Maternal and neonatal primary hemostasis

Saleh, Abdelaziz A.; Alshameeri, Rasheed S.; O’Brien, James M.; Munkarah, Adnan; Dombrowski, Mitchel P.; Bottoms, Sidney F.; Cotton, David B.; Mammen, Eberhard F.

doi:10.1016/0049-3848(94)90087-6

Cited by 14 publications

(16 citation statements)

References 8 publications

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“…Results are con¯icting, most studies using conventional aggregation methods [3,6,14,24] have shown a diminished response to various agonists: platelets of newborns exhibited a low response when induced by collagen and adenosine diphosphate (ADP) [6]; normalization of platelet aggregation response was beginning by the 5th day of life [23]. Platelet aggregation [18] with platelet-rich plasma was markedly impaired in neonatal blood when platelets were stimulated with ADP, epinephrine, collagen, or thrombin, while aggregation with whole blood showed no dierences between neonates and their mothers when ADP and collagen were used as the stimulating agents.…”

Section: Introductionmentioning

confidence: 99%

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Hyporeactivity of neonatal platelets is not caused by preactivation during birth

Grosshaupt

Muntean

Sedlmayr

1997

European Journal of Pediatrics

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Section: Introductionmentioning

confidence: 99%

“…Bleeding time is short in neonates. Using Thrombostat 4000, an in vitro device to measure primary haemostasis in newborns and their mothers [18], the bleeding time was signi®cantly shorter in newborns than in their mothers suggesting an accelerated primary haemostasis in neonates.…”

Section: Introductionmentioning

confidence: 99%

Hyporeactivity of neonatal platelets is not caused by preactivation during birth

Grosshaupt

Muntean

Sedlmayr

1997

European Journal of Pediatrics

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“…There is an apparent contrast between an in vitro hypofunctional state of neonatal platelets regarded as subactivated, and evidence of normal or even short in vivo bleeding times. One reason why the problem is still unresolved may be technical since diculties in assessing platelet function in the neonate arise from the excessive volume of blood needed and from the intrinsic variability of the methods available [3,4,6]. Simple ®rst-line screening procedures have not been available to assess the platelet function in newborns.…”

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confidence: 99%

The in-vitro bleeding time for the screening of platelet function in the newborn: assessment of a normal reference range

et al. 2001

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Sir: The physiological functional state of platelets in newborn babies is a matter of debate. There is an apparent contrast between an in vitro hypofunctional state of neonatal platelets regarded as subactivated, and evidence of normal or even short in vivo bleeding times. One reason why the problem is still unresolved may be technical since diculties in assessing platelet function in the neonate arise from the excessive volume of blood needed and from the intrinsic variability of the methods available [3,4,6]. Simple ®rst-line screening procedures have not been available to assess the platelet function in newborns. The Platelet Function Analyser (PFA100, Dade Behring, Miami, Fla., USA) is a new tool for the quick and fully automated analysis of platelet response to agonists. The PFA100 measures the``in vitro bleeding time'' (IVBT), an ex vivo surrogate of the in vivo bleeding time, using only 800 ll citrate anticoagulated whole blood. Brie¯y, PFA100 controls the blood ow through a substrate-agonist (collagen-epinephrine or collagen-ADP) coated capillary; platelets adhere, become activated, and form plugs, which obstructs the blood¯ow. The plug-dependent capillary obstruction is measured as closure time. Manual operations are restricted to blood pipetting into disposable cartridges (requiring a few seconds); the overall test time up to the printed report is 10±15 min. The infrareplicate coecient of variation is 7%±12%. IVBT measurement has been successfully used for the detection of congenital platelet disorders such as those due to von Willebrand defect [2]. Owing to its intrinsic characteristics, PFA100 seems to be a candidate to enable large-scale platelet function investigations in newborns. In order to assess the normal newborn IVBT reference range, a group of 25 consecutive neonates was investigated.The study group was homogeneous for gestational age (39 1.2 weeks): all were clinically well, including three from preeclamptic mothers. Mothers and newborns were not on drugs known to aect platelet function. The neonates were bled at 0±4 days of age from the antecubital vein using a 21±23 gauge needle. A total of 36 adult blood donors were used as controls. The results (Fig. 1) clustered according to the newborns' age did not show signi®cant dierences (0 vs 4 days, Kruskal-Wallis analysis). Slight dierences in gestational age did not correlate with closure times (linear regression analysis; epinephrine-induced, EPI, closure time: r 2 = 0.0976, ADP time: r 2 = 0.015). The EPI closure time did not dier between the study groups (EPI time; Mann-Whitney U test: P 0.723). One newborn from a pre-eclamptic woman had the longest closure time of the neonate group (222 s), supporting the hypothesis of a close cause±eect relationship between maternal pre-eclamptic status and neonatal platelet function. A slight dierence was evident comparing the ADP induced closure time of the two groups (ADP time; Mann-Whitney U test: P 0.016).Such ®ndings warrant comment. ADP-dependent platelet activation is a very complex event. Two dis...

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“…The discrepancy mentioned is elucidated by technical reasons: thrombin generation in neonates is only impaired when strong activators are used to start clotting and this difference between neonates and adults cannot be shown when small amounts of tissue factor are used as activator [15]. The bleeding time (measured in vitro using a Thrombostat 4000 device) is short in neonates, even shorter than in their mothers [17]. In summary, neonates have an excellent hemostasis, despite the apparent functional immaturity, resulting in relatively few clinical coagulation problems for the healthy term infant.…”

Section: The Neonatal Coagulation Systemmentioning

confidence: 91%

The neonatal coagulation system and the vitamin K deficiency bleeding – a mini review

Pichler¹,

Pichler

2008

Wien Med Wochenschr

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Coagulation factors do not cross the placental barrier but are synthesized independently by the conceptus. At birth, activities of the vitamin K dependent factors II, VII, IX, and X and the concentrations of the contact factors XI and XII are reduced to about 50% of normal adult values. The levels of the factors V, VIII, XIII, and fibrinogen are similar to adult values. Plasma concentrations of the naturally occurring anticoagulant proteins (antithrombin, protein C, and protein S) are significantly lower at birth than during the adult years. Plasminogen is reduced by approximately 50%. Platelet counts are within the normal range, regarding function, however, neonatal platelets seem to be hyporeactive. The von Willebrand factor contains large multimers and its concentration is increased. Properties and functions of vitamin K as well as requirement and plasma concentrations in newborns are reviewed. Regarding vitamin K deficiency bleeding (VKDB), the classical nomenclature is used: "early" (presenting within the first 24 h of life), "classical" (day 1-7 after birth), and "late" (8 days to 6 months). After the presentation of the history of vitamin K prophylaxis, vitamin K levels are described as can be expected after the administration of prophylactic doses at various routes. Subsequently, the actual schedule of vitamin K prophylaxis as recommended by the "Osterreichische Gesellschaft für Kinder- und Jugendheilkunde" is given as follows: i) the oral treatment of healthy full-term babies and orally fed preterm babies, ii) the parenteral treatment of small preterm and sick full-term babies, and iii) the treatment of mothers under medication with enzyme-inducing drugs with vitamin K during the last 15-30 days of pregnancy. The regimes of prophylactic vitamin K treatment of different countries are also given. Finally, the therapeutic use of vitamin K is addressed; the potential use of fresh-frozen plasma, prothrombin complex preparations, and recombinant factor VIIa is discussed.

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Maternal and neonatal primary hemostasis

Cited by 14 publications

References 8 publications

Hyporeactivity of neonatal platelets is not caused by preactivation during birth

Hyporeactivity of neonatal platelets is not caused by preactivation during birth

The in-vitro bleeding time for the screening of platelet function in the newborn: assessment of a normal reference range

The neonatal coagulation system and the vitamin K deficiency bleeding – a mini review

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