Respiratory complications

Pulmonary embolism (PE), like venous thromboembolism (VTE), is a significant risk in the acute phase following SCI due to increased venous stasis and blood coagulability—particularly within the first 2 weeks post-injury, although elevated risk persists for 3-6 months.

These changes are due to trunk and lower limb muscle paralysis, prolonged immobility, as well as cardiovascular changes associated with ANS disruption. Timely and optimal thromboprophylaxis—including both pharmacological and mechanical strategies—is essential to prevent or reduce the incidence of PE. However, chemical thromboprophylaxis does not eliminate the risk entirely. Prompt investigation and treatment of suspected PE is considered a medical emergency.

The risk of PE increases with:

• acute, high-level motor complete SCI
• multi-trauma, especially involving lower limb or pelvic fractures
• increasing age
• history of previous VTE
• delayed or absent thromboprophylaxis
• dehydration.

Signs and symptoms of PE may include:

• chest pain which worsens with breathing
• arrhythmia, including tachycardia (ANS disruption may limit this response)
• shortness of breath and an increased respiratory rate
• reduced air entry on auscultation
• decreasing oxygen (O₂) levels on pulse oximetry and blood gas analysis
• unexplained low-grade fever
• a sense of anxiety, dizziness or syncope
• acute confusion
• CT pulmonary angiography evidence.

For more information on managing the risk of PE following SCI, refer to Venous thromboembolism.

Pulmonary oedema (PO) is a significant risk in the acute phase following SCI due to several contributing factors. PO most commonly results from cardiovascular changes related to ANS disruption. This causes venous and lymph pooling in the periphery, a reduction in cardiac pre-load and output, along with impaired pulmonary capillary tone and permeability. It can also occur in combination with excessive fluid resuscitation for management of neurogenic shock. PO may have a delayed onset and may occur in the absence of other signs of cardiac failure.

The risk of PO increases with:

• acute, high-level motor complete SCI with ANS disruption
• the need for treatment of severe hypotension associated with neurogenic shock.

Signs and symptoms of PO may include:

• extreme shortness of breath, worsening with exertion or lying supine
• sense of suffocating or drowning when lying supine
• cold, clammy skin
• rattling, moist sounds on deep breathing or coughing
• cough producing frothy and possibly blood-stained sputum
• arrhythmia, including tachycardia (ANS disruption may limit this response)
• shortness of breath and an increased respiratory rate
• reduced air entry and added sounds on auscultation
• decreasing oxygen (O₂) levels on pulse oximetry and blood gas analysis
• radiological evidence of fluid in the lung, including pleural effusion.

For more information on managing the risk of PO following SCI, refer to Neurogenic shock.

Aspiration is a significant risk in the acute phase following SCI due to the potential for compromised airway protection.

The risk of aspiration increases with:

• acute, high-level motor complete SCI
• immersion injury, traumatic brain injury, concussion or loss of consciousness
• vomiting while wearing a fixed neck device (e.g. cervical collar or halo brace)

• anterior cervical discectomy and fusion, due to surgical hardware, soft tissue swelling, or recurrent laryngeal nerve injury
• tracheostomy tube insertion
• recent extubation
• insertion of nasogastric, radiologically inserted gastrostomy, or percutaneous endoscopic gastrostomy tubes, particularly when accompanied by overfeeding and paralytic ileus or reduced bowel motility
• assessed changes in laryngeal function
• presence of dysphagia and/or risk-feeding behaviours.

Signs and symptoms of aspiration may include:

• awkward or incomplete swallow: watery eyes, audible or delayed swallow, wet vocal quality, drooling, cough or choking
• increased need for suctioning or coughing
• recurrent respiratory tract infections suggestive of silent aspiration of saliva or risk-feeding behaviours
• arrhythmia, including tachycardia (ANS disruption may limit this response)
• shortness of breath and an increased respiratory rate
• reduced air entry and added sounds on auscultation
• decreasing oxygen (O₂) and increasing carbon dioxide (CO₂) levels on pulse oximetry and blood gas analysis
• radiological evidence of lung collapse and consolidation.

Management of aspiration includes immediate airway clearance/secretion management including antibiotic therapy, along with ventilation support and lung volume augmentation. Addressing the original cause of aspiration will also be important.

For more information on managing the risk of aspiration following SCI, refer to Dysphagia.

Atelectasis is a significant risk in the acute phase following SCI due to respiratory muscle impairment which may result in hypoventilation and sputum retention. Any ANS disruption can further accelerate the development of atelectasis by increasing sputum production and triggering airway bronchospasm.

The risk of atelectasis increases with:

• acute high, level motor complete SCI
• multi-trauma resulting in lung injury (e.g. immersion, pneumothorax, aspiration)
• post-surgical recovery following other injuries, including spinal stabilisation
• pre-existing lung disease such as COPD
• prolonged mechanical invasive ventilation
• extended periods of immobilisation in bed.

Signs and symptoms of atelectasis may include:

• arrhythmia, including tachycardia (ANS disruption may limit this response)
• shortness of breath and an increased respiratory rate
• reduced air entry and added sounds on auscultation
• decreasing oxygen (O₂) and increasing carbon dioxide (CO₂) levels on pulse oximetry and blood gas analysis
• radiological evidence of lung collapse.

Management of atelectasis includes improving overall ventilation and lung volumes using positioning and positive pressure breathing, along with secretion clearance strategies.

For more information on managing the risk of atelectasis following SCI, refer to Ventilation support, Lung volume augmentation, and Secretion management.

Pneumonia is a significant risk in the acute phase following SCI for similar reasons to atelectasis. Inadequate management of atelectasis with significant sputum retention, typically promotes the development of pneumonia. This is particularly a common complication within the initial weeks post-injury, but it can also become problematic with ageing.

The risk of pneumonia increases with:

• acute, high-level motor complete SCI
• multi-trauma resulting in lung tissue injury (e.g. immersion, pneumothorax, aspiration)
• post-surgical recovery following other injuries, including spinal stabilisation
• pre-existing lung disease (e.g chronic obstructive pulmonary disease (COPD))
• presence of atelectasis and sputum retention
• aspiration
• poor infection control practices
• prolonged mechanical invasive ventilation
• extended periods of immobilisation in bed.

Signs and symptoms of suspected pneumonia may include:

• arrhythmia, including tachycardia (ANS disruption may limit this response)
• shortness of breath and an increased respiratory rate
• reduced air entry and added sounds on auscultation
• decreasing oxygen (O₂) and increasing carbon dioxide (CO₂) levels on pulse oximetry and blood gas analysis
• elevated body temperature, white cell count, C reactive protein levels
• increased sputum production and/or change in sputum colour
• positive sputum culture for bacteria etc.
• radiological evidence of lung collapse and consolidation, including pleural effusion.

Management of pneumonia includes antibiotic therapy, along with improving overall ventilation and lung volumes using positioning and positive pressure breathing, as well as secretion management strategies.

For more information on managing the risk of pneumonia following SCI, refer to refer to Ventilation support, Lung volume augmentation, and Secretion management.

Type 2 respiratory failure is a significant risk during the acute phase following spinal cord injury (SCI), primarily due to extensive respiratory muscle impairment, spinal shock, and autonomic nervous system (ANS) disruption. These factors lead to reduced ventilation, impaired secretion clearance, and altered breathing patterns—all of which significantly increase the work of breathing. Without adequate and timely intervention, this will lead to progressive hypoventilation, including worsening hypoxaemia and rising hypercapnia, as well as respiratory fatigue. The transition to respiratory failure quickly occurs (typically between 1-5 days following high-level cervical SCI) and may persist for many weeks.

The risk of developing acute respiratory failure type 2 increases with:

• acute, high-level motor complete SCI
• associated lung injury (e.g. immersion, pneumothorax, aspiration)
• pre-existing lung disease (e.g. COPD)
• presence of other respiratory complications e.g. atelectasis, sputum retention, or pneumonia
• increased work of breathing and inadequate early ventilation support
• attempting mobilisation in sitting too early and/or without adequate ventilation support.

Signs and symptoms of suspected respiratory failure may include:

• bluish skin discolouration (cyanosis)
• drowsiness and reduced alertness
• reduced capacity for speech or slurred speech
• abnormal breathing patterns, including paradoxical breathing
• increased sputum production
• decreased ability to co-operate with coughing
• increased work of breathing
• arrhythmia, including tachycardia (ANS disruption may limit this response)
• shortness of breath and an increased respiratory rate
• reduced air entry and added sounds on auscultation
• decreasing oxygen (O₂) and increasing carbon dioxide (CO₂) levels on pulse oximetry and blood gas analysis: evidence of hypoxaemia (PaO₂ <60 mmHg) and hypercapnia (PaCO₂ >50 mmHg)
• radiological evidence of lung collapse and consolidation, including pleural effusion
• significant decline in spirometry.

For more information on managing the risk of respiratory failure following SCI, refer to Ventilation support, Lung volume augmentation, and Secretion management.

Following SCI, inflammatory responses and progressive oedema can compromise vascular supply to adjacent spinal cord segments. In the days and weeks post-injury, the assessed neurological level of injury (NLI) may worsen due to these secondary processes and makes this an especially high-risk period for neurological deterioration.

Factors contributing to an ascending NLI include:

• initial first aid and emergency retrieval conditions
• timing and methods of medical management or surgical decompression
• acute central nervous system (CNS) neuroinflammatory responses post-injury, arising from the mechanism and energy of trauma or other related pathological processes.

In rare cases, subacute post-traumatic ascending myelopathy (SPAM) may develop several weeks after SCI, though its pathophysiology remains poorly understood. Neurological deterioration may also occur years later as a result of syringomyelia.

Detection of any change in NLI requires careful exploration of the subjective history, as well as objective neurological assessment. Completion of the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) is necessary to confirm any change in the NLI, while Magnetic Resonance Imaging (MRI) of the spinal cord may detect changes such as an expanding haematoma, progressive oedema or the development of a syrinx.

Depending on any assessed ISNCSCI or radiological change, re-assessment of respiratory function may be indicated.

Management of ascending NLI may include conservative approaches or surgical decompression, including insertion of a syringo-subarachnoid shunt.

For more information on managing respiratory function changes related to the ascension of NLI after SCI, refer to Respiratory predictive factors, Respiratory changes, Respiratory assessment, Ventilation support, Lung volume augmentation, and Secretion management.

Sleep-disordered breathing (SDB) may emerge during the acute phase following SCI and often persists as a chronic health issue. Its development is correlated to the neurological level of injury (NLI), with cervical and high thoracic injuries resulting in more significant respiratory muscle impairment and ANS disruption. Additionally, central disruptions to the control of breathing during sleep, contribute to the risk. In combination, these changes result in a reduction in respiratory muscle tone, altered respiratory drive, airway collapse and suboptimal gas exchange.

For more information on managing the risk of sleep-disordered breathing following SCI, refer to Sleep-disordered breathing.