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Upper Lobe (upper + lobe)
Kinds of Upper Lobe Selected AbstractsReoperative Grafting of the LAD System Using the LAST Approach: Technical DetailJOURNAL OF CARDIAC SURGERY, Issue 6 2000Marco Ricci M.D., Ph.D. In such cases, however, the left upper lobe of the lung and the lingula may exert unwanted traction on the newly constructed coronary graft. Herein, we describe a detail of technique that eliminates this inconvenience. [source] Paralysis in the left phrenic nerve after living-donor liver transplantation for biliary atresia with situs inversusLIVER TRANSPLANTATION, Issue 11 2008Yukihiro Sanada A 7-month-old boy with biliary atresia accompanied by situs inversus and absent inferior vena cava (IVC) underwent living-donor liver transplantation (LDLT). Because a constriction in the recipient hepatic vein (HV) was detected during the preparation of the HV in LDLT, a dissection in the cranial direction and a total clamp of the suprahepatic IVC was performed, and the suprahepatic IVC and the graft HV were anastomosed end-to-end. Postoperatively, atelectasis in the left upper lobe and ventilator failure accompanied by an elevation of the left hemidiaphragm were observed and mechanical ventilation was repetitively required. Paralysis in the left phrenic nerve was diagnosed by chest radiograph and ultrasonography. In our patient, conservative treatment was administrated, because weaning him from mechanical ventilation was possible a few days after intubation and the ventilator function was expected to be improved with growth. The disease course was good, and he was discharged from the hospital at 78 days after LDLT. Complications of paralysis in the phrenic nerve after cadaveric liver transplantation have been reported to be high. Although using a conventional technique during the reconstruction of the HV may injure the phrenic nerve directly, use of the piggyback technique with preservation of the IVC is rare. Even if LDLT was undertaken, a dissection of the HV or a total clamp of the suprahepatic IVC as a conventional technique can directly injure the phrenic nerve. Therefore, a dissection of the HV or a total clamp of the suprahepatic IVC at the reconstruction of the HV in LDLT should be carefully performed, and the possibility of paralysis in the phrenic nerve should be considered in patients with a relapse of respiratory symptoms and an elevation of the hemidiaphragm after LDLT. Liver Transpl 14:1659,1663, 2008. © 2008 AASLD. [source] Pulmonary capillary hemangiomatosis incidentally detected in a lobectomy specimen for a metastatic colon cancerPATHOLOGY INTERNATIONAL, Issue 6 2006Suzuko Moritani Pulmonary capillary hemangiomatosis is a rare vascular proliferative disease of unknown etiology. The common clinical features are slowly progressive and finally fatal pulmonary hypertension. The clinical diagnosis is usually difficult. Because most reported cases are of autopsy, little is known about its incipient lesion and natural history. Presented herein is a case of pulmonary capillary hemangiomatosis incidentally detected in a surgically resected lung for a metastatic colon cancer. The patient was a 60-year-old Japanese woman with a history of sigmoid colon cancer 3 years previously. The patient had undergone a right lower lobectomy for a metastatic tumor in the hilar region and a thoracoscopic tumorectomy of the peripheral area of the left upper lobe. Except for an episode of hemoptysis 2 weeks prior to the lung surgery, there were no other clinical symptoms characteristic of pulmonary capillary hemangiomatosis. The non-tumor area of right lower lobe showed multiple foci of capillary proliferation affecting alveolar walls, interlobular septa and pleura associated with patchy hemorrhage. There was a minor degree of vascular and bronchial involvement by capillary proliferation. It is suggested this particular case is an incidentally detected clinically incipient stage of pulmonary capillary hemangiomatosis. Passive congestion secondary to metastatic colon cancer in the hilar region may have contributed to the pathogenesis of this lesion. [source] Case for diagnosis: 4-month-old infant with increasing cough, hemoptysis, and anemiaPEDIATRIC PULMONOLOGY, Issue 9 2007D. Snijders MD Abstract A 4-month-old caucasian infant presented non-productive cough, fever associated with hemoptysis, and increasing anemia. He had mild tachypnoea; routine lab tests were normal. The thoracic HRCT scan showed a very large mass in the right lung adherent to the thorax wall, well defined and limiting the medium and upper lobe; the mass was well vascularized, and with central hypodensic areas. Fiberoptic bronchoscopy and bronchoalveolar lavage (BAL) cytology were normal. The definitive histology of the mass showed the presence of inflammatory cells admixed with fibroblasts and rare Touton giant cells in the lesion suggestive of a juvenile xanthogranuloma (JXG) of the lung. Pediatr Pulmonol. 2007; 42:844,846. © 2007 Wiley-Liss, Inc. [source] Congenital lobar emphysema: Differential diagnosis and therapeutic approachPEDIATRICS INTERNATIONAL, Issue 5 2008Refik Ulku Abstract Background: Congenital lobar emphysema (CLE) is a rare anomaly of lung development that usually presents in the neonatal period with respirator distress and pulmonary lobar hyperinflation. It is commonly confused with pneumothorax. The aim of the present paper was to review the authors' experience in order to emphasize the importance of differential diagnosis with pneumothorax. Methods: Children with CLE treatment at Department of Thoracic Surgery, Dicle University School of Medicine, Turkey, between January 1993 and June 2004, were reviewed. Results: Ten children consisting of six boys and four girls (age range, 6 h,12 months) had CLE. Major presenting symptoms were tachypnea(n = 100%) and respiratory distress in (n = 80%). On chest radiograph, emphysema was seen in all patients, and shift-herniation to the opposite lung, atelectasis were observed. Computed tomography was performed in all patients, which indicated emphysema in the affected lobes in all cases. Pulmonary perfusion scan was performed in two patients, showing loss of perfusion in the affected lobe. The most common affected lobe was the left upper lobe (50%). In the present series, three patients were mistakenly diagnosed as pneumothorax and intercostal drains were inserted in the emergency department. Eight patients underwent lobectomy, and postoperative course was uneventful. Two patients were followed conservatively. Emphysema was detected in all pathological specimens. One patient was lost to follow up. Mean follow-up duration of all patients was 26.8 ± 29.24 months (range, 1,89 months). Conclusions: CLE is established on combined clinical, radiological and scintigraphic imaging. Surgical excision of the affected lobe is the appropriate treatment. Particularly, differential diagnosis should be made between CLE and pneumothorax. [source] A case of pulmonary arteritis with stenosis of the main pulmonary arteries with positive myeloperoxidase-antineutrophil cytoplasmic autoantibodiesRESPIROLOGY, Issue 4 2000Hiroyuki Nakayama A 53-year-old woman was referred to our hospital with the main symptoms of productive cough, fever and exertional dyspnoea. Chest X-ray revealed enlargement of the left hilar shadow and cavitary infiltration in the right upper lobe. 99mTechnetium-macroaggregated albumin (99mTc-MAA) perfusion scintigram showed complete hypoperfusion through the entire right lung. A pulmonary angiogram revealed stenotic lesions in the right and left main pulmonary arteries. Right cardiac catheterization showed an elevated right ventricular systolic pressure. There was no evidence of systemic arterial lesions nor vasculitis. The patient was positive for myeloperoxidase (MPO)antineutrophil cytoplasmic autoantibodies (ANCA) (168 EU). The Mycobacterium avium complex sputum culture was positive. The pulmonary stenotic lesions were surgically resected. The resected pulmonary arterial lesions were pathologically diagnosed as non-specific vasculitis. The cavitary lesion disappeared 6 months after the surgery. Two years after the surgery, although the MPO-ANCA level had decreased to 12 EU, stenosis of the pulmonary arteries reappeared. It is suggested that the patient became positive for MPO-ANCA in association with the Mycobacterium avium complex infection, and that the presence of MPO-ANCA may not be related to the development of pulmonary stenosis of the main pulmonary arteries. [source] Intravascular ultrasound imaging of the pulmonary arteries in primary pulmonary hypertensionRESPIROLOGY, Issue 1 2000Takaaki Nakamoto Objective: Intravascular ultrasound has the unique ability to provide cross-sectional images of the arterial wall. This study examined intravascular ultrasound (IVUS) images of the proximal pulmonary arteries in primary pulmonary hypertension (PPH). Methodology: Study 1: Specimens from four patients who had died of PPH (in vitro PPH group) were compared with those of three patients who had died of subarachnoid haemorrhage but had no evidence of cardiopulmonary disease (in vitro control group). Three-centimetre segments of the following levels were examined by IVUS: pulmonary trunk, eight secondary branch arteries of the upper, middle, and lower lobes of both lungs, and the thoracic descending aorta. Study 2: Four patients with PPH (in vivo PPH group) and five patients without pulmonary hypertension and no evidence of cardiopulmonary disease (in vivo control group) were examined. The IVUS images of the apical segmental artery of the right upper lobe and the descending branch of the right pulmonary artery were studied. Results: Echographic examination of formalin-fixed preparations of secondary branch sections of the pulmonary artery failed to show a clear three-layer structure in the in vitro control group (24 preparations), but a distinct three-layer structure and increased vessel wall thickness were observed in the in vitro PPH group (32 preparations). Similar findings were obtained in the in vivo study. The mean echo density of the proximal pulmonary arterial wall correlated well with the mean pulmonary arterial pressure (mPA) in the in vitro PPH, and also correlated with the mPA in the in vivo study (r = 0.960, P < 0.0001). The echo intensity of secondary branch sections of the pulmonary artery was higher in the in vitro PPH group than in the in vitro control group (180.5 ± 27.0 vs 132.5 ± 26.7 counts, P < 0.001); similar results were obtained in the in vivo study (144.7 ± 23.4 vs 85.0 ± 14.3 counts, P < 0.01). Conclusions: These results suggest that the histological changes detected in the pulmonary artery walls in the PPH group were responsible for the increased echo intensity. [source] | ||||||||||