Pulmonary embolism is a common condition, the exact incidence of which has not been reported and is estimated at 300,000-650,000 patients per year in the United States. The emboli of pulmonary embolism mainly originate from the deep veins of the lower extremities (VTE), and the incidence of VTE is approximately 1/1000 in the population. The incidence of pulmonary embolism increased from 13.9/100,000 in 2001 to 18.9/100,000 in 2007, with 59% of women and 41% of men. More than half of the patients were over 70 years of age (2). There is no accurate epidemiological data in China, but pulmonary embolism is also a relatively common disease in China, with a high rate of underdiagnosis and high untreated mortality, which can be significantly reduced in those with clear diagnosis and active treatment. Chronic pulmonary embolism can cause embolic pulmonary hypertension with poor prognosis. Life expectancy is 3 years when pulmonary artery pressure exceeds 50 mmHg, and surgery is the only effective method. Five patients with chronic embolic pulmonary hypertension have undergone pulmonary artery endarterectomy, and four cases have good results.
Symptoms of pulmonary embolism: Depending on the extent of embolism, pulmonary embolism can be asymptomatic or have typical clinical manifestations such as shortness of breath and chest pain. If the embolism is extensive, it may cause blood pressure drop, shock, or sudden death.
Pulmonary embolism can be divided into acute and chronic depending on the time, acute pulmonary embolism within 2 weeks of onset and chronic over 2 weeks. Most of the acute pulmonary embolism will not turn into chronic because the body’s own thrombolytic mechanism can dissolve the thrombus, which is usually treated with warfarin or heparin anticoagulation for 3-6 months.
Some patients with recurrent pulmonary embolism, even with warfarin or heparin anticoagulation therapy, need to place a device in the inferior vena cava.
When the embolus does not dissolve completely and lasts for more than two weeks, it becomes chronic pulmonary embolism, and the thrombus can be mechanized and fibrotic in the pulmonary vasculature, then continued thrombolytic therapy will no longer work.
Diagnosis of chronic pulmonary embolism.
1 Patient’s symptoms: shortness of breath, or dyspnea
2. Echocardiography: elevated pulmonary artery pressure can be detected
3. Pulmonary CT examination: filling defect, wall thickening and lumen narrowing in the pulmonary artery can be found.
4. Pulmonary arteriogram: It is the most definite diagnostic tool, which can clarify the scope and size of embolism.
When chronic pulmonary embolism is formed, due to the reduction of pulmonary vascular bed, which makes the right heart ejection blood to the lung decrease and the return blood flow to the left heart decrease, together with the reactive pulmonary vasoconstriction and the release of inflammatory factors and other factors, it will cause the increase of pulmonary artery pressure and pulmonary vascular resistance, and this increase will gradually aggravate with time, the patient will have shortness of breath and fatigue, medication may delay the time but cannot prevent it. The treatment option available to many patients in this situation is to continue medication, but when is the end? What does the future hold for him/her? This is also a difficult question for many doctors to answer. This is because traditional surgical treatment has affected and confused many physicians and surgeons due to the high risk of mortality. A welcome turnaround came from the decades-long efforts of cardiac surgeons at San Diego Hospital across the ocean, who reported in 2012 in Ann Thrac Surg, a specialized journal in cardiac surgery, the results of 2700 cases of pulmonary endarterectomy for chronic pulmonary embolism with pulmonary hypertension, with a mortality rate reduced to about 2.2% (3). So which patients with chronic pulmonary embolism pulmonary hypertension are suitable for surgical treatment?
Typing of chronic pulmonary embolism: Patients with chronic pulmonary embolism can be divided into four types according to the embolism involving the pulmonary artery.
Type 1: about 30%, with fresh thrombus in the main pulmonary artery and lobar pulmonary arteries.
Type 2: about 60%, with proximal involvement of pulmonary segmental arteries, with thickening and fibrosis of the intima, with or without mechanized thrombus.
Type 3: about 10%, involving distal or subpulmonary segmental arteries, with thickening and fibrosis of the intima, with reticular changes of the intima, with or without mechanized thrombus.
Type 4: Distal small pulmonary artery vasculopathy without visible thromboembolic lesions.
Current status of foreign treatment of chronic pulmonary embolic disease.
Most of the early patients at San Diego Hospital were type 1,2 patients. With experience, the number of type 3 patients has gradually increased, and most of the recent 500 patients were type 3 patients (3). In other words: type 1,2 and 3 patients can be treated surgically.
Surgical risks: The main one is the postoperative pulmonary edema, caused by the massive increase in pulmonary blood flow after evacuation. Its occurrence is unpredictable and increases with the severity of the disease. The mortality rate is usually in the range of 5-10%. The risk of surgery is also related to the experience of the surgeon, anesthesiologist, and ICU physician.
The procedure is usually performed under extracorporeal circulation, with systemic hypothermia to deep hypothermia, and decompression is necessary to allow for clear and complete removal of the diseased tissue when stripping the mechanized thrombus from the arteries in the pulmonary segment.
Postoperatively, the patient usually requires sedation and remains asleep for several days to allow the lung tissue to adjust to the new blood flow state.
The vast majority of patients have a good prognosis, with significant reduction or complete resolution of symptoms, a decrease in pulmonary artery pressure, improved right heart function, and after a few weeks, they are no longer dependent on oxygen, and the patient’s exercise tolerance increases significantly. Follow-up of 3-5 years has been reported in the literature, with variable deterioration in a minority of patients (18.8%) (4).
Patients require lifelong anticoagulation with warfarin after surgery.
Current status of domestic treatment of chronic pulmonary embolic disease: A few cardiac centers in Beijing, Shanghai and individual hospitals in Guangxi, Guangdong have performed this type of surgery (5-16), but the total number of reported cases is small and the results are still somewhat different from those reported abroad.
The surgeries are performed via a median incisional route, with extracorporeal circulation applying deep hypothermia with low flow and intermittent stopping circulation. Before blocking the ascending aorta, both pulmonary arteries should be carefully released and freed, and the right pulmonary artery should be freed to the opening of the right inferior pulmonary artery, and each pulmonary artery can be covered with small elastic tape to increase the exposure. The left pulmonary artery may be free to the left upper pulmonary artery branch. It is more convenient to position the operator on the opposite side of the operating lung, e.g., on the left side of the patient for right pulmonary artery dissection, and on the right side for left-sided surgery. The right side of the incision starts at the right pulmonary artery trunk and reaches the beginning of the right inferior pulmonary artery, starting with the arterial trunk to peel away the thickened intima. It is important to carefully identify the correct plane, as too shallow may result in incomplete dissection, while too deep may damage the pulmonary vessel wall and lead to postoperative intrapulmonary hemorrhage. Once the correct plane is found, the arteries can be separated downward along this plane until they are inside each pulmonary segment artery. By pulling the stripped tissue outward, the subpulmonary segment artery can be reached, and the tip of the stripped intima can be seen in a bird’s beak shape when the stripping reaches the end. The left pulmonary artery was stripped in the same way. A small stripper with suction function is needed because the pulmonary artery will continue to rebleed when the circulation is stopped, affecting the visual field. The time required for dissection varies slightly depending on the patient’s condition and usually takes about 30 minutes per side. We performed two stop cycles of 15-20 minutes on each side, with recovery times arranged on a 1:1 basis. The minimum temperature was 200 C. The aortic block time was 138-173 min. All patients were able to stop the extracorporeal circulation successfully after rewarming, and the circulation was stable, requiring only low-dose vasoactive drugs. The ventilator was used for 3-5 days postoperatively, and the tracheal intubation was removed only when the oxygenation was normal. Sedation, hyperventilation, alkalinization and other treatments to prevent pulmonary hypertension are done during the period of ventilator use. Various drugs to lower pulmonary arterial pressure can also be applied, such as inhaled NO, intravenous application of prostacyclin, transgastric tube injection of vancomycin, etc. Most patients recovered successfully. The shortness of breath disappeared after activity, all the pulmonary artery pressure decreased significantly, the enlarged right atrium and right ventricle all became smaller, and the cardiac function recovered to grade 1-2.
Figure 1: A sample of left pulmonary artery endothelial denudation (omitted)
When is the appropriate time for surgery?
The information reported by San Diego Hospital in the United States shows that their operative mortality rate has been reduced to about 3%. The reasons for the high surgical mortality rate reported in China (9-12,14) should be multifaceted, including the problem of surgical skill, equipment conditions, level of postoperative ICU monitoring, etc. One important factor is the condition of the patient selected. Tiago Hospital reported an average preoperative pulmonary vascular resistance of 719±383dynes/sec/cm (-5) in their patients; the average pulmonary artery pressure was 45±11.6.