Discussion: In this case, the combination of May- Thurner syndrome along with atrial septal defect created the perfect storm for turbulent blood flow leading to thrombus formation, which resulted in a paradoxical embolism causing ischemic stroke. Atrial septal defect (ASD) with aneurysm has been shown to significantly increase the risk of recurrent stroke and evaluation for closure is prudent. Similarly, iliac vessel narrowing may require stenting to prevent further DVT. Interestingly, there is an increased prevalence of migraine (25-35%) in patients with ASD. Defect closure has been found to decrease migraine burden and severity over time at follow up visits in a prospective study, which may ultimately be seen in this patient in the future.
in this young individual involved an interdisciplinary team with neurology and cardiology. Labs returned with normal lipid panel, HbA1c, thyroid stimulating test, and negative hypercoagulable and autoimmune workup. She was counseled to avoid estrogen-containing medications and triptans indefinitely. A transthoracic echocardiogram with bubble study revealed a small atrial septal defect with an aneurysm that was further characterized on transesophageal echocardiogram. Ultrasound for deep vein thrombosis (DVT) was negative; however, an MR angiogram /MR venogram of the pelvis demonstrated findings consistent with May- Thurner Syndrome. The patient was discharged on antiplatelet and anticoagulation therapy, with close neurology and structural cardiology follow-up.
ZIEVE’S SYNDROME: A ZEBRA OR AN UNDERRECOGNIZED HEMOLYTIC ANEMIA Kati Young, Sarak Kirk, Alexander Say; Louisiana State University School of Medicine, New Orleans, LA.
Introduction: Zieve’s syndrome is a complication of alcohol-induced liver injury that presents with the clinical triad of jaundice, hyperlipidemia, and hemolytic anemia. The syndrome is underreported in patients with alcohol use disorder and not readily recognized in patient care due to low awareness of the syndrome in the medical field. Case: A 50-year-old man with alcoholic cirrhosis complicated by esophageal varices and ascites presented with acute shortness of breath. The patient also reported hematemesis, hallucinations, and worsening fatigue. Initial examination revealed alcohol intoxication, tachycardia, abdominal distention with a positive fluid wave, jaundice, scleral icterus, and peripheral edema. Initial workup was significant for leukocytosis and anemia. During the hospital course, the patient developed melena associated with worsening anemia prompting further investigation into the source of blood loss. A chest x-ray was negative for fluid accumulation in the pleural cavity. Esophagogastroduodenoscopy and colonoscopy were negative for gastrointestinal (GI) blood loss. Peritoneal fluid analysis revealed serum ascites albumin gradient indicative of portal hypertension. Subsequent workup revealed hemolytic anemia with low haptoglobin and fibrinogen and elevated lactate dehydrogenase and reticulocyte count. Immune-mediated hemolysis
was ruled out with negative direct antiglobulin tests (DAT) for IgG and complement. Peripheral smear indicated microangiopathic hemolytic anemia. After no clear source of hemolysis was identified, further workup for Zieve’s syndrome including a lipid panel and vitamin E level was completed and consistent with this process. Supportive care measures with blood transfusions and symptom control were provided, resulting in intermittent improvement; however, ultimately the patient was transitioned to comfort care with hospice. Discussion: Though initial findings hinted towards GI blood loss as the cause of anemia, it is important to consider Zieve’s syndrome resulting in hemolytic anemia in patients with alcohol use disorder. Due to low awareness about this syndrome in the medical community, it is not often considered as a differential diagnosis, though the workup for this syndrome is easily incorporated into an anemia workup. Early consideration may lead to an earlier diagnosis and more efficient management. With more awareness of this syndrome and making the clinical diagnosis, there is likely to be improvement in management of this syndrome and research surrounding pathophysiology and treatment.
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