Early rerupture of cerebral arteriovenous malformations: Beware the progressive hemispheric swelling Ralph Rahme, Alexander G. Weil, Michel W. Bojanowski ⇑ Division of Neurosurgery, Hôpital Notre-Dame du CHUM, University of Montreal, Montreal, Quebec, Canada article info Article history: Received 23 September 2010 Accepted 4 January 2011 abstract While early rerupture of cerebral arteriovenous malformations (AVMs) may not be as rare as previously thought, its determinants and risk factors remain unknown. Impairment of the venous drainage of AVMs is a well known risk factor for rupture and has been linked with the development of perinidal cerebral edema. We propose that a significant proportion of early AVM reruptures are the result of post-hemor- rhagic venous drainage impairment, which may manifest as refractory perihematomal edema. To support this hypothesis, an illustrative case of early AVM rerupture occurring 3 weeks following intracranial hem- orrhage and heralded by progressive perinidal and perihematomal edema is presented. This finding should be viewed as a marker for unstable lesions with a high risk of imminent rerupture and should thus prompt a rapid definitive treatment for the AVM. Ó 2011 Elsevier Ltd. All rights reserved. Introduction Although traditionally considered an infrequent event, early rerupture of cerebral arteriovenous malformations (AVMs) was recently reported to occur in as many as 7.4% of patients [1]. Unfor- tunately, the determinants and risk factors of this serious compli- cation remain largely unknown. We postulate that a significant proportion of AVM reruptures are the result of secondary alterations in the venous drainage pat- tern of the AVM following intracranial hemorrhage. In some cases, this manifests as refractory or progressive perinidal and perihe- matomal edema. We propose that this finding is a marker for unstable lesions, predicting a high risk of imminent rerupture because of underlying venous congestion. Early AVM rerupture: clinical case A 62-year old male patient was referred for AVM-related intra- cranial hemorrhage. Six years earlier, he presented to another hos- pital with spontaneous intraventricular hemorrhage. Cerebral angiography revealed a right temporal AVM fed by branches of the middle cerebral artery. The lesion had both superficial and deep venous drainage with multiple venous ectasias and aneu- rysms (Fig. 1). The patient was treated with temporary external ventricular drainage (EVD) and had an uneventful recovery. No treatment aiming at AVM obliteration was undertaken. Instead, the patient was followed with serial angiograms that documented stability of the lesion. A few days prior to his referral to us, the patient developed sud- den headache with left hemiparesis and rapid deterioration of his level of consciousness to a GCS of 8. Head CT revealed a right tem- poral hematoma with intraventricular extension (Fig. 2A). The pa- tient was intubated and underwent emergent EVD placement. Repeat cerebral angiography failed to demonstrate substantial changes in the size and angioarchitecture of the AVM. The pattern of venous drainage, in particular, was identical to that seen on pre- vious angiograms and there were no new identifiable stenoses or occlusions. Over the following few weeks, the patient remained in the same neurological condition without significant improvement and a nor- mal-high intracranial pressure was persistently recorded despite aggressive medical therapy and EVD. Although serial head CTs doc- umented progressive resorption of the hematoma, there was grad- ually increasing perinidal and perihematomal edema causing significant right hemispheric swelling (Fig. 2B and C). Thrombosis of a draining vein with secondary occlusive hyperemia was strongly suspected and thus repeat cerebral angiography was or- dered in preparation for microsurgical resection of the AVM. Unfortunately, in less than 48 h and before the angiogram could be obtained, the patient suffered acute neurological deterioration to a GCS of 6 with right mydriasis and left hemiplegia. Urgent head CT demonstrated massive AVM rebleed with transtentorial hernia- tion secondary to a large temporal hematoma (Fig. 2D). The patient was taken emergently to the operating room where decompressive craniectomy, hematoma evacuation, and AVM resection were per- formed (Fig. 2E). 0306-9877/$ - see front matter Ó 2011 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2011.01.003 ⇑ Corresponding author. Address: Division of Neurosurgery, Hôpital Notre-Dame du CHUM, 1560 Sherbrooke E, Montreal, Quebec, Canada H2L 4M1. Tel.: +1 514 890 8000x26809. E-mail address: michel.bojanowski.chum@ssss.gouv.qc.ca (M.W. Bojanowski). Medical Hypotheses 76 (2011) 570–573 Contents lists available at ScienceDirect Medical Hypotheses journal homepage: www.elsevier.com/locate/mehy