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Query: UMLS:C0019079 (hemoptysis)
6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

OBJECTIVE: To report a fatal outcome from pulmonary hemosiderosis in an infant with scimitar syndrome after prolonged pulmonary vasodilator therapy. DESIGN: Case report. SETTING: A tertiary care pediatric intensive care unit. SUBJECT: An infant with scimitar syndrome. INTERVENTIONS: Treatment included redirection of anomalous right pulmonary venous drainage and closure of atrial septal defect, assisted ventilation via tracheostomy, and protracted nitric oxide and prostacyclin therapy until his death at 1 yr of age. RESULTS: Inhaled nitric oxide (iNO) and/or prostacyclin (PGI(2)) were administered for 6.5 months. Numerous echocardiograms demonstrated good control of pulmonary pressures and no evidence of pulmonary venous obstruction. Repeated attempts to slowly wean from the pulmonary vasodilators resulted in return of pulmonary pressures to systemic levels. Although there was no clinically apparent hemoptysis, pulmonary infiltrates worsened, prompting an open-lung biopsy that revealed pulmonary hemosiderosis. During the last 4 days of the patient's life, the pulmonary hypertensive crises with suprasystemic pressures and pulmonary infiltrates worsened regardless of aggressive vasodilator therapy with iNO, PGI(2), alkalinization, and isoproterenol. Vasodilator therapy was withdrawn and the patient rapidly died. CONCLUSION: We achieved long-term control of pulmonary hypertension with iNO and/or PGI(2) without apparent tachyphylaxis or other major reported side effects. Although pulmonary hypertension was successfully controlled with prolonged iNO and intravenous PGI(2) administration in this patient with scimitar syndrome, the patient died of hypoxemic respiratory failure from pulmonary hemosiderosis. Early evaluation of roentgenographic infiltrates for hemosiderosis and potential lung transplantation in similar patients may be warranted.
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PMID:Pulmonary hemosiderosis in scimitar syndrome after prolonged management of pulmonary hypertension. 1279 55

A 27 year old man with hereditary haemorrhagic telangiectasia who developed progressive liver dysfunction underwent living related right lobe transplantation. Pulmonary arteriography did not reveal arteriovenous malformation or abnormal intrapulmonary venous channels. The postoperative course was characterised by persistent hypoxaemia and respiratory failure developed. On day 6, a massive haemoptysis developed and the patient died shortly thereafter. The native liver showed a nodular pseudocirrhotic transformation, with highly dilated and irregularly interconnected vein-like or arterial-like structures in the fibrous septa. Pathological examination of both lungs showed irregular thickening of the wall of the arteries, secondary to eccentric and/or concentric myointimal hyperplasia. This case suggests that massive haemoptysis can develop even when arteriovenous malformations are undetectable by pulmonary arteriography, and it questions the role and the appropriateness of living donor liver transplantation in high risk patients.
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PMID:Massive haemoptysis after living donor liver transplantation. 1460 Jan 39

OBJECTIVE: To alert pediatricians about the possibillity of childhood Idiopathic Pulmonary Hemosiderosis, in cases of anemia associated with chronic lung disease. METHODS: This article documents a case of Idiopathic Pulmonary Hemosiderosis in a 6 year-old child, with histopathological documentation, and reviews it against published literature. RESULTS: A 6 year-old child with history of anemia and lung disease characterized by wheezing, recurrent pneumonia and digital clubbing was admitted to the hospital for investigation, where he suffered sudden respiratory failure and hemoptysis.He was submitted to a lung biopsy which showed a histopathological diagnosis compatible with pulmonary hemosiderosis. Therapy with high doses of corticosteroids was initiated with a good early response. After two and a half months of therapy he had a new bleeding episode, culminating in death. CONCLUSIONS: Idiopathic Pulmonary Hemosiderosis should be included as a possible diagnosis of children with anemia and chronic lung disease. This case is a good example.
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PMID:[Idiopathic pulmonary hemosiderosis: case report] 1464 89

To determine the prognostic factors associated with severity and death of leptospirosis, the authors conducted a hospital based cross sectional study by collecting data of adult patients that were admitted to Phrae Hospital for leptospirosis from 1998 to 2001. The serology was confirmed with a microscopic agglutination test (MAT). The variables obtained from the history, examination, behavioral risks, investigations, and initial treatment especially the data of the first day of admission were examined for association with severity. Of 362 patients, 214 were classed as nonsevere patients, 81 were severe with complications (serum creatinine > or = 3 mg/dl and/or patients with respiratory failure) and 67 died. Multivariate logistic regression demonstrated that five factors were independently associated with severity: hemoptysis, platelet count (Plt) < 100,000/mm3, total bilirubin > 2.5 mg/dl, white blood cell count > 13,000/mm3 and hematocrit (Hct) < 30 per cent. Five factors associated with mortality are: respiratory failure (or respiratory rate; RR > 24/min), hemoptysis, oliguria, metabolic acidosis (or bicarbonate < 20 mmol/l) and thrombocytopenia (or Plt < 100,000/mm3). Identification of these factors might provide useful selection criteria for patients who need early admission or transfer to the intensive care unit.
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PMID:Prognostic factors associated with severe leptospirosis. 1465 Jul 4

Bronchiectasis is primarily the result of airway injury and remodeling attributable to recurrent or chronic inflammation and infection. The underlying etiologies include autoimmune diseases, severe infections, genetic abnormalities, and acquired disorders. Recurrent airway inflammation and infection may also be the result of allergic or immunodeficiency states such as allergic bronchopulmonary mycoses or HIV/AIDS. Bronchiectasis should be included in the differentiation diagnosis of any patient with chronic respiratory complaints such as cough and sputum production. Early clinical manifestations may be subtle. Hallmarks of severe bronchiectasis include fetid breath, chronic cough, and sputum production. The associated chronic respiratory infections and airway sepsis are punctuated by episodes of acute exacerbation. Prompt recognition and treatment of bronchiectasis may allow for prevention of disease progression and irreversible loss of lung function. This review of severe non-cystic fibrosis bronchiectasis describes the current pathophysiology, clinical presentations, and management of bronchiectasis. We review how impaired airway clearance and the inability to resolve infection and inflammation creates a vicious cycle of recurrent injury. The common clinical features of bronchiectasis and findings are presented and illustrated by radiographic images. The common species and significance of various organisms often recovered from the distal airways including: tuberculous and environmental mycobacteria, aspergillus, and bacteria such as Pseudomonas aeruginosa will be covered. Management strategies including sputum surveillance, sputum clearance, antimicrobial therapy including antifungal and antimyobacterial agents as well as the evidence for the use of inhalational and anti-inflammatory therapies such as corticosteroids are also discussed. Recommendations for the work-up and therapy of complications including hemoptysis and respiratory failure are presented.
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PMID:Severe bronchiectasis. 1471 69

Around 1 in 1,000 adults in the UK has bronchiectasis, a potential outcome of various underlying lung diseases. It results from a 'vicious circle' of recurrent infection, inflammation, excessive mucus production, reduced mucociliary clearance, and dilatation and destruction of bronchi. Associated damage to blood vessels can lead to haemoptysis, which is usually slight, but may be severe. Bronchiectasis may be limited to one area (localised) or be more widespread (generalised). It can reduce lung function and quality of life, and may lead to respiratory failure and premature death. Here we review the management of patients with bronchiectasis.
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PMID:Management of bronchiectasis. 1472 94

Pulmonary aspergilloma is a saprophytic form of aspergillosis, and the diagnosis is usually based on radiological findings such as thickened cavitary wall and fungus ball, and on positive serum antibody. Up to 58% of the patients with aspergilloma in Japan have medical history of tuberculosis. Serum anti-Aspergillus antigen is almost always positive in aspergilloma patients but aspergillus antigen is usually negative. Massive hemoptysis can be a fatal complication of aspergilloma, and the most common complication was respiratory failure according to our study. Surgical resection is the only promising intervention to cure the aspergilloma, however, low pulmonary function does not allow operation. Antifungal treatment is chosen for those who are out of operation indication, but the efficacy of antifungal treatment against aspergilloma is controversial. Some patients with aspergilloma show progressive form, and we define such aspergillosis as CNPA, chronic necrotizing aspergillosis, although the original entity of CNPA by Binder et al. is different. We make a diagnosis of CNPA only if all the following entity meets, 1; progressive shadows in radiological findings regardless of the presence of aspergilloma, 2; have some symptoms such as cough, sputum, hemosputum, hemoptysis or fever, 3; proof of Aspergillus attribution by mycological or pathological examination, 4; positive systemic inflammatory reaction, 5; neglect of other etiology of pulmonary diseases. Since CNPA is usually progressive, patients with CNPA should be treated with antifungals.
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PMID:[Pulmonary aspergilloma, diagnosis and treatment]. 1473 17

A 69-year-old man presented with progressive dyspnea, hemoptysis and fatigue for the previous 4 weeks. Chest radiograph and CT-scan were suggestive of lung cancer. The patient's condition worsened and within in few days he developed respiratory failure and acute cor pulmonale. Despite intensive care measures directed at suspected lung thromboembolism, the patient died on day 12. Autopsy revealed disseminated obstruction of small pulmonary arteries by microscopic tumor emboli. No signs of venous thromboembolism were found. Pulmonary tumor microembolism should be considered whenever a patient with malignancy presents with unexplained progressive dyspnea or pulmonary hypertension.
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PMID:[Right heart failure due to pulmonary tumor microembolism -- a rare differential diagnosis]. 1521 32

A 29-year-old woman was admitted to our hospital with a 7-day history of elevated temperature to 39.5 degrees C associated with headache and nausea. She had been diagnosed with tuberous sclerosis complex 10 years earlier. Her unconsciousness progressed, and she was diagnosed as having aseptic meningoencephalitis. The next day, she had a generalized seizure with severe hemoptysis, and she suddenly fell into severe respiratory failure (PaO2/FiO2 = 76.9). Transbronchial lung biopsy revealed the findings of lymphangioleiomyomatosis. It was suggested that neurogenic pulmonary edema accompanied with venous flow obstruction by lymphangioleiomyomatosis lesions resulted in diffuse pulmonary hemorrhage with resultant gross hemoptysis accelerating to severe hypoxemia.
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PMID:Acute respiratory failure with gross hemoptysis in a patient with lymphangioleiomyomatosis as part of tuberous sclerosis complex. 1546 81

An 8.5-year-old girl who presented with chronic cough and hemoptysis underwent a CT scan of the chest showing diffuse mediastinal and parenchymal infiltration and pleural effusion, and laboratory findings showed disseminated intravascular coagulation. Disseminated lymphangiomatosis was diagnosed after an open-lung biopsy. She was treated by systemic steroids, interferon, tamoxifen, chemotherapy, and radiation but died of respiratory failure and disseminated intravascular coagulation 2 years after the diagnosis. This patient represents a rare presentation of diffuse pulmonary lymphangiomatosis together with disseminated intravascular coagulation, involving both the mediastinum and pulmonary parenchyma, in a child.
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PMID:Diffuse thoracic lymphangiomatosis with disseminated intravascular coagulation in a child. 1634 79


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