Chronic constrictive pericarditis is a sequela of acute pericarditis. Occasionally, the transition from acute to constrictive pericarditis can be observed clinically, but in most cases, the acute phase is insidious and difficult to detect, so patients often present with constrictive pericarditis at the time of diagnosis. The etiology remains unclear in many cases. Among the known causes, tuberculous pericarditis is the most common, followed by purulent and traumatic pericarditis. Due to long-term prevention and treatment of tuberculosis, the incidence of tuberculous pericarditis has declined in recent years, while cases caused by nonspecific factors, including viral pericarditis, have increased. In constrictive pericarditis, especially when the visceral pericardium or both layers develop fibrous thickening and scar contraction, ventricular diastolic expansion is impaired. This leads to reduced cardiac output on one hand and elevated central venous pressure on the other, resulting in a series of clinical symptoms and signs.

bubble_chart Clinical Manifestations

Symptoms

1. Dyspnea: This is the main symptom of the condition. It usually occurs after activity, which is related to the inability of cardiac output to increase correspondingly during activity. Ascites elevates the diaphragm and impedes breathing. It can also be caused by pulmonary congestion. In severe cases, orthopnea may occur.
2. Abdominal distension: This is caused by ascites and an enlarged liver compressing the abdominal organs.

1. Marked hepatomegaly, which appears early. There is tenderness but no pulsation.
2. Ascites: Large or moderate in amount, with rapid reaccumulation of abdominal mass after fluid withdrawal.
3. Jugular vein distension, which becomes more pronounced during inspiration.
4. The cardiac borders are not enlarged, may even be reduced, and cardiac pulsations are significantly weakened.
5. Pericardial knock: An early diastolic sound is often heard medial to the apex. This is due to constrictive pericarditis causing the ventricular cavity to become smaller and difficult to expand during diastole. Rapid filling quickly fills the ventricle, and the sudden cessation of blood inflow causes the ventricular wall to rebound and vibrate, producing a loud knocking sound—the early diastolic sound or pericardial knock. This sound is loudest medial to the apex.

bubble_chart Auxiliary Examination

1. General examination: Grade I anemia may be present, and in cases with a longer disease course, hypoproteinemia may occur, primarily characterized by decreased albumin levels.
2. X-ray examination: Confirms weakened or absent cardiac pulsations, with a fixed position, normal heart shadow or only Grade I enlargement, rough and indistinct cardiac borders, rigidity, and possible pericardial calcification.
3. Electrocardiogram: Mainly shows low voltage and T-wave changes.
4. Echocardiography: Demonstrates enhanced echoes in the pericardial region and the outer membrane of the left ventricular posterior wall, paradoxical motion of the interventricular septum, and reduced ventricular cavity size.

bubble_chart Treatment Measures

1. First, acute pericarditis should be actively treated to prevent it from progressing into constrictive sexually transmitted disease. Once the latter is diagnosed, pericardial stripping surgery should be considered as early as possible after acute symptoms subside. If the disease course exceeds six months, myocardial atrophy is more likely to occur, which can affect the recovery of cardiac function after surgery.
2. Before surgery, bed rest, a low-salt diet, and the judicious use of diuretics are recommended. Patients with anemia and low serum protein should receive treatment to improve their general condition.
3. For those with significant ascites or pleural effusion before surgery, appropriate treatment should be administered.
4. Generally, there is no need to use digitalis before surgery, but it should be used for a short period postoperatively to prevent heart failure in the atrophied myocardium under increased load.
5. For patients with active subcutaneous nodes, anti-subcutaneous node therapy should be actively pursued before and after surgery.

AD

bubble_chart Differentiation

1. Liver cirrhosis: This condition does not present with cardiac pathology, nor does it exhibit distension or engorgement of the jugular and upper extremity veins. Additionally, venous pressure remains normal.
2. Right heart failure: There is an underlying cardiac condition such as valvular disease or pulmonary hypertension. Following treatment with cardiotonics, diuretics, and rest, the liver may significantly shrink, and venous pressure decreases.
3. Restrictive cardiomyopathy: This condition primarily affects the left ventricle, manifesting as pulmonary venous hypertension and pulmonary circulation congestion, while systemic venous congestion is less pronounced. In contrast, constrictive pericarditis typically encases the ventricles, atria, and the roots of the great vessels, preventing atrial enlargement. This condition, however, only affects the ventricles, impeding atrial blood flow into the ventricles and leading to atrial congestion and enlargement. On X-ray examination, left ventricular pulsations are markedly weakened, while right ventricular pulsations are more prominent, accompanied by left atrial enlargement. In constrictive pericarditis, overall cardiac pulsations are weakened, and there is no atrial enlargement.