Infection Signals Track With Delayed Healing After Anal Fissure Surgery
Delayed recovery after anal fissure surgery is not just a matter of persistent pain. In this prospective cohort, healing time tracked with a cluster of patient factors that included older age, female sex, higher body mass index, multiple fissures, and stool positivity for Entamoeba histolytica, Helicobacter pylori, and Giardia.
The infection findings are the most striking part of the study. After adjustment for age, BMI, and number of fissures, all three organisms remained associated with delayed healing, and Entamoeba plus H. pylori stayed independently associated when modeled together. In a field where postoperative delay is often framed as a local wound problem, the data point toward a wider biologic burden that may be shaping mucosal repair.
What the Cohort Looked Like in Practice
This single-center prospective cohort followed 280 patients after anal fissure surgery over 6 months. Of these, 180 achieved normal and complete healing, while 100 had delayed or no healing. The study period ran from August 2024 to November 2025, and patients younger than 18 years, those with malignancy, inflammatory bowel disease, recurrent fissures, associated anal disease, uncontrolled diabetes, poor medication adherence, or poor hygiene were excluded.
Mean age differed between groups: 40.9 ± 12.4 years in the normal-healing group and 44.5 ± 12.6 years in the delayed-healing group. Age, BMI, fissure number, surgery type, energy source, Entamoeba infestation, H. pylori infection, and Giardia infestation all differed significantly between the two groups. Female sex also tracked with delayed healing, although the association was borderline.
Patients underwent one of five procedures performed by the same surgical team: fissurectomy with posterior sphincterotomy, fissurectomy with lateral internal sphincterotomy, lateral internal sphincterotomy alone, V–Y advancement flap, or laser fissuroplasty. The sequence of procedures was assigned by day of clinic attendance rather than by concealed randomization, which leaves room for selection bias. Still, the cohort offers a useful look at how healing behaves across real-world surgical approaches.
Why These Infections May Matter to a Surgical Wound
Anal fissure surgery creates a wound in tissue already prone to ischemia and sphincter hypertonia. Healing depends on restoring blood flow, limiting inflammation, and allowing mucosal remodeling to proceed without interruption. Enteric and gastric infections can plausibly interfere with that process through persistent inflammatory signaling, altered mucosal immunity, and broader effects on nutritional status or gastrointestinal function, even when symptoms are absent.
The association with H. pylori is especially notable because the organism was confirmed with stool ELISA and PCR rather than inferred clinically. Entamoeba and Giardia were handled the same way. No eradication treatment was given during the study period, which allowed the investigators to examine the infections themselves rather than treatment effects. As a result, the signal seen here is not a medication effect or a short-term postoperative artifact; it is a biologic association between untreated infection and slower wound closure.
Surgery Type Mattered Less After Adjustment Than the Wound Biology
Unadjusted analyses suggested that V–Y advancement flap, laser fissuroplasty, and lateral internal sphincterotomy were linked to lower rates of delayed healing. After adjustment for age, BMI, and number of fissures, only laser fissuroplasty remained statistically significant.
That pattern points to a familiar surgical problem: procedure choice may influence healing, but patient biology can dominate the outcome. Laser fissuroplasty may create a smaller or more controlled injury field than other techniques, which could explain why it retained significance after multivariable modeling. By contrast, the benefit of the other procedures weakened once the baseline differences between patients were taken into account.
The outcome definition was also clinically grounded. Patients without complete healing at 3 months were classified as delayed healing, and those not healed by 6 months were classified as failed or no healing. Follow-up was intensive, with clinic visits twice weekly for 2 weeks and then weekly for 10 weeks, and healing was assessed by the same physician through digital rectal examination and proctoscopy.
The Signal Held Up in Sensitivity Analyses
The study did not rely on a single statistical pass. Sensitivity analyses using Firth’s penalized likelihood logistic regression produced consistent findings for all three infections, and additional models that adjusted for diabetes and muscle tone did the same. Stool-positive Entamoeba histolytica, H. pylori, and Giardia remained linked to delayed healing across these models.
That consistency matters because delayed healing is a multifactorial endpoint. Diabetes and anorectal muscle tone can clearly affect repair, but the infection association persisted even when those variables were added. The result suggests that clinicians evaluating a patient whose fissure remains open after surgery should not think only about the operative field. An occult infectious burden may be part of the reason the wound is stalled.
What This Means at the Bedside
The practical takeaway is narrow but important: postoperative delay after anal fissure surgery may justify broader preoperative and follow-up assessment than surgeons usually apply. Stool testing for Entamoeba histolytica, H. pylori, and Giardia identified a subgroup at higher risk of delayed closure, even in patients without overt symptoms. If those infections are common in a local population, ignoring them may leave a reversible contributor to impaired healing untouched.
The study also reminds clinicians that fissure surgery is not just about relieving sphincter spasm. Healing is the endpoint patients feel, and delayed repair means ongoing pain, persistent symptoms, dissatisfaction, and sometimes the sense that the operation failed despite technically adequate surgery. Older age, female sex, higher BMI, and multiple fissures added to that risk profile, but the infection signal gives the cohort its most actionable hypothesis.
The allocation of procedures by clinic day rather than concealed randomization limits how confidently the surgical comparisons can be interpreted. Thirteen patients were lost to follow-up, and baseline characteristics for those patients were not systematically compared with the analyzed cohort. Even with those caveats, the infection associations remained stable across multiple analytic approaches, which makes the main signal hard to dismiss.
For colorectal surgeons, this study raises a concrete question for future practice: should stool-based screening for enteric infection become part of the preoperative workup in patients with anal fissure who are headed for surgery or at risk of poor healing? The answer is not settled here, but the wound data are strong enough to justify testing the idea in larger cohorts with randomized treatment of identified infections.