Chapter 21: Brain Aneurysm and Arteriovenous Malformation Surgery

In order to make an appropriate treatment decision for this patient, etiology of the sub-arachnoid hemorrhage (SAH), whether aneurysmal or traumatic, must first be determined. Most frequently, intracranial aneurysms present to clinical attention with symptoms of major aneurysmal rupture and, therefore, constitute a distinct clinical entity in the setting of SAH. Although rupture nearly always results in SAH, it may also be accompanied by intracerebral hemorrhage (ICH), intraventricular hemorrhage (IVH), and, less often, subdural hemorrhage. This chapter discusses neurologic intensive care specific to surgical interventions for both ruptured and unruptured aneurysms. For NICU management of SAH and its related complications, see Chapter 1.

Symptoms that support a diagnosis of acute SAH due to aneurysmal rupture include:

• Worst headache of life, often with vomiting.

• Unilateral third cranial nerve palsy.

• Sixth nerve palsy.

• In the setting of concomitant ICH: hemiparesis, aphasia, amnesia, deterioration due to cerebral edema.

• In many cases, patients may present with sudden severe headache, but without any focal neurologic symptoms.

If an aneurysmal rupture is suspected, a noncontrast head CT scan must be performed immediately to assess for subarachnoid blood. In the first 12 hours after the initial bleed, noncontrast head CT has a 98% to 100% sensitivity for SAH, which decreases to 93% at 24 hours^1-5 and to 57% to 85% after 6 days.^6,7 If the head CT does not reveal SAH, a mass lesion, or hydrocephalus, a lumbar puncture with analysis of the cerebrospinal fluid for xanthochromia should be performed.⁸

The gold standard for evaluation of cerebral aneurysms remains digital subtraction angiography (DSA), which demonstrates the source of SAH in approximately 85% of patients. Two less invasive modalities are increasingly being used, magnetic resonance angiography (MRA) and CT angiography. Three-dimensional time-of-flight MRA has a sensitivity to detect cerebral aneurysms between 55% and 93%.^9-12 Dichotomizing by size, the sensitivity is 85% to 100% for aneurysms 5 mm or greater, but only 56% for those less than 5 mm in size.^11,13,14 CT angiography, however, is the more frequently used noninvasive modality, as it is faster and more readily available. In addition, it has sensitivity for aneurysms between 77% and 100% and specificity between 79% and 100%.^15-21

Recommended initial therapy includes:

1. Cefazolin sodium injection 1 g IV q8h

2. Nimodipine oral 60 mg PO q4h

3. Levetiracetam injection 1000 mg IVPB q12h

4. Dexamethasone oral 10 mg PO q6h

5. Esomeprazole oral 40 mg PO daily

6. Acetaminophen oral 650 mg PO q4h

7. Ondansetron injection 4 mg IV q3h

(Figure 21-2)

Newly diagnosed cranial nerve (CN) III involvement in the setting of a posterior communicating artery aneurysm implies expansion of the vascular lesion with impending risk of rebleeding. Rebleeding is the major cause of death in patients who survive the initial hemorrhage but do not undergo surgical intervention.^22-24 Table 21-1 demonstrates common interpretations of emerging neurologic signs with regard to location of an expanding aneurysm.

The progression of neurologic deficits in the setting of aneurysmal rupture plays an integral role in deciding on surgical management of the aneurysm. The grading scale proposed by Hunt and Hess²⁵ (see Chapter 1) is a useful tool, but does not replace a comprehensive neurologic examination that can give an accurate and even quantitative assessment of neurologic deterioration as well as its underlying pathophysiology. Therefore, a careful neurologic examination at admission and subsequent points during the hospital stay is an important tool for assessing the outcomes of surgery and identifying, treating, and preventing postoperative complications.

In untreated SAH, the greatest risk of rebleeding occurs on the first day (4%), with a daily frequency of 1.5% until 13 days. By 2 weeks' post-ictus, the rebleed rate is 15% to 20%, and up to 50% by 6 months.²⁴ In the setting of modern tertiary care medical centers, the rate of rebleeding is nearly 7% when prehospital events are excluded,²⁶ although a number of studies refer to a 10% to 20% incidence of "ultraearly" rebleeds by taking into account events that occur before patients receive neurosurgical attention.^27-30 Overall, rebleed events in the first day are associated with a drastically reduced chance of survival, with functional independence at 3 months (modified Rankin score [mRS], ≤ 4; OR, 0.08; 95% CI, 0.02 to 0.34).²⁶ The goal of surgical and endovascular treatment is to prevent this occurrence, and since the 1980s there has been a shift toward early intervention.³¹

The use of antifibrinolytic therapy for the prevention of rebleeding is controversial, as it has been shown to significantly decrease the incidence of rebleeding by 40% to 60%, but has also been shown to increase the risk of ischemic neurologic deficits by a similar margin.^32,33 However, recent evidence has shown that when antifibrinolytic therapy is prophylactically administered before early surgery, preoperative rebleeding rates can be reduced effectively and ischemic complications can be minimized by postsurgical discontinuation of antifibrinolytics.^28,34 ∊-Aminocaproic acid (36 g/day) or tranexamic acid (6 to 12 g/day) can be used for these purposes.³⁵

Interventions that directly address the aneurysm that caused the initial hemorrhage must be carefully considered alongside supportive and prophylactic therapies that treat the primary brain injury and prevent cerebral vasospasm, delayed ischemia, and hydrocephalus. Surgical treatment of an aneurysm is accomplished through craniotomy and aneurysm neck clipping to definitively exclude it from the circulation, thereby removing the risk of rebleeding.

At admission, large amounts of subarachnoid blood visible on CT, which are related to the development and severity of symptomatic vasospasm,³⁶ make early surgery a strong consideration. In fact, the use of hyperdynamic therapy for the treatment of vasospasm becomes a much safer option once an aneurysm has been secured with surgical clipping. Any conditions that contribute to instability of the aneurysm, including seizures and abrupt changes in blood pressure, may also make early intervention beneficial. However, if a patient has active vasospasm or severe cerebral edema at the time of evaluation, then surgery should be delayed.

The timing of intervention is still a source of debate,³⁷ but there are substantial efforts to carry out early management protocols³¹ on account of broad-based support for their implementation garnered through favorable outcome data.^37-40 There is a widely recognized trade-off between early surgical risk of operative mortality and the benefits it confers in terms of rebleeding prevention. In 1990, the International Cooperative Study on the Timing of Aneurysm Surgery, which prospectively followed 3521 patients, reported no difference in outcome between intervention at 0 to 3 days after the original bleed versus 11 to 14 days, but outcomes were definitively worse in the 7- to 10-day interval.³⁹ No subsequent randomized controlled trials have been performed, but more recent observational studies and meta-analyses have argued that the benefits derived from reduction of rebleeding appear to outweigh the risks of early intervention.^35,37,38,40

At our institution, we favor early surgery to prevent rebleeding. Early intervention is strongly indicated in cases where rebleeding has already occurred at least once. Likewise, any indications of an impending rebleed, such as an increase in aneurysm size on serial angiography or new neurologic deficits, including third nerve palsy in the setting of a posterior communicating artery aneurysm,⁴¹ should prompt the clinician to consider surgical intervention. It is important to note that hyperdynamic therapy and bed rest do not prevent rebleeding.⁴² This patient should receive immediate surgical intervention.

This patient has a Hunt and Hess grade IV SAH. Although good medical and neurologic conditions (Hunt and Hess grade < 4) encourage favorable outcomes,^43,44 surgery also remains an appropriate option for patients in poor neurologic condition, as up to 40% of Hunt and Hess grade IV and V patients have been shown to have a good outcome (modified Rankin score 0 to 3) following surgical intervention.^45,46

While the aneurysm remains unsecured, careful blood pressure and volume management must be performed. As a general guideline, this involves maintenance of a target systolic pressure of less than 180 mm Hg and a target mean arterial pressure between 100 and 120 mm Hg, but a definitive target must be established by taking the patient's baseline blood pressure into account.⁴⁷ Some studies have found that rebleeding is more common when systolic blood pressure is above 150 mm Hg²⁷ or 160 mm Hg,²⁹ while others have found no relationship between blood pressure and rebleed rates.²⁶ Differences among these studies are related to the variable use of antihypertensive medications and inconsistent observation times.⁴⁸ At our center, we aim for blood pressure control with short-acting continuous infusion agents that can be delivered safely and with a reliable dose-response profile, such as nicardipine, labetalol, and esmolol. For specific protocols on blood pressure management, refer to Chapter 24.

Upon admission, patients should be started on prophylactic anticonvulsants because of increased seizure incidence in the setting of aneurysmal rupture, as nearly 8% of patients experience seizures at SAH onset and more than 20% of patients experience them after initial hemorrhage.^49,50 Meperidine (Demerol) should be avoided for analgesia because it can lower the seizure threshold, and fentanyl should be used for pain relief instead of morphine to avoid histamine release. Dexamethasone (Decadron) can be given to relieve headache and neck pain and should be started preoperatively when preparing for craniotomy.

When anticipating early surgery, patients should be held NPO (nothing by mouth), and the clinical team must evaluate platelet count, bleeding time, and clotting parameters. Hematocrit levels above 40% significantly increase serum viscosity, as do levels of serum fibrinogen greater than 250 mg/dL. Serum viscosity may play an important role in the setting of vasospasm prevention and treatment, but this assertion has not been definitively evaluated.⁵¹ A hematocrit above 40% at admission can be corrected with delivery of 5% IV colloids or hypertonic saline.^52,53 A hematocrit between 28% and 32% is considered ideal by many clinicians.⁵⁴ Patients with large hemorrhages may be in a state of catecholamine excess due to hypothalamic dysfunction. Myofibrillar necrosis may occur as a result of prolonged myocardial fiber contraction stimulated by high levels of catecholamines, and therefore serum levels of troponin and creatine kinase must be obtained to evaluate for the possibility of myocardial ischemia.

Hydrocephalus is common in the setting of aneurysmal rupture, occurring in 20% to 30% of cases.³⁵ It should be promptly treated by placement of an external ventricular drain (EVD), as there is class I evidence to demonstrate that ventriculostomy improves neurologic status in patients who are symptomatic.^55-57 Fluid therapy with normal saline and 20 mEq KCl/L at 2 mL/kg per hour should be given to prevent hyponatremia caused by cerebral salt wasting because volume contraction has been shown to be correlated with the incidence of symptomatic vasospasm.⁵⁸ Fludrocortisone⁵⁹ and hypertonic saline⁶⁰ can also be used to improve sodium balance. Management of hypovolemia and hyponatremia in connection with cerebral salt wasting and hypervolemia secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are discussed in Chapter 1.

When ICH occurs in the setting of aneurysmal rupture, radiographic studies will often reveal a hematoma at the middle cerebral artery bifurcation extending down to the circle of Willis. The presence of major ICH with mass effect and focal neurologic deficits favors craniotomy for hematoma evacuation and aneurysm clipping.⁴⁷ Notable in this context, however, are the results from the Surgical Trial in Intracerebral Hemorrhage (STICH), which was based on prospective data of 1033 patients. This randomized controlled trial demonstrated that ICH patients do not significantly benefit from early hematoma evacuation in the first 72 hours compared with conservative management of ICH.⁶¹ In the setting of aneurysmal rupture, craniotomy with hematoma evacuation and duraplasty should be considered carefully in patients with ICH, and intervention should be indicated for large hematomas producing rapid deterioration due to mass effect. Additionally, patients with a > 3-cm diameter cerebellar hemorrhage should be treated with expeditious hematoma evacuation as the procedure can be lifesaving.⁶²

Surgical management of unruptured intracranial aneurysms (UIAs) centers on identifying those patients for whom the risk of aneurysmal rupture and consequent SAH exceeds the risks of procedural intervention. Almost 80% of nontraumatic SAH is due to aneurysmal rupture,⁶³ and the 30-day fatality rate of SAH is estimated to be near 15%.⁶⁴ Therefore, the risk of rupture must be taken very seriously. Unfortunately, management of UIAs continues to be fraught with controversy that is in large part due to a lack of definitive data on the natural history of UIAs.

Although UIAs are common, with an estimated prevalence in the general population of 2%,⁶⁵ their average annual rupture rate is considered to be relatively low, ranging from 0.3% to 0.7%.^66,67 However, the risk of rupture is heavily influenced by aneurysm size, location, and history of prior SAH from a separate but successfully treated aneurysm. In the retrospective arm of the International Study of Unruptured Intracranial Aneurysms (ISUIA), UIAs that were < 10 mm in diameter had a rupture rate of 0.05% per year, but this rate increased to 0.5% for patients who had a history of SAH from a previously treated aneurysm. For aneurysms > 10 mm, the rupture rate was near 1% per year irrespective of SAH history, but for giant aneurysms (> 25 mm), the rate was 6% in the first year.⁶⁶

More recently, the prospective arm of the ISUIA, which followed 1692 patients, reported a cumulative rupture rate of 0%, 2.6%, 14.5%, and 40.0% over 5 years for anterior circulation aneurysms that were < 7 mm, 7 to 12 mm, 13 to 24 mm, and ≤ 25 mm in diameter, respectively. For posterior circulation aneurysms, the rates were 2.5%, 14.0%, 18.4%, and 50.0% over the same 5-year period (Table 21-2).⁶⁷ In summary, larger aneurysms and those located in the vertebrobasilar circulation or the posterior communicating artery are at significantly higher risk of rupture than other aneurysms. Small aneurysms (< 7 mm in the ISUIA) have a very low risk of rupture 5 years from diagnosis unless the patient has a history of SAH.⁶⁷ Other comorbidities, such as history of hypertension, abuse of alcohol or tobacco, and family history of aneurysms and SAH, should be taken into account as they may increase the risk of rupture.⁶⁸

The risk of aneurysmal rupture must be weighed against the risks of morbidity and mortality associated with surgical intervention. In a meta-analysis of 61 studies with 2460 total patients, Raaymakers et al found that surgical clipping of UIAs was associated with a 10.9% morbidity and 2.6% mortality rate.⁶⁹ In this cohort, 54% of the aneurysms were in the anterior circulation and 30% were > 10 mm in diameter.⁶⁹ Conversely, in a meta-analysis that solely included asymptomatic UIAs, morbidity and mortality rates were 4.1% and 1.0%, respectively, but 94% of aneurysms were located in the anterior circulation and 28% were greater than 10 mm, likely favoring better outcomes.⁷⁰

Given these statistics on surgical morbidity and mortality, patients with UIAs must be recommended for surgery only when the risk of rupture under conservative management is high. Age plays a central role in this decision making since rupture risk is significantly higher for younger patients owing to accumulation over a greater number of years. Younger patients are also less prone to suffer adverse effects from surgery and thus may benefit most from surgical clipping. The patients for whom management recommendations are most difficult to make include those with (1) UIAs in the anterior circulation 5 to 10 mm in diameter, (2) UIAs in the posterior circulation 3 to 10 mm in diameter, and (3) any UIAs 3 to 10 mm in diameter when there is a history of SAH. This is because the natural history of these lesions and their surgical risks are similar.⁶⁸ Randomized clinical trials comparing conservative management and surgical intervention will be necessary to define appropriate management guidelines in these situations.

UIAs may present symptomatically when they exert pressure on nearby brain parenchyma or cranial nerves. Mass effect from giant aneurysms can involve brainstem compression resulting in hemiparesis and cranial neuropathies. CN III involvement is the most common cranial neuropathy found with an expanding aneurysm, and Table 21-1 reviews typical neurologic deficits associated with expansion at specific aneurysmal locations. In 2% to 3% of cases, UIAs may manifest as ischemic strokes downstream from the aneurysmal sac.^71,72 Seizures may be coincident with UIAs, but most often arise from localized gliosis rather than aneurysmal expansion per se.⁷² Headaches are a common manifestation of UIAs, and the "worst headache of my life" description can also apply to cases that do not rupture. In cases where the disruption caused by symptoms outweighs the risks of surgical treatment, the UIA should be recommended for surgical clipping.

Currently, the guidelines of the Stroke Council of the American Heart Association, which were issued in 2000, before the results from the prospective phase of the ISUIA, remain applicable to management decisions⁷³:

• The treatment of small incidental intracavernous aneurysms is not generally indicated. For large symptomatic intracavernous aneurysms, treatment decisions should be individualized on the basis of patient age, severity and progression of symptoms, and treatment alternatives. The higher risk of treatment and shorter life expectancy in older individuals must be considered in all patients and favors observation in older patients with asymptomatic aneurysms.

• Symptomatic intradural aneurysms of all sizes should be considered for treatment, with relative urgency for the treatment of acutely symptomatic aneurysms. Symptomatic large or giant aneurysms carry higher surgical risks that require a careful analysis of individualized patient and aneurysmal risks and surgeon and center expertise.

• Coexisting or remaining aneurysms of all sizes in patients with SAH due to another treated aneurysm carry a higher risk for future hemorrhage than do similar-sized aneurysms without a prior SAH history and warrant consideration for treatment. Aneurysms located at the basilar apex carry a relatively high risk of rupture. Treatment decisions must take into account the patient's age, existing medical and neurologic conditions, and relative risks of repair. If a decision is made for observation, reevaluation on a periodic basis with CT/MRA or selective contrast angiography should be considered, with changes in aneurysmal size sought, although careful attention to technical factors will be required to optimize the reliability of these measures.

• In consideration of the apparent low risk of hemorrhage from incidental small (<10 mm) aneurysms in patients without previous SAH, treatment rather than observation cannot be generally advocated. However, special consideration for treatment should be given to young patients in this group. Likewise, small aneurysms approaching the 10-mm diameter size, those with daughter sac formation and other unique hemodynamic features, and patients with a positive family history for aneurysms or aneurysmal SAH deserve special consideration for treatment. In those managed conservatively, periodic follow-up imaging evaluation should be considered and is necessary if a specific symptom should arise. If changes in aneurysmal size or configuration are observed, this should lead to special consideration for treatment.

• Asymptomatic aneurysms of ≤ 10 mm in diameter warrant strong consideration for treatment, taking into account patient age, existing medical and neurologic conditions, and relative risks for treatment.

A thorough radiologic workup is necessary to develop an appropriate surgical strategy. DSA with selective cerebral arterial injection is the gold standard for the imaging of UIAs, but head CT and MRI can also be useful in providing information on these lesions, particularly when calcification or thrombosis is present, which cannot be detected by DSA.⁷⁴ Multislice CT angiography is often used instead of DSA because of its quicker image acquisition, lower cost, and minimal invasiveness, but it is less sensitive and specific than DSA.⁷⁵ Likewise, MRA is a minimally invasive procedure, but its sensitivity for detection significantly decreases at aneurysm sizes below 6 mm.⁷⁴

In addition to a general medical examination and routine preoperative laboratory studies, the importance of a careful neurologic examination, as discussed in the section on aneurysmal rupture above, cannot be emphasized enough for its role in identifying postoperative improvement or morbidity.

During surgery, the most dreaded complication is intraoperative rupture of the aneurysm. High-quality preoperative angiography is absolutely essential to give a detailed understanding of the aneurysm's position and all sources of collateral circulation in case temporary clips need to be applied to trap the aneurysm in the event of rupture or difficult neck dissection.

As prophylaxis against possible intraoperative aneurysm rupture and adverse effects of vascular manipulation during the procedure, patients should receive anticonvulsants (phenytoin [Dilantin] IV loading dose 15 mg/kg), corticosteroids, and calcium channel blockers (nimodipine 60 mg PO q4h). Prophylaxis with H₂ blockers (eg, cimetidine) or proton pump inhibitors (eg, omeprazole) is common against gastrointestinal complications from steroids.

The most important complications after aneurysm surgery that differ from routine craniotomies are rebleeding from an incompletely clipped aneurysm, hydrocephalus secondary to SAH, and delayed cerebral ischemia due to vasospasm or perforator occlusion. The major complications after aneurysm surgery are presented in Table 21-3.

Incomplete occlusion must be followed with serial angiography, and reoperation is necessary in the setting of aneurysmal expansion and rebleeding. Prevention of rebleeding is accomplished through careful surgical clipping and verification with immediate postoperative angiography. Postoperative angiography can reveal the presence of an aneurysmal rest, indicating that the neck is not fully occluded by the surgical clip, unintentional vessel occlusion, or another unclipped aneurysm, all of which may be indications for a secondary procedure for clip adjustment.

Hydrocephalus may often present asymptomatically, but a CT scan should be performed in the presence of even subtle cognitive alterations to assess the role of ventriculomegaly in neurologic deterioration. Little reservation should be given to placement of an EVD if indicated by CT and neurologic deficits. Ventriculoperitoneal shunt placement should also be considered after EVD placement when chronic cerebrospinal fluid (CSF) diversion is necessary.

The most important monitoring is timely and consistent neurologic examination of the patient. Whenever neurologic deterioration occurs, CT scanning is a valuable diagnostic tool. Delayed neurologic deterioration occurring secondary to vasospasm is suspected when the CT is negative for hydrocephalus and hematoma and transcranial Doppler (TCD) monitoring reveals high flow velocities. Vasospasm can be treated with calcium channel blockers, balloon angioplasty, and hyperdynamic therapy, and is reviewed thoroughly in Chapter 1.

CT scans can be used to detect a developing subdural, epidural, or intracerebral hemorrhage. Reexploration is necessary to remove large hematomas. In some cases, meningitis may cause neurologic deterioration, and lumbar puncture is necessary to evaluate CSF for the presence of neutrophils, low glucose, or high protein concentration. Furthermore, electrolyte imbalances from diabetes insipidus or cerebral salt wasting should be monitored by routine laboratory studies and treated with fluid therapy as discussed in Chapter 1.

Electrophysiologic monitoring in the first 48 to 72 hours after surgery must be performed to assess for seizure activity. Therapeutic levels of anticonvulsant drugs should only be withdrawn after patients are definitively seizure-free.

Medically, myocardial infarction may be caused by catecholamine excess and is suspected in the face of unexplained changes in vital signs, a high troponin or creatine kinase level, and electrocardiographic (ECG) abnormalities. Use of 12-lead ECG monitoring in the recovery room, nitrate administration, and avoidance of hypertension are indicated in this setting.

Other medical complications may also occur. Deep venous thrombosis (DVT) may occur in the lower extremity, necessitating Doppler monitoring of this region. Thigh-high compression stockings should be used to avoid DVT complications. An inferior vena cava filter can be used in the acute postoperative setting to prevent pulmonary embolism in the presence of DVT, but heparin and warfarin can be initiated 5 days after surgery. Pulmonary embolism can be suspected from worsening arterial blood-gas and ECG abnormalities, but a pulmonary angiogram is required to definitively confirm the diagnosis.

One of the greatest challenges of microsurgical management of AVMs lies in balancing the risk of surgery against the probability of hemorrhage, neurologic deficit, or seizure from the lesion. Microsurgery is not appropriate for all AVM patients, and a thorough understanding of the natural history of AVMs is important in making clinical decisions regarding possible interventions.

In general, AVMs carry a 2% to 4% annual risk of hemorrhage, which rises to 6% to 18% in the first year after an initial hemorrhage. Over a patient's lifetime, this translates into a 17% to 90% risk of rehemorrhage.^76-81 Multivariate modeling has demonstrated that young⁸² or old⁸³ age may increase hemorrhage risk, but results regarding patient sex have been in disagreement.^82,84 Aneurysms are often found to be associated with AVMs in roughly 7% to 41% of cases. These may form inside or near the AVM nidus, in arterial feeders, or at a distance from the AVM. Potential rupture of such aneurysms increases the risk of AVM hemorrhage and, therefore, must be monitored radiographically.^81,85 The goal of microsurgical intervention for AVMs is complete obliteration of the AVM nidus and to eliminate the risk of hemorrhage.

Most commonly, operative risk is assessed using the Spetzler and Martin (SM) grading system for AVMs, which has been widely validated for outcome prediction following microsurgery.^76,86-89 SM grading factors in such AVM characteristics as location, size, and venous drainage pattern provide a basis for exploring AVM management decisions (Table 21-4). Grade I and II lesions are often treated with microsurgery, especially when the AVM presents with a history of hemorrhage. Favorable outcomes following microsurgical intervention have been observed in 92% to 100% of patients with grade I lesions and 94% to 95% of patients with grade II lesions.^86,87,89 Microsurgery for grade III AVMs produces excellent or good outcomes in 68% to 96% of cases^86,87and in 71% to 75% of cases for grade IV AVMs.^76,86,89 Finally, grade V AVMs have been reported to have a good or excellent outcome in only 50% to 70% of cases, accompanied by a 14% to 25% rate of poor outcome and a 0% to 5% mortality rate.^76,86,87,90

Given these figures, microsurgery with adjunctive endovascular therapy is often recommended for grade I and II patients. Grade III lesions are more successfully treated with endovascular therapy followed by microsurgery if they are greater than 6 cm in size (grade IIIA), or with endovascular therapy followed by radiosurgery if they have deep venous drainage and/or are localized to eloquent areas (cortical M1, S1, or V1 regions, which are areas responsible for speech, hypothalamus, thalamus, internal capsule, brainstem, or cerebellar peduncles or nuclei) of the brain (grade IIIB).⁹⁰ Generally, grade IV and V patients are recommended for observation or, in some cases, multimodality treatment. Figure 21-9 summarizes this approach.⁸¹ In the case above, the patient's lesion would be classified as SM grade IIIA, and therefore should be treated with endovascular embolization followed by microsurgery for definitive resection.

Generally, AVM microsurgery is an elective procedure except in emergent cases in which patients present with ICH or life-threatening hydrocephalus caused by hemorrhage. In these cases, clot removal constitutes the primary objective of surgical intervention and resection is only performed after the hematoma-related complications are resolved and the anatomy of the AVM can be carefully elucidated with angiography. If the AVM is readily visualized during clot removal, such as with superficial AVMs, microsurgical resection can be performed together with clot removal.

The presence of focal neurologic symptoms, including seizures, precipitated by AVM are considered to be a factor that favors surgery since AVM excision can lead to symptom resolution.⁸⁵ For instance, in a series of surgically treated AVMs that included 102 patients at 2 year follow-up, 82% were symptom-free 2 years after microsurgery and almost half improved enough so as to discontinue anticonvulsants.⁹¹ Although good seizure control often results from microsurgery, it is affected by duration of seizures, age at onset, and seizure location. Studies with longer-term follow-up are needed to investigate the continuing effects of microsurgery on seizures secondary to AVMs.^81,92

Overall, the best candidates for microsurgical resection are those with an absence of significant medical comorbidities, with a good life expectancy, and with AVMs < 6 cm in size that are located in noneloquent brain areas. A higher risk of hemorrhage, such as seen with AVMs that have associated aneurysms or obstruction of venous outflow, serves as another indication for microsurgical resection.

Management of patients who are asymptomatic, however, remains controversial. In a recent prospective, population-based study of 114 patients with unruptured AVMs, there was no difference in long-term outcome between patients receiving microsurgery and those undergoing conservative management for their AVM, suggesting that monitoring of such lesions may be the best option if there is no history of hemorrhage.⁹³ However, if nonconservative management is attempted with this patient, then embolization followed by definitive resection of the malformation are recommended as treatment.

AVMs are thought to decrease blood flow to the rest of the brain through vascular steal, thereby compromising autoregulatory function of the cerebral vasculature and producing a state of chronic vasodilation. After AVM resection, blood flow to the rest of the brain increases significantly above normal and can lead to severe edema and hemorrhage. First described by Spetzler et al,⁹⁴ the development of malignant cerebral edema or hemorrhage due to normal perfusion pressure breakthrough is the most important complication following AVM surgery.

When surgical intervention is indicated for a large AVM with a high degree of direct arteriovenous shunting, staged treatment of the lesion is recommended for a more gradual reduction in lesion size. This can be accomplished with staged endovascular embolization of arterial feeders before complete surgical resection, thereby minimizing complications associated with normal perfusion pressure breakthrough.⁹⁵

Postoperative NICU care of AVM patients consists of strict blood pressure control and careful maintenance of euvolemia.⁹⁶ Using an arterial catheter, the systolic blood pressure should be maintained at the patient's baseline blood pressure, and parenteral antihypertensives may be used to lower the systolic pressure to < 110 mm Hg in healthy young patients. An indwelling catheter should be used to control urine output. Normotension should be maintained for at least 24 to 48 hours postoperatively. Neurologic status must be constantly monitored, and any observed changes should immediately be followed by an urgent head CT scan to evaluate for the presence of cerebral hemorrhage or hydrocephalus. Cerebral infarctions can be evaluated on diffusion-weighted imaging with MRI. Antiseizure prophylaxis is also needed after AVM surgery.

Although normal pressure perfusion breakthrough may result in hemorrhage, the most common cause of postoperative hemorrhage remains subtotal resection of the AVM. For this reason, it is imperative to perform an angiogram postoperatively to assess whether there are any remnants of the AVM at the site of surgery. When an angiogram reveals only partial obliteration of the AVM, the patient should return to the operating suite until complete excision is attained. Additionally, any complication in the postoperative period warrants prompt evaluation of the patient by angiogram to help in the diagnosis and treatment intervention.