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Infectious disease and microbiology – Pericarditis
Pericarditis is an inflammatory condition of the pericardium, the sac surrounding the heart, and can result from a wide range of infectious (viral, bacterial, fungal, protozoal) and noninfectious causes. In many cases, especially when no specific pathogen is identified, it is presumed to be viral or idiopathic, often involving an immune-mediated mechanism.
The condition is relatively common in clinical practice, accounting for about 5% of emergency visits for chest pain, though it occurs in only about 0.1% of hospitalized patients. Bacterial pericarditis is much rarer but more severe. There is no specific prevention for idiopathic cases, but early diagnosis and treatment can reduce complications and the need for surgical intervention.
Pathophysiologically, pericarditis may result from direct infection of the pericardium, as seen in bacterial cases, or from an autoimmune response, particularly in idiopathic or viral forms. Tuberculous pericarditis involves immune activation with CD4 lymphocytes and interferon-gamma, while viral infections lead to lymphocytic inflammation of the pericardium.
A wide variety of pathogens can cause pericarditis. Viruses are the most common, especially Coxsackie A and B, along with herpes viruses, influenza, adenovirus, HIV, and others. Bacterial causes often arise from nearby infections like pneumonia or from postoperative or hospital-acquired infections, with organisms such as Staphylococcus aureus, Streptococcus pneumoniae, and gram-negative bacteria. Less commonly, fungi (e.g., Candida, Histoplasma) and protozoa (e.g., Toxoplasma, Entamoeba histolytica) are involved, typically in disseminated disease.
Clinically, patients usually present with sharp, retrosternal chest pain and fever, with pain often relieved by sitting forward, which is a classic feature. Viral prodromal symptoms may be present. In bacterial cases, chest pain may be less prominent. Other findings include tachypnea and tachycardia, and in severe cases, progression to cardiac tamponade. On examination, a pericardial friction rub is characteristic, and signs such as pulsus paradoxus and decreased heart sounds may indicate significant effusion.
Diagnosis relies heavily on electrocardiography (ECG), which typically shows diffuse ST-segment elevation and PR depression, making it one of the most important diagnostic tools. Laboratory findings may include elevated white blood cells and inflammatory markers, and sometimes elevated cardiac troponins. Imaging such as chest X-ray, CT, MRI, or echocardiography helps assess pericardial effusion and structural involvement. Pericardiocentesis or biopsy may be necessary for diagnosis and to relieve tamponade, with fluid analysis aiding in identifying the cause.
Management depends on the underlying etiology. Most cases are treated with nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin or indomethacin, along with colchicine, which reduces symptoms and recurrence. Steroids are generally avoided except in specific situations like tuberculous pericarditis. If a specific pathogen is identified, targeted therapy is required—for example, antivirals (e.g., acyclovir, ganciclovir), antibiotics for bacterial causes, or antituberculous therapy. Supportive measures include bed rest and gastric protection when using NSAIDs.
Severe complications such as cardiac tamponade require urgent intervention with pericardiocentesis, while purulent or constrictive pericarditis may necessitate surgical procedures like pericardiotomy or pericardiectomy. Hospitalization is indicated in high-risk patients, including those with fever, large effusions, immunosuppression, or failure of initial therapy.
The prognosis is generally excellent in idiopathic or viral pericarditis, with recovery in most patients. However, outcomes are worse in tuberculous or untreated bacterial pericarditis, which can be fatal. Important complications include recurrence, constrictive pericarditis, and cardiac tamponade, all of which require careful monitoring and follow-up, often with repeat echocardiography.
Pericarditis is an inflammatory condition of the pericardium, the sac surrounding the heart, and can result from a wide range of infectious (viral, bacterial, fungal, protozoal) and noninfectious causes. In many cases, especially when no specific pathogen is identified, it is presumed to be viral or idiopathic, often involving an immune-mediated mechanism.
The condition is relatively common in clinical practice, accounting for about 5% of emergency visits for chest pain, though it occurs in only about 0.1% of hospitalized patients. Bacterial pericarditis is much rarer but more severe. There is no specific prevention for idiopathic cases, but early diagnosis and treatment can reduce complications and the need for surgical intervention.
Pathophysiologically, pericarditis may result from direct infection of the pericardium, as seen in bacterial cases, or from an autoimmune response, particularly in idiopathic or viral forms. Tuberculous pericarditis involves immune activation with CD4 lymphocytes and interferon-gamma, while viral infections lead to lymphocytic inflammation of the pericardium.
A wide variety of pathogens can cause pericarditis. Viruses are the most common, especially Coxsackie A and B, along with herpes viruses, influenza, adenovirus, HIV, and others. Bacterial causes often arise from nearby infections like pneumonia or from postoperative or hospital-acquired infections, with organisms such as Staphylococcus aureus, Streptococcus pneumoniae, and gram-negative bacteria. Less commonly, fungi (e.g., Candida, Histoplasma) and protozoa (e.g., Toxoplasma, Entamoeba histolytica) are involved, typically in disseminated disease.
Clinically, patients usually present with sharp, retrosternal chest pain and fever, with pain often relieved by sitting forward, which is a classic feature. Viral prodromal symptoms may be present. In bacterial cases, chest pain may be less prominent. Other findings include tachypnea and tachycardia, and in severe cases, progression to cardiac tamponade. On examination, a pericardial friction rub is characteristic, and signs such as pulsus paradoxus and decreased heart sounds may indicate significant effusion.
Diagnosis relies heavily on electrocardiography (ECG), which typically shows diffuse ST-segment elevation and PR depression, making it one of the most important diagnostic tools. Laboratory findings may include elevated white blood cells and inflammatory markers, and sometimes elevated cardiac troponins. Imaging such as chest X-ray, CT, MRI, or echocardiography helps assess pericardial effusion and structural involvement. Pericardiocentesis or biopsy may be necessary for diagnosis and to relieve tamponade, with fluid analysis aiding in identifying the cause.
Management depends on the underlying etiology. Most cases are treated with nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin or indomethacin, along with colchicine, which reduces symptoms and recurrence. Steroids are generally avoided except in specific situations like tuberculous pericarditis. If a specific pathogen is identified, targeted therapy is required—for example, antivirals (e.g., acyclovir, ganciclovir), antibiotics for bacterial causes, or antituberculous therapy. Supportive measures include bed rest and gastric protection when using NSAIDs.
Severe complications such as cardiac tamponade require urgent intervention with pericardiocentesis, while purulent or constrictive pericarditis may necessitate surgical procedures like pericardiotomy or pericardiectomy. Hospitalization is indicated in high-risk patients, including those with fever, large effusions, immunosuppression, or failure of initial therapy.
The prognosis is generally excellent in idiopathic or viral pericarditis, with recovery in most patients. However, outcomes are worse in tuberculous or untreated bacterial pericarditis, which can be fatal. Important complications include recurrence, constrictive pericarditis, and cardiac tamponade, all of which require careful monitoring and follow-up, often with repeat echocardiography.
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