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Review
. 2011 Dec;18(12):1166-85.
doi: 10.1177/1933719111414206. Epub 2011 Jul 20.

Postoperative adhesion development following cesarean and open intra-abdominal gynecological operations: a review

Affiliations
Review

Postoperative adhesion development following cesarean and open intra-abdominal gynecological operations: a review

Awoniyi O Awonuga et al. Reprod Sci. 2011 Dec.

Abstract

In this review, we discuss the pathophysiology of adhesion development, the impact of physiological changes associated with pregnancy on markers of adhesion development, and the clinical implications of adhesion development following cesarean delivery (CD). Although peritoneal adhesions develop after the overwhelming majority of intra-abdominal and pelvic surgery, there is evidence in the literature that suggests that patients having CD may develop adhesions less frequently. However, adhesions continue to be a concern after CD, and are likely significant, albeit on average less than after gynecological operations, but with potential to cause significant delay in the delivery of the baby with serious, lifelong consequences. Appreciation of the pathophysiology of adhesion development described herein should allow a more informed approach to the rapidly evolving field of intra-abdominal adhesions and should serve as a reference for an evidence-based approach to consideration for the prevention and treatment of adhesions.

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Conflict of interest statement

Author AOA, NMF and GMS, declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. Author MPD has the following conflicts of interest with the following companies: Board membership of the American Society for Reproductive Medicine; Consultancy with Genzyme Biosurgery, Neomend, Omirix, ZSX Medical, Sanofi-Aventis, SyntheMed; Contracts with BioSante, Boerhinger Ingleheim.

Figures

Figure 1.
Figure 1.
Proposed scheme for the pathogenesis of peritoneal adhesion development following injury. WBCs, white blood cells.
Figure 2.
Figure 2.
Proposed scheme for the pathogenesis of adhesion development following injury and induction of gene expression. ↑, an increase; ↓, a decrease; BCl-2, B-cell CLL/lymphoma 2; BAX, BCl2-associated X; COX-2, cyclooxygenase 2; ECM, extracellular matrix; HIF, hypoxia-induced factor; IFNy, Interferon-γ; IL, interleukin; iNOS, inducible nitrous oxide synthase; MMP, matrix metalloproteinases; NADP, nicotine adenine dinucleotide phosphate; NO, nitric oxide; NOS, nitric oxide synthase; P53, tumor protein 53; PAI-1, plasminogen activator inhibitor; TGF-β1, transforming growth factor-beta; TIMP, tissue inhibitor of matrix metalloproteinases; tPA, tissue plasminogen activator; VEGF, vascular endothelial growth factor.
Figure 3.
Figure 3.
Proposed scheme for the interaction of operative oxidative metabolic reaction and free radicals associated adhesion development. Cl-, chloride ion; Fe2+ and Fe3+, elemental iron; GSH, glutathione; GSSG, glutathione disulfide; H2O, wáter; H4B, tetrohydrobiopterin; HOCI, hypochlorous acid; MPO, myeloperoxidase; O2, molecular oxygen; O2 •−, superoxide anion; NADP, nicotine adenine dinucleotide phosphate; NO, nitric oxide; iNOS, inducible nitric oxide synthase; ROS, reactive oxygen specie; SOD, superoxide dismutase.
Figure 4.
Figure 4.
Proposed scheme for the interaction of the coagulation cascade and adhesion development in pregnancy. ↑, denote an increase; ↓, a decrease; a, activated; Ca+, elemental calcium; F, coagulation factors; PAI, plasminogen activator inhibitor; tPA, tissue plasminogen.

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