Background

In December 2019, a novel virus, severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), was identified in Wuhan, China. Initially thought to be comparable to influenza, our understanding of COVID-19, caused by SARS-CoV-2 is evolving daily. It has caused a global disturbance due to its high transmission rate. WHO officially labelled COVID-19 as a pandemic on 11 March 2020, with the disease having spread to >190 countries. As of 07 April 2020, there were more than 1 400 000 confirmed cases with over 80 000 deaths.1

SARS-CoV-2 is a non-segmented, positive sense RNA virus that was first isolated from people who had visited the Huanan seafood market in Wuhan, China.2 Coronaviruses are naturally found in bats, which were postulated to be the primary reservoir for zoonotic transmission to humans in prior cases of coronavirus infection.3 4 This is, expectedly also true for SARS-CoV-2 as genetic studies have identified more than 96% similarity in the whole genome sequencing of SARS-CoV-2 and a bat SARS-related coronavirus (RaTG13) in China.5 In addition, pangolins have also been identified as potential reservoirs of coronavirus.6 SARS-CoV-2 binds the ACE2 receptor located on type II alveolar cells and intestinal epithelia. This is the same receptor used by the severe acute respiratory syndrome coronavirus-1 (SARS-CoV-1), hence the technical name for COVID-19 being SARS-CoV-2.7 8

The clinical presentation for SARS-CoV-2 varies from being asymptomatic to developing mild upper respiratory tract infection to severe pneumonia resulting in acute respiratory distress syndrome.9 This has posed challenges in halting the transmission via droplets due to asymptomatic carriers as well as identifying patients who can potentially decompensate later in the clinical course. As we learn more about COVID-19, we need to adapt and identify the means of early diagnosis, its management and most importantly, its prevention. We present a case of an 80-ear-old man who posed a diagnostic dilemma and the thoughts behind our decision-making process which could be useful to other clinicians managing patients with COVID-19.

Case presentation

An 80-year-old man presented to the emergency department with dyspnoea and nausea. His comorbidities included atrial fibrillation requiring cardioversion currently receiving anticoagulation with apixaban, non-ischaemic cardiomyopathy causing biventricular heart failure and left bundle branch block requiring cardiac resynchronisation therapy-defibrillation placement with most recent ejection fraction of 54%, hyperlipidaemia, gastro-oesophageal reflux disease and pseudogout. He was a remote smoker having quit more than 50 years ago, worked as a financial planner and denied any concerning exposures. His dyspnoea was primarily with exertion and had gradually progressed over the preceding 6–8 weeks. His primary residence was in Tennessee but he travelled extensively for work, most recently to New York, almost 4 weeks prior to his presentation. He did not have any known sick contacts. In the week prior to presentation, the patient had an acute change in exertional dyspnoea that resulted in difficulty climbing a flight of stairs. This acute change correlated with new onset nausea and loss of appetite. Notably, he did not have fevers, cough, sputum production, haemoptysis, chest pain, orthopnoea, lower extremity oedema or weight gain. He initially sought recommendations from his local primary care provider a week prior to presentation who temporarily increased the patient’s dose of furosemide. However, this did not alleviate his dyspnoea.

Investigations

In the emergency department, he was afebrile and normotensive with mild tachypnoea and oxygen saturation of 92% on room air. On examination, he was well appearing, had bibasilar rales with a systolic murmur likely from known tricuspid regurgitation, but without significant jugular venous distension or lower extremity oedema. The remainder of his physical examination was unremarkable. Laboratory workup revealed normocytic anaemia with haemoglobin 119 g/L, normal white cell count of 7.5×10⁹/L with reduced absolute lymphocyte count of 0.76×10⁹/L, N-terminal pro brain natriuretic Peptide (NT-pro BNP) 1722 pg/mL (normal 5–128 pg/mL), D-dimer 1392 ng/mL (normal ≤500 ng/mL), C-reactive protein (CRP) 82.6 mg/dL (normal ≤8 mg/dL), high sensitive troponin T 26 ng/L (normal ≤15 ng/L) without significant change after 2 hours, aspartate aminotransferase 61 U/L (normal 8–48 U/L) with otherwise unremarkable liver function tests and a normal renal function panel. A 12-lead ECG showed a paced rhythm without significant changes from prior readings. Chest radiograph revealed new patchy airspace opacities bilaterally. Due to an elevated D-dimer and progressive dyspnoea, a chest CT scan with pulmonary angiogram was obtained. CT chest with pulmonary angiogram was negative for pulmonary embolism but demonstrated diffuse bilateral patchy groundglass opacities predominantly in the mid to lower lung zones, which were consistent with crazy paving pattern (figure 1). These findings were new compared with a scan obtained 12 months prior, which showed an unremarkable pulmonary parenchyma.

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Figure 1

Chest X-ray with bilateral patchy airspace opacities (left), CT chest with bilateral groundglass opacities and crazy-paving pattern.

He was admitted to the inpatient medicine service for further workup under modified contact and droplet isolation (use of gown, gloves, surgical mask and eye shield). Influenza and respiratory syncytial virus PCR were negative. Due to the COVID-19 pandemic, his travel history and reports of community transmission within the USA, a nasopharyngeal swab for SARS-CoV-2 PCR was obtained, which returned negative. The pulmonary medicine team was consulted for consideration of bronchoscopy for further diagnostic workup. Due to high suspicion of infection, haemodynamic stability and immunocompetent status, testing with an extended respiratory pathogen panel and repeat SARS-CoV-2 PCR was recommended. Both tests were negative 24 hours after the initial SARS-CoV-2 PCR. The case was reviewed with the institutional infection prevention and control team who recommended repeating SARS-CoV-2 PCR 48 hours from the initial test. This was subsequently obtained and was positive, consistent with COVID-19 infection. Importantly, due to high clinical suspicion, modified contract and droplet precautions were maintained while the SARS-CoV-2 PCR tests were pending.

Differential diagnosis

The differential diagnosis of his clinical presentation was broad and included viral or atypical infection including pneumocystis pneumonia, inflammatory/interstitial lung disease such as eosinophilic pneumonia, non-specific interstitial pneumonitis or hypersensitivity pneumonitis and heart failure exacerbation. Heart failure exacerbation was less likely due to a stable echocardiogram, normal cardiac device interrogation a week prior to presentation, stable weight and absence of volume overload on examination or imaging.

Treatment

The patient was subsequently transferred to a dedicated medicine service caring for patients positive for COVID-19. Due to reports of sudden acute decompensation in older patients with COVID-19,10 he was observed in the hospital for a longer duration despite being haemodynamically stable.

Outcome and follow-up

His inflammatory markers down-trended (table 1) which correlated with symptomatic improvement and he was discharged in stable condition after a total of 8 days of hospitalisation.