Pathophysiology

Spinal nerve root compression commonly occurs in conditions such as acute herniated disc, spinal stenosis, trauma (e.g., burst fractures), metastatic or primary tumors of the spine, or spinal infections (e.g., epidural abscess) (Box 105-2). Acute CES most commonly presents secondary to lumbosacral intervertebral disc prolapse (Fig. 105-1). However, the pathophysiology of the symptoms and signs related to spinal nerve root compression remains poorly defined.

FIGURE 105-1 Thirty-year-old woman with acute cauda equina syndrome secondary to a large herniated disc at the L5-S1 level. The patient’s initial symptoms included urinary retention (postvoid residual = 200 mL), saddle anesthesia, and S1 motor-sensory radiculopathy. A, T2-weighted midsagittal MRI. B, Axial MRI demonstrating complete occlusion of the spinal canal at L5-S1. C, Axial MRI caudal to area of maximal compression (B) demonstrating displacement of the S1 roots and compression of the central sacral roots. Patient underwent urgent surgical (<24 hours of bladder symptoms) decompression with complete recovery of bladder function, sensation, and radiculopathy.

Several experimental studies have assessed the pathophysiologic mechanism of CES. Delamarter et al.^1,2 developed an animal model of CES, subjecting 30 beagle dogs to L6-7 laminectomy and cauda equina compression. Neurologic recovery was assessed in animals undergoing 75% constriction of the cauda equina followed by immediate, early, or delayed decompression. The first group was constricted and immediately decompressed. The remaining groups were constricted for 1 hour, 6 hours, 24 hours, and 1 week, respectively, before being decompressed. Evoked potentials were measured before and after surgery, before and after decompression, and 6 weeks after decompression. Six weeks after decompression, all dogs were killed, and the neural elements were analyzed histologically. After compression, all 30 dogs had significant lower extremity weakness, tail paralysis, and urinary incontinence. All dogs recovered significant motor function by 6 weeks after decompression. The dogs with immediate decompression typically recovered neurologic function within 2 to 5 days. The dogs receiving 1- and 6-hour compression recovered within 5 to 7 days. Dogs receiving 24 hours of compression remained paraparetic for 5 to 7 days, with bladder dysfunction persisting for 7 to 10 days and tail dysfunction for up to 4 weeks. The dogs with compression for 1 week were paraparetic and incontinent during the duration of cauda equina compression. They recovered the ability to walk by 1 week and regained bladder and tail control by the time of euthanasia. Immediately after compression, all five groups demonstrated at least 50% deterioration of the posterior tibial evoked potential amplitudes.² Delamarter et al.² demonstrated axoplasmic flow blockade and wallerian degeneration of the motor nerve roots distal to the constriction and of the sensory roots proximal to the site of constriction, as well as dorsal column degeneration. Severe arterial narrowing occurred at the level of the constriction with venous congestion of the roots and dorsal root ganglia of the seventh lumbar and first sacral nerves.¹ Evoked potentials were the most sensitive predictor of neural compression, revealing neurologic abnormalities before the appearance of neurologic signs and symptoms.¹ Cystometrograms were not sensitive until severe compression was achieved. Bladder dysfunction was correlated with axoplasmic flow blockade and early sensory changes during neurovenous congestion.

Olmarker et al.^3–7 developed an experimental model of acute, graded compression of the cauda equina in pigs that accurately mimics the neural and vascular anatomy of the human cauda equina. There were structural and vascular differences between spinal nerve roots and peripheral nerves that could contribute to differences in compression susceptibility between these two parts of the nervous system. Pressure transmission from the balloon to the nerve roots permitted determination of occlusion pressures for the arterioles, capillaries, and venules of the cauda equina.⁷ Arteriolar blood flow ceased when the applied pressure approached the mean arterial blood pressure. Capillary blood flow was dependent on flow in connected venules, and the blood flow in some venules ceased at 5 to 10 mm Hg despite venous occlusion pressures ranging from 5 to 60 mm Hg. Compression up to 200 mm Hg for 2 hours did not induce a no-reflow phenomenon upon compression release. However, transient hyperemia was noted at all pressure-time relations studied, indicating nutritional deficit in the compressed segment during compression. Signs of edema were observed in nerve roots exposed to compression for 2 hours at either 50 or 200 mm Hg. The nutritional supply to the cauda equina was impaired at low pressure levels (<10 mm Hg).^4,5 Thus diffusion from adjacent tissues with a better nutritional supply, including the cerebrospinal fluid, could not compensate completely for compression-induced effects on the transport of nutrients. However, a certain nutritional supply to the compressed segment was present even at 200 mm Hg compression. A rapid compression rate resulted in more pronounced effects on the nutritional supply than did a slow compression rate. Nutritional impairment was observed both within and outside the compressed nerve segment. An increase in vascular permeability was induced by compression at 50 mm Hg for 2 minutes.⁶ The magnitude of this permeability increase was dependent on both the magnitude and the duration of compression. The permeability increase was more pronounced for the rapid compression onset rate than for the slow compression onset rate at all pressure-time relations studied. Reduction of muscle action-potential amplitude in tail muscles, after stimulation cranial to the compression zone, was induced by compression at 100 and 200 mm Hg for 2 hours.^4,6

Pedowitz et al.⁸ and Rydevik et al.^9,10 presented an experimental model of compression-induced functional changes of the porcine cauda equina that permits electrophysiologic investigation of the neurophysiologic changes induced by nerve root deformation. In several studies, they compared the effects of various pressures and durations of acute compression on spinal nerve root conduction in the pig cauda equina. Changes in both afferent (compound nerve action potentials) and efferent (compound motor action potentials) conduction were induced at an acute pressure threshold of 50 to 75 mm Hg. Higher compression pressures produced a differential recovery in afferent and efferent conduction.^9,10 Efferent conduction and afferent conduction were monitored during compression for 2 or 4 hours with compression pressures of 0 (sham treatment), 50, 100, or 200 mm Hg. Recovery was monitored for 1.5 hours. No significant deficits in spinal nerve root conduction were observed with 0 or 50 mm Hg compression, whereas significant deficits were induced by 100 and 200 mm Hg compression. Variance analysis demonstrated significant effects of compression pressure and duration on conduction, with a significant difference between efferent and afferent conduction at the end of the recovery period, suggesting a synergistic interaction between biomechanical and microvascular mechanisms in the production of nerve root conduction deficits.⁸

Compression of the spinal nerve roots often occurs at multiple levels simultaneously; however, the basic pathophysiology of multilevel compression is poorly defined. Using a thermal diffusion technique, Takahashi et al.¹¹ quantitated intraneural blood flow in the uncompressed segment between two compressive balloons in the porcine cauda equina. At 10 mm Hg compression, there was a 64% reduction of total blood flow in the uncompressed segment compared with precompression values. Total ischemia occurred at pressures 10 to 20 mm Hg less than the mean arterial blood pressure. After two-level compression at 200 mm Hg for 10 minutes, there was a gradual recovery of the intraneural blood flow toward the baseline. Recovery was less rapid and less complete after 2 hours of compression. Double-level compression of the cauda equina induced blood flow impairment, not only at the sites of compression but also in the intermediate nerve segments located between two compression sites, even at very low pressures.

Cauda Equina Syndrome Secondary to Disc Herniation

Diagnostic Imaging

Diagnosis and treatment are often delayed because of lack of recognition of the condition and failure to appreciate the surgical imperative for its treatment. Once cauda equina compression is recognized or suspected, MRI is the investigation method of choice. If an MRI is contraindicated, of poor quality because of motion artifact (patients with CES are often in severe pain), or unavailable, CT-myelography is recommended. CT alone can be misleading in cases of complete canal occlusion (Fig. 105-2).

FIGURE 105-2 A, Axial CT at L4-5 of a 43-year-old male patient with right L5 radiculopathy and abnormal perineal sensation. Axial (B) and sagittal (C) MRIs of the same patient. As can be seen, the contrasting effect of epidural fat or cerebrospinal fluid in CT can be lost because of massive disc herniations causing near or complete occlusion of the spinal canal. This patient’s CT was interpreted as equivocal for an L4-5 disc herniation. Consequently, MRI and CT-myelography are the imaging modalities of choice for the evaluation of cauda equina syndrome.

Surgical Therapy

Urgent surgical intervention should commence after diagnosis. Choudhury and Taylor²⁰ advocated wide laminectomy with excision of the overhanging facet joints and adequate visualization of the lumbar nerve roots. This yielded good or excellent results in 95% of patients and fair results in the remainder. No postoperative spinal instability or significant morbidity was reported.²⁰

A routine microdiscectomy interlaminar approach necessitates retraction on already severely compromised nerve roots. Furthermore, because of the extent of compression, these roots often have no available canal space; thus, retraction not only increases traction but also may cause direct compression (against the disc or the overlying lamina). For the same reason, the use of large punches with a thick foot plate is also not recommended (compresses underlying roots against the herniated disc) (Fig. 105-3). Consequently, the authors advocate a wide bilateral decompression (laminectomy and medial third facetectomy). To avoid iatrogenic compression of the cauda equina, the surgeon can perform the laminectomy using a high-speed bur to thin out the lamina and then curettes and small punches lateral to the area of maximal compression to release the medial portion of the lamina (see Fig. 105-3). Once the lamina is released, it can be safely lifted away from the cauda equina. The decompression should be adequate enough to allow access lateral to the thecal sac and traversing roots at the level of the affected disc space and/or the sequestered fragment. The surgeon should carefully perform retrieval of the herniated fragment to avoid creating a further mass effect and therefore increased traction on the less mobile central sacral roots. This can be accomplished by performing a lateral anulotomy and discectomy and then pushing the central fragment back into the disc space with a reverse-angle curette. If the fragment is sequestered, it should be manipulated in a lateral direction using a nerve hook or angled curette and then retrieved. Before closure, the surgeon should confirm adequate decompression.

FIGURE 105-3 Sagittal (A) and L5-S1 axial (B) MRIs of a 45-year-old woman with cauda equina syndrome demonstrating severe compression of the cauda equina. C, The cauda equina (outlined in white) is draped over the disc and compressed between the disc and lamina. Removal of the lamina (medial to the black arrows) by sublaminar placement of standard spinal punches (see text) would obviously cause further compression of the roots. Wide bilateral laminectomy is required to gain safe access to the disc. Following appropriate decompression of the cauda equina, care must be taken when retrieving large disc fragments to avoid excessive traction or mass effect on the tented traversing nerve roots.

Cauda Equina Syndrome Resulting from Intradural Disc Rupture

There is a strong association between the presence of intradural disc rupture and the development of CES. Dinning and Schaeffer²⁵ reported that intradural sequestration of disc fragments occurs in 7.5% of cases, although in most other series the rate is less than 1%. Spangfort¹⁴ detected no differences in age or sex distribution. Lower lumbar discs were the most commonly affected levels; however, there was a significantly larger number of high lumbar herniations leading to this problem than to other disc syndromes. Myelography typically demonstrates complete block, and at surgery, intradural fragments of sequestrated disc material can be found (Fig. 105-4). Intradural exploration or transdural sequestrectomy avoids traction on already compromised nerve roots and is often safer than extradural sequestrectomy.

FIGURE 105-4 Patient is a 48-year-old man who presented with a 2-week history of severe low back pain and 24-hour history of progressive frank cauda equina syndrome with complete loss of erectile, bladder, and bowel function, as well as right bilateral L4-S1 leg weakness. He had undergone a right L3-4 microdiscectomy 2 years previously. A, T1-weighted sagittal MRI demonstrating intradural disc herniation (arrow). Because of uncontrollable pain, the patient was unable to lie flat for the rest of the MRI and underwent a CT-myelogram in the lateral decubitus position. B, Sagittal reformatted CT demonstrating complete myelographic block at the rostral aspect of the L3 vertebral body. Patient underwent urgent (<12 hours from presentation to emergency) surgical decompression. C, Intraoperative picture demonstrating wide decompression, release of previous epidural scar, and small defect (5 mm) in the dura. The defect was enlarged, and a massive intradural sequestered disc fragment (white arrow) was removed (D). At 2 years follow-up, the patient has some residual right L5 weakness; a functional bladder with normal postvoid residuals; good, but not normal, bowel function; and incomplete erectile dysfunction that has responded to medical management.

Cauda Equina Syndrome Secondary to Trauma

Patients with sacral fracture or dislocation and CES have been reported. Schnaid et al.²⁸ reported CES complicating acute lumbosacral fracture or dislocation 3 weeks postinjury. Isolated transverse sacral fractures are rare, but extensive neurologic deficits may accompany these injuries. Extradural hemorrhage can accompany these fractures and produce a serious neurologic deficit requiring urgent sacral laminectomy.²⁹

Hilibrand et al.³⁰ reported CES associated with acute spondylolytic spondylolisthesis after major trauma. The deformity progressed from grade III to grade V (spondyloptosis), and the patient developed CES. The patient was treated with dorsal reduction and arthrodesis followed by an anterior arthrodesis, and the neurologic deficits resolved. Although minor or repetitive trauma is often associated with spondylolysis, high-energy trauma may produce a more severe form of spondylolysis with spondylolisthesis. These deformities are more unstable, with instability similar to that of a fracture-dislocation, and they have a greater propensity to progress than does the usual form of spondylolytic spondylolisthesis.³⁰

Dorsal dural lacerations associated with lumbar burst fractures can occur and are produced by dural impaction within a fractured lamina. Neural elements can be extruded outside the dura mater and be trapped in a lamina fracture. Preoperative appreciation of this diagnosis is imperative and is based on clinical presentation, fracture pattern, and radiographic findings. Denis and Burkus³¹ recommended extraction of entrapped neural elements from the fractured lamina by laminoplasty of the dorsal neural arch. Neurologically impaired patients with lumbar burst fractures and radiographic evidence of dorsal displacement of the neural elements in the lamina fracture should undergo dorsal exploration of the spinal canal, extraction of cauda equina neural elements, and repair of the dural laceration before any spinal reduction maneuver is attempted.³¹

Intradural lumbar arachnoid diverticulas are rare but can cause mild compression of the cauda equina and produce debilitating symptoms. A chronic posttraumatic lumbar intradural arachnoid cyst causing CES has been reported.³²

Cauda Equina Syndrome Secondary to Primary or Secondary Neoplasms

Primary extradural or intradural tumors may rarely present with acute CES.²³ For example, myxopapillary ependymomas of the conus or filum may present acutely with subarachnoid hemorrhage and cauda equina dysfunction.^33,34 There are reported cases of paraganglioma of the cauda equina causing compression requiring urgent treatment.³⁵

Metastatic tumors to the lumbosacral spine can create CES by one of two means: (1) cauda equina compression by epidural tumor or (2) vertebral instability resulting in canal compromise and subsequent cauda equina compression (Fig. 105-5). The most common clinical manifestation is pain with or without concomitant nerve root signs. Regardless of the cause, the major goal of treatment is prompt decompression of the neural elements with stabilization or, at a minimum, avoidance of destabilization of the spine.

FIGURE 105-5 Sagittal (A) and L5-S1 axial (B) MRIs of a 39-year-old woman with low back pain and urinary incontinence. She had no leg symptoms. MRI demonstrated multiple spinal metastases of unknown origin with complete compression of the sacral cauda equina by tumor extending posterior from the body of S2. Patient underwent urgent surgical decompression and postoperative palliative radiation. She had rapid resolution of her pain, but at 6-month follow-up, she still required in-and-out catheterization. Her tumor is an adenocarcinoma, but extensive investigations have not identified the origin.

Indications for surgical intervention in patients with CES secondary to metastatic tumors include unknown tumor with rapid compression, previous irradiation precluding further radiotherapy, radioresistant tumor, neurologic deterioration during radiotherapy, and pathologic fracture/instability producing neural compression.

Spiegelmann et al.³⁶ reported a patient with acute myelogenous leukemia with CES as the presenting symptom. Staff et al. reported two patients with metastatic lobular breast adenocarcinoma presenting as CES.³⁷ There have been eight reported cases in the literature of intradural spinal metastasis from renal cell carcinoma causing CES.³⁸ Woo et al.³⁹ reported 97 Chinese patients with multiple myeloma, of whom 23.7% had cauda equina or spinal cord compression. Predictive features for spinal cord compression include paraprotein type, hemoglobin level, and extent of bone lesion at initial hematologic diagnosis. They concluded that vertebral cortex involvement predisposes the patient to spinal cord compression.³⁹ Rarely, patients with gynecologic tumors may present with acute CES.²³There have been two reported cases of CES due to leptomeningeal carcinomatosis of the ovary.⁴⁰

Cauda Equina Syndrome Secondary to Ankylosing Spondylitis

CES may occur as a neurologic complication of long-standing ankylosing spondylitis. The syndrome is uncommon, and its pathophysiology is poorly defined. There are several case reports of slowly progressive CES in patients with long-standing ankylosing spondylitis, with loss of lower spinal motor and sensory root function. The pathogenesis of CES in ankylosing spondylitis may be demyelination, postirradiation ischemia, or compression from spinal arachnoiditis, or it may arise in association with massive dural ectasia.^41–43

Symmetrical neurologic deficits typically progress slowly and occur late in the evolution of spondylitis, long after the onset of the condition and well after the rheumatologic symptoms have abated. The initial symptom is typically disturbance of sphincter control with subsequent changes in ankle reflexes and cutaneous sensation, particularly in the sacral dermatomes. Variable lower nerve root involvement has been reported. Typical findings include cutaneous sensory impairment of the lower limbs and perineum with sphincter disturbances. Motor impairment occurs less commonly, and associated pain is inconsistent. Eventually, patients experience cutaneous sensory loss in the fifth lumbar and sacral dermatomes and develop a lower motor neuron urinary sphincter disturbance with loss of rectal sphincter tone and with incontinence or severe constipation. Some patients have mild to moderate weakness in the lumbosacral myotomes or pain in the rectum or lower limbs.⁴⁴

A cauda equina–like syndrome with neuropathic bladder is a rare but well-described complication of long-standing ankylosing spondylitis. Diverticulas from the subarachnoid space may erode into the lumbosacral vertebrae. These spinal diverticulas can be demonstrated by CT.⁴⁵ Electromyographic (EMG) abnormalities are typically consistent with multiple lumbosacral radiculopathies.⁴⁴ In the setting of ankylosing spondylitis, MRI is valuable in excluding other spinal lesions because it excludes the presence of extrinsic compression of the cauda equina.⁴⁶

The clinical diagnosis of CES can be adequately confirmed with plain radiology, EMG, and CT. CT and MRI represent noninvasive means of establishing the diagnosis of CES in patients with ankylosing spondylitis.⁴³ MRI of the CES in patients with ankylosing spondylitis aids in the diagnosis and may provide valuable insight into the pathophysiology of this condition.⁴⁷ The features observed on MRI are pathognomonic, allowing accurate noninvasive diagnosis of the disorder.⁴⁸

CT-myelography of the lumbosacral spine typically shows dilation of the spinal canal and lumbar sac with multiple dorsal arachnoid diverticulas eroding the laminae and spinous processes. Young et al.⁴⁹ found no compressive lesions with myelography, and foraminal encroachment was not seen. The pathogenesis of these erosions may be related to arachnoiditis in the early phase of the spondylitis.⁵⁰ Recognition of this syndrome, coupled with CT of the lower spinal canal, allows the clinician to avoid myelography, a procedure that is often difficult to perform in these patients because of associated spine abnormalities.

Early investigators concluded that surgery for CES secondary to ankylosing spondylitis was neither beneficial nor indicated and that it should be avoided.^43,44 However, surgery may be indicated in some patients, particularly when there is nerve root compression by the arachnoid cysts and when the patient is treated before irreversible damage to the cauda equina has occurred.⁵¹

Cauda Equina Syndrome Secondary to Arteriovenous Malformation or Hemorrhage

Spinal subdural hematoma is a rare cause of cauda equina compression that can occur in patients with a bleeding diathesis. Johnson et al.⁵² reported a case of subacute lumbar subdural hematoma that was demonstrated by MRI. Laus et al.⁵³ reported three cases of CES resulting from epidural hematoma secondary to warfarin (Coumadin)-induced coagulopathy. They recommended anticoagulant correction with appropriate medications and hemoderivatives, with surgical treatment for the severe cases. Schmidt et al.⁵⁴ presented a patient with acute CES from a ruptured aneurysm in the sacral canal. The lesion was associated with pathologic enlargement of the lateral sacral arteries bilaterally, which occurred to provide cross-pelvic collateral flow in response to the diversion of the right internal iliac artery for renal transplantation. The patient showed signs and symptoms of spontaneous spinal epidural hemorrhage. In addition to angiography and partial embolization of the vascular supply, contrast-enhanced, high-resolution CT was essential in the diagnosis and treatment of this aneurysm.⁵⁴ Brown and Stambough reported a case of CES caused by an epidural hematoma secondary to a rupture of a synovial cyst.⁵⁵ In the literature it is reported that patients who have undergone exploration and evacuation of spinal epidural hematoma experienced the most extensive neurologic recovery within 6 hours of diagnosis. Patients who were surgically treated within 8 hours of diagnosis demonstrated less recovery.^56,57

CES caused by massive spontaneous subarachnoid hemorrhage from an intradural angioblastic meningioma of the filum terminale has been reported.⁵⁸ Kulali et al.⁵⁸ reviewed six cases of spontaneous spinal subarachnoid hematoma caused by subarachnoid hemorrhage from a spinal tumor with acute compression of the adjoining nervous structures. Likewise, Malbrain et al.³⁴ reported a patient with acute CES resulting from intratumoral and spinal subarachnoid hemorrhage from a filum terminale ependymoma after therapy with oral anticoagulants. Only 13 cases of spinal subarachnoid hemorrhage caused by cauda equina ependymoma have been reported.

Cauda Equina Syndrome Secondary to Pregnancy

CES is rarely associated with pregnancy, with few cases reported in literature. Curtin and Rice reported a case of CES in a 37-year-old woman in the first trimester of pregnancy, due to a prolapsed lumbar disc.⁵⁹ Chow et al. reported a case of CES immediately following caesarean section.⁶⁰ We recommend that vigilance be maintained in the neurologic surveillance of pregnant women with known disc disease.

Iatrogenic Cauda Equina Syndrome

Cauda Equina Syndrome Caused by Infection

CES can manifest in association with lumbar spinal infections that result in an epidural abscess or pathologic fracture (Fig. 105-6). CES typically results from direct compression of the cauda equina, but may also occur secondary to subarachnoid vascular injury or thrombosis.⁸¹ Management consists of early detection, antibiotic and surgical decompression, and debridement with or without spinal stabilization.⁸²

FIGURE 105-6 Gadolinium-enhanced T1-weighted MRI of a 70-year-old diabetic woman with cauda equina compression from an epidural abscess.

Arend et al.⁸³ described a patient who developed toxic shock syndrome, meningitis, and CES several days after lumbar laminectomy. Enterotoxin-producing Staphylococcus aureus was cultured from the surgical wound and the cerebrospinal fluid. The patient recovered from toxic shock syndrome but remained partially paralyzed. CES was postulated to result from the neurotoxic effects of the intrathecally produced S. aureus exotoxins.⁸³

Crawfurd et al.⁸⁴ presented five patients who were HIV positive who had symptoms initially thought to be indicative of lumbar disc lesions. Signs of nerve root or cauda equina compression were noted in all five patients, but lumbar imaging studies demonstrated no evidence of compressive lesions. Therefore, physicians must exercise caution in diagnosing nerve root compression in HIV-positive patients. Likewise, Zeman and Donaghy⁸⁵ reported a case of CES in the context of acute infection with HIV and emphasized the importance of considering the possibility of primary HIV infection in a wide range of self-limiting neurologic disorders.

Diagnostic Pitfalls

Tullberg and Isacson⁸⁶ reported on 19 patients with normal lumbar myelograms and symptoms consistent with CES. Two patients had thoracic lesions—one with a tumor and the other with a herniated disc—who were discovered on a second myelogram. One patient was considered to have hysterical paresis. In three other patients, the symptoms were attributed to diseases not related to the spine. Thirteen patients recovered spontaneously. The authors concluded that the prognosis for patients with signs of compression of the cauda equina is favorable, provided the myelography results are normal and surgical exploration is not indicated. However, if severe unexplained symptoms persist and the CT-myelogram is normal, the authors recommend myelography of the thoracic spine.⁸⁶

A large number of patients present to neurosurgical units with symptoms suggestive of CES without radiologic evidence of pathology. In these cases, a high level of suspicion should be maintained. If lumbosacral compression is not demonstrated, then imaging studies should be pursued to rule out a proximal lesion.⁸⁷

Prognosis for Recovery of Bladder Dysfunction

CES must be considered for prompt surgical intervention because spontaneous neurologic recovery is uncommon. If incontinence is present, prompt surgery can possibly lessen the likelihood of future urinary dysfunction and maintain whatever function still remains. Similarly, severe paresis or paraplegia merits the consideration for prompt and generous decompression. Patients with CES should undergo emergent radiologic evaluation and urgent surgical intervention if indicated.

Gleave and MacFarlane¹⁶ reviewed 932 patients who underwent surgery for prolapsed lumbar intervertebral disc and identified a group of 33 with acute urinary retention. No identifiable factor predisposed this group of patients to CES. The mean duration of bladder paralysis before operation was 3.6 days. Ultimately, 79% of patients claimed full recovery of bladder function, but only 22% were left without sensory deficits in the limbs or perineum. There was no correlation between recovery and the duration of bladder paralysis before surgery, except in three patients in whom there was no sciatica and in whom the correct diagnosis was delayed for many days. Retention developing less than 48 hours after acute prolapse was associated with a worse prognosis.

Hellstrom et al.⁸⁸ urodynamically evaluated bladder function after surgery in 17 patients with CES caused by lumbar intervertebral disc herniation. At the 3-year follow-up, 10 patients (59%) reported normal bladder function, whereas 7 patients (41%) noted obstruction or incontinence. Urodynamic function was normal in four patients (24%), three patients (18%) had no detrusor contraction, two patients (12%) used the detrusor but strained during voiding, and three patients (18%) had an unstable detrusor; the remaining five patients (29%) had either an increased bladder capacity or a decreased maximal flow rate. Neurologic findings were normal in two patients (12%). Bladder function is often substantially disturbed in patients with asymptomatic CES, and therefore urodynamic testing is warranted in all patients with CES. Urgent surgical intervention may improve long-term bladder function. Regeneration of the autonomic nervous supply to the bladder and genitals often requires several months or even years.

Nielsen et al.⁸⁹ reported that among 1972 patients undergoing surgery for lumbar disc herniation in a 7-year period (from 1971 to 1978), CES was diagnosed in 26 patients. Twenty-two patients had follow-up visits 4 to 72 months postoperatively (average, 37 months). At follow-up, half of the patients had a history of normal micturition, and only six patients had a serious complaint of micturition. One third of the patients were free from lumbar or sciatic pain, whereas two thirds complained of distressing pain and neurologic symptoms. The urodynamic investigation revealed complete bladder emptying in all but one patient. In half of the patients, normal detrusor contraction was demonstrated, whereas one third of the patients voided by straining only. Preoperative micturition symptoms exceeded 2 days in almost all patients voiding by straining. This finding indicates a connection of early diagnosis and treatment with the degree of detrusor damage.

Summary

CES is a complex of low back pain, saddle anesthesia, bowel and bladder dysfunction or incontinence that is often associated with radiculopathy, and lower-extremity motor weakness that occasionally progresses to paraplegia.

Patients with CES should undergo rapid radiologic evaluation and surgical intervention. It is prudent to adhere to a few simple principles during evaluation of patients with acute back pain or lumbosacral trauma (Box 105-3). It is important to maintain a high index of suspicion for the diagnosis of CES and its implications both diagnostically and prognostically. It is essential that these patients are specifically asked about urinary incontinence and retention and that their bladder and bowel functions are monitored vigilantly. If the clinician is suspicious, he or she should obtain a postvoid residual urine volume. In addition, trauma patients often receive an indwelling catheter at the time of admission to the emergency department. This catheter should be removed and checked for postvoid residual urine volume as quickly as possible. A rectal examination and evaluation of perianal sensation is mandatory when assessing any patient with acute onset of severe back pain or significant lumbosacral trauma. Imaging studies to determine the nature of the lesion (e.g., disc herniation, fracture, hematoma, tumor) must be performed expeditiously. If one imaging study (e.g., MRI) is inadequate, a complementary study (e.g., CT-myelography) should be obtained. If surgical management is indicated, meticulous surgical technique is critical so as to avoid additional nerve root traction or compression.

References

The complete reference list is available online at expertconsult.com.