PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “DEFECTS, CONGENITAL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources
PubMed1976

[Acute complications of hernias caused by congenital defects of the diaphragm].

Following a classification of the various types of congenital hernia of the diaphragm, the acute complications that may be caused by such defects of diaphragmatic morphogenesis are reviewed. Relative physiopathology is considered, particularly as regards the thoracic dimension of large hernias of the cupola. As regards visceral hernia, the most typical pictures of the two commonest complications, volvulus and strangulation, are described among other aspects. The clinical situation is outlined bearing in mind the diversity of anatomoclinical pictures in relation to the age of the patient, the type of hernia involved, and the period in which the observation was made. The surgical problems involved in acute complications concern the approach--although agreement is almost unanimous depending on the type of hernia--viscous reduction modalities and the type of plastic surgery which is required on each occasion. Postoperative complications and the prognosis for these hernias are reviewed briefly.

Diaphragm↗
PubMed1988

Management of pregnancy in women with antithrombin III congenital defect: report of four cases.

Four pregnant women with antithrombin III congenital deficiency underwent thrombosis prophylaxis including oral anticoagulants administered from the 16-18th week to the 36-37th week of pregnancy, subcutaneous heparin before the 16-18th week and after the 36-37th week, and a single infusion of AT III concentrate in the peripartum period in order to obtain a minimal level of 0.8 U/ml of AT III functional activity. The level of circulating AT III after the concentrate infusion needs to be evaluated by functional methods, because of a consistent amount in the concentrates of inactive AT III immunoreactive material. No thrombotic or haemorrhagic complication occurred after starting prophylaxis in any woman either in any newborn.

Administration, Oral↗
PubMed1991

Haemostasis in oral surgery--the possible pathogenetic implications of oral fibrinolysis on bleeding. Experimental and clinical studies of the haemostatic balance in the oral cavity, with particular reference to patients with acquired and congenital defects of the coagulation system.

Activation and inhibition of the haemostatic system was reviewed including the interaction between the four biological systems involved in haemostasis: the vessel wall, the platelets, the coagulation system and the fibrinolytic system. The haemostatic mechanism is initiated at the site of injury through local activation of surfaces and release of tissue thromboplastin, resulting in formation and deposition of fibrin. The coagulation process is regulated by physiological anticoagulants. Activation of fibrinolysis is triggered by the presence of fibrin, and the role of tissue-type plasminogen activators (t-PA) at the site of fibrin formation in particular is emphasized. The process is regulated by physiological inhibitors, of which alpha 2-antiplasmin, histidine-rich glycoprotein and plasminogen activator inhibitor are reported to be of major physiological significance. The role of fibrinolysis in the regulation of the dynamic haemostatic balance is discussed, elucidated through examples of congenital deficiencies of the coagulation and the fibrinoytic system. Pharmacological inhibitors of fibrinolysis (i.e. epsilon-aminocaproic acid and tranexamic acid) and their possible effect on the haemostatic system are described. The systemic effects on the fibrinolytic system of surgery and oral surgery is reviewed, and it is concluded, that oral surgery has insignificant effects on blood fibrinolysis. In contrast, oral surgery induces changes of fibrinolysis in the oral environment; initially the fibrinolytic activity of saliva is reduced, due to the presence of inhibitors of fibrinolysis originating from the blood and the wound exudate. When bleeding and exudation cease, the fibrinolytic activity of the saliva will increase. Plasminogen and plasminogen activator, identified as t-PA are present in the oral environment under physiological conditions. Plasminogen is secreted in the saliva and the sources of t-PA include oral epithelial cells and gingival crevicular fluid. The presence of plasminogen and t-PA in the oral environment implies that when fibrin is present (i.e. after surgery), fibrinolysis is triggered. Haemorrhagic complications to oral surgery in patients without known defects of the coagulation system is reviewed. It is concluded that the investigations conducted to the present day do not permit final conclusions with respect to the pathophysiological role of defects in the coagulation and the fibrinolytic systems for the development of bleeding after oral surgery. Further investigations are necessary in order to clarify these aspects, and should include extensive laboratory analyses to reveal rare congenital defects such as factor XIII- and alpha 2-antiplasmin deficiencies.(ABSTRACT TRUNCATED AT 400 WORDS)

Anticoagulants↗