Acute urinary retention as a complication of primary varicella-zoster infection of childhood – a second reported case
To the Editor: We discuss the case of a child with acute urinary retention and constipation following primary varicella-zoster infection (chickenpox). To our knowledge, this unusual complication has only been reported once before.1
An 8-year-old boy presented 2 days after developing urinary retention. Chickenpox had been diagnosed 2 weeks previously and treated with paracetamol and topical calamine lotion. There was no similar preceding history, trauma, use of anti-cholinergic medication, or other urinary or neurological signs or symptoms. The child was HIV-negative. He was fully ambulant, well hydrated and apyrexial. His urinary bladder was abdominally palpable and was catheterised at the referring hospital, draining clear urine. The trunk and extremities had healing primary varicella-zoster (chickenpox) skin lesions. No evidence of sacral or perineal shingles rash (secondary varicella-zoster infection) or neurological deficit was found. Urine dipstix, renal function tests, blood electrolytes, full blood count and C-reactive protein were normal. Lumbar puncture and serology for varicella-zoster virus were not done.
After excluding urethral and bladder outlet obstruction, anti-cholinergic use, urinary tract or bladder infection and transverse myelitis, primary varicella-zoster virus-related urinary retention and constipation was tentatively diagnosed. He was admitted and given oral acyclovir (400 mg 8-hourly for 10 days) and laxatives. After 3 doses of acyclovir, the catheter was temporarily removed and the child gradually began to urinate and resumed passing stools. There were no further similar complaints after discharge. Informed consent for publication was obtained from the patient.
The varicella-zoster virus is an exclusively human virus belonging to the Alphaherpesvirinae subfamily of the Herpesviridae.2 It is neurotropic and very contagious, and is spread mostly by virus-filled respiratory droplets and, to a lesser degree, from skin lesions.3 Varicella-zoster causes 2 distinct clinical syndromes: chickenpox/varicella, the initial or primary infection of the host; and shingles/zoster, corresponding to reactivation of latent infection.2
In healthy children, chickenpox usually has no prodrome, is self-limiting, and is characterised by a distinct pruritic exanthum (macules progressing to papules and virus-rich vesicles before crusting), malaise and low-grade fever. Treatment is symptomatic.
Once the self-limiting initial infection is contained by the immune system, the virus establishes itself within the spinal cord ganglia (dorsal root/sensory ganglia being the most common site) and becomes latent. Transport to the ganglia is thought to be via retrograde axonal transport (from the skin) and via haematogenous spread.2
Re-activation of dormant varicella-zoster virus occurs when cell-mediated immunity is weakened, allowing viral replication within the infected ganglia. Viral spread along the nerves associated with the affected ganglia causes symptoms associated with nerve dysfunction.3 Re-activation within sensory ganglia results in a painful dermatomal zoster rash whereas signs of re-activation within the autonomic sacral ganglia include urinary retention, zoster cystitis, or ano-rectal dysfunction.2 We found 1 report in the English literature of urinary retention complicating primary varicella-zoster infection.1 Their case differed in having a large primary varicella-zoster vesicle on the glans penis obstructing the urethral meatus.1 Incision and removal of the vesicle did not resolve the retention, necessitating suprapubic catheterisation and dilatation of a meatal stricture, with gradual regaining of full micturition control. The authors speculated that the retention was due to combined neurogenic effects of the primary varicella-zoster infection on the sacral ganglia (i.e. the virus establishing itself within the sacral ganglia before becoming latent) and obstruction caused by the vesicle and stricture.1
Having excluded other pathology, we believe that our patient’s presentation was congruent with the hypothesis that, towards the end of primary varicella-zoster infection, virus infecting a specific ganglion (prior to becoming latent) may cause transient neurological effects. As this was the patient’s first varicella-zoster infection, we believe that, should infection be re-activated (by old age or immune suppression), he may again develop urinary dysfunction and constipation.
David M Favara
East London Hospital Complex
1. Nicholas RM, Sharpe S, Graham WJ, Templeton JL. Acute urinary retention: a unique complication of primary varicella infection of childhood. Br J Urol 1990;66(5):546-547.
2. Gilden D, Mahalingam R, Nagel MA, Pugazhenthi S, Cohrs RJ. Review: The neurobiology of varicella zoster virus infection. Neuropathol Appl Neurobiol 2011;37(5):441-463. [http://dx.doi.org/10.1111/j.1365-2990.2011.01167.x].
3. Dinh A, Salomon J, Schoindre Y, et al. Acute urinary retention due to viral coinfections (HIV, HBV, VZV). J Int Assoc Physicians AIDS Care (Chic) 2010;9(1):20-22. Epub 18 December 2009.
4. Rix GH, Carroll DN, MacFarlane JR. Herpes zoster producing temporary erectile dysfunction. Int J Impot Res. 2001;13(6):352-353.
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