High transverse skin incisions may reduce wound complications in obese women having cesarean sections: a pilot study.

OBJECTIVE: Women having cesarean section have a high risk of wound complications. Our objective was to determine whether high transverse skin incisions are associated with a reduced risk of cesarean wound complications in women with BMI greater than 40. METHODS: A retrospective cohort study was undertaken of parturients ages 18-45 with BMI greater than 40 having high transverse skin incisions from January 2010 to April 2015 at a tertiary maternity hospital. Temporally matched controls had low transverse skin incisions along with a BMI greater than 40. The primary outcome, wound complication, was defined as any seroma, hematoma, dehiscence, or infection requiring opening and evacuating/debriding the wound. Secondary outcomes included rates of endometritis, number of hospital days, NICU admission, Apgar scores, birth weight, and gestational age at delivery. Analysis of outcomes was performed using two-sample t-test or Wilcoxon rank-sum test for continuous variables and Fisher's exact test for categorical variables. RESULTS: Thirty-two women had high transverse incisions and were temporally matched with 96 controls (low transverse incisions). The mean BMI was 49 for both groups. There was a trend toward reduced wound complications in those having high transverse skin incisions, but this did not reach statistical significance (15.63% versus 27.08%, p = .2379). Those having high transverse skin incisions had lower five minute median Apgar scores (8.0 versus 9.0, p = .0021), but no difference in umbilical artery pH values. The high transverse group also had increased NICU admissions (28.13% versus 5.21%, p = .0011), and early gestational age at delivery (36.8 versus 38.0, p = .0272). CONCLUSION: High transverse skin incisions may reduce the risk of wound complications in parturients with obesity. A study with more power should be considered.

Evaluating maternal hyperglycemic exposure and fetal placental arterial dysfunction in a dual cotyledon, dual perfusion model.

BACKGROUND: Gestational diabetes affects almost 1 in 10 pregnancies and is associated with adverse outcomes including fetal demise. Pregnancy complications related to diabetes are attributed to placental vascular dysfunction. With diabetes, maternal hyperglycemia is thought to promote placental vasoconstriction. However, it remains poorly understood if and how hyperglycemia leads to placental vascular dysfunction or if humoral factors related to maternal diabetes are responsible. METHODS AND RESULTS: Utilizing a human placenta dual cotyledon, dual perfusion assay we examined the arterial pressure response to the thromboxane mimetic U44619, in cotyledons exposed to normal vs. a hyperglycemic infusion into the intervillous space. Tissues were then analyzed for the activity of key signaling molecules related to vascular tone; eNOS, Akt, PKA and VEGFR2. Results indicate a significant increase in fetal vascular resistance with maternal exposure to hyperglycemia. This response corresponded with a reduction in the phosphorylation of eNOS at Ser1177 and Akt at Thr308. In contrast, VEGFR2 at Tyr1175 and PKA at Thr197 were not different with hyperglycemia. CONCLUSION: Reductions of eNOS and Akt phosphorylation at key residues implicated in nitric oxide production suggest that hyperglycemia alters the vasodilatory signaling of placental vessels. In contrast, acute hyperglycemic exposure may not alter vasoconstriction via VEGF and PKA signaling. Altogether our results link hyperglycemic exposure in human placentas to nitric oxide signaling; a mechanisms that may account for the elevations in vascular resistance commonly observed in diabetic pregnancies.

Evaluation of Sildenafil and Tadalafil for Reversing Constriction of Fetal Arteries in a Human Placenta Perfusion Model.

Fetal growth restriction resulting from reduced placental blood perfusion is a major cause of neonatal morbidity and mortality. Aside from intense surveillance and early delivery, there is no treatment for fetal growth restriction. A potential treatment associated with placental vasoconstriction is the class of PDE5 (phosphodiesterase type 5) inhibitors such as sildenafil, which is known to cross the placenta. In contrast, tadalafil, a more potent and selective PDE5 inhibitor has not been studied in pregnancy or experimental models of fetal growth restriction. Therefore, we compared the efficacy of these 2 PDE5 inhibitors for reversing vasoconstriction in an ex vivo human placental model and evaluating molecular and physiological responses. Sildenafil and tadalafil were infused into the intervillous space in a preconstricted human placental dual cotyledon, dual perfusion assay for the comparison of arteriole pressures and molecular indicators of drug inhibition. Results indicate a decrease arterial pressure with sildenafil citrate compared with controls, whereas tadalafil showed no difference. PDE5 and endothelial nitric oxide synthase activity were altered with sildenafil but not tadalafil. Sildenafil citrate improved preconstricted placental arterial perfusion in a human placental model, whereas tadalafil showed no response. It is possible that tadalafil did not cross the human placental barrier or was degraded by trophoblasts. This study supports human clinical trials exploring sildenafil as a potential treatment for improving fetal blood flow in fetal growth restriction associated with vasoconstriction.