Antenatal risk prediction of shoulder dystocia: influence of diabetes and obesity: a multicenter study.

PURPOSE: To estimate the risk of shoulder dystocia (SD) in pregnancies with/without maternal diabetes or obesity; to identify antenatal maternal and fetal ultrasound-derived risk factors and calculate their contributions. METHODS: A multicenter retrospective analysis of 13,428 deliveries in three tertiary hospitals (2014-2017) with fetal ultrasound data ≤ 14 days prior to delivery (n = 7396). INCLUSION CRITERIA: singleton pregnancies in women ≥ 18 years old; vertex presentation; vaginal delivery at ≥ 37 weeks of gestation. Estimated fetal weight (EFW) and birth weight (BW) were categorized by steps of 250 g. To evaluate risk factors, a model was performed using ultrasound data with SD as the dependent variable. RESULTS: Diabetes was present in 9.3%; BMI ≥ 30 kg/m2 in 10.4% and excessive weight gain in 39.8%. The total SD rate was 0.9%, with diabetes 2.0% and with obesity 1.9%. These increased with BW 4250-4499 g compared to 4000-4249 g in women with diabetes (12.1% vs 1.9%, P = 0.010) and without (6.1% vs 1.6%, P < 0.001) and at the same BW threshold for women with obesity (9.6% vs 0.6%, P = 0.002) or without (6.4% vs 1.8%, P < 0.001). Rates increased similarly for EFW at 4250 g and for AC-HC at 2.5 cm. Independent risk factors for SD were EFW ≥ 4250 g (OR 3.8, 95% CI 1.5-9.4), AC-HC ≥ 2.5 cm (OR 3.1, 95% CI 1.3-7.5) and diabetes (OR 2.2, 95% CI 1.2-4.0). HC/AC ratio, obesity, excessive weight gain and labor induction were not significant. CONCLUSION: Independent of diabetes, which remains a risk factor for SD, a significant increase may be expected if the EFW is ≥ 4250 g and AC-HC is ≥ 2.5 cm.

Platelet activation and increased tissue factor expression on monocytes in reperfusion injury following orthotopic liver transplantation.

Platelets have been implicated in the pathogenesis of liver damage after orthotopic liver transplantation (OLT). Early graft dysfunction is frequently caused by reperfusion injury subsequent to cold ischemia (IRI). Therefore, we investigated activation of the pivotal haemostatic cells, platelets and monocytes, from patients with elevated markers of IRI and from patients with uneventful course (control-group), respectively during the first week after OLT. Flow cytometry analysis of citrate anticoagulated blood samples revealed that platelets from IRI patients became significantly activated within 48 h after OLT in vivo, with increased surface presentation of P-selectin, CD40L, thrombospondin-1 and tissue-factor. Platelet activation in IRI patients on post-transplant day 2 was accompanied by significantly enhanced tissue-factor expression on peripheral blood monocytes, significant elevated levels of C-reactive protein and hepatocellular damage. Towards post-transplant day 4, levels of platelet-derived microparticles rose significantly in IRI patients if contrasted to control patients. Thus, activated cellular haemostasis is involved in the early inflammatory response of hepatocellular damage subsequent to reperfusion of the transplanted liver. Targeting distinct activation patterns of platelets and monocytes in an early phase of hepatic grafting may counteract the extent of IRI via inhibition of micro-thrombus formation and inflammation without exacerbating the existing bleeding risk.