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Table of Contents
CASE REPORT
Year : 2021  |  Volume : 9  |  Issue : 3  |  Page : 183-186

When pulmonary embolism mimics pneumonia: An interesting case report


Department of Internal Medicine, MVJ MC and RH, Hoskote, Karnataka, India

Date of Submission23-Jan-2020
Date of Decision28-Jan-2020
Date of Acceptance15-Feb-2020
Date of Web Publication16-Jul-2021

Correspondence Address:
Dr. Shreyashi Ganguly
309, Sai Charita Green Oaks, Horamavu Main Road, Bengaluru - 560 043, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AJIM.AJIM_3_20

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  Abstract 


The classic presentation of pulmonary embolism is rather uncommon. The lack of pathognomonic signs and symptoms makes the diagnosis of PE difficult. Here, we report a patient presented with symptoms suggestive of pneumonia and ultimately diagnosed as PE. A 75 years old male patient with no known co-morbidity, presented with of breathlessness for 1 week, cough for one week, productive in type, with scanty sputum, chest pain since one week, sharp, aggravated on coughing. His respiratory system examination revealed increased VF/VR in right mammary and left infrascapular areas, equal air entry with normal vesicular breath sounds, crepitations in the right mammary and left infrascapular areas. He was initially treated as pneumonia but did not respond. His chest X-ray PA view showed probable mass lesion in the right para cardiac region, ECG– sinus tachycardia with right axis deviation and RV strain pattern. CECT Thorax- Intraluminal thrombus in Rt and Lt pulmonary artery consistent with acute pulmonary thromboembolism.The patient was lysed with Inj. Streptokinase and subsequently improved over the next 6 days. Whilst established criteria aid in ruling in or out the diagnosis in a setting, the gestalt of a clinician is the most appropriate defence against a missed diagnosis especially in settings of confounded presentation. Therefore, until conclusively proven with the help of imaging and lab-work, PE should be a diagnosis that needs be considered in any case of atypical pneumonia who is not responding to first line therapies.

Keywords: Acute pulmonary thromboembolism, masquerader, pneumonia, thrombolysis


How to cite this article:
Sooraj C S, Kamath V, Ganguly S. When pulmonary embolism mimics pneumonia: An interesting case report. APIK J Int Med 2021;9:183-6

How to cite this URL:
Sooraj C S, Kamath V, Ganguly S. When pulmonary embolism mimics pneumonia: An interesting case report. APIK J Int Med [serial online] 2021 [cited 2021 Jul 29];9:183-6. Available from: https://www.ajim.in/text.asp?2021/9/3/183/321658




  Introduction Top


Pulmonary thromboembolism is defined as the obstruction of a pulmonary artery or one of its branches, usually produced by a blood clot. Acute pulmonary embolism (PE) is a component of venous thromboembolism, which may prove fatal if not suspected and subsequently treated.[1] The classic presentation of PE with abrupt onset pleuritic chest pain, hypoxia, hemoptysis, and dyspnea is rather uncommon with an incidence of 5%–7%.[2] The lack of pathognomonic signs and symptoms makes the diagnosis of PE difficult. Well-timed diagnosis and management of PE are necessary with the aim of decreasing mortality.[3] Up to 70% of misdiagnosed PEs are detected postmortem. However, 40% of dead patients had visited a clinician for ambiguous symptoms in the weeks before their death.[4] This significant amount of misdiagnosis highlights the importance to review different possible presentations of this fatal medical condition. Here, we report a patient presented with symptoms suggestive of pneumonia and ultimately diagnosed as PE.


  Case Report Top


A 75-year-old male patient with no known comorbidity, presented with complaints of breathlessness for 1–week which was insidious in onset and progressive in nature. He had a history of cough for 1 week, productive in type, with scanty sputum, which was mucoid, white in color, and nonblood tinged. He also had history of chest pain for 1–week, sharp, aggravated on coughing. There was no history of fever.

On examination, the pulse rate was 110/min, respiratory rate of 24/min, blood pressure of 110/70 mm Hg, and SpO2 of 88% on room air which improved to 94% with 4L O2. His temperature was 98.6°F. His respiratory system examination revealed increased vocal fremitus/vocal resonance in the right mammary and left infrascapular areas, equal air entry with normal vesicular breath sounds, crepitations in the right mammary and left infrascapular areas. The rest of his physical examination was within the normal limits.

A detailed laboratory workup was done for him. It is elucidated in [Table 1].
Table 1: Investigations in the patient

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Chest X-ray [Figure 1] posteroanterior view showed a mass lesion in the right paracardiac region.

Electrocardiogram (ECG) showed sinus tachycardia with right axis deviation and right ventricular (RV) strain pattern.

Initially, the patient was managed in the intensive care unit as a case of pneumonia and started on intravenous antibiotics, nebulization, and steroid. Chest X-ray was suggestive of mass lesion in the hilar area. The patient was advised contrast-enhanced computed tomography (CECT) for confirmation of the diagnosis.
Figure 1: Chest X-ray posteroanterior view showing mass lesion in the right paracardiac region

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CECT (thorax) done on September 10, 2019, revealed [Figure 2] intraluminal thrombus in the right and left pulmonary arteries distal to the upper lobar branches and extension of thrombi into segmental branches with consolidation of medial and lateral segments of the right middle lobe and basal segments of the left lower lobe. This is consistent with acute pulmonary thromboembolism. His PE severity index was calculated to be 125 points putting him in Class IV (high risk: 4.0%–11.4% 30-day mortality in this group).[5]
Figure 2: Contrast-enhanced computed tomography thorax showing intraluminal thrombus in the right and left pulmonary artery distal to the upper lobar branches and extension of thrombi into segmental branches with consolidation of medial and lateral segments of the right middle lobe and basal segments of the left lower lobe

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Emergency cardiothoracic surgeon opinion was taken. The patient was not found to be a candidate for thrombectomy. The patient was lysed with injection streptokinase 2.5 lakh IU over 30 min. Subsequently, the patient improved over the next 6 days, following which he was discharged under the cover of anticoagulation.


  Discussion Top


PE is a serious medical emergency. The incidence of PE is around 0.5–1 case/1000. Nevertheless, it is difficult to diagnose PE. The Wells criteria for PE is a risk stratification score and clinical decision rule to estimate the probability for acute PE, and the PE rule-out criteria (PERC) may be utilized to negate the need for further PE workup in patients who are deemed low risk for PE but in whom the diagnosis is being considered.[6]

The clinician should have a low threshold to consider its diagnosis in atypical presentations, particularly in the elderly. However, many affected individuals' silent PE can develop in up to 40%–50% of patients and remain asymptomatic throughout life.

Thrombosis is caused by the interaction of three Virchow factors, that is, hypercoagulability, endothelial injury, and stasis. There are acquired and genetic risk factors responsible for thromboembolism.

Recent surgery, trauma, immobilization, pregnancy, and oral contraceptives are the most common acquired factors which are most of the time, temporary in nature. Other factors such as malignancies, for example, hematological, lung, and pancreatic and brain cancers, pose the greatest risk for PE, and cancer association is a predictor of increased mortality. Smoking, obesity, atherosclerosis, hypertension, and infection in hospitalized patients are also common causes for PE. Deep vein thrombosis (DVT) is present in 79% of cases of PE, and 40%–50% of DVT is complicated by PE.[7] In our case, there is no risk factor for pulmonary thromboembolism, and several studies showed that up to 30% of cases of PE develop idiopathically without risk factors.

Symptoms of PE include sudden-onset dyspnea (90%), syncope (14%), and pleurisy (5%). Signs or PE may include tachypnea (96%), tachycardia (44%), hypoxemia (75%), hypotension (20%), features of RV dysfunction (distended jugular veins), and ECG showing RV strain (34%), S1Q3T3 (20%), right bundle branch block (18%), and T-inversion in leads V1–V4 (50%).[8] Our patient had sinus tachycardia with right axis deviation and RV strain pattern.

Up to 10% of symptomatic PEs are fatal within the 1st h of symptoms. Classical triad of chest pain, hemoptysis, and dyspnea is present <20% of cases.[9] In the elderly who are more likely to have risk factors for thromboembolic disease, immobility, and malignancy, PE should be considered in the differential for subtle symptoms such as weakness, malaise, or dizziness. Medications such as beta-blockers and narcotics, and cognitive decline can also contribute to the blunted responses to critical insults.[10] In one review, the most common symptoms of PE in patients over 65 were dyspnea, tachypnea, and tachycardia rather than chest pain. Initial symptoms in PE, dominated by dyspnea and/or pleuritic chest pain were significantly different from those in community-acquired pneumonia, dominated by fever, chills, and/or cough. In a study done by Hsiao et al., the patient presented with symptoms suggesting shortness of breath, pleuritic chest pain, coughing, orthopnea, hemoptysis, and fever.[11]

In another study of Zhang et al., chest pain, shortness of breath, hemoptysis, and fever were identified as independent risk factors of a PE in patients initially diagnosed with pneumonia.[12] On the other hand, Söderberg et al. highlighted the presence of dyspnea and/or chest pain in PE and fever, chills, and/or cough in community-acquired pneumonia.[11] There were only 3.3% of patients in their study, who were suffering from pneumonia but diagnosed as acute PE in the end. Our patient was initially suspected to have atypical pneumonia, however the subsequent lack of response to therapy, and additional diagnostics, alerted to the need to revise the diagnosis.

Conventionally, the patients with PE are treated in the hospital (usually for 24 h but up to 5 or 6 days) for initiation of anticoagulation therapy and monitoring for any clinical deterioration. The introduction of low-molecular-weight heparin (LMWH) and the non-Vitamin K-dependent oral anticoagulants, together with the increased ability to accurately stratify patients according to their risk of short-term clinical deterioration, have made it potentially feasible and safe to manage selected low-risk patients in the outpatient setting either entirely or after a short in-hospital observation period. Our patient was initially managed in the intensive care, but once diagnosed and appropriately treated, he was able to be discharged under the cover of oral anticoagulation in 6 days.


  Conclusion Top


PE is known as the “great masquerader” for a reason. The classic textbook presentation of PE abrupt onset pleuritic chest pain, hypoxia, hemoptysis, and dyspnea is uncommon. PE is more likely to be diagnosed in a setting where it is a diagnosis of exclusion.

Criteria such as Wells' score and PERC aid in ruling in or out the diagnosis in a setting. However, the gestalt of a clinician is the most appropriate defense against a missed diagnosis, especially in settings of confounded presentation.

With the advent of thrombectomy, thrombolysis, LMWH, and Vitamin K-independent anticoagulation, the management of PE has become more streamlined and rewarding. The crux of the problem lies in not diagnosing a patient in time. Therefore, until conclusively proven with the help of imaging and laboratory work, PE should be a diagnosis that needs to be considered in any case of atypical pneumonia who is not responding to first-line therapies.

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

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
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2.
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Parambil JG, Savci CD, Tazelaar HD, Ryu JH. Causes and presenting features of pulmonary infarctions in 43 cases identified by surgical lung biopsy. Chest 2005;127:1178-83. doi:10.1378/chest.127.4.1178.  Back to cited text no. 3
    
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Misra P, Ghosh AK, Assar A. Autopsy findings in an atypical case of occult massive fatal pulmonary embolism in a backdrop of hyperhomocysteinemia. Indian J Pathol Microbiol 2018;61:116-9.  Back to cited text no. 4
[PUBMED]  [Full text]  
5.
Aujesky D, Obrosky DS, Stone RA, Auble TE, Perrier A, Cornuz J, et al. Derivation and validation of a prognostic model for pulmonary embolism. Am J Respir Crit Care Med 2005;172:1041-6.  Back to cited text no. 5
    
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Masotti L, Ray P, Righini M, Le Gal G, Antonelli F, Landini G, et al. Pulmonary embolism in the elderly: A review on clinical, instrumental and laboratory presentation. Vasc Health Risk Manag 2008;4:629-36. Review. PubMed PMID: 18827912; PubMed Central PMCID:PMC2515422.  Back to cited text no. 6
    
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Thorneycroft IH, Goldzieher JW. Venous thromboembolism. A review. J Reprod Med 2003;48(11 Suppl):911-20.  Back to cited text no. 7
    
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Nahar S, Momenuzzaman G, Begum F, Khan KN, Anisuzzaman Q, Dhar R, et al. Pulmonary embolism. Univ Heart J 2016;12:11-3.  Back to cited text no. 8
    
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Morrone D, Morrone V. Acute Pulmonary Embolism: Focus on the Clinical Picture [published correctionappears in Korean Circ J 2018;48:661-663]. Korean Circ J 2018;48:365-381. doi:10.4070/kcj.2017.0314.  Back to cited text no. 9
    
10.
Konstantinides S. Clinical practice. Acute pulmonary embolism. N Engl J Med 2008;359:2804-13.  Back to cited text no. 10
    
11.
Söderberg M, Hedström U, Sjunnesson M, L&#s228;rfars G, Jorup-Rönström C. Initial symptoms in pulmonary embolism differ from those in pneumonia: A retrospective study during seven years. Eur J Emerg Med 2006;13:225-9.  Back to cited text no. 11
    
12.
Zhang Y, Zhou Q, Zou Y, Song X, Xie S, Tan M, et al. Risk factors for pulmonary embolism in patients preliminarily diagnosed with community-acquired pneumonia: A prospective cohort study. J Thromb Thrombolysis 2016;41:619-27.  Back to cited text no. 12
    


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