Cerebellar hemorrhage in patients treated with edoxaban for portal vein thrombosis after hepatobiliary surgery: a report of two cases.

BACKGROUND: The standard therapeutic agent administered for portal vein thrombosis (PVT) in patients with or without cirrhosis is warfarin or low-molecular weight heparin. However, therapy with edoxaban appears to be one of the most promising treatments for patients who require anticoagulation therapy. We encountered two cases of cerebellar hemorrhage in patients treated with edoxaban for PVT after hepatobiliary surgery during the past 2 years. CASE PRESENTATION: Case 1 A 67-year-old male underwent cholecystectomy and choledocholithotomy with choledochoduodenostomy to treat choledocholithiasis after cholangitis. Enhanced computed tomography (CT) on the 1st postoperative day (POD) revealed thrombosis in the left and anterior segment of the portal vein branches. We administered antithrombin III concentrate with heparin for 5 days; thereafter, we switched to 60 mg edoxaban. A sudden decrease in the patient's level of consciousness was observed due to cerebellar hemorrhage on POD 27. Cerebellar hemorrhage was successfully treated with craniotomy hematoma evacuation and ventricular drainage; however, the patient died from aggravation of hepatic failure due to PVT and intra-abdominal infection. Case 2 A 67-year-old male received laparoscopic microwave coagulation therapy for two hepatic nodules suggestive of hepatocellular carcinoma in the left lobe of the liver due to alcoholic hepatitis. Enhanced CT on POD 5 revealed a thrombosis in the 4th segment branch of the portal vein, and the patient was treated with 60 mg edoxaban. Cerebellar hemorrhage with ventricular perforation occurred on POD 15. Cerebellar hemorrhage was successfully treated by craniotomy hematoma evacuation with ventricular drainage. Prolonged consciousness disorder persisted, and the patient was transferred to another medical facility for rehabilitation 49 days after brain surgery. CONCLUSIONS: Although edoxaban is recently described to be one of the options for patients with PVT who require anticoagulation therapy instead of heparin or warfarin, it should be used with caution, given its propensity to induce severe hemorrhagic adverse events in cases such as those described above. The monitoring of hepatic dysfunction and decision for continuation of drug may be required during edoxaban use for PVT, especially after hepatobiliary surgery.

[Comparison of intrathecal morphine and buprenorphine for postoperative analgesia in cesarean delivery].

BACKGROUND: It has become a popular practice to add opioids to spinal solutions to enhance and prolong intraoperative and postoperative analgesia in cesarean section. Morphine is the opioid most widely used for this purpose, but there are few reports about intrathecal buprenorphine. We evaluated the postoperative analgesic effect of intrathecal buprenorphine compared with intrathecal morphine after cesarean section. METHODS: We retrospectively compared group B (n = 20) receiving tetracaine 10mg plus intrathecal buprenorphine 0.05 mg with group M (n = 24) receiving tetracaine 10 mg with intrathecal morphine 0.1 mg in elective cesarean section under spinal anesthesia. RESULTS: There were no significant differences between the groups in time to first postoperative supplemental analgesics, times of using postoperative supplemental analgesics and antiemetics within 24 hours after operation, and the incidence of postoperative nausea and vomiting and pruritus. CONCLUSIONS: It is concluded that intrathecal buprenorphine 0.05 mg provides similar postoperative analgesic effect with intrathecal morphine 0.1 mg without any increases of side-effects in cesarean section.

Cytotoxic edema and interleukin-6 in hypertensive encephalopathy.

We report a female, 10 years of age, with juvenile rheumatoid arthritis accompanied by hypertensive encephalopathy. The patient developed a cytotoxic brain lesion, as revealed by the high signal intensity on diffusion-weighted magnetic resonance imaging, which corresponded to the hypoperfusion area on single-photon emission computed tomography scan using (99m)Tc-ethylcysteinatedimer. Cerebrospinal fluid interleukin-6 activity was elevated when the hypertensive encephalopathy revealed active central nervous system disease, and its activity decreased when the encephalopathy recovered from the central nervous system manifestations. We speculated that the cytotoxic edema and associated parenchymal damage in hypertensive encephalopathy were closely related to the intrathecal overproduction of interleukin-6.