bubble_chart Overview

Traumatic hemopericardium refers to the accumulation of blood in the pericardial cavity caused by trauma. It is often a complication resulting from cardiac trauma, injury to major blood vessels within the pericardium, or pericardial injury, mostly caused by sharp or firearm injuries to the precordial region, and in some cases, severe closed chest injuries. Cardiac perforation leading to hemopericardium may also occasionally occur after cardiac surgery or interventional cardiac procedures. The severity of hemopericardium is closely related to the extent of cardiac injury, the volume of blood accumulated in the pericardial cavity, and the rate of accumulation. If the amount of blood in the pericardial cavity is small and does not cause compressive symptoms, it is referred to as hemopericardium. Hemopericardium does not significantly impair cardiac function and thus presents no clinical symptoms or signs. X-ray examination may sometimes show a slightly enlarged cardiac shadow, while ultrasound may reveal fluid levels within the pericardium.

When the accumulation of blood in the pericardial cavity causes compressive symptoms, it is termed acute cardiac tamponade. This occurs when a relatively large amount of blood rapidly enters the pericardial cavity, and the pericardial sac cannot stretch and expand quickly enough, leading to increased intrapericardial pressure. This impedes ventricular diastolic filling, resulting in decreased cardiac output, obstructed venous return, and elevated venous pressure. The body compensates by increasing peripheral vascular resistance, heart rate, and pulse pressure to boost cardiac output. However, once these compensatory mechanisms are exceeded (when intrapericardial pressure reaches approximately 15 cm H2O), signs of tamponade such as decreased blood pressure will appear. If the intrapericardial pressure is not reduced (by draining the blood), cardiac arrest will occur when the pericardial pressure exceeds that of the superior and inferior vena cava, leading to death.

In cases of acute hemopericardium, an accumulation of 150–200 ml of blood within a short period can be sufficient to cause compression and fatal cardiac tamponade. Therefore, after open-heart surgery, if chest drainage increases, close monitoring for potential tamponade is essential. The incidence of cardiac tamponade after open-heart surgery ranges from 3.4% to 8.8% and can often be life-threatening, with a mortality rate of around 7%.

The three classic signs of acute cardiac tamponade (Beck’s triad) are elevated venous pressure, decreased pulse pressure, and distant heart sounds. However, only 35–40% of patients exhibit these typical signs. Based on hemodynamic changes (the body’s compensatory mechanisms), acute cardiac tamponade first manifests as elevated venous pressure (or oliguria, which may appear earlier than decreased pulse pressure), followed by decreased pulse pressure. These two stages are crucial for diagnosis and treatment. The former is an important early diagnostic indicator, while the latter signifies a critical condition requiring immediate intervention without delay.

bubble_chart Clinical Manifestations

1. Symptoms of acute cardiac tamponade: chest tightness, dysphoria, pale complexion, cold and clammy skin, difficulty breathing, and even loss of consciousness.
2. Signs: rapid breathing, possible cyanosis. Distended neck veins, rapid and weak pulse, decreased blood pressure, narrowed pulse pressure, elevated central venous pressure, wound in the precordial area (blood oozing with respiration or heartbeat), weakened or absent apical impulse, distant and faint heart sounds. Pulsus paradoxus may be present (marked weakening or disappearance of the pulse during inspiration, becoming stronger at the end of expiration). Kussmaul's sign may also occur (marked distension of the neck veins during inspiration).

bubble_chart Diagnosis

1. There is a history of chest trauma, especially a history of sharp instrument injury in the precordial area.
2. There are signs of acute cardiac tamponade.
3. Chest X-ray shows weakened cardiac pulsation under fluoroscopy, and the chest film reveals normal or slightly enlarged cardiac shadow.
4. Electrocardiogram: No specific changes or generalized low voltage and ST-T changes in all leads.
5. Echocardiography: Can assess the presence of blood in the pericardial cavity.
6. Magnetic resonance (MR) examination: Can be performed for stable patients to confirm the presence of blood in the pericardial cavity.
7. Pericardiocentesis: Can confirm the diagnosis and immediately relieve symptoms of cardiac tamponade.
8. Limited pericardial exploration: For cases with high clinical suspicion of cardiac tamponade but unconfirmed by pericardiocentesis, limited pericardial exploration may be performed.

bubble_chart Treatment Measures

1. Pericardiocentesis: Can immediately relieve symptoms of cardiac tamponade and improve hemodynamics. The puncture site is usually approached subxiphoid or at the fourth intercostal space in the precordial region. For blunt trauma-induced cardiac tamponade with a slow progression, pericardiocentesis may allow temporary observation under close monitoring. If tamponade symptoms recur, surgical exploration should be considered.
2. Surgical Treatment: Incision of the pericardium to remove pericardial blood or clots, relieve cardiac tamponade, repair injuries to the heart or major blood vessels, and eliminate the source of bleeding in the hemopericardium. While administering anti-shock therapy, rapid progression of cardiac tamponade due to closed injury often indicates cardiac injury, and immediate surgery is required, similar to penetrating cardiac wounds. Even if pericardiocentesis effectively alleviates tamponade, surgical intervention is still necessary. A negative pericardiocentesis does not rule out cardiac injury, and prompt surgical exploration should be performed based on signs.
3. The treatment of acute cardiac tamponade particularly emphasizes timeliness and effectiveness to prevent severe consequences caused by tamponade.
4. To maintain ventricular filling pressure, vasodilators can be used to increase stroke volume. Isoproterenol increases heart rate and myocardial contractility, enhances stroke volume, and reduces peripheral vascular resistance, making it useful for improving cardiac output in tamponade patients. In contrast, norepinephrine, an α-receptor agonist, increases vascular resistance, and digitalis (e.g., Rehmannia) may elevate afterload, neither of which improves stroke volume in tamponade and should therefore be avoided.
5. Appropriate use of antibiotics is recommended to prevent infection.

Traumatic hemopericardium is a complication caused by injury to the heart, major intrapericardial vessels, or the pericardium, leading to acute cardiac tamponade. It can also occur after open-heart surgery and is often life-threatening.

For patients with chest trauma, hypotension and jugular venous distension (without other symptoms of tension pneumothorax), or severe shock disproportionate to the volume of blood loss from thoracic injury, strongly suggest acute cardiac tamponade.

After open-heart surgery, if chest drainage is excessive, urine output is low, and blood pressure fluctuates with positional changes, cardiac tamponade should be diagnosed. If in doubt, echocardiography or two-dimensional B-mode ultrasound can be performed.

In penetrating cardiac injuries with tamponade, 60% of cases involve intrapericardial clots, so pericardiocentesis yields a false-negative rate of 15–25%. A negative pericardiocentesis does not exclude the presence of tamponade.

After acute cardiac tamponade occurs, venous pressure rises first, followed by a decrease in pulse pressure. Early diagnosis and decisive management are crucial. Waiting for a drop in pulse pressure to confirm diagnosis means the condition has already reached an advanced stage. For acute tamponade, anti-shock measures and therapeutic pericardiocentesis should prioritize minimizing unnecessary diagnostic tests and shortening preoperative preparation time to expedite surgical decompression and save the patient’s life.

bubble_chart Cure Criteria

1. Cure: Symptoms and signs disappear (healing of chest wall wound), no pericardial effusion (blood) detected by ultrasound or echocardiography, and no complications.
2. Improvement: Symptoms and signs are alleviated, and other complications show improvement.
3. No cure: Symptoms and signs do not improve, other complications persist, and pericardial effusion (blood) is still present as detected by ultrasound or echocardiography.