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 Table of Contents  
Year : 2020  |  Volume : 22  |  Issue : 3  |  Page : 128-132

Atypical presentations in COVID-19-lung abscess, pulmonary thromboembolism and ST-elevation myocardial infarction: Diagnosis and management in a temporary COVID-19 hospital

1 Department of Internal Medicine AFMC, Pune, Maharashtra, India
2 Department of Anaesthesiology and Critical Care, AFMC, Pune, Maharashtra, India

Date of Submission09-Aug-2020
Date of Decision18-Aug-2020
Date of Acceptance21-Aug-2020
Date of Web Publication29-Sep-2020

Correspondence Address:
Sqn Ldr Sourya Mohakuda
Assistant Professor, Department of Internal Medicine, AFMC, Solapur Road, Pune-40, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jmms.jmms_110_20

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COVID-19 pandemic has adversely affected every tenet of societies all across the world. The gruesome disease, which is primarily a respiratory illness, as is being unmasked with each passing day, has been reported to have a variety of presentations. Here, we report three such cases with atypical manifestation in COVID-19 who were managed in a resource-limited makeshift COVID-19 temporary hospital in Northern India. The dictum to avoid unnecessary exposure by restricting investigations or procedures that would not directly aid in management has been reiterated in this series of cases.

Keywords: Atypical, COVID-19, lung abscess, pulmonary thromboembolism, ST-elevation myocardial infarction

How to cite this article:
Harikrishnan P, Mohakuda S, Pathak B, Singh AR, Tilak T, Srinath R, Singh S, Paul S. Atypical presentations in COVID-19-lung abscess, pulmonary thromboembolism and ST-elevation myocardial infarction: Diagnosis and management in a temporary COVID-19 hospital. J Mar Med Soc 2020;22, Suppl S1:128-32

How to cite this URL:
Harikrishnan P, Mohakuda S, Pathak B, Singh AR, Tilak T, Srinath R, Singh S, Paul S. Atypical presentations in COVID-19-lung abscess, pulmonary thromboembolism and ST-elevation myocardial infarction: Diagnosis and management in a temporary COVID-19 hospital. J Mar Med Soc [serial online] 2020 [cited 2021 Jun 20];22, Suppl S1:128-32. Available from: https://www.marinemedicalsociety.in/text.asp?2020/22/3/128/296566

  Introduction Top

In December 2019, a cluster of patients having pneumonia and other respiratory symptoms emerged in Wuhan, Hubei Province, China, which was later identified to be due to a novel virus belonging to severe acute respiratory syndrome (SARS) coronavirus family.[1],[2],[3] Over half a year since its first detection in China, the disease has wreaked havoc across the globe-spanning over 200 countries, infecting over 18 million people and claiming over 6 lakh lives.[4] With transmission dynamics similar to other common respiratory viruses, and the presence of human-to-human transmission, the virus continues to spread despite stringent interdisciplinary tactics adopted by the governments and health-care agencies globally.[5]

COVID-19 infection is characterized by wide array symptomatology ranging from mild disease with fever, cough, fatigue, anorexia, myalgias, and diarrhea to severe forms with dyspnea, hypoxemia and rapid progression to respiratory failure and death.[6],[7],[8] Apart from these, COVID-19 is also known to have a variety of atypical presentations.[9] Here we report a series of cases with atypical COVID-19 presentations in a dedicated 1000-bedded hospital in Northern India. The hospital is a makeshift facility with limited tertiary care diagnostic modalities available that has restricted our diagnoses primarily to be based on basic investigations and clinical parameters. Possible exposures and unwanted movement of patients for investigations which would not lead to a change in management were avoided.

  Case Presentations Top

Case 1: COVID-19 with lung abscess and septic shock

Sixty-seven-year-old diabetic female had presented with fever and cough with expectoration of 3 days duration with no history of chest pain, syncope, palpitation, or dyspnea.

She was tested positive for COVID-19 by SARS-CoV2 reverse transcription polymerase chain reaction (RT PCR).

An initial evaluation in the triage area revealed that she was afebrile, had a pulse rate of 108/min, respiratory rate of 24/min, and oxygen SpO2 of 88% at room air, which improved up to 97% with oxygen at a rate of 10 L/min through the face mask. Her blood pressure (BP) was 100/70 mmHg. She had pallor. There was no icterus cyanosis, clubbing or pedal edema.

She was assessed in the COVID-19 intensive care unit (ICU) in detail, where her systemic examination revealed reduced breath sounds in the left mammary region with bronchial breath sounds. Further characters of auscultation could not be assessed due to a very high ambient sound in the ICU of the makeshift hospital. About 6 h since admission, she became hypotensive with bounding peripheral pulses and elevated serum lactate levels (4.12 mmol/L), which was managed as septic shock with intravenous (IV) fluids and inotropes.

Her chest radiograph was suggestive of an abscess involving the upper lobe of the left lung [Figure 1]. Initial laboratory evaluation revealed neutrophilic leucocytosis and normocytic normochromic anemia. The rest of her investigations were essentially normal, including serum procalcitonin levels. Furthermore, she was started on injection remdesivir and broad-spectrum parenteral antibiotics with anaerobic cover in view of lung abscess with sepsis. She has responded well to the treatment and is presently maintaining oxygen saturation >97% at room air. In view of improving the clinical course, no invasive diagnostic strategy was adopted to minimize the interventions. Her chest radiograph 3 days postantibiotics shows resolution of the abscess [Figure 2]. She is planned for discharge with advice for high-resolution computed tomography (HRCT) chest and further workup to rule out active tuberculosis.
Figure 1: Chest X-ray AP and lateral view: Lung abscess with air fluid level left upper lobe (Blue Arrows)

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Figure 2: Chest X-ray showing resolution of lung abscess post antibiotic therapy (Red arrow)

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Case 2: A case of acute pulmonary thromboembolism in COVID-19 patient

Fifty-one-year-old male, a resident of Delhi Cantonment, with no prior comorbidities had presented with chief complaints of fever and cough with expectoration of 5 days duration and nonradiating, left-sided, pleuritic chest pain with the Modified Medical Research Council Grade 3 dyspnoea of 1 day duration. There was no history of palpitation, syncope, hemoptysis, or wheeze. His SARS-CoV2 RT PCR was positive.

On examination, he was afebrile, had a pulse rate of 128/min and respiratory rate of 45/min with SpO2 of 88% with room air that improved up to 99% with oxygen supplementation at a rate of 8 L/min through the face mask. He was normotensive (BP: 124/86 mmHg). There was no pallor, icterus, cyanosis, clubbing, or pedal edema. Jugular venous pressure was not elevated. His systemic examination was unremarkable.

His baseline electrocardiograph (ECG) revealed sinus tachycardia with S1Q3T3 pattern and precordial leads showing evidence of Right ventricular strain [Figure 3]. He had a modified Well's criteria score of 4.5 placing him in a moderate risk for pulmonary thromboembolism (PTE) with pulmonary embolism severity index score of 121, indicating high risk of mortality and morbidity.[10] His laboratory evaluation revealed normal blood counts, with significantly elevated D-Dimer (560 ng/ml) and Aspartate Transaminase (AST), 251 IU/L >5 times of upper limit of normal. The rest of the liver and kidney function tests, and his chest X-ray was normal. Serological markers for common hepatotropic viruses were negative. Serum B-TYPE Natriuretic Peptide levels were not elevated (<10.0 pg/mL). Troponin I was negative. The facility for CT-Pulmonary angiography (CTPA) was not available in the temporary makeshift COVID-19 Hospital. In view of adequate clinical (Wells Score-4.5) and laboratory evidence, the patient was managed as a case of acute PTE. He was started on twice-daily therapeutic doses of low-molecular-weight heparin. The decision to thrombolyze the patient was reserved for worsening hemodynamic parameters only. He was also started on IV parenteral antibiotics along with tablet hydroxychloroquine and IV fluids. He has responded well to this conservative approach and shows significant improvement. After 10 days of stay in the COVID-19 ICU, he is maintaining oxygen saturation > 97% at room air, with a normal respiratory rate. The ECG has reverted to normal sinus rhythm, his D-dimer, C-reactive protein (CRP), erythrocyte sedimentation rate, and AST levels have normalized. He is being planned for discharge with advice to review in a tertiary care facility with CTPA and to decide on the continuation of oral anticoagulants after 3 months.
Figure 3: Electrocardiograph depicting changes suggestive of pulmonary thromboembolism sinus tachycardia, S1Q3T3 (red, blue and purple arrows) and Right ventricular strain pattern (green arrows)

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Case 3: A case of COVID-19 with ST-elevation myocardial infarction

Sixty-five-year-old male, a resident of South Delhi, with poorly controlled Diabetes Mellitus (HBA1C-12.9%), had presented with chief complaints of intermittent fever with chills, nonproductive cough without diurnal variation of 5 days duration and dyspnea at rest of 3 days duration. He was received in the ICU of the dedicated COVID-19 hospital after his SARS-CoV2 RT PCR came positive.

Clinical evaluation revealed a temperature of 100.4°F, pulse rate of 118/min, BP of 146/84 mmHg, respiratory rate of 35/min, and oxygen saturation (SpO2) of 37% with Bilevel Positive Airway Pressure (BiPAP: IPAP16/ePAP6 cm). On auscultation of the respiratory system, air entry was comparable in both sides, and there were bilateral coarse crackles all across lung fields. Rest of the systemic examination were normal.

In view of continuing severe hypoxemia (SpO2-37-40%) despite noninvasive ventilation, he was started on invasive mechanical ventilation, which improved the oxygen saturation to 66%–70%. His basic hematological workup revealed neutrophilic leucocytosis with mild thrombocytopenia. His serum lactate levels were suggestive of severe sepsis (7.29 mmol/L). Serum ferritin (3000 ng/ml) and CRP (157 mg/L) levels were markedly elevated [Table 1]. His baseline ECG was essentially normal, with no ST-T segment changes. One hour postadmission in view of poor response to mechanical ventilation and worsening clinical state, a repeat ECG revealed ST-segment elevation of inferolateral leads (II, III, aVF, V4-V6) [Figure 4]. His cardiac biomarkers were normal (suggesting a hyperacute ST-elevation myocardial infarction [STEMI]). In view of an anticipated time of shifting the patient to the nearest percutaneous coronary intervention facility being >120 min, which was attributable to the patient being on ventilator, the patient was thrombolyzed with accelerated 90 min regimen of IV Alteplase. Chest radiograph revealed extensive bilateral ground-glass opacities with a blood gas analysis consistent with severe acute respiratory distress syndrome (PaO2/FiO2: 56). He was also started on broad-spectrum parenteral antibiotics, and IV fluids to cater for on-going septicemia. His respiratory drive kept worsening and about an hour into thrombolysis, he had a cardiac arrest and succumbed to the illness.
Table 1: Relevant laboratory investigations of the patients

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Figure 4: Electrocardiogram showing ST-elevation (orange arrows)

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  Discussion Top

At the dawn of the 21st century, the world is faced with one of the most dreadful pandemics that have affected humankind. The COVID-19 pandemic has shattered the scaffolding of even the most powerful economies in the world and has put the health-care preparedness of every nation to test. The disease, as is known, is caused by the SARS-CoV2 virus belonging to the larger family of coronaviruses, which is primarily a respiratory pathogen.[11] In the setting of a pandemic by a novel agent, the knowledge of its transmission dynamics and spectrum of clinical presentation is vital to tackle the condition more effectively.

Fever, dry cough, sore throat, dyspnea, fatigue, and myalgia constitute the commonest symptoms of COVID-19. However, multiple cases of atypical presentations that have posed diagnostic and management dilemmas in patients with COVID-19 have been reported.[12],[13]

COVID-19 with lung abscess and septic shock

Patients of COVID-19 suffer serious lung injuries attributable to direct injury by viral replication, which is worsened by consequent cytokine storm and inflammatory damage.[14] Although lung abscess is known to occur in COVID-19 in up to 11% of cases,[15] very few cases have been reported about the same. Lung abscess is presumed to be the result of bacterial or fungal superadded infections.[16],[17] In our patient, despite formidable clinical and radiographic evidence of a lung abscess, which was further complicated by septic shock as evidenced by high serum lactate levels, the normal values of serum procalcitonin warrant special attention. Furthermore, the positive response to antimicrobials without antifungals consolidates the likelihood of a possible bacterial superinfection as opposed to a fungal pathogen. Serum procalcitonin levels, although a useful indicator for bacterial infection, may thus not always be relied upon in our approach toward the management of possible bacterial sepsis. This is supported by ATS/IDSA clinical practice guideline on the diagnosis and treatment of adults with community-acquired pneumonia of 2019,[18] which aided in our empirical management of the patient with a positive outcome. Low procalcitonin levels in our patient may be attributed to the more sequestered nature of bacterial products within the lung abscess, such that the bacterial endotoxin was underexposed to rest of the systems. Although an HRCT chest and possibly a diagnostic aspiration was indicated in our patient, the clinical course was very promising with our management protocol, which enabled us to postpone more detailed investigations to a later date postdischarge, which is of course also limited by the lack of higher imaging facility in our makeshift COVID-19 hospital.

Pulmonary thromboembolism in COVID-19

Thrombotic complications are well known to occur in COVID-19 patients.[19] Although the precise mechanism behind these thrombotic complications is not known, virus-mediated endothelial cell activation, excess of tissue factor, and resultant augmentation of coagulation cascade seem to play a key role.[20] The presence of neutrophil extracellular traps in both arteries and veins from autopsy specimens also points toward a possible cause for intravascular coagulation.[21],[22] The interaction of CD147 expressed on various hematopoietic cells with SARS-CoV2 spike protein is also implicated in arterio-venous thrombosis.[23] Furthermore, studies on pulmonary thrombosis in COVID-19 suggest more of an in situ process as opposed to an embolic event.[24] The more severe the disease higher would be the risk of thrombosis as reflected by higher levels of D-Dimer levels. Role of anticoagulants both in prophylactic and therapeutic doses, thus cannot be refuted as they are known to reduce morbidity and mortality in COVID-19 patients with the more severe disease more so with elevated D-Dimer levels.[25]

COVID-19 and cardiovascular manifestations

Several mechanisms have been postulated by which SARS-CoV2 virus leads to cardiovascular complications. Direct myocardial injury by altering angiotensin-converting enzyme 2 signaling pathways or indirectly as a part of cytokine storm-related multi-organ dysfunction are known to cause cardiovascular involvement.[26],[27],[28] Hypoxia and respiratory failure and the ensuing demand-supply mismatch are also detrimental to the myocardium. Furthermore, the prothrombotic state, which is established by the disease, could impede coronary flow and lead to the acute coronary syndrome. The latter two causes seem to be the most likely precipitating factor in our patients with STEMI.

As our experience and approach toward COVID-19 cases continue to be in its infancy phase, such atypical presentation would surely pose challenges not only to our clinical assessment of cases but also in crucial decision making. With number of cases of COVID-19 still in its surge, more makeshift facilities with limited resources are likely to come in action, wherein avoidance of unwarranted investigations and exposure will be vital as have been depicted in our series of cases.

  Conclusion Top

COVID-19 pandemic has affected the world as a whole and has certainly exposed our limitations in tackling such an outbreak. After almost 8 months post the outbreak and a myriad of research eyeing to counter the disease, our case series brings forth some atypical presentations of COVID-19, which would surely benefit clinicians in framing their approaches towards such cases. The common notion of COVID-19 being a respiratory illness, although true in a majority of cases must be sought with caution as these atypical clinical manifestations of COVID-19 will surely bring forth challenges to our existing protocols and practice guidelines.

Based on our experience, we suggest a higher index of suspicion for acute coronary syndrome and PTE in patients with COVID 19 and thereby frequent ECGs, cardiac biomarkers, and prophylactic anticoagulants may be helpful in timely management of the patients. Furthermore, our decisions on levels of intervention is to be weighed for risks and benefits involved not only to the patient but also to the health care workers involved in managing such cases as has been exhibited in our case with lung abscess. On the flipside, it would also be wise to emphasize that any patient reporting to our emergency departments with these diagnoses are to be tested for COVID-19 infection.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

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