SPINAL STABILITY

A spinal injury is considered unstable if normal physiologic loads cause further neurologic damage, chronic pain, and unacceptable deformity.

White and Punjabi

Defined scoring criteria have been developed for the assessment of clinical instability of spine fractures (Tables 10.1 and 10.2).

 

 

 

 

 

 

Denis‌

The three-column model of spinal stability (Fig. 10.12 and Table 10.3) is as follows:

 

 

 

 

 

 

1. Anterior column: anterior longitudinal ligament, anterior half of the vertebral body, and anterior annulus‌

2. Middle column: posterior half of vertebral body, posterior annulus, and posterior longitudinal ligament

3. Posterior column: posterior neural arches (pedicles, facets, and laminae) and posterior ligamentous complex (supraspinous ligament, interspinous ligament, ligamentum flavum, and facet capsules)

   • Instability exists with disruption of any two of the three columns.

   • Thoracolumbar stability usually follows the middle column: If it is intact, then the injury is usually stable.

Three degrees of instability are recognized:

First degree (mechanical instability): potential for late kyphosis

• Severe compression fractures

• Seat belt–type injuries

  Second degree (neurologic instability): potential for late neurologic injury

• Burst fractures without neurologic deficit

  Third degree (mechanical and neurologic instability):

• Fracture-dislocations

• Severe burst fractures with neurologic deficit

  McAfee

  This author noted that burst fractures can be unstable, with early progression of neurologic deficits and spinal deformity as well as late onset of neurologic deficits and mechanical back pain.

• Factors indicative of instability in burst fractures:

  • 50% canal compromise

  • >15 to 25 degrees of kyphosis

  • >40% loss of anterior body height

     

    GUNSHOT WOUNDS

• In general, fractures associated with low-velocity gunshot wounds are stable fractures. This is the case with most handgun injuries. They are associated with a low infection rate and can be prophylactically treated with 48 hours of a broad-spectrum antibiotic. Transintestinal gunshot wounds require special attention. In these cases, the bullet passes through the colon, intestine, or stomach before passing through the spine. These injuries carry a significantly higher rate of infection. Broad-spectrum antibiotics should be continued for 7 to 14 days. High-energy wounds, as caused by a rifle or military assault weapon, require open debridement and stabilization.

• Neural injury is often secondary to a blast effect in which the energy of the bullet is absorbed and transmitted to the soft tissues. Because of this unique mechanism, decompression is rarely indicated. One exception is when a bullet fragment is found in the spinal canal between the level of T12 and L5 in the presence of a neurologic deficit. Rarely, delayed bullet extraction may be indicated for lead toxicity or late neurologic deficits owing to migration of a bullet fragment. Steroids after gunshot wounds to the spine are not recommended because they have demonstrated no neurologic benefit and appear to be associated with a higher rate of nonspinal complications.

  PROGNOSIS AND NEUROLOGIC RECOVERY

  Bradford and McBride

• The authors modified the Frankel grading system of neurologic injury for thoracolumbar injuries, dividing Frankel D types (impaired but functional motor function) based on degree of motor

  function as well as bowel and bladder function:

  Type A: Complete motor and sensory loss

  Type B: Preserved sensation, no voluntary motor

  Type C: Preserved motor, nonfunctional

  Type D1: Low-functional motor (3+/5+) and/or bowel or bladder paralysis

  Type D2: Midfunctional motor (3+ to 4+/5+) and/or neurogenic bowel or bladder dysfunction Type D3: High-functional motor (4+/5+) and normal voluntary bowel or bladder function Type E: Complete motor and sensory function normal

• In patients with thoracolumbar spine fractures and incomplete neurologic injuries, greater neurologic improvement (including return of sphincter control) was found in those treated by anterior spinal decompression versus posterior or lateral spinal decompression.

  Da l and Stauffer

• They prospectively examined neurologic injury and recovery patterns for T12–L1 burst fractures with partial paralysis and >30% initial canal compromise.

• Conclusions

  • Severity of neurologic injury did not correlate with fracture pattern or amount of CT-measured canal compromise.

  • Neurologic recovery did not correlate with the treatment method or amount of canal

    decompression.

  • Neurologic recovery did correlate with the initial fracture pattern (four types):

    Type I: <15 degrees of kyphosis; maximal canal compromise at level of ligamentum flavum

    Type II: <15 degrees of kyphosis; maximal compromise at the bony posterior arch

    Type III: >15 degrees of kyphosis; maximal compromise at the bony arch

    Type IV: >15 degrees of kyphosis; maximal compromise at the level of the ligamentum flavum

• Type I or type II: Significant neurologic recovery occurred in >90%, regardless of the severity of the initial paralysis or treatment method.

• Type III: Significant neurologic recovery occurred in <50%.

• Type IV: The response was variable.

  Camissa et al.

• They associated dural tears in 37% of burst fractures with associated laminar fractures; all patients had neurologic deficits.

• They concluded that the presence of a preoperative neurologic deficit in a patient who had a burst fracture and an associated laminar fracture was a sensitive (100%) and specific (74%) predictor of dural laceration, as well as a predictor of risk for associated entrapment of neural elements.

  Keenen et al.

• They reported an 8% incidence of dural tears in all surgically treated spine fractures and 25% in lumbar burst fractures.

• In patients with burst fractures and a dural tear, 86% had neurologic deficits versus 42% in those with burst fractures without a dural tear.