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Neurology India, Vol. 52, No. 1, January-March, 2004, pp. 111-115 Case Report Normal perfusion pressure breakthrough in arteriovenous malformation surgery: The concept revisited with a case report Kumar S, Kato Y, Sano H, Imizu S, Nagahisa S, Kanno T Department of Neurosurgery, Fujita Health University, 1-98 Dengakubakubo, Kutsukake-cho, Toyoake, Aichi-470-1192 Code Number: ni04030 Abstract The pathophysiological mechanisms and the salient features of normal perfusion pressure breakthrough (NPPB) are discussed on the basis of an operated case of arteriovenous malformation. Introduction Multifocal hemorrhage along with cerebral edema can be a frightening and sometimes catastrophic postoperative complication in high flow cerebral arteriovenous malformation (AVM) surgery. This phenomenon, termed as ′normal perfusion pressure breakthrough′ (NPPB), has been attributed to the diversion of bloodflow from the AVM, after its resection, into the adjacent cortical blood vessels. A case of arteriovenous malformation is presented and the changes in the hemodynamics during and after surgery are assessed. Case Report A 44-year-old male presented with frequent episodes of generalized seizures. There was no neurological deficit. Investigations revealed arteriovenous malformation in the left parieto-occipital lobe. Left carotid and vertebral angiograms showed large high flow feeders to the AVM from the posterior cerebral, middle cerebral as well as anterior cerebral arteries. The venous phase delineated the draining veins to the superior sagittal sinus as well as to the internal cerebral veins [Figure - 1]. C-99M Single photon emission computed tomography (SPECT) showed a hypervolemic lesion adjacent to the nidus. In 123I-IMP SPECT scan, the left parietal cortex adjacent to the nidus showed abnormally decreased perfusion. DIAMOX activated 123I-IMP SPECT scan showed perifocal hypoperfusion in the area within the left parietal lobe as well as the limitation of cerebral vasodilatory capacity in the perinidal area [Figure - 2]. The patient was operated with standard microsurgical techniques. Through a subtemporal approach the main feeder from the posterior cerebral artery (PCA) was clipped. Through the interhemispheric approach, temporary clips were applied to the middle cerebral artery (MCA) and the anterior cerebral artery (ACA) feeders. The lesion was subsequently completely excised. Intraoperatively, the local cortical blood flow (lcoBF) was more than 20 ml/100 gm/min, when the temporary clip was placed on the main feeder from the MCA [Figure - 3]. CT scan brain on postoperative Day 1 showed cerebral edema and an enlarged vascular tubular enhancement in the left parieto-occipital lobe, suggesting hyperemia [Figure - 4] upper). Significant hyperperfusion was found in the left frontoparietal lobe in the dynamic scan image of 123I-IMP SPECT scan. However, on postoperative Day 1 and Day 8 static images of the0123 I-IMP SPECT scan study showed an area of hypoperfusion in and adjacent to the nidus site. This suggested that the hyperperfusion had disappeared on postoperative Day 8 [Figure - 5]. CT scan also showed an improvement in the hyperemic state. CT scan done 3 weeks later showed marked reduction in the cerebral edema [Figure - 4] Lower). Postoperative angiogram done on Day 5 showed stagnation in the feeders and delayed circulation [Figure - 6]. One month later, the angiograms showed normalization of flow in the stagnating arteries. There was no postoperative neurological deficit. Discussion AVM surgery can be complicated by postoperative cerebral edema and hemorrhage in the adjacent brain tissue. Various theories have been put forward to explain the hemodynamic basis for this phenomenon, which include disordered autoregulation causing NPPB and obstruction of venous drainage leading to occlusive hyperemia. 1. Concept of normal perfusion pressure breakthrough (NPPB) Al-Rodhan et al[2] presented an alternative concept of occlusive hyperemia. They argued that postoperative intracranial bleeding or edema may result in (1) occlusion of the draining venous system in the brain surrounding the AVM, followed by passive hyperemia and stagnation; and (2) stagnation in the feeding artery for the AVM and in the blood flow in the parenchymatous branching of the artery, followed by exacerbation of pre-existing hypoperfusion, ischemia, or edema. Wilson et al[3] argue that this condition is observed frequently following embolization. Rapid neurological deterioration follows thrombus formation in a main draining vein. This is called "venous overload". They state that venous overload can be "malignant" if venous occlusion occurs in the presence of nidus remnant. 2. Histopathological assessment of brain surrounding the AVM 3. Prediction of NPPB occurrence 4. Is NPPB present?[10] Causes of intraoperative NPPB occurrence 5. Prevention of intraoperative NPPB occurrence[10] (1) Feeder embolization refers to the occlusion of feeding arteries not easily accessible with a remnant nidus and thus requiring a pre-operative session/sessions. In the case of proximal occlusion of a main feeder only, prevention of NPPB is non-significant because of increased hemodynamic stress on the small feeders in the surrounding area and elevated inflow into a non-occluded remnant nidus of low vascular resistance. (2) Nidus embolization refers to an embolization extending from a feeding artery to the nidus. This technique is thought to accelerate a natural course of thrombogenesis by inducing stagnation of blood flow from other feeders via rapidly decreasing outflow into the drainers. This approach is expected to decrease the nidus in size and lower the A-V shunt volume, leading to resumption of autoregulation in the surrounding area and hence NPPB prevention. In patients who underwent an actual operation, the state of the surrounding brain did not change considerably when the operation was conducted 1-2 weeks after embolization, but in those subjected to operation at about 1 month after embolization, vasoparalysis of the surrounding brain improved, suggesting NPPB prevention.[1] On the other hand, embolization extending into the nidus involves risks such as venous occlusion by an embolizing material, resulting in increased intra-nidus pressure; or isolated nidus formation by an embolizing material migrated postoperatively, causing bleeding. Risk of venous occlusion is particularly high in cases of multifeeders coupled with a single drainer. Important points in intraoperative bleeding control 1) Management of feeders over 1 mm in diameter Coagulation is to be achieved underwater, by holding a vessel gently without closing the bipolar completely (wet-bipolar coagulation system) and by decreasing blood flow through mechanical pressure applied centrally. When these measures do not achieve satisfactory hemostasis, applying pressure to the bleeding site with compactly folded oxycel cotton moistened with Biobond ® may work. If bleeding does not stop by applying pressure only, caution is required, because intracerebral hematoma may develop right below the compressed site. Coagulation must be ensured for expanded capillaries prior to complete occlusion of veins, and for vessels supplying the normal side of the brain. Failure to achieve hemostasis at the capillary level: The source of hemorrhage should be located by tracking down the capillary to the arteriole level as and when required, to achieve complete arrest of bleeding. Prediction and countermeasures for intra- and postoperative perifocal hyperemic state and NPPB occurrence. Caution should be exercised for patients who show an intense steal phenomenon in the area surrounding the nidus, which is indicated by low perfusion detected by postoperative SPECT and decreased vasodilative reaction in the Diamox ® loading test, and who show increased peripheral blood flow, by clipping of feeding arteries, as perfusion breakthrough-associated complications may develop postoperatively.[7],[10] In these patients who are presumably prone to developing a hyperemic state postoperatively, blood pressure should be maintained below 150 mmHg during and after the operation, and the barbiturate dose should be adjusted downward about a few days to one week after the operation. Conclusion NPPB is responsible for massive hemorrhage and cerebral edema even after meticulous hemostasis during AVM surgery. SPECT study and local cerebral blood flow study should be performed. Preoperative 1) feeder embolization and 2) nidus embolization are available for selective embolization of feeding arteries for prevention of NPPB. Intraoperative bleeding control should be tackled by the management of feeders over 1mm in diameter, with hemo clips along with adequate capillary coagulation. References
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