Complications
In general, the risk of seizure in a person with an AVM is 8% over 5 years, and this increases to 23% if there is a focal neurologic deficit or ICH. After a first seizure, the risk of subsequent seizures increases, and the 5-year risk of epilepsy is 58%.[59] In patients presenting with an AVM without seizures, 18.4% had de novo seizures after surgical treatment.[94]
A systematic review reported that 82% of patients were seizure-free after obliteration of an AVM by any modality, and 41% were seizure-free after incomplete obliteration.[95]
The severity of the hemorrhage may be conferred by its size, laterality, location, degree of mass effect, and Glasgow Coma Scale score of the patient. In patients with a ruptured arteriovenous malformation (AVM), emergent surgical evacuation of the intracerebral hematoma and control of acute bleeding may be required.[61] During an acute intracranial hemorrhage (ICH) episode, blood pressure lowering and reduction in blood pressure variability can reduce hematoma expansion with improved functional outcomes.[45]
Neurologic deficit secondary to AVM rupture or the "steal phenomenon" depends on location of the AVM and size of the hematoma or area of ischemia. Hospital-based survival cohorts suggest that the morbidity secondary to AVM-associated intracerebral hemorrhage (ICH) is less than with other causes of ICH.[93] Theoretically, lower morbidity could be explained by a younger cohort of patients, less vasospasm, low-pressure bleeds, improved detection of small ICH, and redistribution of cognitive function.[2]
Neurologic deficits may be a complication of treatment, due to hemorrhage, edema, or stroke following surgery, or due to radionecrosis or stroke (late) following stereotactic radiosurgery.
Patients presenting with focal neurologic deficits should undergo computed tomography and magnetic resonance imaging brain imaging.
The risks of stroke from angiograms for AVMs (0.5%) are lower than following angiograms for transient ischemic attack or stroke.[55][56] Complications at the femoral puncture site include false aneurysms and hematomas ranging from groin to significant retroperitoneal hematomas. The risks of endovascular occlusion include stroke from arterial occlusion or thromboembolic events, aneurysmal rupture, hemorrhagic infarction following inadvertent venous occlusion, arterial dissection, and revascularization due to recanalization or the development of collaterals.
Large AVMs are embolized in a staged manner to reduce the risk of hemodynamic stress and bleeding from residual feeders.
Postoperative hemorrhage: early postoperative hemorrhage is uncommon (<5% incidence).[30] It is attributed to normal perfusion pressure breakthrough (NPPB), which is attributed to loss of local autoregulation. Following the removal of high-flow, low-resistance AVMs that pose increased risk of local ischemia, the risk of postoperative NPPB is increased, but there is little other evidence to support the NPPB theory.[30] In the event of a postoperative hematoma, other reversible causes such as coagulopathies should be excluded and hypertension avoided. Cerebral angiography should be performed to exclude residual AVM.
Other complications include postoperative edema, surgical site infection, neurologic deficit, new-onset epilepsy, and stroke. The Spetzler-Martin grading system is used to predict the risk of surgery.[6]
Overall, there is a 5% to 7% risk of complications secondary to stereotactic radiosurgery (SRS). AVMs take approximately 2 to 5 years to resolve following SRS.[62] During this time the risk of hemorrhage is unchanged.
The incidence of radiation-associated imaging changes after SRS is approximately 35%, while 10% of patients have temporary neurologic deficits and 4% have permanent deficits.[96] Delayed cyst formation or neoplasia can occur 10 years after SRS.
Superficial AVMs are difficult to treat with SRS due to the risk of local hair loss and radiation damage to overlying skin. Other complications of SRS are delayed and include failure to obliterate the AVM, stroke, and radionecrosis causing neurologic deterioration.
Hyponatremia due to syndrome of inappropriate secretion of antidiuretic hormone (SIADH) or cerebral salt wasting (CSW) is a frequent finding in patients with brain injury such as intracerebral hemorrhage or following surgery.
SIADH results from a failure to excrete water and is treated primarily with fluid restriction.
CSW results from renal sodium loss with consequent reduction in intravascular volume. It is treated with sodium replacement. Fluid restriction is contraindicated.
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