Case Report: Acute Urinary Retention and Fever in a Man

A 74-year-old man presents with five days of fever and urinary incontinence. He has a history of diabetes mellitus type 2. Vital signs are: blood pressure, 117/68; heart rate, 89; resting heart rate, 16; temperature, 37.7 degrees C (99.9 degrees F). On physical examination, he is confused and incoherent. What is the best management of this condition?

Acute urinary retention (AUR) is generally defined as a “painful, palpable, or percussable bladder, when the patient is unable to pass any urine.”1 It is typically seen in males older than 60 years and has a significantly higher incidence in men with benign prostatic hyperplasia.2

However, AUR presenting simultaneously with fever is a particularly concerning presentation, due to a number of rare and severe etiologies. While AUR may occur due to obstruction, infectious etiologies, trauma, surgical complications, multiple drug interactions, neurogenic etiologies, and miscellaneous causes such as severe constipation, the simultaneous presentation of AUR and fever in the ED presents a narrower differential.2-4

Infectious etiologies may cause fever and urinary retention. Acute prostatitis, presenting with fever, back pain, perineal pain, and rectal pain, may be a cause of AUR and fever.5 Although not all males will develop the acute form, up to 50 percent will “develop some form of prostatitis during their lifetime,” and in males presenting with fever and urinary symptoms, prostatitis is the underlying condition in more than 90 percent of cases “in the absence of pyelonephritis symptoms.”6-7 Typically caused by gram-negative bacteria, Escherichia coli is “the predominant organism in acute prostatitis and occurs in 75 percent of all cases.”6 Some studies estimate that E. coli is the causative organism in up to 80 percent of all cases.7

Diagnosis of acute prostatitis is made through the patient’s clinical presentation and through the presence of bacteria in urine analysis.6 Rectal examination should be performed only cautiously—prostate massage “can release bacteria and inflammatory cytokines, triggering an abrupt clinical decompensation.”7 Postvoid residual urine volume and levels of prostate-specific antigen are useful for diagnostic purposes, as well as possible CT scan or ultrasound to evaluate for an enlarged and inflamed prostate.7

For immediate relief of the patient’s AUR, catheterization should be performed.7 Most cases of acute prostatitis respond well to oral antimicrobials, due to the relatively easy penetration of the prostate’s cellular membrane in an acute inflammatory reaction. While therapy should be specifically tailored to the organism responsible, medications such as trimethoprim/sulfamethoxazole and/or fluoroquinolones are often therapeutically successful, provided that the length of therapy is prolonged (four to six weeks).6 Repeat urine cultures during the patient’s treatment course should be performed to ensure that the causative organisms are thoroughly eliminated.7

While acute prostatitis is a relatively common disease with a bimodal distribution, meningitis-retention syndrome (MRS) is a significantly rarer disease that is more likely to present in young, healthy adults.6,8

MRS will typically present with neurological signs highly suggestive of aseptic meningitis, including “headache, drowsiness, fever… nuchal rigidity and positive Kernig and/or Brudzinski signs.”8 However, in many cases, the neurological signs may be so mild that the predominant symptom appears to be “isolated acute urinary retention.”9 One of the most notable presentations of MRS is the fever and AUR that patients with it will eventually develop. Only newly reported in the literature, the cause of MRS remains undetermined in most cases.8

Distinguishing it further from acute prostatitis, MRS patients will display a neurogenic bladder during urodynamic studies.8 Unusually, MRS patients will not display any evidence of lower motor neuron involvement—with a “lack of leg numbness and paresthesias help(ing) to differentiate MRS from Guillain-Barre syndrome, polyneuropathies and conditions affecting the lower motor neurons.”8 It is theorized that MRS affects upper motor neurons in the central nervous system responsible for the detrusor muscle.8 Likewise, patients with MRS display normal peripheral nerve conduction.9

The presence of MRS may be confirmed with lumbar puncture, which will display “lymphocytic pleocytosis, elevated protein levels, and mildly decreased glucose levels.”8 MRI of the brain and spinal cord will not reveal any abnormalities—nor will blood or urine cultures.9 Patients with MRS should have their AUR treated by catheterization and be admitted for observation. There is no evidence to suggest that treatment with steroids, antibiotics, or antivirals improves the disease course or hastens recovery.9 Fortunately, the disease is self-limiting over a period of several weeks, and there is no evidence of long-term neurological sequelae.8

In elderly patients, pharmacological causes of AUR with fever should also be considered, given the “decreased clearance, drug interactions, altered drug sensitivity and multiple comorbid medical conditions more common with advancing age.”10

Pharmacologic etiologies account for up to 10 percent of AUR cases.2 Drugs with anticholinergic effects should be strongly considered. Even localized anticholinergic drugs, such as short-acting and long-acting anticholinergic bronchodilators such as ipratropium and oxitropium, may cause AUR. Atropine eye drops have also been found to induce AUR.2 Other medications at risk for causing AUR include antihistamines, class 1 antiarrythmics including disopyramide and flecainide, antipsychotic drugs, tricyclic antidepressants, fluoxetine, benzodiazepines, NSAIDs, calcium channel blockers, recent epidural analgesics, and D1 and D2 agonists for the treatment of Parkinson’s disease.2 The street drug—3,4-methylenedioxy—amphetamine (MDMA or ecstasy) has also been found to be associated with AUR.2–4

Ultimately, in elderly patients presenting with AUR and fever of an unclear etiology, rapid decompression of the bladder through catheterization should be achieved.10 Afterward, the patient’s medication list—including the use of over-the-counter medications such as NSAIDs—should be carefully reviewed for signs of any causative agents.2,10

In the case described, a postvoid residual ultrasound showed that the patient was retaining approximately 700 mL of urine. His bladder was successfully drained with the placement of a urethral catheter, and a UA showed him to have significant bacteriuria. Due to the possibility of acute prostatitis, a digital rectal exam was deferred. Ultrasound imaging showed evidence of a heterogeneous, inflamed prostate, and the patient was diagnosed with acute prostatitis. While the urine culture was pending, the patient was empirically started on a broad-spectrum intravenous antibiotic and admitted to the hospital, where he rapidly improved. 48 hours later, the patient’s urine culture grew E. coli colonies, sensitive to trimethoprim/sulfamethoxazole. The patient was discharged on a four-week course of oral antibiotics, and followed up in clinic for repeat urine cultures. Ultimately, the patient made a full recovery.


Dr. Turner is an emergency medicine intern at Hershey Medical Center in Hershey, PA.

Dr. Marco is professor of emergency medicine at Penn State Health-Milton S. Hershey Medical Center and associate editor of ACEP Now.

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  2. Verhamme KM, Sturkenboom MC, Stricker BH, et al. Drug-induced urinary retention: incidence, management and prevention. Drug Safety. 2008;31:373-88.
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