Thromboembolism pulmonary artery(PE) - occlusion of one or more pulmonary arteries by blood clots that form elsewhere, usually in the large veins of the lower extremities or pelvis.
Risk factors are conditions that impair venous flow and cause endothelial damage or dysfunction, especially in patients with hypercoagulable states. Symptoms of pulmonary embolism (PE) include shortness of breath, pleuritic chest pain, cough, and in severe cases, fainting or cardiac and respiratory arrest. Detected changes are vague and may include tachypnea, tachycardia, hypotension, and increased pulmonary component of the second heart sound. Diagnosis is based on ventilation-perfusion scanning, CT angiography, or pulmonary arteriography. Treatment of pulmonary embolism (PE) involves anticoagulants, thrombolytics, and sometimes surgery to remove the clot.
Pulmonary embolism (PE) affects approximately 650,000 people and causes up to 200,000 deaths per year, accounting for approximately 15% of all hospital deaths per year. The prevalence of pulmonary embolism (PE) in children is approximately 5 per 10,000 admissions.
ICD-10 code
I26 Pulmonary embolism
I26.0 Pulmonary embolism with mention of acute cor pulmonale
I26.9 Pulmonary embolism without mention of acute cor pulmonale
Causes of pulmonary embolism
Almost all pulmonary emboli are the result of thrombosis in the lower extremities or pelvic veins (deep venous thrombosis [DVT]). Blood clots in any system can be silent. Thromboemboli can also occur in the veins of the upper extremities or in the right side of the heart. Risk factors for deep venous thrombosis and pulmonary embolism (PE) are similar in children and adults and include conditions that impair venous inflow or cause endothelial damage or dysfunction, especially in patients with an underlying hypercoagulable state. Bed rest and limited walking, even for several hours, are common precipitating factors.
Once deep venous thrombosis develops, the clot may break off and travel through the venous system to the right side of the heart, then lodge in the pulmonary arteries, where it partially or completely occludes one or more vessels. The consequences depend on the size and number of emboli, the reaction of the lungs and the ability of the person’s internal thrombolytic system to dissolve the clot.
Small emboli may not have any acute physiological effects; many begin to lyse immediately and dissolve within hours or days. Large emboli may cause a reflex increase in ventilation (tachypnea); hypoxemia due to ventilation-perfusion (V/P) mismatch and shunting; atelectasis due to alveolar hypocapnia and surfactant disturbances and increased pulmonary vascular resistance caused by mechanical obstruction and vasoconstriction. Endogenous lysis reduces most emboli, even large ones, without treatment, and physiological responses decrease within hours or days. Some emboli are resistant to lysis and can organize and persist. Sometimes chronic residual obstruction leads to pulmonary hypertension (chronic thromboembolic pulmonary hypertension), which can develop over years and lead to chronic right ventricular failure. When large emboli occlude large arteries or when many small emboli occlude more than 50% of the distal arteries of the system, pressure in the right ventricle increases, causing acute right ventricular failure, failure with shock (massive pulmonary embolism (PE)), or sudden death in severe cases. The risk of death depends on the degree and frequency of increased pressure in the right side of the heart and on the patient's previous cardiopulmonary status; higher blood pressure is more common in patients with pre-existing heart disease. Healthy patients can survive pulmonary embolism that occludes more than 50% of the pulmonary vascular bed.
Risk factors for deep venous thrombosis and pulmonary embolism (PE)
- Age > 60 years
- Atrial fibrillation
- Cigarette smoking (including secondhand smoke)
- Estrogen receptor modulators (raloxifene, tamoxifen)
- Limb injuries
- Heart failure
- Hypercoagulable states
- Antiphospholipid syndrome
- Antithrombin III deficiency
- Factor V Leiden mutation (activated protein C resistance)
- Heparin-induced thrombocytopenia and thrombosis
- Hereditary defects in fibrinolysis
- Hyperhomocysteinemia
- Factor VIII increase
- Factor XI increase
- Increased von Willebrand factor
- Paroxysmal nocturnal hemoglobinuria
- Protein C deficiency
- Protein S deficiency
- Gene defects of prothrombin G-A
- Tissue factor pathway inhibitor
- Immobilization
- Placement of venous catheters
- Malignant neoplasms
- Myeloproliferative diseases (increased viscosity)
- Nephrotic syndrome
- Obesity
- Oral contraceptives/estrogens replacement therapy
- Pregnancy and postpartum period
- Previous venous thromboembolism
- Sickle cell anemia
- Surgery in the previous 3 months
Pulmonary infarction occurs in less than 10% of patients diagnosed with pulmonary embolism (PE). This low percentage is attributed to the dual blood supply to the lungs (i.e., bronchial and pulmonary). Infarction is typically characterized by a radiographic infiltrate, chest pain, fever, and occasionally hemoptysis.
Nonthrombotic pulmonary embolism (PE)
Pulmonary embolism (PE), which develops from a variety of nonthrombotic sources, causes clinical syndromes that are distinct from thrombotic pulmonary embolism (PE).
An air embolism occurs when a large amount of air is injected into the systemic veins or into the right heart, which then moves into the pulmonary arterial system. Causes include surgery, blunt or barotrauma (eg, mechanical ventilation), use of defective or uncovered venous catheters, and rapid decompression after diving. The formation of microbubbles in the pulmonary circulation can cause endothelial damage, hypoxemia and diffuse infiltration. With a large-volume air embolism, obstruction of the pulmonary outflow tract may occur, which can lead to rapid death.
Fat embolism is caused by the entry of fat or bone marrow particles into the systemic venous circulation and then into the pulmonary arteries. Causes include long bone fractures, orthopedic procedures, capillary occlusion or bone marrow necrosis in patients with sickle cell disease crisis and, rarely, toxic modification of native or parenteral serum lipids. Fat embolism causes a pulmonary syndrome similar to acute respiratory distress syndrome, with severe, rapid-onset hypoxemia, often accompanied by neurological changes and petechial rash.
Amniotic fluid embolism is a rare syndrome caused by amniotic fluid entering the maternal venous system and then into the pulmonary arterial system during or after childbirth. The syndrome can sometimes occur during prenatal manipulation of the uterus. Patients may have cardiac shock and respiratory distress due to anaphylaxis, vasoconstriction causing acute severe pulmonary hypertension, and direct pulmonary capillary damage.
Septic embolism occurs when infected material enters the lungs. Causes include drug use, infective endocarditis of the right valves, and septic thrombophlebitis. Septic embolism causes symptoms and manifestations of pneumonia or sepsis and is initially diagnosed by the identification of focal infiltrates on chest radiography, which may increase peripherally and abscess.
Foreign body embolism is caused by the entry of particles into the pulmonary arterial system, usually due to the intravenous administration of inorganic substances, such as talc by heroin addicts or mercury by patients with mental disorders.
Tumor embolism is a rare complication of malignant neoplasms (usually adenocarcinoma), in which tumor cells from the tumor enter the venous and pulmonary arterial system, where they linger, multiply and impede blood flow. Patients typically present with symptoms of shortness of breath and pleuritic chest pain, as well as signs of cor pulmonale, which develop over weeks to months. Diagnosis that is suspected in the presence of fine nodular or diffuse pulmonary infiltration, can be confirmed by biopsy or sometimes by cytological examination of aspirated fluid and histological examination of pulmonary capillary blood.
Systemic gas embolism is a rare syndrome that occurs during barotrauma during mechanical ventilation with high airway pressure, which leads to the breakthrough of air from the lung parenchyma into the pulmonary veins and then into the systemic arterial vessels. Gas emboli cause central nervous system lesions (including stroke), cardiac lesions, and livedo reticularis in the shoulders or anterior chest wall. The diagnosis is based on the exclusion of other vascular processes in the presence of established barotrauma.
Symptoms of pulmonary embolism
Most pulmonary emboli are small, physiologically insignificant, and asymptomatic. Even when present, symptoms of pulmonary embolism (PE) are nonspecific and vary in frequency and intensity depending on the extent of pulmonary vascular occlusion and preexisting cardiopulmonary function.
Large emboli cause acute shortness of breath and pleuritic chest pain and, less commonly, cough and/or hemoptysis. Massive pulmonary embolism (PE) causes hypotension, tachycardia, syncope, or cardiac arrest.
The most common symptoms of pulmonary embolism (PE) are tachycardia and tachypnea. Less commonly, patients have hypotension, a loud second heart sound (S2) due to an increase in the pulmonary component (P), and/or crackles and wheezes. In the presence of right ventricular failure, there may be clearly visible swelling of the internal jugular veins and bulging of the right ventricle, and a gallop rhythm of the right ventricle may be heard (third and fourth heart sounds)
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