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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 9  |  Issue : 2  |  Page : 229-233

Disseminated tuberculosis presenting as cardiac tamponade—Uncommon presentation in common disease


1 Department of Laboratory Medicine, Yashoda Hospital—Malakpet, Malakpet, Hyderabad, Telangana, India
2 Department of Interventional Cardiologist, Yashoda Hospital—Malakpet, Malakpet, Hyderabad, Telangana, India
3 Department of Medicine, Yashoda Hospital—Malakpet, Malakpet, Hyderabad, Telangana, India
4 Department of Radiology, Yashoda Hospital—Malakpet, Malakpet, Hyderabad, Telangana, India

Date of Submission17-Aug-2021
Date of Acceptance23-Mar-2022
Date of Web Publication17-Jun-2022

Correspondence Address:
Dr. Majed A B Momin
Department of Laboratory Medicine, Yashoda Hospital—Malakpet, Nalgonda x-roads, Hyderabad 500036, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mgmj.mgmj_62_21

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  Abstract 

Tuberculosis is the most common infection in India, and its incidence accounts for approximately one-fifth of the global burden. Cardiac tamponade resulting from the liver abscess with subdiaphragmatic rupture communicating with pericardial cavity presenting as disseminated tuberculosis is uncommon. Here, we reported a case of a 63-year-old man who presented with the shortness of breath for 3 days with orthopnea. Imaging studies reveal pericardial effusion, left liver lobe loculated lesion, and enlarged right supraclavicular lymph node. Further image-guided pericardiocentesis, left liver lobe aspiration cytology, and right supraclavicular lymph node cytology reveal granulomatous inflammation with positive acid-fast bacillus in the liver aspirate. The patient was managed in the emergency room symptomatically initially and was then successfully treated with antituberculous treatment.

Keywords: Cardiac tamponade, cytology and imaging, disseminated tuberculosis, liver abscess


How to cite this article:
Momin MA, Poddar P, Sarda AK, Borad DK. Disseminated tuberculosis presenting as cardiac tamponade—Uncommon presentation in common disease. MGM J Med Sci 2022;9:229-33

How to cite this URL:
Momin MA, Poddar P, Sarda AK, Borad DK. Disseminated tuberculosis presenting as cardiac tamponade—Uncommon presentation in common disease. MGM J Med Sci [serial online] 2022 [cited 2022 Sep 28];9:229-33. Available from: http://www.mgmjms.com/text.asp?2022/9/2/229/347701




  Introduction Top


Disseminated tuberculosis (DTB) is defined as the presence of two or more noncontiguous sites resulting from hematogenous dissemination of Mycobacterium tuberculosis, occurring as a result of progressive primary infection and the reactivation of a latent focus with subsequent spread.[1] A pericardial effusion with enough pressure to adversely affect heart function is called cardiac tamponade. Extrapulmonary tuberculosis in immunocompetent patients constitutes 15%–20% of all tuberculosis, in which cardiac tamponade presentation is seen in less than 2%.[2] Hepatic involvement in the absence of miliary tuberculosis and its association with pericardial effusion are very rare. A lymph node is the most common site for extrapulmonary tuberculosis.

The diagnosis of DTB poses a particular challenge for clinicians because of its atypical presentation and a lack of imaging facilities such as computed tomography (CT) and 2D echocardiography, particularly in rural areas. Cardiac tamponade is a life-threatening condition and requires acute treatment to avoid its fatal outcome. Here, we present a case of DTB with pericardium, liver, and lymph node involvement. In a thorough review of literature, cardiac tamponade from a ruptured liver abscess is not published so far, and such acute presentation secondary to chronic inflammation is rare.


  Case history Top


A 63-year-old man, agricultural worker, presented to the emergency room (ER) with sudden onset of the shortness of breath, orthopnea, and bilateral pedal edema for 3 days. On general examination, the patient is moderately built, conscious, and tachypneic. Pulse rate was 124 beats/minute, blood pressure was 70 mmHg, respiratory rate was 44 breaths/minute, and he is afebrile. Saturation SpO2 is 77% with room air and 95% with oxygen support. The right supraclavicular lymph node is palpable, having a size of 2 × 2cm, firm in consistency, mobile, and nontender. Systemic examination was normal except for mild hepatomegaly. Electrocardiogram shows sinus rhythm with low-voltage QRS complexes. The 2D echocardiography shows pericardial effusion and tamponade. Chest X-ray shows increased cardiothoracic ratio and the obliteration of the left costophrenic angle [Figure 1]. Ultrasound abdomen shows an abscess in the left liver lobe. Pericardiocentesis was done and around 700 mL of fluid aspirated. It was a brownish pus-like chocolate-colored fluid.
Figure 1: Chest X-ray shows an increased cardiothoracic ratio and the obliteration of the left costophrenic angle

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CT chest and abdomen [Figure 2] show pericardial effusion [Figure 2A], and the left liver lobe shows loculated lesion [Figure 2B] with subdiaphragmatic rupture communicating with the pericardial cavity, large matted lymph node in the left supraclavicular region measuring 3 × 2 cm [Figure 2C], and the right paratracheal and subcarinal subcentimeter lymph nodes. Pigtail catheter was seen in the left in situ [Figure 2D].
Figure 2: A, Computed tomography (CT) abdomen (axial plane), pericardial effusion (red arrow); B, pericardial effusion (red arrow) with left liver lobe loculated lesion (blue arrow); C, CT thorax (axial plane), supraclavicular lymph node (blue arrow); D, CT abdomen (axial plane), pigtail catheter (blue arrow) and subdiaphragmatic rupture communicating with pericardial cavity (red arrow)

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Laboratory investigation revealed hemoglobin of 12.7 g% (12–15 g%), increased white blood cells of 20,500/mm3 (4,000–10,000/mm3), thrombocytosis of platelets, 6 lakhs/mm3 (1.5–4.1 lakhs/mm3) with neutrophil predominant, 90% (40%–75%) in peripheral smear examination. Erythrocyte Sedimentation Rate (ESR) was 40 mm at the end of 1 hour. The coagulation profile was normal. Biochemical parameters show normal kidney function test and normal liver function except hypoproteinemia 4.5 g/dL (albumin, 2.1 g/dL, and globulin, 2.4 g/dL). Serological examination was negative for human immunodeficiency virus, hepatitis B surface antigen, and hepatitis C virus. Pericardial fluid biochemical examination results show high adenosine deaminase (ADA), 124 U/L, protein, 5.2 g/dL, and sugar, 20 mg/dL. Pericardial fluid cell count was high, 18,000/mm3, and cytology smears revealed mixed inflammatory cells consisting of polymorphonuclear neutrophils and lymphocytes [Figure 3]A against the hemorrhagic background.
Figure 3: Cytology smears of ascitic fluid, supraclavicular lymph node, and liver aspirate. A; Pericardial fluid cytology with neutrophils and lymphocytes, B; supraclavicular fine-needle aspiration cytology (FNAC) cytosmear with granuloma (blue arrow), C; supraclavicular FNAC cytosmear with epithelioid cells (blue arrow), D; FNAC liver aspirate with Z-N staining with positive acid-fast bacilli (red arrow)

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Ultrasound-guided fine-needle aspiration cytology (FNAC) performed from the right supraclavicular lymph node and left liver lobe lesion shows granulomatous inflammation [[Figure 3B] and C] and suppurative inflammation with a positive acid-fast bacillus [[Figure 3D], respectively. The Gene Xpert MTB/RIF (cartridge-based nucleic acid amplification test to identify Mycobacterium tuberculosis and resistance to rifampicin) came positive for Mycobacterium tuberculosis with no resistance to rifampicin in liver abscess sample, whereas E. histolytica antigen came negative. The patient after the initial supportive treatment was finally treated with antitubercular therapy. The treatment response was difficult to assess as the patient did not have symptoms of tuberculosis. However, a chest x-ray after 3 weeks of the initiation of treatment showed a normal study [Figure 4].
Figure 4: Chest X-ray after 3 weeks of the initiation of treatment

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  Discussion Top


Tuberculosis affects almost all organs, systems, and body cavities. Cardiac involvement in tuberculosis includes acute pericarditis, pericardial effusion, and cardiac tamponade. The pathogenesis of pericardial effusion is due to hypersensitivity to tubercular protein.[3] In the present case, possible pathogenesis of the pericardial involvement results from direct extension from progressive primary infection from the liver than the lymphohematogenous route. The common clinical presentation in such cases is chest pain, cough, and dyspnea; however, nonspecific constitutional symptoms such as evening-rise temperature, night sweats, loss of weight, and appetite may also be seen. Patients may present acutely as massive pericardial effusion leading to cardiac tamponade and subacutely with constrictive pericarditis.[4] In our case, a patient presented with acute onset cardiac tamponade, which was aggressively managed in ER symptomatically, and related imaging findings give clues for underlying etiology and which was confirmed by laboratory results. In the review of literature, cardiac tamponade secondary to rupture liver abscess and subdiaphragmatic, communicating with a pericardial cavity, has not been published so far.

Liver tuberculous involvement is usually associated with either an active pulmonary or miliary tuberculosis and rarely localizes as a mass-mimicking tumor. Pathogenesis in such focal hepatic tuberculosis is the portal of entry of tubercle bacilli via the portal vein and hepatic artery in case of miliary tuberculosis. As a result of the antigenic response, granulomas are formed. These granulomas are more commonly seen in periportal areas (zone 1 of Rappaport) but rarely seen in zones 2 and 3. Granulomas are seen in both caseous and noncaseous forms. Many granulomas come together to form a large tuberculoma—tumor-like mass, which further undergoes extensive caseation or liquefaction necrosis to form an abscess. These abscesses are confused with hepatoma, pyogenic liver abscess, and amoebic liver abscess.[5] Tuberculous lymphadenitis is the most frequent form of extrapulmonary tuberculosis and is responsible for up to 43% of peripheral lymphadenopathy in developing countries. Most commonly involved superficial nodes are the anterior or posterior cervical group of lymph nodes, and supraclavicular, submandibular, preauricular, inguinal, and axillary group of lymph nodes also involved. Lymphadenopathy is often bilateral and noncontagious. Clinical presentation is usually nonspecific and presents with accidentally noticed swelling.[6]

Image-guided FNAC has emerged as the first line of investigation in the assessment of radiologically detected lesions. This is a safe, less traumatic, rapid, economical, and easy method compared to open biopsy and easier to repeat, if necessary.[7] The rapid detection of M. tuberculosis and rifampin (RIF) resistance in infected patients using GeneXpert real-time Polymerase Chain Reaction (PCR) is essential for disease management and the emergence of multidrug-resistant tuberculosis and extensively drug-resistant tuberculosis. Culture is the “gold standard” for final determination, but it is slow and may take up to 2–8 weeks, although smear microscopy for acid-fast bacilli (AFB) is rapid and inexpensive. Thus, rapid identification is essential for earlier treatment initiation and improved patient outcomes.[8] ADA is an enzyme marker of cell-mediated immune response activity to M. tuberculosis. The measurement of ADA is not diagnostic but supplementary diagnostic test as negative Ziehl-Neelsen staining and culture of AFB are common in pericardial fluid.

The treatment of DTB is on the same lines as for pulmonary tuberculosis. A 6- to 9-month regimen (2 months of isoniazid, rifampin, pyrazinamide, and ethambutol, followed by 4–7 months of isoniazid and rifampin) is recommended as an initial therapy for all forms of DTB.[9] Adjunctive corticosteroids may be beneficial in patients with tuberculous pericarditis or miliary tuberculosis with refractory hypoxemia, as it might be associated with fewer deaths, less frequent need for pericardiocentesis, or pericardiectomy.[10]


  Conclusion Top


To conclude, though tuberculosis is common, DTB presenting as cardiac tamponade resulting from the left lobe liver abscess leading to subdiaphragmatic rupture and communicating with the pericardial cavity is the rarest encounter. As cardiac tamponade has a fatal outcome, it needs aggressive treatment in the form of pericardiocentesis, and clinicians should also include tuberculous etiology among differential diagnoses to treat underlying etiology and avoid a fatal outcome. Imaging and cytology findings play a crucial role in final diagnosis and prognosis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Ethical consideration

Institutional Ethics Committee, Yashoda Academy of Medical Education and Research (IEC-YAMER), Secunderabad, India has permitted to undertake the proposed study on Disseminated Tuberculosis Presenting as Cardiac Tamponade—Uncommon Presentation in Common Disease at Yashoda Group of Hospital, vide letter no. DC/PP-02/2022 dated March 19, 2022. The study was retrospective; hence informed consent was waived off.



 
  References Top

1.
Khan FY, Dosa K, Fuad A, Ibrahim W, Alaini A, Osman L Disseminated tuberculosis among adult patients admitted to Hamad General Hospital, Qatar: A five-year hospital-based study. Mycobact Dis 2016;6:212.  Back to cited text no. 1
    
2.
Rai DK, Kumar A A rare case of cardiac tamponade due to tuberculosis. Int J Adv Med 2017;4:296-9.  Back to cited text no. 2
    
3.
Agrawal S, Radhakrishnan S, Sinha N Echocardiographic demonstration of resolving intrapericardial mass in tuberculous pericardial effusion. Int J Cardiol 1990;26:240-1.  Back to cited text no. 3
    
4.
Reuter H, Burgess LJ, Doubell AF Epidemiology of pericardial effusions at a large academic hospital in South Africa. Epidemiol Infect 2005;133:393-9.  Back to cited text no. 4
    
5.
Reynolds TB, Campra JL, Peters RL Hepatic granulomata. In: Zakim D, Boyer TD, editors. Hepatology—A Textbook of Liver Diseases. 2nd ed. Philadelphia, PA: WB Saunders; 1990.  Back to cited text no. 5
    
6.
Dandapat MC, Mishra BM, Dash SP, Kar PK Peripheral lymph node tuberculosis: A review of 80 cases. Br J Surg 1990;77: 911-2.  Back to cited text no. 6
    
7.
Swamy MC, Arathi C, Kodandaswamy C Value of ultrasonography-guided fine needle aspiration cytology in the investigative sequence of hepatic lesions with an emphasis on hepatocellular carcinoma. J Cytol 2011;28:178-84.  Back to cited text no. 7
    
8.
Centers for Disease Control and Prevention (CDC). Updated guidelines for the use of nucleic acid amplification tests in the diagnosis of tuberculosis. MMWR Morb Mortal Wkly Rep 2009;58:7-10.  Back to cited text no. 8
    
9.
World Health Organization. Treatment of Tuberculosis: Guidelines. 4th ed. Geneva: WHO; 2009.  Back to cited text no. 9
    
10.
Golden MP, Vikram HR Extrapulmonary tuberculosis: An overview. Am Fam Physician 2005;72:1761-8.  Back to cited text no. 10
    


    Figures

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



 

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