You see a patient with pleuritic chest pain. The EKG shows ST segment elevation in the inferior leads as well as V2-V5. The closest cardiac catheterization laboratory is 120 miles away, and you normally give thrombolytics for STEMI. But is this STEMI or pericarditis? Can the history and physical examination help?
It has been estimated that as many as 5% of emergency department patients with noninfarction chest pain have pericarditis. (NEJM 2004)
Recognizing pericarditis is important because administration of thrombolytics may lead to hemorrhagic complications and even death.
The diagnosis of pericarditis rests on the right clinical story along with a confirmatory finding on physical examination, EKG, or echocardiogram. Describing the sensitivity and specificity of these findings is difficult because there is often no independent gold standard for diagnosis and there are no known large studies on the clinical findings in pericarditis in the emergency department.
Classic symptoms include pain localized at the area of the heart. The pain is classically pleuritic and worse with inspiration. It is relieved with leaning forward. The pain can radiate to any cardiac referral area, but pain referred to the trapezius ridge might be more specific, caused by irritation of the phrenic nerve(NEJM 2004).
The incidence of a friction rub appears to be somewhat low, perhaps 18-34%(Cohen). It is easier to hear at the left lower sternal border with the patient leaning forward at end expiration. In the emergency department, however, an additional maneuver for improving audibility is lowering ambient noise. The rub is often transient and serial examination improves the sensitivity. (NEJM 2004, Spodick JAMA 2003). Because of the poor sensitivity and specificity of clinical diagnosis, adjunctive testing is generally needed for diagnosis.
Electrocardiographic findings depend on the stage of illness. Classically the disease starts with diffuse ST-segment elevation, which then resolves, followed by diffuse T-wave inversions, which then resolves. Diffuse PR segment depression may in fact be earlier and more sensitive than ST elevation.
Laboratory support for the diagnosis is said to include elevation in C-reactive protein and erythrocyte sedimentation rate. However, the sensitivity and specificity for these laboratory markers for pericarditis in emergency department patients with chest pain is not known. Troponin elevations occur in 35 to 50% , so this can not always help differentiate myocardial infarction from pericarditis.(NEJM)
Finally, an echocardiogram can be used when there is doubt about the differential diagnosis of myocardial infarction and pericarditis. Regional wall motion abnormalities would support myocardial infarction whereas pericardial effusion, present in 58% of cases, would support pericarditis (Cohen 2008)
The patient’s pain is pleuritic but there are no additional specific signs of pericarditis. You call the cardiologist and ask for an echocardiogram to ensure no regional wall motion abnormalities. The cardiologist comes and though there is no effusion, there is also no regional wall movement abnormalities, so you both decide not to give thrombolytics. Because of diagnostic uncertainty however, you transfer the patient for cardiac catheterization, and the arteries turn out to be clean. The patient’s discharge diagnosis is pericarditis. The clinical diagnosis of pericarditis and the decision to withhold thrombolytics was felt to be courageous but well-justified, and ultimately protected the patient from exposure to hemorrhagic risks.
Summary: Confirmatory findings include
Exam – Pericardial friction rub
EKG – Classic diffuse ST elevation
Echo – Pericardial effusion