Delayed Ischemic Neurological Deficit after Uneventful Elective Clipping of Unruptured Intracranial Aneurysms

Cerebral vasospasm and subsequent delayed ischemic neurological deficit is a typical sequela of acute subarachnoid hemorrhage after aneurysm rupture. The occurrence of vasospasms after uncomplicated surgery of an unruptured aneurysm without history of suspected rupture is extremely rare. The pathogenesis and severity of cerebral vasospasms is typically correlated with the amount of blood breakdown products extravasated during subarachnoid hemorrhage. In rare cases, where vasospasms occur after unruptured aneurysm surgery, the pathogenesis is most likely multifactorial and unclear. We present two cases of vasospasms following uncomplicated clipping of middle cerebral artery (MCA) aneurysms and a review of literature. Early diagnosis and therapy of this rare complication are necessary to achieve optimal clinical outcomes.

Management of cerebral vasospasm in subarachnoid hemorrhage

Subarachnoid hemorrhage (SAH) has been shown to result in cerebral vasospasm at day 4 to day 14, which is the main cause of mortality and morbidity after SAH. Outcome after SAH depends on many factors, including the severity of the event, medical management, and prevention of several serious complications. The principal goal in management of vasospasm after SAH is to prevent delayed ischemic neurological deficit (DIND) by decreasing intracranial pressure (ICP), optimizing cerebral oxygen demand rate and improving cerebral blood flow (CBF). Therapeutic management has been applied to prevent or treat vasospasm, including hemodynamic therapy, and endovascular therapy. Endovascular therapies, including mechanical angioplasty and chemical angioplasty with administration of intra-arterial (IA) vasodilator, have been widely used and given a good outcome. The purpose of this article is to describe the management of vasospasm including medical management and endovascular treatment. This review will describe the treatment modalities and management strategies to treat vasospasm.Abbreviations: SAH – subarachnoid hemorrhage; aSAH – aneurysmal subarachnoid hemorrhage; TCD – transcranial Doppler; ROS – reactive oxygen species; ICAM – intercellular adhesion molecule; VCAM – vascular cell adhesion molecule; IL – interleukin; CTA – computed tomography angiography; MRA – magnetic resonance angiography; CBF – cerebral blood flow; DIND – delayed ischemic neurological deficit; RCT - randomized controlled trialsCitation: Prahaztuti D, Hidayati HB, Sani AF. Management of cerebral vasospasm in subarachnoid hemorrhage. Anaesth Pain & Intensive Care 2018;22(3 Suppl 1):S58-S66.Received: 19 Oct 2018 Reviewed: 4, 11 Nov 2018 Accepted: 12 Nov 2018

Defisit Neurologis Iskemik Tertunda pada Perdarahan Subaraknoid akibat Rupture Aneurisma yang dilakukan Tindakan Coiling

Stroke dapat terjadi akibat terhentinya aliran darah ke otak, yang terjadi secara mendadak. Penyebab terbanyak stroke adalah berkurangnya pasokan darah ke otak (stroke iskemik). Penyebab stroke lainnya adalah perdarahan (stroke hemoragik). Perdarahan subaraknoid (SAH) biasanya dapat terjadi baik karena ruptur aneurisma, atau karena trauma. Perempuan, 46 tahun dengan GCS 14 (E4M6V4) dengan hipertensi tidak terkontrol mengalami nyeri kepala hebat. Dari pemeriksaan CT scan memperlihatkan adanya perdarahan subaraknoid dan edema sereberi. Pasien ini dilakukan tindakan coiling aneurisma cito dengan anestesia umum. Pasca coiling pasien dirawat di ruang intensive care unit (ICU). Pasca perawatan 1 hari di ICU, pasien dipindahkan ke ruang high care unit (HCU), dengan kondisi stabil. Penurunan kesadaran mulai terjadi saat perawatan hari kedua, sempat dilakukan pemasangan lumbar drain pada hari ketiga, untuk membantu mengurangi hidrosefalus dan juga menurunkan tekanan intra kranial. Pada perawatan hari ketigabelas kesadaran menurun drastis menjadi E1M1V1, pasien dipindahkan ke ruang ICU, dan meninggal esok harinya. Penurunan kesadaran pasca coiling diakibatkan oleh peningkatan tekanan intra kranial, yang pada kasus ini disebabkan oleh edema sereberi luas. Early Brain Injury ¬ditambah dengan adanya vasopasme menyebabkan terjadinya delayed ischemic neurological deficit. Terapi yang sudah dikerjakan baik farmakologis maupun non farmakologis, tetap tidak bisa memperbaiki keadaan pasien. Delayed Ischemic Neurological Defisit (DIND) Pasca Coiling Subarachnoid Hemorrhage (SAH) e.c Ruptur AneurismaAbstractStroke can occur due to the cessation of blood flow to the brain, which occurs suddenly. The most common cause of stroke is reduced blood supply to the brain (ischemic stroke). Another cause of stroke is bleeding in the brain (hemorrhagic stroke). Subarachnoid hemorrhage (SAH) usually results from ruptured aneurysms or because of trauma. Women, 46 years old with GCS 14 (E4M6V4) with uncontrolled hypertension experienced severe headache since 2 days before admitted to the hospital. The CT scan examination showed subarachnoid hemorrhage and edema of the brain. This patient then performed emergency coiling of aneurysm with general anesthesia. During the procedure the patient is in stable condition. Post coiling the patient was sent to the ICU room. After 1 day in ICU, the patient was transferred to high care unit (HCU) room, with stable condition. Decreased of consciousness began to occur during the second day of treatment, had done lumbar drain installation on the third day, to help reduce the hydrocephalus and also improve intra-cranial pressure. On the thirteenth day care GCS was decrease suddenly to E1M1V1, the patient was transferred to the ICU room, the next day the patient was declared dead. The decrease of consciousness post coiling results from an increase in intra-cranial pressure, which in this case is due to severe brain edema. Earlu brain injury along with the occurence of vasospasm lead to delayed ischemic neurological deficit. Pharmacological and non-pharmacological therapy had been given to the patient still couldn’t improve the patient condition

Statins for aneurysmal subarachnoid haemorrhage: Another loss in translation

Experimental evidence suggests that statin attenuates inflammation, oxidation, platelet aggregation and excitotoxicity. In brain ischemic models, statin administration produces vasodilatation and reduces neuronal apoptosis. It was hypothesized that statin administration may improve outcome by reducing delayed ischemic neurological deficit after aneurysmal subarachnoid haemorrhage. Earlier pilot trials suggested demonstrated encouraging results but the recent Simvastatin in Aneurysmal Subarachnoid Haemorrhage Trial, using simvastatin 40 mg per day, failed to demonstrate a benefit. Even at larger doses, simvastatin 80 mg per day did not reduce delayed ischemic neurological deficit. In common with many other interventions, statin represents another translational failure of presumed neuroprotective agents.

Method of Aneurysm Treatment Does Not Affect Clot Clearance After Aneurysmal Subarachnoid Hemorrhage

BACKGROUND Patients undergoing neurosurgical clipping or endovascular coiling of a ruptured aneurysm may differ in their risk of vasospasm. OBJECTIVE Because clot clearance affects vasospasm, we tested the hypothesis that clot clearance differs in patients depending on method of aneurysm treatment. METHODS Exploratory analysis was performed on 413 patients from CONSCIOUS-1, a prospective randomized trial of clazosentan for the prevention of angiographic vasospasm in patients with aneurysmal subarachnoid hemorrhage (SAH). Clot clearance was measured by change in Hijdra score between baseline computed tomography and one performed 24 to 48 hours after aneurysm treatment. Angiographic vasospasm was assessed by the use of catheter angiography 7 to 11 days after SAH, and delayed ischemic neurological deficit (DIND) was determined clinically. Extended Glasgow Outcome Score (GOSE) was assessed 3 months after SAH, and poor outcome was defined as death, vegetative state, or severe disability. Multivariable ordinal and binary logistic regression were used. RESULTS There was no significant difference in the rate of clot clearance between patients undergoing clipping or coiling (P = .56). Coiling was independently associated with decreased severity of angiographic vasospasm (odds ratio [OR] 0.53, 95% confidence interval [CI] 0.33-0.86), but not with DIND or GOSE. Greater clot clearance decreased the risk of severe angiographic vasospasm (OR 0.86, 95% CI 0.81-0.91), whereas higher baseline Hijdra score predicted increased angiographic vasospasm (OR 1.17, 95% CI 1.11-1.23) and poor GOSE (OR 1.09, 95% CI 1.04-1.14). CONCLUSION Aneurysm coiling and increased clot clearance were independently associated with decreased severity of angiographic vasospasm in multivariate analysis, although no differences in clot clearance were seen between coiled and clipped patients.