Treatment Of Symptomatic Vasospasm Research Articles

Sub arachnoid hemorrhage and vasospasm

Spontaneous sub arachnoid hemorrhage develops vasospasm in the 3-8 days. It should be dealt with conservative symptomatic treatment in this risky phase. Commonest presentation of vasospasm is headache. Usually headache increases with the onset of vasospasm at day 3 and diminishes as the vasospasm subsides after 8-10 days. Surgical interventions like clipping and coiling should be avoided in this period and patients should be given plenty of fluids (hemodilution, hypervolemia and hypertension). This triple H therapy holds good for asymptomatic vasospasms but were found less effective in symptomatic patients of SAH. Constipation should be avoided. Grade is supported by evidence from placebo-controlled study. There are some guidelines available for the prevention and the treatment of cerebral vasospasms with Nimodipine (oral). The use of triple H treatment as a preventative measure is a grade B recommendation. The treatment of symptomatic vasospasm with therapeutic hypertensive hypervolemia hemodilution is advised, however no prospective trials are available (grade C recommendation). There is no evidence that antifibrinolytics, steroids, or anticonvulsive prophylaxis should be used routinely. Current prophylaxis and treatment of cerebral vasospasm are still insufficient, according to clinical data, and vigorous triple-H-therapy is linked to an increased risk of sequelae.

Ca ++ 拮抗薬 Diltiazem による遅発性脳血管攣縮の予防と治療

Ca ++ 拮抗薬 Diltiazem による遅発性脳血管攣縮の予防と治療

Medical management of cerebral vasospasm: present and future

Cerebral vasospasm is one of the major complications of subarachnoid hemorrhage. The delayed occurrence of this complication allows for preventive management and early therapeutic interventions. Yet, accurate and timely diagnosis remains challenging and therapeutic options are rather limited. This review discusses new developments in the diagnosis and medical management of cerebral vasospasm made possible by technological advances and growing understanding of the complex pathophysiology of this disorder. CT protocols including CT perfusion and MRI with diffusion and perfusion sequences are increasingly employed in the evaluation of patients with suspected vasospasm. These radiological studies can add important information to that provided by transcranial Doppler and conventional angiography. Nimodipine for the prevention of delayed functional sequelae and hemodynamic augmentation therapy for the treatment of symptomatic vasospasm remains the mainstay of medical management. Novel strategies under investigation include the use of endothelin receptor antagonists, magnesium sulphate and statins. The value of albumin is being formally studied in an ongoing trial. Interventions to enhance nitric oxide may prove viable in the near future.

Emergency surgical management for prevention of symptomatic vasospasm and normal pressure hydrocephalus after subarachnoid hemorrhage due to ruptured cerebral aneurysm

Various pieces of research have been done on prevention or treatment of symptomatic vasospasm and normal pressure hydrocephalus after subarachnoid hemorrhage due to ruptured cerebral aneurysm. However, this important issue is still unresolved. In this preliminary report, we introduce our surgical strategy and techniques of subarachnoid hemorrhage due to ruptured cerebral aneurysm and discuss the prevention of symptomatic vasospasm and normal pressure hydrocephalus in the surgical aspect.

Aneurysmatische Subarachnoidalblutung

Despite substantial improvement in the management of patients with aneurysmal subarachnoid hemorrhage (SAH), including early aneurysm occlusion by endovascular techniques and surgical procedures, a significant percentage of patients with SAH still experience serious sequelae of neurological or cognitive deficits as a result of primary hemorrhage and/or secondary brain damage. Available neuromonitoring methods for early recognition of ischemia include, among others, measurement of brain tissue O(2) partial pressure, brain metabolism with microdialysis and monitoring of regional blood flow. The triple-H therapy (arterial hypertension, hypervolemia and hemodilution) is the treatment of choice of a symptomatic vasospasm and leads to an enduring recession of ischemic symptoms, if initiated early after the onset of a vasospasm-linked ischemic neurological deficit. Further promising therapy approaches are the administration of highly selective ET(A) receptor antagonists and intracisternal administration of vasodilators in depot form. This review summarizes the major neurological and non-neurological complications following aneurysm occlusion. Possible neuromonitoring techniques to improve diagnosis and therapy for treatment of symptomatic vasospasm as well as extracranial complications are discussed.

Neurointerventional treatment of vasospasm

Objectives: To review the historical development and current status of endovascular techniques used in the treatment of symptomatic vasospasm following aneurysmal subarachnoid hemorrhage.Methods: This article summarizes the relevant literature on neurointerventional therapy for vasospasm, namely instillation of intraarterial medication (papaverine, nicardipine, verapamil) and transluminal balloon angioplasty. The authors synthesize the available literature with their own experience using the various endovascular modalities to treat vasospasm at high volume cerebrovascular centers.Technique: Indications for the use of neurointerventional therapy as well as a summary of the technique for transluminal angioplasty to treat vasospasm as employed by the authors is described.Discussion: Neurointerventional treatment of vasospasm following aneurysmal hemorrhage has been proven to be a safe and successful technique for those patients suffering symptomatic vasospasm refractory to medical management. The techniques contunue to undergo refinement as endovascular technology advances. We currently favor the use of balloon angioplasty over intraarterial antispasmotics due to the increased durability and long-lasting effects of the former and lower risk profile.

Recommendations for the management of patients with aneurysmal subarachnoid hemorrhage

After SAH, primary and secondary complications are frequent and often require neurosurgical interventions to avoid secondary brain damage. The authors of the present paper have summarized the available data about the treatment modalities often used for patients with SAH. The present recommendations have been developed as a neurosurgical and neuroanestesiological consensus. Evidence from prospective, randomized, double blind, placebo-controlled studies support grade A recommendations (standard) for the prophylaxis and treatment of cerebral vasospasm with oral Nimodipine in good grade patients. For intravenous Nimodipine or for oral nimodipine treatment in poor grade patients, available data only support grade C recommendations (options). Despite the lack of data supporting standards (grade A) or guidelines (grade B), avoidance and rigorous treatment of hypotension and hypovolemia remains the mainstay in the prophylaxis and treatment of a delayed ischemic neurological deficit (DIND). Prophylactic hypervolemia or prophylactic hypertension and hypervolemia was shown to be ineffective in reducing symptomatic vasospasm and improving outcome (grade B). Therapeutic hypertensive hypervolemic hemodilution is recommended as a treatment of symptomatic vasospasm but no prospective studies are available (grade C recommendation). Suggested target values for moderate triple-H-therapy are CPP 80— 120 mmHg (MAP 90-130), CVP >7 mmHg and Hk 0.25-0.40. Balloon angioplasty should be considered for treatment of DIND cause by focal, proximal cerebral vasospasm. There is no evidence supporting the routine use of antifibrinolytica, steroids or anticonvulsive prophylaxis. Clinical data indicate that current prophylaxis and treatment of cerebral vasospasm is still insufficient and aggressive triple-H-therapy is associated with an increased incidence of complications.

Endovascular Treatment of Cerebral Vasospasm and Ischaemia

Currently the most widely used treatment for symptomatic vasospasm remains hypervolemia and hemodilution combined with pharmacologically induced hypertension using pressor agents (Triple-H therapy), despite the fact that evidence of its efficacy is lacking in controlled studies. Triple-H therapy can be difficult to regulate for any length of time and poor patient tolerance and frequent cardiac and cerebral complications limit its use.

Empfehlungen zum Management der aneurysmatischen Subarachnoidalblutung

After SAH, primary and secondary complications are frequent and often require neurosurgical interventions to avoid secondary brain damage. The authors of the present paper have summarized the available data about the treatment modalities often used for patients with SAH. The present recommendations have been developed as a neurosurgical and neuroanestesiological consensus. Evidence from prospective, randomized, double blind, placebo-controlled studies support grade A recommendations (standard) for the prophylaxis and treatment of cerebral vasospasm with oral Nimodipine in good grade patients. For intravenous Nimodipine or for oral nimodipine treatment in poor grade patients, available data only support grade C recommendations (options). Despite the lack of data supporting standards (grade A) or guidelines (grade B), avoidance and rigorous treatment of hypotension and hypovolemia remains the mainstay in the prophylaxis and treatment of a delayed ischemic neurological deficit (DIND). Prophylactic hypervolemia or prophylactic hypertension and hypervolemia was shown to be ineffective in reducing symptomatic vasospasm and improving outcome (grade B). Therapeutic hypertensive hypervolemic hemodilution is recommended as a treatment of symptomatic vasospasm but no prospective studies are available (grade C recommendation). Suggested target values for moderate triple-H-therapy are CPP 80- 120 mmHg (MAP 90-130), CVP > 7 mmHg and Hk 0.25-0.40. Balloon angioplasty should be considered for treatment of DIND cause by focal, proximal cerebral vasospasm. There is no evidence supporting the routine use of antifibrinolyticals, steroids or anticonvulsive prophylaxis. Clinical data indicate that current prophylaxis and treatment of cerebral vasospasm is still insufficient and aggressive triple-H-therapy is associated with an increased incidence of complications.

Persistent Autoregulatory Disturbance after Angioplasty for Cerebral Vasospasm

Hyperdynamic therapy, consisting of hypervolemia, haemodilution, and hypertension, is an established treatment for cerebral vasospasm following subarachnoid haemorrhage. Angioplasty has emerged as an additional, effective treatment for symptomatic vasospasm. Loss of autoregulation, however, can occur despite effective angioplasty, underscoring the need for treatment with hyperdynamic therapy in combination with angioplasty. A 43-year-old woman underwent endovascular coiling of a ruptured left posterior communicating artery aneurysm. The patient went on to develop symptomatic vasospasm and was treated with hyperdynamic therapy and angioplasty. Autoregulation was assessed with xenon CT cerebral blood flow (CBF) measurement. An initial CBF study was obtained when the patient received dopamine and dobutamine infusions to maintain systolic blood pressure at 160 mmHg. The vasopressor drips were then temporarily held for twenty minutes, allowing the patient's systolic blood pressure to drop to 140 mmHg, and a repeat CBF study was obtained. Several days after angioplasty, CBF decreased significantly when the patient was taken off vasopressors, indicating impaired autoregulation. Hyperdynamic therapy was continued, and another CBF study one week later showed a return of autoregulation and normalization of CBF without induced hypertension. Autoregulation is disturbed during vasospasm. Although angioplasty can improve large artery blood flow during vasospasm, hyperdynamic therapy is also needed to maintain cerebral perfusion, particularly in the face of impaired autoregulation. Quantitative CBF measurement permits the maintenance of optimal CBF and monitoring of response to therapy.

Multicenter Evaluation of the Efficacy of Endovascular Treatment for Symptomatic Vasospasm unresponsive to Hypervolemic and Hypertensive Therapy in Patients with Subarachnoid Hemorrhage.

P231 BACKGROUND AND PURPOSE: Symptomatic vasospasm remains an important cause of morbidity and mortality in patients with subarachnoid hemorrhage (SAH). Endovascular techniques have recently been introduced for treatment of vasospasm resistant to medical treatment. We performed this study to determine the safety and efficacy of these techniques in a large series of patients with SAH. METHODS: We reviewed the medical records, angiograms, and computed tomographic (CT) scans for patients who underwent endovascular treatment for symptomatic vasospasm at 3 university-affiliated centers. The following outcomes were analyzed; angiographic improvement, neurological improvement, ability to prevent cerebral infarction as demonstrated by serial CT scans, and outcome at 3 months using Glasgow Outcome Scale (GOS). RESULTS: Forty-five patients (mean age 51 ±10 years; 13 were men) were treated for symptomatic vasospasm. The vasospasm was graded as severe (n=27), moderate (n=16), and mild (n=2) by angiographic criteria. Angioplasty was performed in 26 patients; intra-arterial papaverine was administered as adjunctive therapy in 11 procedures. Nineteen patients were treated with intra-arterial papaverine alone. Angiographic improvement was documented in all patients. Cerebral infarction was observed in 29 (64%) of 45 patients on follow-up CT scan. Good outcome (minimal or no disability by GOS) was seen in 12 (27%) patients. CONCLUSIONS: Although endovascular treatment of symptomatic vasospasm results in good angiographic response, a high proportion of cerebral infarction and poor outcomes is still observed in patients who failed medical treatment. New strategies need to be developed to improve outcome in this subset of patients with SAH.

Multicenter Evaluation of the Efficacy of Endovascular Treatment for Symptomatic Vasospasm unresponsive to Hypervolemic and Hypertensive Therapy in Patients with Subarachnoid Hemorrhage.

P231 BACKGROUND AND PURPOSE: Symptomatic vasospasm remains an important cause of morbidity and mortality in patients with subarachnoid hemorrhage (SAH). Endovascular techniques have recently been introduced for treatment of vasospasm resistant to medical treatment. We performed this study to determine the safety and efficacy of these techniques in a large series of patients with SAH. METHODS: We reviewed the medical records, angiograms, and computed tomographic (CT) scans for patients who underwent endovascular treatment for symptomatic vasospasm at 3 university-affiliated centers. The following outcomes were analyzed; angiographic improvement, neurological improvement, ability to prevent cerebral infarction as demonstrated by serial CT scans, and outcome at 3 months using Glasgow Outcome Scale (GOS). RESULTS: Forty-five patients (mean age 51 ±10 years; 13 were men) were treated for symptomatic vasospasm. The vasospasm was graded as severe (n=27), moderate (n=16), and mild (n=2) by angiographic criteria. Angioplasty was performed in 26 patients; intra-arterial papaverine was administered as adjunctive therapy in 11 procedures. Nineteen patients were treated with intra-arterial papaverine alone. Angiographic improvement was documented in all patients. Cerebral infarction was observed in 29 (64%) of 45 patients on follow-up CT scan. Good outcome (minimal or no disability by GOS) was seen in 12 (27%) patients. CONCLUSIONS: Although endovascular treatment of symptomatic vasospasm results in good angiographic response, a high proportion of cerebral infarction and poor outcomes is still observed in patients who failed medical treatment. New strategies need to be developed to improve outcome in this subset of patients with SAH.

Endovascular Therapy of Carotid Cavernous Fistulas

The clinical manifestations of carotid cavernous fistulas, regardless of the type, depend on the pattern of venous drainage from the fistula. Venous drainage toward the orbit produces the usual syndrome of proptosis, chemosis, and arterialization of scleral veins. If the venous drainage is toward the brain, the signs and symptoms may not be as apparent, but the risk for catastrophic hemorrhage is much higher. Although many of these lesions may be managed in a conservative fashion, there are indications for urgent treatment to prevent a devastating hemorrhage or loss of vision. Direct carotid cavernous fistulas can usually be managed by transarterial embolization, most commonly with detachable balloons. The transvenous approach is most efficacious for treating indirect carotid cavernous fistulas.

Endovascular Treatment of Vasospasm

Angioplasty has become an important tool in the treatment of symptomatic vasospasm. The recent advent of intra-arterial papaverine infusion for the treatment of vasospasm serves to complement angioplasty. The use of these techniques in the treatment of symptomatic vasospasm is discussed.