Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of unilateral pulmonary vein atresia in a 20-month-old girl is described in this report. A chest X-ray revealed a reticular shadow on the right side, while an electrocardiogram revealed right ventricular hypertrophy. After cardiac catheterization and angiography, a diagnosis of a ventricular septal defect, patent ductus arteriosus, severe pulmonary hypertension, and atresia of the right pulmonary vein was made. The patient underwent an operation for the ventricular septal defect and ligation of the patent ductus arteriosus. During the operation, the right pulmonary vein was found to be atretic, and unrepairable. Pneumonectomy was not performed because the pulmonary arterial pressure decreased to 41 mmHg after the surgical treatment of the intracardiac lesions. Pneumonectomy will be necessary if one or more complications such as persistent hemoptysis, repeated pulmonary infections or the development of pulmonary hypertension, may occur in future.
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PMID:[Unilateral pulmonary vein atresia]. 268 12

A 24-year-old patient presented with hemoptysis. Pulmonary evaluation was unrevealing. After being lost to follow-up, he again presented with worsening symptoms and physical findings of severe pulmonary hypertension. A large left atrial mass was found on echocardiogram. This was subsequently found to be a malignant fibrous histiocytoma. He also had pseudothrombocytopenia due to platelet cold agglutinins. Left atrial masses must be considered in unexplained hemoptysis.
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PMID:Malignant fibrous histiocytoma of the heart presenting as hemoptysis. Association with pseudothrombocytopenia. 283 43

Pulmonary arterial rupture due to the use of a Swan-Ganz catheter is a rare accident, with an estimated 2% incidence rate. It is fatal in almost 50% of cases. Predisposing factors are age greater than 60 years, pulmonary arterial hypertension and anticoagulant treatment. In patients older than 60 years, changes in the arterial wall increase the risk of rupture; pulmonary hypertension leads to too distal a movement of the catheter, and a concomitant treatment with anticoagulant drugs increases the amount of blood lost. Handling errors when setting up the catheter are often the cause of these accidents, especially a balloon too blown up and a catheter pushed too far. A subsequent movement of the catheter can be a cause of rupture during cardiac surgery. Haemoptysis is the major symptom of this accident, being found in 90% of cases. It can however be of minor importance; if it is ignored, this can lead to a secondary overwhelming haemorrhage. The haemorrhage can be life-threatening because of the cardiovascular collapse and acute respiratory failure by asphyxia. The treatment can only be carried out in intensive care. It will depend on the severity of the accident. It can go from an expectant wait after partial or total removal of the catheter, to an emergency thoracotomy for vascular suture, segmentectomy or even lobectomy. Intermediate measures include turning the patient onto the healthy side, injecting adrenaline or a clot of the patient's blood by the distal end of the catheter, placing a Fogarty catheter in the affected bronchus, or tracheal intubation with a double-lumen catheter and using mechanical ventilation with PEEP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Perforation of the pulmonary artery following Swan-Ganz catheterization]. 306 41

A congenital deficiency of factor VII and protein C was found in a 21-year-old female suffering from recurrent and progressive attacks of dyspnea and hemoptysis over the last four years. She has been followed in our Department since the age of 17 under a diagnosis of peripheral pulmonary artery stenosis and pulmonary hypertension as confirmed by cardiac catheterization and angiography. Prolonged prothrombin time repeatedly examined during this time period prompted us to perform detailed coagulation studies. We found that factor VII and protein C were both half normal in activity as well as in antigen. Three other members of her immediate family were also found to be affected with this combined deficiency. Since the genes encoding factor VII and protein C are located in different chromosomes, the 13th and the second chromosomes, respectively, expression of the combined hereditary deficiency is a random and very rare association on the basis of frequencies of 1:50,000 for factor VII and 1:16,000 for protein C deficiencies.
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PMID:Combined factor VII and protein C deficiency found in a patient with peripheral pulmonary artery stenosis accompanied by progressive pulmonary hypertension and hemoptysis. 318 53

Elevation of pulmonary arterial pressure may be secondary to many diseases of the lungs, chest wall, and heart. From a pathophysiologic viewpoint, pulmonary hypertension is secondary to vascular obstruction, vasoactivity, increased circulation, and passive forces. Clinically, the entities that result in secondary pulmonary hypertension present with a picture that identifies the primary disease. Patients with primary pulmonary hypertension may be difficult to identify. Pulmonary hypertension may present early with dyspnea and fatigue, while syncope and hemoptysis are late symptoms. In many instances, pulmonary hypertension can be diagnosed utilizing physical examination and noninvasive tests. Eventually, right heart catheterization is necessary to confirm the diagnosis and to monitor trials of therapy with vasodilators. Treatment may be specific (closure of a septal defect, thromboendarterectomy) or generic (vasodilators). These have been used recently for both secondary and primary pulmonary hypertension in an effort to reduce pulmonary vascular resistance, thereby decreasing right ventricular afterload and improving cardiac output and oxygen delivery. The success of these treatments has not been demonstrated.
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PMID:Pulmonary hypertension: etiology and clinical evaluation. 333 61

A 70-year-old woman with pulmonary hypertension due to severe chronic obstructive pulmonary disease and long-standing mitral stenosis developed hemoptysis and a right upper lobe infiltrate during manipulation of a balloon-tipped flow-directed pulmonary artery catheter. Hemoptysis resolved spontaneously over several minutes, and the right upper lobe infiltrate cleared over several weeks, during which time a new right upper lobe nodule became apparent. Angiography disclosed the presence of a late-filling well-circumscribed saccular pseudoaneurysm. This was obliterated with an acute infiltrate with or without hemoptysis in the area subtended by a flow-director pulmonary artery catheter, and particularly when it is associated with manipulation of that catheter, the differential diagnosis should include pulmonary artery perforation as well as infarction. If the patient survives the episode, the possibility that a pseudoaneurysm has formed must be actively entertained and aggressively evaluated, since pseudoaneurysm is a potentially fatal lesion that is treatable.
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PMID:Pulmonary artery pseudoaneurysm. A potential complication of pulmonary artery catheterization. 334 43

We report a case of pulmonary hemoptysis induced by a balloon-tipped catheter. The bleeding ceased spontaneously. Factors known to be associated with pulmonary artery rupture such as pulmonary hypertension, anticoagulant therapy, and advanced age were absent in our patient. Bleeding occurred despite careful consideration of the guidelines for right heart catheterization suggested by Swan and Ganz in 1974. We conclude that hemoptysis may be a complication of balloon-tipped right heart catheterization even in the absence of risk factors for this procedure. Therefore the indication for this intervention should be considered carefully.
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PMID:[Lung hemorrhage as a sequela of heart catheterization study]. 368 15

Congenital stenosis of individual pulmonary veins is uncommon. Of the 49 cases reported, four were seen at the IWK Hospital for Children and are reported here. Plain radiographs show a shift of the heart toward the side of major involvement, Kerley B lines, fluid in the fissures, and interstitial edema of the affected lobes. These findings, while subtle, should nevertheless suggest stenosis. Technetium-99m macro-aggregate lung perfusion scans show absence of or diminished perfusion of the affected lobes. The diagnosis can usually be confirmed with angiography. Congenital stenosis of individual pulmonary veins should be considered in children with repeated pulmonary infections, dyspnea, failure to thrive, hemoptysis, or unexplained pulmonary hypertension.
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PMID:Stenosis of individual pulmonary veins: radiologic findings. 376 52

A patient presenting with the rare association of congenital unilateral pulmonary venous atresia in one lung and pulmonary veno-occlusive disease in the other is described. The patient first presented at the age of 3 1/2 years with anemia, hemoptysis, and pulmonary hypertension. After cardiac catheterization and angiocardiography, a diagnosis of atresia of the left pulmonary veins was made for which left pneumonectomy was done. Four years later the patient presented with right-sided congestive failure and radiologic evidence of right-sided pulmonary edema from which death resulted. At autopsy, the right lung showed changes of pulmonary veno-occlusive disease, while the major veins were not involved.
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PMID:Congenital unilateral pulmonary venous atresia with pulmonary veno-occlusive disease in contralateral lung: an unusual association. 382 68

The clinical signs associated with heartworm disease are the result of changes in the pulmonary arterial system. These clinical signs are the result of either pulmonary hypertension or lung parenchymal disease associated with vascular changes. An increase in pulmonary arterial pressure produces an increase in right ventricular afterload, which may lead to exercise intolerance, syncope, and right-sided congestive heart failure. Coughing, dyspnea, and hemoptysis are the results of pulmonary parenchymal disease.
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PMID:Pulmonary manifestations of heartworm disease. 390 12


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