Shyam Shankar

Thyrotoxic Periodic Paralysis and Cardiomyopathy in a Patient with Graves’ Disease

Thyrotoxic periodic paralysis (TPP) and cardiomyopathy are two established complications of thyrotoxicosis. Emergent management is essential as TPP and cardiac events secondary to thyrotoxic cardiomyopathy can be fatal. We report a unique case of a patient with Graves’ disease presenting with symptoms secondary to both these complications. A 34-year-old Hispanic male, diagnosed with Graves’ disease, non-compliant with his medications, presented to the emergency room (ER) with complaints of generalized weakness, palpitations, chest pain and multiple episodes of nausea and vomiting for one day. On presentation, the patient was tachycardiac, had a systolic flow murmur and decreased motor strength in all extremities. Blood work showed a potassium of 1.8 millimoles per liter, cardiac troponin of 0.04 nanograms per milliliter and a thyroid panel consistent with hyperthyroidism. Electrocardiogram showed atrial flutter. In the ER, Propranolol, Propylthiouracil and Hydrocortisone were administered to prevent thyroid storm. Potassium was repleted, and the patient developed rebound hyperkalemia. He was given calcium gluconate, insulin, sodium polystyrene and admitted to the medical intensive care unit (MICU) for further management. Echocardiogram revealed severely decreased left ventricular systolic function and an ejection fraction of 26-30%. He was diagnosed with cardiomyopathy secondary to thyrotoxicosis. He was stabilized with Methimazole, Propranolol, Lisinopril and discharged on day nine with these medications and an outpatient follow-up appointment. Thyrotoxicosis can be life-threatening. This case shows a unique instance where a Hispanic patient presented with two complications of this phenomena. The pathogenesis of TPP involves increased responsiveness of the beta-adrenergic receptors, which leads to increased activity of the Sodium/Potassium (Na+/K+) ATPase pump and a transcellular shift of potassium into cells. The condition can resolve acutely with the administration of potassium. It is important to monitor the rate of potassium replacement as rebound hyperkalemia can occur, as this case demonstrates. Propranolol is an integral part of treatment as it is a beta-adrenergic receptor blocker and blocks the peripheral conversion of thyroxine (T4) to triiodothyronine (T3) in high doses. Thyrotoxic cardiomyopathy is one of the many cardiac complications that can be precipitated by Graves’ disease. One probable cause is the chronic tachycardia that patients with hyperthyroidism develop. Treatment entails managing the hyperthyroidism by starting the patient on beta blockers and anti-thyroid drugs or radioactive iodine uptake. Diuretics can be started to manage patients with heart failure. It is important to identify and treat the condition immediately to prevent grave complications.

Candida Tropicalis Cholangitis in a Patient Without Underlying Malignancy

Candida tropicalis is a rare cause of acute cholangitis, predominantly seen in patients with underlying hematological malignancies. Here, we describe a case of acute cholangitis caused by mixed organisms (Candida tropicalis, Candida albicans, and Enterococcus durans) without a known risk factor.

Bilateral Femoral Neuropathy Following Psoas Muscle Hematomas Caused by Enoxaparin Therapy

Patient: Female, 64 Final Diagnosis: Bilateral femoral neuropathy Symptoms: Inability to walk Medication: — Clinical Procedure: None Specialty: Critical Care Medicine Objective: Adverse events of drug therapy Background: Femoral neuropathy as a result of retroperitoneal hemorrhage most commonly occurs following pelvic and lower extremity trauma, but has been described to develop as a less frequent complication of anticoagulation. Case Report: We present the case of a 64-year-old white woman who was being treated for pulmonary embolism and deep venous thrombosis with enoxaparin. In the course of her treatment, she was noted to be hypotensive, with a sudden drop in hematocrit. She had been previously ambulatory, but noted an inability to move her bilateral lower extremities. A diagnosis of bilateral femoral neuropathy as a result of psoas hematomas caused by enoxaparin was made. Anticoagulation was discontinued and she was treated conservatively, with an excellent outcome. At the time of discharge to a rehabilitation center, she had regained most of the motor strength in her lower extremities. Conclusions: We believe this is the first reported case of bilateral femoral nerve neuropathy following use of enoxaparin. A full neurological examination should always be performed when there is sudden loss of function. The constellation of bilateral groin pain, loss of lower extremity mobility, and decreased hematocrit raised the suspicion of massive blood loss into the cavity/compartment. Thus, a high index of suspicion should be maintained by clinicians when presented with such symptoms and signs, as there can be significant morbidity and mortality when prompt diagnosis is not made.

1619: SEPSIS-INDUCED ISOLATED RIGHT VENTRICULAR STRESS CARDIOMYOPATHY MASQUERADING AS PULMONARY EMBOLISM.

Learning Objectives: Stress cardiomyopathy (SC) is a type of transient non-ischemic acute cardiomyopathy which is characterized by wall motion abnormalities of the heart in which intense physical or emotional stress can lead to sudden and severe heart muscle weakness. We present a rare case of sepsis/ respiratory distress induced stress cardiomyopathy with isolated right ventricle (RV) involvement, which was initially thought to be secondary to pulmonary embolism. Methods: A 84 year old woman with past medical history of chronic obstructive pulmonary disease (COPD) presented to the emergency room with shortness of breath and lethargy. The patient was started on anticoagulation for suspected pulmonary embolism (PE) and was admitted to the intensive care unit for hemodynamic instability requiring vasopressor support and respiratory failure. Echocardiogram (ECHO) showed severely decreased RV function, RV ballooning and normal left ventricular (LV) wall motion. Computed tomography angiography showed small chronic sub-segmental PE in the right upper lobe, which was not significant enough to cause the degree of hemodynamic instability in this patient. ECHO done two weeks prior to admission showed normal RV function. Electrocardiogram showed new V2-V4 “T” wave inversions with rising serum troponin levels. Coronary angiography showed clean coronary arteries. Cultures confirmed the diagnosis of urinary tract infection leading to sepsis and with appropriate treatment of sepsis and COPD exacerbation, patient showed clinical improvement and improved RV function on repeat ECHO. Results: SC most commonly involves the apical segment of the left ventricle. Isolated involvement of the RV has rarely been described in the literature, apart from few sporadic cases. To the best of our knowledge, this is the first case of isolated of RV stress cardiomyopathy masquerading as massive PE on initial presentation. This case makes it imperative to further study this new, emerging variant of SC in the future since it can be easily misdiagnosed as massive PE potentially leading to inappropriate thrombolytic therapy.