Management of a Ruptured Cerebral Aneurysm – Decision Making and Dilemmas
Sri Varsha Pulijal, MD, Resident
Eman Nada, MD, PhD, Assistant Professor
University of Massachusetts Medical School
Department of Anesthesiology and Perioperative Medicine
|Sri Varsha Pulijal, MD|
|Eman Nada, MD, PhD|
If the patient survives the initial aneurysmal subarachnoid hemorrhage (SAH), the most common early complication is rebleeding with reported incidences of 8% to 23% in the first 72 hours. The consequences of rebleeding are severe, with reported mortality rates ≤ 60%. Urgent repair of the ruptured aneurysm by endovascular coiling or neurosurgical clipping is thus of utmost importance. Once the aneurysm is successfully repaired, the chance of a rebleeding is negligible.
Various scales are used for classification and prediction of the prognosis. The Hunt-Hess score is correlated with clinical outcomes. Another scale is the World Federation of Neurological Surgeons clinical grading scale. The radiographic assessment using the modified Fisher score and was found to correlate with the risk of vasospasm.1
Treatment and Monitoring Patients with Ruptured Cerebral Aneurysm
Definitive treatment of ruptured cerebral aneurysm should be done to prevent further bleeding. The American Heart Association guidelines recommend open clipping for patients with large intraparenchymal hematomas and middle cerebral artery aneurysms, whereas endovascular coiling should be done for patients older than 70 years with high-grade SAH, and/or giant basilar apex aneurysms.2
A 69-year-old female with past medical history of coronary heart disease, chronic obstructive lung disease (COPD) on home oxygen, and morbid obesity, presented to the emergency department (ED) after sudden onset of severe headache followed by brief loss of consciousness and fall. Her past surgical history included abdominal aortic aneurysm repair and posterior communicating artery (PCOM) aneurysm coiling eight years ago. The CT scan of the head revealed an extensive subarachnoid hemorrhage with mild distension of the third and lateral ventricles. Fifty gm of Mannitol and 1000 mg of Levetiracetam were administered in the ED. The patient was transferred to the interventional neuroradiology suite for a diagnostic cerebral angiogram and possible coiling of an aneurysm.
On arrival to the interventional radiology suite, the patient’s Glasgow Coma Scale was 14, and she was alert and oriented to person, place and time. Suddenly, she became unresponsive and started to seize. A face mask ventilation was initiated, followed by immediate intubation. Intubation was facilitated using Propofol, Succinyl Choline and Fentanyl. Head CT showed marked increase of the SAH and the presence of significant hydrocephalus. A neurosurgeon was called for the placement of an endoventricular drain (EVD). Immediately prior to EVD placement, the blood pressure increased to 180/90 and the heart rate dropped to 30 beats/minute consistent with Cushing reflex. Cerebrospinal fluid was drained and the intracranial hypertension improved.
Anesthetic management included the placement of an arterial line for tight blood pressure control, sevoflurane 0.5 MAC, propofol and remifentanil infusion were used for maintenance. Phenylephrine infusion to maintain the systolic blood pressure (SBP) of less and equal 160 mmhg. When the Cushing reflex happened glycopyrrolate, boluses of propofol, fentanyl, and nicardipine were administered and hyperventilation was initiated and the cerebrospinal fluid (CSF) was drained as soon as the EVD was placed. Imaging has shown a new POCM aneurysm that was successfully coiled and the case continued uneventfully. Then the patient was transferred to the intensive care unit intubated and mechanically ventilated.
Postoperatively, the patient received seizure prophylaxis and nimodipine, and was monitored for vasospasm. She was extubated on the post-op day five. She was neurologically intact except for a right third nerve palsy. The EVD was later transitioned to a ventriculoperitoneal shunt. The patient was discharged to a rehabilitation facility on postoperative day 14 and subsequently went home.
- What are the challenges of the case?
- What is the incidence of rebleeding after a cerebral aneurysm rupture?
- What are the phases of treatment of a rupture aneurysm and acute care goals?
- What are goals of acute treatment of a ruptured cerebral aneurysm?
- What are the common complications of a ruptured aneurysm?
- How a ruptured cerebral aneurysm is monitored post the acute phase?
- What are the hemodynamic goals of ruptured cerebral aneurysm following coiling?
- What are the common complications of aneurysmal subarachnoid hemorrhage?
- What is the treatment of a cerebral vasospam following a ruptured cerebral aneurysm?
Challenges of the Case
One challenge is the need for an emergent intubation at a remote location in a patient with low oxygen reserve secondary to severe COPD. Fortunately, the event occurred close to the angiosuite where induction medications and airway equipment were prepared. The development of Cushing Reflex before placement of the EVD is another challenge.
Treatment of Ruptured Cerebral Aneurysm Includes:
- Stabilization of life-threatening conditions: ensuring a secure airway, normalizing cardiovascular function, and treating seizures.
- Acute care recommendations:
- Early repair of the unsecured aneurysm with surgical clipping or endovascular coiling.3, 4
- Serial neurological examination for monitoring clinical deterioration/improvement.
- Blood pressure control: The goal is to maintain SBP <160 mmHg or mean arterial pressure (MAP) <110 mmHg, as recommended by guidelines.2
- Maintenance of euvolemia and normal electrolyte balance: Hypovolemia is a risk factor for ischemic complications and should be avoided. Hyponatremia is common and sodium levels should be checked daily.
- Prophylactic use of Nimodipine: Nimodipine 60 mg every four hours is administered to all patients with aneurysmal SAH. Nimodipine has been demonstrated to improve outcomes in SAH and is the standard of care in these patients.5
Treatment of Complications
Rebleeding usually occurs in the first 24-hours and significantly worsens mortality. Risk factors for rebleeding include aneurysm size, clinical severity of SAH, and systolic pressure of greater than 160 mm Hg. Nicardipine, labetalol, and esmolol are considered first-line agents for BP reduction. Nitroglycerin and sodium nitroprusside should be avoided because they can cause cerebral vasodilation and worsen ICP.6
Cerebral Vasospasm and Delayed Cerebral Ischemia
Symptoms can occur as early as post-bleed day three, usually peak by day 7-10, and begin to resolve by day 14-21. Vasospasm occurs in 40-60% of patients and is associated with symptoms in about 20-30% of cases. Vasospasm causes regional cerebral hypoperfusion and delayed cerebral ischemia and infarction. Vasospasm is suspected with the development of a new focal neurological deficit or global decline in level of consciousness. Transcranial Doppler Ultrasound (TCD) is used as a screening tool for cerebral vasospasm. Mean flow velocities of the middle cerebral artery territories of greater than 120 cm/s and a Lindegaard ratio (MCA velocity/extracranial internal carotid artery velocity) of three or higher are used as thresholds for screening of vasospasm. Vasospasm can be confirmed by CTA or digital subtraction angiography. Other methods for detection include SPECT scans or CT or MR perfusion studies. Nimodipine is the only proven prophylaxis for vasospasm. The traditional treatment was the Triple H therapy. Currently hemodynamic augmentation only is considered the first-line therapy. It is done by maintaining euvolemia and induced hypertension. For refractory vasospasm, endovascular balloon angioplasty and selective intraarterial vasodilator therapy using papaverine, nicardipine and verapamil is used.7
Increased Intracranial Pressure and Hydrocephalus
Increased ICP results from a number of factors including hemorrhage volume, reactive hyperemia, irritation of arachnoid granulation and obstruction of the third ventricle causing obstructive hydrocephalus. If severe, it is treated by endoventricular drainage.8
Acute seizures occur in six to 18% of patients with SAH. Seizures occurring prior to aneurysm treatment are often a sign of early rebleeding. Patients with acute seizures after SAH are treated with antiepileptic medications to prevent recurrence.9
- Electrocardiographic (EKG) abnormalities.
- Neurogenic stunned myocardium (Takotsubo cardiomyopathy) can occur in severe cases. It is usually diagnosed by the presence of elevated troponins, and presence of EKG changes.
- Pulmonary edema develops in 4-42% of SAH patients. It can result from volume overload or neurogenic pulmonary edema thought to be due to high circulating catecholamines. 10
Disruption of the hypothalamic pituitary adrenal axis can occur resulting in supraphysiological levels of cortisol and the loss of diurnal variation. Hyperglycemia can result from elevated circulating cortisol.
Serum Sodium Imbalance
Two common causes of hyponatremia are syndrome of inappropriate diuretic hormone (SIADH) and cerebral salt wasting syndrome (CSWS). Both syndromes present with hyponatremia, however, in patients with CSWS, hypovolemia is present with hyponatremia.
Most cerebral aneurysms don’t rupture. However, when cerebral aneurysms do rupture, they can result in devastating outcomes, including death and disability. Prompt identification and resuscitation followed by early definitive treatment of coiling or clipping is necessary, tight blood pressure control, monitoring the neurologic condition, the prophylactic use of nimodipine are keys to successful treatment. Postoperative treatment includes monitoring and treatment of complications.
- Larsen CC, Astrup J. Rebleeding after aneurysmal subarachnoid hemorrhage: a literature review. World Neurosurg. 2013;79(2):307-12.
- Connolly ES, Rabinstein AA, Carhuapoma JR, Derdeyn CP, Dion J, Higashida RT, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012;43(6):1711-37.
- Lawton MT, Vates GE. Subarachnoid Hemorrhage. N Engl J Med. 2017;377(3):257-66.
- Diringer MN, Bleck TP, Claude Hemphill J, Menon D, Shutter L, Vespa P, et al. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society's Multidisciplinary Consensus Conference. Neurocrit Care. 2011;15(2):211-40.
- Philippon J, Grob R, Dagreou F, Guggiari M, Rivierez M, Viars P. Prevention of vasospasm in subarachnoid haemorrhage. A controlled study with nimodipine. Acta Neurochir (Wien). 1986;82(3-4):110-4.
- Tang C, Zhang TS, Zhou LF. Risk factors for rebleeding of aneurysmal subarachnoid hemorrhage: a meta-analysis. PLoS One. 2014;9(6):e99536.
- Bauer AM, Rasmussen PA. Treatment of intracranial vasospasm following subarachnoid hemorrhage. Front Neurol. 2014;5:72.
- Chen S, Luo J, Reis C, Manaenko A, Zhang J. Hydrocephalus after Subarachnoid Hemorrhage: Pathophysiology, Diagnosis, and Treatment. Biomed Res Int. 2017;2017:8584753.
- Raper DM, Starke RM, Komotar RJ, Allan R, Connolly ES. Seizures after aneurysmal subarachnoid hemorrhage: a systematic review of outcomes. World Neurosurg. 2013;79(5-6):682-90.
- Lele A, Lakireddy V, Gorbachov S, Chaikittisilpa N, Krishnamoorthy V, Vavilala MS. A Narrative Review of Cardiovascular Abnormalities After Spontaneous Intracerebral Hemorrhage. J Neurosurg Anesthesiol. 2019;31(2):199-211.