Permanent Urinary Incontinence After Subarachnoid Anesthesia with 0.5% Hyperbaric Bupivacaine

Abstract

To the Editor: Basaranoglu et al. (1) described transient urinary incontinence in a patient after spinal anesthesia using 0.5% hyperbaric bupivacaine. We report a case of permanent urinary incontinence after spinal anesthesia using hyperbaric bupivacaine. A 70-yr-old, 175 cm, 94 kg, woman was scheduled to undergo hammer toe surgery. Medical history revealed five term-pregnancies without birth trauma, appendectomy, hysterectomy, cholecystectomy, and surgery for colon carcinoma. Results of all laboratory tests, as well as EKG and chest radiograph, were normal. Spinal anesthesia was administered with the patient in the sitting position using a 22-gauge Quincke spinal needle at the L3-4 interspace and 0.5% hyperbaric bupivacaine. She was then positioned supine, and after 2 min, the segmental level of sensory block achieved a Ramsey score of 2; moreover, a Bromage score of 3 lasted for about 210 min. No free flow of clear cerebral spinal fluid was observed before or after administration of the bupivacaine. Furthermore, there were no paresthesias. Surgery lasted 54 min with no hypotension, nausea, vomiting, brachycardia, or arrhythmia. After signs of sensory and motor recovery, the patient complained of urinary incontinence, which did not respond to 20 mg dexamethasone, 0.375 mg hyoscyamine sulfate, or 5 mg oxybutynin chloride, and has persisted for more than 2 yr. Our patient had no history of a neurological disorder or neurotoxic drug use of any kind. The subarachnoid block was easily performed on the first attempt, and there were no signs of hematoma, abscess, or other causes of spinal cord or nerve root compression. Combined radiological studies (i.e., tomography and magnetic resonance imaging) did not reveal any volumetric, morphological, or structural alterations in the surrounding organs and glands (i.e., liver, pancreas, kidneys, adrenal glands, and spleen). Moreover, no stones were present in the lower or upper urinary tract, and urethrocystoscopy showed a normal urethra. Cystomanometry revealed that the detrusor was unstable and the bladder was insensible to filling and bladder hyperreflexia was manifested. Lastly, the patient was unable to void in the presence of detrusoral contractions of high amplitude (detrusoral pressure = 31.9 cm H2O) and when the bladder volume was 150 mL. As stated by Basaranoglu et al. (1), hyperbaric solutions of local anesthetics could lead to an increased risk of nerve-root toxicity in the lower parts of the spinal canal. Because the dorsal roots of L5 and S1 have the most dorsal position with the patients' supine, they would be the most exposed to the hyperbaric solution. Conversely, if the lesion occurred in the sacral roots, depending on the lesion site, a flabby or spastic or paraplegia would have been observed. In this latter case, hypertonus, spasticity, local anesthesia, fecal, and urinary incontinence generally associated with incomplete bladder emptying would appear. Initially, the bladder would be areflexic and acontractile and only subsequently hyperreflexic associated with dyssynergia of the striated sphincter to which a dyssynergia of the smooth sphincter would follow. Emilio Di Genova, MD SS. Filippo and Nicola Hospital Via G. Di Vittorio Avezzano, Italy Gabriele D'Andrea, MD University of L'Aquila School of Medicine Via Vetoio L'Aquila, Italy [email protected]