A 44-year-old otherwise healthy man presents to an emergency department in Baltimore, noting that for the past 24 hours he has had a sharp pain in his chest that worsens when he breathes deeply. He says he is also short of breath even when he is at rest, feels feverish, and is having chills.

The patient has no past medical conditions to explain these symptoms. Initial assessment reveals sinus tachycardia with rates of 140 to 150 seconds and a blood pressure of 143/73 mm Hg. Physical examination identifies a large pericardial friction rub.

Clinicians perform a preliminary electrocardiogram (ECG) that reveals sinus tachycardia, frequent premature ventricular contractions of outflow tract morphology, and mild diffuse ST elevations with PR segment depression.

Results of laboratory tests are notable for leukocytosis of 12,000 cells/mm3 and elevated C-reactive protein of 206.0 mg/L. Clinicians order a chest x-ray that shows mild cardiomegaly, but there is no sign of pulmonary edema.

Subsequently, an echocardiogram demonstrates a small pericardial effusion, thus fulfilling the diagnostic criteria for acute pericarditis.

The patient is started on treatment with colchicine and ibuprofen. However, his symptoms do not improve and he undergoes several transthoracic echocardiograms (TTE) over the next 4 days. Imaging reveals an enlarging circumferential pericardial effusion and with depressed ejection fraction of 40%-45%, without evidence of tamponade.

Echocardiogram showing large pericardial effusion, without evidence of tamponade physiology.

Day 5

Pericardiocentesis is performed resulting in drainage of 450 cc of straw-colored fluid. Analysis shows 100,000 white blood cells with neutrophilic predominance. Placement of a pericardial drain removes an additional 450 mL of fluid over the following 48 hours, and clinicians then remove the drain.

Fluid culture findings included polymicrobial growth of Micromonas micro, Prevotella intermedia, and Fusobacterium species, all anaerobic flora of the oral cavity, and treatment is started with ceftriaxone.

Day 8

Within 48 hours of the removal of the pericardial drain, a repeat TTE shows that pericardial fluid has re-accumulated, and there is partial diastolic collapse of right atrial and right ventricular, indicating echocardiographic tamponade.

The patient's systolic blood pressure is noted to have fallen by 30 mm Hg. Urgent pericardiocentesis is performed, removing 550 mL of purulent thick fluid that, again, has a high white blood cell count, consistent with purulent pericarditis.

Day 9

A repeat TTE the following day shows no further re-accumulation of fluid. However, a few hours later, a transesophageal echocardiogram (TEE) and subsequent computed tomography (CT) scan of the chest shows that pericardial fluid is indeed again re-accumulating.

On the mediastinal-view scan, clinicians also note evidence of gas in the pericardium with an enhancing rim suggestive of infection, along with evidence of new nodules in the lungs that raise concern for septic emboli. A repeat echocardiogram shows large, echo-dense circumferential pericardial effusion, as well as "septal bounce" suggestive of constrictive physiology.

Clinicians decide that the patient requires a pericardial window, and perform another TEE prior to the surgery, with the results consistent with tamponade physiology.

The pericardial window procedure is completed, and 750 cc of pus is removed under pressure. The esophagram is negative, confirming there is no path from the upper gastrointestinal tract to the pericardial area.

Day 10 Follow-up

Blood cultures drawn on days 1, 8, and 10 indicate that the patient was never bacteremic. Likewise, an extensive infectious work-up was negative, consistent with primary pericarditis. The patient is discharged with 4 weeks of intravenous ceftriaxone from the time of the pericardial window, and he subsequently has a full clinical recovery.

Discussion

Clinicians reporting this case of primary bacterial purulent pericarditis with cardiac tamponade in a healthy immunocompetent adult male note that this is a rare phenomenon, virtually unheard of in immunocompetent patients without underlying infection.

Because acute bacterial purulent pericarditis can progress rapidly into cardiac tamponade, early diagnosis and treatment are critical to reduce mortality and improve clinical outcomes. Of patients who do receive treatment, about 40% develop fatal cardiac tamponade, constrictive pericarditis, and septic shock.

The case authors note that most cases of acute pericarditis are of an unknown etiology, which may or may not be infectious in nature. However, bacteria -- usually gram-positive cocci -- have been reported as the cause of spontaneous pericarditis leading to clinical and echocardiographic tamponade. For instance, while a bacterial cause was identified in up to a third of purulent pericarditis cases in a 1977 study, the rate of gram-positive bacteria as the cause of bacterial pericarditis has fallen slowly with increasing use of antibiotics.

Similarly, a 20-year retrospective review published in 1993 by researchers in Spain reported a bacterial cause of pericarditis in about 5.5% of cases, 42% of which were diagnosed postmortem.

The anaerobic bacteria implicated in cases of purulent pericarditis were most commonly Peptostreptococcus, Clostridium, Fusiform, Bifidobacterium, and Actinomyces spp.

Risk factors for purulent pericarditis have notably been alcohol abuse, immunosuppression, and chest trauma. However, the case authors note that none of these applied to this patient, whose pericarditis was due to normal flora from the oropharynx.

Most commonly, patients develop a secondary bacterial pericarditis as either an extension of infection from within the thorax, through hematologic spread if the patient is bacteremic, direct inoculation via trauma, or spread from site of infection within the heart.

Complications

As in this case, patients with purulent pericarditis may develop complications such as cardiac tamponade and constrictive pericarditis; additional complications include aortic mycotic aneurysms and left ventricular pseudoaneurysms.

Purulent pericarditis generally presents with non-specific symptoms such as fever and chills. Clinicians reporting this case note that although this patient had pleuritic chest pain, pericardial friction rub, and diffuse ST segment elevation, these symptoms may be seen more commonly in pericarditis with a viral rather than a bacterial cause.

Suspected cases of bacterial pericarditis should immediately receive an echocardiogram to evaluate for cardiac tamponade. Echocardiographic signs of tamponade, such as diastolic collapse of the right ventricle, can precede clinical symptoms of tamponade, the case authors note. They advise urgent pericardiocentesis to relieve pressure and analysis of the pericardial aspirate for cytology examination, as well as bacterial and fungal cultures. Despite initial pericardiocentesis, 40% of patients ultimately require a surgical pericardial window.

Although there have been reports of cases of bacterial pericarditis that involved Fusiform species, there have been only two documented cases of Prevotella, both in patients receiving cancer chemotherapy.

Early antibiotic treatment is necessary to prevent recurrence of bacterial pericardial effusion, the authors note, adding that oral anaerobic bacteria are generally sensitive to beta-lactam antibiotics. This patient was successfully treated with 4 weeks of intravenous ceftriaxone.

Conclusions

The authors conclude that when patients present with non-specific symptoms and pleuritic chest pain, clinicians should have a high level of suspicion for purulent pericarditis due to its high level of mortality.

Last Updated March 09, 2020

Disclosures

The case report authors noted no conflicts of interest.

View post:
Pleuritic Chest Pain, Other Vague Symptoms -- What Could It Be? - MedPage Today