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At least 523 records · Page 29Linked to original sources
PubMed2001

Disseminated intravascular coagulation.

Healthy pregnancy is accompanied by changes in the haemostatic system which convert it into a hypercoagulable state vulnerable to a spectrum of disorders ranging from venous thromboembolism to disseminated intravascular coagulation (DIC). This latter is always a secondary phenomenon triggered by specific disorders such as abruptio placentae and amniotic fluid embolism due to release of thromboplastin intravascularly or endothelial damage resulting from pre-eclampsia and sepsis. In modern obstetric practice the most common cause is haemorrhagic shock with delay in resuscitation leading to endothelial damage. The initial management of massive obstetric haemorrhage is the same whether associated with coagulopathy initially or not. Low-grade DIC, associated with pre-eclampsia, is monitored haematologically by serial platelet counts and serum fibrin degradation products (FDPs). Supportive measures and removal of the triggering mechanism are the key to successful management. Outcome depends primarily on our ability to deal with the trigger and not on direct attempts to correct the coagulation deficit.

Abortion, Therapeutic↗
PubMed1986

Squamous and trophoblastic cells in the maternal pulmonary circulation identified by invasive hemodynamic monitoring during the peripartum period.

The antemortem diagnosis of amniotic fluid embolism has traditionally relied on the identification of amniotic fluid debris in the maternal circulation by central venous or pulmonary arterial catheterization. Pulmonary artery blood specimens from 14 term pregnant women with severe pregnancy-induced hypertension suggest that squamous or trophoblastic cells may be normally present in the maternal pulmonary circulation during the peripartum period and that their presence is not pathognomonic of clinically significant amniotic fluid embolism.

Amniotic Fluid↗
PubMed1991

Amniotic fluid contains tissue factor, a potent initiator of coagulation.

A primary clinical manifestation of amniotic fluid embolism is coagulopathy. Prior studies have identified a poorly characterized yet potent procoagulant property in amniotic fluid that increases with gestational age. One possible source of procoagulant activity is tissue factor, a primary biologic initiator of coagulation. We used sensitive immunoassays and functional assays to identify substantial quantities of tissue factor antigen and tissue factor-specific procoagulant activity in amniotic fluid, which increased with gestational age. Moreover, tissue factor accounted for virtually all of the coagulant potential of amniotic fluid. Amniotic tissue factor appeared intact and membrane bound and, when reconstituted into synthetic microvesicles of optimal phospholipid content, displayed nearly full activity. Calcium chelation and sonication experiments suggested that the presence of inhibitors and the physical configuration of membrane-bound tissue factor in amniotic fluid might explain the modest reduction in tissue factor procoagulant activity relative to total antigen levels observed in vivo. We postulate that the substantial quantities of functionally active tissue factor in amniotic fluid account for the coagulation changes accompanying amniotic fluid embolism and could indirectly contribute to the characteristic hemodynamic derangements of amniotic fluid embolism.

Amnion↗
PubMed1994

Sudden maternal deaths probably due to obstetrical pulmonary embolism in Malaysia for 1991.

Obstetric pulmonary embolism forms the most serious vascular problem during pregnancy. The following report is a retrospective study into maternal deaths in Malaysian mothers probably due to obstetrical pulmonary embolism. Obstetric pulmonary embolism can be divided into amniotic fluid embolism and obstetric blood clot embolism. There were 37 maternal deaths attributable to this cause -9.9 per cent of all maternal deaths to blood clot embolism and 6.7 per cent to amniotic fluid embolism. Most cases were diagnosed clinically because a postmortem examination was not done. Eleven cases of embolism were associated with Caesarean delivery. The typical profile of a Malaysian mother dying from obstetrical pulmonary embolism is that of a Malay mother in the "non-risk" parities of one to four and usually aged between 31-35 years. In the management of these patients, there should be an urgency in diagnosis and improvement in diagnostic procedures. Health staff at all levels should be trained to pick up patients who present with features of deep vein thrombosis.

Adult↗
PubMed2005

[Activity and role of tryptase after entrance of amniotic fluid into blood in rats].

OBJECTIVE: To investigate the activity and role of tryptase after entrance of amniotic fluid into blood in rats. METHODS: Thirty female Wistar rats (20 day pregnancy) were divided into the control group (10, injected with normal saline), amniotic group (10, injected with amniotic fluid), meconium group (10, injected with 1% meconium). After injection, pulmonary tissue was taken out. Tryptase activity was measured by special substrate. The histology of pulmonary tissue was determined by immunohistochemistry (HE). RESULTS: (1) Dropsy, hemorrhage, and infiltration of neutrophil (PMN), macrophage, leukomonocyte were observed in two experimental groups, but no such changes were found in control group. (2) After injection, tryptase activity in meconium group 176.4 +/- 8.6 and amniotic fluid group 165.4 +/- 7.4 was significantly higher than preexperimental groups 146.8 +/- 8.9 and 147.8 +/- 9.5, respectively (t = 7.58 and t = 4.64, P < 0.01); tryptase activity in control group was 145.3 +/- 10.6 before injection and 146.9 +/- 9.4 after injection, respectively, there was no difference (t = 0.37, P > 0.05). After injection, tryptase activity in meconium and amniotic fluid groups was significantly increased than that in control group (F = 30.66, P < 0.05). CONCLUSION: The activity of tryptase was significantly increased after entrance of amniotic fluid into blood in rats. Degranulation of mast cells to release tryptase may be the important cause of the pathophysiologic change after entrance of amniotic fluid into blood. These results suggest a role for mast cell activation in the mechanism of amniotic fluid embolism. This method is sensitive and effective for diagnosis of amniotic fluid embolism in clinic.

Amniotic Fluid↗
PubMed1993

Amniotic fluid embolus.

A case report of a 27-yr-old healthy patient for Caesarean section under epidural anaesthesia is presented. The patient suffered an acute cardiorespiratory collapse when the infant's head was being delivered through the anterior abdominal wall. The patient remained cyanosed after proper tracheal intubation and pulmonary ventilation with 100% O2. Hypotension was difficult to treat but returned to normal 25 min after the event. A pulmonary artery catheter inserted three hours after the event showed normal pressures and a high cardiac output. The patient suffered permanent neurological damage. The differential diagnosis is discussed and current concepts of the aetiology and management of amniotic fluid embolism reviewed.

Adult↗