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.

Descripción de los cambios en la velocidad media de flujo sanguíneo cerebral en posición supino y sedente, en pacientes con hemorragia subaracnoidea aneurismática con vasoespasmo asintomático o sin vasoespasmo: Serie de casos / Changes in cerebral blood flow velocity in supine and sitting position in patients with aneurysmal subarachnoid hemorrhage

Background: Early mobilization in intensive care units (ICU) provides respiratory, neurological and cardiovascular benefits in hospitalized patients. However, the orthostatic effects of changing from a supine to a sitting position may interfere with cerebral hemodynamics of patients with aneurysmal subarachnoid hemorrhage (aSAH). Aim: To describe the changes in mean cerebral blood flow velocity (MCBFV) in supine and sitting position, in adult patients with aSAH, with asymptomatic vasospasm (AVS) or without vasospasm (VS) at a neurosurgical ICU. Material and Methods: Descriptive case series study in 21 patients with aSAH, both with and without VS. They were positioned in a supine 30° position and then seated at the edge of bed for six minutes. MCBFV was measured by transcranial Doppler (TCD), and hemodynamic variables in both positions were registered. After this basal assessment and for 21 days after the episode of SAH, patients were seated once a day and signs of VS were recorded. Results: No significant changes in MCBFV or hemodynamic variables were detected during position changes, except for an increase in heart rate in the sitting position. No patient with AVS at the onset, had symptomatic VS during the 21 days of follow up when patients were seated. Among patients with a normal MCBFV at baseline, five patients (24%) had VS at a mean of three days after the first time that they were seated on the edge of bed. Conclusions: Sitting patients at the edge of the bed is a safe mobilization alternative for patients who suffered aSAH who did not have VS or had AVS.

Erythropoietin in vasospasm. From bench to bedside? / Eritropoietina no vasoespasmo. Da bancada do laboratório para a beira do leito?

Aneurysmal subarachnoid haemorrhage is one of the most deleterious acute neurological diseases. The cerebral ischemia secondary to arterial vasospasm occurring after aneurysmal subarachnoid haemorrhage is still responsible for the considerable morbidity and mortality in these patients. Besides the knowledge of basic mechanisms of cerebral vasoespasm following aneurysmal subarachnoid haemorrhage, the prophylaxis and treatment of this pathology however still remain suboptimal. There issome evidence that acute erythropoietin treatment may reduce the severity of cerebral vasospasm and eventually improve outcome in aneurysmal subarachnoid haemorrhage patients. There are underlying mechanisms extend far beyond erythropoiesis: like enhancing neurogenesis, decreasing inflammation and apoptosis inhibition. In this review the authors describe many of the biologic effects, especially experimental studies and clinical studies that reported why the erythropoietin could be beneficial topatients with aneurysmal subarachnoid haemorrhage.

A hemorragia subaracnóidea é uma das doenças neurológicas agudas mais graves. A isquemia cerebral secundária ao vasoespasmo arterial após a hemorragia ainda é responsável por considerável morbidade e mortalidade nesses pacientes. Ao lado do conhecimento dos mecanismos básicos do vasoespasmo na hemorragia subaracnóidea, a profilaxia e o tratamento dessa entidade ainda são insuficientes. Há evidências de que o uso da eritropoietina na fase aguda pode reduzir a gravidade do vasoespasmo e,eventualmente, melhorar o prognóstico desses pacientes. Há mecanismos de ação da eritropoietina que vão além da eritropoiese como neurogênese, redução da inflamação e inibição da apoptose. Nesta revisão, os autores elucidam inúmeros efeitos biológicos, principalmente aqueles demonstrados nos estudos experimentais e clínicos que descrevem por que a eritropoietina pode ser benéfica em pacientes com hemorragia subaracnóidea.

Fisher revised scale for assessment of prognosis in patients with subarachnoid hemorrhage / Avaliação prognóstica com escala de Fisher modificada em pacientes com hemorragia subaracnóidea

The Fisher revised scale (FRS) presents an alternative for evaluating patients with subarachnoid hemorrhage (SAH). In this study, we compared the prognosis of patients with SAH and vasospasms (VSP). METHOD: This was a prospective study on patients with a diagnosis of aneurysmal SAH, 72 hours after the initial event. Sequential neurological examinations and Hunt and Hess (HaH) score were performed on the 1st, 7th and 14th days. Transcranial Doppler was used to assess vasospasms. RESULTS: Out of the 24 patients studied, ten (41.66 percent) presented a delayed neurological deficit, such as diminished consciousness, decreased HaH score or death. The single patient classified as FS-1 did not have any delayed neurological deficit, while such deficits evolved in one patient out of five with FS-2 (20 percent); two out of seven with FS-3 (28.57 percent) and seven out of 11 with FS-4 (63.63 percent). CONCLUSION: Level three of the FS and FRS seemed to be compatible with regard to predicting the likelihood of progression to severe VSP.

A escala revisada de Fisher (FRS) representa uma alternativa para avaliação de pacientes com hemorragia subaracnóidea (HSA). Neste estudo comparamos a evolução prognóstica referente ao vasoespasmo (VSP) nos pacientes com HSA. MÉTODO: Estudo prospectivo em pacientes com diagnóstico de HSA, com 72 horas após o evento inicial. Escala de Hunt e Hess (HeH) foi realizada no 1º, 7º, 14º dia. Utilizamos Doppler transcraniano para avaliação de VSP. RESULTADOS: Dos 24 pacientes estudados dez (41,66 por cento) tiveram déficit neurológico tardio (DNT), como diminuição da consciência, grau de HeH ou morte. Um paciente de cinco classificados como FS-2 (20 por cento), dois de sete pacientes com FS-3 (28,57 por cento) e sete de 11 pacientes com FS-4 (63,63 por cento) evoluíram com DNT. Para o FRS não encontramos piora neurológica precoce no paciente com FRS-0. CONCLUSÃO: O nível três da FS e FRS parecem ser comparáveis, quando se trata de predizer a probabilidade de progressão para VSP grave.

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.

Hemodynamic monitoring in the neurological intensive care unit.

The neurointensivist needs to have a thorough understanding of hemodynamic issues and the interaction of the brain and the cardiovascular system. Before one decides to intervene and try to correct an apparent "abnormal hemodynamic parameter" one needs to think whether such an intervention is indeed warranted and what effect the intervention would have on the cerebral circulation. The neurointensivist thus needs to approach these issues differently from the approach an internist or general intensivist would take.