Cytology of tracheobronchial aspirates in horses. (9/163)

Tracheobronchial aspirates were obtained from 27 normal horses and from 57 horses with respiratory disease. Aspirates from normal horses contained mainly ciliated columnar epithelial cells, mononuclear cells, a few neutrophils and mucus. Aspirates from horses with acute suppurative bronchopneumonias or chronic bronchiolitis had predominantly neutrophils and usually large amounts of mucus; in severe suppurative inflammatory diseases, many of the cells were degenerated, and there were coils of fibrinous material resembling Curschmann's spirals. Eosinophils were rarely found, even from horses with histories suggestive of allergic respiratory disease. Aspirates from horses with epistaxis frequently had macrophages with intracytoplasmic green globules (hemosiderin). Tracheobronchial aspirates occasionally revealed subclinical lung disease. Four horses with no clinical signs of lung disease and lungs that were unremarkable on percussion and normal on auscultation had adpirates suggestive of inflammation; histologic examination confirmed bronchiolitis.  (+info)

Aggressive undifferentiated carcinoma of unknown primary site complicated by lactic acidosis after bleeding: a case report. (10/163)

Undifferentiated carcinoma of unknown primary site complicated by lactic acidosis has not been documented. We describe a young female with undifferentiated carcinoma of unknown primary site manifested by widespread lymph node and hepatic infiltration, hyperuricemia and very high levels of lactate dehydrogenase. She developed lactic acidosis suddenly after an episode of bleeding following nasal biopsy. The bleeding episode is likely to have caused subclinical hepatic hypoperfusion and hypoxemia, thereby aggravating lactate overproduction by tumor cells and clearance impairment due to diffuse hepatic infiltration to result in rapidly fatal acidosis before cytotoxic agents could be instituted. Although uncommon, when a critical event occurs in aggressive malignancies with massive hepatic involvement, the clinician should be alert for the development of lactic acidosis because the life-threatening metabolic complication is best avoided by prompt and effective cytoreduction therapy.  (+info)

Epistaxis and conjunctival contamination--are our ENT trainees at risk? (11/163)

The aims of this study were to assess the risk of conjunctival contamination with blood during the treatment of epistaxis and to identify if certain patients and treatments may pose a higher risk. Protective eye-wear worn by ENT trainees during the ward management of epistaxis was examined for contamination with blood splashes. This occurred in 18% of cases. The incidence of contamination was higher when two treatment modalities were required and when treating elderly female patients.  (+info)

An unusual epistaxis. (12/163)

The case of a man who presented complaining of epistaxis is reported. He had coarctation repair 18 years previously. Subsequent investigation revealed an aortobronchial fistula resulting from false aneurysm formation distal to the original vessel anastamosis. This was repaired at surgery, the patient suffering a minor stroke, before rehabilitation and good recovery.  (+info)

Hereditary haemorrhagic telangiectasia (Osler-Weber-Rendu syndrome): a view from the 21st century. (13/163)

Hereditary haemorrhagic telangiectasia (HHT) affects one in 5-8000, and no longer can be viewed as solely causing anaemia (due to nasal and gastrointestinal bleeding) and characteristic mucocutaneous telangiectasia. Arteriovenous malformations commonly occur, and in the pulmonary and cerebral circulations demand knowledge of risks and benefits of asymptomatic screening and treatment. HHT is inherited as an autosomal dominant trait and there is no age cut off when apparently unaffected offspring of an individual with HHT can be told they are unaffected. This review focuses on the evolving evidence base for HHT management, issues regarding pregnancy and prothrombotic treatments, and discusses the molecular and cellular changes that underlie this disease.  (+info)

Visceral manifestations in hereditary haemorrhagic telangiectasia type 2. (14/163)

Hereditary haemorrhagic telangiectasia (HHT) is a genetic vascular disorder characterised by epistaxis, telangiectases, and visceral manifestations. The two known disease types, HHT1 and HHT2, are caused by mutations in the endoglin (ENG) and ALK-1 genes, respectively. A higher frequency of pulmonary arteriovenous malformations (AVMs) has been reported for HHT1 while HHT2 is thought to be associated with a lower penetrance and milder disease manifestations. In this study, we present 10 families with an ALK-1 genotype. Visceral manifestations were detected in 24 (26%) of the 93 HHT2 patients from nine of the families and included gastrointestinal bleeding (14%), intrahepatic shunts (6%), and AVMs in the lung (4%) and brain (3%). Gastrointestinal bleeding, the most frequent visceral manifestation, was reported in six of the 10 families, mostly in patients over the age of 50. These patients also had frequent epistaxis and suffered from anaemia, often requiring blood transfusions. The identification of ALK-1 mutations in subjects with a suspected diagnosis and without clinical signs of HHT argue in favour of a molecular diagnosis. We also analysed the data published on 44 families with HHT2 and conclude that visceral manifestations occur in 26 of these families and affect 30% of HHT2 patients. This is considered an underestimate given incomplete and variable screening for lung, brain, and/or liver involvement in different clinical centres. These findings, however, stress the need for an early diagnosis of HHT that can be useful for the early control of associated visceral involvement.  (+info)

Massive epistaxis related to petrous carotid artery pseudoaneurysm after radiation therapy: emergency treatment with covered stent in two cases. (15/163)

Two patients had acute left carotid rupture from radiation therapy-induced pseudoaneurysms, resulting in hemodynamic collapse. Because the patients were semicomatose and in shock, an immediate salvage procedure was needed. Location of the pseudoaneurysm at the skull base made surgical treatment less possible. Endovascular therapy was the treatment of choice. Preserving patency of the carotid artery was a desirable option. The successful use of a covered stent in the emergency treatment of massive epistaxis due to active bleeding from pseudoaneurysm in the petrous internal carotid artery (ICA) is described.  (+info)

Hereditary haemorrhagic telangiectasia: a questionnaire based study to delineate the different phenotypes caused by endoglin and ALK1 mutations. (16/163)

BACKGROUND: Hereditary haemorrhagic telangiectasia (HHT) is an autosomal dominant vascular dysplasia characterised by mucocutaneous telangiectasis, epistaxis, gastrointestinal haemorrhage, and arteriovenous malformations in the lung and brain. Causative mutations for HHT have been identified in two genes, endoglin and ALK1, which encode proteins involved in serine-threonine kinase signalling in the endothelial cell. METHODS: A number of people affected with HHT had completed a postal questionnaire as part of an international study to delineate the HHT phenotype. We identified questionnaires completed by subjects in whom we had identified a mutation in endoglin or ALK1. Further questionnaires were sent to families with known mutations. Data were only included from questionnaires returned by people known to carry disease causing mutations. RESULTS: Questionnaires were completed by 83 subjects with known mutations. Of these, 49 had endoglin mutations (HHT1) and 34 had ALK1 mutations (HHT2). Subjects with HHT1 reported an earlier onset of epistaxis (p=0.01) and telangiectasis (p=0.0001) than those with HHT2. Pulmonary arteriovenous malformations were only reported in the endoglin mutation group in our study (p<0.001). CONCLUSIONS: Our questionnaire based study provides evidence that the HHT phenotype caused by mutations in endoglin (HHT1) is distinct from, and more severe than, HHT caused by mutations in ALK1 (HHT2). This has significant implications for diagnosis, screening, and treatment in the two different forms of HHT, as well as for understanding the pathogenesis of the disease.  (+info)