The Impact of Antithrombotic Medications on Postoperative Bleeding Events Following Hemorrhoidectomy.

BACKGROUND: Bleeding complications are a risk associated with hemorrhoid procedures. Despite the prevalence of anticoagulant and antiplatelet therapies, including newer direct oral anticoagulants (DOACs) in the aging patient population there is a paucity of data regarding the impact of the use of antithrombotic therapy (AT) especially DOACs, on bleeding complications of hemorrhoid procedures. METHODS: We retrospectively reviewed charts of patients who had undergone a total of 1152 procedures, including hemorrhoid excision and ligation, at a single institution in the years 2016-2018. We noted whether they were prescribed AT, the indication for therapy, perioperative medication management, whether a PBE occurred, and how the PBE was managed. RESULTS: PBE's were noted in 5.92% of patients on ATs, as opposed to 2.66% of patients not on ATs (P = .014.) The odds ratio of having a PBE when on ATs vs not on ATs is 2.3 (95% CI 1.21 to 4.38, P = .011). Seven out of 40 (17.5%) total PBE's required hospital admission or repeat procedure, and this was not associated with AT use. Surprisingly, although males represented most of the patients on ATs, females were statistically more likely to have a PBE following a hemorrhoidectomy if on ATs. DISCUSSION: Patients on AT have an elevated risk of PBE compared to patients not on AT. No significant difference was found between the two groups when considering only those PBE's severe enough to require hospital admission or repeat procedure. Further research is required to establish clear guidelines regarding the perioperative management of AT for hemorrhoid procedures.

Mitigation of autophagy ameliorates hepatocellular damage following ischemia-reperfusion injury in murine steatotic liver.

Ischemia-reperfusion injury (IRI) is a common clinical consequence of hepatic surgery, cardiogenic shock, and liver transplantation. A steatotic liver is particularly vulnerable to IRI, responding with extensive hepatocellular injury. Autophagy, a lysosomal pathway balancing cell survival and cell death, is engaged in IRI, although its role in IRI of a steatotic liver is unclear. The role of autophagy was investigated in high-fat diet (HFD)-fed mice exposed to IRI in vivo and in steatotic hepatocytes exposed to hypoxic IRI (HIRI) in vitro. Two inhibitors of autophagy, 3-methyladenine and bafilomycin A1, protected the steatotic hepatocytes from HIRI. Exendin 4 (Ex4), a glucagon-like peptide 1 analog, also led to suppression of autophagy, as evidenced by decreased autophagy-associated proteins [microtubule-associated protein 1A/1B-light chain 3 (LC3) II, p62, high-mobility group protein B1, beclin-1, and autophagy-related protein 7], reduced hepatocellular damage, and improved mitochondrial structure and function in HFD-fed mice exposed to IRI. Decreased autophagy was further demonstrated by reversal of a punctate pattern of LC3 and decreased autophagic flux after IRI in HFD-fed mice. Under the same conditions, the effects of Ex4 were reversed by the competitive antagonist exendin 9-39. The present study suggests that, in IRI of hepatic steatosis, treatment of hepatocytes with Ex4 mitigates autophagy, ameliorates hepatocellular injury, and preserves mitochondrial integrity. These data suggest that therapies targeting autophagy, by Ex4 treatment in particular, may ameliorate the effects of IRI in highly prevalent steatotic liver.