0
Selected Reports |

Purulent Pericarditis With Tamponade in a Postpartum Patient Due to Group F Streptococcus* FREE TO VIEW

Richard W. Snyder, MD, FCCP; Todd I. Braun, MD
Author and Funding Information

*From Abington Memorial Hospital, Abington, PA.



Chest. 1999;115(6):1746-1748. doi:10.1378/chest.115.6.1746
Text Size: A A A
Published online

Bacterial pericarditis with cardiac tamponade is a life-threatening disorder that has been associated with a variety of organisms. There is usually an associated underlying condition or a seeding of the pericardium from an infection elsewhere. We report the development of cardiac tamponade and a subsequent pericardial constriction due to group F streptococcus purulent pericarditis. We believe this to be the first report of a postpartum patient with purulent pericarditis.

Purulent pericarditis is an infrequent but fulminant and frequently lethal disease. Its clinical recognition is difficult due to insidiously subtle and varied presentations.1Unfortunately, the diagnosis is most often made at autopsy, and mortality remains high in diagnosed cases despite aggressive drainage and prolonged antibiotic therapy. Therapeutic advances have been associated with a changing spectrum of pathogens over the past 50 years.2 We report an uncommon pathogen that caused purulent pericarditis in a postpartum patient presenting with cardiac tamponade and subsequently developing pericardial abscess and constriction.

A 20-year-old woman was evaluated with pleuritic pain and fever 1 week after the uncomplicated vaginal delivery of her first child. She had noted fever with a nonproductive cough, and headache, nasal congestion, sore throat, and chest discomfort 1 to 2 weeks prior to delivery. At the time of delivery, she was afebrile and without evidence of acute illness; after discharge, she noted increasing dyspnea and pleuritic right chest discomfort. An emergency department evaluation 1 week after delivery revealed tachypnea, hypoxia, a heart rate of 134 beats/min, hypertension, and no fever. Pulsus paradoxus was not assessed. A physical examination further revealed nondistended cervical veins, a regular heart beat without rub, dullness with diminished breath sounds at both lung bases, and diffuse abdominal tenderness with no organomegaly. The laboratory evaluation included a chest radiograph remarkable for bilateral pleural effusions and a WBC count of 25 × 103/μL. Piperacillin and gentamicin therapy was instituted, but the patient continued to decline rapidly with hypotension and an increase in heart rate to 150 beats/min. Within hours of presentation, intubation and assisted ventilation were required. The patient suffered a cardiopulmonary arrest, and 150 mL of purulent material was recovered by pericardiocentesis during resuscitative measures. Pericardial fluid analysis revealed Gram-positive cocci on smear and group Fβ -hemolytic streptococci on culture. Echocardiography revealed a pericardial effusion with a collapse of the right atrium and right ventricle consistent with cardiac tamponade. Following pericardiocentesis, the patient’s BP and heart rate briefly improved, but within 1 h, the patient’s condition worsened again. Echocardiography was again performed to aid in the guided aspiration of an additional 60 mL of purulent pericardial fluid that again revealed Gram-positive cocci on smear and group F β-hemolytic streptococci on culture. A right heart catheter was placed; the pulmonary artery pressure was 38/22 mm Hg, and the central venous pressure was 19 mm Hg. A subxiphoid pericardial resection was performed, and subsequent echocardiography revealed pericardial thickening without tamponade. The heart rate improved to 120 beats/min, and a fever of 38.8°C developed. Blood cultures and paracentesis fluid cultures revealed no growth. The patient’s hospitalization was further complicated by multisystem organ failure that required prolonged assisted ventilation and dialysis. Echocardiography continued to reveal a thickening pericardium without fluid over the next 4 weeks. A repeat right heart catheterization was prompted by recurrent hypotension with tachycardia improving after intravascular infusion of fluids; right atrial pressure was 15 mm Hg with prominent x and y descents, and pulmonary artery wedge pressure was 15 mm Hg, suggesting pericardial constriction. CT and MRI scans of the thorax revealed pericardial thickening and a density adjacent to the heart. Five weeks after hospitalization, a median sternotomy and an anterior hemipericardectomy with epicardial stripping were performed. An abscess cavity adjacent to the right atrial appendage was resected and debrided. Epicardial thickening up to 1 cm in width was noted. Postoperative pulmonary artery diastolic pressure and central venous pressure were lower than their preoperative measurements of 22 mm Hg, respectively: 16 vs 10 mm Hg. Following lengthy supportive care and rehabilitation, the patient was discharged to home.

The spectrum of purulent pericarditis has changed over the last 50 years.1,,2 Prior to the current antibiotic era, Streptococcus pneumoniae was the most frequently identified organism, with Gram-negative bacilli becoming relatively more common during the past 50 years. Clinically, purulent pericarditis is an acute illness with a usual duration prior to hospitalization of just a few days (range, 1 to 6 days). The disease is characterized by high spiking fevers, rigors, and cardiorespiratory complaints such as dyspnea, cough, and (to a lesser degree) chest pain. Tachycardia is the most common physical finding, with a friction rub noted in less than half of cases. Purulent pericarditis usually occurs in a clinical setting of another illness, such as surgical wound infection, intrathoracic infection, or bacteremia.

Streptococci are broadly classified using three schemes that overlap and are therefore potentially confusing. The Streptococcus milleri group is made up of three species: Streptococcus intermedius, Streptococcus anginosus, and Streptococcus constellatus. Lancefield groups are characterized according to serologically active carbohydrates, and the hemolytic reaction on sheep blood agar is further used to characterize these strains. We suspect that the isolate described in our case report belongs to the S constellatus group, in view of the group F antigen and theβ -hemolytic reaction noted.

Group F streptococci of the S milleri group are normal resident flora of the oropharynx, GI tract, and perineum.3 They have rarely been associated with life-threatening infection and are uncommonly associated with gynecologic infection. Purulent pericarditis due to S milleri, allowing for the difficulty in classification, has only rarely been reported,4,,5,,6,,7 and no group F β-hemolytic streptococci were noted.

The possibility of purulent pericarditis complicating preceding nonsuppurative pericardial disease was first suggested by Solomon et al,8 who cultured streptococci from the pericardium during a postmortem examination of four patients with uremic pericarditis. Two of 26 patients reported at the Massachusetts General Hospital between 1960 and 1974 appeared to have preexisting nonsuppurative pericarditis prior to the onset of purulent pericarditis.1 The superinfection of viral pericarditis has been speculated on elsewhere as well.9

We speculate that our patient’s infection derived from transient bacteremia occurring at the time of her uncomplicated vaginal delivery with subsequent seeding of the pericardium. Puerperal bacteremia has been reported in 16 of 327 women with an interval between delivery and venipuncture ranging from 1 to 45 min, with streptococci most commonly recovered.10 Additionally, our patient may have had viral pericarditis weeks before delivery. Following the development of purulent pericarditis, she developed a constrictive pericardial disorder that required surgical intervention.

This case is unique in that the patient was early in the postpartum period when she developed purulent pericarditis with an organism known to be present in the perineum. This case is also interesting because the group F streptococcus, as well as the entire S milleri group, have only rarely been the causative agent of pericarditis. Vigilance regarding the development of this condition is needed in view of the significant morbidity and potential for death. In a series from Johns Hopkins,2 35% of patients with purulent pericarditis died. Furthermore, of 55 patients with purulent pericarditis at autopsy, only 10 patients had purulent pericarditis diagnosed antemortem.

Last, we would like to emphasize the potential for the development of a pericardial abscess or a constrictive disorder following purulent pericarditis that would necessitate surgical intervention.

Correspondence to: Richard W. Snyder, MD, FCCP, Abington Memorial Hospital, Suite 121, 1235 Old York Road, Abington, PA 19001

Rubin, RH, Moellering, RC (1975) Clinical, microbiologic, and therapeutic aspects of purulent pericarditis.Am J Med59,68-78. [PubMed] [CrossRef]
 
Klacsmann, PG, Bulkley, BH, Hutchins, GM The changed spectrum of purulent pericarditis.Am J Med1977;63,666-673. [PubMed]
 
Libertin, CR, Hermans, PE, Washington, JA Beta-hemolytic group F streptococcal bacteremia: a study and review of the literature.Rev Infect Dis1985;7,498-503. [PubMed]
 
Akashi, K, Ishimaru, T, Tsuda, Y, et al Purulent pericarditis caused byStreptococcus milleri.Arch Intern Med1988;148,2446-2447. [PubMed]
 
Reder, RF, Raucher, H, Cesa, M, et al Purulent pericarditis caused byStreptococcus anginosus-constellatus.Mt Sinai J Med1984;51,295-297. [PubMed]
 
Hauser, AM, et al Myocardial infarction and purulent pericarditis.Cardiovasc Rev Reports1983;4,971-974
 
Gopalakrishna, KU, Kwon, KH, Shah, A Metastatic myocardial abscess due to group F streptococci.Am J Med Sci1977;274,329-332. [PubMed]
 
Solomon, C, Robert, JE, Lisa, JR The heart in uremia. Am J Pathol. 1942;;18 ,.:729. [PubMed]
 
Case records of the Massachusetts General Hospital: weekly clinicopathological exercises; case 49–100; a 47-year-old Cape Verdean man with pericardial disease. N Engl J Med 1990; 323:1614–1624.
 
Everett, ED, Hirschmann, JV Transient bacteremia and endocarditis prophylacxis: a review.Medicine1977;56,61-75. [PubMed]
 

Figures

Tables

References

Rubin, RH, Moellering, RC (1975) Clinical, microbiologic, and therapeutic aspects of purulent pericarditis.Am J Med59,68-78. [PubMed] [CrossRef]
 
Klacsmann, PG, Bulkley, BH, Hutchins, GM The changed spectrum of purulent pericarditis.Am J Med1977;63,666-673. [PubMed]
 
Libertin, CR, Hermans, PE, Washington, JA Beta-hemolytic group F streptococcal bacteremia: a study and review of the literature.Rev Infect Dis1985;7,498-503. [PubMed]
 
Akashi, K, Ishimaru, T, Tsuda, Y, et al Purulent pericarditis caused byStreptococcus milleri.Arch Intern Med1988;148,2446-2447. [PubMed]
 
Reder, RF, Raucher, H, Cesa, M, et al Purulent pericarditis caused byStreptococcus anginosus-constellatus.Mt Sinai J Med1984;51,295-297. [PubMed]
 
Hauser, AM, et al Myocardial infarction and purulent pericarditis.Cardiovasc Rev Reports1983;4,971-974
 
Gopalakrishna, KU, Kwon, KH, Shah, A Metastatic myocardial abscess due to group F streptococci.Am J Med Sci1977;274,329-332. [PubMed]
 
Solomon, C, Robert, JE, Lisa, JR The heart in uremia. Am J Pathol. 1942;;18 ,.:729. [PubMed]
 
Case records of the Massachusetts General Hospital: weekly clinicopathological exercises; case 49–100; a 47-year-old Cape Verdean man with pericardial disease. N Engl J Med 1990; 323:1614–1624.
 
Everett, ED, Hirschmann, JV Transient bacteremia and endocarditis prophylacxis: a review.Medicine1977;56,61-75. [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Find Similar Articles
CHEST Journal Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543