Sialorrhea & aspiration control - A minimally invasive strategy uncomplicated by anticholinergic drug tolerance or tachyphylaxis.

Sialorrhea complicated by aspiration is a primary source of morbidity and mortality in neurologically impaired children. Anticholinergics are an effective treatment option, but have traditionally been considered only adjuncts due to tachyphylaxis and drug tolerance. Similarly, Botox-A^® salivary gland injections are also considered adjunctive due to the need to repeat treatment every 3 months. This retrospective case series assessed these two adjunctive strategies used in combination as definitive minimally invasive primary treatment.

112 subjects diagnosed with sialorrhea and treated at UPMC Children's Hospital of Pittsburgh between 2004 and 2011 were identified. Charts were carefully reviewed for pertinent information regarding the treatment of their sialorrhea and related outcomes.

Over half of the subject undergoing BTX-A injections were able to reduce their dosage of anticholinergics after receiving injection (58%, n = 28 for glycopyrrolate users and 61%, n = 20 for scopolamine users). Subjects experienced a significant reduction in days spent in the hospital in the year following Botox-A^® injection (P-Value = 0.03), and the number of pneumonia episodes in the year following injection (P-Value = 0.04).

Patients treated effectively with both BTX-A injections into their salivary glands and anticholinergics developed neither tachyphylaxis nor drug tolerance with up to 9.6 years of continuous treatment. During the year following combined therapy, patients' average length hospital stay was reduced by a full week and the number of pneumonia episodes was statistically decreased. The failure rate of combined therapy was below that reported for any other intervention or combination of interventions in the literature. Finally, patients did not require BTX-A re-injection at the reported frequency. We hypothesize that anticholinergic medications competitively block acetylcholine attachment to post-synaptic receptors while BTX-A inhibits acetylcholine release at the pre-synaptic terminal, tachyphylaxis/drug tolerance mechanisms resulting in up-regulation of post-synaptic receptors are disrupted. Although salivary production may increase in the year following BTX-A injection, there is enough remaining activity at a molecular level to inhibit release of acetylcholine allowing salvage with anticholinergic medications at tolerable dosages.