Patient: Female, 52Final Diagnosis: Hypothyroidism induced rhabdomyolysisSymptoms: Bilateral leg pain • fatigueMedication: Levothyroxine • Calcitriol • Calcium GluconateClinical Procedure: —Specialty: Endocrinology and MetabolicObjective:Unusual clinical courseBackground:Muscular symptoms, including stiffness, myalgia, cramps, and fatigue, are present in the majority of the patients with symptomatic hypothyroidism, but rhabdomyolysis, the rapid breakdown of skeletal muscle, is a rare manifestation. In most patients with hypothyroidism who develop rhabdomyolysis, precipitating factors, such as strenuous exercise or use of lipid-lowering drugs, can be identified.Case Report:We report a case of a 52-year-old Hispanic woman with a history of hypothyroidism, hypertension, and type 2 diabetes mellitus who presented with fatigue, severe generalized weakness, bilateral leg pain, and recurrent falls. She reported poor medication compliance for the preceding month. Initial laboratory testing showed elevated thyroid stimulating hormone (TSH) and creatine kinase (CK) levels, indicating uncontrolled hypothyroidism with associated rhabdomyolysis. Supportive treatment with intravenous fluids and intravenous levothyroxine were initiated and resulted in dramatic clinical improvement.Conclusions:We report a case of rhabdomyolysis, which is a rare but potentially serious complication of hypothyroidism. Screening for hypothyroidism in patients with elevated muscle enzymes should be considered, since an early diagnosis and prompt treatment of hypothyroidism is essential to prevent rhabdomyolysis and its consequences.

Patient: Female, 21Final Diagnosis: Anti-NMDA receptor encephalitisSymptoms: Altered mental status • headacheMedication: Intravenous immunoglobulin • methylprednisolone • cyclophosphamide • rituximabClinical Procedure: Cardiac pacemaker • bilateral salpingo-oophorectomySpecialty: Neurology • Critical CareObjective:Unusual clinical courseBackground:Anti-N-methyl D-Aspartate (anti-NMDA) receptor encephalitis is a rare autoimmune panencephalitis that typically presents with acute psychiatric disturbances and neurological deficits. Anti-NMDA receptor encephalitis is associated with certain tumors, most commonly ovarian teratomas. First-line therapy typically involves immunotherapy and tumor resection, if present, with up to 53% of patients experiencing improvement within 4 weeks. Cardiac arrhythmias and increased intracranial pressure have been reported in anti-NMDA receptor encephalitis, but these complications have usually been self-limited.Case Report:We report the case of a previously healthy, obese 21-year-old female who presented with acute encephalopathy. Her psychiatric and neurological function rapidly deteriorated, warranting intubation and mechanical ventilation. Lumbar puncture was performed. Cerebrospinal fluid (CSF) opening pressure was elevated and a lumbar drain was placed. Infectious disease work-up was negative and anti-NMDA receptor antibodies were present in the CSF and serum. Initial treatment included intravenous immunoglobulin (IVIG) therapy, plasmapheresis, methylprednisolone, and bilateral salpingoophorectomy, without clinical improvement. Second-line immunotherapy with cyclophosphamide and rituximab was then administered. The patient also developed intermittent episodes of severe bradycardia and asystole that remained refractory to treatment and required placement of a permanent cardiac pacemaker.Conclusions:Anti-NMDA receptor encephalitis presents with rapidly progressive psychiatric and neurologic dysfunction and can develop a severe and prolonged course with limited response to treatment. Patients can develop severe autonomic dysfunction with bradycardia and asystole that may require placement of permanent cardiac pacemakers. Elevated intracranial pressure may also be associated with anti-NMDA receptor encephalitis, and might contribute to the autonomic instability.

Background. Pituitary apoplexy (PA) is a clinical syndrome caused by acute ischemic infarction or hemorrhage of the pituitary gland. The typical clinical presentation of PA includes acute onset of severe headache, visual disturbance, cranial nerve palsy, and altered level of consciousness. Case Report. A 78-year-old man presented to the emergency department with one-day history of ptosis and diplopia and an acute-onset episode of altered level of consciousness which was resolving. He denied having headache, nausea, or vomiting. Physical examination revealed third-cranial nerve palsy and fourth-cranial nerve palsy both on the right side. Noncontrast computed tomography (CT) scan of the head was unremarkable. Brain magnetic resonance imaging (MRI) showed a pituitary mass with hemorrhage (apoplexy) and extension to the right cavernous sinus. The patient developed another episode of altered level of consciousness in the hospital. Transsphenoidal resection of the tumor was done which resulted in complete recovery of the ophthalmoplegia and mental status. Conclusion. Pituitary apoplexy can present with ophthalmoplegia and altered level of consciousness without having headache, nausea, or vomiting. A CT scan of the head could be negative for hemorrhage. A high index of suspicion is needed for early diagnosis and timely management of pituitary apoplexy.

Patient: Male, 32Final Diagnosis: Miller Fisher syndromeSymptoms: Ataxia • headache • ophthalmoplegiaMedication: —Clinical Procedure: PlasmapheresisSpecialty: NeurologyObjective:Rare co-existance of disease or pathologyBackground:Miller Fisher Syndrome is characterized by the clinical triad of ophthalmoplegia, ataxia, and areflexia, and is considered to be a variant of Guillain-Barre Syndrome. Miller Fisher Syndrome is observed in approximately 1–5% of all Guillain-Barre cases in Western countries. Patients with Miller Fisher Syndrome usually have good recovery without residual deficits. Venous thromboembolism is a common complication of Guillain-Barre Syndrome and has also been reported in Miller Fisher Syndrome, but it has generally been reported in the presence of at least one prothrombotic risk factor such as immobility. A direct correlation between venous thromboembolism and Miller Fisher Syndrome or Guillain-Barre Syndrome has not been previously described.Case Report:We report the case of a 32-year-old Hispanic male who presented with acute, severe thromboembolic disease and concurrently demonstrated characteristic clinical features of Miller Fisher Syndrome including ophthalmoplegia, ataxia, and areflexia. Past medical and family history were negative for thromboembolic disease, and subsequent hypercoagulability workup was unremarkable. During the course of hospitalization, the patient also developed angioedema.Conclusions:We describe a possible association between Miller Fisher Syndrome, thromboembolic disease, and angioedema.