bubble_chart Overview

Constrictive pericarditis develops from acute pericarditis and is a severe form of chronic pericarditis. It occurs when fibrous tissue proliferates extensively in the pericardium of some patients with acute pericarditis, forming thick scar tissue that compresses and restricts the contraction and relaxation of the heart. This leads to a series of circulatory disorders, such as reduced cardiac output and elevated venous pressure, which characterize constrictive pericarditis.

bubble_chart Etiology

1. Acute pericarditis: The vast majority of constrictive pericarditis cases are sequelae of acute pericarditis, especially subcutaneous nodular, purulent, and nonspecific pericarditis. If treatment is deficient or incomplete, these conditions can evolve into constrictive pericarditis. Among the causes of constrictive pericarditis, subcutaneous nodular pericarditis accounts for the majority. Although the clinical progression from acute pericarditis to constrictive pericarditis can sometimes be observed, in most cases, the acute stage is insidious and goes unnoticed, with patients presenting as constrictive pericarditis by the time they seek medical attention.
2. Other causes such as pericardial trauma, pericardial tumors, radiation therapy, and hemodialysis for uremia may occasionally lead to this condition.

bubble_chart Pathological Changes

The visceral and parietal layers of the pericardium are extensively adhered, thickened, and calcified due to massive fibrous tissue proliferation, reaching a thickness of 0.5 cm or more, even leading to occlusion of the pericardial cavity. This forms a rigid shell around the heart, tightly encasing and compressing the heart and the outlets of the great vessels, impairing normal myocardial metabolism and resulting in myocardial atrophy. The size of the heart may be normal or smaller.

The compression and restriction cause diastolic dysfunction, reducing ventricular filling and cardiac output. Simultaneously, venous return is obstructed, and the decreased cardiac output can lead to renal retention of water and sodium, increasing blood volume and causing venous congestion. This manifests as elevated venous pressure, jugular vein distension, hepatomegaly, ascites, and lower limb edema. Pericardial adhesions and constriction can also affect cardiac systolic function, particularly in the advanced stage of constrictive pericarditis, where myocardial atrophy further reduces myocardial contractility, significantly exacerbating the decrease in cardiac output.

bubble_chart Clinical Manifestations

Symptoms

1. The onset of this disease is insidious, with pericardial constriction typically developing months or years after acute pericarditis.
2. Dyspnea is a prominent symptom, initially occurring after exertion and progressively worsening, even to the point of inability to lie flat or requiring an upright sitting position. This is due to reduced cardiac output, pulmonary congestion, and pleural or peritoneal effusions. Liver enlargement and significant ascites compressing abdominal organs may lead to abdominal distension and pain. Additionally, dizziness, lack of strength, decreased appetite, weight loss, cough, and other symptoms are commonly observed.

Signs

1. Cardiac signs: The apical impulse is weakened or absent, the cardiac dullness border may be normal or grade I enlarged, and heart sounds are faint and distant. In some patients, a pericardial knock—heard approximately 0.1 seconds after the second heart sound at the left sternal border in the 3rd or 4th intercostal space during early diastole—may be present, caused by the abrupt restriction of ventricular filling due to pericardial constriction. Arrhythmias such as atrial fibrillation or premature beats may also occur.
2. Signs of pericardial constriction and occlusion: These include signs of impaired venous return, such as jugular vein distension, hepatomegaly, ascites, pleural effusion, and lower limb edema. A few patients may exhibit Kussmaul's sign (marked jugular vein distension during inspiration) or Friedreich's sign (sudden collapse of the jugular vein in early diastole, caused by a sharp drop in pressure in the overfilled right atrium upon tricuspid valve opening). Due to reduced cardiac output, systolic blood pressure decreases, pulse pressure narrows, and the pulse often becomes rapid and thready.

bubble_chart Auxiliary Examination

1. Laboratory tests: Grade I anemia may be present. In cases with prolonged disease course, liver congestion may lead to abnormal liver function and hypoalbuminemia.
2. X-ray examination: The heart shadow may appear normal in size or show Grade I enlargement, with weakened or absent cardiac pulsation, straight and rigid cardiac borders, and possible pericardial calcification. The shadow of the superior vena cava may widen, and the hilar shadows may enlarge.
3. Electrocardiogram (ECG): The main manifestations include low QRS complex voltage, flattened or inverted T waves (the depth of inversion correlates with the degree of myocardial involvement), and a fixed electrical axis. Some cases may exhibit widened or notched P waves, right ventricular hypertrophy, incomplete right bundle branch block, or atrial fibrillation.
4. Echocardiography: Reduced motion amplitude of the right ventricular anterior wall and left ventricular posterior wall, decreased ventricular volume, and atrial enlargement. If a small amount of pericardial effusion remains for contrast, thickening of the pericardial parietal layer may be observed.
5. Venous pressure measurement: Venous pressure is significantly elevated, generally above 2.4 kPa (250 mmH₂O) and may sometimes reach 3.9 kPa (400 mmH₂O).

bubble_chart Diagnosis

1. If symptoms and signs of venous return obstruction and reduced cardiac output appear months or years after acute pericarditis, the possibility of constrictive pericarditis should be considered.
2. There are symptoms and signs caused by constriction and occlusion of the pericardial cavity.
3. Based on positive findings from auxiliary examinations such as X-ray, echocardiography, venous pressure, and electrocardiogram.

bubble_chart Treatment Measures

Early pericardiectomy is the key to treating this disease, with approximately 75% of cases achieving lasting hemodynamic and clinical symptom improvement postoperatively. Otherwise, most patients die within 6 months to 2 years. If subcutaneous nodes remain active after surgery, anti-subcutaneous node therapy should be continued. Due to the slow recovery of atrophied myocardium, successful surgery often results in satisfactory outcomes only gradually 4 to 6 months postoperatively.

Symptomatic treatment

1. For ascites, a low-salt diet and diuretics are recommended, and ascites drainage may be considered if necessary.
2. For heart failure or rapid atrial fibrillation, appropriate use of digitalis preparations may be considered.

bubble_chart Prevention

Actively prevent and treat

acute pericarditis, especially subcutaneous nodular, purulent, and nonspecific pericarditis, to prevent the formation of constrictive pericarditis.

disease cause Prevention and treatment

Actively preventing and treating subcutaneous nodular disease, wind-dampness heat, sepsis, and viral infections are important measures to prevent pericarditis.

Prevention of constrictive pericarditis:

1. Pericardial puncture and drainage: For purulent pericarditis and subcutaneous nodular pericarditis with significant effusion, pericardial puncture and fluid drainage, if performed inadequately, may lead to pericardial adhesions and constriction, resulting in constrictive pericarditis. Therefore, pericardial puncture and drainage are not only diagnostic and therapeutic measures for acute pericarditis but also a means to prevent constrictive pericarditis.
2. Use of adrenal corticosteroids: For subcutaneous nodular and nonspecific pericarditis, early application of adrenal corticosteroids is recommended to reduce exudation, fibrous tissue proliferation, and granuloma formation, thereby preventing the occurrence of constrictive pericarditis.
3. Pericardiotomy and drainage: If drug therapy for purulent pericarditis is ineffective, pericardiotomy and drainage may be performed to prevent progression to constrictive pericarditis.

bubble_chart Differentiation

1. Diseases primarily manifested as ascites: Constrictive pericarditis. Since ascites is one of the main manifestations, it is clinically prone to misdiagnosis as diseases primarily manifested as ascites, such as cirrhosis and subcutaneous nodular peritonitis, and differentiation should be noted:
   1. Although cirrhosis presents with ascites similar to constrictive pericarditis, in cirrhosis the liver shrinks, liver function injury is more severe, there is no jugular vein distension or elevated venous pressure, nor a history of acute pericarditis. Additionally, there is no weakened cardiac impulse, distant heart sounds, narrowed pulse pressure, or pericardial calcification.
   2. Subcutaneous nodular peritonitis. This condition presents with generalized abdominal distension, a doughy and resistant abdominal wall, tenderness, and rebound tenderness. The ascites is exudative, without symptoms or signs of obstructed venous return or reduced cardiac output.
2. Cardiac insufficiency: A history of pre-existing heart disease may include murmurs caused by valvular damage, significant cardiac enlargement, generalized edema more prominent than ascites, and responsiveness to digitalis preparations, which differ from constrictive pericarditis and aid in differentiation.