Spinal Cord Injury: Respiration

Respiratory complications are the most common cause of mortality following a spinal cord injury. The extent of respiratory compromise is highly dependent on the level of the injury. High cervical lesions will affect respiration to a much greater extent than lesions lower in the spinal cord.

Above C3: Patients are likely to be fully ventilator dependent due to diaphragm paralysis.

C3-C4: Diaphragm function likely severely impaired, but patients may be able to have some time off ventilator while awake and seated.

C5: Often need ventilator support initially but long term may be able to be weaned from ventilator. Loss of accessory muscles of respiration (intercostals, abdominal muscles) leads to decreased tidal volumes and weakened cough.

C6-C8: Able to breath independently. Other muscles, such as pectoral muscles, may be used to support cough.

T1-T4: Intercostal muscles remain intact to support inspiration and forced expiration. Lack of abdominal muscles leads to weakened cough.

T4-T12: Improvement in strength of abdominal muscles with descending lesions.

Below T12: Respiratory function essentially normal.

Immediately following a spinal cord injury there is a period of flaccid paralysis which lasts for a few weeks to a few months. During this time the weakness of the intercostal muscles can create an unstable chest wall, which leads to paradoxical motion of the chest during respiration (collapse of chest wall during inspiration due to negative intrathoracic pressure). With time the chest wall will tend to stiffen, and the upper motor neuron injury can lead to spasticity of the intercostals, which will tend to decrease the paradoxical chest motion.