Reduction of pulmonary edema after SAH with a pulmonary artery catheter-guided hemodynamic management protocol

Introduction: The frequency of pulmonary edema, which occurs with high frequency following subarachnoid hemorrhage (SAH), can be worsened by hypervolemic, hypertensive, hemodilution therapy for vasospasm. This study compares the complication rates for patients with SAH before and after institution of a pulmonary artery catheter-guided hemodynamic management protocol. Methods: Complication and outcome data were prospectively collected on 453 patients with spontaneous SAH. The patients were divided into groups treated from July 1998 through January 2000 (n=174) and from February 2002 through June 2002 (n=279). In group I, treatment consisted of hypervolemia (central venous pressures: >8 mmHg) and hypertension (mean arterial pressure: 110–130 mmHg). In group II, normovolemia was the goal, defined using a pulmonary artery catheter (wedge pressure: 10–14 mmHg). Cardiac output was enhanced (index: >4.5 L/minute/m2), and blood pressure elevations were moderated (mean pressure: >100 mmHg). Results: The average age, comorbidity, hemorrhage severity, and incidence of vasospasm were almost identical between the two groups. Statistically significant reductions were noted in patients in group II for two types of complications as well as for mortality. The rate of pulmonary edema (from 14 to 6%) and the rate of sepsis (from 14 to 6%) were both decreased (p≤0.03). Mortality decreased from 34 to 29% (p=0.04). Other complications, such as myocardial infarction, were not affected. Conclusions: These data show that a significant reduction in the frequency of pulmonary edema after SAH can be attained using a pulmonary artery catheter-guided hemodynamic management protocol.     

Combined extracranial and intracranial atherosclerosis in Korean patients

OBJECTIVES: To evaluate the frequency of intracranial atherosclerosis among patients with steno-occlusive extracranial carotid artery disease and to determine if there are factors related to the combined intracranial atherosclerosis. DESIGN: Cross-sectional study. SETTING: A tertiary referral hospital.Patients We studied 142 consecutive patients who had atherosclerotic steno-occlusive lesions (defined as > or =30% narrowing of the luminal diameter or occlusion) of an extracranial carotid artery confirmed by conventional angiography. We excluded patients who had potential cardiogenic sources of embolism. Potential vascular risk factors for each patient were obtained from medical records.Main Outcome Measure We determined the location and severity of atherosclerotic lesions by conventional angiography. We compared the vascular risk factors between patients with steno-occlusive extracranial carotid artery disease alone and patients with combined intracranial atherosclerosis and extracranial carotid artery disease. RESULTS: Intracranial steno-occlusive lesions (> or =30% stenosis or occlusion) were found in 80 patients (56.3%). Of 121 patients with significant (> or =50% stenosis or occlusion) extracranial carotid artery disease, 58 (47.9%) also had significant lesions of intracranial arteries. Univariate and multivariate analyses showed that diabetes mellitus was the only significant factor associated with combined intracranial atherosclerosis in patients with extracranial carotid artery disease. CONCLUSIONS: Intracranial atherosclerosis is common in Korean patients with steno-occlusive extracranial carotid artery disease. Diabetes mellitus is associated with intracranial atherosclerosis in patients who had steno-occlusive extracranial carotid artery disease.     

Neurogenic pulmonary edema during intracranial endovascular therapy

Neurogenic pulmonary edema (NPE) is a well-known complication of acute brain injury. Neurogenic stunned myocardium (NSM) occurs clinically in a significant subset of patients with NPE. A 49-year-old woman developed refractory cerebral vasospasm requiring angioplasty following a subarachnoid hemorrhage. During angioplasty, NPE with NSM manifested as acute pulmonary edema associated with elevated pulmonary artery occlusion pressure and reduced cardiac output. Evaluations disclosed a right insular infarction, cardiac wall motion abnormalities, and electrocardiographic characteristics of NSM. The NSM completely resolved, and the neurological outcome was good. A 56-year-old woman developed NPE during complicated coil embolization of an internal carotid artery aneurysm. Cardiac function was normal, and the NPE resolved with a brief period of mechanical ventilation and diuresis. The delayed appearance of NSM and NPE during endovascular therapy in these patients implies a degree of risk for sympathetically mediated cardiopulmonary dysfunction during complex intracranial endovascular procedures.     

三种方法制作大鼠蛛网膜下腔出血模型

目的探讨三种方法制作大鼠蛛网膜下腔出血(SAH)模型的应用价值。方法分别采用颈内动脉穿刺法(PIC)、枕大池2次注血法(ACM)和交叉前池注血法(APC)制作大鼠SAH模型。观察不同模型的病死率、蛛网膜下腔血液分布及含量、脑血管痉挛程度及持续时间、伴发脑水肿、血-脑屏障(BBB)通透性等方面的改变。结果三种方法均成功制作SAH模型。病死率:PIC为46.2%,ACM为25.0%,APC为11.1%。血管痉挛高峰时间:PIC与APC均为第2天,第3～5天恢复正常;ACM为第5天,持续7 d。蛛网膜下腔血液量:ACM为(240.50±25.38)lμ,APC为(172.15±25.45)μl;PIC模型变异大,为60～520 lμ,平均(267.12±45.86)μl。PIC模型脑水肿最重,ACM与APC模型脑水肿相对较轻。PIC模型造成严重的BBB通透性损害,另两组损害程度相近。结论三种方法制成的模型适用于研究SAH不同病理生理改变的需要。PIC脑水肿重,病死率高,适用于SAH后脑损害的机制研究;ACM脑血管痉挛的时间特征与人SAH后血管痉挛接近,适用于血管痉挛的机制研究;APC血液恒定分布于前循环,病死率低,...     

氢气盐水治疗迟发性脑血管痉挛实验研究

目的研究饱和氢气盐水对脑血管痉挛其及缺血性脑损害的治疗作用。方法 70只新西兰兔随机分为3组,分别为假手术组(n=10)、生理盐水组(n=30)和氢水治疗组(n=30)。于建模后第3 d、第5 d和第7 d处死动物,脑组织切片后行苏木精-伊红(HE)染色及末端脱氧核苷酸转移酶介导的生物素脱氧尿嘧啶核苷酸缺口末端标记法(TUNEL)染色,观察基底动脉直径及海马神经元凋亡情况。结果氢水治疗组与生理盐水组比较,仅在第5 d氢气治疗可明显减少海马神经元的凋亡(P=0.039),其他各组数据均无统计学差异。结论饱和氢气盐水注射不能显著改善蛛网膜下腔出血后的血管痉挛,但能减轻痉挛高峰期的缺血性脑损害。     

Transiente kortikale Blindheit bei EPH-Gestose infolge zerebraler Vasospasmen

The pathogenesis of cortical blindness as a rare complication in severe preeclampsia is still unclear. The case of a women with postpartum blindness is reported in which CT and MRI initially showed cortical and subcortical edema in the parieto-occipital lobes. At this time cerebral angiography and transcranial color-coded sonography (TCCS) revealed widespread cerebral vasospasm. Mean blood flow velocities in the middle and posterior cerebral artery and carotid syphon initially reached 380 cm/s and normalized within 2 weeks. While the patient's vision improved rapidly, follow-up MRI disclosed ischemic lesions and petechial hemorrhage in the occipital cortex. This case provides rare documentation that transient blindness in patients with preeclampsia may result from parieto-occipital ischemia due to cerebral vasospasm. In such patients TCCS may be useful to detect vasospasm associated with preeclampsia/eclampsia.     

Experimental model of symptomatic vasospasm in rabbits

The common carotid arteries were ligated bilaterally 2 weeks before induction of subarachnoid hemorrhage in rabbits. The rabbits were observed closely for clinical symptoms, and angiographic and pathologic investigations were performed. Thirteen experimental rabbits showed a progressing neurologic deficit that was worst on the fourth or fifth day after the subarachnoid hemorrhage. This symptomatic change did not occur in five rabbits without previous carotid ligation. Presumably, the rabbits with carotid ligation became symptomatic because they no longer had a collateral blood flow to compensate for the reduced blood flow in the basilar artery after subarachnoid hemorrhage. Our model of symptomatic vasospasm after subarachnoid hemorrhage may be beneficial for future studies.     

Cilostazol attenuates cerebral vasospasm after experimental subarachnoid hemorrhage

Abstract

Background and purpose: Cerebral vasospasm is a major cause of morbidity and mortality in patients with subarachnoid hemorrhage (SAH). Cilostazol, a selective inhibitor of phosphodiesterase 3, is a peripheral vasodilator, an anti-inflammatory, and causes antiplatelet aggregation. We investigated these effects on cerebral vasospasm after rat SAH.

Methods: Thirty-eight Sprague–Dawley rats were randomly divided into three groups: SAH + normal feed (SAH group; n=14), SAH + feed containing 0·1% cilostazol (cilostazol group; n=12) and sham-operated rats (sham group; n=12). The basilar arteries (BA) of all groups were analysed by measuring wall thickness, internal luminal perimeter and cross-sectional area on day 7. Immunohistochemical study with RM-4, an anti-rat macrophage/dendritic cells monoclonal antibody and ultrastructural study with transmission electron microscopy were performed.

Results: Although most animals in the SAH group presented with typical vasospasm, the means of inner perimeter and cross-section area of the BA in the cilostazol group were significantly greater than the SAH group (836 ± 134 μm versus 771 ± 125 μm and 39177 ± 15405 μm² versus 33098 ± 13871 μm², respectively). Wall thickness of the BA in the cilostazol group demonstrated significant decrease, compared with the SAH group (17·4 ± 2·3 versus 21·0 ± 2·7 μm). In immunohistological study, SAH induced an obvious increase in mean perivascular RM-4-positive cell count, whereas cilostazol significantly reduced it by 59%. Ultrastructural study depicted cilostazol markedly attenuating structural deterioration of the vascular wall due to SAH.

Conclusions: This work demonstrates that cilostazol attenuates cerebral vasospasm after SAH in rat, possibly in part due to the anti-inflammatory effect.     

Anti-apoptotic and neuroprotective effects of Tetramethylpyrazine following subarachnoid hemorrhage in rats

This study was designed to explore the effects of Tetramethylpyrazine on cerebral vasospasm and early brain injury and its underlying mechanisms after experimental SAH in rats. Male Sprague-Dawley rats (n=164) were allocated randomly to SAH+TMP, SAH+vehicle (sodium chloride), or sham-operated group. The SAH model was induced through perforating internal carotid artery. TMP (30 mg/kg) or the vehicle was injected via vena caudalis 60 min before the perforation. Mortality, neurological scores, water content of brain and cerebral vasospasm were recorded at 24 h after SAH. Apoptosis of cerebral cortex was determined by TUNEL staining; caspase-3, bax and bcl-2 by Western blotting; P53 expression by immunohistochemical staining. TMP administrated in advance improved neurological scores, ameliorated cerebral edema and cerebral vasospasm. TUNEL-positive cells were reduced significantly in TMP-treated group. P53 was not found significantly different between TMP-treated and vehicle-treated group, while P53 positive cells were markedly higher in SAH group than that in sham-operated group. Cleaved caspase-3 protein was decreased significantly in TMP-treated group, while bax, bcl-2 protein expression did not differ statistically among the three groups. In conclusion, TMP ameliorated cerebral vasospasm and early brain injury after experimental SAH in rats. The underlying mechanisms may be partly related to inhibition of caspase-3 dependent proapoptosis pathway.     

Adult onset moyamoya disease: institutional experience

Moyamoya disease is a progressive steno-occlusive disease of bilateral carotid forks with the formation of fine collateral vascular network and is an angiographic diagnosis. We analyzed case records of 11 patients with "adult-onset moyamoya disease." Six patients presented with intracranial hemorrhage (intracerebral and/or intraventricular) and 5 with focal ischemia. Angiography revealed bilateral Internal carotid artery involvement in 8 patients and unilateral involvement in 3. Posterior cerebral artery involvement was seen in 3 patients. Saccular aneurysm involving posterior circulation was seen in only 1 patient. Although rare, adult-onset moyamoya disease should be considered as one of the causes for intracerebral and intraventricular hemorrhage in adults.     

Vasogenic Edema of the Basal Ganglia after Intra-Arterial Administration of Nimodipine for Treatment of Vasospasm

The intra-arterial administration of nimodipine (IAN) is commonly used for cerebral vasospasm refractory to medical treatments. We report two cases of vasogenic edema after IAN. Our patients with aneurismal subarachnoid hemorrhage presented with vasospasm, which was treated by IAN. Consequently, vasogenic edema developed in the basal ganglia. Reperfusion following IAN for vasospasm may have the potential for inciting vasogenic edema in the ischemic brain.     

兔症状性脑血管痉挛模型的改进

目的完善单侧兔颈总动脉结扎后枕大池二次注血法致症状性脑血管痉挛（CVS）动物模型的血管形态学研究。方法实验兔随机分为单侧颈总动脉结扎后枕大池二次注血组（S-SAH组）与单纯枕大池二次注血组（SAH组）,每组各10只。比较两组神经功能改变,并分别于注血前、注血后（d1,d5）行基底动脉脑血管造影。结果各组均出现神经功能障碍,两组d5发生CVS数量与注血前比较均有显著性差异（P〈0.05）;各组同时间段CVS程度无显著差异（P〉0.05）。结论单侧兔颈总动脉结扎后枕大池二次注血法制作CVS动物模型方法可行,模型稳定,改良制作方法有助于提高成功率。     

颈内动脉狭窄程度和血流速度与颈内动脉支架置入术后高灌注损伤的相关性研究

目的 探讨颈内动脉狭窄程度和血流速度与颈内动脉支架置入术后高灌注损伤的相关性。方法 选取2014年1月-2019年2月本院收治的298例颈内动脉狭窄患者为研究对象,全部患者采取颈内动脉支架置入术治疗,根据术后是否发生高灌注脑出血将其分为高灌注脑出血组(观察组,n=8)与未发生高灌注脑出血组(对照组,n=290); 采用改良RANKIN量表(mRS评分)评估2组受试者手术前、手术30 d后残疾程度,分别于手术前、手术后3 d采用彩色多普勒超声测定2组受试者患侧颈内动脉狭窄程度及血流速度,应用经颅多普勒TCD测定2组受试者患侧大脑中动脉血流速度; 采用NIHSS评分评估2组受试者手术前、手术30 d后神经功能缺损程度,采用LOGSTIC多元回归分析颈内动脉支架置入术后高灌注脑出血的影响因素。结果 观察组手术30 d后mRS评分高于对照组(P<0.05); 观察组手术前患侧颈内动脉狭窄程度高于对照组(P<0.05); 观察组手术前患侧大脑中动脉动脉血流速度(Vm)低于对照组(P<0.05); 观察组手术30 d后NIHSS评分高于对照组(P<0.05); Logistic多因素回归分析显示,颈内动脉支架置入术后高灌注脑出血与术前颈内动脉狭窄程度、血流速度、术后3 d患侧大脑中动脉血流速度(Vm)呈正相关(P<0.05),与术前患侧大脑中动脉血流速度(Vm)呈负相关(P<0.05)。结论 颈内动脉狭窄程度和血流速度是颈内动脉支架置入术后发生高灌注脑出血的独立影响因素。     

Cerebral hemodynamics and metabolism in postoperative cerebral vasospasm and treatment with hypertensive therapy

A 24-year-old woman developed subarachnoid hemorrhage from an aneurysm at the bifurcation of the right internal carotid artery. Following successful clipping of the aneurysm she developed a left hemiplegia associated with focal cerebral vasospasm, which markedly improved when systemic blood flow and oxygen utilization were significantly depressed in both cerebral hemispheres, while blood volume was significantly elevated only on the side with vasospasm. Oxygen extraction was significantly elevated in both hemispheres, indicating a generalized impairment in oxygen delivery to the brain.     

A 70-year-old woman with poor grade subarachnoid hemorrhage complicated by carotid stenosis, cerebral vasospasm, and cerebral rebleed

Introduction: Subarachnoid hemorrhage is one of the most common entities encountered in neurocritical care units. Knowledge of disease sequelae and their management is paramount for all neurointensivists. Materials and Methods: This study relates the case of a 70-year-old woman with poor grade subarachnoid hemorrhage who underwent endovascular detachable coil embolization of a right internal carotid artery aneurysm. Her hospital course was subsequently complicated by symptomatic carotid stenosis and cerebral vasospasm requiring intervention. Discussion: The discussants present their views regarding five main questions pertaining to management of the patient regarding the choice of endovascular versus surgical aneurysm occlusion, stent-supported angioplasty in a patient with a recent subarachnoid hemorrhage, and treatment options for vasospasm.     

Nonenzymatic derived lipid peroxide, 8-iso-PGF2α, participates in the pathogenesis of delayed cerebral vasospasm in a canine SAH model

Abstract

We studied whether 8-iso-PGF_2α, nonenzymatic arachidonyl peroxide, participated in the pathogenesis of delayed vasospasm using a canine subarachnoid hemorrhage (SAH) model. Fourteen adult mongrel dogs were divided into two groups, two-hemorrhage SAH group (n = 8) and control group (n = 6). The contents of 8-iso-PGF _2α in CSF, the basilar artery segment, and subarachnoid clot were measured by enzyme immunoassay kit. The CSF 8-iso-PGF_2α content on Day 7 in the SAH group was 67.9 ± 29.9 pg ml^-1 (n = 8), which was significantly higher than 27.1 ± 13.8 (n = 8) on Day 0 in the SAH group, and 33.2 ± 14.4 pg ml^-1 (n = 5) on Day 7 in the control group. The 8-iso-PGF_2α content in the basilar artery segment with spasm on Day 7 in the SAH group was 13.5 ± 1.9 pg mg^-1 wet weight (n = 8), significantly higher than 8.7 ± 1.9 (n = 6) in the control group. The 8-iso-PGF_2α content in subarachnoid clot was 1.7 ± 1.4 ng g^-1 wet weight (n = 8). Significant elevation of the 8-iso-PGF_2α contents in the CSF and the basilar artery segment occurred on Day 7 in the SAH group. The subarachnoid clot enclosed the basilar artery on Day 7, contained a considerable amount of 8-iso-PGF_2α. These results suggested that 8-iso-PGF_2α could play a crucial role in the pathogenesis of the delayed cerebral vasospasm. [Neurol Res 2002; 24: 301-306]     

Myocardial damage (myocytolysis) caused by subarachnoid hemorrhage

A case of subarachnoid hemorrhage complicated by neurogenic pulmonary edema and neurogenic myocardial damage is reported. A 50-year-old woman was admitted following the sudden onset of headache and disturbance of consciousness due to a ruptured internal carotid posterior communicating artery aneurysm on the right side. She showed respiratory failure due to pulmonary edema, which subsequently improved with the mechanical ventilation. After that, she manifested chest distress and hypotensive episode then occurred. An ECG showed QS wave and ST elevation which suggested the presence of inferolateral myocardial damage. Subsequent rises in serum GOT, GPT, LDH and CPK were noticed. CPK-MB and LDH I and V isozyme levels rose. An echo cardiogram showed hypokinesis of the apical half of the left ventricular septum. The patient died on 5th hospital day due to rerupture of the cerebral aneurysm. Autopsy revealed diffuse myocytolysis with coagulation necrosis of the heart muscle without occlusion of coronary arteries. A small hemorrhagic lesion was found in the hypothalamus. We suggested that a hypothalamic lesion due to subarachnoid hemorrhage stimulated the sympathetic nervous system which in turn discharged endogenic catecholamine. This was probably accompanied by vasospasm of the coronary arteries and systemic peripheral arterioles. Furthermore, myocardial oxygen consumption could have been increased by the increase in catecholamine. Finally, it gave rise to neurogenic pulmonary edema and extensive diffuse myocytolysis of the heart occurred.     

First emerging objective experimental evidence of hearing impairment following subarachnoid haemorrhage; Felix culpa,phonophobia, and elucidation of the role of trigeminal ganglion

Objective: The exact mechanism of phonophobia induced by subarachnoid hemorrhage (SAH) has not been understood well. This subject was investigated.

Material and methods: This study was conducted on 25 rabbits. They divided into three groups: Five as control, five as SHAM, 20 as SAH group. All animals objected to 85?dB impulse noise by daily periods, and their phonophobic score values were examined by daily periods for 20 days. Their brains, trigeminal ganglia were extracted bilaterally. The normal and degenerated neuron densities of trigeminal ganglia were examined by stereological methods and compared with phonophobia scores.

Results: Phonophobic score was 19-17, mean live neuron density (LND) of the trigeminal ganglia was 16.321?±?2.430/mm³, and degenerated neuron density (DND) was 1.15?±?0.120/mm³ in animals of control groups (n?=?5). The phonophobic score was 17-14, LND: 14.345?±?1.913/mm³, DND of the trigeminal ganglia was 1.150?±?0.110/mm³ in SHAM group (n?=?5). The phonophobic score was 14-8, LND: 12.987?±?1.966/mm³, mean DND of the trigeminal ganglia was 2.520?±?510/mm³ in animals with high phonophobia scores (n?=?6). The phonophobic score was 7-4, LND: 9.122?±?1.006, mean DND of the trigeminal ganglia was 5.820?±?1.610/mm³, in animals with fever phonophobia scores (n?=?9).

Conclusion: An inverse relationship between DND trigeminal ganglion (TGG) and phonopobic score was found. The paralysis of tensor tympani muscle owing to trigeminal ganglia ischemia may be responsible for phonophobic clinical state in animals with SAH. In addition, there seems to be an important concern for the verbal component of GCS in SAH. These two important findings have not been published previously.     

The effects of endothelin antagonist BQ-610 on cerebral vascular wall following experimental subarachnoid hemorrhage and cerebral vasospasm

Abstract. Endothelin, a potent vasoconstrictor, has been found to increase in the cerebrospinal fluid and serum of patients following subarachnoid hemorrhage (SAH) and to play a major role in the development of cerebral vasospasm. The aim of this study is to investigate the role of endothelin-A antagonist BQ-610 in the experimentally performed cerebral vasospasm following SAH. Thirty New Zealand rabbits were divided into three groups (each n = 10): group A, control group; Group B, SAH group; Group C, treatment (endothelin antagonist BQ-610 treated) group. In the study, the rabbits developed vasospasm after injection of intracisternal autolog blood into the cisterna magna. After cerebral vasospasm development, in group C, endothelin antagonist BQ-610 was injected intracisternally. Morphometrically, basilar artery lumen was constricted 25% and 62% compared to the control group (group A) in the endothelin treated group (group C) and the endothelin untreated group (group B), respectively. Histopathological findings of the basilar artery wall confirmed the therapeutic effect of endothelin antagonist in vasospasm development. Endothelin-A receptor antagonist BQ-610 has a therapeutic effect in the cerebral vasospasm following experimentally performed subarachnoid hemorrhage when used intracisternally.     

Transcranial Doppler in cerebrovascular disease

Doppler analysis of flow in intracranial arteries is now possible using a 2 MHz probe allowing sufficient penetration of bone to obtain signals noninvasively. Thirty-two normal subjects, and 11 patients with cerebrovascular diseases including vasospasm following subarachnoid hemorrhage, middle cerebral artery stenosis, and extracranial internal carotid artery stenosis were studied by transcranial Doppler. Increased peak velocity and spectral broadening of the reflected signal corresponded to clinical and angiographic evidence of middle cerebral artery vasospasm or stenosis. Decreased peak velocity and blunted waveforms occurred in the middle cerebral artery ipsilateral to severe extracranial internal carotid stenosis with poor crossfilling from the contralateral carotid artery. Abnormalities resolved following carotid endarterectomy. Transcranial Doppler identifies vasospasm or stenosis of the middle cerebral artery and may allow noninvasive evaluation of collateral flow across the anterior circle of Willis in patients with extracranial carotid artery stenosis.