Sunday, June 16, 2013

Priapism in acute spinal cord injury

Why priapism in acute spinal cord injury? The pathophysiology

It is assumed that the mechanism of priapism in most patients with SCI is that abrupt loss of sympathetic input to the pelvic vasculature leads to increased parasympathetic input and uncontrolled arterial inflow directly into the penile sinusoidal spaces.

The sympathetic outflow arises from the thoracolumbar spine, that is, the spinal cord from approximately T2 to the conus (L1-2). The sympathetic outflow to the penis and clitoris arises from the lowest levels of the spinal cord, the conus, which is the reason why a lesion at any level in the spinal cord from the brainstem to the conus can be associated with priapism.

(Ref: Keoghane SR, Sullivan ME, Miller MA. The aetiology, pathogenesis and management of priapism. BJU Int 2002; 90: 149–154.)

Therefore, if a patient is unconscious because of a traumatic brain injury, the presence of priapism is an indication of coexisting SCI.

(Ref: Sneed RC, Stover SL. Undiagnosed spinal cord injuries in brain-injured children. Am J Dis Child 1988; 142: 965–967.)

However, priapism can occur in both:
  • Complete spinal cord injury (anatomical/physical damage to the motor and sensory pathways in the spinal cord) OR
  • Spinal shock (physiological; reversible, typically over several hours or days)
Nonetheless, spinal shock is rare; most patients with traumatic SCI who have complete motor and sensory paraplegia on first assessment have irreversible lesions, which is the reason why the presence of priapism usually carries a poor prognosis for neurological or functional recovery (unless reversibility demonstrated subsequently)

The timing of the occurrence of the priapism is important.
  • If priapism occurs at the time of first assessment, this suggests a complete spinal cord injury occurred within the past few hours
  • If, however, on first assessment there was no penile erection and priapism was subsequently identified, this suggests that the complete SCI was not a consequence of the primary injury, but occurred subsequently as a secondary neurological deterioration, possibly can be due to excessive movement at the level of an unstable fracture and/or dislocation.

Todd NV. Priapism in acute spinal cord injury. Spinal Cord.  Oct;49(10):1033-5.

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