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.