How we manage the haematological aspects of major obstetric haemorrhage

Allard, Shubha; Green, Laura; Hunt, Beverley J.

doi:10.1111/bjh.12605

Cited by 50 publications

(61 citation statements)

References 105 publications

(85 reference statements)

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“…At term, haemostasis is tipped towards a prothrombotic state, with levels of all procoagulant factors, except factor XI, increased [12][13][14]. This is especially marked for fibrinogen, von Willebrand factor and factor VIII [14], with levels typically increased by more than 100%.…”

Section: Changes In Haemostasis At Termmentioning

confidence: 99%

“…The type, severity and rate of onset of coagulopathy vary with the aetiology of the bleeding [12,13]. Uterine atony, surgical and genital tract traumainduced bleeding is often associated with no significant coagulopathy, even with relatively large blood loss [27].…”

Section: Haemostatic Changesmentioning

confidence: 99%

“…Consumption results from dysregulated activation of coagulation and a reduction in coagulation factors, especially fibrinogen and platelets [12,13,31]. Although PPH is often thought to be associated with DIC, this is an uncommon event and very few cases fulfil internationally agreed criteria [12,13,27,32,33].…”

mentioning

confidence: 99%

“…Although PPH is often thought to be associated with DIC, this is an uncommon event and very few cases fulfil internationally agreed criteria [12,13,27,32,33]. The consumptive coagulopathies associated with PPH are often localised to the placental bed (e.g.…”

mentioning

confidence: 99%

“…in many cases of abruption), or related to coagulation factors being consumed into inter-uterine clots (e.g. in atony) [12]. True DIC is seen with amniotic fluid embolus, in some cases of severe pre-eclampsia or HELLP syndrome and more severe cases of abruption [29].…”

mentioning

confidence: 99%

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Haemostatic management of obstetric haemorrhage

2014

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SummaryThe haemostatic management of major obstetric haemorrhage remains challenging, and current published guidance relies heavily on experience from the non-pregnant population and expert opinion. In recent years, an interest in the implications of relative hypofibrinogenaemia, point-of-care monitoring of coagulation abnormalities, and the potential to give goal-directed therapy to correct coagulopathies, have created the possibility of significantly challenging and changing guidance. There is evidence that the haemostatic impairment in the pregnant population is different from trauma-induced bleeding, and the type and rate of onset of coagulopathies differ depending on the underlying cause. This review examines areas such as possible intervention points, describes evidence for overtransfusion of fresh frozen plasma in some situations and challenges conventional thinking on formulaic management. It also examines the rationale for other therapeutic options, including fibrinogen concentrate and tranexamic acid.

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Section: Changes In Haemostasis At Termmentioning

confidence: 99%

Section: Haemostatic Changesmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Haemostatic management of obstetric haemorrhage

2014

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Acquired Bleeding Disorders

O’Sullivan

Hunt

2015

Encyclopedia of Life Sciences

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Acquired bleeding disorders include disseminated intravascular coagulation ( DIC ), vitamin K deficiency, massive transfusion, renal and liver disease and hyperfibrinolysis. A history of a bleeding tendency should be followed by appropriate laboratory investigations. DIC is characterised by consumption of platelets and coagulation factors and increased fibrinolytic activity. The treatment of the underlying condition is key to DIC management. In major bleeding, serial coagulation tests should be performed to guide use of blood components. Vitamin K deficiency occurs in neonates and malabsorptive states. Abnormalities in liver disease involve coagulation and fibrinolytic defects and platelet dysfunction, whereas in renal disease, abnormal platelet function and adhesion is the primary abnormality. Hyperfibrinolysis involves excessive fibrinolytic activity causing disproportionately elevated FDPs (fibrinogen degradation products) (D‐dimer levels) and should be considered in patients with liver disease and disseminated cancers. Acquired coagulation inhibitors result from immune‐mediated inhibition of a coagulation factor in patients with inherited bleeding disorder or previously normal haemostasis. Key Concepts Key to management of DIC is treatment of the underlying condition. Only replace coagulation proteins and platelets in bleeding patient or for planned interventions. Early use of fresh frozen plasma to prevent coagulopathy development is currently recommended. Tranexamic acid should be given in all patients at risk of or with significant bleeding. Vitamin K prophylaxis should be offered to all neonates at birth. Prothrombin complex concentrate is recommended when rapid reversal of vitamin K antagonist therapy is required. Vitamin K given either orally or intravenously will reverse the effects of VKAs in 6 h. In liver disease, asymptomatic patients with abnormal coagulation tests do not routinely require replacement therapy. Abnormalities of platelet function and adhesion are the major causes of bleeding in renal disease. Acquired coagulation inhibitors can occur in patients with congenital coagulation factor deficiencies or in patients with previously normal haemostasis.

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