Case for diagnosis

A 35-year-old woman presented to the emergency room with a very severe acute chest pain. The pain had started with a “sudden onset” a few hours ago, it was sharp and gnawing in character and reflecting to her back, neck and mandibula, it was worsening with deep breath and any motion. Her medical history revealed only non-productive cough since last 2 days and an urticaria with paracetamol tablet 500 mg 2 days ago. She had cesarian section 2 years ago without any complication, she was using no oral contraceptives, alcohol or cigarettes.

On admission, the patient was bending forward and dyspneic because of very severe pain. Physical examination revealed tachypnea (36/min), tachycardia (120/min), arteriel blood pressure 110/60 mmHg, normal breath and heart sounds without cyanosis, edema or clubbing. The abdomen was nondistended, nontender without organomegaly or masses. There were no focal neurological findings. Arterial O₂ saturation was 95% in room air. A chest radiograph was normal and ECG revealed negative T waves in front leads. Blood tests including cardiac enzymes, sedimentation,CRP, whole blood count, biochemistry were within normal limits. She was given Aldolane i.v. but her chest pain did not resolve. A computerised tomography (CT) of thorax has been wanted (Fig 1)

What is your diagnosis?

In the thorax CT of the patient minimal pericardial thickening with some hiperdense areas were evaluated without any mediastinel or pulmonary parencymal or pleural lesion. Then a transthoracic echocardiographic examination had been performed in the emergency room and revealed pericardial effusion.

Discussion

The basic clinical symptom of acute pericarditis is chest pain. The onset of pain usually occurs relatively rapidly, but not as rapidly as in an acute myocardial infarction. Pain will be prolonged (generally lasting several days), and located in the precordial or retrosternal region, but may radiate to the neck, back, and left shoulder and arm. Pain will also often spread to the supraclavicular region and the trapezial region due to involvement of the phrenic nerves that enter the diaphragm. Pain may be exacerbated by breathing in, chest movements, decubitus position, and coughing but eased by sitting with the trunk leaning forward. It should be emphasized that, even though it is fairly characteristic, the diagnosis of pericarditis cannot be established on the type of pain alone. Frequently, patients have been diagnosed with pericarditis solely on the grounds of their pain, and often because of relatively nonspecific chest pain. Other common symptoms are dyspnea, which not only affects patients with cardiac tamponade but also patients without hemodynamic compromise because the pain itself may limit deep breathing. Fever, cough, and asthenia may also occur.

The main pathognomonic sign of acute pericarditis is pericardial friction rub, detected by auscultation in approximately 60% to 85% of the cases. Such a finding allows definitive diagnosis of acute pericarditis, but diagnosis cannot be discarded in its absence. Friction rub is a scratchy superficial sound that is heard most strongly in the mesocardium and the lower left parasternal edge and that varies in strength with respiratory movements. It is normally louder when breathing in.. Friction rub can be present in pericarditis regardless of whether effusion is present or whether effusion is extensive, even in patients with cardiac tamponade. When the pericarditis involves extensive effusion, signs of tamponade may appear.

Electrocardiographic findings are abnormal in 80% of the patients with acute pericarditis. In the most typical cases, ECG changes can be described in 4 stages. Stage I consists of a diffuse ST-segment elevation with upward concavity (indicative of subepicardial injury) and positive T waves. The PQ or PR segments may be depressed (indicative of atrial injury). These changes may last several hours or a few days. In Stage II, the ST segment returns to the isoelectric position. Stage III is characterized by the appearance of negative T waves that may return to normal in a few days, but they often remain negative for weeks or months. This should not be interpreted as persistence of the disease. Stage IV corresponds to normalization of the ECG. The changes in stage I may be confused with those of myocardial infarction and with the normal variant of repolarization known as “early repolarization.” No PR-segment depression occurs in myocardial infarction, ST-segment elevation is upwardly convex and may have a mirror image in some opposing leads, and Q waves may often appear. In pericarditis, on the other hand, Q waves do not appear and arrhythmias other than sinus tachycardia are rare. Early repolarization is a normal variant characterized by ST-segment elevation with upward concavity and positive T waves that resemble changes seen in acute pericarditis. The most reliable differential finding is the ratio of the ST-segment elevation to T-wave amplitude in the V6 lead: pericarditis is indicated when the ratio is greater than 0.24. Nevertheless, the normal variant of early repolarization can be definitively distinguished from acute pericarditis in the ECG if the ST segment changes over time, because the ST segment remains unchanged in early repolarization. In the event of extensive pericardial effusion, the amplitude of the QRS complex may decrease or follow cyclic changes (electrical alternation), particularly in patients with tamponade.

Echocardiography is the most useful diagnostic technique for identifying the presence of pericardial effusion and quantifying its extent. Nevertheless, echocardiography should not be considered as essential for establishing diagnosis of acute pericarditis, which, as mentioned earlier, should be based on other criteria. The course of acute pericarditis may not include effusion and, in contrast, not all cases of pericardial effusion are due to acute pericarditis. Echocardiography can also provide very useful information for establishing diagnosis of tamponade, essentially by detecting right atrial or ventricular collapse and abnormal mitral and tricuspid valve flow.

Corresponding Author

Nese Dursunoglu Pamukkale University Medical Faculty Department of Chest, Kınıklı, 20200, Denizli / Turkey Phone: (+90) 258-211 85 85 Fax: (+90) 258 213 49 22 E-mail: ndursunoglu@yahoo.com