PERICARDIUM AND PERICARDITIS
(serous, fibrinous, purulent, suppurative, caseous, and hemorrhagic)

The pericardium is a serous membrane that surrounds the heart, providing mechanical protection, reducing friction during cardiac motion, and contributing to the maintenance of intrathoracic pressure. It consists of two layers:

• The parietal pericardium, the outermost layer, which is closely connected to the pleura and diaphragm.
• The visceral pericardium, also called the epicardium, which adheres directly to the heart and major vessels.

Between these two layers, there is a virtual space known as the pericardial cavity, containing a small amount of serous fluid (about 10-50 mL) with a lubricating function, produced by pericardial capillaries and reabsorbed by lymphatic vessels.

Pathophysiology of Pericarditis

Pericarditis is an inflammatory process affecting the pericardium, leading to a series of structural and functional alterations of the pericardial membrane. Inflammation results in:

• Increased vascular permeability → leading to the leakage of plasma proteins into the pericardial fluid.
• Activation of the immune system → with the recruitment of leukocytes and the release of pro-inflammatory mediators (IL-1, IL-6, TNF-α).
• Alterations in pericardial fluid → transforming from a serous transudate into a pathological exudate.

Pericarditis and Pericardial Effusion

Pericarditis is not always associated with a significant effusion: small amounts of fluid may also be present in healthy individuals or patients with systemic conditions (heart failure, nephrotic syndrome).

When present, pericardial effusion can vary in amount and composition, influencing clinical presentation:

• Moderate effusion → usually well tolerated, without hemodynamic compromise.
• Large effusion → may lead to cardiac compression with a risk of cardiac tamponade.
• Chronic effusion → may progress to constrictive pericarditis, with fibrosis and calcifications.

Classification of Pericarditis

Pericarditis is classified based on the characteristics of the exudate:

• Serous pericarditis: clear exudate, free of fibrin.
• Serofibrinous pericarditis: cloudy exudate with fibrin presence.
• Fibrinous pericarditis: fibrin-rich exudate with little fluid.
• Purulent pericarditis: dense exudate, rich in bacteria and leukocytes.
• Caseous pericarditis: characterized by necrotic material, typical of tuberculosis.
• Hemorrhagic pericarditis: exudate mixed with blood, common in neoplasms and advanced tuberculosis.

This classification has important clinical implications, as the different forms can have distinct etiologies, progression, and prognosis.

Clinical Presentation and Symptoms

The clinical manifestations of pericarditis can vary depending on the severity of inflammation and the amount of pericardial fluid accumulated. The most common symptoms include:

• Chest pain: typically pleuritic, worsened by deep breathing and the supine position, relieved by sitting up.
• Dyspnea: related to pericardial irritation or an effusion affecting cardiac mechanics.
• Fever and malaise: especially in infectious or autoimmune forms.
• Pericardial friction rub: a distinctive auscultatory sign, due to the presence of fibrin between pericardial layers.

Diagnosis of Pericarditis

Diagnosis is based on a combination of clinical, laboratory, and instrumental findings:

• ECG: diffuse ST-segment elevations (concave upwards), PR-segment depression.
• Echocardiography: useful for assessing the presence of effusion and cardiac function.
• Cardiac MRI: indicated in doubtful cases to confirm pericardial inflammation.
• Blood tests: increased CRP, ESR, and leukocytosis in inflammatory forms.
• Pericardial fluid analysis: performed in cases of significant effusion to determine the etiology.

Treatment of Pericarditis

Treatment varies based on the cause and severity of pericarditis:

• NSAIDs (ibuprofen, aspirin): first-line therapy in viral and idiopathic pericarditis.
• Colchicine: used to reduce the risk of recurrence.
• Corticosteroids: indicated only in autoimmune or refractory cases.
• Antibiotics: required in bacterial or suppurative pericarditis.
• Pericardiocentesis: indicated in cases of large effusion or cardiac tamponade.

Prognosis and Evolution

The prognosis of pericarditis depends on the underlying cause:

• Viral or idiopathic forms → generally benign, with spontaneous resolution.
• Autoimmune forms → possible recurrences, requiring immunosuppressive treatment.
• Bacterial or tuberculous forms → high risk of progression to constrictive pericarditis.

A proper echocardiographic follow-up is essential to monitor the resolution of inflammation and prevent complications.

Serous Pericarditis

Serous pericarditis is the mildest and most frequently self-limiting form of pericardial inflammation. It is characterized by the presence of a clear or slightly turbid exudate, rich in proteins, monocytes, and lymphocytes, but devoid of fibrin. This distinction is crucial as it prevents the formation of adhesions between the pericardial layers.

The inflammatory process is mediated by the production of pro-inflammatory cytokines (IL-1, IL-6, TNF-α), which increase capillary permeability and facilitate the passage of fluid into the pericardial cavity. However, in the absence of fibrin, resolution is usually spontaneous and does not result in fibrotic sequelae.

Main Causes

The primary causes of serous pericarditis include:

• Viral infections: Coxsackievirus, Echovirus, Cytomegalovirus, Herpesvirus, HIV.
• Autoimmune diseases: systemic lupus erythematosus (SLE), rheumatoid arthritis.
• Uremia: typical in patients with advanced chronic kidney disease.
• Post-infarction reactions: Dressler syndrome.

Evolution and Prognosis

Serous pericarditis has a favorable prognosis, with spontaneous resolution in most cases.

In some patients, however, it may evolve into:

• Serofibrinous pericarditis → with fibrin deposition and possible fibrotic evolution.
• Chronic pericarditis → with recurrent episodes of pericardial effusion.

Treatment is generally symptomatic with NSAIDs and colchicine. In more complex cases, corticosteroids may be necessary.

Serofibrinous Pericarditis

Serofibrinous pericarditis represents an intermediate stage between serous pericarditis and fibrinous pericarditis. It is distinguished by the presence of a turbid exudate, rich in inflammatory proteins and fibrin strands, which may deposit on the pericardial surfaces.

This condition is associated with a more intense inflammatory process, with increased activation of mediators such as IL-1, IL-6, and TNF-α, which enhance vascular permeability and promote inflammatory cell recruitment.

Distinctive Features

• Turbid exudate with fibrin: the pericardial fluid is denser and rich in inflammatory proteins.
• Thickened and opaque pericardial surfaces: loss of mesothelial lining with possible subepicardial inflammatory infiltration.
• Presence of pericardial friction rubs: due to friction between the pericardial layers partially covered with fibrin.

Main Causes

The causes of serofibrinous pericarditis overlap in part with those of serous pericarditis but involve more intense and prolonged inflammation. The main causes include:

• Viral infections (Coxsackievirus, Echovirus, Influenza, HIV).
• Dressler syndrome (post-infarction pericarditis).
• Advanced uremia (chronic kidney disease).
• Autoimmune diseases (SLE, rheumatoid arthritis).
• Neoplasms involving the pericardium.

Evolution and Prognosis

Serofibrinous pericarditis may evolve into:

• Complete resolution → with resorption of fluid and fibrin.
• Fibrinous pericarditis → if fibrin accumulates and organizes.
• Chronic pericarditis → with possible recurrences.
• Constrictive pericarditis → in cases where inflammation leads to fibrosis and calcifications.

Treatment includes NSAIDs and colchicine, with possible corticosteroid use in cases secondary to autoimmune diseases.

Fibrinous Pericarditis

Fibrinous pericarditis represents an advanced stage of serofibrinous pericarditis, characterized by a pericardial exudate that is almost exclusively fibrinous, with minimal liquid component. The reduced lubrication between the pericardial layers leads to the characteristic pericardial friction rub, a hallmark clinical sign of this condition.

Distinctive Features

• Fibrin-rich exudate: minimal serous component with fibrin deposits on the pericardial surface.
• Thickened and rough pericardium: "bread and butter" appearance due to fibrin layering.
• Friction between pericardial layers: causes the pericardial rub, audible on auscultation.

Main Causes

The causes of fibrinous pericarditis include:

• Advanced uremia → most common cause in renal failure.
• Myocardial infarction → early phase or Dressler syndrome.
• Autoimmune diseases → SLE, rheumatoid arthritis, vasculitis.
• Viral and bacterial infections → early stages before suppuration.

Evolution and Prognosis

Fibrinous pericarditis may evolve into:

• Spontaneous resolution → with fibrin resorption.
• Chronic pericarditis → with recurrent episodes.
• Purulent pericarditis → if bacterial infection supervenes.
• Constrictive pericarditis → in cases of advanced fibrosis.

Treatment involves NSAIDs and colchicine, with drainage if an associated effusion is present.

Purulent or Suppurative Pericarditis

Purulent pericarditis, also known as suppurative pericarditis, is a severe form of pericardial inflammation caused by bacterial, fungal, or, more rarely, parasitic infections. It is characterized by a dense, yellowish exudate rich in pus, with a high infiltration of neutrophils and a significant risk of structural complications.

Distinctive Features

• Purulent exudate: opaque, thick fluid filled with cellular debris.
• Highly inflamed pericardium: thickened, hyperemic, with possible necrosis.
• High risk of fibrosis and calcifications: increased likelihood of developing constrictive pericarditis.

Main Causes

Bacterial infections reach the pericardium through:

• Hematogenous spread → from sepsis or endocarditis.
• Contiguous spread → from pneumonia, mediastinitis, or subdiaphragmatic abscesses.
• Direct inoculation → from trauma or cardiac surgical procedures.

The most common pathogens include:

• Staphylococcus aureus → frequently found in hospitalized patients.
• Streptococcus pneumoniae → common in respiratory infections.
• Mycobacterium tuberculosis → when evolving into caseous pericarditis.

Evolution and Prognosis

Purulent pericarditis progresses aggressively and can lead to:

• Cardiac tamponade → due to rapid accumulation of pus.
• Constrictive pericarditis → resulting from massive post-infectious fibrosis.
• Septicemia → with high mortality if not treated promptly.

Treatment

Unlike other forms, purulent pericarditis requires:

• Targeted antibiotic therapy → based on pericardial fluid culture.
• Pericardial drainage → to prevent cardiac tamponade.
• Pericardiectomy → in cases of advanced fibrosis.

Early treatment is essential to prevent irreversible complications.

Caseous Pericarditis

Caseous pericarditis is a rare form of pericardial inflammation, typically associated with tuberculosis and, more rarely, chronic fungal infections such as histoplasmosis. It is characterized by a granulomatous, dense, yellow-white exudate, with caseous necrosis and lymphomonocytic infiltration.

Distinctive Features

• Caseous necrosis: tissue destruction with yellowish deposits resembling cheese.
• Granulomas with Langhans giant cells: a hallmark of tuberculosis.
• High risk of constrictive pericarditis: due to strong fibrotic and calcification tendencies.

Main Causes

Caseous pericarditis is almost always secondary to:

• Tuberculous infection → Mycobacterium tuberculosis.
• Chronic fungal infections → Histoplasma capsulatum, Coccidioides spp.
• Sequelae of bacterial pericarditis → evolution of purulent pericarditis.

Evolution and Prognosis

Caseous pericarditis has a strong tendency to evolve into constrictive pericarditis, due to progressive deposition of fibrotic tissue and calcifications.

Frequent complications include:

• Fibrosis and pericardial thickening → leading to reduced ventricular compliance.
• Widespread calcifications → a hallmark of advanced forms.
• Risk of cardiac tamponade → in cases of massive effusion.

Treatment

The management of caseous pericarditis includes:

• Antituberculous therapy → prolonged treatment with isoniazid, rifampin, pyrazinamide, and ethambutol.
• Pericardial drainage → in cases with significant effusion.
• Pericardiectomy → in patients with constrictive pericarditis.

Early treatment is essential to avoid irreversible damage.

Hemorrhagic Pericarditis

Hemorrhagic pericarditis is a severe form of pericardial inflammation characterized by the presence of a bloody exudate, mixed with fibrin and, in some cases, pus. This condition often indicates advanced systemic diseases or neoplastic processes infiltrating the pericardium.

Distinctive Features

• Hemorrhagic exudate: blood-tinged pericardial fluid, with fibrin and cellular debris.
• Focal pericardial necrosis: possible in severe cases.
• High risk of cardiac tamponade: due to rapid accumulation of pericardial fluid.

Main Causes

The main causes of hemorrhagic pericarditis include:

• Infiltrating neoplasms → lung cancer, breast cancer, mesothelioma, and lymphomas.
• Tuberculous pericarditis → frequently associated with hemorrhagic effusion.
• Coagulopathies → anticoagulant use, thrombocytopenia, DIC.
• Cardiac trauma → iatrogenic perforations or post-surgical injuries.

Evolution and Prognosis

The main complications of hemorrhagic pericarditis include:

• Cardiac tamponade → due to rapid fluid accumulation.
• Pericardial fibrosis → with possible evolution into constrictive pericarditis.
• Chronic recurrences → in cases of neoplasms or coagulation disorders.

Treatment

The management of hemorrhagic pericarditis depends on the underlying cause and includes:

• Treatment of the primary condition → chemotherapy for neoplasms, antituberculous therapy.
• Pericardiocentesis → to relieve cardiac tamponade.
• Hemodynamic monitoring → for patients at risk of circulatory instability.

Prognosis depends significantly on the underlying pathology and the promptness of treatment.

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