Pulmonary arteriovenous malformation

The lungs are the most important part of the human body. Once a disease occurs, it is difficult to treat and even more difficult to recover. Therefore, attention should be paid to timely treatment. Everyone's physical condition is completely different, so the lung disease problems are also different. Then pulmonary arteriovenous malformation should be a more serious problem, so proper attention should be paid to treatment. It’s just that people often find that lung infections are treated according to their own conditions, so what should be done about pulmonary arteriovenous malformations?

Pulmonary arteriovenous malformation (PAVM) is a typical disease caused by congenital developmental abnormalities. About 70% of PAVM patients have hereditary hemorrhagic telangiectasia. Genetics suggests that chromosomal abnormalities may lead to the disease. Some authors also believe that PAVM may be caused by trauma, schistosomiasis and tumors. The basic pathological change is that the artery directly passes into the enlarged vein through a thin aneurysmal sac.

Treatment

Traditionally, it is believed that not all PAVMs require treatment. Treatment is warranted only in patients with progressive lesions, paradoxical embolism, and symptomatic hypoxemia. However, recent studies have found that many asymptomatic patients or patients with minimal lesions may also develop serious neurological complications (such as stroke, brain abscess, etc.). Therefore, White et al. advocate that all PAVMs patients with a feeding artery diameter ≥ 3 mm should be treated regardless of whether they have symptoms or not. The purpose of treatment is to improve symptoms of hypoxia and prevent the occurrence of serious complications such as stroke, brain abscess, and hemoptysis. The current methods for treating PAVMs include surgery, transcatheter embolization, and drug therapy. The various methods are summarized as follows:

Surgery is a radical treatment measure. The surgical indications include: single solitary PAVMs with symptoms, large shunt volume and HHT, regardless of complications; multiple PAVMs, lesions limited to one lobe or one side of the lung; diameter A2. Murmur: 3/6SM can be heard at the apex and L2. Routine blood test: White blood cell count: 2.04/L, severe anemia.

X: Cystic masses with smooth edges and multiple lobes were observed in the posterior basal segments of the right middle and lower lobes of the lung, and were closely related to the pulmonary vessels. No consolidation was observed in the rest of the lung. Heart-chest ratio: 0.65. Multiple pulmonary arteriovenous fistulas were considered. On February 21, 2002, right lower pulmonary arteriovenous fistula closure was performed.

Occlusion process: Under local anesthesia, the right femoral vein was punctured, and a 12F delivery sheath was inserted into the right lower pulmonary artery trunk. A 30mm diameter domestic LifeTech ASD occluder was selected to occlude the proximal right lower pulmonary artery and the arterial end of the giant aneurysm sac. The femoral artery blood oxygen saturation immediately increased from 65% before the operation to 93%. Then pulmonary angiography was performed, which showed that a pulmonary artery branch in the anterior segment of the right upper lung was still affected, and the tumor sac was visible. The diameter of the proximal pulmonary artery was about 13 mm. Therefore, a 9F delivery sheath was placed proximal to the branch and the tumor sac, and a 14/12 diameter domestic LifeTech PDA occluder was selected to occlude the distal end of the branch. The femoral artery oxygen saturation rose again to 97%; repeated pulmonary angiography showed no visualization of the tumor sac. The operation went smoothly, the patient did not complain of discomfort, and 150 ml of iodine was used in total.

Blood oxygen saturation: before occlusion: 65%; after occlusion: 97%.

Pulmonary artery pressure: before occlusion: 30/10(18); after occlusion: 37/17(25).

Second Zhang Huan: Female, 16 years old, had heart murmur and cyanosis since childhood. He underwent pulmonary artery fistula embolization three times between 1997 and 2002. In January 2002, the right pulmonary artery (right lower pulmonary artery trunk) was occluded with an AGA16/14mm occluder. After the occlusion, the blood oxygen saturation was 84%. Today, the symptoms of paroxysmal chest tightness and shortness of breath have worsened, so I sought treatment again. In April 2004, the aorta was occluded again with AGA26mmASD occluder.

Pulmonary angiography + right pulmonary artery fistula embolization was performed under local anesthesia. The bilateral right femoral veins were punctured, a 6F sheath was inserted, and angiography was performed through the right femoral vein, which showed extensive arteriovenous fistula in the right pulmonary artery. After angiography with a 6F pigtail tube inserted through the left femoral vein, a 26mm ASD occluder was selected. There were no adverse reactions during the trial occlusion and no increase in pulmonary artery pressure.

Pulmonary artery pressure: 20/16 before embolization (19), 35/10 after embolization (22)

Pulmonary artery blood oxygen: 75.6% before embolism; 90% after embolism.