DISCUSSION
Pericardial effusion after acute myocardial infarction could lead to pericardial rupture, which occurs in 0.01–0.5% of acute myocardial infarctions and is a fatal complication.1 Emergency surgery is required to stop the bleeding to save the patient’s life. Other causes of rapid pericardial effusion after acute myocardial infarction include bleeding complications such as aortic dissection and coronary artery hemorrhage.
This case was diagnosed as acute myocardial infarction based on ST changes in ECG leads II, III, and aVF, decreased wall motion of the right ventricle, tendency to bradycardia, and abnormal levels of myocardial enzymes. Coronary angiography also showed occlusion of the right coronary artery. After catheterization, the bradycardia and the chest symptoms were relieved. Echocardiography before and after catheterization showed no pericardial effusion.
In the present case, a patient who had an acute myocardial infarction of the right coronary artery developed cardiac tamponade and went into shock on the second day after catheterization. We considered the possibility of cardiac rupture following acute myocardial infarction based on the clinical course of the patient. However, reports of right ventricular rupture are rare,2 and we considered the possibility of bleeding due to catheter complications such as aortic dissection or bleeding from the coronary artery. However, plain CT did not reveal an aortic dissection. In the preoperative blood test, CRP was high, indicating some kind of infection. However, the blood pressure was notably low, and we judged that the cardiac tamponade needed to be removed first to improve the patient’s hemodynamics. We performed hemostasis through a median incision rather than via puncture, considering the possibility of hemorrhage. The pericardial fluid was white, cloudy, and non-bloody, a finding that suggested pericardial effusion due to infection. Subsequently, MSSA was detected in the pericardial fluid and blood cultures. It is possible that the patient developed purulent pericarditis simultaneously or acute myocardial infarction after the onset of purulent pericarditis. However, there were no symptoms of infection before the acute myocardial infarction and no pericardial fluid before or immediately after the catheterization, and the pericardial fluid suddenly accumulated on the second day of treatment. The detection of MSSA suggested the possibility of bacteremia from the skin related to the catheterization and the spread of infection into the pericardial sac. There is a report of myocardial abscess associated with acute myocardial infarction, followed by purulent pericarditis.3 however, the presence of a myocardial abscess was not evident in the intraoperative findings.
Although purulent pericarditis is rare in the modern antibiotic era, it is a rapidly progressive condition with a poor prognosis, and early diagnosis and response are necessary to prevent mortality. The routes of infection include chest trauma, surgery, intrathoracic, myocardial, and subdiaphragmatic spread, as well as hematogenous spread from distant sites. In this case, the CT scan showed only gallstones and no obvious infection in the adjacent organs. S. aureus , Haemophilus influenzae , Neisseria meningitides , and Streptococcus pneumoniae have been reported as causative organisms of purulent pericarditis.4-8
Although pericardial infection after catheterization for acute myocardial infarction is rare, it should be considered when the inflammatory response is high, and the intraoperative pericardial fluid is white and cloudy instead of bloody, as in this case. In such a case, the shock state may be caused not only by pericardial tamponade but also by sepsis, and an appropriate response is required for the infection.
Postoperatively, the patient was treated for sepsis with antibiotics and endotoxin adsorption, and although a large amount of catecholamine transiently increased the blood pressure, the state of shock was prolonged, and the patient died.
There have been reports of patients who recovered after pericardiocentesis and antibiotic therapy. Thus, in the future, when a patient with purulent pericarditis presents with shock to the extent that circulation cannot be maintained, it may be necessary to consider not only early antibiotic administration and drainage but also thorough removal of the source of infection, such as continuous irrigation with the chest open. This report details our experience in treating purulent pericarditis complicating an acute myocardial infarction. In the case of sudden pericardial effusion after acute myocardial infarction, cardiac rupture or acute aortic dissection should be considered first; however, if the inflammatory response is high, purulent pericarditis should be included in the differential diagnosis. In such cases, hypotension may not only be due to cardiac tamponade but also to septic shock, and if purulent pericarditis is suspected intraoperatively, thorough treatment of the infection, including drainage and antibiotics, may be necessary.