Anesthetic Management of Intracranial AVMs

Introduction

Intracranial arteriovenous malformations (iAVMs) are relatively rare vascular abnormalities thought to be congenital in etiology; however, angiogenic and inflammatory processes may also play a role in their development. AVMs are a complex tangle of vessels, referred to as the nidus, with feeding arteries and draining vein(s) that lack a true intervening capillary bed (see Chapter 1 ). In contrast to normal cerebral vascular beds, an iAVM is a low-resistance, high-flow system, with shunt flow proportional to the size of the lesion. Accordingly, the risk of spontaneous rupture is thought to be higher in smaller iAVMs due to the higher intranidal pressure and venous hypertension.

The anesthesiologist will encounter patients with iAVMs scheduled for diagnostic imaging and therapeutic treatment in the operating room (OR), interventional neuroradiology suite, or stereotactic radiosurgery suites. Optimal perioperative anesthetic management necessitates knowledge of the basic physiologic and pharmacologic principles inherent to neuroanesthesia as well as intimate understanding of the physiology of iAVMs and the common complications that may arise in the perioperative period. This chapter reviews basic cerebral vascular physiology unique to iAVMs as well as anesthetic goals and considerations for elective treatment; the management of perioperative complications is addressed in Chapter 26 .

Presentation

The most common clinical presentation is related to sequelae of intracranial hemorrhage. Diagnosis is typically made in relatively young patients, with 75% of the hemorrhagic presentations occurring before the age of 50. Clinical manifestations can include seizures, headache, and focal neurologic findings from mass effect of the lesion on surrounding tissues. Although the long-term risk of hemorrhage is controversial and dependent on specific characteristics, natural history studies suggest an annual hemorrhage risk of 2%–3%. The risk of rehemorrhage appears to be higher than the risk of initial hemorrhage for some modest period of time. The primary goal of treatment is complete obliteration of the lesion to prevent future hemorrhages.

Treatment

Intracranial AVMs are typically treated electively by microsurgical resection, interventional neuroradiology (INR) embolization, stereotactic radiosurgery, or a combination of these modalities. Staged INR embolization prior to microsurgical resection is commonly performed to reduce the lesion size, decrease intraoperative blood loss, occlude deep feeding vessels that are anatomically challenging during open resection, and provide staged flow reduction to the nidus, thus potentially reducing the incidence of postoperative complications due to large acute changes in flow dynamics.

Infrequently, emergent craniotomy may be required to evacuate a life-threatening hematoma due to a ruptured iAVM. In such cases, superficial iAVMs may be resected in conjunction with hematoma evacuation. Resection of more complicated iAVMs is typically deferred until the anatomy is well defined with a diagnostic cerebral angiogram and the patient is otherwise optimized for surgery.

From an anesthesia perspective, microsurgery involves three basic components: (1) obliteration of arterial feeders, (2) circumferential resection of the nidus, and (3) ligation of draining veins. It is critically important that arterial input is controlled prior to sacrificing venous drainage, or malignant edema may result.

Cerebrovascular Physiology

AVMs are vascular abnormalities with high flow and low resistance due to direct connection of arteries to veins without true intervening capillaries. The result is that blood preferentially travels the path of least resistance and thus is shunted away from parallel vascular beds that perfuse the brain as an end organ.

Consequently, relative arterial hypotension occurs in neighboring beds sharing the same vascular supply. In larger iAVMs with high flow, perfusion pressures may be below the normal range of autoregulation. Despite this, ischemic symptoms are very rare, cerebral blood flow (CBF) may be normal, and autoregulation preserved. These findings suggest an adaptive autoregulatory response. This adaptive response has been explained by displacement of the autoregulation curve to the left as opposed to the rightward shift seen in chronic hypertension. This helps explain why CO ₂ responsiveness may be preserved preoperatively (though diminished in the arterial feeders), and nearly universally postoperatively. In summary, prior to AVM resection, a subset of patients may have local cerebrovascular beds with reduced CBF or near-normal CBF with perfusion pressures that approximate the lower limit of autoregulation. Further reductions in cerebral perfusion pressure may increase the risk of ischemia, particularly when combined with brain retraction and surgical manipulation.

Following iAVM resection, feeding artery pressure increases due to loss of the pathologic low-resistance pathway previously offered by the AVM. Feeding arteries are commonly dilated and do not return to normal caliber immediately after iAVM resection. Therefore based on the Poiseuille equation, there will be less pressure reduction than would typically occur along the length of the vessel. The increased vessel diameter may also increase reflection waves, resulting in higher peak pressures. Although there is evidence that autoregulation is intact following iAVM resection, it is possible that a small subset of patients do have impaired local autoregulation. At the very least, if local cerebral perfusion pressure exceeds the left-shifted local autoregulatory capacity of the resistance arterioles, the patient may be at risk of hyperemia causing cerebral edema and/or hemorrhage (normal perfusion pressure breakthrough). Alternatively, in contrast to the previous concern, patients may be at risk of stagnation or thrombosis in both veins and arteries following iAVM resection due to abnormal vessel modeling resulting from the previous high flow. Resection of an iAVM may thus reduce vessel runoff below that which is required to prevent stagnation (occlusive hyperemia). In response to these opposing hemodynamic concerns, the ideal postresection hemodynamic management remains controversial due to risk for both hyperemia-induced edema with or without hemorrhage and stagnation-induced ischemia or hemorrhage due to venous back pressure. For this reason, many centers focus on strict normotension, which is most commonly defined by the patient’s preoperative blood pressure.