Cases reported "Hypoxia-Ischemia, Brain"

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1/3. Acute pancreatic damage associated with convulsive status epilepticus: a report of three cases.

    Three cases involving a previously unreported association of acute pancreatic damage following convulsive status epilepticus (SE) are presented. A review of literature failed to reveal a similar association between SE and acute pancreatic damage. As possible pathophysiological mechanisms of this so far unknown sequel of SE, increased intraduodenal pressure during SE leading to the reflux of the duodenal contents into the pancreatic duct, along with altered metabolism of oxygen-derived free radicals during a prolonged seizure with hypoxia and ischemia resulting in acinar cell injury are suggested. We believe that SE should be considered as an additional risk factor of acute pancreatitis and that pancreatic enzymes should be monitored in patients who have prolonged seizures.
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2/3. Novel applications of therapeutic hypothermia: report of three cases.

    Therapeutic hypothermia can provide neuroprotection in various situations where global or focal neurological injury has occurred. hypothermia has been shown to be effective in a large number of animal experiments. In clinical trials, hypothermia has been used in patients with postanoxic injury following cardiopulmonary resuscitation, in traumatic brain injury with high intracranial pressure, in the perioperative setting during various surgical procedures and for various other indications. There is thus evidence that hypothermia can be effective in various situations of neurological injury, although a number of questions remain unanswered. We describe three patients with unusual causes of neurological injury, whose clinical situation was in fundamental aspects analogous to conditions where hypothermia has been shown to be effective.
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3/3. Return of vision after transarterial coiling of a carotid cavernous sinus fistula: case report.

    BACKGROUND: Carotid cavernous sinus fistulae are abnormal communications between the carotid circulation and cavernous sinus that may arise spontaneously or develop after craniocerebral trauma. They may present with a constellation of signs and symptoms characteristic of raised cavernous sinus pressure, including orbital or retro-orbital pain, pulsatile proptosis, chemosis, ocular or cranial bruit, deterioration of visual acuity, or ophthalmoplegia. Visual loss is likely the result of multiple insults to the visual system, including reversal of venous drainage from the fistula, arterial flow into the superior ophthalmic vein, increased intraocular venous pressure, venous stasis retinopathy, and eventually ischemic optic neuropathy [Brodsky MC, Hoyt WF, Halbach VV, et al. Recovery from total monocular blindness after balloon embolization of carotid-cavernous fistula. Am J Ophthalmol 1987;104:86-87; Sanders MD, Hoyt WF. Hypoxic ocular sequelae of carotid-cavernous fistulae: study of the causes of visual failure before and after neurosurgical treatment in a series of 25 cases. Br J Ophthalmol 1969;53:82-97]. CASE DESCRIPTION: With few exceptions, the literature is replete with evidence of persistent blindness despite successful treatment of the CCF [Albuquerque FC, Heinz GW, McDougall CG. Reversal of blindness after transvenous embolization of a carotid-cavernous fistula: case report. neurosurgery 2003;52:233-237; Brodsky MC, Hoyt WF, Halbach VV, et al. Recovery from total monocular blindness after balloon embolization of carotid-cavernous fistula. Am J Ophthalmol 1987;104:86-87; Weinstein JM, Rufenacht DA, Partington CR, et al. Delayed visual loss due to trauma of the internal carotid artery. Arch Neurol. 1991;48:490-497]. Here, we report a patient who experienced recovery of vision after endovascular obliteration of the offending CCF. DISCUSSION: To our knowledge, this is the second reported case of recovery of visual function in a patient presenting with loss of light perception after treatment of a direct CCF.
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