Case Report: COVID-19 Pneumonia Complicated by Lung Abscess
Rebecca McAteer, MD, Dmitriy Gagarkin, MD
Phelps-Northwell Family Medicine Residency Program (Sleepy Hollow, NY)
INTRODUCTION
The emergence of the present COVID-19 global pandemic has presented myriad challenges in the diagnosis and management of infected patients. The illness typically presents as an acute viral syndrome, often with significant elevations in inflammatory markers and radiographic findings of bilateral interstitial pulmonary infiltrates. While the majority of confirmed PCR-positive patients will only experience mild symptoms, 14% of patients go on to develop severe disease and 5% will end up in a critical condition (1). A recent U.S.-based study postulates that as many as 45% of adults are at risk of developing complications associated with the virus due to preexisting risk factors (2), including venous and thromboembolic events (3,4,5), encephalopathy (6,7) and arrhythmias or other cardiac events (8,9).
While it is difficult to predict which patients will develop these complications, elevations in certain biomarkers have been associated with worse outcomes. Procalcitonin has been utilized as an effective biomarker to reliably distinguish viral from bacterial infections in the lower respiratory tract (10), and has been associated with bacterial co-infection and progression to severe disease in patients infected with SARS-CoV-19 (11). We here describe a case of COVID-19 respiratory failure complicated by a proteus mirabilis lung abscess in the context of a negative procalcitonin and non-specific chest radiograph findings.
CASE REPORT
A 63-year-old Ecuadorian male presented to the emergency department on April 4, 2020 with three days of progressively worsening shortness of breath, cough, fatigue and subjective fevers. His medical history was significant for acquired hypothyroidism, for which he took 50 mcg levothyroxine daily, and diet-controlled hypertension. He worked in construction, lived alone, and denied any known sick contacts or international travel in the preceding three months.
On presentation, the patient was tachycardic (HR 106), tachypneic (RR 22), febrile (T 100.6 F), and hypoxic (SpO2 80% on room air). Admission weight was 77.2 kg. Physical examination revealed an ill-appearing man in acute respiratory distress, with significant tachypnea and increased work of breathing; pulmonary auscultation revealed diffuse bilateral rales. Initial laboratory results demonstrated a neutrophil-predominant leukocytosis (WBC 12,500, N 91%) and elevated inflammatory markers (C-reactive protein 317.4 mg/L, D-dimer 825 ng/mL, LDH 2165 U/L). A chest radiograph demonstrated bilateral moderate to extensive patchy parenchymal opacities suspicious for multilobar infiltrates. His SARS-CoV-2 PCR nasopharyngeal swab was positive.
The patient had improved oxygenation on a non-rebreather (SpO2 95%) and was admitted to the family medicine teaching service for further management. Due to increasing oxygen requirements he was intubated from 4/13- 4/16, subsequently transitioned to high flow nasal cannula oxygen, and again intubated from 4/25–4/27. Based on institutional protocols at the time, he was treated with azithromycin (total of 2 grams over 7 days), hydroxychloroquine (total of 2400 mg over 5 days), acetazolamide (1.25 grams over 5 days), enoxaparin (40 mg daily), tocilizumab (weight-based protocol), anakinra (weight-based protocol) and convalescent plasma.
Following his second extubation, on 5/5/20, he was noted to have a progressive leukocytosis with thrombocytosis, uptrending CRP and D-Dimer levels (peak D-Dimer 24,658), and a repeat chest radiograph showing interval progression of his prior patchy bilateral airspace opacities. Blood cultures and repeat COVID-19 nasopharyngeal swab PCR were negative; a procalcitonin drawn at that time was 0.09 ng/mL, falling below the standard threshold of 0.25 ng/mL. Nevertheless, he empirically received standard-dose meropenem and linezolid due to progressive clinical decompensation that was felt to be infectious in nature, with the suspected source being pulmonary, likely a bacterial superinfection.
A CT-angiogram of the chest revealed a large left upper lobe septated cavitary lung abscess (FIGURE 1) and a right lower lobe subsegmental pulmonary thrombus of undetermined acuity. Nasopharyngeal and sputum cultures were subsequently positive for proteus mirabilis, and his antibiotic regimen was narrowed to ceftriaxone based on sensitivity results. A CT-guided pigtail catheter was placed into the abscess by interventional radiology, and abscess fluid culture confirmed growth of proteus mirabilis. Of note, a urine culture earlier in his admission had demonstrated growth of proteus mirabilis (50–100k CFU/mL on a catheter specimen), although blood cultures remained negative throughout.
DISCUSSION
To our knowledge, there are no cases described in the literature of a pulmonary abscess complicating an infection with the 2019 novel coronavirus, particularly with a negative procalcitonin, which is generally viewed as a useful marker of bacterial infection. Normally, physiological levels of procalcitonin are fairly low (less than 0.05 ng/mL). This concentration can be increased by orders of magnitude as a result of endotoxin stimulation of liver, pancreas, kidney or lung tissues. In this way, an acute elevation of procalcitonin can be a signal of endotoxin and thus bacterial exposure. Conversely, procalcitonin synthesis has been found to be suppressed by cytokines such as interferon-gamma, which is released following a viral infection.
However, procalcitonin remains one indicator among many in a constellation of findings in a given clinical presentation, and over-reliance on any one such finding should be avoided. This is consistent with the 2019 ATS/IDSA Clinical Practice Guideline on the Diagnosis and Treatment of Adults with Community-acquired Pneumonia, which recommends that empiric antibiotic therapy be initiated in adults with clinically suspected and radiographically confirmed CAP, regardless of initial serum procalcitonin level (12), as was implemented in this case in a timely fashion despite the negative procalcitonin result.
While it is unclear why procalcitonin was suppressed despite the presence of a confirmed bacterial abscess, one possibility is the “walled off nature” of an abscess and lack of systemic exposure to the endotoxin. The reliability of procalcitonin is thought to be low in such a setting, though this has not been fully characterized in the literature. Another possibility is that procalcitonin is suppressed by released interferon due to the active COVID infection, though this is less likely in the above case given that a repeat nasopharyngeal COVID swab collected concurrently was negative.
In retrospect, this case demonstrated a progressive uptrending of various inflammatory markers and gradually worsening plain-film imaging findings, with ongoing need for high-flow nasal cannula and difficulty weaning his oxygen requirements, which preceded a sudden clinical decompensation four weeks into his hospital stay. Apart from the initial CT done on admission, radiographic assessment was performed only with serial chest X-rays as clinically indicated; a repeat CT scan of his chest was not done until he demonstrated an acute clinical change, which is consistent with best practice guidelines regarding the use of CT imaging in hospitalized adults. However, retrospectively, CT imaging may have been warranted earlier in his hospital stay, given his sluggish response to treatment and ongoing oxygen requirements, with subtle evidence of an ongoing systemic inflammatory response.
CONCLUSION
Providers should remain vigilant for complications associated with the novel coronavirus, and be aware that the marker procalcitonin may be inaccurate in some types of superimposed bacterial infections, such as pulmonary abscesses. Use of imaging modalities, particularly computed tomography, can aid in the diagnosis and should be considered early in the clinical course, especially in the context of slow treatment response or evidence of ongoing systemic infection despite usual care consistent with guidelines recommendations.
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