Effect of amniotic fluid on coagulation and platelet function in pregnancy: an evaluation using thromboelastography*

Harnett, Miriam; Hepner, David L.; Datta, Sanjay; Kodali, Bhavani Shankar

doi:10.1111/j.1365-2044.2005.04373.x

Cited by 48 publications

(18 citation statements)

References 19 publications

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“…When AF is added to blood from pregnant women, the R time, which reflects the time to first clot formation, is significantly decreased with the addition of as little as 10 mL to 330 mL blood. This substantiates the hypothesis that coagulation profile changes are invariable accompaniments of AFE [106]. The Thrombelastograph1 test may therefore be useful in assessing coagulopathy during or after AFE [107].…”

Section: Pathophysiologysupporting

confidence: 58%

Nonthrombotic pulmonary embolism

Jorens¹,

Marck²,

Snoeckx³

et al. 2009

European Respiratory Journal

153

127

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Nonthrombotic pulmonary embolism (NTPE) is defined as embolisation to the pulmonary circulation of different cell types (adipocytes, haematopoietic, amniotic, trophoblastic or tumour), bacteria, fungi, foreign material or gas. The purpose of this article is to describe the clinical signs, pathogenesis, diagnosis and treatment of the different NTPE subtypes.The complex and diverse pathogenesis of different subtypes of emboli is subject to continuing speculation and is certainly far more complex than ''simple'' mechanical obstruction after embolisation of vascular thrombi. Nonthrombotic emboli may also lead to a severe inflammatory reaction both in the systemic and pulmonary circulation, as well as in the lung.NTPE presents a formidable diagnostic challenge, as the condition often presents with very unusual and peculiar clinical signs that are frequently overlooked. They range from very dramatic acute presentations such as acute respiratory distress syndrome to signs observed late in the disease course. Pathological observations play a key role in the exact diagnosis, and sometimes carefully aspirated blood from the pulmonary artery or specific staining of cells recovered from bronchoalveolar lavage fluid may be helpful. Frequently, lung biopsies revealing severe granulomatous reaction or unfortunate post-mortem pathological investigations of pulmonary tissue are necessary to confirm the diagnosis. Here, we also aim to familiarise the reader with the atypical radiological features of NTPE. Thin-section computed tomography of the lungs showing peculiar radiographic findings, such as a feeding vessel, the so-called tree-in-bud pattern or the appearance of micronodules distributed at the termination of bronchovascular bundles, may be observed in certain forms of NTPE.Increased awareness of NTPE as an underestimated cause of acute and chronic embolism, which may result in acute and chronic pulmonary hypertension, is needed. Despite the fact that detailed descriptions of several forms of NTPE have existed for nearly 100 years, well-designed trials have never been performed to evaluate therapy in the different subsets of these patients.

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Section: Pathophysiologysupporting

confidence: 58%

Nonthrombotic pulmonary embolism

Jorens¹,

Marck²,

Snoeckx³

et al. 2009

European Respiratory Journal

153

127

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“…Harnett et al, 78 using thromboelastography analysis, have demonstrated that the addition of amniotic fluid to blood from pregnant women causes a hypercoagulable state related to the procoagulant activity of amniotic fluid and enhanced platelet activation, but there was no evidence of fibrinolysis, suggesting that the primary cause of bleeding in AFE is consumption coagulopathy. Similar results were reported by Liu et al, 79 using blood from non pregnant women.…”

Section: Resultsmentioning

confidence: 99%

“…Amniotic fluid contains epithelial squamous cells from the fetal skin, mucin derived from meconium excreted by the fetal intestine, fat derived from the vernix caseosa, and hair. 2,78 These constituents can be specifically identified by using immunohistochemical markers for cytokeratin AE1/AE3, Alcian blue or mucicarmine staining, oil red O staining, and polarized light, respectively. 81–83 Kobayashi et al, 84 reported that immunohistochemical staining using monoclonal antibody TKH-2 is a more sensitive method to detect meconium and amniotic fluid-derived mucin in the lung sections of patients with AFE than conventional hematoxylin eosin or Alcian blue staining.…”

Section: Resultsmentioning

confidence: 99%

Amniotic fluid embolism: an evidence-based review

Conde-Agudelo

Romero

2009

American Journal of Obstetrics and Gynecology

232

276

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We conducted an evidence-based review of information bout amniotic fluid embolism (AFE). The estimated incidence of AFE is 1:15,200 and 1:53,800 deliveries in North America and Europe, respectively. The case fatality rate and perinatal mortality associated with AFE are 13–30% and 9–44%, respectively. Risk factors associated with an increased risk of AFE include advanced maternal age, placental abnormalities, operative deliveries, eclampsia, polyhydramnios, cervical lacerations, and uterine rupture. The hemodynamic response in AFE is biphasic, with initial pulmonary hypertension and right ventricular failure, followed by left ventricular failure. Promising therapies include selective pulmonary vasodilators and recombinant activated facto Vlla. Important topics for future research are presented.

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“…110 Abciximab has been added to celite-activated TEG ® assays to distinguish between platelet and fibrin(ogen) components of clotting in pregnant patients, 111 to demonstrate elevated fibrin-based clot formation after in vitro fertilization, 112 and to dissect the effects of contaminating blood with amniotic fluid in vitro . 113 However, no evidence was identified for the use of platelet-inhibited TEG ® assays during PPH.…”

Section: Teg® and Rotem®; Intraoperative Assessment And Haemostatic Tmentioning

confidence: 99%

Haemostatic monitoring during postpartum haemorrhage and implications for management

Solomon

Collis

Collins

2012

British Journal of Anaesthesia

175

161

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SummaryPostpartum haemorrhage (PPH) is a major risk factor for maternal morbidity and mortality. PPH has numerous causative factors, which makes its occurrence and severity difficult to predict. Underlying haemostatic imbalances such as consumptive and dilutional coagulopathies may develop during PPH, and can exacerbate bleeding and lead to progression to severe PPH. Monitoring coagulation status in patients with PPH may be crucial for effective haemostatic management, goal-directed therapy, and improved outcomes. However, current PPH management guidelines do not account for the altered baseline coagulation status observed in pregnant patients, and the appropriate transfusion triggers to use in PPH are unknown, due to a lack of high-quality studies specific to this area. In this review, we consider the evidence for the use of standard laboratory-based coagulation tests and point-of-care viscoelastic coagulation monitoring in PPH. Many laboratory-based tests are unsuitable for emergency use due to their long turnaround times, so have limited value for the management of PPH. Emerging evidence suggests that viscoelastic monitoring, using thrombelastography- or thromboelastometry-based tests, may be useful for rapid assessment and for guiding haemostatic therapy during PPH. However, further studies are needed to define the ranges of reference values that should be considered ‘normal’ in this setting. Improving awareness of the correct application and interpretation of viscoelastic coagulation monitoring techniques may be critical in realizing their emergency diagnostic potential.

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Effect of amniotic fluid on coagulation and platelet function in pregnancy: an evaluation using thromboelastography*

Cited by 48 publications

References 19 publications

Nonthrombotic pulmonary embolism

Nonthrombotic pulmonary embolism

Amniotic fluid embolism: an evidence-based review

Haemostatic monitoring during postpartum haemorrhage and implications for management

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