scholarly journals A case report on the management of severe vasospasm in subarachnoid hemorrhagic patients using intra-arterial nimodipine, intrathecal sodium nitroprusside and intra-arterial papaverine

2020 ◽  
Vol 11 (4) ◽  
pp. 7334-7337
Author(s):  
Sheen Reynold ◽  
Jiya Marium George ◽  
Athul Gopan ◽  
Anila KN ◽  
Sreehari NR ◽  
...  

Management and prevention of vasospasm in subarachnoid haemorrhage are one of the complex dictums so far. Aneurysmal subarachnoid haemorrhage (aSAH) is the condition in which bleeding occurs in subarachnoid space. Vasospasm is a complex immunologically active phenomenon which requires a multimodality approach in the treatment of established vasospasm. Various treatment strategies for vasospasm and related disabilities include vasodilators such as nimodipine, sodium nitroprusside and papaverine. Intra-arterial nimodipine shows drastic improvement in several patients by resolving and preventing vasospasm. Intra-arterial administration of nimodipine can cause hypotension which can be easily managed. Papaverine is also an efficient drug-producing vasodilatory action on cerebral arteries. Papaverine is considered as the first intraarterial agent to reduce angiographic cerebral vasospasm which has the side effect of elevated intracranial pressure. Besides, the intrathecal administration of sodium nitroprusside has also demonstrated the effect in ischemic vasospasm after subarachnoid haemorrhage. Intraarterial administration of this drug can induce arterial hypotension which is not a recommended method. Vomiting is the main side effect of sodium nitroprusside, which can be managed with antiemetics such as ondansetron. Here we present a case of management of cerebral vasospasm in subarachnoid patients using the combination of these three effective drugs which showed a remarkable improvement in the resolution of aneurysmal vasospasm.

1987 ◽  
Vol 9 (3) ◽  
pp. 188-192 ◽  
Author(s):  
Robert R. Smith ◽  
Ben R. Clower ◽  
J.M. Cruse ◽  
Yutaka Honma ◽  
J.L. Haining

2016 ◽  
Vol 44 (3) ◽  
pp. 125-129 ◽  
Author(s):  
Md Nazmul Hasan ◽  
Md Azharul Hoque ◽  
Kazi Mohibur Rahman ◽  
Md Harisul Hoque ◽  
Md Rasul Amin ◽  
...  

The present study was undertaken to evaluate the morphological anatomy of cerebral vessels in patients of aneurysmal subarachnoid hemorrhage. The cross-sectional observational study was carried out in the Department of Neurology, Dhaka Medical College Hospital, Dhaka from January 2013 to June 2013. Adult patients of spontaneous subarachnoid haemorrhage (SAH), diagnosed clinically and confirmed by CT scan of the head were included in the study. However, patients who are not capable financially of undergoing Digital Subtraction Angiography (DSA), traumatic subarachnoid haemorrhage, intracerebral haemorrhage and patients taking antiplatelet and anticoagulant drugs and with comorbidities were excluded. A total of 30 subjects meeting the above eligibility criteria were selected consecutively from the study population. The present study demonstrated that 80% of the patients were 50 or younger than 50 years old (mean age 45.0 ± 9.4 years) with a male preponderance (60%). Sudden headache accompanied by vomiting was invariably complained by the patients at onset of Athe disease. On admission two-thirds (66.7%) of the patients were unconscious. 4 out of 30(16.65%) patients exhibited neurological deficit. Of the risk factors, hypertension and smoking demonstrated their significant presence (around 45%) among the patients studied. Based on Glasgow Coma Scale, 7(23.3%) patients out of 30 in the present study were in grade-v. Our data showed that the common site of aneurysm was anterior communication artery (36.7%) followed by middle cerebral artery (26.7%) and posterior communicating artery (23.3%). Saccular aneurysms formed the main bulk (93%) of the cases irrespective of anatomical distribution of aneurysm. In aneurysmal subarachnoid haemorrhage, aneurysms are mainly located in anterior communicating and middle cerebral arteries and of medium-sized. Majority are saccular type and narrow-necked.Bangladesh Med J. 2015 Sep; 44 (3): 125-129


2008 ◽  
Vol 8 (2) ◽  
pp. 177-182
Author(s):  
Kemal Dizdarević

Intracranial aneurysmal rupture is the common cause of spontaneous subarachnoid haemorrhage (SAH). This haemorrhage is typically diffuse and located in extracerebral subarachnoid space in which main cerebral arterial branches are situated. The intimate and long-term contact of arterial wall and blood products in the closed space causes the cerebral vasospasm as a serious and frequent complication of SAH. It is connected with significant morbidity and mortality due to developing of focal cerebral ischaemia and subsequently cerebral infarction. The aim of our experimental research was to create the animal model of vasospasm using the femoral artery due to examination of reduced basic dilator activity cause in arterial wall after SAH. The important characteristic of major cerebral arteries is their localization in the closed subarachnoid space which enables their to have long-term contact with blood products after haemorrhage. Thirty six femoral arteries (FA) of eighteen female rats weighing about 300 g were used. In vivo, femoral arteries are microsurgically prepared in both inguinal regions in all rats. Eighteen arteries were encompassed by polytetrafluoroethylene (PTFE) material forming closed tube and autologous blood was injected in the tube around the arterial wall. Additional eighteen arteries, as a control group, were also put in PTFE tube but without exposing to the blood. All rats are left to live for eight days. Afterwards, rats were sacrificed and their arteries were in vitro examined including an isometric tension measurement and histological changes analysis. The tension was measured during application of vasoconstrictors and vasodilatators (nitric oxide, NO). FA exposed to periadventitial blood exhibit hyper reactivity to constrictors (KCl, phenylephrine, acetylcholine) compared to control group. It was also found that NO donor (sodium nitroprusside) diminished arterial spasm induced by blood and vasoconstrictors. In conclusion, FA can be used as a model for vasospasm correlating with cerebral vasospasm after SAH and therefore this model can be utilized in future experiments assessing cerebral vasospasm. The reduced basic dilator activity of spastic femoral artery is caused by an absence of gaseous messenger NO next to the arteries but not by diminished response vasculature to NO. Absence of NO after SAH probably causes the reduced basic dilator activity of cerebral arteries as well. The guanylate-cyclase level in the arterial wall is consequently reduced after SAH primary due to absence of NO but not due to direct reduction of enzyme activities caused by process of blood degradation inside of subarachnoid space.


2020 ◽  
Vol 18 (1) ◽  
pp. 70-78
Author(s):  
Ieva Buce-Satoba ◽  
Daina Rozkalne ◽  
Jevgenijs Stepanovs ◽  
Biruta Mamaja ◽  
Gaida Krumina ◽  
...  

SummaryIntroductionAneurysmal subarachnoid haemorrhage (SAH) is associated with high mortality and morbidity. Rebleeding, cerebral vasospasm (VS) with delayed cerebral ischemia (DCI) are major complications after SAH associated with poor neurological outcome.Aim of the studyTo summarize the existing research data on the SAH from incidence, risk factors and clinical presentation to diagnostic, monitoring and treatment options after SAH.Materials and MethodsLiterature review was carried out to identify factors associated with SAH using specific keywords (aneurysmal subarachnoid haemorrhage, rebleeding, cerebral vasospasm, delayed cerebral ischemia) in the PUBMED database. In the time period from 2000 to 2019, 34 full articles were reviewed.ResultsAccording to the literature, the key risk factors for cerebral aneurysms and the SAH are hypertension, smoking, chronic alcohol abuse, family history of intracranial aneurysms in first-degree relatives and female sex. The key risk factor for early complication - rebleeding after SAH - is hypertension. The factors responsible for late complications - cerebral VS and DCI after SAH - are initially lower Glasgow coma scale and higher grades of Fisher scale, where grade IV and III predict cerebral VS in 31–37%. Furthermore, hyperglycaemic state, hyponatremia, hypotension and cerebral hypoperfusion, increased level of Troponin correlate with the incidence of cerebral VS and DCI. Although the golden standard to detect cerebral VS is digital subtraction angiography, CT angiography has become a routine examination. Transcranial doppler sonography is recommended and regional cerebral oximetry also seems to be promising. To avoid rebleeding for wide-necked, gigantic aneurysms or when SAH is combined with intraparenchymal hematoma, surgical clipping is preferred. For posterior circulation aneurisms, poor grade SAH and patients with age >70 years superior is endovascular treatment. To avoid late complications, the pharmacological method is used with Nimodipine.ConclusionsSAH is still associated with poor clinical outcome due to the development of early and late complications. The highest risk patients are those with low Glasgow coma scale and high grades of Fisher scale. Timely performed obliteration methods of the ruptured aneurysm are crucial and Nimodipine is the main agent to prevent cerebral VS and DCI.


1993 ◽  
Vol 15 (3) ◽  
pp. 209-211 ◽  
Author(s):  
Takakazu Kawamata ◽  
Nobuhiko Aoki ◽  
Tatsuo Sakai ◽  
Koji Arai

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