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INTRODUCTION: We present a patient who presented to the ICU after successful resuscitation from cardiac arrest who was subsequently diagnosed with AEN. CASE PRESENTATION: A 66-year-old female presented after cardiac arrest in which return of spontaneous circulation was achieved within 7 minutes after the initiation of CPR. She was intubated on the scene and found to have coffee ground emesis in her bathroom when found unresponsive. Due to the hemodynamically significant GI bleed, patient was started on IV proton pump inhibitor, octreotide, and levophed. Subsequent endoscopy showed diffuse severe mucosal changes characterized by blackness, erythema, friability, granularity, inflammation, and decreased vascular pattern in the middle third of the esophagus and in the lower third of the esophagus. DISCUSSION: AEN is a rare syndrome with a prevalence ranging from 0.001 to 0.2% of EGD. This patient is especially rare as this patient was female and had AEN in the middle esophagus along with lower esophagus. The pathophysiology in this patient is hypothesized that she had cardiac arrest secondary to acute upper GI hemorrhage. Subsequent low-flow state (cardiac arrest) in addition to being in the setting of severe alcohol abuse led to esophageal necrosis.
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A 37-year-old woman with known glioblastoma multiforme was admitted for treatment of new deep vein thrombosis. Anion gap and plasma lactate levels were found to be elevated. Magnetic resonance imaging of the brain showed a stable, advanced glioblastoma multiforme. All causes of lactic acidosis, including infections and medications, were ruled out. Aggressive tumors have been shown to produce lactate levels in minute quantities in their microenvironment, which helps them metastasize and evade immune response and even radiation.
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A 60-year-old man was treated in the hospital for mesenteric vein thrombosis and discharged home on anticoagulation. On warfarin the patient started to bleed profusely from the nose and tongue. He was evaluated by ENT (ears, nose and throat); a nasal endoscopy revealed several vascular ectasias. Subsequent detailed history and general physical examination established the diagnosis of hereditary haemorrhagic telangiectasia also known as Osler-Weber-Rendu syndrome. On further evaluation, pulmonary arteriovenous malformations were diagnosed on imaging and treated by intervention radiology. In hindsight, the diagnosis could have been made in the general practitioner's office with just a routine thorough history and a physical examination at a new patient visit. We report this case to stress upon the importance of vigilant clinical, medical and family history and a thorough examination to establish an early diagnosis of this not-so-rare entity.
