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CASE REPORT
Year : 2019  |  Volume : 12  |  Issue : 3  |  Page : 278-280  

Peripheral pulmonary embolism: A missed entity


Department of Medicine, Military Hospital, Chennai, Tamil Nadu, India

Date of Submission03-Sep-2018
Date of Acceptance10-Oct-2018
Date of Web Publication15-May-2019

Correspondence Address:
J Sankar
Graded Specialist Medicine, Military Hospital, Ekkaduthangal, Chennai - 600 032, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mjdrdypu.mjdrdypu_144_18

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  Abstract 


Pulmonary embolism (PE) is common, but often under-diagnosed or misdiagnosed entity. Pulmonary infarct is often caused by embolus in the peripheral branches, and timely diagnosis is often more challenging. Although peripheral pulmonary infarct is not fatal, it can be misdiagnosed as pneumonia or pleural effusion. Accurate diagnosis is also essential not only to rule out risk factors and prothrombotic states but also to prevent future thrombotic events. We report a case of 35-year-old male who presented with a history of isolated right-sided pleuritic chest pain of 1-week duration, diagnosed as a case of PE with a peripheral infarct. After 3 months of anticoagulation, he underwent screening for thrombophilia and detected to have factor V Leiden mutation. This case report highlights the fact that PE should be considered in the differential diagnosis of pleuritic chest pain.

Keywords: Pleuritic chest pain, pulmonary embolism, pulmonary infarct


How to cite this article:
Sankar J, Unniyal M, Ramprasad R, Khullar A. Peripheral pulmonary embolism: A missed entity. Med J DY Patil Vidyapeeth 2019;12:278-80

How to cite this URL:
Sankar J, Unniyal M, Ramprasad R, Khullar A. Peripheral pulmonary embolism: A missed entity. Med J DY Patil Vidyapeeth [serial online] 2019 [cited 2019 May 25];12:278-80. Available from: http://www.mjdrdypv.org/text.asp?2019/12/3/278/258202




  Introduction Top


Pulmonary embolism (PE) is known as “the great masquerader.” The diagnosis of PE is challenging because of nonspecific signs and symptoms.[1],[2] While massive PE presents with dyspnea, syncope, hypotension, and cyanosis, small PE presents with severe pleuritic chest pain. Pulmonary infarct is an uncommon manifestation of PE. Even though PE remains a differential diagnosis of pleuritic chest pain, PE without any other ominous signs is often overlooked. Although peripheral pulmonary infarct is not a catastrophe, it is extremely important in correct diagnosis to rule out underlying causes, and recurrent episodes may be devastating. Here, we report a case of 35-year-old male admitted with persistent pleuritic chest pain without any other symptoms, eventually diagnosed to have PE with a peripheral infarct. After 3 months of anticoagulation, he underwent screening for thrombophilia and detected to have factor V Leiden mutation and currently on oral anticoagulants under follow-up.


  Case Report Top


A 35-year-old male patient, without any comorbidities, admitted to our hospital with a history of right-sided chest pain for 1 week. Chest pain was pricking in nature aggravates on inspiration. He denied a history of fever, cough, hemoptysis, dyspnea, syncope, palpitations, or weight loss. He also denied any such episode in the past. He was initially evaluated in some other hospital for the same, diagnosed as a case of musculoskeletal chest pain, prescribed nonsteroidal anti-inflammatory drugs with some relief. On clinical examination at this center, he was hemodynamically stable and systemic examination was unremarkable. He was investigated for all possible etiologies of pleuritic chest pain in our scenario such as pneumonia, tuberculosis, pericarditis, and pleurisy due to viral infection. His hematological and biochemical parameters were normal. Chest X-ray posteroanterior view, electrocardiography (ECG), and two-dimensional (2D) echocardiography did not reveal any abnormalities. However, he continued to have worsening persistent pleuritic chest pain that prompted us to evaluate for other rare etiologies. On the 2nd day of admission, he underwent a contrast-enhanced computed tomography (CT) of the chest which revealed focal area of collapse consolidation involving the posterior segment of the right lower lobe [Figure 1]. His D dimer was also significantly elevated, raising the suspicion of possible peripheral pulmonary infarct. He was sent for urgent CT pulmonary angiography which revealed features, suggestive of PE in the terminal pulmonary artery branch supplying the posterior segment of right lower lobe causing its infarct [Figure 2]. He was started on parental low-molecular-weight heparin along with oral anticoagulant. Color Doppler of both lower limbs was done to rule out deep vein thrombosis (DVT). After 1 week, the target international normalized ratio was achieved and symptomatically improved. He was evaluated for inherited causes of thrombophilia after 3 months of anticoagulation and detected to have factor V Leiden mutation, the most common cause of inherited thrombophilia. At present, he is on oral anticoagulants under regular follow-up.
Figure 1: Collapse consolidation (pulmonary infarct) in the posterior segment of right lower lobe

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Figure 2: Filling defect in the terminal branch of pulmonary artery

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  Discussion Top


PE is common, but often under-diagnosed or misdiagnosed, and most of the cases of PE are diagnosed by postmortem.[3] Most patients of massive PE present with sudden-onset dyspnea, chest pain, syncope, or hemoptysis. Pulmonary infarction indicates small embolus, and it is exquisitely painful due to the peripheral lodging of thrombus, near the innervations of pleural nerves.[4] The diagnosis requires an integrated approach which includes multiple mode of investigations which include nonimaging and imaging diagnostic modalities. Nonimaging modalities include D dimer, cardiac biomarkers, and ECG. D dimer is sensitive, but not specific; it can be elevated in various other conditions. Cardiac biomarkers can be elevated due to right ventricular (RV) microinfarction. ECG findings are sinus tachycardia (most common), S1Q3T3 seen in only 20% of cases. T-wave inversion in V1–V3 can also be seen. Imaging modalities are Doppler ultrasonography to rule out DVT. The diagnosis of DVT is certain when thrombus is visualized. Chest X-ray is normal in most of the cases.[5] Classical findings in literature include focal oligemia (Westermark's sign), peripheral wedge-shaped density above the diaphragm (Hampton's hump), and an enlarged right descending pulmonary artery (Palla's sign). 2D echocardiography is used to assess the impact of PE on RV function. “McConnell's sign” described as akinesia of RV free wall with normal apical contractility can be seen. Chest CT with pulmonary angiography with evidence of intraluminal filling defect is the gold standard of diagnosing PE.[6] Treatment in hemodynamically stable patients includes low-molecular-weight heparin.[7] In the absence of contraindications, the American College of Chest Physicians (ACCP) carries Grade 1B level evidence for thrombolysis in massive acute PE with hemodynamic instability.[7] For unprovoked PE, the ACCP recommends indefinite anticoagulation, and in other cases, 3–6 months is considered sufficient. Novel anticoagulants are promising for prolonged anticoagulation.

In our case, pleuritic chest pain was only presenting complaint with other basic investigations apparently normal. Persistent pleuritic chest pain in peripheral PE is multifactorial due to ischemia, release of vasoactive cytokines, and peripheral lodging of emboli near the pleural nerve causing excruciating pain. Differential diagnosis considered in these patients was pneumonia, tuberculosis, costochondritis, and pleurisy due to viral infection. This case report is to highlight the fact that physicians should consider PE in the differential diagnosis of isolated persistent pleuritic chest pain.

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.
Wenger NK, Stein PD, Willis PW 3rd. Massive acute pulmonary embolism. The deceivingly nonspecific manifestations. JAMA 1972;220:843-4.  Back to cited text no. 1
    
2.
Bell WR, Simon TL, DeMets DL. The clinical features of submassive and massive pulmonary emboli. Am J Med 1977;62:355-60.  Back to cited text no. 2
    
3.
Stein PD. Prevalence, Risks, and Prognosis of Pulmonary Embolism and Deep Vein Thrombosis. In Pulmonary Embolism. 2nd ed. Oxford(UK): Blackwell Publishing; 2007. p. 3-15.  Back to cited text no. 3
    
4.
Islam M, Filopei J, Frank M, Ramesh N, Verzosa S, Ehrlich M, et al. Pulmonary infarction secondary to pulmonary embolism: An evolving paradigm. Respirology 2018;doi:10.1111/resp. 13299. [Epub ahead of print].  Back to cited text no. 4
    
5.
Worsley DF, Alavi A, Aronchick JM, Chen JT, Greenspan RH, Ravin CE, et al. Chest radiographic findings in patients with acute pulmonary embolism: Observations from the PIOPED study. Radiology 1993;189:133-6.  Back to cited text no. 5
    
6.
Konstantinides S. Clinical practice. Acute pulmonary embolism. N Engl J Med 2008;359:2804-13.  Back to cited text no. 6
    
7.
Kearon C, Kahn SR, Agnelli G, Goldhaber S, Raskob GE, Comerota AJ, et al. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th edition). Chest 2008;133:454S-545S.  Back to cited text no. 7
    


    Figures

  [Figure 1], [Figure 2]



 

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