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[Surgical treatment of active infective endocarditis].

OBJECTIVE: To summarize the recent experience of surgical management of the active infective endocarditis (IE) disease in Fuwai Hospital. METHODS: From October 1, 1996 to December 31, 2003, 54 patients with active IE underwent heart operation in Fuwai Hospital. There were 41 males, 13 females, with an average age of 35 years old and an average weight 58 kg. Of the cases, 23 had congenital anomalies of the heart, and 1 had rheumatic valvulitis. Streptococci were found in 20 patients, staphylococci in 3, enterococci in 1, enterococcus in 2 and G(+) cocci in 1. Pre-operative cardiac classification (NYHA): class I was in 6 cases, class II in 12 cases, class III in 7 cases and class IV in 29 cases. Systemic embolization occurred in 23 cases and pulmonary infarction in 2 cases. Emergent operations were performed in 27 cases because of heart failure (8 cases), embolism (4 cases), aggressive infection (3 cases), heart failure plus embolism (2 cases), heart failure with aggressive infection (4 cases), aggressive infection with embolism (2 cases) and all the three factors (4 cases). The operations included aortic valve replacement (25 cases), aortic and mitral valves replacement (15 cases), mitral valve replacement (6 cases), mitral valve repair (3 cases), pulmonic valve replacement (1 case) and intracardiac shunt repair (4 cases). RESULTS: The operative mortality was 17% (5 operative death and 4 lost in following-up after being discharged). All of operative deaths were due to infection. Fourteen patients had operative complications. The morbidity included peri-prosthetic leakage (8 cases), prosthetic IE (5 cases), residual intracardiac shunt (2 cases), complete heart block (2 cases), myocardial infarction, ventricular fibrillation, pulmonary trunk stenosis, and mitral regurgitation (1 case in each). Post-operative cardiac classification (NYHA): class I was in 41 cases, class II in 3 cases, class III in 1 case. Two patients were re-operated because of peri-prosthetic leakage, and then they were cured. Re-operation was also performed in other 3 patients. Unrelated late sudden death occurred in 1 patient and hemiplegia caused by anticoagulant intracranial hemorrhage in another patient. CONCLUSION: Acceptable results can be achieved with active surgical intervention in active patients with IE.

Adolescent↗

Pulmonary angiitis and granulomatosis: a review.

Vasculitis is a clinical-pathological process characterized by inflammation and necrosis of blood vessels. It has been effectively classified by Fauci. Granulomatosis in the lung may be angiocentric or bronchocentric in distribution. The angiocentric forms of granulomatosis and vasculitis include Wegener's granulomatosis, allergic angiitis and granulomatosis of Churg and Strauss, lymphomatoid granulomatosis, and necrotizing sarcoid granulomatosis. Wegener's granulomatosis is a well-defined syndrome characterized by necrotizing granulomatous vasculitis of the upper and lower respiratory tracts, segmental necrotizing glomerulonephritis, and systemic small vessel vasculitis. Allergic angiitis and granulomatosis is a less common multisystem vasculitis with many features similar to polyarteritis nodosa. Lymphomatoid granulomatosis is an angiocentric and angiodestructive lymphoreticular proliferative and granulomatous disease involving predominantly the lungs and resembling lymphoma. Necrotizing sarcoid granulomatosis is probably a variant of sarcoidosis in which an angiitis is a prominent feature. Because the radiology of these diseases can be similar, their important differences are highlighted. The appearance of multiple nodules, often with cavities, and pleural-based consolidations resembling pulmonary infarcts should suggest pulmonary angiitis and granulomatosis, especially if improvement occurs in one area while disease is progressing elsewhere. Bronchocentric granulomatosis is not a primary vasculitis but is discussed because of its similarity to the other diseases.

Adult↗

[Amyloidosis in rheumatoid arthritis--clinical study of 124 histologically proven cases].

The diagnosis of secondary amyloidosis due to rheumatoid arthritis (RA) was confirmed by positive tissue staining using Congo-red and antiserum to amyloid A protein. Biopsied specimens were obtained mainly from gastro-intestinal tracts; small salivary glands of the lips as well as abdominal adipose tissues were also studied in a small number. The results were as follows: 1. Gastro-intestinal fiberscopies and biopsies were performed on 789 RA patients for the purpose of routine screening and follow-up for amyloidosis. Seventy-seven cases (10.5%) turned out positive for amyloid. Among the biopsied specimens taken from three different sites, the proportion of amyloid-positivity was 68.9% for gastric antrum, 76.5% for duodenal cap and 88.6% for the second portion of the duodenum, suggesting the higher sensitivity and efficacy of duodenal biopsy in studying secondary amyloidosis in RA. 2. 124 patients of RA complicated with secondary amyloidosis were studied clinically with special reference to its clinical characteristics and prognosis. (1) The mean duration of RA at diagnosis of amyloidosis was 15.4 years and all patients but two were in stage III or IV (Steinbrocker). (2) Gastro-intestinal symptoms were present in 58.1% of the cases, abnormal renal signs in 58.9%, cardiac symptoms in 39.5%, respectively. All of these findings had a significant association with poorer prognosis in secondary amyloidosis due to RA. (3) The 4-year survival rate of all the cases was 57.8%, while the 3-year survival rate for the group without symptoms and signs about amyloidosis was 100%. (4) The causes of death in 36 cases were renal failure (14 cases), infection (13 cases), cerebral bleeding (2 cases), myocardial infarction (1 case), pulmonary infarction (1 case), suicide (1 case) and unknown (4 cases). Patients with intractable diarrhea were mostly susceptible to the ensuing fatal bacterial infection.

Adult↗

Current status of hemodynamic monitoring: indication, diagnoses, complications.

Indications for hemodynamic monitoring include the need to assess left ventricular function, to estimate patient prognosis, to monitor cardiac performance, to study the cardiac response to drugs, to evaluate new methods of treatment, and to diagnose and treat cardiac dysrhythmias. Diagnoses which may be made or clinically facilitated include cardiogenic shock, hypovolemic shock, right ventricular infarction, ruptured ventricular septum, mitral regurgitation, low cardiac output syndrome, cardiac tamponade, and pulmonary embolism. Potential complications of hemodynamic monitoring include dysrhythmias, balloon rupture, knotting of the catheter, pulmonary infarction, pulmonary artery rupture, infection, and deep vein thrombosis.

Acute Disease↗

Transcatheter occlusion of pulmonary arterial circulation and collateral supply: failures, incidents, and complications.

Failures and complications were analyzed retrospectively in 45 patients treated with embolotherapy or occlusion of pulmonary arterial circulation. Pulmonary arterial branches were occluded with steel coils in 19 patients with pulmonary arteriovenous malformations, 17 with hemoptysis of pulmonary artery (PA) origin, and one with massive parenchymal shunt. Bronchial arterial supply to the lung was embolized with small particles in eight cases of hemoptysis and systemic to pulmonary arterial antegrade shunt secondary to chronic thromboembolism. Asymptomatic incidents included catheterization failures, vascular damage, partial occlusion, partial recanalization of the thrombus, ectopic deposition of a coil, and delayed bacterial contamination of the thrombus. A few cases of transient clinical and radiologic signs of pulmonary infarction were observed after complete occlusion of the PA and bronchial artery embolization. This complication was never observed after complete occlusion of main right or left PA, inferior right or left PA, or segmental branches. The management and prevention of these complications, the role of bronchial arterial collateral pathways, and the importance of the site of PA occlusion in the development of pulmonary infarction are discussed.

Arteriovenous Malformations↗

Iliofemoral vein thrombosis and pulmonary embolism associated with a transient ischemic attack in a patient with antiphospholipid syndrome.

Several clinical conditions, such as deep vein thrombosis, cerebral infarct, pulmonary infarct, skin ulcers, renal failure, and habitual abortion, are thought to be associated with the antiphospholipid syndrome. The authors describe a 32-year-old woman who had characteristics of the antiphospholipid syndrome including increased immunoglobulin G-cardiolipin antibody titers, iliofemoral vein thrombosis, pulmonary embolism, headache, visual disturbances, and habitual abortion. During hospitalization, she suddenly experienced right-sided weakness. A Tc-99m HMPAO brain scan showed the probability of a transient ischemic attack in the left frontotemporal cortex.

Adult↗

Transcatheter closure of a huge pulmonary arteriovenous fistula with embolization coils.

A 46-year-old female with bilateral pulmonary arteriovenous fistulas was treated with Gianturco coil occlusion. The small right lung fistula was closed with a 6 mm coil, whereas the huge left lung fistula was occluded with three coils (one 10-mm and two 8-mm). Angiography 3 d later demonstrated recanalization of the left fistula. Two 8 mm coils were inserted to achieve complete obstruction again. She developed pulmonary infarction in the left lung 2 d later, which recovered without sequelae. We conclude that coil embolization for huge pulmonary arteriovenous fistula is feasible but may result in pulmonary infarction.

Adult↗

Hypoxemia in pulmonary embolism, a clinical study.

The cause of hypoxemia was studied in 21 patients with no previous heart or lung disease shortly after an episode of acute pulmonary embolism. The diagnosis was based on pulmonary angiography demonstrating distinct vascular filling defects or "cutoffs." It was found that virtually all of the hypoxemia in patients with previously normal heart and lungs could be accounted for on the basis of shunt-like effect. The magnitude of the shunting did not correlate with the percent of the pulmonary vascular bed occluded nor with the mean pulmonary artery pressure. The shunts tended to gradually recede over about a month after embolism. Patients without pulmonary infarction were able to inspire 80-111% of their predicted inspiratory capacities, and this maneuver temporarily diminished the observed shunt. Patients with pulmonary infarcts were able to inhale only to 60-69% of predicted inspiratory capacity, and this did not reverse shunting. These data suggest that the cause of right-to-left shunting in patients with pulmonary emboli is predominantly atelectasis. When the elevation of mean pulmonary artery pressure was compared to cardiac index per unit of unoccluded lung, it fell within the range of pulmonary hypertension predicted from published data obtained in patients with exercise in all except one case. This observation suggests that pulmonary vasoconstriction following embolism is not important in humans, although these data are applicable only during the time interval in which our patients were studied and in patients receiving heparin.

Adult↗

Pulmonary gas exchange in acute myocardial infarction with low pulmonary capillary wedge pressure.

To evaluate the clinical characteristic of pulmonary gas exchange in patients with low pulmonary capillary wedge pressure (PCW less than 18 mmHg) in the early phase of acute myocardial infarction, we investigated 48 patients admitted within 24h from the onset of chest pain. The alveolar-arterial oxygen tension difference (AaDO2) and arterial blood gas parameters were obtained while breathing room air on admission. The disturbance of pulmonary gas exchange, as revealed by the high value of AaDO2, existed without left ventricular dysfunction, and AaDO2 had no significant relationship with any of the hemodynamic parameters including the difference between plasma colloid osmotic pressure and PCW. Multiple regression analysis was performed using 9 variables related to pulmonary gas exchange, to identify those which were important. As a result, QRS score (p less than 0.01) and age (p less than 0.05) were identified as significant variables related to AaDO2. Thus, the disturbance of pulmonary gas exchange in patients with low PCW was caused by mechanisms other than left ventricular failure which may reflect the extent of ischemic myocardium.

Aged↗

Wegener granulomatosis: CT features of parenchymal lung disease.

Chest CT from eight patients with pulmonary Wegener granulomatosis were reviewed. The CT features of parenchymal lung involvement included multiple nodules or masses (seven of eight; 88%), ranging in size from 0.3 to 5.0 cm. Lung nodules demonstrated distinct feeding vessels in seven of eight patients (88%); and lesions similar to pulmonary infarcts, i.e., peripheral wedge-shaped lesions abutting the pleura, were identified in seven cases (88%). Scarring, spiculation, and pleural tags emanating from pulmonary nodules were prominent features (seven of eight; 88%). Other findings included cavitation (four of eight; 50%), air bronchograms through nodules (two of eight; 25%), and pleural effusions (two of eight; 25%). One patient on immunosuppressant therapy also demonstrated scattered ground glass infiltrates due to complicating pneumocystis pneumonia. In comparison to corresponding conventional chest radiography, CT examinations revealed more parenchymal lesions in five of eight cases (63%) and bilateral disease instead of unilateral disease in one of eight cases (13%). Feeding vessels were only identified on CT. Wegener granulomatosis is a primary necrotizing granulomatous vasculitis, and when it affects the lung it demonstrates CT features that are similar to other vessel-related disorders of the lung such as septic emboli, pulmonary infarcts, and tumor emboli of hematogenous metastases. We believe that these CT features--nodules with feeding vessels and wedge-shaped lesions abutting the pleura--are related to the necrotizing angiitis that affects pulmonary arteries and veins in this disease.

Adult↗

High prevalence of pulmonary arterial thrombi in donor lungs rejected for transplantation.

BACKGROUND: Donor hypoxemia is a common reason for the rejection of lungs for transplantation. Organ donors are at high risk for venous thromboembolism. Pulmonary arterial thrombosis could contribute to donor hypoxemia. The primary objective of this study was to prospectively quantify the incidence of pulmonary arterial thrombosis in organ donors whose lungs were rejected for transplantation. The secondary objective was to better define the spectrum of histologic abnormalities in the same group of lungs. METHODS: A complete gross pathologic and histologic analysis of whole lung specimens was done on lungs from 17 donors whose lungs were rejected for transplantation. Lungs had not been flushed with a pulmonary preservation solution. RESULTS: Overall, 35% of the donors had gross or microscopic evidence of either pulmonary arterial thrombosis, pulmonary infarction, or both. Clinical characteristics, including oxygenation, were not significantly different between donors who had thrombi or infarction and donors who did not. Other pathologic findings included bronchopneumonia (focal or early in 4/17, moderate or severe in 8/17), respiratory bronchiolitis (7/17) and centriacinar emphysema (7/17). CONCLUSIONS: Pulmonary arterial thrombosis and/or pulmonary infarction are very common in organ donors whose lungs are rejected for transplantation and might contribute to lung dysfunction both in lung donors and lung recipients. Further studies are needed to define the incidence of pulmonary arterial thrombosis in organ donors whose lungs are used for transplantation and to better assess the adverse clinical consequences of donor pulmonary arterial thrombosis in lung recipients.

Adult↗