8%), IUGR (∼15%) [44], [45], [46], [47],

[48], [49], [50]

8%), IUGR (∼15%) [44], [45], [46], [47],

[48], [49], [50], [51] and [52], stillbirth (0.1% by 36 weeks [equivalent to risk at 41 weeks in low risk pregnancies]), and NICU admission (up to 50%) [54], CP-868596 cell line [55], [56], [57], [58] and [59]. This appears at ⩾20 weeks. By ABPM, ≈30% of women with hypertension at ⩾20 weeks demonstrate white coat effect (≈70% in third trimester) [60]. Associated risks depend on gestational age at presentation and progression to preeclampsia; gestational hypertension at <34 weeks is associated with a ∼35% risk of preeclampsia which takes an average of 5 weeks to develop [61], [62], [63], [64], [65] and [66]. This is the HDP associated with the greatest risks, particularly when it is severe or present at <34 weeks. The risk of SGA infants is primarily among find more women who

present at <34 weeks, with macrosomia more common with term preeclampsia [67]. ○ The pathogenesis of preeclampsia Preeclampsia results from a mismatch between uteroplacental supply and fetal demands, leading to its systemic inflammatory maternal (and fetal) manifestations (Fig. 1) [68] and [69]. The most common maternal manifestations define preeclampsia clinically: hypertension and proteinuria. Other manifestations reflect end-organ dysfunction and are non-specific. Stroke [2] and [25], and pulmonary oedema are leading causes of maternal death in preeclampsia [25]. Jaundice is a late finding or may reflect another diagnosis (e.g., acute fatty liver of pregnancy). Eclamptic seizures are usually isolated [70], [71], [72], [73], [74], [75] and [76]. Fetal manifestations

may occur before, with, or in the absence of maternal manifestations [77], and consist of oligohydramnios, IUGR (up to 30%) [78], abnormal umbilical artery Doppler velocimetry, decreased fetal middle cerebral artery resistance, an abnormal ductus venosus waveform, and/or stillbirth. ○ Definition of preeclampsia Preeclampsia is most commonly defined by new-onset proteinuria and potentially, other end-organ dysfunction. Hypertension and proteinuria are discussed under ‘Diagnosis of hypertension’ and ‘Proteinuria’. Women with preeclampsia may have Casein kinase 1 a diminished or no nocturnal BP decrease [10]. Table 2 outlines the end-organ dysfunction of preeclampsia: ‘adverse conditions’ and ‘severe complications.’ ‘Adverse conditions’ consist of maternal symptoms, signs, and abnormal laboratory results, and abnormal fetal monitoring results that may herald development of severe maternal orfetal complications (including stillbirth). The ‘adverse conditions’ are those that we wait for and respond to (e.g., low oxygen saturation) to avoid the severe complications that we wish to avoid entirely (e.g., pulmonary oedema).

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