONCLUSIONS: These findings are consistent with the hypothesis that accelerated enzymatic degradation of collagens and other structural proteins compromises the mechanical integrity of the cerebral vessel wall and leads to conditions that favor aneurysm formation.

Prevention of chronic cerebral vasospasm in dogs with milrinone.

OBJECTIVE: Delayed cerebral ischemia resulting from vasospasm is a major cause of morbidity and death in patients with aneurysmal subarachnoid hemorrhage. Milrinone, because it inhibits Type IV cyclic adenosine monophosphate-specific phosphodiesterase enzyme in both cardiac and vascular smooth muscle, is a powerful inotrope and vasodilator, but it has little effect on heart rate or blood pressure. Because of these properties, milrinone is an attractive potential therapy after subarachnoid hemorrhage. The purpose of the present study was to investigate the effect of milrinone on chronic experimental cerebral vasospasm. METHODS: A double-hemorrhage canine model of vasospasm was used to study the efficacy of milrinone. Angiographic vasospasm and systemic hemodynamics were compared in a treatment group of animals that received a loading dose of milrinone (0.05 mg/kg, intravenously) and then slow-release (0.05 microgram/kg/min) milrinone pellets (n = 10) and a control group that received placebo pellets (n = 9), over an 8-day period after the initial subarachnoid hemorrhage. The hemorrhage was created by injection of 4 ml of autologous, nonheparinized, arterial blood into the cisterna magna on Days 1 and 3. Hemodynamic measurements, including cardiac output determinations, were made on Days 0, 1, 3, 6, and 8 with a pulmonary artery catheter, and angiographic vasospasm was assessed on Day 8 by comparison with baseline angiograms. RESULTS: Treatment with milrinone caused no significant changes in systemic hemodynamics. Angiographic vasospasm, however, was significantly reduced in the Day 8 angiograms for the treated group, compared with the control group (98.28 +/- 14.06 and 67.89 +/- 13.06% of original vessel cross-sectional area, respectively; P < 0.001). CONCLUSION: Milrinone is effective in preventing chronic cerebral vasospasm in a canine model of experimental chronic cerebral vasospasm. This effect is independent of changes in systemic hemodynamics. Milrinone and related drugs warrant further investigation for the treatment of cerebral vasospasm.

Specific repression of the preproendothelin-1 gene in intracranial arteriovenous malformations.

Cerebrovascular arteriovenous malformations (AVMs) display abnormal vascular development and dysautoregulation of blood flow. Genetic mechanisms that contribute to the pathogenesis and phenotype of cerebral AVMs are unknown. As a first step in understanding the pathophysiology of AVMs, the authors investigated the hypothesis that endothelial dysfunction-specifically, deregulation of endothelin-1 (ET-1) secretion-contributes to the abnormal vascular phenotype and the lack of hemodynamic autoregulation elaborated by these lesions. Endothelin-1 peptide and preproendothelin-1 (ppET1) messenger RNA were not detected in the intranidal vasculature of all 17 patients with AVMs studied, but were prominently expressed in human control subjects with normal cerebrovasculature (p < 0.01). Although AVM vasculature lacked ET-1, its expression was prominent in vasculature distant from these lesions, suggesting local repression of the ppET-1 gene. Local repression of ET-1 was specific to AVMs; ET-1 in vascular malformations of patients with Sturge-Weber disease was actually elevated compared to normal controls (p < 0.01). Repression of the ppET-1 gene was an intrinsic phenotype of AVM endothelial cells and was not due to factors in the AVM microenvironment. The authors also showed that ETA receptor expression was low in AVM vasculature compared to normal controls. Together, these results demonstrate that the ppET-1 gene is locally repressed in AVM lesions and suggest a role for abnormal ppET-1 gene regulation in the pathogenesis and clinical sequelae of cerebral AVMs.

Normal pressure perfusion breakthrough after resection of arteriovenous malformation.

UNLABELLED: Objectives. The syndrome of normal pressure perfusion breakthrough (NPPB) follows the surgical resection of a small fraction of cerebral arteriovenous malformations (AVM). Although intraoperative hyperemia occurs in NPPB, the relationship and temporal profile of vasomotor paralysis to NPPB are unknown. In the present study, serial transcranial Doppler (TCD) studies (static and stress) were correlated with clinic observations to determine the relationship and temporal profile of vasomotor paralysis to NPPB. Methods. Thirty-five patients underwent complete AVM removal with preservation of the normal arteries and veins. Serial TCD examinations were performed under static and stress conditions (CO(2), Diamox, or blood pressure challenge). Vasomotor paralysis was considered present when CO(2) or Diamox challenge produced less than a 10% change in flow velocity or when flow velocity changed with blood pressure over physiological ranges. Results. Two of 35 patients (6%) developed NPPB immediately after AVM resection. Results of TCD studies were consistent with vasomotor paralysis. NPPB and vasomotor paralysis abated together in both patients on postoperative day 3 to 4. In one patient, NPPB and vasomotor paralysis reoccurred on postoperative day 8 after liberalization of blood pressure control. CONCLUSIONS: NPPB occurs in a small fraction of patients after AVM resection. The occurrence of NPPB correlates with vasomotor paralysis, and both are present immediately postoperatively and last several days. Improving vasomotor tone and clinical condition do not imply complete normalization of the cerebral circulation because NPPB and vasomotor paralysis can reoccur after liberalization of blood pressure control.

Is image subtraction necessary in the clinical interpretation of single-day split-dose stress cerebral perfusion single-photon emission tomography using technetium-99m compounds?

The aim of this study was to validate a simplified semiquantitative method of evaluating a single-day stress cerebral perfusion test to obtain cerebrovascular reserve capacity (CVRC) for routine clinical uses. A split-dose protocol was tested in 36 pairs of technetium-99m hexamethylpropylene amino oxime baseline (low dose) and acetazolamide (high dose) stress brain single-photon emission tomographic (SPET) studies from 16 patients with cerebrovascular disease. The images were displayed on a semiquantitative color scale with (corrected) and without (uncorrected) image subtraction, dose adjustment, and decay correction. The representative CVRC was determined by placing 3x3 pixel regions of interest on midthalamic and midcerebellar slices. The corrected and uncorrected relative changes in CVRC were correlated using linear regression. The relative changes of corrected (x) and uncorrected (y) CVRC by quantitative analysis were highly correlated in a linear fashion (y=0.67x+0.002, r=0.998, P<0.0005). As predicted by theory, the slope was related to the ratio of split dose and independent of ROI sampling. Single-day split-dose stress brain SPET can be accurately performed without image subtraction and complicated dose adjustment or decay correction for clinical studies.

Sex differences in the management of patients hospitalized with ischemic cerebrovascular disease.

BACKGROUND AND PURPOSE: Previous studies suggest that the management of coronary artery disease differs for women compared with men. We examined this issue for ischemic cerebrovascular disease. METHODS: We reviewed the use of angiography and carotid endarterectomy among patients discharged from Connecticut hospitals during 6 years over the past decade. Crude and age-adjusted rates of angiography and endarterectomy were determined for each sex. RESULTS: Among 22,582 female and 19,729 male patients discharged, the rate of cerebral angiography was 11.8% for men and 7.2% for women; the age-adjusted odds ratio was 0.77 (95% confidence interval [CI], 0.72 to 0.82). The rate of endarterectomy was 10.6% for men and 5.7% for women; the age-adjusted odds ratio was 0.67 (95% CI, 0.62 to 0.72). The distribution of cerebrovascular disease type differed by sex, however, with carotid artery disease representing a larger proportion of men (12.2% [2415/19,729]) than women (6.9% [1554/22,582]) (chi 2 = 355.8, P < .0001). When restricted to this diagnosis, no sex differences exist (odds ratio for angiography, 1.00 [95% CI, 0.87 to 1.14] and for endarterectomy, 0.93 [95% CI, 0.81 to 1.07]). CONCLUSIONS: Overall, women hospitalized for ischemic cerebrovascular disease undergo fewer angiograms and are less likely to have carotid endarterectomy than men. These differences are not found when analysis is restricted to subjects with carotid disease and suggest that part of the difference in management may be due to biological differences between men and women.

Seasonal fluctuation in the incidence of intracranial aneurysm rupture and its relationship to changing climatic conditions.

Seasonal and climatic variations have been linked to the occurrence of some types of cerebrovascular disease; however, the conditions that lead to intracranial aneurysm rupture are not known. The purpose of the present study was to determine whether seasonal and climatic conditions are related to intracranial aneurysm rupture. Data provided by the Connecticut Health Information Management and Exchange were analyzed for all patients with a primary diagnosis of aneurysmal subarachnoid hemorrhage (SAH) for the fiscal years 1981, 1983, 1985, 1987, 1988, and 1989. Patient records were correlated with climatic conditions for the years 1981 to 1989 obtained from the National Climatic Data Center, National Oceanic and Atmospheric Administration, National Environmental Satellite Data, and Information Service. During the time periods studied, 1487 patients with a primary diagnosis of aneurysmal SAH were treated by reporting hospitals. Seasonal variation in the incidence of aneurysmal SAH and admission clustering were observed but differed significantly between men and women. Men showed a single large peak in late fall (Roger's r = 11.5, p < 0.005), whereas women had an annual peak occurring in late spring (Roger's r = 10.3, p < 0.01). Substantial climatic change occurred during the 72 hours prior to 10 of the 14 clusters of men who were admitted (p < 0.01, Yates' corrected chi-square 7.33, df = 1). In contrast, clusters of women admitted were not related to preceding climatic change (p > 0.25, Yates' corrected chi-square 0.06, df = 1). Hospital admissions for aneurysmal SAH display seasonal fluctuation, with women showing a different seasonal pattern from men. Changing climatic conditions precede aneurysm rupture in men but not in women, which suggests that weather is causally related to aneurysm rupture in men, and that factors that lead to aneurysm rupture in women may be different from those in men. These data do not explain why weather fronts or gradients are associated with aneurysm rupture in men.

Exposure rates to patients' blood for surgical personnel.

BACKGROUND: Surgical personnel are at risk of contracting blood-borne diseases through exposure to patients' blood. Exposure rates for each surgical subspecialty have not been previously reported. The purpose of this study was to determine the rates of exposure to patients' blood for operating room personnel. METHODS: The study was conducted at Yale-New Haven Hospital, a level I trauma center and tertiary care hospital. During a 3-month period, exposed personnel were interviewed by a study nurse immediately after a cutaneous exposure to blood or after a sharp injury. RESULTS: During 2292 surgical procedures, 70 sharp injuries and 168 cutaneous exposures to blood were reported. The combined exposure rate (skin contact and sharp injury) was 10.4 per 100 procedures (95% confidence interval, 9.1 to 11.6) and ranged from 21.2 for general surgery to 3.3 for pediatric surgery (goodness-of-fit chi-squared, p < 0.001). The combined exposure rates were also significantly different among types of surgery and ranged from 18 for laparotomies to 4.3 for craniotomies (chi-squared, p < 0.001). The overall sharp injury rate was 3.1 per 100 procedures (95% confidence interval, 2.3 to 3.8) and ranged from 4.3 for general surgery to 1.3 for vascular surgery. CONCLUSIONS: The rate of exposure to blood for operating room personnel, which differ from prior studies, was 10.4 per 100 procedures and was highest for general surgical procedures. The differences in rates among studies might be attributable to different surgical technique, dissimilar case-mix, or different research methods relating to definition or ascertainment of exposure.