A contraction response of the internal anal sphincter to Botulinum toxin: does low-pressure chronic anal fissure have a different pathophysiology?

Aim A subset of low-pressure fissures is not associated with typical internal anal sphincter hypertonia and may involve a different pathophysiological mechanism. We aimed to assess the manometric response of the internal anal sphincter to botulinum toxin in low-pressure fissures compared to high-pressure fissures. Method Twenty five units of botulinum toxin (Botox (TM)) were injected directly into the internal anal sphincter. Maximum resting pressure (MRP) and maximum squeeze increment (MSI) were documented at baseline and four weeks after injection. Results Nine (31%) of 29 patients had a low-pressure fissure. Those with an anterior fissure had a significantly lower median baseline MRP than those with a posterior fissure (66 vs 83 mmHg, P = 0.009). Significantly more patients with low-pressure fissures developed a contraction or no response (78% vs 30%, difference 48%, 95% CI 14-82%, P = 0.006). Those developing a contraction response had a lower mean baseline MRP than those developing a relaxation response (56 vs 86 mmHg, difference 30 mmHg, 95% CI 17-43%, P < 0.001). Conclusion Botulinum toxin appears to have an atypical contraction effect on the internal anal sphincter in low-pressure (usually anterior) fissures. This may be accounted for by blockade of acetylcholine released at parasympathetic nerve terminals and the sympathetic ganglion (relaxation). Low pressure fissures may be physiologically different from high-pressure fissures.