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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The triennial Confidential Enquiries into Maternal Deaths in England and Wales report 235 maternal deaths directly due to pregnancy or childbirth in 1973-75. The inquiry covers 94% of maternal deaths, and the figure is 4 times lower than the 1950s report. 37 deaths were attributed to obstetric anesthesia, some of which could have been prevented if the practising house officer had been more knowledgeable. Amniotic fluid deaths numbered 15 and were largely unpreventable. While maternal mortality rates have declined, amniotic fluid embolisms have remained steady since the 1960s. From 1973-75 the causes of death were as follows: hypertensive disease of pregnancy, 47; pulmonary embolism, 61; abortion, 81; sepsis, 70; ectopic pregnancy, 34; uterine hemorrhage, 27.
Lancet 1979 Sep 22
PMID:George Stroh. 9 Mar 22

Venous thrombosis is often asymptomatic in patients in whom major pulmonary embolism develops. When used expectantly, iodine 125-labeled fibrinogen scanning is a very sensitive method for detecting subclinical leg vein thrombi. Fibrinogen scanning is less useful for the diagnosis of established venous thrombosis, but is valuable for detecting extension of venographically diagnosed calf vein thrombosis. The technique is safe if fibrinogen is obtained from carefully screened donors. The limitations of the method include its inability to distinguish between superficial and deep venous thrombi, and its sensitivity to fibrin in hematoma and inflammatory exudates. Though the results agree closely with those of phlebography, scanning seems less reliable for detecting femoral vein than calf vein thrombi and is insensitive to thrombi above the inguinal ligament. Screening for these major thrombi may be improved by combining fibrinogen scanning with impedance plethysmography or ultrasonic examination.
JAMA 1975 Sep 01
PMID:125-I-labeled fibrinogen scanning. Use in the diagnosis of venous thrombosis. 12 51

The authors report 6 cases of acute respiratory failure complicating chronic bronchial and lung disease admitted to hospital with the diagnosis of: heart disease, 3 cases, pulmonary oedema, pulmonary embolism, atrial flutter; status asthmaticus : one case; neuro-psychiatric disease : 2 cases (toxic coma and agitation). The authors emphasize the frequency of chronic bronchial disease and recall the signs of acute decompensation discussing the possible difficulties in diagnosis and the therapeutic implications.
Sem Hop 1977 Sep
PMID:[Deceptive and revealing clinical forms of acute respiratory insufficience in chronic bronchopneumopathies]. 19 94

The authors report 12 cases of pulmonary embolism with misleading signs and discuss the difficulty in diagnosis: 1) the frequency of incomplete forms; 2) lack of specificity of the clinical and paraclinical picture of pulmonary embolism which may simulate pulmonary or heart disease; 3) difficulties in interpretation of the signs of pulmonary embolism in cases of prior heart or pulmonary disease.
Sem Hop 1977 Sep
PMID:[Misleading pulmonary emboliu]. 19 95

Pulmonary embolism is unique among cardiorespiratory diseases because of its high frequency of both overdiagnosis and underdiagnosis. The lack of specific and consistent clinical, laboratory, roentgen, and electrocardiographic features lead to this paradox. While the lung scan may be diagnostic in selected cases, the pulmonary angiogram is the most accurate method of demonstrating emoboli short of operative or pathological examination.
Prim Care 1978 Sep
PMID:Pulmonary embolism: dilemmas in diagnosis and therapy. 25 22

Using the radiofibrinogen test and perfusion lung scanning (2-phase pharmacoscintigraphy), the incidence of postoperative thrombosis and pulmonary embolism was determined in a group of 362 operated patients. Low-dose heparin administration (twice 5000 IU daily) was given to 162, combined heparin and dihydroergotamine administration (5000 IU heparin and 0.5 mg dihydroergotamine daily) to 150, while 50 patients received no prophylactic treatment. There was a significant decrease in thrombo-embolism in the heparin/DHE group (8.7% deep-vein thrombosis; 2.7% pulmonary embolism) compared with the heparin group (19.8% and 5.5%, respectively) and the control group (30% and 14%, respectively).
Dtsch Med Wochenschr 1977 Sep 30
PMID:[Prevention of postoperative thrombo-embolism by heparin/dihydroergotamine (author's transl]. 33

Prostaglandin D2 (PGD2) produced by platelets can inhibit aggregation via activation of platelet adenylate cyclase. PGD2 activation of platelet cyclase in platelet membrane fractions was studied in 20 consecutive patients hospitalized with acute deep-vein thrombosis and/or pulmonary embolism. In nine patients, PGD2-stimulated enzyme activity was decreased at all concentrations of PGD2 studied. This altered enzyme sensitivity was specific for PGD2 as basal enzyme activity, and prostaglandin E1, prostaglandin I2, and sodium fluoride stimulated adenylate cyclase was normal. The effect of PGD2 on platelet aggregation and 14C-serotonin release was also studied in one patient where a four-fold higher concentration of PGD2 was required to inhibit collagen-induced 14C-serotonin release. Binding studies using [3H]PGD2 as a radioligand indicated that this patient's platelets bound 10 fmole PGD2/10(8) platelets compared to 30 fmole/10(8) platelets in a normal control. Five patients had follow-up studies between 2 and 7 mo after their acute thrombotic event, and PGD2-stimulated adenylate cyclase activity returned towards normal in four. Since PGD2 is synthesized in platelets at concentrations sufficient to inhibit aggregation and activate adenylate cyclase, diminished platelet sensitivity to this prostaglandin could result in "hyperactivity" and contribute to the thrombosis observed in these patients.
Blood 1979 Sep
PMID:Diminished platelet adenylate cyclase activation by prostaglandin D2 in acute thrombosis. 38 Jun 88

Two patients with multiple myeloma are described in whom an unusual complication developed: pleural effusion containing myeloma cells. There are 7 previously reported cases of myeloma in the English literature with this type of effusion. Pleural effusion in myeloma may be due to plasma cell infiltration of the pleura, congestive heart failure, pulmonary embolism, nephrotic syndrome, and second neoplasms. In view of these multiple etiologies, diagnostic thoracentesis should be performed in order to treat the effusion appropriately.
Cancer 1979 Sep
PMID:Pleural effusion in multiple myeloma. 38 71

Ten patients with matching ventilation-perfusion lung scan defects and corresponding pulmonary infiltrates were evaluated with segmental pulmonary angiography. All ten patients presented with sudden onset of pleuritic chest pain and fever. Pulmonary emboli were documented in three of the ten patients (30%). The remaining seven patients had pneumonia or atelectasis. The findings emphasize the non-diagnostic nature of lung scans which show only matching ventilation and perfusion defects in regions of pulmonary infiltrates. Segmental pulmonary angiography is recommended for differentiating pulmonary embolism from atelectasis or pneumonia in these patients.
J Can Assoc Radiol 1979 Sep
PMID:Pulmonary embolism with unilateral lung scan defects and matching infiltrates. 46 74

An infant with primary congenital lipoid nephrosis then developed left renal vein thrombosis and secondary hepatic vein obstruction. This was shown by inferior venacavography. The thrombus detached subsequently, and the child died from massive pulmonary embolism.
J Can Assoc Radiol 1979 Sep
PMID:Congenital lipoid nephrosis with left renal vein thrombosis and Chiari's syndrome. 46 79


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