Characteristics of aneurysmal subarachnoid hemorrhage associated with rheumatic disease

Neurosurgical Review - Spontaneous subarachnoid hemorrhage (SAH) occurs due to intracranial aneurysm rupture in most cases. Rheumatic disease may cause vessel wall inflammation, which can increase...     

Two cases of transient left ventricular apical ballooning syndrome associated with subarachnoid hemorrhage

Electrocardiogram (ECG) abnormalities secondary to subarachnoid hemorrhage are well known, but the etiology remains unclear. Transient left ventricular apical ballooning syndrome is characterized by acute onset myocardial infarction-like symptoms, transient (reversible) cardiac dysfunction, and shapes resembling ampulla on left ventriculography. We managed general anesthesia for two patients with transient left ventricular apical ballooning and ECG abnormalities associated with subarachnoid hemorrhage. During anesthesia, their hemodynamic status was almost stable although their cardiac performance analyzed by transthoracic echocardiography and transesophageal cardiography was poor. Anesthetic management of this syndrome may be simplified if less cardiosuppressive anesthetic management is used. We recommend evaluating cardiac function with transthoracic echocardiography or transesophageal cardiography when an subarachnoid hemorrhage patient has ECG abnormalities.     

A study of left ventricular rupture associated with acute myocardial infarction

A report is presented on 9 cases of left ventricular rupture associated with acute myocardial infarction experienced at Tsuchiya Hospital from January 1983 to August 1987. These cases accounted for 2.6% of the 384 cases of acute myocardial infarction admitted during the same period. Cases of cardiac rupture were classified according to clinical symptoms and hemodynamic findings obtained into three types, blow out type, subacute type, and our newly added intermediate type. In the intermediate type, there is depression of blood pressure to the level of losing consciousness but improvement of blood pressure and consciousness through medical treatment and time is available to permit surgical treatment in comparison with the blow out type. The therapeutic results were studied by the types. Among the four cases of blow out type, closure of the ventricular rupture was made under the extracorporeal circulation in one case, release of tamponade only under thoracotomy in the CCU in one case, and medical treatment only in two case, but none of the cases survived. Surgical closure of the ventricular rupture was made in all the three cases of the subacute type and all the cases are surviving. Of the two cases of the intermediate type who underwent surgical closure of the ventricular rupture, only one case could be salvaged. In examining the risk factors of cardiac rupture, a high rate of cardiac rupture was observed in initial cases of myocardial infarction without a past history of angina attack and in cases of coronary occlusion without evidence of peripheral collateral flow by emergency coronary angiography.     

Ampulla cardiomyopathy associated with aneurysmal subarachnoid hemorrhage: report of 6 patients

BACKGROUND: The authors report 6 cases of aneurysmal SAH associated with ampulla cardiomyopathy, which has been considered a unique type of stunned myocaridum. CASE DESCRIPTION: All patients were female, ranged from 35 to 79 years, and their echocardiograms revealed typical cardiac wall motions: the hypokinesia in the apical area of the left ventricle associated with the hyperkinesia in the basal area. In all, the cardiac function started to recover in the first few days; however, associated pulmonary congestions delayed aneurysmal surgeries in 3 patients. Among 3 patients whose surgeries were delayed, one died due to rerupture of aneurysm and another due to severe pneumonia. The other 4 patients recovered well, although one had left ventricular mural thrombus, which was treated successively with anticoagulant. CONCLUSIONS: It is considered highly important for neurosurgeons to be familiar with this clinical entity, since this transient cardiac function disturbance can be diagnosed at the initial presentation with a unique wall motion. The significance and clinical features of ampulla cardiomyopathy are discussed.     

An introduction to the pathophysiology of aneurysmal subarachnoid hemorrhage

Pathophysiological processes following subarachnoid hemorrhage (SAH) present survivors of the initial bleeding with a high risk of morbidity and mortality during the course of the disease. As angiographic vasospasm is strongly associated with delayed cerebral ischemia (DCI) and clinical outcome, clinical trials in the last few decades focused on prevention of these angiographic spasms. Despite all efforts, no new pharmacological agents have shown to improve patient outcome. As such, it has become clear that our understanding of the pathophysiology of SAH is incomplete and we need to reevaluate our concepts on the complex pathophysiological process following SAH. Angiographic vasospasm is probably important. However, a unifying theory for the pathophysiological changes following SAH has yet not been described. Some of these changes may be causally connected or present themselves as an epiphenomenon of an associated process. A causal connection between DCI and early brain injury (EBI) would mean that future therapies should address EBI more specifically. If the mechanisms following SAH display no causal pathophysiological connection but are rather evoked by the subarachnoid blood and its degradation production, multiple treatment strategies addressing the different pathophysiological mechanisms are required. The discrepancy between experimental and clinical SAH could be one reason for unsuccessful translational results.     

A case of aneurysmal subarachnoid hemorrhage associated with bilateral common carotid artery occlusion

Cerebral aneurysm may occur in some cases of major cerebral artery occlusion. However, according to our search of the literature, only four cases of aneurysmal subarchnoid hemorrhage (SAH) associated with bilateral common carotid artery occlusion (CCAO) have been reported in addition to the case we report here with a summary of the previously reported cases. A healthy 82-year-old female was found unconscious and admitted to our hospital where her neurological state was diagnosed as Hunt & Kosnik grade II, World Federation of Neurosurgical Societies grade II. General physical examination yielded no abnormal findings. A computed tomography (CT) scan of the head revealed a subarachnoid hemorrhage (Fisher's classification group 3). An aortogram demonstrated the presence of both vertebral arteries (VA), but the origins of the common carotid arteries (CCAS) were not visible at all. The left vertebral angiogram (VAG) revealed anastomosis between the muscle branch of the VA and the occipital artery, with retrograde blood flow through the external carotid artery supplying the internal carotid artery (ICA). These findings were also visible on the right VAG, but there was severe stenosis of the C2 portion of the right ICA. The right enlarged posterior communicating artery (Pcom) supplied the right ICA. Two saccular aneurysms arising from the junction of the right posterior cerebral artery (PCA) and the enlarged right Pcom and the P2 segment of right PCA, respectively were also observed. Aneurysm formation in this case was probably caused by hemodynamic stress secondary to bilateral CCAO induced by arteriosclerosis.     

The predictive value of serum myeloperoxidase for vasospasm in patients with aneurysmal subarachnoid hemorrhage

Vasospasm is a major contributor to morbidity and mortality in aneurysmal subarachnoid hemorrhage (SAH), with inflammation playing a key role in its pathophysiology. Myeloperoxidase (MPO), an inflammatory marker, was examined as a potential marker of vasospasm in patients with SAH. Daily serum samples from patients with aneurysmal SAH were assayed for MPO, and transcranial Doppler (TCDs) and neurological exams were assessed to determine vasospasm. Suspected vasospasm was confirmed by angiography. Peak MPO levels were then compared with timing of onset of vasospasm, based on clinical exams, TCDs and cerebral angiography. Patients with vasospasm had a mean MPO level of 115.5?ng/ml, compared to 59.4?ng/ml in those without vasospasm, 42.0?ng/ml in those with unruptured aneurysms, and 4.3?ng/ml in normal controls. In patients who experienced vasospasm, MPO was elevated above the threshold on the day of, or at any point prior to, vasospasm in 10 of 15 events (66.7%), and on the day of, or within 2?days prior to, vasospasm in 8 of 15 events (53.3%). Elevated serum MPO correlates with clinically evident vasospasm following aneurysmal SAH. The potential utility of MPO as a marker of vasospasm is discussed.     

Factors associated with the development of vasospasm after planned surgical treatment of aneurysmal subarachnoid hemorrhage

OBJECT: The goal of this study was to determine factors associated with the development of symptomatic vasospasm among patients with aneurysmal subarachnoid hemorrhage (SAH) who participated in the randomized, double-blind, placebo-controlled trials of tirilazad between 1991 and 1997. METHODS: Data obtained from 3567 patients entered into trials of tirilazad were analyzed using uni- and multivariate logistic regression to determine factors that predict the development of symptomatic vasospasm. Symptomatic vasospasm was defined by clinical criteria accompanied by laboratory- and radiologically determined exclusion of other causes of neurological deterioration. Transcranial Doppler ultrasonographic and/or angiographic confirmation was not required. In these patients, the aneurysms were scheduled to be treated surgically, and no patient undergoing endovascular treatment was included. A multivariate analysis showed that factors significantly associated with vasospasm were age 40 to 59 years, history of hypertension, worse neurological grade, thicker blood clot on the cranial computerized tomography (CT) scan obtained on hospital admission, larger aneurysm size, presence of intraventricular hemorrhage (IVH), prophylactic use of induced hypertension, and not participating in the first European tirilazad study. CONCLUSIONS: Symptomatic vasospasm was associated with the amount of SAH on the CT scan, the presence of IVH, and the patient's neurological grade. The association with patient age may reflect alterations in vessel reactivity associated with age. A history of hypertension may render the brain more susceptible to symptoms from vasospasm. The explanation for the relationships with aneurysm size, use of prophylactic induced hypertension, and the particular study is unclear.     

The role of catecholamines in the pathogenesis of neurogenic pulmonary edema associated with subarachnoid hemorrhage

Background

Neurogenic pulmonary edema (NPE) occurs frequently after aneurysmal subarachnoid hemorrhage (SAH), and excessive release of catecholamines (epinephrine/norepinephrine) has been suggested as its principal cause. The objective of this retrospective study is to evaluate the relative contribution of each catecholamine in the pathogenesis of NPE associated with SAH.

Methods

Records of 63 SAH patients (20 men/43 women) whose plasma catecholamine levels were measured within 48?h of SAH onset were reviewed, and the clinical characteristics and laboratory data of those who developed early-onset NPE were analyzed thoroughly.

Results

Seven patients (11?%) were diagnosed with NPE on admission. Demographic comparison revealed that the NPE+ group sustained more severe SAH than the NPE? group. Cardiac dysfunction was also significantly more profound in the former, and the great majority of the NPE+ group sustained concomitant cardiac wall motion abnormality. There was no significant difference in the plasma epinephrine levels between NPE+ and NPE? group (324.6?±?172.8 vs 163.1?±?257.2?pg/ml, p?=?0.11). By contrast, plasma norepinephrine levels were significantly higher in the NPE+ group (2977.6?±?2034.5 vs 847.9?±?535.6?pg/ml, p?<?0.001). Multivariate regression analysis revealed that increased norepinephrine levels were associated with NPE (OR, 1.003; 95?% CI, 1.002–1.007). Plasma epinephrine and norepinephrine levels were positively correlated (R?=?0.48, p?<?0.001). According to receiver operating characteristic curve analysis, the threshold value for plasma norepinephrine predictive of NPE was 2,000?pg/ml, with an area under the curve value of 0.85.

Conclusions

Elevated plasma norepinephrine may have more active role in the pathogenesis of SAH-induced NPE compared with epinephrine, although both catecholamines may be involved via multiple signaling pathways.     

Effects of pre-existing left ventricular hypertrophy on ventricular dysfunction and remodeling following myocardial infarction in rats.

BACKGROUND: Myocardial hypertrophy is a characteristic component of left ventricular (LV) remodeling that may, at least initially, have a beneficial effect on LV function following myocardial infarction (MI). In the present study, we examine the effects of pre-existing left ventricular hypertrophy (LVH) on LV function and chamber enlargement following MI in inbred Lewis rats. METHODS: The one-kidney, one-clip model (1K1C) of hypertension was used to produce LVH. Four weeks after 1K1C, rats were randomized to left anterior descending coronary artery ligation (LVH + MI group, n = 8) or sham ligation (LVH group, n = 11). Another group of rats underwent sham 1K1C. Four weeks later, they were randomized to coronary ligation (MI group, n = 12) or sham ligation (Sham group, n = 12). LV end-diastolic pressure (EDP, mm Hg), end-diastolic volume (EDV, ml), end-systolic volume (ESV, ml) and ejection fraction (EF) (determined by angiography) were measured in all groups 2 months after MI. RESULTS: LV EDP was 20 +/- 2 mm Hg in the LVH + MI group compared with 9 +/- 1 mm Hg in the MI group (p < 0.05). LV EDV and ESV were significantly greater with LVH + MI than with MI alone (EDV 0.90 +/- 0.03 vs 0.75 +/- 0.02 ml; ESV 0.68 +/- 0.02 vs 0.50 +/- 0.03 ml; p < 0.05). Pre-existing LVH resulted in a greater reduction in EF following MI (25 +/- 2% for LVH + MI vs 34 +/- 2% for MI alone; p < 0.05). CONCLUSIONS: Pre-existing LVH is an important determinant of progressive LV dysfunction and remodeling following MI in Lewis inbred rats.     

Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage

OBJECT: Subarachnoid hemorrhage (SAH) has been associated with cardiac injury and left ventricular (LV) dysfunction. The incidence and natural history of neurocardiogenic injury after SAH remains poorly understood. The objective of this study was to describe the incidence, time course, recovery rate, and segmental patterns of LV dysfunction after SAH. METHODS: Echocardiography was performed three times over a 7-day period in 173 patients with SAH. The incidence of global (ejection fraction [EF] < 50%) and segmental (any regional wall-motion abnormality [RWMA]) LV dysfunction was measured. The time course of LV dysfunction was determined by comparing the prevalence of LVEF less than 50% and RWMA at 0 to 2, 3 to 5, and 6 to 8 days after SAH. The recovery rate was defined as the proportion of patients with partial or complete normalization of function. The distribution of RWMAs among 16 LV segments was also determined. An LVEF less than 50% was found in 15% of patients, and 13% had an RWMA with a normal LVEF. There was a trend toward increased dysfunction at 0 to 2 days after SAH, compared with 3 to 8 days after SAH. Recovery of LV function was observed in 66% of patients. The most frequently abnormal LV segments were the basal and middle ventricular portions of the anteroseptal and anterior walls. The apex was rarely affected. CONCLUSIONS: Left ventricular systolic dysfunction occurs frequently after SAH and usually improves over time. The observed segmental patterns of LV dysfunction often do not correlate with coronary artery distributions.     

The value of computerized tomography in aneurysmal subarachnoid hemorrhage. The concept of the CT score

Of 256 patients with aneurysmal subarachnoid hemorrhage, 131 underwent computerized tomographic (CT) scanning within 7 days of the ictus. These scans were analyzed in order to assess the quantity of blood in the main subarachnoid cisterns and cerebral fissures. The method of quantification used recognized the horizontal and vertical components of the largest clot visible on the CT scan and expressed this as the "CT score." Angiographic vasospasm was assessed and graded, based on reduction in the caliber of the major cerebral vessels. The CT score was then compared to 1) the incidence of angiographic vasospasm, 2) the clinical course, and 3) the eventual outcome. Of the patients who showed no blood on the initial CT scan, 87% were admitted in good clinical grades, whereas among patients with higher CT scores the number admitted in poor clinical grades increased. The degree of angiographic vasospasm did not relate as closely as the CT score to the clinical grade on admission or to the subsequent clinical course. The final outcome was assessed on follow-up review, and those acquiring neurological deficits from ischemic neurological dysfunction (IND) were identified. Ninety percent of patients with no blood on the CT scan (CT score 0) had a good outcome, while 5% sustained the effects of IND. The incidence of IND gradually increased with a rise in the CT score until, with scores of 8 and above, 90% of patients suffered the ill effects of IND. The CT score proved to be a simple yet accurate prognostic indicator of the outcome of IND.     

The value of perfusion computed tomography in predicting clinically relevant vasospasm in patients with aneurysmal subarachnoid hemorrhage

Delayed cerebral ischemia remains a severe potential complication of aneurysmal subarachnoid hemorrhage (SAH) possibly leading to death and disability. We evaluated a semiquantitative and visual analysis of perfusion computed tomography (PCT) as a predictor of clinically relevant vasospasm (CRV) in patients with aneurysmal SAH. Thirty-eight patients with aneurysmal SAH were analyzed yielding 145 PCT scans. PCT, clinical examination, and transcranial Doppler ultrasound (TCD) were performed on days 3, 7, 10, and 14 after hemorrhage. Cerebral blood flow, cerebral blood volume, and time to peak (TTP) were analyzed semiquantitatively using six regions of interest, and visually for signs of cerebral hypoperfusion. CRV was defined as secondary cerebral infarction (CI) seen on cranial computed tomography scans and/or delayed neurological deterioration (DND). CI occurred in 13 (34.2 %) and DND in 11 patients (28.9 %). With TCD as pretest, TTP had a sensitivity of 90 % and a specificity of 72 % (cutoff value, 0.963) as predictor for CI. TTP’s sensitivity as predictor for DND was 90 % with a specificity of 61.1 % (cutoff value, 0.983). Visual analysis of TTP showed a negative predictive value of 100 % with a positive predictive value of 52 %. TTP is a sensitive and specific perfusion parameter in predicting CI in patients with SAH. Its use in the clinical setting may optimize the early treatment of patients at risk for vasospasm before the onset of clinical deterioration, especially when applying TCD as pretest. Further investigation in a larger patient population is required.     

Comparison of rapid and gradual weaning from external ventricular drainage in patients with aneurysmal subarachnoid hemorrhage: a prospective randomized trial

OBJECT: The goal of this study was to compare rapid and gradual weaning from external ventricular drainage in patients with aneurysmal subarachnoid hemorrhage (SAH) in a prospective, randomized trial. METHODS: Between December 2001 and December 2002, 81 patients with aneurysmal SAH in whom external ventricular drains (EVDs) had been placed were enrolled in the study: 41 patients were randomized to the rapidly weaned group and 40 were randomized to the gradually weaned group. The two groups were well matched with respect to age, sex, posterior aneurysm location, Fisher grade, Hunt and Hess grade, intraventricular hemorrhage on admission, and hydrocephalus on admission. Rapid weaning was defined as weaning that occurred within 24 hours with immediate closure of the EVD, whereas gradual weaning took place over a 96-hour period with daily, sequential height elevations of the EVD system followed by drain closure for 24 hours. All patients in whom EVD weaning failed underwent shunt placement. Rates of shunt implantation, days in the intensive care unit (ICU), and overall duration of hospitalization were compared. There was no significant difference in rates of shunt implantation between the rapidly weaned (63.4%) and gradually weaned (62.5%) groups. Nevertheless, patients in the gradually weaned group spent a mean of 2.8 more days in the ICU (p = 0.0002) and 2.4 more days in the hospital (p = 0.0314) than patients in the rapidly weaned group. CONCLUSIONS: Compared with rapid weaning, gradual, multistep EVD weaning provided no advantage to patients with aneurysmal SAH in preventing the need for long-term shunt placement and prolonged ICU and hospital stays.