Respiratory Function After Spinal Cord Injury (SCI) 

Respiratory complications are one of the most common causes of morbidity and mortality across the life continuum following a spinal cord injury (SCI).  

An accurate and comprehensive assessment of respiratory function, as well as early management planning and intervention, is time critical following acute SCI. It is also important in treating individuals with chronic SCI.  

An acute SCI involving loss of motor control above the neurological level of T12, may result in respiratory muscle flaccid paralysis and weakness, altering chest wall and lung compliance and therefore breathing biomechanics. In addition to this, a cervical and high thoracic SCI above T6, may result in autonomic dysfunction impacting the physiological functioning of the respiratory and associated cardiovascular system. Respiratory compromise can be further complicated by concomitant injuries, age and comorbidities. 

Typically, respiratory complications result from low lung volumes and weakened cough causing a cyclical pattern of 

  • hypoventilation and CO2 retention 
  • atelectasis  
  • secretion retention 
  • reduced pulmonary and chest wall compliance  

This heightens the risk of  

  • hypoxaemia and hypercapnia from decreased mechanical efficiency of ventilation 
  • pneumonias from accumulating bacterial growths and atelectasis due to secretion retention 
  • respiratory fatigue from increased work of breathing  
  • respiratory failure from ventilation perfusion mismatch  

In the acute phase following a SCI, all potential respiratory complications must be anticipated.  

Early management planning and intervention is critical to provide sufficient respiratory support and treatment to minimise secondary complications. 

For individuals with chronic SCI, the following may need to be addressed  

  • chronic hypoventilation 
  • altered pulmonary and chest wall compliance 
  • sputum load 
  • speech and voice generation  
  • sleep-disordered breathing
  • impact of posture and seating
  • respiratory demands for ADL

Overview of risk factors after spinal cord injury (SCI) 

Below is a list of risk factors and considerations that can impact respiratory function in people with SCI with acute and chronic injuries.  

Also refer to Respiratory Complication Risks and SCI; Respiratory Management for Acute SCI; Respiratory Function and Long Term SCI Changes

Acute SCI 

Cervical and thoracic injuries above T6  

  • presence of spinal and/or neurogenic shock due to disruption in the sympathetic nervous system and a dominance of the parasympathetic nervous system, resulting in:
    • generalised pattern of airway constriction/bronchospasm including blockage of nasal passages and an increase in sputum load: mucous plugs can occur within 1 hour
    • altered cardiovascular function leading to an increased risk of pulmonary oedema, pulmonary emboli and potential for bradycardia when performing tracheal suctioning
    • changes in muscle tone affecting breathing mechanics, including paradoxical breathing patterns
    • resolution of spinal shock typically improves stability of the rib cage, improves paradoxical breathing patterns and lung volumes
  • increased risk of pulmonary embolism
  • increased risk of aspiration
  • increased risk of pneumonia
  • significant risk of respiratory fatigue and failure
    • is highest for C1-C6 levels of injury
    • usually occurs within 1-5 days post injury
    • results from
      • paradoxical breathing patterns/increased work of breathing from respiratory muscles flaccid paralysis or weakness and altered chest wall and lung complianc For more information refer to Respiratory Function Assessment and SC
      • increased secretions and bronchospasm
      • increasing hypoventilation, CO2 retention, atelectasis, secretion retention and ultimately hypoxaemia and hypercapnia
  • risk of ascension of SCI level: results from increasing inflammation and bleeding around the spinal cord, including delayed spinal decompression

Concomitant injuries and presentations

  • immersion in water-based injuries/other aspiration risks including saliva 
  • high velocity mechanism of injury can result in aortic, rib, sternal and intrabdominal injuries that require planning for treatment methods 
  • other fractures eg. rib/sternal that can impede management or positioning  
  • traumatic brain injury: can cause overlying issues with respiratory function 
  • pain: affecting ability to breathe deeply and engage in active therapy 
  • post-surgical recovery ie. spinal discectomies and fusions, intra-abdominal repairs 
  • presence of intubation tube, tracheostomy or mechanical ventilation  
  • altered level of consciousness  
  • altered psychological state 

Acute and Chronic SCI 

Cervical and thoracic injuries above T6  

  • high level cervical injury: impacting motor, sensory and sympathetic nervous system regulation of respiratory system  
  • completeness of injury: variably affecting respiratory function eg. right and left hemi-diaphragm

Concomitant injuries 

  • traumatic brain injury: can cause overlying issues with respiratory function 
  • pain: affecting ability to breathe deeply and engage in active therapy 
  • presence of intubation tube, tracheostomy or mechanical ventilation  
  • altered level of consciousness  
  • altered psychological state 

Additional ventilatory support 

  • unique considerations for tracheostomies and mechanical ventilation 

Biochemistry 

  • electrolyte imbalances and hypoalbuminemia can increase respiratory complications 

Gastrointestinal impact 

  • paralytic ileus can result in build-up of gastric contents and gases that impedes the descension of the diaphragm during inspiration and further increases the work of breathing
  • significant constipation can reduce diaphragm movement and impact ease of breathing with early and chronic SCI

Medical history 

  • pre-existing medical conditions: history of smoking, chronic lung disease, advanced age with other comorbidities 

Medications 

  • post-surgery: general anaesthetic can reduce respiratory drive 
  • medications such as opioids can cause sedation or respiratory depression 

Physical changes with chronic SCI 

  • changes in lung volumes, chest wall and lung compliance, sputum load and incidences of respiratory infections, prevalence of sleep disordered breathing, activity level and fitness  

Australian and New Zealand Clinical Practice Guidelines for the Physiotherapy management of Spinal Cord Injury Guidelines Documents | SCI Physiotherapy Clinical Practice Guidelines (sciptguide.com) 

Berlowitz DJ, Wadsworth B, Ross J. (2016) Respiratory problems and management in people with spinal cord injury. Breathe 12: 328–340.  

Galeiras Vázquez R, Rascado Sedes P, Mourelo Fariña M, Montoto Marqués A, Ferreiro Velasco ME. (2013) Respiratory management in the patient with spinal cord injury. Biomed Res Int.:168757.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781830/ Respiratory management in the patient with spinal cord injury 

Henke A, Billington Z, Gater D. (2022) Autonomic Dysfunction and Management after Spinal Cord Injury: A Narrative Review. J Pers Med. Jul 7;12(7):1110. doi: 10.3390/jpm12071110. PMID: 35887607; PMCID: PMC9320320. 

Mullen, E., Faltynek, P., Mirkowski, M., Benton, B., McIntyre, A., Vu, V & Teasall, R. (2022) Acute Respiratory Management Following Spinal Cord Injury. In: In: Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, Sproule S, McIntyre A, Querée M, editors. Spinal Cord Injury Rehabilitation Evidence. Version 6.0. Vancouver: p. 1-51. acute-respiratory_V7.pdf (scireproject.com) 

Sheel AW, Welch JF, Townson AF (2018) Respiratory Management Following Spinal Cord Injury. In:Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, Sproule S, McIntyre A, Querée M, editors. Spinal Cord Injury Rehabilitation Evidence.Version6.0. Vancouver: p. 1-72. 

Wulf MJ and Tom VJ (2023) Consequences of spinal cord injury on the sympathetic nervous system. Front. Cell. Neurosci. 17:999253 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10011113/pdf/fncel-17-999253.pdf