THE COMPANY YOU KEEP: A CASE OF REFRACTORY HYPOXEMIC RESPIRATORY FAILURE, THYROID STORM, AND SYSTOLIC HEART FAILURE IN THE POSTPARTUM PERIOD

Abstract

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: We present a case of acute hypoxemic respiratory failure from flash pulmonary edema in a new mother with Graves’ disease. CASE PRESENTATION: A 36 year old woman, four days postpartum with history of Graves’ disease and pre-eclampsia presented in acute respiratory distress. On admission, she had a systolic BP > 200 mmHg, sinus tachycardia to 150 BPM, bilateral patchy pulmonary infiltrates, and profound hypoxemia requiring intubation. Severe hypoxemia persisted despite paralysis and lung recruitment maneuvers, therefore airway pressure release ventilation (APRV) was used as a rescue strategy. Thyroid studies suggested evidence of thyroid storm (low TSH, high free T3, normal free T4 and a Burch-Wartofsky score of 70). Intravenous esmolol was initiated to achieve peripheral beta blockade but was complicated by PEA arrest. Return of spontaneous circulation was achieved after five minutes of CPR. An echocardiogram showed biventricular failure and ejection fraction of 30%. Hydrocortisone, propylthiouracil, and iodine were initiated for thyroid storm and eventually she was extubated. Repeat echocardiogram revealed recovered ejection fraction of 60%. She was discharged in stable condition on methimazole with close follow-up. DISCUSSION: Therapies invariably consist of both positive and negative effects. The role of an intensivist is to weigh these risks and benefits, make sound judgement, and adapt to unintended consequences. This patient presented in extremis with hypoxemic respiratory failure from flash pulmonary edema. Her history of Graves’ disease combined with laboratory and clinical data pointed strongly to thyroid storm. The best evidence suggests that early treatment of thyroid storm is crucial and mortality rates rise to 75% with delays in therapy. While beta-blockade is considered first line therapy to treat the effects of uncontrolled thyroid hormone, in this case it undoubtedly led to cardiac arrest. Following the successful resuscitation, it was clear that RV dysfunction paired with high intrathoracic pressures generated by APRV mode should be seen as a death knell if paired with beta blockade. Opposing the sympathetic surge and tachycardia required to maintain cardiac output, our patient quickly decompensated, with loss of chronotropy and RV failure leading to cardiac arrest. Rapid removal of the short-acting agent esmolol, along with resuscitative efforts were able to quickly correct the untoward effects and the patient made a full recovery. CONCLUSIONS: This case offers a unique presentation of thyroid storm and highlights the duality of therapies. A high level of suspicion is required for timely diagnosis of thyroid storm and early treatment is critical. Despite this, the benefits of therapy cannot be seen in a vacuum and we must strive to understand the potential negative consequences in our quest to provide exceptional critical care. Reference #1: Chiha M, Samarasinghe S, Kabaker AS. Thyroid Storm: An Updated Review. Journal of Intensive Care Medicine. August 5, 2013. Volume: 30 issue: 3, page(s): 131-140. Reference #2: Karger S, Führer D. Thyroid storm--thyrotoxic crisis: an update. Dtsch Med Wochenschr. 2008;133(10):479-484. doi:10.1055/s-2008-1046737 DISCLOSURES: No relevant relationships by Paul Cooper, source=Web Response No relevant relationships by Dustin Fraidenburg, source=Web Response No relevant relationships by Janae Gonzales, source=Web Response No relevant relationships by Malvika Kaul, source=Web Response No relevant relationships by Shuvani Sanyal, source=Web Response No relevant relationships by Christen Vagts, source=Web Response