Subarachnoid haemorrhage of unknown aetiology

Summary The authors review the literature on subarachnoid haemorrhage of unknown aetiology (SAHUE) and analyze a personal series of 212 patients diagnosed as SAHUE. These patients represent 30% of all cases of primary SAH admitted over a 14.5 year period.The age, sex, antecedents and initial clinical presentation of patients with SAHUE were indistinguishable from those of patients with subarachnoid haemorrhage due to ruptured aneurysm (SAHRA). However, the present series of SAHUE compare favourably with both a personal and a previously reported series of SAHRA insofar as clinical grade on admission (94% of patients in grades I–II of Botterell), presence of blood on CT (51%), vasospasm (5%), ischaemic deficits (3.3%), persistent hydrocephalus (3.5%), rebleeding (6%) and fatal result (3.9%) are concerned.The amount of blood on CT scan in our patients with SAHUE was associated with a significantly higher incidence of brain ischaemia and hydrocephalus but did not correlate with the Botterell grade on admission or final outcome, which were good in the majority of cases regardless of the presence or not of visible cisternal haemorrhage. The results of the present series confirm that the final prognosis of patients with primary SAH showing normal four-vessel cerebral angiography is essentially favourable.     

血浆ET-1和CGRP含量测定对脑出血病人的应用价值

目的 :探讨血浆内皮素 (ET)和降钙素基因相关肽 (CGRP)在脑出血病人急性期与恢复期中的变化。方法 :采用放射免疫分析技术 ,对 4 2例脑出血病人的急性期与恢复期 ,分别测定血浆ET和CGRP含量 ,并用 35例健康对照人员作比较。结果 :脑出血病人血浆ET含量明显高于对照组 (p <0 0 1) ,治疗后有所下降 ;而血浆CGRP含量 ,在脑出血的急性期 ,显著高于对照组 (p <0 0 1) ,恢复期降为正常。结论 :血浆ET和CGRP在脑出血的急性期显著升高 ,并与脑损伤程度有关 ,提示神经肽参与出血性脑损伤的发生发展过程     

Baroreflex control of jejunal blood flow and fluid transport in cats; effects of yohimbine,an α.-adrenergic antagonist

The aim of the study was to test the hypothesis that baroreceptor unloading increases jejunal fluid absorption rate via an α₂-adrenergic effect on electrogenic active transport. In 13 chloralose-anaesthetized cats, the carotid sinus baroreceptors were isolated and perfused with arterial blood, and we studied the effects of a graded decrease in carotid sinus pressure on intestinal vascular resistance, net fluid absorption rate and the potential difference between the intestinal lumen and the peritoneal cavity (PD). Experiments were performed in seven control animals and in six animals pretreated with yohimbine, an α₂-adrenergic antagonist, at a dose of 0.1 mg kg^-I i.v. Yohimbine per se had no significant effects on systemic arterial pressure, intestinal vascular resistance, net fluid absorption rate or PD. In the control animals, baroreceptor unloading induced an increase in systemic arterial pressure, intestinal vascular resistance and net fluid absorption rate, and a decrease in the PD. Yohimbine pretreatment did not significantly affect the systemic blood pressure response to baroreceptor unloading, but abolished the effect on intestinal vascular resistance and PD. After yohimbine treatment, decreases in carotid sinus pressure still enhanced net fluid absorption rate, but this response was observed in a higher range of carotid sinus pressures than in control animals. We conclude that (1) a major component of the increase in jejunal absorption rate during baroreceptor unloading is due to a non-electrogenic mechanism, which may be either active or passive; (2) this component of the response is not blocked by yohimbine at a dose sufficient for an effect on presynaptic α₂-receptors; (3) the absorptive response to baroreceptor unloading is not a phenomenon secondary to the concomitant jejunal vasoconstriction.     

Fertility and pregnancy outcomes following hypogastric artery ligation for severe post-partum haemorrhage

BACKGROUND: Hypogastric artery ligation is a therapeutic option for severe post-partum haemorrhage. Little is known about the outcomes of subsequent fertility and pregnancy. We studied these parameters in women who required hypogastric artery ligation for severe post-partum haemorrhage in our institution over a 13-year period. METHODS: All patients who required hypogastric artery ligation for severe intractable post-partum haemorrhage from January, 1989 to April, 2001 were included. Data were retrieved from medical files and telephone interviews. RESULTS: A total of 68 patients required hypogastric artery ligation during the study period. Seventeen patients had 21 pregnancies with 13 term deliveries, two ectopic pregnancies, three miscarriages, and three abortions. Twenty-eight patients did not want a new pregnancy and one patient refused the interview. Twenty-three (34%) patients were lost to follow up. None of the patients suffered subsequent infertility and pregnancy was achieved in <12 months once planned. Pregnancy outcomes were normal. Fifty-four percent had vaginal deliveries. Three patients suffered a threatened post-partum haemorrhage that was easily treated medically. CONCLUSIONS: This is the largest reported series of pregnancies following hypogastric artery ligation. Hypogastric artery ligation for post-partum bleeding >1 l appears to be a safe procedure that does not impair subsequent fertility and pregnancy outcomes.     

Prenatal diagnosis of a complete mole coexisting with a dichorionic twin pregnancy: case report

A complete mole coexisting with dichorionic twins was diagnosed by the combined use of sonography and chorionic villus sampling at 10 weeks gestation. The pregnancy resulted in the death of one fetus at 31 weeks from presumed feto-maternal haemorrhage, while the other fetus survived in good condition. A summary of the available literature, combined with this report, reveals a total of seven pregnancies with twins and a coexistent complete mole. Only two out of 14 fetuses survived. Maternal complications included one case of pre-eclampsia and one persistent trophoblastic tumour. Accurate diagnosis of complete mole is possible by genetic analysis of chorionic villi obtained with standard transabdominal sampling. Twins with a coexistent complete mole will usually undergo miscarriage. However, fetal survival is possible and the maternal risks seem limited. A concomitance between gestational trophoblastic disease and the occurrence of feto-maternal haemorrhage is observed.     

Different roles of arteriosclerosis in the rupture of intracranial dissecting aneurysms

AIMS: Although intracranial dissecting aneurysm (IDA) is a newly described variant of the brain aneurysms that affects mainly the vertebrobasilar arterial system, its pathogenesis remains obscure. We aimed to clarify the role of arteriosclerosis in the pathogenesis of IDA based on histopathological findings in seven autopsy cases of IDA. METHODS AND RESULTS: All cases exhibited systemic hypertension or left ventricular hypertrophy. Macroscopically, all cases exhibited subarachnoid haemorrhage. Two types of dissection were recognized in the vertebral artery. Six of seven IDA cases showed a widespread disruption of the entire thickness of the arterial wall with the formation of a dilated pseudoaneurysm, which consisted of thin adventitia (arterial wall disruption type). Medial disruption of the arterial wall and subadventitial dissecting haemorrhage were also found, resulting in the formation of a false lumen and stenosis of the 'true' lumen of the artery. However, these lesions were connected to the site of rupture of the entire arterial wall. Within 1 day after onset of IDA, the autopsy cases showed formation of fibrin thrombus, marked leucocyte infiltration and necrosis of the arterial wall at the site of the lesion. Cases that survived more than 1 week showed smooth muscle cell proliferation, macrophage accumulation and lymphocytic infiltration in the lesions. These cases showed no atherosclerotic plaque, but non-atherosclerotic fibrocellular intima. The thickness of intima and media was significantly less in the vertebral artery of IDA patients than that of non-IDA patients with systemic hypertension. On the other hand, the remaining case showed severe atherosclerosis with haemorrhage into the lipid core without connection to the arterial lumen (intra-atheromatous plaque haemorrhage type). However, unusual arterioles and neovascularization of the intra-and peri-arterial walls were observed. CONCLUSIONS: Our results suggest that disruption of the entire arterial wall may be a critical event in the development of IDA and result in the medial disruption and subadventitial haemorrhage. Non-atheromatous intima might function as a protective factor in arterial wall disruption. On the other hand, atherosclerosis may predispose to intra-atheromatous plaque haemorrhage type of IDA through intramural haemorrhage originating from the newly formed vessels.     

Temporal profile of potassium channel dysfunction in cerebrovascular smooth muscle after experimental subarachnoid haemorrhage

The pathogenesis of cerebral vasospasm after subarachnoid haemorrhage (SAH) involves sustained contraction of arterial smooth muscle cells that is maximal 6–8 days after SAH. We reported that function of voltage-gated K⁺ (K_V) channels was significantly decreased during vasospasm 7 days after SAH in dogs. Since arterial constriction is regulated by membrane potential that in turn is determined predominately by K⁺ conductance, the compromised K⁺ channel dysfunction may cause vasospasm. Additional support for this hypothesis would be demonstration that K⁺ channel dysfunction is temporally coincident with vasospasm. To test this hypothesis, SAH was created using the double haemorrhage model in dogs and smooth muscle cells from the basilar artery, which develops vasospasm, were isolated 4 days (early vasospasm), 7 days (during vasospasm) and 21 days (after vasospasm) after SAH and studied using patch-clamp electrophysiology. We investigated the two main K⁺ channels (K_V and large-conductance voltage/Ca²⁺-activated (K_Ca) channels). Electrophysiologic function of K_Ca channels was preserved at all times after SAH. In contrast, function of K_V channels was significantly decreased at all times after SAH. The decrease in cell size and degree of K_V channel dysfunction was maximal 7 days after SAH. The results suggest that K_V channel dysfunction either only partially contributes to vasospasm after SAH or that compensatory mechanisms develop that lead to resolution of vasospasm before K_V channels recover their function.     

Maternal death associated with ovum donation twin pregnancy.

A case of maternal death due to sub-arachnoid haemorrhage in an ovum donation twin pregnancy complicated by hypertension is described. Attention is drawn to a forecasted increase in maternal morbidity and mortality in in-vitro fertilization (IVF) pregnancies, which occur in older women and are often multiple.     

Prevention of cerebral vasospasm with OKY-046 an imidazole derivative and a thromboxane synthetase inhibitor. A preliminary co-operative clinical study

Summary The prevention of cerebral vasospasm with OKY-046, an imidazole derivative and a thromboxane synthetase inhibitor, was studied co-operatively at ten neurosurgical services. Intravenous administrations of 2, 5 or 10 /kg/minute of OKY-046 were given continuously from the earliest possible day to the 14th SAH-day to 82 pateints with ruptured cerebral aneurysm. Sixty-eight patients (83%) showed moderate to high high-density (SAH) in their initial CTs. Angiographic vasospasms were seen in 58 patients, representing 71% of all cases or 81% of the 72 cases for which angiograms were available; the vasospasms of 45 patients (55 or 63%) were moderate to severe. Symptomatic vasospasm occurred, however, only in 27 patients (33%); in 18 of those cases, moreover, the symptoms were mild or transient. The conditions of the patients at one month after the SAH were classified into 9 grades from 0 (normal) to 8 (deceased). Fifty-two patients (63%) were classified as 0 or 1, and 64 (78%) as better than 3 (possible daily life unaided). The administration of OKY-046 was proven to decrease TXB₂ in the blood.This paper emphasizes the effectiveness of the drug for symptomatic vasospasm, and supports our previous contention that cerebral microthrombosis may play an important role in the pathogenesis of cerebral vasospasm.