A major cause of morbidity seen in spinal cord injury are related to respiratory complications. Typically, thoracic spinal cord lesions do not cause respiratory compromise related to ventilatory muscle compromise. However, because the diaphragm is the major muscle of ventilation and inspiration (C3-C5 nerve roots), chronic respiratory failure may develop. We present the case of a patient whose initial spinal lesion caused by a gun-shot wound would not have contributed to persistent hypercapnia, however he developed a syringomyelia extending into the cervical area which led to chronic ventilatory insufficiency.
A 49 year old male with history of parapalegia secondary to gunshot wound to the back suffered in 1997 with spinal cord injury at the level of T5, was admitted to the medical intensive care unit for urosepsis and concomitant acute hypercapnic hypoxic respiratory failure. He required mechanical ventilation for the treatment of respiratory distress and was subsequently found to have Pseudomonal infection in the urine and methicillin resistant staphylococcus aureus bacteremia. He responded well to antibiotics and defervesced after approximately 24 hours, but the patient experienced hypercapnia during attempted ventilator weaning. Review of laboratory testing prior to his infectious complications revealed a persistently elevated serum bicarbonate (range 30–36) over the past month. He was successfully extubated to BiPAP on day 4 of his ICU course and was ultimately transitioned to BiPAP at night.An MRI of the spine was done (see Panel A) after extubation to assess the cause for his chronic respiratory failure and hypoventilation as a spinal lesion at the T5 level should not result in persistent hypercapnia. He was found to have a syrinx that had extended from the level of C4 –T11 of the spine.
Syringomyelia is the development of a fluid-filled cavity or syrinx within the spinal cord. 50% of cases are due to congenital defects that become more apparent as the person develops (usually into adolescence or young adulthood), the vast majority of which are caused by Arnold-Chiari malformations. The other 50% are due to causes such as spinal cord tumor or hemorrhage, scarring due to previous spinal trauma, or kyphoscoliosis. Progressive post-traumatic cystic syringomyelia is an uncommon but a potentially clinically serious complication of spinal cord injury. Post-traumatic delayed development of syringomyelia, once thought to occur in only 1–4% of cases, is now increasingly recognized as a major cause of morbidity. Progressive signs and symptoms can develop as early as three months after spinal cord trauma or can occur as late sequelae as late as 32 years after spinal cord injury.It is likely that our patient developed chronic hypoventilation from the extension of the syrinx to the level of C4 which can cause weakness in both the diaphragm and other muscles of respiration. As was noted in the case described, the risk of chronic ventilator dependence is greatest among patients with injuries close to the C3 level and in patients older than 50 with underlying lung disease. Some patients with injuries at this level may, with aging, insidiously develop chronic hypoventilation which requires chronic ventilatory support decades after spinal cord injury.Though the patient seemed to do well with improvement on BiPAP at night, he may ultimately require continuous mechanical ventilation.
In the case just described, as the original lesion at T4 should not have affected the patient’s ventilatory status further investigations for this relatively uncommon complication of spinal cord injury was warranted. The possibility of syringomyelia should be considered in any patient who develops chronic hypercapnia following a spinal cord injury as extension of a syrinx can lead to progressive respiratory failure.
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