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.

Introduction Acquired hemophilia A (AHA) also known as acquired factor VIII (FVIII) deficiency is an acquired inhibition of coagulation by antibodies that either inhibit the activity or increase the clearance of a clotting factor (FVIII). Mortality in patients presenting with AHA is related to bleeding and hemorrhage, therefore rapid diagnosis and effective treatment are needed. Case presentation We present a case of a 59-year-old male with acquired VIII deficiency presenting with diffuse ecchymosis and bleeding diathesis. The patient was treated successfully with steroids and rituximab. Clinical discussion It is a rare autoimmune disorder caused by neutralization of Factor VIII by IgG antibodies. This can lead to severe, life threatening bleeding. Treatment involves replacement of FVIII and immunosuppression. Conclusion A key point to successfully treating AHA is to remove inhibitors and stop bleeding. Mortality in patients presenting with AHA is related to the bleeding and hemorrhage, therefore rapid diagnosis and effective treatment are needed.

Nitrous oxide is clinically used as an inhaled anesthetic in surgical and dental procedures. It is also used as an inhaled recreational drug and can be incredibly addictive. It tends to irreversibly oxidize cobalamin (Vitamin B12), rendering it inactive as a coenzyme in the production of methionine. Methionine is required in myelin sheath phospholipid production, and thus overuse of this anesthetic can affect myelin formation. Furthermore, other substrates that require this coenzyme (such as methylmalonate and propionate) accumulate and get incorporated in the myelin sheath, resulting in subacute combined degeneration of the spinal cord. We present a case of a young, avid hunter with a history of polysubstance use to include inhaled nitrous-oxide abuse, prior cocaine use, current marijuana use, and tobacco abuse, who presented with ascending paresthesias without appreciable motor dysfunction. Initial labs showed isolated macrocytosis without anemia in the setting of low vitamin B12 levels. Relevant studies showed elevated methylmalonic acid, normal anti-parietal cell, and anti-intrinsic factor antibodies. Heavy metals screens were negative for high levels of lead, iron, copper, or zinc. Cervical spine MRI demonstrated dorsal cord signal abnormalities without enhancement, in a pattern consistent with vitamin B12 deficiency. The patient was diagnosed with subacute combined degenerative disease secondary to depleted vitamin B12 as a result of recreational inhaled nitrous-oxide abuse. After cessation of nitrous oxide abuse, in addition to three months of B12 replacement, he reported complete resolution of symptoms.

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.

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.