Methods: A retrospective review was performed of patients who had resection of PVL at three centers between 1990 and 2018. Patients' demographics, comorbidities, tumor characteristics, intraoperative data, and oncologic and graft-related outcomes were recorded. Survival analysis was performed using Kaplan-Meier curves and Cox proportional hazards regression. Results: Seventy patients with a diagnosis of PVL were identified between 1990 and 2018. Fifty-four patients (77%) had PVL of the inferior vena cava (IVC) and 16 (23%) had peripheral PVL. Mean follow-up for the series was 55.0 months (range, 1-217 months). Of the patients with IVC PVL, 51 (96%) needed caval reconstruction and 3 (4%) had resection only; 17 patients (31%) received neoadjuvant radiation, 6 patients (11%) received neoadjuvant chemotherapy, and 3 (6%) patients received both. There were no deaths within 30 days of surgery. Five patients (9%) required early reintervention, including one (2%) IVC stent. Thirtyone patients (57%) developed metastatic disease, and 11 (20%) of these patients developed local recurrence. Sixteen peripheral PVLs were identified. Eight patients (50%) had venous reconstructions performed and eight (50%) had the vein resected without reconstruction. There were no deaths within 30 days. Nine patients (56%) developed metastasis and three (19%) developed local recurrence. Five-year survival was 57.5% for IVC PVLs and 70.0% for peripheral PVLs. Kaplan-Meier survival analysis for IVC and peripheral PVLs revealed no difference in overall survival (P ¼ .624) and tumor-free survival (P ¼ .644) at 5 years. Cox proportional hazards regression analysis for overall survival revealed neoadjuvant radiation and need for venous reconstruction to be associated with decreased survival (Table). Conclusions: PVL is a rare and aggressive disease even with surgical resection. We found no difference in survival between IVC and peripheral lesions, suggesting that aggressive management is warranted for PVL of any origin. IVC resection and replacement can be done safely if needed. The role for adjuvant therapies remains undefined.
Compartment syndrome is caused by increased pressure within fascial compartment. We present a unique case of a thigh compartment syndrome that occurred after overnight catheter delivered Tissue plasminogen activator (tPA) thrombolysis of an acutely thrombosis femoral-to above knee popliteal artery Propaten® PTFE (WL Gore & Associates, Flagstaff, AZ) bypass graft. The condition was treated by emergency fasciotomy and the patient recovered uneventfully.
Figure 1. (A) Magnetic resonance cholangiopancreatography (MRCP) of the pancreatic tail cyst. (B) Endoscopic ultrasound (EUS) of the pancreatic tail cyst.
Introduction: Fluoxetine is a commonly prescribed antidepressant with generalized gastrointestinal side effects that can include nausea and diarrhea. While fluoxetine is metabolized in the liver, fewer than 1% of patients develop a mild and self-limited transaminitis. Here, we present a unique case of clinically apparent drug-induced liver injury (DILI) soon after fluoxetine initiation. Case Description/Methods: A 28-year-old male with schizophrenia and bipolar disorder was admitted to the hospital due to a 3-day history of worsening right upper quadrant (RUQ) abdominal pain with a 2day history of yellowing of the skin and eyes. A thorough history revealed that he was on chronic citalopram and olanzapine therapy but was started fluoxetine (20 mg daily) 5-days prior. Additionally, he denied use of alcohol, recreational drugs, and herbal supplements, and denied a history of known liver disease. On admission, the patient was alert and oriented x4 with jaundice, scleral icterus, and asterixis. Laboratory work demonstrated WBC 15,000, platelets 235,000, ammonia 131, AST 3219, ALT 6574, ALP 181, total bilirubin 22.9, and INR 1.97. Acetaminophen and salicylate levels were unremarkable. Fluoxetine was held immediately, and the patient was empirically given N-acetylcysteine. RUQ ultrasound was unremarkable. MRCP demonstrated fatty infiltration of the liver without nodularity or biliary dilation. A thorough workup including viral hepatitis (A, B, C, E), EBV, CMV, HIV, hemochromatosis, Wilson's disease, and autoimmune hepatitis was unremarkable. A liver biopsy was performed, and pathology was consistent with mixed-pattern DILI. With the removal of fluoxetine, the patient's liver function tests and clinical symptoms continued to improve, and on hospital day 10 he was discharged in stable condition. Discussion: Transaminitis from fluoxetine is typically mild, asymptomatic, and self-limited. Our case highlights a rare instance where fluoxetine precipitated DILI. It is unclear whether polypharmacy with his other psychiatric medications, or underlying hepatic steatosis, were predisposing factors to developing fluoxetine-associated DILI. Higher awareness of fluoxetine-associated hepatotoxicity is needed and caution should be used when considering current medications and underlying liver pathology when starting this medication.
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