What Is Lung Infarction?

Pulmonary infarction is the necrosis of the lung tissue caused by the blockage of blood flow after pulmonary embolism. The common emboli causing pulmonary embolism is deep vein thrombosis. Clinical manifestations are chest tightness, shortness of breath, dyspnea, chest pain, low fever, and hemoptysis. It has a sudden onset, a fierce onset, a critical condition, and a high mortality rate. However, it is complicated by clinical manifestations due to secondary to other diseases. It is often easily misdiagnosed as pneumonia, pleurisy, pulmonary edema, atelectasis, etc., and should be identified with it. Pulmonary infarction can be cured by accurate diagnosis and active treatment, such as immediate thrombectomy, thrombolysis or anticoagulation.

Pulmonary infarction

Pulmonary infarction is the necrosis of the lung tissue caused by the blockage of blood flow after pulmonary embolism. The common emboli causing pulmonary embolism is deep vein thrombosis. Clinical manifestations are chest tightness, shortness of breath, dyspnea, chest pain, low fever, and hemoptysis. It has a sudden onset, a fierce onset, a critical condition, and a high mortality rate. However, it is complicated by clinical manifestations due to secondary to other diseases. It is often easily misdiagnosed as pneumonia, pleurisy, pulmonary edema, atelectasis, etc., and should be identified with it. Pulmonary infarction can be cured by accurate diagnosis and active treatment, such as immediate thrombectomy, thrombolysis or anticoagulation.

Introduction to pulmonary infarction

Pulmonary embolism is a common disease. Pulmonary embolism is a pulmonary circulation disorder that occurs after the branches of the pulmonary artery are blocked by emboli. Pulmonary infarction is the necrosis of lung tissue that occurs as a result of blood flow blockage after pulmonary embolism.
Pulmonary infarction is not uncommon. Pulmonary infarction occurs in about 10-15% of pulmonary embolisms. It has a sudden onset, a fierce onset, a critical condition, and a high mortality rate. However, it is complicated by clinical manifestations and secondary to other diseases. And lack of understanding, it is very easy to cause clinical misdiagnosis or imaging misdiagnosis. Misdiagnosis directly affects patients and increases the financial burden on patients. Timely and accurate diagnosis is the key to treatment.

Pathogenesis of pulmonary infarction

Due to the dual supply of blood from the bronchial artery and the pulmonary artery, only a small number of embolisms cause ischemic necrosis of the tissue and cause infarction. Pulmonary infarction is the necrosis of the lung tissue caused by the blockage of blood flow after pulmonary embolism. The common emboli that cause pulmonary embolism are
Pulmonary infarction
Deep vein thrombosis.
The origin of thrombosis is the deep veins of the lower limbs, accounting for 80% to 90%, followed by pelvic, prostate veins and heart disease. Deep venous thrombosis can occur due to chronic bedridden, pregnancy, major surgery and cardiac insufficiency, which is the cause of pulmonary embolism.
The thrombosis of rheumatic heart disease and the thrombosis that originates in the pulmonary artery are also the causes of the disease. The emboli entering the pulmonary circulation can also be fat, tumor emboli, and gas.
The pathological changes of pulmonary embolism depend on the size of the emboli and the state of pulmonary blood circulation.
The size of the emboli ranges from small emboli in the microvessels to riding thrombi in the aorta. Smaller emboli are less likely to cause blood circulation disorders when they fail to completely block blood vessels. Multiple small emboli can cause multiple embolization of small arterial branches, and the main or large branches of the pulmonary artery are blocked by large emboli, which can cause acute right heart failure and cause death. Pulmonary embolism in patients with severe pulmonary congestion can lead to pulmonary infarction.
The lobe below the pulmonary infarction is more common, with a tapered shape and a pointed tip toward the hilum. The center of the lesion is a necrotic area with edema and bleeding around. Edema and bleeding are resorbable, and fibrosis occurs when the necrotic area heals.

Clinical manifestations of pulmonary infarction

The patient became acutely ill, had difficulty breathing, chest pain, and coughing up blood. Hemoptysis indicates a pulmonary infarction. Single branch embolism is mild or without obvious discomfort, large branch or pulmonary artery main embolism, or small branch extensive embolism has severe dyspnea and cyanosis. On auscultation, dry or wet rales can be heard in the lungs. Noise and abnormal heart rate can be heard in the anterior heart area. About 10% of patients with acute pulmonary embolism die within 1 hour of onset. Without timely diagnosis and treatment, approximately 30% of patients die due to recurrent pulmonary embolism. Patients often have chronic heart disease, recent surgery, a history of trauma, thrombocclusive phlebitis, pregnancy, long-term bedridden, hyperviscosity and other causes.

Pulmonary infarction, sudden chest tightness, shortness of breath, and difficulty breathing

Patients often cannot lie supine since their onset, sit and breathe, and have difficulty falling asleep. This is caused by inadequate lung ventilation, hypoxemia, and inability to breathe deeply in chest pain after partial lung tissue infarction.

Pulmonary infarction chest pain

Chest pain is another prominent clinical feature. Sudden acute chest pain is pleural pain. Patients often dare not take deep breaths, cannot lie on the affected side, or even fall asleep. This is due to the supply of blood from the lungs to the visceral pleura and edema and necrosis of the visceral pleura after infarction.

Pulmonary infarction

The body temperature was normal at the time of onset, and then gradually increased, mostly between 38 ~ 38.5 , fell to normal in about 1 week, due to ischemic necrosis of lung tissue. The prominent clinical symptoms, the increased breathing pulse and the low-temperature fever are obvious contradictions. This is another clinical feature of this disease, which is different from general infectious diseases.

Pulmonary infarction

More patients began to cough blood on the second to third day after the onset, from bloodshot sputum to cough purple and black blood clots, which lasted about 3 to 33 days, and more common in 10 to 15 days. Long duration of hemoptysis is another feature of the disease.

Assistant diagnosis of pulmonary infarction

Pulmonary embolism can be examined by plain radiography, angiography, CT and MR, and nuclide scanning.
X-rays of single pulmonary embolism in the small branches of the pulmonary arteries showed no abnormalities, and X-rays of the large branches and multiple small branch embolisms showed abnormal X-rays.
(1) Pulmonary ischemia: When pulmonary lobe or pulmonary segment arterial embolism occurs, the corresponding range of lung texture decreases or disappears, and the transmittance increases, which is called the Westmark sign. Multiple arterial embolism causes extensive pulmonary ischemia.
(2) Pulmonary artery abnormality: The diseased pulmonary artery becomes thicker due to thrombus impaction, and the distal end becomes thinner due to reduced blood flow. SCT shows clear.
(3) Reduced lung volume: Lower lobe pulmonary embolism is more common, so lung volume reduction is also common in the lower lobe, causing elevated ridges and lower hilar and interlobular fissures. And can be combined with disc atelectasis.
(4) Heart shadow enlargement: Heart shadow enlargement is caused by enlargement of right ventricle, which is seen in embolism of large pulmonary artery or multiple pulmonary embolism.
X-ray, SCT and MRI can be identified.
Angiography, nuclide scans, etc. can also help with diagnosis.
D-dimer negative can exclude acute PTE, positive is not a specific test for PTE

Differential diagnosis of pulmonary infarction

This disease is often misdiagnosed as pneumonia, pleurisy, pulmonary edema, atelectasis, etc., and should be identified.
Pneumonia patients have fever first, symptoms of systemic poisoning are obvious, body temperature, pulse, and breathing increase synchronously, chest pain is mild, rust-colored sputum has a short duration, rapid absorption after treatment, no acute pulmonary heart disease, no hilar truncation sign, and is different from pulmonary infarction. There was no cone consolidation in the pleurisy and no symptoms of hemoptysis. Pulmonary edema is mostly bilateral, with no severe chest pain, no hilar truncation, and cone consolidation. It is absorbed quickly after treatment and is different from pulmonary infarction.
Because pulmonary infarction mostly occurs in patients with cardiopulmonary disease, if pulmonary heart disease, pulmonary congestion, and pulmonary edema are seen on the chest radiograph at the same time, the possibility of the lung becoming pulmonary infarction should be considered. In patients without cardiopulmonary disease, pulmonary infarction can cause pulmonary hemorrhage without pulmonary infarction. At this time, the X-ray manifestation of pulmonary hemorrhage is not easy to distinguish from pulmonary infarction. Beware that no other significant changes in the lungs may indicate a high possibility of pulmonary hemorrhage. Pulmonary hemorrhage alone can completely disappear in 7-10 days or less, and there are no residual traces. The resolution of pulmonary infarction is relatively slow. It takes about 20 days on average and can last up to 5 weeks. In most cases, fibrous scars can remain. Striped shadows.

Prevention of pulmonary infarction

More than half of the lung emboli come from veins in the lower limbs. In addition, emboli in the pelvic cavity, iliac vein, and right atrium can cause pulmonary infarction. Therefore, if patients with deep phlebitis of the lower limbs, fractures, childbirth, postoperative surgery, or history of atrial fibrillation, etc., should not be paralyzed once they have symptoms similar to pneumonia, they should go to the hospital for early diagnosis and active treatment, such as immediately Embolization
Pulmonary infarction
Pulmonary infarction can be cured with thrombolytic or anticoagulant treatment.
The elderly have high blood viscosity, slow blood flow, and trauma to the lower limbs, especially after fractures, will cause the blood vessel wall to be non-smooth. If you stay in bed for a long time after surgery, thrombosis in the lower limbs or pelvis is likely to occur, and emboli may cause pulmonary infarction. Therefore, patients with fractures, especially elderly patients undergoing surgical treatment after fractures of the lower limbs, should get up as soon as possible after surgery. Patients who need to stay in bed for a long time can often take deep breaths and move their lower limbs in bed (or with the help of family members) to prevent venous embolism. For patients who have been diagnosed with venous embolism in the lower limbs, the emboli in the body are like time bombs, and they may fall off at any time and cause pulmonary infarction. Therefore, in addition to the active treatment of patients, patients should often change their positions, do not sit still for a long time, so as to avoid pulmonary infarction.

Typical cases of pulmonary infarction

1. There was a 73-year-old uncle Wang who sat cross-legged and played Mahjong all afternoon. When he stood up, he suddenly felt severe pain in his left chest, especially when he deflated, and did not dare to gasp. Uncle Wang didn't care. Until two days later, he vomited a few mouthfuls of blood before going to the hospital for treatment. After pulmonary CT and pulmonary angiography, the doctor was diagnosed with pulmonary thromboembolism. After three days of hospitalization, Mr. Wang Bo's calf swelled. Doppler ultrasound examination revealed embolism in the deep vein of the left lower extremity. It turned out that the pulmonary infarction detected three days ago was caused by venous thrombosis of the lower extremities.
2. The 77-year-old Professor Zhang accidentally fell while walking, causing a fracture of the femoral neck of his left lower extremity, and rested in bed for several months. One day, a nurse had a lower limb massage while talking with Professor Zhang. The professor suddenly developed chest tightness, shortness of breath, and died after rescue. At first the doctor thought that Professor Zhang had died of a myocardial infarction, but after autopsy it was discovered that the old professor died of a pulmonary infarction, and those emboli that affected the lungs were formed due to a lack of exercise for a long time after a fracture of the lower limb.
3, Bayi women's basketball player Wang Fan died on February 15, 2010 due to pulmonary infarction, at the age of 26. Wang Fan suddenly fainted in the training before the Bayi Women's Basketball Team against the Beijing Women's Basketball Team on January 24. According to teammates, "At the time the team started to warm up and did not have much physical activity, Wang Fan suddenly fainted." After emergency rescue, Wang Fan woke up. But after entering the hospital, Wang Fan went to the bathroom only once and fell into a coma. Until February 15, Wang Fan left the world. After the death of Comrade Wang Fan, in view of the actual situation and peacetime performance of her sacrifice in the WCBA competition, the General Political Department of the PLA approved Wang Fan as a "revolutionary martyr."

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