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 neurological 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.[93]
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.[94]
The severity of the haemorrhage 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 haematoma and control of acute bleeding may be required.[61] During an acute intracranial haemorrhage (ICH) episode, blood pressure lowering and reduction in blood pressure variability can reduce haematoma expansion with improved functional outcomes.[45]
Neurological deficit secondary to AVM rupture or the 'steal phenomenon' depends on location of the AVM and size of the haematoma or area of ischaemia. Hospital-based survival cohorts suggest that the morbidity secondary to AVM-associated intracerebral haemorrhage (ICH) is less than with other causes of ICH.[92] 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]
Neurological deficits may be a complication of treatment, due to haemorrhage, oedema, or stroke following surgery, or due to radionecrosis or stroke (late) following stereotactic radiosurgery.
Patients presenting with focal neurological 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 ischaemic attack or stroke.[55][56] Complications at the femoral puncture site include false aneurysms and haematomas ranging from groin to significant retroperitoneal haematomas. The risks of endovascular occlusion include stroke from arterial occlusion or thromboembolic events, aneurysmal rupture, haemorrhagic infarction following inadvertent venous occlusion, arterial dissection, and revascularisation due to recanalisation or the development of collaterals.
Large AVMs are embolised in a staged manner to reduce the risk of haemodynamic stress and bleeding from residual feeders.
Post-operative haemorrhage: early post-operative haemorrhage 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 ischaemia, the risk of post-operative NPPB is increased, but there is little other evidence to support the NPPB theory.[30] In the event of a post-operative haematoma, other reversible causes such as coagulopathies should be excluded and hypertension avoided. Cerebral angiography should be performed to exclude residual AVM.
Other complications include post-operative oedema, surgical site infection, neurological 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 haemorrhage is unchanged.
The incidence of radiation-associated imaging changes after SRS is approximately 35%, while 10% of patients have temporary neurological deficits and 4% have permanent deficits.[95] 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 neurological deterioration.
Hyponatraemia 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 haemorrhage 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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