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Year : 2017  |  Volume : 19  |  Issue : 2  |  Page : 129-132

Pyopericardium − A fatal presentation: A case report

Department of Emergency Medicine and Trauma, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, India

Date of Web Publication15-Nov-2017

Correspondence Address:
K.N.J. Prakash Raju
Department of Emergency Medicine and Trauma, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry 605006
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jomt.jomt_4_17

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Pyopericardium is an uncommon presentation of tuberculosis (TB) and has been reported in 6.98% of the cases of pyopericardium. Pyopericardium has been documented in <3% of the cases of large TB pericardial effusions, even in the high-prevalence areas of TB and human immunodeficiency virus infection. Pulmonary TB affects the pericardium in 1–2% of the cases, and pericardial TB is responsible for 7% of the cases of cardiac tamponade. Pericardial TB is usually an insidious illness and may present as acute pericarditis, chronic pericardial effusion, cardiac tamponade, or pericardial constriction; however, purulent pericarditis is rare. To the best of our knowledge, there are no previous case reports from India on acute pyopericardium with tamponade. Purulent pericarditis or pyopericardium is a rare entity and is associated with very high mortality. A 50-year-old woman was brought to the Emergency Department with respiratory distress and shock. Screening echocardiography suggested pericardial effusion with cardiac tamponade. The pericardial aspirate was frankly purulent, but she sustained a cardiac arrest, and resuscitative attempts were futile. The case is highlighted because of its rarity and fatal outcome, especially with late diagnosis and management. The following core competencies are addressed in this article: medical knowledge and patient care.

Keywords: Cardiac tamponade, purulent pericarditis, pyopericardium

How to cite this article:
Raju KP, Juvva G, Prakash R, Pandit VR, Anandhi D. Pyopericardium − A fatal presentation: A case report. J Med Trop 2017;19:129-32

How to cite this URL:
Raju KP, Juvva G, Prakash R, Pandit VR, Anandhi D. Pyopericardium − A fatal presentation: A case report. J Med Trop [serial online] 2017 [cited 2023 Jun 6];19:129-32. Available from:

  Introduction Top

Purulent pericarditis is the most serious manifestation of bacterial pericarditis, characterized by gross pus in the pericardium or microscopically purulent effusion.[1] In this modern antibiotic era, bacterial pericarditis has become very rare with an incidence of 1/18,000.[2] It is a rapidly progressive and highly fatal infection, with mortality rate reaching 100% if left untreated;[3] it is often diagnosed postmortem in half of the cases.[2],[4] It is commonly seen as a complication of pneumonia among children and young adults[3] and is also reported in immunocompromised individuals.[4] Herewith, we report a case of acute fulminant purulent pericarditis without an obvious focus of primary infection.

  Case report Top

A 50-year-old woman without any previous comorbidities presented to the Emergency Department (ED) with complaints of epigastric pain and nonbilious, nonprojectile vomiting. Her clinical examination revealed the following: pulse rate was 90/min, blood pressure was 100/60 mmHg, Jugular venous pressure (JVP) was not elevated, and cardiovascular system (CVS) was S1S2 heard, with no murmurs; her abdominal examination was normal. Her complete blood count showed total leukocyte counts (TLCs) of 12,000 cells/cumm, 70% neutrophils, and 20% lymphocytes; her urea level was 30 mg/dL and creatinine level was 1.1 mg/dL. Her electrocardiogram was normal; abdominal ultrasonography and chest X-ray [Figure 1A] were essentially normal. After observing for a few hours, surgical consultation was obtained. She was prescribed proton-pump inhibitors and discharged home. A week later, she was brought to the ED in a hemodynamically unstable condition with complaints of worsening of breathlessness over 4–5 days. She was also complaining of intermittent high-grade fever associated with retrosternal chest pain.

On arrival, she was conscious, but restless and tachypneic with a respiratory rate of 40/min. She had cold and clammy peripheries with feeble peripheral pulses at a rate of 120/min. Her room air oxygen saturation was 80%, and systolic blood pressure was 70 mmHg. In view of respiratory distress and shock, she was triaged as Emergency Severity Index level 1 and moved to the resuscitation zone. Along with resuscitative measures, her clinical examination revealed distended neck veins and muffled heart sounds. Electrocardiogram showed sinus tachycardia with low-voltage QRS complex duration in electrocardiogram (QRS) complexes. Chest X-ray disclosed a marked enlargement of the cardiac silhouette [Figure 1]. Bedside 2D echocardiography performed in the ED suggested large pericardial effusion with swirling echogenic material and septae as well as diastolic collapse of the right ventricle [Figure 2]. With a diagnosis of acute cardiac tamponade, emergent pericardiocentesis was performed, and about 20 ml of foul-smelling, frank pus was aspirated from the pericardial space by the subxiphoid approach. Meanwhile, the patient suddenly collapsed and went into pulseless electrical activity. After 5 min of cardiopulmonary resuscitation, return of spontaneous circulation was achieved. Immediately, 60 ml of frank pus was aspirated from the pericardial cavity; however, the patient went into cardiac arrest again, and further resuscitation efforts became futile.
Figure 1: (A) Chest X-ray during the first visit is essentially normal. (B) Chest X-ray during the second visit showing gross cardiomegaly

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Figure 2: (A) Subxiphoid view of 2D echocardiography suggestive of a large pericardial effusion filled with echogenic material and septae. (B) Frank pus, which was aspirated from the pericardial cavity

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Her laboratory reports showed TLCs of 12,100 cells/cumm, 80% neutrophils, 20% lymphocytes, Erythrocyte sedimentation rate (ESR) of 32 mm/h, hemoglobin level of 11 g/dL, blood sugar level of 120 mg/dL, urea level of 20 mg/dL, and creatinine level of 1.7 mg/dL. Her liver function tests were within normal limits.

Ziehl–Neelsen and auramine–rhodamine staining of the pus sample showed plenty of acid-fast bacilli. Pus samples were inoculated into sheep blood agar, MacConkey agar (for aerobic and anaerobic culture), Lowenstein–Jensen (LJ) medium, and Sabouraud dextrose agar. There was no growth on the routine bacteriological media after 48 h of both aerobic and anaerobic incubations.

  Discussion Top

Purulent pericarditis or pyopericardium is diagnosed when pus is drained from the pericardial space or when bacteria are cultured from the pericardial fluid.[5] It is an acute, fulminant illness with fever in virtually all patients. Chest pain is uncommon. Typically, patients with acute pericarditis present with nonspecific systemic inflammatory response syndrome, and often the classic manifestations of pericarditis such as chest pain, pulsus paradoxus, and pericardial friction rub as well as electrocardiographic changes may be absent.[2],[6]

Direct extension from pneumonia or empyema accounts for the majority of the cases, but hematogenous spread during bacteremia, thoracic surgery, and trauma can also cause pyopericardium.[7] Complications of amoebic liver abscess involve rupture of the abscess causing spread into the peritoneum, pleural space, or pericardium. Rupture into the pleuropulmonary system occurs in up to 40% of the patients with amoebic liver abscess, whereas peritoneal rupture occurs in only 7% of the patients.[8] In our case, the patient did not have any obvious focus of infection, and chest X-ray on her previous visit a week ago was normal. Nor did she have any underlying chronic illness or diabetes mellitus. Classical signs were absent during the initial course of illness. Pyopericardium cases due to different etiological agents have been reported worldwide and are commonly caused by Staphylococcus, Pneumococcus, Streptococcus, Haemophilus, and Mycobacterium tuberculosis. Tuberculous infection may present as acute pericarditis, cardiac tamponade, silent relapsing pericardial effusion, effusive-constrictive pericarditis, and acute, subacute, or chronic constriction.

In case of pericardial effusion, tuberculosis as the etiological cause can be established through demonstration of Acid fast bacillus (AFB) in smear or culture of pericardial fluid or pericardial biopsy specimen and a histological examination of pericardial biopsy specimen revealing caseating granulomatous inflammation. The diagnostic yield of AFB from smear and culture of pericardial fluid was variable and was 53% with conventional culture method using LJ medium and increased up to 75% with prompt bedside culture in double strength liquid medium of Kirchner.[9] Myocardial biopsy could be useful in making the diagnosis.[10]

Ultrasound-guided pericardiocentesis has been established as the gold standard, because it results in lower complication rates and allows the physician to choose the safest approach. Medical treatment of pyopericardium involves mainly antibiotic therapy and antitubercular therapy in case of tubercular pericardial effusion. In addition to a standard antituberculosis regimen, the treatment of tuberculous pericarditis may include adjuvant therapy with corticosteroids, pericardiocentesis, and/or pericardiectomy.[11] Purulent pericarditis or pyopericardium is an emergency, which, if untreated, progresses to constrictive pericarditis or cardiac tamponade, and the prognosis is usually fatal.[11]

This rare disease is often diagnosed late when severe hemodynamic compromise develops due to pericardial tamponade. Death is mostly due to cardiac tamponade, systemic toxicity, cardiac decompensation, and constriction.

  Conclusion Top

Timely judgment and diagnosis by the clinician along with accurate microbiological diagnosis will definitely determine the prognosis in pyopericardium. The case is reported for its rarity and fatal clinical outcome if diagnosis is delayed. All emergency physicians should be trained in pericardiocentesis procedure. Ultrasound-guided pericardiocentesis is preferred to reduce the complications related to procedure.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Gowrinath K, Phani Krishna B, Raghavendra C, Sai Ravi Shankar A. Unusual cause of pyopericardium with tamponade. J Clin Sci Res 2015;4:61-4.  Back to cited text no. 1
Sagrista-Sauleda J. Purulent pericarditis: Review of a 20-year experience in a general hospital. J Am Coll Cardiol 1993;22:1661-5.  Back to cited text no. 2
McClure RS, Burgess JJ, Bayes AJ, Cohen JJ. Primary purulent pericarditis due to group C Streptococcus. Can J Cardiol 2004;20:1479-80.  Back to cited text no. 3
Klacsmann PG. The changed spectrum of purulent pericarditis: An 86 year autopsy experience in 200 patients. Am J Med 1977;63:666-73.  Back to cited text no. 4
Hall IP. Purulent pericarditis. Postgrad Med J 1989;65:444-8.  Back to cited text no. 5
Rubin R, Moellering RJ. Clinical, microbiologic and therapeutic aspects of purulent pericarditis. Am J Med 1975;59:68-78.  Back to cited text no. 6
Thebaud B, Sidi D, Kachaner J. Purulent pericarditis in children: A 15-year-experience. Arch Pediatr 1996;3:1084-90. [in French].  Back to cited text no. 7
Wuerz T, Kane JB, Boggild AK, Krajden S, Keystone JS, Fuksa M et al. A review of amoebic liver abscess for clinicians in a nonendemic setting. Can J Gastroenterol 2012;26:729-33.  Back to cited text no. 8
Lee JH, Lee CW, Lee SG, Yang HS, Hong MK, Kim JJ et al. Comparison of polymerase chain reaction with adenosine deaminase activity in pericardial fluid for the diagnosis of tuberculous pericarditis. Am J Med 2002;113:519-21.  Back to cited text no. 9
Danbauchi SS, Odigie VI, Rafindadi AH, Kalayi GD, Mohammed I. Tuberculous myocarditis: A case report. Niger Postgrad Med J 2001;8:199-202.  Back to cited text no. 10
Ahluwalia G, Ahluwalia A, Sikolsky L, Sayal A. Prompt diagnosis and therapy are keys to reducing mortality − Extrapulmonary tuberculosis. J Respir Dis 2007;28:278-82.  Back to cited text no. 11


  [Figure 1], [Figure 2]


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