Case Presentation: A 60-year-old man with type 2 diabetes presented with dyspnea and chest pain for 5 days during the COVID-19 pandemic. He arrived in acute hypoxic respiratory failure, with an oxygen saturation of 45% on room air. Physical exam revealed coarse lung sounds bilaterally and accessory muscle use. Initial labs were notable for leukocytosis 17.3 K/cumm (49% N 41% L), D-dimer 0.82 mg/mL, BNP 610 pg/mL, hypercapnia (CO2 79 mm Hg) and lactic acidosis (lactate 6.3 mmol/L). The patient was emergently intubated for acute hypoxic respiratory failure. Troponin was undetectable. ECG was notable for <1mm ST elevation in leads V1-V2, without any other ST or T-wave abnormalities. A contrast-enhanced chest CT revealed bilateral patchy airspace opacities concerning for multifocal viral versus bacterial pneumonia. Antibiotic therapy was initiated. Additionally, dexamethasone was initiated for severe COVID-19 pneumonia. On the first day of hospitalization the patient’s COVID-19 PCR test returned negative. The patient’s respiratory status quickly improved, and he was successfully extubated on hospital day 2.On hospital day 3, the patient unexpectedly experienced a severe episode of squeezing chest pain. The patient was administered sublingual nitroglycerin with resolution of chest pain after the third dose. Further interview revealed recurrent exertional and rest angina that coincided with the dyspnea leading to his presentation. Laboratory evaluation revealed a troponin of 0.11 µg/L, and an ECG showed T- wave inversions in leads V3-V4. The patient was transferred to the cardiac intensive-care unit to manage his NSTEMI. Coronary angiography performed the following morning showed multivessel coronary artery disease. The patient received an intra-aortic balloon pump, followed by triple coronary artery bypass grafting without complication.
Discussion: Acute coronary syndrome (ACS) is a common cause of hospitalization in the United States with an incidence of over 780,000 cases per year. Approximately 70% of ACS patients have NSTEMI. ACS and COVID-19 pneumonia can present similarly, with chest pain and dyspnea. In this case, the patient’s severe hypoxic respiratory failure, as well as the prevalence of COVID-19 pneumonia in our hospital, led to a presumed diagnosis of COVID-19. The initial leukocytosis, lactic acidosis, lack of troponin or ECG findings, and multifocal opacities on a chest CT contributed further to confirmation bias and premature closure. This case highlights how premature closure, availability heuristic, and anchoring bias can be exacerbated during a pandemic. Additionally, our case highlights how keeping alternative diagnoses in mind when a patient’s hospital course deviates from what is expected can lead to a correct diagnosis. It is important for hospitalists, even in the setting of a global pandemic, to keep a broad differential and be aware that biases can delay or impede a correct diagnosis.
Conclusions: Hospitalists should maintain a broad differential even in the setting of a global pandemic. Although a pandemic requires hospitalists to learn about a brand-new disease, it is important to remember how bias can impact clinical diagnosis. Avoiding premature closure requires keeping a broad differential, but also reevaluating the working diagnosis if the patient’s hospital course is unexpected.