Abstract
Aneurysm rebleed can lead to catastrophic deterioration in clinical condition with worsening of Glasgow Coma Scale score and increased subarachnoid/ intraventricular blood, leading to impaired cerebral perfusion. Rebleeding carries a high mortality of greater than 60%. The risk of rebleeding is highest in 2 to 12 hours after a subarachnoid hemorrhage. Early treatment can reduce the risk of rebleeding. Aggressive treatment in the endovascular suite, surgical suite, or medical management in the critical care unit have led to a reduction in poor outcomes. Intraoperative rupture of aneurysms carries a 6% to 8% mortality rate with surgical- as well as anesthesia-related factors. Hypertension is the single most contributing factor. The goals of management of aneurysmal rebleed are an intricate balance between blood pressure, intracranial pressure, fluid management, and temperature regulation.
Keywords
aneurysm rebleeding, intracranial aneurysm. aneurysm rupture, neuroanesthesia emergency, subarachnoid haemorhage, transmural pressure gradient, vasospasm
Case Synopsis
A 55-year-old man undergoing craniotomy for clip-ligation of a right anterior communicating artery aneurysm 12 hours after initial subarachnoid hemorrhage becomes acutely hypertensive and experiences bradycardia during the induction of anesthesia.
Acknowledgment
The authors wish to thank Dr. Philippa Newfield for her contribution to the previous edition of this chapter.
Problem Analysis
Definition
Intracranial aneurysms are outpouching of arteries developing secondary to turbulent flow and hemodynamic stress. Aneurysmal rebleeding is defined as a rerupture of the aneurysm, causing sudden clinical deterioration (a decrease in Glasgow Coma Scale [GCS] score in awake patients) with a concomitant increase of subarachnoid, intracerebral, or intraventricular blood.
Rebleeding raises intracranial pressure (ICP), leading to impairment of cerebral perfusion, causing neurologic deterioration. Many complications may ensue ( Table 60.1 ). Sudden clot deposition throughout the subarachnoid space blocks the passage of cerebrospinal fluid (CSF) through the basal subarachnoid cisterns, producing acute hydrocephalus. Brain infarction may also occur due to direct, hematoma-induced brain destruction or shifts in the intracranial contents, along with vascular compromise. The larger the volume of subarachnoid blood and the greater the ICP, the more likely it is that cerebral blood flow (CBF) will be reduced and the patient’s neurologic condition will worsen. Subarachnoid hemorrhage (SAH) also impairs autoregulation, the ability of the brain to maintain CBF fairly constant over mean arterial pressures (MAPs) between 50 and 150 mm Hg.
| Early | Late |
|---|---|
| Hematoma, ↑ ICP, rebleeding, seizures, hydrocephalus | Rebleeding, hydrocephalus, vasospasm, infarction, epilepsy |
| Nerve palsy, hemiparesis, reduced LOC | Permanent hemiparesis, cognitive disabilities |
| Cardiac arrhythmias | Myocardial infarction, pneumonia, hepatic and renal dysfunction |
| Transient ↑ BP | Persistent ↑ BP |
| Impaired vision | Vitreous hemorrhage |
| Fluid and electrolyte imbalance | Neurologic deterioration, death |
Epidemiology
Overall prevalence of unruptured intracranial aneurysms is 3.2%, and subarachnoid hemorrhage (SAH) from the rupture of an intracranial aneurysm (ICA) occurs with a frequency of 0.002% to 0.016% in most Western populations. Rates of ICA rupture are 0.05% to 6% per year, depending on the size and location of the aneurysm. Most (80% to 85%) of the ICAs are located in the anterior circulation, with a propensity to rupture when larger than 7 mm. The risk of rupture is 11 times greater in patients who present with a previous SAH than in those patients who present with symptomatic unruptured aneurysms.
Rebleeding following SAH can be catastrophic, with poor prognosis for functional recovery in survivors, and carries a mortality rate of greater than 60%. The risk of rebleeding is maximal in the first 2 to 12 hours, with up to 13.6% within the first 24 hours and up to 23% over the first 72 hours. In fact, more than one-third of rebleeds occur within 3 hours and nearly half within 6 hours of symptom onset, and early rebleeding is associated with worse outcome than later rebleeding. Van Donkelaar and colleagues suggested that a modified Fisher grade of 3 to 4 ( Table 60.2 ) was a predictor for an in-hospital rebleeding within 24 hours after onset of prodromal signs. Also, the initiation of external cerebrospinal fluid drainage was independently associated with a rebleeding within 24 hours. In their study, cumulative in-hospital rebleeding rates were 5.8% within 24 hours and 1.2% between 24 to 72 hours after onset of prodromal signs. Early treatment of the ruptured aneurysm can reduce the risk of rebleeding. In the Cerebral Aneurysm Rerupture After Treatment (CARAT) study, recurrent aneurysmal SAH (aSAH) was predicted by incomplete obliteration of the aneurysm and occurred a median of 3 days after treatment but rarely after 1 year. Patients with adequately obliterated aneurysms after aSAH have a low risk of recurrent aSAH for at least 5 years, although some coiled aneurysms require retreatment. In patients presenting later for definitive treatment, during the vasospasm window, delayed obliteration of aneurysm is associated with a higher risk of rebleeding than early obliteration of aneurysm. If untreated, 50% of ruptured ICAs rebleed within 6 months of the initial SAH. About 20% to 30% of ruptured ICAs rebleed within 30 days of the initial SAH. Another 10% to 15% of patients rebleed during the ensuing 5 months.
| Group 1 | No blood detected |
| Group 2 | Diffuse deposition of subarachnoid blood less than 1 mm thick |
| Group 3 | Localized clots and/or vertical layers of blood 1 mm or greater in thickness |
| Group 4 | Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots are present |
The incidence of intraoperative aneurysm rupture (IAR) ranges from 6% to 8%. It varies among institutions and depends on the size and location of the aneurysm. It results from a complex interaction of etiologic factors of aneurysm formation, as well as factors related to anesthesia, surgery, or other interventions. Surgical causes of aneurysm rupture and rebleeding, in decreasing order of frequency, are dissection, brain retraction, hematoma evacuation, and opening of the dural and arachnoid membranes. Induction of anesthesia can precipitate IAR (1% to 2% incidence), with very poor prognosis and mortality rate of 75%. The majority of ruptures occurred during coughing on intubation, indicating that airway manipulation and the resultant sympathetic surge could be the contributing factor.
Recognition
Signs of rebleeding with reruptured ICAs are largely due to intracerebral hemorrhage. This is because adhesions from the prior SAH seal off the aneurysm from the subarachnoid space and deflect any new bleeding into the brain parenchyma.
After ICA rebleeds, the level of consciousness (GCS score) deteriorates in an awake patient, and patients develop focal neurologic deficits (aphasia, hemiplegia), abnormal vital signs (hypertension, bradycardia, arrhythmias, irregular respirations), and temperature elevation. They also have fluid and electrolyte imbalance (especially hyponatremia), and retinal hemorrhage may be evident on ophthalmologic examination ( Box 60.1 ). Patients in an already poor clinical condition and who are intubated and sedated and closely monitored in the intensive care unit may already have an external ventricular catheter. In case of a sudden change of blood pressure (BP), pupil size, or fresh blood coming out of the CSF drainage system, computed tomography would confirm a rebleeding.
Direct brain destruction
Disturbance of CSF flow → hydrocephalus
↑ ICP from hematoma, intracerebral hemorrhage, intraventricular hemorrhage
Cerebral infarction from ↓ CBF
Fluid and electrolyte imbalance
Cardiac arrhythmias, ↑ BP
Respiratory impairment
BP, Blood pressure; CBF, cerebral blood flow; CSF, cerebrospinal fluid; ICP, intracranial pressure.
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