Establishing a peripartum perineal trauma clinic: a narrative review.

INTRODUCTION AND HYPOTHESIS: Obstetric anal sphincter injury (OASI) is not rare, and its consequences are multiple and potentially severe, especially for young women. Some dedicated perineal clinics have been established to improve the management of OASI. Despite their obvious importance, these specific clinics are underrepresented and underdeveloped. The objectives of this review are to explore various options for developing a peripartum perineal clinic and to compare the different practices regarding the mode of delivery for subsequent pregnancies after an OASI. METHODS: This narrative review covers information from patients' questionnaires specific to anal incontinence, anal physiology assessment, pelvic floor and anal sphincter imaging, and the arguments for choosing the mode of delivery after an OASI. RESULTS: This review highlights the extensive range of practices regarding the delivery mode after an OASI throughout national professional organizations and experienced perineal clinics. CONCLUSION: This review summarizes the different choices in developing a perineal clinic to facilitate their development in promoting health care and education specific for peripartum women concerning the perineal consequences of delivery for obstetrician-gynaecologists, family doctors, and residents.

Surgical treatment of intractable pelvic, groin, and perineal neuropathic pain in a gynaecologic patient: triple neurectomy.

BACKGROUND: Gynaecologists who are asked to assess patients with pain in the genital area are not generally trained to consider neurogenic causes for the pain, nor are they generally familiar with the surgical procedures that can eliminate this pain. CASE: A 54-year-old woman who had undergone multiple laparotomies for Caesarean section, abdominal hysterectomy, treatment of ovarian cysts, and lysis of adhesions through a transverse abdominal approach presented with a seven- to eight-month history of severe neuropathic left-sided groin, labial, and perineal pain. Neurectomy involving the iliohypogastric, ilioinguinal, and genitofemoral nerves was performed. Postoperatively the patient experienced complete resolution of the pain. CONCLUSION: Neuropathic pain should be considered in the differential diagnosis of women with an extensive history of lower abdominal surgery. Neurectomy is an effective treatment for this.

Contexte : Les gynécologues à qui l'on demande d'évaluer des patientes qui présentent des douleurs affectant les organes génitaux ne disposent généralement pas de la formation qui leur permettrait de tenir compte des causes neurogènes de la douleur; d'ordre général, les interventions chirurgicales permettant d'éliminer cette douleur ne leur sont également pas familières. Cas : Une femme de 54 ans qui avait subi de multiples laparotomies (césarienne, hystérectomie abdominale, prise en charge de kystes ovariens et libération d'adhérences) par l'intermédiaire d'une approche abdominale transversale connaissait de graves douleurs neuropathiques inguinales, labiales et périnéales affectant le côté gauche depuis 7-8 mois. Une neurectomie visant les nerfs ilio-hypogastrique, ilio-inguinal et génitocrural a été menée. À la suite de l'intervention, la patiente en est venue à connaître une résolution totale de la douleur. Conclusion : La présence de douleurs neuropathiques devrait être envisagée dans le cadre du diagnostic différentiel chez les femmes qui présentent des antécédents importants de chirurgie abdominale basse. La neurectomie constitue alors un traitement efficace.

Dexamethasone inhibits the action of TNF on ENaC expression and activity.

We have reported that TNF, a proinflammatory cytokine present in several lung pathologies, decreases the expression and activity of the epithelial Na(+) channel (ENaC) by approximately 70% in alveolar epithelial cells. Because dexamethasone has been shown to upregulate ENaC mRNA expression and is well known to downregulate proinflammatory genes, we tested if it could alleviate the effect of TNF on ENaC expression and activity. In cotreatment with TNF, we found that dexamethasone reversed the inhibitory effect of TNF and upregulated alpha, beta, and gammaENaC mRNA expression. When the cells were pretreated for 24 h with TNF before cotreatment, dexamethasone was still able to increase alphaENaC mRNA expression to 1.8-fold above control values. However, in these conditions, beta and gammaENaC mRNA expression was reduced to 47% and 14%, respectively. The potential role of TNF and dexamethasone on alphaENaC promoter activity was tested in A549 alveolar epithelial cells. TNF decreased luciferase (Luc) expression by approximately 25% in these cells, indicating that the strong diminution of alphaENaC mRNA must be related to posttranscriptional events. Dexamethasone raised Luc expression by fivefold in the cells and augmented promoter activity by 2.77-fold in cotreatment with TNF. In addition to its effect on alphaENaC gene expression, dexamethasone was able to maintain amiloride-sensitive current as well as the liquid clearance abilities of TNF-treated cells within the normal range. All these results suggest that dexamethasone alleviates the downregulation of ENaC expression and activity in TNF-treated alveolar epithelial cells.

Downregulation of ENaC activity and expression by TNF-alpha in alveolar epithelial cells.

Sodium absorption by an amiloride-sensitive channel is the main driving force of lung liquid clearance at birth and lung edema clearance in adulthood. In this study, we tested whether tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine involved in several lung pathologies, could modulate sodium absorption in cultured alveolar epithelial cells. We found that TNF-alpha decreased the expression of the alpha-, beta-, and gamma-subunits of epithelial sodium channel (ENaC) mRNA to 36, 43, and 16% of the controls after 24-h treatment and reduced to 50% the amount of alpha-ENaC protein in these cells. There was no impact, however, on alpha(1) and beta(1) Na(+)-K(+)-ATPase mRNA expression. Amiloride-sensitive current and ouabain-sensitive Rb(+) uptake were reduced, respectively, to 28 and 39% of the controls. A strong correlation was found at different TNF-alpha concentrations between the decrease of amiloride-sensitive current and alpha-ENaC mRNA expression. All these data show that TNF-alpha, a proinflammatory cytokine present during lung infection, has a profound influence on the capacity of alveolar epithelial cells to transport sodium.

Alveolar liquid clearance and sodium channel expression are decreased in transplanted canine lungs.

To determine the impact of transplantation-associated injury on the clearance mechanisms of pulmonary edema, we created a canine single lung transplant model. After 3 hours of preservation and 4 hours of reperfusion, right native lungs and left transplanted lungs were used to measure alveolar liquid clearance (ALC) in ex vivo liquid-filled lung preparations. We also examined the role of the pulmonary circulation in edema clearance in in vivo liquid-filled lungs between 4 and 8 hours of reperfusion. To study molecular modifications in ALC, we also measured expression levels of the epithelial sodium channel (ENaC) and sodium-potassium-adenosine triphosphatase (ATPase). We found that ALC was significantly lower in transplanted than in right native lungs ex vivo (p < 0.05) and that transplanted lungs did not respond to the beta-adrenergic agonist terbutaline. Our in vivo study confirmed the ex vivo results. Molecular analyses revealed that ENaC messenger RNA but not sodium-potassium-ATPase was significantly decreased in transplanted lungs (p < 0.01). Furthermore, there was a significant decrease in ENaC protein expression. Therefore, we conclude that the current investigation indicates that the lung injury caused by lung preservation and transplantation significantly reduces the edema clearance ability of transplanted lungs.