Case Review: A Young Woman with Chest Pain and Shortness of Breath
Erica Wachtmeister, DO
A 20 year old female presented to the emergency room with a one week history of chest discomfort. The chest pain was described as sharp, constant, and rated 9/10 on the pain scale. The pain was worse with inspiration, and no alleviating factors were identified. She denied any fever or chills over the past week. The patient also reported back pain, dyspnea, orthopnea, and a nonproductive cough. The back pain was described as “achy”, constant, and 5/10 on the pain scale. The cough was worse with laying flat. She denied any leg pain or tenderness. She had been seen in the emergency room approximately one week prior for a pharyngitis and received a course of penicillin. At that time there was no complaint of chest pain or discomfort. In spite of antibiotic treatment, the pharyngitis had not improved, and her new symptoms prompted her return to the emergency department for further evaluation.
The patient had no significant past medical history including heart disease. She was on no medications and specifically denied oral contraceptive use. She denied a history of tobacco, alcohol or illicit drug use. The patient was physically active without any recent periods of immobilization. She had no recent travel. She also denied significant family history including heart disease.
On physical exam, the patient was afebrile, her blood pressure was 138/85 mmHg, heart rate was 100 beats per minute, respiratory rate was 18 breaths per minute, and pulse oximetry was 100% on 2L nasal cannula. The patient was alert and in mild discomfort. There was no jugular venous distension or lymphadenopathy. The patient was tachycardic with no murmurs, gallops, or rubs appreciated. Chest exam revealed equal chest wall expansion bilaterally with lungs clear to auscultation bilaterally. Her abdomen was soft, non-tender with no hepatojugular reflux. No edema, clubbing, or cyanosis of the extremities was appreciated.
DIFFERENTIAL DIAGNOSIS
Based on the patient’s history and physical exam, the differential diagnosis remains broad. Acute pericarditis was a strong possibility, especially in the setting of a recent upper respiratory infection. Although pulmonary embolism was high on the differential, the patient had no obvious risk factors and was not hypoxic. Acute myocardial infarction was less likely as the patient was young, had pleuritic pain, and prolonged symptoms. In addition, there was no family history of premature heart disease. There was no recent history of trauma to suggest a musculoskeletal etiology of the pain. Metabolic disorders were considered less likely due to the acute onset of symptoms and the lack of family or past medical history. Aortic dissection, drugs, toxins, autoimmune disorders, and malignancy were also in the differential.
LABORATORY DATA
Table 1: Complete Blood Count on admission *
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* Note: (H) signifies high
Table 2: Basic Metabolic Panel and Cardiac Enzymes/Troponin on admission
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An electrocardiogram showed sinus tachycardia at a rate of 107 beats per minute with T wave inversions in the inferior and anterior leads.
A chest x-ray revealed a slightly prominent cardiac-pericardial silhouette, unchanged from the patient’s previous study. No acute processes were identified.
CT-angiography of the chest revealed a large pericardial effusion, measuring up to 1.5cm in maximal thickness. It also showed non-specific mediastinal lymphadenopathy and segmental atelectasis of the left lung. No pulmonary embolus was identified.
An echocardiogram revealed normal left ventricular systolic function and a moderate circumferential pericardial effusion with findings of tamponade physiology.
HOSPITAL COURSE
A diagnosis of acute pericarditis was made based on the patient’s recent history of upper respiratory infection, ECG abnormalities, and presence of a pericardial effusion. The patient was admitted to the hospital for further evaluation and management. The patient’s dyspnea and chest pain became progressively worse. The cardiothoracic surgery service was consulted for emergent pericardiocentesis, given the patients progressive symptoms and supporting echocardiogram. Approximately 500 milliliters of serosanguinous fluid was initially drained and a pericardial window was created.
Post-operatively, the patient’s symptoms improved and therapy with indomethicin was initiated. The pericardial drain was removed three days later and a repeat echocardiogram revealed normal biventricular systolic function and a significantly smaller pericardial effusion as compared to the prior study.
During her hospitalization, the patient was tested for potential causes of acute pericarditis including HIV, tuberculosis, rheumatological conditions, viral diseases, and thyroid disease. HIV counseling was initiated, and test results were still pending at the time of discharge from the hospital. Fungus cultures and acid fast bacilli (AFB) smear of the pericardial fluid were negative. Antinuclear antibody (ANA) and Ebstein-Barr virus (EBV) antibody titers were also negative. Thyroid disease was essentially ruled out given her normal thyroid studies. The patient remained afebrile and her symptoms resolved, she was safely discharged home on indomethacin.
DISCUSSION
Anatomy& Physiology
The pericardium is composed of two layers: the parietal pericardium, a fibrous outer layer, and the visceral pericardium, a serous inner layer. These two layers are attached by connective tissue and separated by up to 50 ml of pericardial fluid. The pericardium has multiple functions that include acting as a barrier against infection and the spread of malignancy, limiting excessive cardiac movement, reducing friction between the heart and other organs, and the maintaining intrapericardial pressure. This pressure is normally negative and has an important role in allowing distention of the cardiac chambers in diastole (1, 6).
In pericarditis, the pericardium becomes acutely inflamed and becomes infiltrated with polymorphonuclear (PMN) leukocytes. Often, the pericardium exhibits a fibrinous reaction with exudates and adhesion and a serous or hemorrhagic effusion may develop. A granulomatous pericarditis may occur with tuberculosis, fungal infections, rheumatoid arthritis (RA), and sarcoidosis.
Acute pericarditis is the most common disease state affecting the pericardium. Most cases are idiopathic or viral in nature. Other etiologies including bacterial and fungal infections, rheumatologic conditions, Crohn’s disease, Ulcerative Colitis, drug reactions, malignancy, uremia, pregnancy, and immunologic disorders.
Presenting Symptoms & Physical Exam
Chest pain is the primary presenting symptom of acute pericarditis. The pain is typically described as sharp and pleuritic in nature that is relieved on sitting upright and leaning forward. The pain is commonly felt over the anterior chest, but can radiate to the trapezius ridge, shoulder, arm, or epigastrium. Other non-specific symptoms include hiccups, fever, cough, hoarseness, palpitations, nausea, and vomiting.
A pericardial friction rub is the cardinal physical finding in acute pericarditis. Typically seen in about 85 percent of patients with pericarditis, a pericardial friction rub is described as harsh, scratching, grating and high pitched noise. It is best heard on end expiration while the patient is leaning forward.
Diagnosis
Initial evaluation of suspected acute pericarditis should include an ECG, laboratory studies to measure markers of myocardial injury, chest x-ray, and echocardiogram. Markers of myocardial injury include Creatinine Kinase-MB and cardiac Troponin-I. ECG abnormalities are found in up to 90% of cases and are broken down into four phases, though progression through all four stages occurs in less than 50% of patients. Stage 1 is seen in the first hours to days and is characterized by diffuse ST-segment elevation and depression of PR-segments. The ST- and PR-segments normalize in Stage 2. In Stage 3, there is development of diffuse T wave inversions. Finally, Stage 4 is characterized by either normalization of the T waves or indefinite persistence of T wave inversions. The most sensitive finding is diffuse ST-segment elevation.
Imaging in the evaluation of pericarditis includes chest radiography and echocardiography. Chest radiography usually has a limited role in the evaluation of acute pericarditis but in the presence of a large pericardial effusion of at least 250 ml, a radiograph may show an enlarged cardiac silhouette. An echocardiogram is recommended in patients in whom cardiac tamponade or pericardial effusion is suspected. In fact, the use of echocardiography was given a Class I recommendation by a 2003 task force of the American College of Cardiology, the American Heart Association, and the American Society of Echocardiography.
Once a diagnosis of acute pericarditis has been made, other tests should be considered to determine the etiology. Tests to consider include an ANA titer, HIV serology, tuberculin skin testing, rheumatoid factor, antistreptolysin (ASO) antibody titer, and thyroid hormone studies. These studies may help corroborate the diagnosis and refine therapy.
Complications
Complications of idiopathic acute pericarditis include recurrent pericarditis, cardiac tamponade, and constrictive pericarditis. The most common complication is recurrent pericardial inflammation, which develops in 15-32% of patients. Risk factors include chronic illnesses such as malignancy and connective tissue disease. The presence of systemic arterial hypotension, tachycardia, elevated jugular venous pressure, and pulsus paradoxus suggests cardiac tamponade. In tamponade, the accumulation of pericardial fluid increases the intrapericardial pressure to the point that it equals or exceeds the pressure in the right side of the heart. Due to the elevated intrapericardial pressure, venous return and ventricular filling are restricted which results in decreased stroke volume and pulse pressure along with tachycardia and increased venous pressure. The right ventricle is reduced in diameter with late diastolic inward collapse of the right ventricle and right atrium. The result is right heart failure and decreased cardiac output.
Treatment
Treatment of acute pericarditis involves addressing the underlying etiology, pain control, and resolution of inflammation. Treatment is usually supportive as the majority of cases are idiopathic or viral in origin. The mainstay of therapy is non-steroidal anti-inflammatory drugs (NSAIDS) such as aspirin, indomethacin, naproxen, and ketorolac, which aid with symptomatic improvement and prevent further inflammation. If there is failure of monotherapy, aspirin can be added to the regimen. Combination therapy should be continued for seven to fourteen days with tapering of NSAIDs over another two weeks. Ibuprofen is preferred over indomethacin due to its relatively limited adverse effects.
Studies suggest that corticosteroid therapy, if used as initial treatment, increases the risk of recurrent pericarditis and should be reserved for patients whose symptoms are refractory to NSAID therapy. Colchicine, an anti-inflammatory agent, has been successful in the treatment of recurrent pericarditis. In recalcitrant cases, immunosuppressive therapy with high-dose corticosteroids, cyclophosphamide, or azathioprine has been used with variable success.
References
- Ross, A, Grauer S. Acute Pericarditis: Evaluation and treatment of infectious and other causes. Postgraduate Medicine. 2004, Vol.115 No.3.
- Marinella, M. Electrocardiographic Manifestations and Differential Diagnosis of Acute Pericarditis. American Family Physician. 1998. Vol.57 No.4