002;!-534 7 /90/1436-1223$02.00/0 THE JOURNAL OF UROLOGY Copyright© 1990 by AMERICAN UROLOGICAL ASSOCIATION, INC.

Vol. 143, June

Printed in U.S.A.

LYME DISEASE PRESENTING AS URINARY RETENTION MICHAEL B. CHANCELLOR, VIRGINIA M. DATO

AND

JOHNY. YANG

From the Department of Urology, College of Physicians and Surgeons, Columbia University, New York, New York

ABSTRACT

We report a case of Lyme disease that presented with urinary retention. The individual then experienced lower extremity paralysis. Paralysis and urinary retention resolved with intravenous ceftriaxone antibiotic. To our knowledge this is the first report of a urological manifestation as the initial clinical presentation of Lyme disease. Recognition of clinical symptoms and urological complications of Lyme disease also are discussed. (J. Ural., 143: 1223-1224, 1990) Almost 14,000 cases of Lyme disease were reported in 43 states to the Centers of Disease Control from 1980 through 1988. 1 Because the Centers of Disease Control use a strict case definition the true number of cases in this country may be much higher. Lyme disease is caused by a spirochete, Borrelia burgdorferi. The initial clinical manifestations include a characteristic rash called erythema chronicum migrans. 2 With more advanced stages of Lyme disease central and peripheral neurological dysfunction can occur. 3 We report on a woman with Lyme disease and meningoencephalomyelitis in whom the first noticeable manifestation of a neuropathic condition was urinary retention. CASE REPORT

A 42-year-old right-handed woman presented to the emergency room of a community hospital unable to urinate for 24 hours. She had a history of fatigue, numbness of the body and pressure behind both eyes for the last week, which she attributed to chronic sinusitis. The history and examination were otherwise unremarkable. Catheterization produced 1 1. clear urine and the patient was discharged from the hospital. However, she was unable to void during the next 48 hours and returned to the emergency room twice for catheterization. Further evaluations by the emergency room physician were unremarkable and she was told that she did not drink enough fluids. After another 24 hours of inability to void the patient consulted a urologist. The bladder was drained and a pelvic neurological examination revealed decreased pinprick sensation of the perianal region, decreased anal sphincter tone and an absent bulbocavernosus reflex. There also was bilateral lower extremity weakness. The patient was referred to a neurologist immediately and she was hospitalized with the tentative diagnosis of acute myelitis. During the next 24 hours increasing weakness of both legs developed until the patient was unable to walk. The medical history was remarkable for Bell's palsy on the right side 5 years ago, which resolved spontaneously. During the ensuing years she occasionally took oral antibiotics for respiratory infections although she did not remember the names and dosages of the medications. She denied allergies and was not taking any medications. The patient lives on the edge of the New Jersey Pine Barrens in an area endemic for Lyme disease. She did not recall any tick bites or rashes. Physical examination revealed no skin lesions. The fundi were normal, pupils were equal and reactive to light, and extraocular muscles were intact. The face was symmetrical and the tongue was midline. Speech was normal, affect was euphoric and the mental status was otherwise normal. There was severe weakness of the legs, especially of the proximal muscles. Sensory examination revealed decreased pinprick sensation and temperature sensation up to the T3 level bilaterally. The deep Accepted for publication December 18, 1989.

tendon reflexes were hyperreflexic and Babinski's sign was positive. Myelography and computerized tomography of the thoracic and lumber spines were normal. Chest x-ray and magnetic resonance imaging of the brain also were normal. Three lumbar punctures showed a moderately elevated protein level of 41 to 83 mg./dl. and leukocytosis of 125 to 224 white blood cells per mm.3, and 80% lymphocytes were present. Cerebrospinal fluid rapid plasma reagent and serum venereal disease tests for syphilis were negative. Cerebrospinal fluid oligoclonal bands were negative on 2 occasions. Cerebrospinal fluid immunoglobulin G (lgG) was 8.5 mg./dl. (normal 0.5 to 6.1). Serum antinuclear antibody, rheumatoid factor, infectious mononucleosis screening test, thyroid function tests and fibril agglutinins were all within normal limits. Cryptococcus antigen was not detected and cerebrospinal fluid viral culture isolated no viruses. Lyme titers done by the enzyme-linked immunosorbent assay technique were positive for lgG at 1 to 1,024, lgM at 1 to 128 in the serum, and lgG at 1 to 8 and lgM at 1 to 2 in the cerebrospinal fluid, respectively. The Lyme titers were repeated and remained elevated. The patient was treated with ceftriaxone (1 gm. intravenously twice a day) for 3 weeks. Cystometrography 2 weeks after hospitalization revealed no voluntary or involuntary detrusor contractions to a volume of 500 ml., although she did have sensations of fullness. She was initially managed with an indwelling Foley catheter, and than taught intermittent selfcatheterization. Hospitalization was complicated by a pulmonary embolus requiring anticoagulation. The patient was transferred to a rehabilitation facility 6 weeks after hospitalization where she remained for another 4 months. At the rehabilitation hospital the Lyme titers increased again and she received another 3-week course of ceftriaxone. Subsequently, improvement progressed from paralysis to walking but she still has a sensory deficit level of approximately TIO, and has tingling and numbness sensation in the legs. The bladder function recovered 5 months after the initial urinary retention. DISCUSSION

Lyme disease takes its name from Lyme, Connecticut, where the illness was first described in 1975. The spirochete Borrelia burgdorferi has been identified as the cause of the disease and it is transmitted predominately by the deer tick. 4 Lyme disease has been called "The latest great imitator" in reference to the fact that, like syphilis, it can manifest itself with many different symptoms. 5 Steere and associates suggested dividing the clinical findings of Lyme disease into 3 stages on the basis of a chronological relationship to the original tick bite. 6 The initial clinical manifestations include a characteristic rash, called erythema chronicum migrans, which typically appears as an erythematous papule that expands to form an annular lesion with a partial clearing in the center. 2 Systemic symptoms may be present at this time. Treatment at this stage with oral antibiotics generally will result in cure. Blood tests at

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this stage are not generally positive. Stage 2 occurs weeks to months later, and is characterized by neurological and cardiac manifestations. Aseptic meningitis, peripheral radiculoneuritis and cranial palsies may occur at this time in approximately 15% of the untreated patients. 4 •7 Stage 3 has been classified typically as the presence of arthritis8 but it is becoming increasingly clear that central neurological manifestations may occur at this stage. 9 A spectrum of neurological disorders has been associated with Lyme disease. Menigitis, cranial neuritis and radiculoneuritis have been reported to be the most common forms of nervous system involvement. Myelopathy, encephalopathy, psychiatric disorders and a multiple sclerosis-like illness are reported less frequently. 10- 12 We believe that the symptoms in our patient were secondary to Lyme disease on the basis of 6 factors: 1) the presence of a high titer of Lyme antibody in the peripheral blood, 2) the presence of Lyme antibody and elevated protein in the cerebrospinal fluid, 3) the fact that the individual lived in an area endemic for Lyme disease, 4) the lack of any other documented cause, 5) the response to ceftriaxone and 6) the presence of Bell's palsy 5 years previously in this patient. Our patient probably had stage 3 Lyme disease based on the history of cranial nerve palsy. The symptoms described by this woman are reminiscent of the first "great imitator", syphilis. Syphilis is caused by another spirochete, Treponema pallidum. Cranial nerve involvement, although present in less than 1% of the individuals with secondary syphilis, does occur. In addition, secondary syphilis if untreated can progress to late syphilis. General paralysis and tabes dorsalis (spinal cord damage) are well described complications. Bladder function disturbances and impotence can occur.13 What was so unusual about the Lyme neuroborreliosis in our patient is that initially she and the physicians did not notice any neurological abnormalities beside the urinary retention. The cystometrogram and neurological examination were con sistent with suprasacral detrusor areflexia. Similar to the fact that the urological dysfunction preceded the paralysis, the paralysis resolved before the bladder dysfunction. Since Lyme disease is a problem of increasing national and international importance, urologists must be aware that bladder dysfunction can be a manifestation. Our patient was misdiagnosed initially with psychogenic retention. A variety of neu-

ropathic conditions, including meningoencephalopathy, transverse myelitis, demylinating process and psychiatric dysfunction, have been described. Therefore, a variety of urodynamic findings are possible, including detrusor hyperreflexia, areflexia and detrusor-sphincter dyssynergia. In most cases of neuroborreliosis the illness is reversible. If bladder function is disturbed, intermittent catheterization in addition to antibiotics would be the most appropriate conservative treatment. Clinical studies to define further the complications of the disease and to evaluate treatment regimens are needed. REFERENCES

1. Lyme disease-Connecticut. MMWR, 37: 1, 1988. 2. Steere, A. C., Broderick, T. F. and Malawista, S. E.: Erythema chronicum migrans and Lyme arthritis: epidemiologic evidence for a tick vector. Amer. J. Epidemiol., 108: 312, 1978. 3. Halperin, J. J., Luft, B. J., Anand, A. K., Roque, C. T., Alvarez, 0., Volkman, D. J. and Dattwyler, R. J.: Lyme neuroborreliosis: central nervous system manifestations. Neurology, 39: 753, 1989. 4. Burgdorfer, W., Barbour, A. G., Hayes, S. F., Benach, J. L., Grunwaldt, E. and Davis, J. P.: Lyme disease: a tick-borne spirochetosis? Science, 216: 1317, 1982. 5. Stechenberg, B. W.: Lyme disease: the latest great imitator. Ped. Infect. Dis. J., 7: 402, 1988. 6. Steere, A. C., Grodzicki, R. L., Kornblatt, A. N., Craft, J. E., Barbour, A.G., Burgdorfer, W., Schmid, G. P., Johnson, E. and Malawista, S. E.: The spirochetal etiology of Lyme disease. New Engl. J. Med., 308: 733, 1983. 7. Steere, A. C., Pachner, A. R. and Malawista, S. E.: Neurological abnormalities of Lyme disease: successful treatment with highdose intravenous penicillin. Ann. Intern. Med., 99: 767, 1983. 8. Steere, A. C., Green, J., Schoen, R. T., Taylor, E., Hutchinson, G. J., Rahn, D. W. and Malawista, S. E.: Successful parenteral penicillin therapy of established Lyme arthritis. New Engl. J. Med., 312: 869, 1985. 9. Pachner, A. R.: Borrelia burgdorferi in the nervous system: the new "great imitator". Ann. N. Y. Acad. Sci., 539: 56, 1988. 10. Steere, A. C.: Lyme disease. New Engl. J. Med., 321: 586, 1989. 11. Rousseau, J. J., Lust, C., Zangerle, P. F. and Bigaignon, G.: Acute transverse myelitis as presenting neurological feature of Lyme disease. Letter to the Editor. Lancet, 2: 1222, 1986. 12. Sterman, A. B., Nelson, S. and Barclay, P.: Demyelinating neuropathy accompanying Lyme disease. Neurology, 32: 1302, 1982. 13. Tramont, E. C.: Treponema pallidum (syphilis). In: Principles and Practice of Infectious Disease, 2nd ed. Edited by G. L. Mandell, R. G. Douglas, Jr. and J.E. Bennett. New York: Wiley Medical Publications, chapt. 194, pp. 1323-1333, 1985.

Lyme disease presenting as urinary retention.

We report a case of Lyme disease that presented with urinary retention. The individual then experienced lower extremity paralysis. Paralysis and urina...
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