Successful Perimortem Cesarean Section With Cardiopulmonary Resuscitation and Anesthesia: A Report of an Unique Case.

Cardiac arrest after acute pulmonary edema in pregnancy is an uncommon event but one with a potentially disastrous outcome. We report the case of a pregnant woman with preeclampsia who presented with rapidly advancing pulmonary edema and subsequently went into cardiac arrest on arrival at the operating room. A perimortem cesarean section was performed in addition to cardiopulmonary resuscitation and anesthesia. These simultaneous treatments resulted in excellent maternal and neonatal outcomes. Moreover, therapeutic brain hypothermia was performed. To our knowledge, this is the first case report of a patient undergoing a cesarean section during cardiac arrest and treated with brain hypothermia. We discuss some of the issues arising from the case in this report.

A case of craniocervical junction pial arteriovenous fistula causing postoperative medullary and spinal cord edema.

OBJECTIVES: Pial arteriovenous fistulas (pAVFs) are direct connections between the pial artery and vein without an intervening nidus. We report a rare case of craniocervical junction (CCJ) pAVF causing medullary and spinal cord edema resulting from surgical removal of the varix with remnant shunt after coil embolization. CASE DESCRIPTION: A 16-year-old man presented with subarachnoid hemorrhage. Digital subtraction angiography revealed a CCJ pAVF with multiple fistulas at the 2 varices (varix A and varix B), which was fed by the bilateral lateral spinal arteries and anterior spinal artery (ASA), and drained into the median posterior vermian vein with varix (varix C) and anterior spinal vein (ASV). Varices A and B were embolized using coils, but the shunts remained in varix C. Then, varix C was surgically removed. After this operation, medullary and spinal cord edema occurred. Digital subtraction angiography showed the ASV drainage responsible for edema. Finally, surgical removal of varices A and B was performed. However, arteriovenous shunts, supplied by the ASA and drained into the ASV via the intrinsic vein, were found in the medulla oblongata and coagulated, resulting in disappearance of edema. CONCLUSIONS: Edema was probably caused by concentration of drainage from the arteriovenous shunt in the medulla oblongata into the ASV by surgical removal of varix C acting as another draining route. High flow AVF can induce angiogenesis and secondary arteriovenous shunt. Precise analysis of the angioarchitecture is important to treat such cases without complications.

An autopsy case of amyloid angiopathy-related cerebellar hemorrhage.

An 80-year-old man with dementia demonstrated cerebellar hemorrhage. Autopsy revealed pathology compatible with Alzheimer's disease and cerebral amyloid angiopathy (CAA). CAA was more prevalent in the occipital lobe than in the frontal, parietal, and temporal lobes; however, amyloid-ß (Aß)-containing senile plaques were less abundant in the occipital cortex than in the other cortices. In the cerebellum, abundant CAA-involved vessels were observed in the subarachnoid space and molecular layer and to a lesser extent in the Purkinje and granule layers. On consecutive sections, Aß1-42 immunohistochemistry revealed senile plaques and CAA-involved vessels with strong immunoreactivity whereas Aß1-40 immunohistochemistry identfied CAA-involved vessels with strong immunoreactivity and senile plaques with weak immunoreactivity in the cerebellar cortices.

Spinal epidural arteriovenous fistulas with unusual manifestation of sudden onset of severe neurological deficits: case report.

Spinal epidural arteriovenous fistulas with perimedullary venous drainage cause venous hypertension, and usually manifest as slowly progressive myelopathy. We treated two patients presenting with sudden onset of severe neurological deficits. Moreover, in Case 1, the venous drainage was exclusively epidural and no perimedullary venous drainage was present. Angiographic findings of this patient were characterized by a slow-flow fistula with marked retention of the epidural venous drainage. Rapidly progressing thrombosis of the epidural venous plexus may have caused the sudden onset of the symptoms. In Case 2, hematomyelia may also be possibly associated with the sudden onset of the symptoms. Early diagnosis and treatment are essential to achieve favorable outcome in such cases because venous congestion results in irreversible venous infarction within a short period.

Clinical and angiographic characteristics of cavernous sinus dural arteriovenous fistulas manifesting as venous infarction and/or intracranial hemorrhage.

INTRODUCTION: Cavernous sinus (CS) dural arteriovenous fistulas (DAVFs) rarely cause venous infarction (VI) and/or intracranial hemorrhage (ICH) despite the presence of cortical venous drainage (CVD). The present study investigated the characteristics of CS DAVFs manifesting as VI/ICH. MATERIALS AND METHODS: Fifty-four patients treated for CS DAVFs were retrospectively studied. RESULTS: Six patients presented with VI/ICH. Two of the three patients presenting with ICH had CVD only to the superficial sylvian vein (SSV) or the deep sylvian vein (DSV). Three patients presenting with VI had multiple drainages, and angiography of these patients showed a varix on the SSV, drainage into the DSV with agenesis of the second and third segment of basal vein of Rosenthal, and thrombosis of the distal petrosal vein. CS DAVF with CVD only carries higher risk of VI/ICH than multiple drainages. Many CS DAVFs presenting with VI, especially those with drainage into the petrosal vein, have multiple drainages in the early stage. Thrombosis of the inferior and superior petrosal sinuses and superior orbital vein gradually increases pressure of the CVD, and then, VI may occur. In contrast, CS DAVFs with CVD only from the beginning, common in the patients with drainage into the SSVs and DSVs, are likely to cause ICH. CONCLUSION: Angiographic risk factors causing VI/ICH are CVD only, varix formation, agenesis of the second and third segment of basal vein of Rosenthal, and thrombosis of the superior orbital vein, lateral half of the superior petrosal sinus, and distal CVD.

Urgent stenting for patients with acute stroke due to atherosclerotic occlusive lesions of the cervical internal carotid artery.

Acute symptomatic occlusion of the cervical internal carotid artery (ICA) can be treated by intravenous administration of tissue plasminogen activator, percutaneous transluminal angioplasty, and carotid endarterectomy. Carotid artery stenting (CAS) is now indicated for cervical ICA stenosis, but the safety and the efficacy of urgent CAS have not been established. We retrospectively reviewed 10 patients treated by urgent CAS for atherosclerotic occlusive lesions of cervical ICA with acute stroke. Five patients had complete occlusions and five had near total occlusions. Five of the 10 patients had intracranial tandem occlusions. Indication for urgent CAS was determined by mismatch of diffusion-weighted and perfusion-weighted magnetic resonance imaging findings. Stents were successfully deployed in all lesions. Three of five patients with concomitant intracranial tandem occlusions were treated by additional intraarterial fibrinolysis after the CAS. Intracranial artery occlusions were completely recanalized in one patient, and partially recanalized in two by fibrinolysis. Hyperperfusion syndrome did not occur in any of the patients. A favorable outcome (modified Rankin Scale < or =1) was obtained in all of the five patients with isolated cervical ICA occlusion and one of the five patients with intracranial tandem occlusions. Urgent CAS is a safe and effective treatment in patients with isolated cervical ICA occlusion. Treatment of intracranial tandem occlusions is an issue that must be resolved.

Management of intracranial vertebral artery dissections initially presenting without subarachnoid hemorrhage.

OBJECTIVE: The clinical and angiographic follow-up results for intracranial vertebral artery (VA) dissections that initially presented without subarachnoid hemorrhage (SAH) were retrospectively investigated, to clarify their management. METHODS: Twenty-one patients with VA dissections that initially presented without SAH were studied. Initial angiography revealed aneurysmal dilation in 11 cases (typical pearl-and-string sign in 8 cases, aneurysmal dilation only in 2, and aneurysmal dilation with double-lumen sign in 1), occlusion in 7, double-lumen sign in 2, and string-like stenosis in 1. Nine patients (six with pearl-and-string sign, one with occlusion with aneurysmal dilations, and two with double-lumen sign), including three patients who experienced subsequent SAH, underwent endovascular proximal parent artery occlusion. The other 12 patients were treated conservatively. All patients were monitored with magnetic resonance angiography or digital subtraction angiography. RESULTS: Three patients experienced subsequent SAH, 1 day (two patients) or 51 months after onset. Follow-up angiographic assessments of the 20 patients demonstrated complete resolution in five cases, reduction of aneurysmal dilation in one case, and partial recanalization in one case. However, enlargement or formation of an aneurysmal dilation was recognized in four cases and progression of dissection was observed in one case. Eighteen patients experienced good recoveries, and three patients demonstrated moderate disabilities as a result of the initial ischemic insult. CONCLUSION: The risk of bleeding from unruptured VA dissections is higher than previously considered. Therefore, endovascular treatment should be considered for patients with VA dissections with relatively large or growing aneurysmal dilations.