Rosen & Barkin's 5-Minute Emergency Medicine Consult (137 page)

354.0 Carpal tunnel syndrome

BASICS

Compression of lumbar and sacral nerve fibers in cauda equina region:

• Nerve fibers below conus medullaris
  
• Fibers end at L1–L2 interspace.
  

• Neoplasm
  
• IV drug use
  
• Immunocompromised state
  
• Trauma
  

• Herniated disc most common:
  
  • L4–L5 discs > L5–S1 > L3–L4
    
  • Most common in 4th and 5th decades of life
    
• Mass effect from:
  
  • Myeloma, lymphoma, sarcoma, meningioma, neurofibroma, hematoma
    
  • Spine metastases (breast, lung, prostate, thyroid, renal)
    
  • Epidural abscess (especially in IV drug users)
    
• Blunt trauma
  
• Penetrating trauma
  
• Spinal anesthesia
  

DIAGNOSIS

• Low back pain
  
• Sciatica/radicular pain (unilateral or bilateral)
  
• Lower-extremity numbness or weakness
  
• Difficulty ambulating owing to weakness or pain
  
• Bladder or rectal dysfunction:
  
  • Retention or incontinence
    

• Lumbosacral (LS) tenderness
  
• Lower-extremity sensory or motor deficits:
  
  • May be asymmetric
    
• Decreased foot dorsiflexion strength
  
• Decreased quadriceps strength
  
• Decreased deep tendon reflexes
  
• Saddle hypalgesia or anesthesia
  
• Decreased anal sphincter tone
  

• Neurologic exam most essential:
  
  • Straight-leg raise
    
  • Lasègue sign:
    
    • With patient supine, flex hip and dorsiflex foot.
      
    • Pain or spasm in posterior thigh indicates nerve irritation.
      
  • Perineal sensation
    
  • Rectal tone
    
  • Anal wink: Reflex contraction of external anal sphincter with gentle stroking of skin lateral to anus
    
• Postvoid residual volume:
  
  • Estimate by bladder catheterization or using US.
    
  • >50–100 mL is considered abnormal.
    
  • Residual increases with age.
    
  • Diagnosis unlikely if normal
    

• Based on differential diagnoses
  
• CBC, urinalysis, ESR, and C-reactive protein (CRP)
  

• Radiographs of LS spine
  
• MRI of spine is definitive study.
  
• CT myelogram if MRI unavailable
  

• Osteoarthritis, LS strain, sciatica
  
• Vertebral fracture (pathologic and nonpathologic)
  
• Osteomyelitis
  
• Spinal epidural abscess
  
• Conus medullaris or higher cord compression
  
• Ankylosing spondylitis, spinal stenosis
  
• Abdominal aortic aneurysm dissection
  
• Vascular claudication
  
• Hip pathology
  
• Acute transverse myelitis
  

TREATMENT

• Manage airway and traumatic injuries as indicated.
  
• If evidence of trauma, patient should be transported with full spine immobilization.
  

• Spine immobilization if trauma or unstable spine lesion suspected
  
• Analgesia
  
• NPO until evaluated by neurosurgery
  

• Repeat neurologic exams to detect progression.
  
• For acute spinal cord trauma (<8 hr), begin high-dose methylprednisolone protocol.
  
• Immediate neurosurgical consultation in all cases
  
• Initiate antibiotics for epidural abscess in consultation with neurosurgery.
  
• Controversy exists regarding urgency of decompression:
  
  • Recommendations range from within 6 hr of onset to within 24 hr.
    

• Methylprednisolone (high-dose steroid protocol): 30 mg/kg IV bolus, then 5.4 mg/kg/h infusion over next 23 hr. Should be started within 8 hr of injury.
  

FOLLOW-UP

• All patients with acute cauda equina syndrome must be admitted to neurosurgical service.
  
• Patients have good prognosis with rapid surgical decompression.
  
• Treatment should not be delayed.
  
• Patients presenting late (>48 hr) also benefit from surgical decompression.
  

Patients with established cauda equina syndrome with prior complete evaluation and no new neurologic deficits may be discharged with close follow-up with their neurosurgeon.

Ideally, diagnose patients in early phase before irreversible neurologic dysfunction:

• Back pain out of proportion
  
• Fever and back pain
  
• Back pain in high-risk groups; screen with ESR/CRP when infection suspected
  

• Fraser S, Roberts L, Murphy E. Cauda equina syndrome: A literature review of its definition and clinical presentation.
  Arch Phys Med Rehabil
  . 2009;90(11):1964–1968.
  
• Hussain SA, Gullan RW, Chitnavis BP. Cauda equina syndrome: Outcome and implications for management.
  Br J Neurosurg
  . 2003;17(2):164–167.
  
• Kingwell SP, Curt A, Dvorak MF. Factors affecting neurological outcome in traumatic conus medullaris and cauda equina injuries.
  Neurosurg Focus
  . 2008;25(5):E7.
  
• Ma B, Wu H, Jia LS, et al. Cauda equina syndrome: A review of clinical progress.
  Chin Med J (Engl)
  . 2009;122(10):1214–1222.
  
• Mauffrey C, Randhawa K, Lewis C, et al. Cauda equina syndrome: An anatomically driven review.
  Br J Hosp Med (Lond)
  . 2008;69(6):344–347.
  
• Olivero WC, Wang H, Hanigan WC, et al. Cauda equina syndrome (CES) from lumbar disc herniations.
  J Spinal Disord Tech
  . 2009;22(3):202–206.
  
• Rooney A, Statham PF, Stone J. Cauda equina syndrome with normal MR imaging.
  J Neurol
  . 2009;256(5):721–725.
  
• Todd NV. An algorithm for suspected cauda equina syndrome.
  Ann R Coll Surg Engl
  . 2009;91(4):358–359; author reply 359–360.
  

CODES

• 344.6 Cauda equina syndrome
  
• 344.60 Cauda equina syndrome without mention of neurogenic bladder
  
• 344.61 Cauda equina syndrome with neurogenic bladder
  

BASICS

• Alkalis:
  
  • Dissociate in the presence of H
    ₂
    O to produce hydroxy (OH
    ⁻
    ) ions, which leads to liquefaction necrosis
    
  • Postingestion—mainly damages the esophagus:
    
    • Gastric damage can occur (see “Acids”).
      
  • Esophageal damage (in the order of increasing damage) consists of:
    
    • Superficial hyperemia
      
    • Mucosal edema
      
    • Superficial blisters
      
    • Exudative ulcerations
      
    • Full-thickness necrosis
      
    • Perforation
      
    • Fibrosis with resulting esophageal strictures
      
  • Do
    not
    directly produce systemic complications.
    
• Acids:
  
  • Dissociate in the presence of H
    ₂
    O to produce hydrogen (H
    ⁺
    ) ions, which leads to a coagulation necrosis with eschar formation
    
  • Postingestion—damages the stomach because of rapid transit time through esophagus:
    
    • Esophageal damage can occur (see “Alkalis”).
      
  • Gastric damage (in the order of increasing damage) consists of:
    
    • Edema
      
    • Inflammation
      
    • Immediate or delayed hemorrhage
      
    • Full-thickness necrosis
      
    • Perforation
      
    • Fibrosis with resulting gastric outlet obstruction
      
  • Well-absorbed and can cause hemolysis of RBCs and a systemic metabolic acidosis