Cerebellar infarct following orchidopexy under spinal anesthesia / Infarto cerebelar após orquidopexia sob raquianestesia

Abstract The report describes a case of peri-operative stroke that presented as diplopia and gait difficulty on 2nd post-operative day after routine orchidopexy under spinal anesthesia in an otherwise healthy young boy. Magnetic resonance imaging of the brain revealed acute infarct in bilateral cerebellar hemispheres, left half of medulla and left thalamus. A diagnosis of acute stroke (infarct) was made and patient was started on oral aspirin 75 mg.day-1, following which his vision started improving after 2 weeks. Possible mechanisms of development of stroke in the peri-operative period are discussed, but, even after extensive investigations, the etiology of infarct may be difficult to determine. Acute infarct after elective non-cardiac, non-neurological surgery is rare; it may not be possible to identify the etiology in all cases. Clinicians must have a high index of suspicion to diagnose such unexpected complications even after routine surgical procedures in order to decrease the morbidity and long term sequelae.

Resumo O presente relato descreve um caso de acidente vascular cerebral perioperatório que resultou em diplopia e dificuldade de marcha no segundo dia após orquidopexia de rotina sob raquianestesia em um jovem, em outros aspectos, saudável. Ressonância magnética cerebral revelou infarto agudo em hemisférios cerebelares bilaterais, metade esquerda do bulbo e tálamo esquerdo. Um diagnóstico de acidente vascular cerebral agudo (infarto) foi feito e o paciente começou a receber tratamento com aspirina oral (75 mg.dia-1), após o qual sua visão começou a melhorar após duas semanas. Possíveis mecanismos de desenvolvimento de acidente vascular cerebral no período perioperatório são discutidos, mas, mesmo após extensas investigações, a etiologia do infarto pode ser difícil de determinar. O infarto agudo após cirurgia eletiva não cardíaca e não neurológica é raro; talvez não seja possível identificar a etiologia em todos os casos. Os médicos devem ter um elevado grau de suspeita para diagnosticar essas complicações inesperadas, mesmo após procedimentos cirúrgicos de rotina, para diminuir a morbidade e as sequelas em longo prazo.

Massive Life-threatening Lower Gastrointestinal Hemorrhage Caused by an Internal Hemorrhoid in a Patient Receiving Antiplatelet Therapy: A Case Report / 대한소화기학회지

A Dieulafoy lesion in the rectum is a very rare and it can cause massive lower gastrointestinal bleeding. An 83-year-old man visited our hospital. He had chronic constipation and had taken aspirin for about 10 years because of a previous brain infarction. He was admitted because of a recent brain stroke. On the third hospital day, he had massive hematochezia and suddenly developed hypovolemic shock. Abdominal computed tomography showed active arterial bleeding on the left side of the mid-rectum. Emergency sigmoidoscopy showed an exposed vessel with blood spurting from the rectal wall. The active bleeding was controlled successfully by an injection of epinephrine and two hemoclippings. On the fourth day after the procedure, he had massive recurrent hematochezia, and his vital signs were unstable. Doppler-guided hemorrhoidal artery band ligation was performed urgently at two sites. However, he rebled on the third postoperative day. Selective inferior mesenteric angiography revealed an arterial pseudoaneurysm in a branch of the superior rectal artery, as the cause of rectal bleeding, and this was embolized successfully. We report a rare case of life-threatening rectal bleeding caused by a Dieulafoy lesion combined with pseudoaneurysm of the superior rectal artery which was treated successfully with embolization.

Massive Life-threatening Lower Gastrointestinal Hemorrhage Caused by an Internal Hemorrhoid in a Patient Receiving Antiplatelet Therapy: A Case Report / 대한소화기학회지

A Dieulafoy lesion in the rectum is a very rare and it can cause massive lower gastrointestinal bleeding. An 83-year-old man visited our hospital. He had chronic constipation and had taken aspirin for about 10 years because of a previous brain infarction. He was admitted because of a recent brain stroke. On the third hospital day, he had massive hematochezia and suddenly developed hypovolemic shock. Abdominal computed tomography showed active arterial bleeding on the left side of the mid-rectum. Emergency sigmoidoscopy showed an exposed vessel with blood spurting from the rectal wall. The active bleeding was controlled successfully by an injection of epinephrine and two hemoclippings. On the fourth day after the procedure, he had massive recurrent hematochezia, and his vital signs were unstable. Doppler-guided hemorrhoidal artery band ligation was performed urgently at two sites. However, he rebled on the third postoperative day. Selective inferior mesenteric angiography revealed an arterial pseudoaneurysm in a branch of the superior rectal artery, as the cause of rectal bleeding, and this was embolized successfully. We report a rare case of life-threatening rectal bleeding caused by a Dieulafoy lesion combined with pseudoaneurysm of the superior rectal artery which was treated successfully with embolization.

Aminoguanidine reduces infarct volume and improves neurological dysfunction in transient model of focal cerebral ischemia in rat

Focal cerebral ischemia [Stroke] is the cessation or severe reduction of blood flow to an area of the brain that through activation of a complex cytotoxic cascade results in neuronal cell death. The present study was designed to examine the effects of post-ischemic treatment with aminoguanidine [AG] on cortical, striatal infarct volume as well as neurological dysfunctions. Rats [n=23] were allocated to sham, saline or AG [300 mg/kg]-treated groups. Ischemia was induced by 90 minutes middle cerebral artery occlusion, followed by 24 hrs reperfusion. Saline or AG was administered intraperitoneal at one hour after induction of ischemia. At the end of 24hrs reperfusion, neurological deficit score was tested and cortical, striatal infarct volumes were determined by Triphenyltetrazolium chloride staining. Administration of AG [300 mg/kg] at one hours after ischemia resulted in a significantly lower cortical [85 +/- 25 vs. 210 +/- 13 mm[3]], striatal [35 +/- 5 vs. 58 +/- 10 mm[3]] infarct volumes, and neurological deficit score [1.88 +/- 0.23vs.2.67 +/- 0.21]. Our findings indicate that aminoguanidine is a potent neuroprotective in rat model of transient focal cerebral ischemia. The future studies are required to clear cerebroprotective mechanism of aminoguanidine and possible use of this agent as a therapeutic target in stroke patients