Purulent Pericarditis Due to Pneumococcal Bacteremia Caused by Acupuncture: An Autopsy Case Report
Purulent pericarditis is an infection of the pericardial cavity that produces a purulent fluid, commonly caused by Streptococcus pneumoniae ( ). However, pericarditis caused by S. pneumoniae is commonly an intrapleural infection and is rarely caused by bacteremia ( ). Pneumococcal bacteremia seldom occurs due to skin and soft tissue infection ( ). We herein report an autopsy case of a patient who died as a result of purulent pericarditis caused by pneumococcal bacteremia owing to acupuncture-induced skin and soft tissue infection. 

A 65-year-old man visited the emergency room with a 1-month history of left thigh and knee pain as well as a 5-day history of dyspnea and a fever. The patient had been receiving regular acupuncture treatment at his lower back and thighs for chronic pain every other month; the last acupuncture treatment had been performed one week prior to the onset of the pain of his left thigh. He denied any chest pain, cough, or sputum. Furthermore, the patient had been taking 4 mg/day of oral prednisolone for a few years to treat ureteral stricture due to retroperitoneal fibrosis, with which he had been diagnosed approximately 4 years prior to admission. Additional medical history included hypertension, hyperlipidemia, and chronic back pain, for which he had received amlodipine, telmisartan, pitavastatin, and indomethacin; he had not received the pneumococcal vaccine. On admission, the patient was conscious, his body temperature was 37.8°C, respiratory rate was 24 breaths/minute, SpO 2 was 90% (room air), blood pressure was 101/68 mmHg, pulse rate was 81 bpm, and a fever and hypoxemia were present. On a physical examination, a coarse crackle of the left lung was heard, but the heart sounds were clear without any abnormal heart murmur or pericardial friction. There was a fever in the left thigh and knee joint, with swelling and tenderness also present. The painful site on his left thigh coincided with the site where the patient had received acupuncture before the onset of the pain. Blood sampling data showed an elevated inflammatory response, with a white blood cell count of 22,500 /μL and a C-reactive protein level of 33.84 mg/dL ( ). We performed cardiocentesis and drained 280 mL of fluid. We also performed arthrocentesis of the patient's left knee and placed a drainage tube. Thoracentesis was not performed because it was difficult to perform due to a low pleural fluid volume. The pericardial effusion and joint fluid were both purulent, with a high white blood cell count and low glucose level ( ). On computed tomography (CT), a left thigh abscess contiguous to the left intra-articular knee abscess was observed ( ). In the chest, bilateral pleural effusions and pericardial effusion without pleural thickening were observed ( ). A chest radiograph showed an enlarged heart and bilateral pleural effusion; an electrocardiogram showed PQ elevation at the I, II, and aVR leads and ST elevation at the I, II, aVF, and precordial leads. Transthoracic echocardiographic findings showed no abnormalities in the left ventricular motion or moderate pericardial effusion. There were no findings of verrucous or valve destruction. We diagnosed the patient with purulent pericarditis, pyogenic arthritis of the left knee, and a left femoral muscle abscess. Therefore, we initiated antibiotic therapy with ceftriaxone and vancomycin. On the second day of admission, blood and joint fluid cultures grew S. pneumoniae ; however, culture of the pericardial effusion was negative. The diagnosis of invasive pneumococcal infection with pericarditis and arthritis was made, and sequential typing later revealed that the pneumococcal serotype was 15A (serotyping by Quellung capsule swelling using Statens Serum Institute antisera). On the same day, vancomycin was discontinued based on the results of the culture. On the fifth day of admission, liver enzymes were elevated, and the antibiotic was switched to penicillin G. On the ninth day of hospitalization, chest radiographs showed that cardiomegaly had improved, bilateral pleural effusions had almost disappeared, and no new lung lesions had appeared. In addition, the inflammatory response had improved according to the blood test results. However, no significant improvement was observed in the patient's dyspnea. Regarding the knee joint drainage, the amount of drained fluid gradually decreased, and the tube was removed on the 10th day of hospitalization. Furthermore, due to strong patient dissatisfaction with frequent penicillin G infusions, the antibiotic was changed to cefazolin on the 11th day of hospitalization. Despite the antibiotics and drainage, the fever and dyspnea worsened, and hypoxia appeared on the 13th day of hospitalization. We performed whole-body CT and found that pericardial effusion, pleural effusion, and left knee joint fluid reappeared. We considered local drainage to be inadequate and repeated pericardial effusion and left knee drainage the following day. We also administered diuretics for pleural effusion and hypoxia. As a result, his hypoxia and pleural effusion improved, but the dyspnea did not. On the 17th day, the patient suddenly experienced cardiopulmonary arrest, and despite resuscitation efforts, the patient unfortunately died. On the same day, at the request of the family, an autopsy was performed, which revealed massive purulent deposits in the epicardium and pericardial sac and partial adhesion of the epicardium and pericardial sac ( ). However, there was no valve destruction or verrucous adherence, suggesting a low probability of purulent pericarditis due to direct spillover from infective endocarditis. A microscopic examination showed marked inflammatory cell infiltration and granulation in the epicardium. This condition was considered similar to constrictive pericarditis. Microscopic findings showed lobular central hepatocyte atrophy and impaired reflux in other organs, suggesting that the direct cause of death was decreased cardiac output due to purulent pericarditis. There was no evidence of inflammation or inflammatory scarring in the pleura or lungs, and there was significant pulmonary congestion. The pleural effusion was culture-negative and transudative, suggesting that it was associated with cardiac failure. Autopsy findings were not suggestive of intrathoracic infection. Therefore, the development of pericarditis from the thoracic cavity was ruled out, and a bloodstream infection developing from left knee arthritis was considered as the cause, which is atypical. The clinical course during hospitalization is shown in . 

We encountered a case of purulent pericarditis caused by S. pneumoniae that developed from a left femoral muscle abscess and pyogenic knee arthritis. There are two noteworthy points about this case: the autopsy results revealed that pneumococcal purulent pericarditis had been caused by a bloodstream infection rather than a thoracic cavity infection, and the pneumococcal bacteremia was thought to be caused by a skin and soft tissue infection associated with acupuncture treatment. Purulent pericarditis is an infection in the pericardial space that produces macroscopically or microscopically purulent fluid. There is also the possibility of pericardial stenosis and constrictive pericarditis after improvement. Therefore, surgical treatment, such as pericardiectomy, may be performed if the treatment of purulent pericarditis with pericardial drainage is deemed inadequate. To avoid invasive procedures, intrapericardial thrombolysis may also be performed ( ). However, even with treatment, the mortality rate in patients treated for bacterial endocarditis is 40%, mostly due to cardiac tamponade, toxicity, and constriction ( ). Staphylococcus aureus is the most common cause of purulent pericarditis, although S. pneumoniae is also a common cause ( ). There are several mechanisms by which patients develop purulent pericarditis, including contiguous spread from an intrathoracic site, hematogenous spread, extension from a myocardial site, perforating injury or surgery, and extension from a subdiaphragmatic site ( ). Pneumococcus is commonly associated with contiguous spread from an intrathoracic site, such as the lungs, while S. aureus is often involved in hematogenous spread ( ). The occurrence of pericarditis due to pneumococcal bacteremia is also rare, with a previous report indicating that only 3 out of 844 patients hospitalized for pneumococcal bacteremia developed pneumococcal pericarditis ( ). In the present case, there was no evidence of pleural enhancement suggestive of pleurisy on CT upon admission. In addition, there was no inflammation or inflammatory scarring suggestive of intrathoracic infection at the autopsy, although the possibility of modification due to antibiotic administration prior to the autopsy cannot be ruled out. In contrast, S. pneumoniae was detected in the knee joint fluid and blood. Considering the onset of dyspnea symptoms after the onset of left knee pain in the patient's history, it was likely that bacteremia triggered by the skin and soft tissue infection preceded purulent pericarditis, as described below. Therefore, the cause of purulent pericarditis was more likely to be bloodstream infection with S. pneumoniae than intrathoracic infection. There have been a few cases of S. pneumoniae associated with bacteremia without thoracic infection ( , , ). Pneumococcal purulent pericarditis, as in this case, can occur due to hematogenous infection even in the absence of pneumonia or pleurisy. Therefore, it is important to recognize that pneumococcal purulent pericarditis can occur even in patients with invasive pneumococcal infections without pulmonary involvement. Invasive pneumococcal infection, defined as an infection confirmed by the isolation of S. pneumoniae from a normally sterile site, is a highly lethal disease ( ). In our patient, S. pneumoniae was detected in the pericardial fluid, joint fluid, and bloodstream. The main focal diagnosis of pneumococcal bacteremia in adults is usually due to respiratory tract infections ( ), but there are occasional cases that are not associated with this focal infection ( ). Furthermore, pneumococcal arthritis in adults is often caused by bacteremia, but the primary focus is not identified in many cases. There is a hypothesis that pyogenic arthritis in such cases arises from joint seeding during transient bacteremia with a mucous membrane source ( ). Therefore, it is difficult to completely exclude the possibility that transient bacteremia was the cause of the knee arthritis, thigh muscle abscess, and purulent pericarditis in the present case. However, there are three reasons to believe that the bacteremia in our patient was likely caused by pneumococcal infection of the skin and soft tissues with skin entry. The first rationale is that cutaneous and soft tissue pneumococcal infections with skin entry are not common but are often reported ( ). Risks have been reported with underlying disease, the use of immunosuppressive drugs and local trauma, such as surgical wounds and burns ( ). Both risks were present in our patient: oral corticosteroid use and local trauma caused by acupuncture. The second rationale is the medical history of left thigh pain, which appeared after the acupuncture treatment; it was the initial symptom, followed by dyspnea. This may support a course of evolution from a femoral muscle abscess to pyogenic arthritis and then to pericarditis via bloodstream infection. The third rationale is the physical and imaging findings of a femoral muscle abscess in the same area where acupuncture had been performed several weeks prior and the fact that pyogenic knee arthritis was contiguous with the abscess. These findings support the hypothesis that acupuncture-induced thigh abscesses occurred first, followed by the development of pyogenic arthritis. Acupuncture has been used as an integrative or complementary therapy for pain ( ). However, it can carry the risk of skin and soft tissue infections; acupuncture site infections are mainly caused by inadequate skin disinfection, the use of contaminated needles, and poor adherence to hand hygiene by medical personnel ( ). S. aureus , Mycobacteriaceae , and Enterobacteriaceae pathogens are commonly reported as the causative agents of acupuncture site infections ( , ). S. pneumoniae rarely causes acupuncture site infections, and only one case has been reported in the literature ( ). It is necessary to recognize that S. pneumoniae may be the organism responsible for skin and soft tissue infections caused by trauma, such as acupuncture, in immunosuppressed patients. Conclusion Pneumococcal purulent pericarditis occasionally results from a bloodstream infection instead of a thoracic infection. If pneumococcal pericarditis is found, it may be necessary to confirm bacteremia in addition to confirming thoracic infection. Furthermore, pneumococcal skin and soft tissue infections can occur due to trauma, such as acupuncture, in immunosuppressed patients and can cause pneumococcal bacteremia. For this reason, a case of pneumococcal bacteremia may require confirmation of a skin and soft tissue infection. 

Pneumococcal purulent pericarditis occasionally results from a bloodstream infection instead of a thoracic infection. If pneumococcal pericarditis is found, it may be necessary to confirm bacteremia in addition to confirming thoracic infection. Furthermore, pneumococcal skin and soft tissue infections can occur due to trauma, such as acupuncture, in immunosuppressed patients and can cause pneumococcal bacteremia. For this reason, a case of pneumococcal bacteremia may require confirmation of a skin and soft tissue infection. 

