Résumé
Background Cardiogenic shock is a rare complication of influenza myocarditis and multisystem inflammatory syndrome. We present the case of a 32-year-old female in cardiogenic shock who met criteria for both entities. Case A 34-year-old female with hypothyroidism presented after being found down and covered in feces. She had cough and weakness the preceding days. She was febrile and hypotensive. Point of care ultrasound showed severe biventricular dysfunction and she was started on norepinephrine. She was influenza A positive with a lactate of 5.1. Right heart catheterization on 2ug/kg/min of norepinephrine showed a cardiac index (CI) of 2.82 L/min/m2 and a systemic vascular resistance (SVR) of 300 dynes/sec/cm-5. She was started on vasopressin, stress dose steroids, and oseltamivir. She received 6 amps of bicarbonate with aggressive electrolyte repletion. CI as per the Fick equation was within normal limits but lactate continued to rise. Thermodilution showed a CI of 1.6 L/min/m2 and an SVR of 2200 dynes/sec/cm-5, indicating mixed cardiogenic and distributive shock. The patient developed severe abdominal pain and was found to have elevated COVID-19 spike domain and nucleocapsid antibodies, meeting criteria for multisystem inflammatory syndrome (MIS-A). Decision-making The patient was started on dobutamine after thermodilution showed decreased CI. Intravenous immunoglobulin was started after meeting criteria for MIS-A. Her pressor requirements were weaned and then her dobutamine requirements. Follow up cardiac MRI showed mild global hypokinesis of the left ventricle and subtle hypokinesis of the right ventricular inferior wall. Left ventricular ejection fraction was 51%. The patient's cardiac MRI findings were not specific. However, her rapid improvement was suggestive of MIS-A. Additionally, consistent discordance between Fick and thermodilution resulted in confusion regarding optimization of pressors and inotropes. Conclusion The patient responded to dobutamine and MIS-A treatment after an initial impression of myocarditis. Infectious processes should be considered in any patient with new onset heart failure.Copyright © 2023 American College of Cardiology Foundation
Résumé
Introduction: Nephrogenic diabetes insipidus (NDI) is caused by reduced renal response to vasopressin. NDI affects up to 40% of patients on lithium. We present a case of partial NDI secondary to lithium use. Case Description: A 66 year old male with bipolar disorder on lithium presented with shortness of breath, chest tightness and cough. On exam he was cachectic, lethargic, tremulous with decreased skin turgor and dry mucous membranes found to have COVID-19 with initial unremarkable blood work. Received treatment for COVID and subsequently developed worsening encephalopathy, follow up blood work revealed elevated serum sodium of 168 mg/dl, with urine osmolality of 382 and lithium level was elevated at 1.6 mEq/L. He received adequate IV fluid hydration with hypotonic fluids and free water. Serum sodium remained elevated with polyuria. Follow up labs showed urine osmolality decrease to 94 mosml/L therefore nephrogenic diabetes insipidus was suspected. A desmopressin stimulation test was performed and hourly urine osmolality was obtained [Table 1] confirming the diagnosis of nephrogenic diabetes insipidus with a partial response to desmopressin compatible with lithium-induced partial diabetes insipidus. Treatment was started initially with chlorthalidone with inappropriate response, then dose increased to 100mg daily with further addition of amiloride 10mg twice daily with subsequent response and decrease of sodium level from 167 to 147 mEq/L. Discussion(s): Lithium-induced NDI is explained by downregulation of aquaporin 2 channel expression in the principal cells due to accumulation of toxic concentrations of lithium and reduction of the kidneys' ability to preserve water in response to vasopressin. NDI usually presents with polyuria, polydipsia, severe dehydration, and electrolyte imbalance. A less than 50% increase in urine osmolality following desmopressin administration proves NDI. Treatment options include high doses of desmopressin, low sodium diet, thiazide diuretics, amiloride, and NSAIDs. (Table Presented).