Nardine Abdelsayed

Gastroparesis is a known complication in patients with diabetes mellitus (DM). This disorder has been known to make glycemic control difficult due to diabetic autonomic neuropathy, resulting in an increase in hypoglycemic episodes. On occasion, gastroparesis may be so severe that prokinetic medications and gastric pacemakers are not sufficient to control the symptoms, in which case some patients need to supplement their diet through a jejunal tube (J-tube) to bypass the stomach. Severe or long-lasting hypoglycemia may rarely be associated with epileptic seizures. We present a case of a 47-year-old female with a history significant for type 1 DM complicated by gastroparesis requiring a gastric pacemaker and J-tube placement who presented to the emergency department after having a witnessed seizure. Her glucose at that time was 27 mg/dl (normal 70-110 mg/dl) and she was treated appropriately with dextrose 25% solution and her glucose recovered to 110 mg/dl. Subsequently, seizure activity ceased.

Patent foramen ovale (PFO) occurs in about 25% of the population. PFO closure has been shown to decrease the risk of stroke in patients with recurrent strokes as compared to those treated with medical therapy alone, with more benefit in those with larger PFO sizes. Percutaneous PFO closure, although minimally invasive, does carry surgical risks, which must also be taken into account. We present a case of a 31-year-old female presenting with a left middle cerebellar artery (MCA) stroke and persistent deficits who was found to have both a PFO and presumed fibroelastoma on her aortic valve. She was treated with aspirin and apixaban and advised to follow up with cardiothoracic surgery once she recovered from her stroke for ultimate PFO closure and removal of the fibroelastoma. Unfortunately, she presented again less than one month later with recurrent cerebrovascular accidents (CVA) requiring urgent PFO closure. Our case stresses the importance of tools such as the Risk of Paradoxical Embolism (RoPE) score index when determining treatment plans for patients with PFO, and possible confounding factors such as the presence of an aortic valve fibroelastoma.

Schwannomatosis is a rare subset of neurofibromatosis. It is a disease process with a predisposition to schwannomas in the absence of bilateral vestibular schwannomas, which differentiates it from neurofibromatosis 2 (NF2). It is occasionally associated with certain tumors such as malignant peripheral nerve sheath tumors or rhabdoid tumors. Currently, there is limited literature to suggest an association between schwannomatosis and glioblastoma (GB). We present a case of a 55-year-old female with a history significant for schwannomatosis who presented after a witnessed first-time seizure with left facial weakness and slurred speech. She was found to have a 3 cm right-sided ring-enhancing lesion that was excised and found to be a grade IV Isocitrate dehydrogenase (IDH) wildtype GB.

A patent foramen ovale (PFO) is an embryological remnant. Hypoxia in the setting of a PFO is generally attributed to pulmonary hypertension resulting in an increase in right atrial pressure and mixing of venous blood from the right atrium with blood in the left atrium resulting in a right-to-left interatrial shunt (RLIAS), thus deoxygenating it. We present a case of a 64-year-old male with a past medical history of coronary artery disease (CAD) who presented with two weeks of dyspnea on exertion and intermittent chest pressure. He was found to be hypoxic at 87% (normal >95%) with largely normal workup except for left anterior descending (LAD) stenosis, which was stented, and a PFO that was found on transesophageal echocardiogram with normal pulmonary artery pressure (PAP). This case of hypoxia in the setting of a PFO without pulmonary hypertension puts into question the pathophysiology of hypoxia in a PFO and RLIAS.

Celiac artery compression syndrome is a rare and poorly understood condition. Compression of the celiac artery by the median arcuate ligament causes intractable nausea, vomiting, and postprandial pain. We present a case of a 55-year-old male with a 50-pound unintentional weight loss and intractable vomiting, whose symptoms persisted despite robotic median arcuate ligament release. He later returned to the emergency department where he was found to have a low gallbladder ejection fraction on imaging indicative of biliary dyskinesia, for which he underwent a cholecystectomy. Eventually, his symptoms improved, and he was able to return to his baseline body weight.

Meloxicam is a widely used nonsteroidal anti-inflammatory drug (NSAID) that is used to treat pain and some inflammatory disorders. One rare side effect is drug-induced thrombocytopenia (DITP), which can result in hemorrhage and death if not treated urgently. This diagnosis can be missed if mistaken for other conditions such as ITP, which is problematic since the mainstay of treatment is medication cessation. We present a case of a 42-year-old Hispanic female who was recently started on meloxicam and presented with petechiae, ecchymosis, and a platelet count of 2 (normal 150-350 K/mm3).

Round atelectasis (RA) is a rare disorder most commonly occurring in the presence of chronic pleural effusions due to the formation of adhesions and resultant pulmonary collapse. The most common culprit to this disease is asbestosis, but other causes of pleural effusions such as congestive heart failure and pneumonia are reported in the literature. RA can occasionally mimic pulmonary cancers and should be identified to prevent the associated morbidity of tumor workup. We present a case of RA seen on echocardiogram, and then later on computed tomography mimicking a pleural tumor in a 58-year-old female with preexisting heart failure and recurrent pleural effusions. Consultation with radiology and recognition of RA prevented the unnecessary potential morbidity and mortality of further workup.

Acquired thrombotic thrombocytopenic purpura (TTP) is an uncommon microangiopathic disorder that can have variable presentations and can be precipitated by a multitude of stressors to the body, most commonly sepsis. TTP is caused by a deficiency of ADAMTS13 leading to intravascular clotting causing thrombocytopenia and microangiopathic hemolytic anemia. TTP can be associated with various other pathologic conditions. One such rare association has been reported with diabetic ketoacidosis (DKA). Here, we present an even less appreciated presentation in association with DKA. A 62-year-old African American male with previously diagnosed prediabetes presented with DKA and developed hemodynamically significant bleeding. He was confirmed to have TTP that responded to plasmapheresis. TTP is a life-threatening illness if not treated urgently with plasmapheresis with or without rituximab. As acquired TTP most commonly occurs during stress on the body, it is important to treat the underlying stressor. Early identification and initiation of appropriate interventions are crucial to reducing mortality associated with TTP. Furthermore, we need to appreciate less commonly associated conditions such as DKA among patients.