tailieunhanh - Critical Care Obstetrics part 49

Critical Care Obstetrics part 49 provides expert clinical guidance throughout on how you can maximize the chances of your patient and her baby surviving trauma. In this stimulating text, internationally recognized experts guide you through the most challenging situations you as an obstetrician are likely to face, enabling you to skillfully:Recognize conditions early-on which might prove life threatening, Implement immediate life-saving treatments in emergency situations, Maximize the survival prospects of both the mother and her fetus | Anaphylactoid Syndrome of Pregnancy Amniotic Fluid Embolism identical fever is unique to septic shock and cutaneous manifestations are more common in anaphylaxis. Nevertheless the marked similarities of these conditions suggest similar pathophysiologic mechanisms. Detailed discussions of the pathophysiologic features of septic shock and anaphylactic shock are presented elsewhere in this text. Both of these conditions involve the entrance of a foreign substance bacterial endotoxin or specific antigens into the circulation which then results in the release of various primary and secondary endogenous mediators Figure . Similar pathophysiology has also been proposed in non-pregnant patients with pulmonary fat embolism. It is the release of these mediators that results in the principal physiologic derangements characterizing these syndromes. These abnormalities include profound myocardial depression and decreased cardiac output described in both animals and humans pulmonary hypertension demonstrated in lower primate models of anaphylaxis and disseminated intervascular coagulation described in both human anaphylactic reactions and septic shock 44-53 . Further the temporal sequence of hemodynamic decompensation and recovery seen in experimental AFE is virtually identical to that described in canine anaphylaxis 49 . An anaphylactoid response is also well described in humans and involves the non-immunologic release of similar mediators 44 . It is also intriguing that on admission to hospital 41 of patients in the AFE registry gave a history of either drug allergy or atopy 5 . The ability of arachidonic acid metabolites to cause the same physiologic and hemodynamic changes observed in human AFE has been noted 54 . Further in the rabbit model of AFE pretreatment with an inhibitor of leukotriene synthesis has been shown to prevent death 28 . These experimental observations further support the clinical conclusions of the National AFE Registry analysis that this condition .

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