Animated biofeedback is an established treatment for pediatric dysfunctional voiding. Bowel dysfunction is closely associated with dysfunctional voiding. We evaluated the efficacy of animated biofeedback urotherapy in bowel and voiding dysfunction in children with dysfunctional elimination syndrome. A total of 80 children with dysfunctional elimination syndrome were randomly assigned to undergo animated biofeedback (group A, 40 patients) or conservative therapy (group B, 40 patients). Group A underwent animated biofeedback along with pelvic floor muscle exercises and behavioral modification (hydration, high fiber diet, scheduled voiding). Group B underwent behavioral modification only. Dysfunctional voiding symptom score, constipation and fecal soiling episodes per week (according to Paris Consensus on Childhood Constipation Terminology criteria), and uroflowmetry parameters were evaluated before and 6 and 12 months after treatment in both groups. Subjective and objective voiding problems were significantly improved. Vesicoureteral reflux resolved in 7 of 9 children (78%) and urinary tract infection did not recur in 10 of 14 children (71%) within 1 year. Bladder capacity and voided volume did not significantly improve. Post-void residual and voiding time decreased considerably, while maximum and average urine flow increased significantly. All children with fecal soiling and 17 of 25 with constipation (68%) in group A were symptom-free within 1 year after treatment. Animated biofeedback therapy was more efficient than nonbiofeedback management regarding objective and subjective voiding problems and bowel dysfunction (p <0.05). Animated biofeedback effectively treats bowel and voiding dysfunction in children with dysfunctional voiding. Pelvic floor muscle exercises coordinate breathing and pelvic floor muscle contractions, and are beneficial in improving bowel dysfunction.

The new virus SARS-CoV-2 is savagely spreading out over the world. The biologic studies show that the target receptor for the virus might be angiotensin-converting enzyme 2 (ACE2). This peptide is responsible for converting angiotensin II (Ang II), which is a profoundly active peptide, into Ang 1-7 with quite a balancing barbell function. It is emphasized that the direct target of the virus is ACE2 underlining the obvious difference with ACE. Nevertheless, we hypothesized that a back load build up effect on Ang II may usurp the ACE capacity and subsequently leave the bradykinin system unabated. We think there are clinical clues for dry cough and the presumed aggravating role of ACE inhibitors like captopril on the disease process. Thereby, we speculated that inhibition of bradykinin synthesis and/or blockade of bradykinin B2 receptor using Aprotinin/ecallantide and Icatibant, respectively, may hold therapeutic promise in severe cases and these molecules can be advanced to clinical trials.