Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tissue type plasminogen activator (tPA) plays a role in differentiation of neurones and activity-dependent structural changes in neurones. We hypothesised that tPA would also be present in CSF during fibrinolysis after intraventricular haemorrhage. We measured tPA antigen in CSF from 13 normal newborn infants and 14 infants with post-haemorrhagic ventricular dilatation (PHVD). tPA was undetectable or at the limit of detection (1 microgram/l) in normal CSF. The CSF tPA concentration ranged from 1.3 to 3.5 micrograms/l in the infants with PHVD. Serial tapping in one infant showed persistence of tPA in the CSF from 3 to 8 weeks of age. We conclude that endogenous tPA may be part of the physiological response to intraventricular haemorrhage or may be present as a result of passive diffusion into the CSF.
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PMID:Endogenous tissue plasminogen activator in neonatal cerebrospinal fluid. 877 26

Previous studies have indicated that intraventricular administration of tissue-type plasminogen activator (TPA) might improve the prognosis of patients with intraventricular haemorrhage (IVH). In aneurysmal IVH, fibrinolytic treatment was always preceded by surgical repair of the aneurysm, since the risk of recurrent haemorrhage from a non-occluded aneurysm was estimated to be high. We reviewed a series of patients with IVH secondary to ruptured aneurysms (n = 4) or arteriovenous malformation (AVM; n = 1) who underwent emergency intraventricular administration of TPA before repair of the bleeding source. Fibrinolysis resulted in rapid decrease of haematoma volume and of ventricular dilatation, and prevented ventricular catheters from becoming obstructed. No intracranial haemorrhages or other complications occurred. The results suggest that the presence of recently ruptured aneurysms or AVM is not necessarily a contraindication for intraventricular administration of TPA. The potentially life saving benefits might outweigh the inherent risks of recurrent haemorrhage in carefully selected patients with massive IVH, in whom ventricular distension, periventricular brain compression, obstruction of CSF flow, and elevated ICP appear to be major determinants for the outcome.
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PMID:Fibrinolytic treatment of intraventricular haemorrhage preceding surgical repair of ruptured aneurysms and arteriovenous malformations. 1061 79

Pulmonary embolism (PE) is extremely common and is a leading cause of death in all age groups. Unfortunately the diagnosis is most often missed than it is made. Prompt diagnosis and treatment can dramatically reduce the mortality and morbidity. This study was done to evaluate the patients with acute PE, assess the utility of laboratory tests and potential of high resolution spiral computed tomogram angiography of pulmonary arteries (sCTPA) as the confirmatory diagnostic tool. Twenty six consecutive patients with acute PE admitted to CCU of Narayana Hrudayalaya of Banglore were followed prospectively. There were 15 male and 11 female (M:F=1:3:1); age range was 32-58 yrs. (mean 45+/-13 yrs). Pre-testing probability assessment of PE was done by a combined approach of history, physical examination and presence of risk factors. D-dimer and cardiac troponin I (TnI) estimation and sCPTA done by contrast enhanced 64-slice spiral CT scanner in all patients. In addition to the typical findings of PE, sCTPA included and revealed features of cardiac and venous CT imaging. Doppler study of leg veins were done to exclude deep vein thrombosis. Trans-thoracic echocardiography assessed right ventricular dilatation and presence of pulmonary hypertension. Nineteen patients (73.0%) had sub-massive PE, 5 patients (19.2%) had non-massive and 2 patients (7.6%) presented with massive PE. A raised D-dimer (0.5mugm/ml) was found in all the cases (100.0%). An elevated a trponin I (TnI) was found in 18 patients (69.2%). RV dilatation, (i.e. RV/LV>0.9) was found in 21 patients (80.7%). All patients (100.0%) received unfractionated heparin. Thrombolysis with alteplase, without concomittent heparin was administered in 11 patients (42.3%). Inferior venacaval filter were implanted in 9 patients (34.6%) with sub massive PE and recurrent events despite anticoagulation. Embolectomy done in one patients with massive PE, offered satisfactory recovery. Pulmonary endarterectomy were undertaken in 6 patients with acute on chronic thromboembolic pulmonary hypertension. Thus sCTPA detected PE, source of PE and provided prognostic information.
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PMID:Pulmonary embolism: an observational study at Narayana Hrudayalaya Institute of Cardiac Sciences, Bangalore, India. 2063 34

A triad of circulatory collapse, right ventricular dilatation, and large alveolar dead space is proposed for the rapid diagnosis and treatment of massive pulmonary embolism. A 17year-old female on oral contraceptives collapsed at home becoming incoherent with shallow breathing. Paramedics initiated mechanical chest compression and transported the patient to our emergency department, arriving minimally responsive with undetectable blood pressure but having positive corneal reflexes and bradycardia with wide QRS. The trachea was intubated and goal-directed echocardiography revealed marked right ventricular dilatation with septal flattening. The arterial PCO2 was 40mmHg with an end-tidal PCO2 of 8mmHg, revealing a large alveolar dead space. Persistent hypotension, bradycardia, and fading alertness despite epinephrine and norepinephrine infusions prompted resumption of chest compression. Intravenous alteplase (10mg bolus over 10min followed by 90mg over 110min) begun 125min after collapse improved hemodynamic function within 10min allowing discontinuation of chest compression. Five and a half hours after starting alteplase, the patient was hemodynamically stable and had normal end-tidal PCO2. A CT-angiogram showed the pulmonary arteries free of emboli but a thrombus in the right common iliac vein. The patient recovered fully and was discharged home on warfarin 8days later. Based on this and other reports, we propose a triad of circulatory collapse, right ventricular dilatation, and large alveolar dead space for the rapid diagnosis and treatment of massive pulmonary embolism, with systemic fibrinolysis as the first-line intervention.
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PMID:Circulatory collapse, right ventricular dilatation, and alveolar dead space: A triad for the rapid diagnosis of massive pulmonary embolism. 2883 Jun 38