Chemical Angioplasty with Nitroglycerin for Vasospasm after Subarachnoid Hemorrhage: Case Series and Review

Introduction Vasospasm is a common and potentially devastating complication in patients with subarachnoid hemorrhage, causing high morbidity and mortality. There is no effective and consistent way to prevent or treat cerebral vasospasm capable of altering the morbidity and mortality of this complication. Animal and human studies have attempted to show improvement in aneurysmal vasospasm. Some sought their prevention; others, the treatment of already installed vasospasm. Some achieved only angiographic improvement without clinical correlation, others achieved both, but with ephemeral duration or at the expense of very harmful associated effects. Endovascular techniques allow immediate and aggressive treatment of cerebral vasospasm and include methods such as mechanical and chemical angioplasty. These methods have risks and benefits. Objectives To analyze the results of chemical angioplasty using nitroglycerin (GTN). In addition, to performa comprehensive review and analysis of aneurysmal vasospasm. Methods We describe our series of 77 patients treated for 8 years with angioplasty for vasospasm, either mechanical (with balloon), chemical (with GTN) or both. Results Eleven patients received only balloon; 37 received only GTN; 29 received both. Forty-four patients (70.1%) evolved with delayed cerebral ischemia and 19 died (mortality of 24.7%). Two deaths were causally related to the rupture of the vessel by the balloon. The only predictors of poor outcome were the need for external ventricular drainage in the first hours of admission, and isolated mechanical angioplasty. Conclusions Balloon angioplasty has excellent results, but it is restricted to proximal vessels and is not without complications. Chemical angioplasty using nitroglycerin has reasonable but short-lived results and further research is needed about it. It is restricted to vasospasm angioplasties only in hospitals, like ours, where better and more potent vasodilator agents are not available.

Simultaneous Endovascular Treatment of Ruptured Cerebral Aneurysms and Vasospasm

OBJECTIVE: The management of patients with ruptured cerebral aneurysms and severe vasospasm is subject to considerable controversy. We intended to describe herein an endovascular technique for the simultaneous treatment of aneurysms and vasospasm. MATERIALS AND METHODS: A series of 11 patients undergoing simultaneous endovascular treatment of ruptured aneurysms and vasospasm were reviewed. After placement of a guiding catheter within the proximal internal carotid artery for coil embolization, an infusion line of nimodipine was wired to one hub, and of a microcatheter was advanced through another hub (to select and deliver detachable coils). Nimodipine was then infused continuously during the coil embolization. RESULTS: This technique was applied to 11 ruptured aneurysms accompanied by vasospasm (anterior communicating artery, 6 patients; internal carotid artery, 2 patients; posterior communicating and middle cerebral arteries, 1 patient each). Aneurysmal occlusion by coils and nimodipine-induced angioplasty were simultaneously achieved, resulting in excellent outcomes for all patients, and there were no procedure-related complications. Eight patients required repeated nimodipine infusions. CONCLUSION: Our small series of patients suggests that the simultaneous endovascular management of ruptured cerebral aneurysms and vasospasm is a viable approach in patients presenting with subarachnoid hemorrhage and severe vasospasm.

Three Interesting Case Reports of Intracranial Aneurysm Managed with Triple 'H' Therapy.

Anaesthesia for aneurysm surgeries is highly specialized and unique. Vasospasm is the most important determinant for morbidity and mortality in intracranial aneurysms. For prevention and management of vasospasm Triple-H therapy (Hypertension, Hypervolemia and Haemodilution) is recommended. Triple-H therapy is gold standard in neuroanaesthesia in intracranial aneurysm surgeries in order to increase cerebral blood flow in areas affected by vasospasm and avoid damage caused by ischemia. First patient was 52 years old female with Right vertebral artery posterior inferior cerebellar artery aneurysm of size 1cm, operated successfully who became unconscious 22 hours after surgery and treated with Triple-H therapy for vasospasm. Second case was 48 years old male patient of right anterior cerebral artery aneurysm of 9mm size operated successfully after intraoperative rupture of aneurysm and subsequent vasospasm. Third case was 35 years pregnant female patient of anterior communicating artery aneurysm of 5mm size treated with triple H therapy for vasospasm.

Terapia endovascular no vasoespasmo cerebral secundário à hemorragia subaracnóidea / Endovascular therapy for the cerebral vasospasm after subarachnoid hemorrhage

O vasoespasmo cerebral é uma complicação relativamente frequente após episódios de hemorragia subaracnóidea de etiologia aneurismática. É responsável pela mortalidade de aproximadamente 30% dos pacientes e por sequelas neurológicas em 50% dos sobreviventes. Revisão de literatura realizada em julho de 2012. Foram pesquisadas as bases de dados PubMed e BVS e selecionados 37 artigos em português e inglês. A terapia do triplo H, largamente utilizada, diminui complicações isquêmicas, mas pode piorar comorbidades. A nimodipina ainda é a única droga que melhora comprovadamente o prognóstico do paciente. O tratamento endovascular pode ser baseado em angioplastia por balão, que dilata mecanicamente os vasos estreitados, ou em administração intra-arterial de agentes vasodilatadores, como a papaverina. Angioplastia profilática em determinados segmentos arteriais pode reduzir em até 10,4% as complicações isquêmicas. A angioplastia terapêutica tem melhores resultados quando realizada nas duas primeiras horas após a instalação do vasoespasmo sintomático. A papaverina induz melhora angiográfica em até 66% dos pacientes, mas pode estar relacionada à neurotoxicidade. A terapia endovascular parece ter resultados muito positivos para o tratamento do vasoespasmo cerebral. Pela falta de evidências, no entanto, deve ainda ser reservada para pacientes refratários ao tratamento clínico ou com complicações que o impeçam.

Cerebral vasospasm is a relatively frequent complication after aneurysmal subarachnoid hemorrhages. It leads to a 30% mortality rate of patients who survived the hemorrhage and the development of neurologic deficits for 50% of the remaining. This is a literature review performed in July, 2012. Two databases were surveyed: PubMed and VHL. Thirty-seven articles in English and Portuguese were selected. ?Triple-H? therapy, widely employed, reduces ischemic complications, but can deteriorate patient?s comorbidities. Nimodipine still the only certified drug for the treatment of vasospasm. Endovascular treatment can be performed through percutaneous transluminal balloon angioplasty (TBA), which enlarges vessels mechanically, or intra-arterial administration of vasodilating agents, such as papaverine. Prophylactic angioplasty in selected arterial segments can reduce ischemic complications in until 10.4%. Therapeutic angioplasty presents better outcome when performed in the first two hours after the development of symptomatic vasospasm. Papaverine induces angiographic improvement in 66% of patients, but can be related with neurotoxicity. Endovascular therapy seems to present very positive results for the treatment of cerebral vasospasm. However, due to the lack of evidences, it should be reserved for when clinical treatment fails or cannot be performed.

Effect of cervical sympathetic block on cerebral vasospasm after subarachnoid hemorrhage in rabbits

PURPOSE: Cerebral vasospasm (CVS) is a major complication after subarachnoid hemorrhage (SAH) induced by the rupture of intracranial aneurysms. The aim of the present study was to investigate the effect and mechanism of cervical sympathetic block on cerebral vasospasm of the rabbits after SAH. METHODS: After successful modeling of cervical sympathetic block, 18 healthy male white rabbits were randomly divided into three groups (n=6), ie, sham operation group (Group A), SAH group (Group B) and SAH with cervical sympathetic block group (Group C). Models of delayed CVS were established by puncturing cisterna magna twice with an injection of autologous arterial blood in Groups B and C. A sham injection of blood through cisterna magna was made in Group A. 0.5 ml saline was injected each time through a catheter for cervical sympathetic block after the first injection of blood three times a day for 3 d in Group B (bilateral alternating). 0.5 ml of 0.25% bupivacaine was injected each time through a catheter for cervical sympathetic block after the first injection of blood three times a day for 7 d in Group B. 2 ml venous blood and cerebrospinal fluid were obtained before (T1), 30 min (T2) and 7 d (T3) after the first injection of blood, respectively, and conserved in a low temperature refrigerator. Basilar artery value at T1, T2 and T3 was measured via cerebral angiography. The degree of damage to nervous system at T1 and T3 was recorded. RESULTS: There was no significant difference in diameter of basilar artery at T1 among three groups. The diameters of basilar artery at T2 and T3 of Groups B and C were all smaller than that in Group A, which was smaller than Group C, with a significant difference. There was no significant difference in NO and NOS in plasma and cerebrospinal fluid among three groups. The NO and NOS contents at T2 and T3 of Groups B and C were all lower than Group A; Group C was higher than Group B, with a significant difference. The nerve function at T3 of Groups B and C were all lower than Group A and that of Group C higher than Group B, with a significant difference. CONCLUSION: Cervical sympathetic block can relieve cerebral vasospasm after subarachnoid hemorrhage and increase NO content and NOS activity in plasma and cerebrospinal fluid to promote neural functional recovery.

Depresiones corticales propagadas y su posible rol en la fisiopatología del daño neuronal subsecuente a la hemorragia subaracnoidea / Cortical spreading depressions and their role in the pathophysiology of neuronal damage subsequent to aneurysmal subarachnoid hemorrhage

El vasoespasmo cerebral es la principal causa potencialmente tratable de mortalidad e incapacidad en pacientes que sufren hemorragia subaracnoidea aneurismática (HSA). Sin embargo, a la fecha no existe un tratamiento eficaz para el mismo. La reciente demostración de la falta de respuesta clínica a la reversión farmacológica del espasmo arterial a consecuencia de HSA ha obligado un replanteo de los fundamentos fisiopatológicos de los déficits neurológicos isquémicos tardíos (“delayed ischemic neurologic déficit”, DIND) a consecuencia de HSA, los cuales se creían en relación al espasmo arterial observado en pacientes con HSA. Desde la demostración de hallazgos electrocorticográficos de depresión cortical propagada (“cortical spreading depression”, CSD) en pacientes con HSA, un interés creciente se ha despertado respecto del rol de estos fenómenos en la fisiopatología de los DIND observados en pacientes con HSA. Cuando inducidas en un cerebro saludable, las CSD se asocian con un aumento del flujo sanguíneo cerebral, facilitando la entrega del cerebro de los sustratos energéticos necesarios. En un cerebro que ha sido lesionado, sin embargo, la CSD se asocia con una reducción en flujo sanguíneo cerebral, lo cual, en el contexto de un aumento de las necesidades de energía, conduce a la insuficiencia energética y la hipoxia, empeorando así el daño cerebral. Estas observaciones sugieren que el déficit de energía producida por la CSD es un factor clave en la patogénesis de los DIND observados a consecuencia de HSA. Este resumen detalla características sobresalientes de las CSD y su potencial relevancia en la fisiopatología del vasoespasmo.

Cerebral vasospasm is the leading potentially treatable cause of mortality and disability in patients with aneurysmatic subarachnoid hemorrhage (SAH). However, to date there is no effective treatment for this entity. The recently demonstrated lack of clinical response to pharmacologic reversal of arterial spasm as a result of SAH has spurred a reassessment of the pathophysiological concepts on delayed ischemic neurologic deficits (DIND) that follow SAH, which were long believed the effect of the arterial spasm observed in patients with SAH. Since the discovery of electrocorticographic cortical spreading depressions (CSD) in patients with SAH, increasing interest has been shown on the role of these phenomena in the pathophysiology of DIND observed in patients with HSA. When induced in a healthy brain, CSD are associated with an increase in cerebral blood flow by facilitating the delivery of the necessary energy substrates. In a brain that has been injured, however, CSD are associated with a reduction in cerebral blood flow, which, in the context of increased energy requirements leads to energy shortage and hypoxia, thus worsening brain damage. These observations suggest that the energetic deficit produced by the CSD is a key factor in the pathogenesis of DIND observed as a result of HSA. This review details striking characteristics of CSD and their potential relevance in the pathophysiology of vasospasm.

Hemodinâmica do vasoespasmo: [revisão] / Cerebral hemodynamic alterations due to vasospasm: [review]

Os autores descrevem as alterações hemodinâmicas encefálicas que ocorrem na vigência do vasoespasmo após a hemorragia subaracnoidea por aneurismas. O conhecimento dessas alterações facilita o entendimento das medidas terapêuticas.

The authors describe the hemodynamic encephalic alterations that occur during the vasospasm after aneurysmal subarachnoid hemorrhage. The knowledge of these alterations promotes better understanding of the therapeutic procedures.