Thyrotoxicosis, also known as hyperthyroidism, is a condition characterized by the excessive production of thyroid hormones by the thyroid gland. Besides Graves\' disease, other common causes of thyrotoxicosis include toxic multinodular goiter, toxic adenoma, and subacute thyroiditis. The treatment of thyrotoxicosis depends on the underlying cause and may include medications (e.g., antithyroid drugs, beta-blockers), radioactive iodine therapy, or surgical removal of the thyroid gland (thyroidectomy). In this report, we present two instances of thyrotoxicosis where conventional high doses of antithyroid treatment failed to control the condition effectively. This failure prompted the exploration of alternative therapeutic interventions. These cases highlight the intricacies involved in managing thyrotoxic crises that do not respond to methimazole (MMI), emphasizing the necessity for innovative approaches such as plasmapheresis and thyroidectomy. Understanding such scenarios is vital for enhancing the care provided to patients encountering resistance to standard treatments. The distinct clinical pathways and treatment strategies adopted in these cases offer valuable insights into this disease management, particularly concerning resistance to MMI.

Thyrotoxicosis can exhibit overlapping symptoms of psychosis in the general population. Each of these pathologies has well-established workups and management. Rare presentations of thyroiditis and psychosis in the postpartum state have been seen in case studies mostly, but data on the prevalence of postpartum psychosis in association with postpartum thyroiditis are not available. Here, we present a unique case of a patient with a history of bipolar disorder who originally presented with postpartum thyroiditis that was worked up and managed appropriately. However, on follow-up, the patient was found to have progressed into prominent psychosis. Both thyroiditis and psychosis were managed individually with full remission upon discharge and is doing well today. The co-occurrence of postpartum psychosis and thyroiditis presents a unique challenge for timely diagnosis and management. We present a case of a young woman initially diagnosed with postpartum thyroiditis needing further management of postpartum psychosis due to persistent symptoms. Clinical presentation supported with a prior history of mood disorder increases the likelihood of these diagnoses together.

The development of heart failure and cardiomyopathy has been identified as an infrequent but life-threatening complication of thyrotoxicosis or thyroid storm. Thyrotoxicosis-induced cardiomyopathy and cardiogenic shock have been shown to be one of the major causes of sudden mortality in adults. However, the treatment of thyrotoxicosis with non-cardioselective beta-blockers has been implicated in the development of severe decompensation and even cardiogenic shock if cardiac function is not known and often requires a multidisciplinary care team to address it. Here, we have reported the case of a 63-year-old male with a past medical history of hyperthyroidism who presented to the emergency room with persistent shortness of breath. Vital signs were notable for hypotension, tachycardia with an irregular heartbeat, with ECG suggestive of atrial fibrillation with a rapid ventricular rate. The thyroid function test was significant for severely suppressed TSH, and the Burch-Wartofsky Score was >45. The patient rapidly decompensated shortly after being given IV metoprolol, subsequently requiring intubation and pressor support. Two-dimensional (2D) echocardiography (or echo) done afterward was significant for four-chamber dilation with mild global hypokinesis and reduced left ventricular ejection fraction. Endocrinology, Cardiology, and Pulmonary Critical Care teams were consulted to assist in multi-modality management. The administration of a non-cardioselective beta-blocker in decompensated heart failure was suggested as the cause of the rapid deterioration. Through a multi-modality management approach, the patient subsequently improved and was eventually discharged with the resolution of thyroid storm and cardiogenic shock, and with close follow-up with the primary care provider, endocrinologist, and cardiologist. This case illustrates the significance of a multidisciplinary team approach in the acute management of thyrotoxicosis-induced cardiogenic shock, as recommendations from the team were instrumental in helping the patient recover from the acute phase of the illness. Also, this case further highlights the significance of assessing the cardiac function, preferably performing echo before starting the patient on beta-blockers.

Hyperthyroidism directly affects the cardiovascular system, altering the heart\'s normal function and leading to high cardiovascular mortality. Excess thyroid hormones are associated with significantly increased risk and prevalence of cardiac arrhythmias, particularly atrial fibrillation (AF). This article reviewed the hemodynamic changes and the risk of cardiac arrhythmias, including atrial and ventricular arrhythmias associated with hyperthyroidism. It has also discussed the multi-level pathophysiology of thyrotoxic AF, sinus tachycardia, and different treatment modalities such as anti-thyroid drugs, beta-blockers, and the role of cardioversion and catheter ablation. This article has explored different studies that have concluded that AF and sinus tachycardia are the most common arrhythmias associated with thyrotoxicosis.