{
  "abstract": "Introduction High grade dural arteriovenous fistulas (BordenII/III dAVFs) have chronic venous hypertension and reduced A-V gradient that renders cerebral perfusion highly pressure-dependent. During DSA arterial phase, high-pressure contrast preferentially enters the low-resistance fistula, augmenting shunt flow and causes a steal. In early venous phase, rapid opacification of cortical veins causes acute elevation of cortical venous pressure which increases intracranial venous blood volume and may raise ICP such that CPP declines. In late venous phase, delayed washout and venous stagnation further signify impaired outflow and sustained elevation of venous pressure, which compromises capillary perfusion and may result in neurological deficits and venous ischemia. We present a case of the same.Materials and Methods Pubmed search of case reports/series.Results A 59-year-old man with hypothyroidism, BPH presented with 4-5 months of cognitive decline, word-finding difficulty, tinnitus, dizziness, gait instability. CTA head neck showed multifocal prominent vessels over posterior fossa and left tentorium, suspicious for high flow vascular malformation/dAVF. MRI brain showed diffusely dilated veins over bilateral cerebral/cerebellar hemispheres. Cerebral angiogram under local anesthesia confirmed a Borden grade 2 dAVF of left transverse sinus with arterial feeders from left parietal branch middle meningeal artery, left medial tentorial artery, bilateral transosseous branches of the occipital arteries, and posterior meningeal artery, with cortical venous reflux into deep venous system (FigA). Additionally there was bilateral traverse sigmoid sinus stenoses and abnormal bihemispheric venous drainage through cortical veins onwards to cavernous sinuses. Immediately after DSA, the patient became aphasic with left gaze deviation and right hemiparesis. Repeat emergent DSA didn’t show LVO. Patient was noted to have a suspected seizure followed by respiratory decompensation requiring intubation. Subsequent MRI brain showed cortical diffusion restriction affecting parieto-temporo-occipital regions in a nonvascular territory (FigB). Despite maximal therapy with sedatives, mannitol, hypertonic saline, steroids, BP control, seizure prophylaxis, the course was complicated by refractory intracranial hypertension and malignant cerebral edema as demonstrated by CSF opening pressure of > 55 on lumbar puncture. Emergent external ventricular drain (EVD) was placed, but refractory ICP elevation persisted. EEG showed severe bilateral cerebral dysfunction but no seizures. The next day patient’s pupils became nonreactive with poor exam and later transitioned to comfort measures only.Conclusion Cerebral angiogram in Borden type II/III dAVFs can transiently convert a compensated state of venous hypertension into acute hemodynamic decompensation through augmentation of cortical venous reflux, increased venous pressure, and reduction of the effective perfusion gradient.Disclosures M. Ismail: None. I. Quraishi: None. R. Goldstein: None. E. Biag: None.Abstract E-299 Figure 1",
  "authors": [
    {
      "affiliations": [
        "Neurology, University of New Mexico Hospital, Albuqerque, NM"
      ],
      "name": "M Ismail"
    },
    {
      "affiliations": [
        "Neurology, University of New Mexico Hospital, Albuqerque, NM"
      ],
      "name": "I Quraishi"
    },
    {
      "affiliations": [
        "Neurology, University of New Mexico Hospital, Albuqerque, NM"
      ],
      "name": "R Goldstein"
    },
    {
      "affiliations": [
        "Neurology, University of New Mexico Hospital, Albuqerque, NM"
      ],
      "name": "E Biag"
    }
  ],
  "title": "E-299 Fulminant cerebral autoregulation failure in high grade dural arteriovenous fistula after cerebral angiogram",
  "uid": "58223422-81b2-54c9-8255-f9aeb58671c7"
}