Bladder Outlet Obstruction (& Anti-cholingeric drugs)

Bladder outlet obstruction generally presents with any or all of the following symptoms:

• reduction in urine output
• bladder spasms
• incontinence
• lower urinary tract infection (cystitis)
• abdominal or suprapubic pain,
• a feeling of abdominal fullness.

The etiology of bladder outlet obstruction includes:

• mechanical causes (eg, tumor, posterior urethral valves)
• neurogenic bladder (eg, due to spinal deformity)
• medication (eg, anticholinergics). 

To understand how anticholinergics cause bladder outlet obstruction, it is important to review the muscular anatomy and neural innervation of the bladder. Normal bladder function depends on the central and peripheral nervous systems and the detrusor muscle and external sphincter of the bladder. Muscular fibers in the bladder interdigitate around the bladder neck, resulting in the formation of a sphincter, which controls the outflow of urine. The somatic and autonomic nervous systems (ANS) control bladder function. The ANS involves sympathetic (from T10 and L1) and parasympathetic (from S2 to S4) control. The sympathetic nervous system stimulates alpha- and beta-receptor sites  in the bladder smooth muscle. The primary neurotransmitter for sympathetic control is norepinephrine (NE). When NE interacts with alpha receptors in the  bladder, the bladder smooth muscle tone increases, allowing for stretch. Stimulation of beta receptors in the bladder by NE results in relaxation of the detrusor muscle. Thus, NE allows the bladder to expand, thereby accommodating the inflow of urine from the kidneys and ureters. The primary neurotransmitter of the parasympathetic nervous system is acetylcholine (ACH). Release of ACH from the parasympathetic nervous system results in bladder contraction. Combined with reduced output from the sympathetic nervous system, the bladder releases urine into the urethra.

Because ACH is a cholinergic substance, anticholinergic medications may counteract its effects, including promotion of bladder emptying. For patients taking anticholinergic medication, the bladder is under only sympathetic control, with a net result of prolonged bladder filling and expansion. In the absence of bladder emptying, spasms inevitably ensue. The effect is identical to that seen in children who have spinal cord lesions at S2 to S4, in which parasympathetic stimulation is reduced.
 
Treatment for bladder spasms due to anticholinergic therapy is discontinuation of the medication. Antiarrhythmics, antihistamines, antipyretics, and antitussives all have significant adverse effects, but they do not include abnormalities in neural stimulation of the urinary bladder.

References:
Atala A, Bauer SB. Bladder dysfunction. In: Barratt TM, Avner ED,
Harmon WE, eds. Pediatric Nephrology. 4th ed. Baltimore, Md:
Lippincott Williams & Wilkins; 1999:913-914
Kaefer M, Zurakowski D, Bauer SB, et al. Estimating normal bladder
capacity in children. J Urol. 1997;158:2261-2264