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   defined as 
    
       low back pain, unilateral or usually bilateral sciatica, saddle sensory disturbances,  bladder
and bowel dysfunction variable lower extremity motor and sensory loss. Pathophysiology
  may result from any lesion that compresses CE nerve rootsnerve roots are particularly susceptible to injury, 
    
      poorly developed epineurium.  When well developed, as in peripheral nerves,
they protect against compressive and tensile stresses.  microvascular systems
of nerve roots have a region of relative hypovascularity in their proximal thirdIncreased vascular permeability and subsequent diffusion from the
surrounding cerebral spinal fluid supplement the nutritional supply. increased permeability may be related to the tendency toward oedema formation of the nerve roots, which may result in
        oedema compounding initial and
sometimes seemingly slight injury. Epidemiology
(US) 
  CES is uncommon, both atraumatically as well as traumaticallyCES is not fatal.  Morbidity is variable, depending on the aetiology of the syndrome.Race: No predilection exists on the basis of race.Sex: No predilection exists on the basis of sex.Age: Traumatic CES is not age specific. Atraumatic CES occurs primarily in
adults. History
  Low back painAcute or chronic radiating painUnilateral or bilateral lower extremity motor and/or sensory abnormalityBowel and/or bladder dysfunctionUsually with associated saddle (perineal) anesthesia (examiner can inquire if
toilet paper feels different when wiping)Bladder dysfunction may present as incontinence, but often presents earlier as
difficulty starting or stopping a stream of urine. Examination
  Pain often is localized to the low back; 
    
       local tenderness to palpation or
percussion may be present.
Reflex abnormalities may be present; 
    
      typically include loss or diminution
of reflexes.  Hyperactive reflexes may signal spinal cord involvement and exclude
the diagnosis of CES.Pain in the legs (or radiating to the legs) is characteristic of CES
Sensory abnormality may be present in the 
    
       perineal area 
        
          Light touch in the perineal area should be testedlower extremitiesMuscle weakness may be present in muscles supplied by affected roots.
    
       Muscle
wasting may occur if CES is chronicPoor anal sphincter tone is characteristic of CES
Babinski sign or other signs of upper motor neuron involvement suggest a
diagnosis other than CES, possibly a diagnosis of spinal cord compressionAnesthetic areas may show skin breakdownAlteration in bladder function may be assessed empirically by obtaining urine
via catheterization. 
    
       A significant volume with little or no urge to void, or as
a post-void residual, may indicate bladder dysfunction Causes:
  TraumaLumbar disc diseaseAbscessSpinal anesthesiaTumor, metastatic, or CNS elementsLate-stage ankylosing spondylitisIdiopathic
 Investigations
  Plain radiography - 
    
       Unlikely to be helpful, but perform in search of
destructive changes, disc space narrowing, or spondylolysisCT with and/or without contrast - Lumbar myelogram followed by CTMRI
    
       Superiority of MRI over CT only suggested by case reports (early
consultation with appropriate subspecialty is encouraged to guide imaging
studies)Catheterization
    
       for residual urine volume may reveal urinary retention
suggesting a neurogenic bladder.
 Treatment
  Prehospital Care:
    
      Stabilize acute life-threatening conditions.Immobilize spine if traumatic.Emergency Department Care:
    
       No proven medical treatment exists, and therapy
generally is directed at the underlying cause of CES.Some may suggest methylprednisolone in a regimen similar to that for
traumatic spinal cord injury or another regimen of steroid for the acute
syndrome.For penetrating trauma, steroids have not shown significant benefit. Surgery is
controversial. The timing of decompression is controversial, with immediate,
early, and late surgical decompression showing varying results.Steroids may be recommended in acute or traumatic CES. Early consultation
regarding the use of steroids and any specific regimen is encouraged. Steroids have anti-inflammatory properties and cause profound and varied
metabolic effects. In addition, these agents modify the body's immune response
to diverse stimuli. They may decrease oedema around nerve root segments. A regimen of methylprednisolone (Solu-Medrol, Depo-Medrol) may be used. One
possible regimen may be the dose employed in traumatic spinal cord injuries, but
no studies exist to support this over any other regimen.Further Inpatient Care
    
      Admit patients to appropriate service (usually neurology, neurosurgery, or
        orthopaedic surgery) with frequent neurological checks. Ideally, the admitting
physician or service should examine the patient at the time of admission.Further Outpatient Care
    
      Patients in whom acute CES is being considered should not be treated or
investigated on an outpatient basis without evaluation by a consultant and/or
appropriate imagingTransfer:
    
      Consider patients with CES for transfer if appropriate subspecialty care is
not available Complications
  Residual weakness,  incontinence, impotence, and/or  sensory abnormalities are
potential problems if therapy is delayed. Prognosis
  The prognosis for CES improves if a definitive cause is identified and
appropriate treatment occurs early in the course. Surgical decompression may be
performed emergently, or, in some patients, delayed, depending on the etiology. |