Liver Abscess and Portal Vein Thrombosis Due to Ileal Diverticulitis Mediated by Barium Fluoroscopy.

We report a case of liver abscess and portal vein thrombosis, which occurred due to diverticulitis at the terminal ileum in a 59-year-old man. The patient underwent a barium fluoroscopic examination 1 month before presenting to our hospital. He also showed liver dysfunction due to thrombosis at the superior mesenteric and portal veins. His inflammation gradually subsided after the initiation of treatment, but the recovery was not sufficient. Thus, surgery was performed. The patient condition improved after surgery and he was discharged. Barium examinations are relatively safe, but can sometimes cause severe adverse effects in patients with certain risk factors, and an appropriate diagnosis and treatment are necessary when symptoms appear.

Acute subdural hematoma after intra-arterial thrombolysis for acute ischemic stroke--case report.

A 79-year-old man with a cardiac pacemaker for bradycardia fell down and presented with sudden onset of right hemiplegia and aphasia. Initial computed tomography (CT) showed no cerebral infarction but angiography revealed occlusion of the left middle cerebral artery (MCA). Local intra-arterial thrombolysis with tissue plasminogen activator (tPA; tisokinase, 1,600,000 units) was performed 3 hours after the onset, and the MCA was partially recanalized. Further administration of tPA was suspended because of nosebleed. However, the patient's neurological findings did not improve. His consciousness gradually deteriorated to coma and quadriplegia with dilation of the left pupil 2.5 hours after thrombolysis. CT disclosed marked mass effect with a left acute subdural hematoma and a small intracerebral hematoma in the left frontal lobe. He underwent urgent craniotomy and removal of the subdural hematoma. The subdural hematoma originated in a frontal cerebral contusion. He died of severe brain edema 2 days after surgery. Acute subdural hematoma is a very rare complication of intra-arterial thrombolysis. Presumably he had suffered head trauma at the first onset. Evidence of head trauma should be considered a contraindication for the use of thrombolytic agents in a patient with acute stroke.

[A surgical case of subdural hematoma with hemophilia A].

A 54-year-old man presented with unconsciousness. Computed tomography revealed acute subdural hematoma. Emergency evacuation of hematoma was performed showing any excessive tendency to bleed or difficulty to stop bleeding during the operation. However transfusion of fresh frozen plasma was needed to stop continuous bleeding from the surgical wound after the operation. The patient underwent craniotomy again 18 days after the operation because he suffered hemorrhagic infarction and recurrence of acute subdural hematoma. After the second operation, a coagulability examination revealed that his activated partial thromboplastin test was prolonged (74.5 seconds) and his plasma factor VIII level was 20% of normal, so he was diagnosed as having mild hemophilia A. Cranioplasty was accomplished with replacement therapy, and he was discharged with mild recent memory disturbance and homonymous hemianopsia.

[A case of duret hemorrhage demonstrated by computed tomography].

Brainstem hemorrhage in descending transtentorial herniation is well known as Duret hemorrhage. However, CT or MRI rarely reveals Duret hemorrhage. The authors report a case of brainstem hemorrhage after craniotomy of spontaneous acute subdural hematoma. A 47-year-old man suffered sudden onset of severe headache and progressive consciousness disturbance. Initial CT scan demonstrated a right acute subdural hematoma and a marked shift of the midline structures to the left. Emergency craniotomy was performed but he remained comatose. CT scan after 8 days showed multiple petechial hemorrhages in the brainstem. We reported a rare case of Duret hemorrhage diagnosed by CT scan. Duret hemorrhage is almost fatal.

Factors affecting successful palliative surgery for malignant bowel obstruction due to peritoneal dissemination from colorectal cancer.

BACKGROUND: Nonresectable colorectal cancer often causes malignant intestinal obstruction due to peritoneal dissemination. However, no previous report has specifically investigated which patients, with peritoneal dissemination from colorectal cancer, would actually benefit from palliative surgery. This study defines the selection criteria for patients who are likely to benefit from palliative surgery. METHODS: Twenty-one patients underwent palliative surgery for malignant bowel obstruction due to peritoneal dissemination from colorectal cancer. In all cases, the advanced and nonresectable nature of the tumor was confirmed at laparotomy. Clinical factors such as age, gender, serum level of carcinoembryonic antigen, amount of ascites, location of the primary cancer, surgical procedure, and postoperative chemotherapy were analyzed for prognostic significance in symptom-free and overall survival using the Kaplan-Meier product limit method and the log-rank test. RESULTS: All the postoperative courses were uneventful. Obstruction recurred after a median symptom-free interval of 61 days in the group with less than 100 ml of ascites, whereas it recurred after 9 days in the group with more than 100 ml of ascites. Symptom-free survival rates in patients who manifested ascites were significantly lower than in those without ascites (P = 0.0321, log-rank method). The symptom-free and overall survival rates in patients who underwent postoperative chemotherapy were significantly higher (P = 0.0225 and 0.0003). CONCLUSIONS: Palliative surgery can be performed effectively for patients without ascites. For patients who do not meet this criterion, a non-surgical procedure may be preferable.

Hippocampal injury and neurobehavioral deficits are improved by PD 81,723 following hyperglycemic cerebral ischemia.

We investigated the effects of PD 81,723, an allosteric enhancer for the adenosine A(1) receptor subtype, on hippocampal injury and Morris water maze (MWM) performance following hyperglycemic cerebral ischemia and reperfusion (4-VO, 10 min) in the rat. PD 81,723 (3 or 10 mg/kg) or the equivalent volume of saline was administered intraperitoneally 30 min prior to ischemia. Moderate hyperglycemia was achieved by administration of D-glucose (3g/kg, i.p.) 15 min prior to induction of ischemia. Morris water maze trials were performed on the 6th, 7th, and 8th days after the ischemic insult. The rat brains were sectioned (8 microm), stained with cresyl violet/acid fuchsin, and evaluated for hippocampal ischemic injury by an experimenter blinded to the treatment conditions. At the higher dose, PD 81,723 (10 mg/kg) had no effect on hippocampal injury or MWM performance following hyperglycemic ischemia compared to corresponding saline-treated animals. In contrast, a lower dose of PD 81,723 (3 mg/kg) resulted in significant (P < 0.05, n = 8) reduction of hippocampal injury following hyperglycemic ischemia. Furthermore, corresponding Morris water maze performance (latency, learning index, and cumulative distance swum) was significantly improved by PD 81,723 (P < 0.05, n = 8). The results of the present study suggest that, in the presence of PD 81,723, an A(1) allosteric enhancer, endogenously produced adenosine is sufficient to exert significant neuroprotection during hyperglycemic ischemia. Moreover, the present study provides further evidence for a neuromodulatory role of adenosine during hyperglycemic ischemia.

Transcortical transchoroidal fissure approach for ruptured distal posterior cerebral artery (P2-P3 junction) aneurysm associated with packed intraventricular hemorrhage--two case reports.

A 56-year-old man with ruptured right P2-P3 junction aneurysm and a 66-year-old man with ruptured left P2-P3 junction aneurysm of the posterior cerebral artery associated with acute-stage packed intraventricular hemorrhage. The aneurysms were successfully clipped through the transcortical transchoroidal fissure approach. This approach requires less retraction of the temporal lobe, provides a wider surgical field, and the P2 segment can be easily reached. The present approach is very useful for the treatment of ruptured aneurysms at the P2-P3 junction, in particular for acute stage surgery associated with packed intraventricular hemorrhage.

Preoperative portal embolization in patients with hepatocellular carcinoma.

The factors that contribute to the effect of portal vein embolization before hepatectomy for hepatocellular carcinoma are unclear. Sixty-six patients with hepatocellular carcinoma were enrolled in the study. Changes in liver function, portal vein pressure, and liver volume after embolization were examined. A multiple linear regression analysis was performed to identify factors that independently contributed to the effects of portal vein embolization. The acceptable volume ratio of the remnant liver was calculated from liver function and compared with the volume ratio of the non-embolized liver. No postoperative deaths were observed after portal vein embolization or hepatectomy. Serum total bilirubin and prothrombin time did not change significantly after portal vein embolization. In patients who underwent arterial embolization before portal vein embolization, aminotransferase levels increased significantly. The only factor that could significantly predict the atrophy effects of portal vein embolization was previous arterial embolization. The volume ratio of the non-embolized liver was smaller than the acceptable volume ratio of the remnant liver in 18 of 40 patients and increased over the acceptable volume ratio in all cases after portal vein embolization. Portal vein embolization induced atrophy or hypertrophy of the embolized or non-embolized liver sufficiently, even when the liver was dysfunctional or cirrhotic. The atrophy effects were significant, especially when arterial embolization had been performed before portal vein embolization.

Hippocampal injury and neurobehavioral deficits following hyperglycemic cerebral ischemia: effect of theophylline and ZM 241385.

OBJECT: The effects of the adenosine receptor antagonists theophylline (for A1 and A2) and ZM 241385 (for A2A) on hippocampal injury and Morris water maze (MWM) performance in rats were investigated following normoglycemic and hyperglycemic cerebral ischemia (induced by four vessel occlusion for 10 minutes). METHODS: Theophylline (36 mg/kg), ZM 241385 (1 mg/kg), or an equivalent volume of saline was administered to rats intraperitoneally 30 minutes before ischemia was induced. Moderate hyperglycemia was achieved by intraperitoneal administration of D-glucose (3 g/kg, 15 minutes before induction of ischemia). Morris water maze trials were performed on the 6th. 7th, and 8th days after ischemic insult. After the conclusion of the performance tests, the rat brains were cut into 8-microm sections, stained with cresyl violet and acid fuchsin, and evaluated in a blinded fashion to determine the extent of injury. Theophylline worsened injury in the hippocampus following normoglycemic and hyperglycemic ischemia. Moreover, theophylline significantly (p < 0.05, six animals) worsened latency and learning index (LI) scores during the MWM trials in both normoglycemic and hyperglycemic animals. On the other hand, ZM 241385 had no effect on either ischemic injury or MWM performance in normoglycemic animals. In the animals in the hyperglycemic ischemia group, however, ZM 241385 significantly (p < 0.05, five animals) reduced injury in the CA1 (94.6 +/- 1.7% compared with 79.2 +/- 10.9%), CA3 (26 +/- 12.5% compared with 11.2 +/- 4.3%), and hilum (22.4 +/- 8.1% compared with 11 +/- 5.5%) regions. In addition, ZM 241385 significantly improved latency (52 +/- 29.7 seconds compared with 24.8 +/- 11.2 seconds, p < 0.05) and LI scores (203.2 +/- 33.3 compared with 152.1 +/- 31.8, p < 0.05) in the MWM trials. A statistically significant correlation was also found between hippocampal injury (CA1, CA3, and hilum) and MWM performance. CONCLUSIONS: The results of this study provide further evidence for a neuromodulatory role of adenosine during normoglycemic and hyperglycemic ischemia.