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Query: UMLS:C0010200 (cough)
23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibrosing alveolitis is a rare, diffuse lung disease characterized by varying combinations of two histological features: thickening of alveolar walls and the presence of large mononuclear cells in the alveolar spaces. Clinical details of 10 children with fibrosing alveolitis are reported. The main symptoms in children are tachypnoea or dyspnoea, cough, poor weight gain, and cyanosis. The condition is similar to that in adults, but it is usually a more acute illness, and if untreated, more predictably fatal. Respiratory failure, pulmonary hypertension, and cardiac failure are the major complications. Less commonly, superimposed bacterial infection and pneumothorax occur. Chest x-rays often show a sequence of changes with a ground-glass appearance and fine mottling in the early stage of the disease, progressing to a picture of mainly hilar linear markings in those children who recover. The histological features at lung biopsy or necropsy are described; these correlated poorly with the radiological features, steroid responsiveness, and clinical course. Lung function tests in 3 older children showed evidence of markedly reduced lung volumes in 2. Static lung compliance in 4 children in the acute stage of the illness was normal in 3 and diminished in one. The response to steroid therapy was analysed in cases from the literature and the 10 reported cases. No spontaneous remissions occurred, all the survivors having been treated with corticosteroids. In children fibrosing alveolitis is almost always a corticosteroid-responsive disease. An appropriate course of prednisolone would be of at least 4 week's, but preferably of 8 weeks' duration, at a minimum daily dose of 2 mg/kg. After improvement the steroid withdrawal should be cautious and protracted, comprising at least a year's continuous treatment.
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PMID:Fibrosing alveolitis in infancy and childhood. 83 51

A statistical correlation between anamnestic and hemodynamic data was performed in 40 patients with chronic obstructive lung disease and pulmonary hypertension at rest. Cardiopulmonary hemodynamic performance was significantly correlated with some of the assessed parameters, especially duration of illness and symptoms generally related with airway obstruction as dyspnea, cough and sputum.
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PMID:Some anamnestic and clinical parameters correlated to longterm pulmonary hypertension development in patients with chronic obstructive lung disease. 93 90

To determine whether a better understanding of primary pulmonary hypertension has affected its clinical presentation, natural history, and prognosis, we retrospectively compared patients with primary pulmonary hypertension presenting to our institution during two different periods: 1962 to 1978 (group 1, n = 38) and 1979 to 1989 (group 2, n = 33). Demographic characteristics were similar in both groups. Dyspnea on exertion was the most frequent presenting symptom in both groups. Fatigue, cough, dizziness, right heart failure, and cyanosis were more frequent in group 1. The electrocardiographic, radiographic, and echocardiographic findings did not differ between groups. Hemodynamic measurements revealed severe pulmonary hypertension and a normal pulmonary capillary wedge pressure and cardiac index; these measurements were similar in both groups. Complications related to cardiac catheterization were more frequent in group 1 (32%) than in group 2 (3%). Causes of death were comparable in both groups, the most frequent being progressive right heart failure, sudden death, and death of unknown cause. Patients from both groups received standard treatment with digitalis, diuretics, and vasodilators; however, group 2 had a higher probability of survival than group 1. We conclude that patients with pulmonary hypertension seen in more recent years tend to present at earlier stages of disease, have fewer complications during cardiac catheterization, and probably survive longer than those seen several decades ago. A clear cause for the longer survival could not be identified, although it may be partly related to earlier presentation in the course of disease.
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PMID:Primary pulmonary hypertension, then and now: 28 years of experience. 152 74

A patent foramen ovale (PFO) is present in 25-35% of people at all ages of life and its size tends to increase with age. It is now possible to detect PFO's by contrast echocardiography and it has been shown that there exists quite frequently a spontaneous transient right-to-left shunt during systole and, moreover, a right-to-left shunt during Valsalva maneuver and coughing. Acute or chronic pulmonary hypertension are also causes of shunt. Besides, a highly statistical correlation has been found between PFO's and strokes of uncertain or absent cause. From 1984 to 1990 the authors have collected 29 cases with 47 embolic cerebral events. Twenty-five cases with 30 embolic cerebral events and a neurological report have been found in the literature from 1930 to 1986. The analysis of these 77 cerebral embolic events is presented. All ages and both sexes are equally affected. Several symptoms and signs can suggest the diagnosis: onset of the neurological disorders during an activity implying a Valsalva maneuver; onset during a recognized phlebitis of the legs of pelvis or, more often, in a clinical setting suggesting the possibility of phlebitis without overt symptoms and signs: post-partum, post-operative conditions with prolonged bed rest; concomitant pulmonary and cerebral embolism. In the authors series of 227 cerebral emboli, such paradoxical emboli account for 12.8% of the cases ant it is likely that the condition is still underdiagnosed.
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PMID:[Paradoxal cerebral embolism: role of patent oval foramen]. 208 18

Several well controlled epidemiologic and hemodynamic studies suggest that about 20% of sleep apnea syndrome (SAS) patients will have chronic obstructive pulmonary disease (COPD), and the majority of these patients (with combined diseases) will have pulmonary hypertension. Indeed it has been suggested that only patients with underlying hypoxemia, such as that from COPD, will develop right heart failure in the OSA setting. Experience shows that apnea/COPD patients will have severe hypersomnolence associated with the OSA, cough and dyspnea with the airways disease, and edema and plethora related to chronic hypoxemia. Many patients present with respiratory failure and are diagnosed at the time of initial intubation and mechanical ventilation. Episodic nocturnal hypoxemia may be worsened by a steeper rate of desaturation due to lower alveolar and blood oxygen stores, and longer apneas perhaps contributed to by depressed chemosensitivity. Daytime hypoxemia may also add to the severe hemodynamic disturbances. Since COPD cannot be cured, aggressive treatment of SAS is critical. Past studies have shown that tracheostomy or nasal CPAP in this setting not only leads to resolution of episodic nocturnal desaturation but may lead to rapid improvement in daytime oxygenation in many patients. Pulmonary hypertension and other measures of cardiopulmonary function improve when apnea is cured. Elimination of the SAS may disclose nonapneic REM related desaturation that could require supplemental oxygen therapy in addition to tracheostomy or nasal CPAP. Pulmonary function testing in SAS patients with smoking histories, followed by aggressive treatment of SAS, is recommended.
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PMID:Chronic lung disease in the sleep apnea syndrome. 211 88

It is sometimes necessary for the practitioner to transfuse the ruminant with whole blood or plasma. These techniques are often difficult to perform in practice and are time-consuming, expensive, and stressful to the animal. Acute loss of 20-25% of the blood volume will result in marked clinical signs of anemia, including tachycardia and maniacal behavior. The PCV is only a useful tool with which to monitor acute blood loss after intravascular equilibration with other fluid compartments has occurred. An acutely developing PCV of 15% or less may require transfusion. Chronic anemia with PCV of 7-12% can be tolerated without transfusion if the animal is not stressed and no further decline in erythrocyte mass occurs. Seventy-five per cent of transfused bovine erythrocytes are destroyed within 48 hours of transfusion. A transfusion rate of 10-20 ml/kg, recipient weight, is necessary to result in any appreciable increase in PCV. A nonpregnant donor can contribute 10-15 ml of blood/kg body weight at 2-4 week intervals. Sodium citrate is an effective anticoagulant, but acid citrate dextrose should be used if blood is to be stored for more than a few hours. Blood should not be stored more than 2 weeks prior to administration. Heparin is an unsuitable anticoagulant because the quantity of heparin required for clot-free blood collection will lead to coagulation defects in the recipient. Blood crossmatching is only rarely performed in the ruminant. In field situations, it is advisable to inject 200 ml of donor blood into the adult recipient and wait 10 minutes. If no reaction occurs, the rest of the blood can probably be safely administered as long as volume overload problems do not develop. Adverse reactions are most commonly seen in very young animals or pregnant cattle. Signs of blood or plasma transfusion reaction include hiccoughing, tachycardia, tachypnea, sweating, muscle tremors, pruritus, salivation, cough, dyspnea, fever, lacrimation, hematuria, hemoglobinuria, collapse, apnea, and opisthotonos. Intravenous epinephrine HCl 1:1000 can be administered (0.2 to 0.5 ml) intravenously or (4 to 5 ml) intramuscularly if clinical signs are severe. Pretreatment with antipyretics and slowing the administration rate may decrease the febrile response. Blood or plasma administered too rapidly will also result in signs of cardiovascular overload, acute heart failure, and pulmonary hypertension and edema. Furosemide and slower administration of blood or plasma should alleviate this problem.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of blood and blood products. 217 38

Mediastinal fibrosis, a rare cause of pulmonary hypertension, may produce cough, dyspnea, and hemoptysis. Steroid therapy has been suggested for individuals with progressive symptoms, but data demonstrating the efficacy of such therapy are lacking. We present a case of pulmonary hypertension secondary to fibrosing mediastinitis. Hemodynamic and scintigraphic studies performed before and after a trial of corticosteroid therapy were unable to demonstrate any therapeutic benefit from the corticosteroids. In order to achieve better use of steroids for the treatment of this disease, we suggest that similar determinations be made on other patients with mediastinal fibrosis who receive such treatment.
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PMID:The effects of steroid therapy on pulmonary hypertension secondary to fibrosing mediastinitis. 175 29

The patient was a 29-year-old woman. She was well until autumn 1983, when she presented with polyarthralgia, fever above 39 degrees C, hepatosplenomegaly, swelling of lymphnode and salmon pink rash. Laboratory tests revealed marked leucocytosis with shift to the left, elevated ESR, strong positivity of CRP and abnormal liver function tests. However, anti-nuclear antibody and RA factor were negative. She was diagnosed as adult onset Still's disease (AOSD) by characteristic clinical course and laboratory data. During her disease course these abnormal findings could be well controlled neither by nonsteroidal anti-inflammatory drugs, immunosuppressive agents nor corticosteroids. Two and half years after the first admission, she began to complain of dry cough, dyspnea on efforts. Auscultation revealed an increased pulmonic sound and systolic murmur of cardiac apex. Chest X-Rays showed enlarged main pulmonary arteries. The lung fields were normal. Pulmonary function tests gave no evidence of a significant obstructive or restrictive defect but showed the low DLco and hypoxemia. Ventilation-perfusion lung scanning failed to reveal pulmonary embolism. Finally, right heart catheterization confirmed the pulmonary precapillary hypertension. Her pulmonary hypertension has progressed rapidly, strongly suggesting poor prognosis. Her pulmonary hypertension associated with no apparent parenchymal involvement was thought to be caused by a pulmonary vascular change probably related to AOSD. This case is a first case of AOSD with pulmonary hypertension.
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PMID:[A case of adult Still's disease with pulmonary hypertension]. 237 40

Radiation pneumonitis is a life-threatening result of therapeutic thoracic irradiation, yet its mechanisms are poorly understood. We studied the effects of unilateral lung irradiation (3,000 rad) in sheep from the immediate response to the later development of radiation pneumonitis. We defined radiation pneumonitis by its diagnostic clinical feature, radiographic infiltration of the irradiated zone with a straight margin corresponding to the radiation port. The immediate response in the few hours after irradiation was characterized by cough, labored respiration, hypoxemia (arterial PO2 decreased 19 Torr), mild pulmonary hypertension (pulmonary arterial pressure increased 20%), and lymphopenia. Hemodynamics and gas exchange returned to normal by day 2 but became abnormal again before or during radiation pneumonitis at 32 +/- 2 days. Respiratory distress, hypoxemia, and pulmonary hypertension recurred during radiation pneumonitis. Bronchoalveolar lavage during radiation pneumonitis contained increased neutrophils (19 +/- 4%, control = 7%), increased protein (0.27 +/- 0.1 g/dl, control = 0.12 +/- 0.03), and severely impaired ability to lower surface tension. Alveolar macrophages from both lungs during unilateral radiation pneumonitis exhibited impaired generation of superoxide after phorbol myristate (only a 30% increase). Normal control alveolar macrophages increased superoxide production after stimulation greater than 400%. We conclude that unilateral lung irradiation in sheep causes a mild immediate response followed by radiation pneumonitis at 1 mo. Unilateral radiation pneumonitis in this model is associated with ipsilateral neutrophilic alveolitis, increased bronchoalveolar lavage protein, and impaired surfactant function, as well as bilateral functional abnormalities of alveolar macrophages.
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PMID:Unilateral radiation pneumonitis in sheep: physiological changes and bronchoalveolar lavage. 254 Jan 44

A 16 year old white female presented with paroxysmal cough and hemoptysis of recent onset. Cardiac evaluation was consistent with pulmonary hypertension. Cor triatriatum sinister was diagnosed by echocardiography. The clinical presentation and the echocardiographic features of this anomaly are discussed.
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PMID:Cor triatriatum sinister: echocardiographic assessment. 261 25


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