Jump to:



Spinal cord injury (SCI) commonly results in some degree of respiratory dysfunction due to weakness or paralysis of the respiratory muscles, reduced vital capacity (VC), increased respiratory secretions, ineffective cough, reduction in lung and chest wall compliance, and increased oxygen cost of breathing due to respiratory system impairment. The range of respiratory complications following SCI includes dyspnea, respiratory failure, pulmonary thromboembolism, pulmonary edema, bronchitis, atelectasis, pneumonia, sleep disordered breathing, and dysphonia.1 The more rostral the level and the more complete the SCI, the more likely the injury will affect ventilation.  Respiratory complications from SCI are most prevalent within the first year of injury but patients continue to experience complications for the rest of their life.2 In patients with spinal cord injury, there is a significantly increased mortality rate from pneumonia compared to the general population, particularly in people with tetraplegia.3 Although, risk of death within the first year has been declining, respiratory dysfunction is a major cause of morbidity and mortality in patients with SCI.4 In addition, the number of respiratory complications are important determinants of length of hospital stay as well as risk of rehospitalization.3


Normal respiration requires coordination between somatic control of the respiratory muscles and autonomic control of the bronchopulmonary tree.5 Inspiratory muscle impairment prevents deep breaths, leading to atelectasis and abnormalities of gas exchange and lung compliance.  Expiratory muscle dysfunction results in impaired cough and secretion clearance, increased airway resistance, and persistence of infection when it occurs.4 Loss of sympathetic autonomic signaling to the bronchopulmonary tree results in changes in mucus production and airway tone. The level and completeness of the SCI determine the severity of the respiratory dysfunction; greater impairment occurs with higher and more complete injuries.5 Respiratory decline associated with SCI results in decreased  Forced Expiratory Reserve Volume (FEV1), Forced Vital Capacity (FVC), inspiratory capacity, Total lung capacity (TLC), and increased Residual volume (RV).3 Patients with complete, high cervical injuries may be unable to sustain spontaneous ventilation. Those with lower or incomplete injuries typically demonstrate restrictive impairments and a weakened cough.

Epidemiology including risk factors and primary prevention

The incidence of respiratory complications varies, depending on the SCI population being studied. The most important risk factors for respiratory complications associated with spinal cord injuries are lesions above C5 and American Spinal Injury Association (ASIA) A impairment scale score.1 Not surprisingly, the incidence of respiratory dysfunction is higher in patients with cervical SCI. It has been shown to occur in 70% of cases with complete, cervical SCI and in 26.8% of cases with incomplete, cervical SCI.6 Pneumonia, atelectasis, and other respiratory complications reportedly occur in 40-70% of patients with tetraplegia, and are the leading cause of mortality in these patients.7 Other predictors of respiratory dysfunction in those with acute SCI include a history of cervicothoracic trauma, advanced age, and prior cardiopulmonary disease.1, 6 Independent risk factors for respiratory dysfunction include a lower forced expiratory volume in one second (FEV1) and a history of pneumonia or bronchitis since the SCI occurred. Patients with a history of smoking or chronic obstructive pulmonary disease (COPD) are also at increased risk for respiratory dysfunction.8, 9


The degree of respiratory dysfunction associated with a traumatic injury to the spinal cord depends on the level of the spinal cord lesion.  Functional impairment worsens as the level of the injury moves more rostral. Typically injuries above the C5 level can cause dysfunction of the diaphragm leading to respiratory dysfunction.1  Injuries to level C1-C2 are associated with severe diaphragm paralysis will most likely require mechanical ventilation. Injuries to levels C3-C4 will have reduced diaphragm function and will often require nighttime ventilation with eventual ventilation weaning when appropriate. Patients with injuries at the level of C5 can have independent respiration but will often need delayed respiratory support due to intercostal and abdominal muscle fatigue. Injuries to levels C6-C8 often have independent breathing although are noted to have increased accessory muscle use with inspiration. Injuries to levels T1-T4 are associated with decreased cough reflex most likely due to weakness of abdominal muscles. Patients with injuries below T12, typically do not have respiratory impairment.2, 3 An injury classified as ASIA impairment scale score A results in greater functional impairment and increased risk for pulmonary complications than an incomplete injury in the ASIA impairment scale score B–D categories.1

Respiratory dysfunction in tetraplegia and high thoracic paraplegia results from compromise to the somatic and autonomic nervous systems.5

Somatic nervous system

  • The phrenic nerve, originating from C3-5, innervates the diaphragm, which is the primary muscle of inspiration. As such, preservation of the C3-C5 spinal cord segments is critical for maintaining spontaneous respiration.5 Patients with complete lesions at C1 and C2 cannot maintain effective spontaneous ventilation.1, 10
  • Patients with incomplete or lower cervical SCI typically maintain spontaneous respiration, but due to partial or complete paralysis of other inspiratory muscles, often demonstrate more restrictive impairment than patients with thoracolumbar SCI.5
  • In neurologically intact individuals, maximal VC is achieved through contributions from the intercostal and scalene muscles. Abdominal muscle dysfunction limits the patient’s ability to raise abdominal pressure during inspiration, impairing optimal diaphragmatic contraction.
  • Loss of control of the abdominal and intercostal muscles impairs expiratory function including the ability to generate a forceful cough for airway clearance.5 To compensate, patients with tetraplegia may recruit the clavicular portion of the pectoralis major muscle to deflate the rib cage during expiration.10

Autonomic nervous system

  • Sympathetic: The cell bodies of preganglionic sympathetic neurons are located in the lateral grey column of the spinal cord from T1-L2/3. These neurons synapse with postganglionic neurons in paravertebral ganglia.
  • Parasympathetic: The cell bodies of the parasympathetic nervous system are located in the brainstem (CN III, VII, IX, X) or the sacral spinal cord (S2-S4).  The vagus nerve provides parasympathetic innervation to the lungs.
  • Contrary to sensory and motor dysfunction, which are localized to the level of the lesion, the effects of SCI on the autonomic nervous system are diffuse due to the anatomic distribution of sympathetic nervous system.2
  • In acute, severe cervical and high thoracic SCI, much of the sympathetic tone is lost, leaving the parasympathetic nervous system to provide the dominant autonomic control of the bronchopulmonary system.5
  • Loss of sympathetic modulation of the parasympathetic outflow tract likely contributes to unopposed bronchoconstriction.5
  • In the acute phase of injury, airway secretions are produced in large volumes due to unopposed vagal tone in patients with cervical SCI.10 The secretions contribute to acute respiratory distress, hypoxemia, worsening hypercapnia, and the need for intubation for ventilatory support and airway suctioning. These events may be avoided when the expiratory muscles are assisted to help eliminate secretions.10 Tracheostomy tube placement has also been noted to increase respiratory secretions.3

Disease progression including natural history, stages of disease, and disease trajectory (changes in clinical features over time)


  • Respiratory failure following acute SCI may occur because of partial or complete respiratory muscle paralysis, fatigue of remaining intact muscles, or in association with pleuropulmonary pathology.10 In addition, flaccid paralysis of the intercostal muscles worsens vital capacity, with the rib cage moving inward with diaphragm contraction during inspiration due to paradoxical depression. Following injury, there is a reduction of vital capacity to 20-60% in tetraplegia and 80-90% in paraplegia.2
  • Common respiratory complications during the first month after SCI include atelectasis, pneumonia, edema, pulmonary embolism, and aspiration. These account for the increased mortality rate during this time.6


  • Improvements in respiratory function over time may be due to enhanced neurologic function in the cord segments at or above the level of injury with improved diaphragm function as tone increases, providing a more rigid rib cage and better lever arm for the diaphragm to work against.10
  • Studies have shown a significant improvement in VC within the first 5 weeks after SCI, with doubling of VC occurring within 3 months of the injury.6


  • The severity of the SCI and a past history of tobacco smoking predict lung function impairment in chronic SCI.4
  • In the year following SCI, improvements may be seen in both FEV1 and VC. This has been attributed to an improvement in diaphragm performance, reflex activity in the abdominal and intercostal muscles, enhanced performance of the accessory muscles of the neck, and improvement in the diaphragm neural supply.4


  • Respiratory dysfunction is the most common causes of death in the SCI population.10

Specific secondary conditions and complications

  1. Sleep-disordered breathing: There is a high prevalence of sleep-disordered breathing in patients with tetraplegia.  Sleep disordered breathing is most prevalent within 6-20 weeks (64%-83%) and decreases in prevalence during the chronic phase (40-60%), which is much higher than the general population (9-24%).3  Most demonstrate an obstructive sleep apnea (OSA) pattern thought to be related to unopposed parasympathetics, abnormal chest wall function from neurologic deficits, obesity, and medications used for management of SCI.3 Polysomnography is the gold standard for OSA diagnosis. A machine that provides continuous positive airway pressure (CPAP), or in some cases bilevel positive airway pressure (BiPAP), can be helpful in managing OSA.7
  2. Aspiration and dysphagia: Risk factors for aspiration in the SCI population include: supine position, spinal shock, gastric reflux, inability to turn the head to spit out regurgitated material, medications that decrease GI motility or cause nausea and vomiting, recent anterior cervical spine surgery, presence of a tracheostomy, and advanced age. The presence of a tracheostomy is the strongest predictor of dysphagia in this population.7

Essentials of Assessment


When assessing a patient’s risk of respiratory dysfunction, one should consider:7

  • Relevant past medical history, including a history of smoking and prior lung disease
  • Current medications, with particular attention being paid to bronchodilators, deliriogenic agents, and those that may impair respiratory drive such as opioids
  • Neurologic impairment, the strongest predictor of respiratory dysfunction after SCI
  • Coexisting injuries, such as a traumatic brain injury, rib fractures, and acute lung injury all of which influence a patient’s respiratory status

Physical examination

Signs of deteriorating respiratory function that may indicate the development of atelectasis and pneumonia include:1, 3, 7, 11

  • Fever and other constitutional symptoms
  • Dyspnea and increasing respiratory rate
  • Increasing anxiety
  • Increased volume and tenacity of secretions
  • Increased levels of carbon dioxide
  • Declining oxygen saturation
  • Declining VC: VC < 15 cc/kg may indicate impending a need for assisted ventilation
  • Declining peak expiratory flow rate (especially during cough)

Functional assessment

Serial determination of VC, peak expiratory flow rate, negative inspiratory force (NIF), and oxygen saturation of blood should be performed.7 Signs of impending respiratory failure include hypoxia coupled with a rising respiratory rate, VC < 15 cc/kg, NIF < 20 cm H2O, hypercapnia, fatigue, and tachycardia.9 If any of these changes are noted, a chest radiograph should be performed.7

Laboratory studies

Following acute SCI, the initial assessment should include:7

  • Arterial blood gas
  • Routine laboratory analysis (CBC, BMP, coagulation profile, urinalysis, toxicology screen, cardiac enzymes)
  • Electrocardiogram
  • Chest radiographs


  • Diaphragm fluoroscopy may be used to assess diaphragm movement.7 Phrenic nerve conduction studies can be used to assess phrenic nerve function.4
  • Chest radiographs can be used to identify atelectasis, pneumonia, or effusion.7
  • Pulmonary CT angiography (CTA) can be used to diagnose pulmonary emboli.
  • Ultrasonography of the diaphragm may be utilized to assess diaphragm thickness and excursion which correlate with pulmonary function in persons with cervical spinal cord injury.12

Supplemental assessment tools

Periodic assessments of respiratory function should include:7

  • Physical examination of the respiratory system
  • Chest imaging as appropriate
  • Continuous pulse oximetry
  • Assessment of respiratory muscles function, including VC and NIF
  • FEV1 or peak cough flow
  • Neurologic status and extent of impairment
  • Polysomnography

Early predictors of outcome

The two most important markers that predict the need for intubation in the acute setting are the level of the injury and the ASIA impairment classification. Complete lesions above C5 require intubation in almost 100% of cases.13, 14 Mechanical ventilation is likely indicated if there is:

  1. One or more signs of respiratory distress15
  2. Hypercarbia with PaCO2 > 50 mmHg15
  3. Hypoxia with PaO2 < 50 mmHg that is unresponsive to oxygen therapy15
  4. The inability to handle oral secretions15
  5. A decline in VC to < 10-15cc/kg of ideal body weight (approximately 1000cc for the average 80 kg person)7

Life expectancy for any age or level of SCI is reduced if the patient remains ventilator-dependent.16


Ventilator-dependent patients and their caregivers must plan in advance for emergencies. This includes maintenance of portable ventilators, ancillary respiratory equipment, power generators, and emergency call systems.7

When tetraplegic patients are traveling by air, meticulous advanced planning is required. Patients with respiratory compromise at ground level may require supplemental oxygen to avoid the hypoxemia that can develop at altitude. In addition, mucous plugging can be particularly problematic if the patient breathes dry air cycled from outside the aircraft. To combat mucous plugging, inspired air should be humidified when possible and suctioning equipment should be readily accessible during transport.17

Social support system

Important things to consider when treating patients with respiratory dysfunction due to SCI include:7

  • Establishing an effective communication system
  • Ensuring that family and caregivers receive adequate training
  • Assessing for possible concomitant traumatic brain injury
  • Assessing the patient’s adjustment to SCI
  • Considering the impact of medication side effects

Professional Issues

Given the quality of life issues that can arise in cases of ventilator-dependent tetraplegia, the presence of advance directives can help the treatment team formulate a clinical plan. In the rare situation where a patient wishes to withdraw treatment, it is important to address the medical as well as social factors that contribute to the patient’s expressed wishes. Specific procedures may involve assessing the patient’s capacity to make such decisions and the consistency of the decision, exposing the patient to other similarly injured individuals, consulting with the institutional ethics committee, and ensuring a humane end of life.7

Rehabilitation Management and Treatments

Current treatment guidelines

Consortium for Spinal Cord Medicine Clinical Practice Guidelines are available for respiratory management following spinal cord injury.7

At various disease stages

Ventilatory support:

  1. Glossopharyngeal breathing: performed by rapidly “gulping” a series of mouthfuls of air, forcing the air into the lungs, and then exhaling the accumulated air.4
  2. CPAP and BiPAP: may be used to rest the non-intubated patient and to give the patient a deep breath to help manage secretions.4
  3. Intermittent positive-pressure breathing: can be administered with mechanical devices or with a bag valve mask. It assists lung expansion by introducing large volumes of air. The pressure should be set at 10–15 cmH2O then gradually increased, never to exceed 40 cmH2O to decrease risk of atelectasis but also prevent barotrauma.3, 7
  4. Phrenic nerve pacing: requires intact phrenic nerve function and allows for at least part-time freedom from mechanical ventilation.4
  5. Intramuscular diaphragm pacing: often requires a period of gradually increasing stimulation (reconditioning period) due to diaphragm atrophy.4

Secretion management/cough:

  1. Assisted cough: requires another person forcefully applying pressure to the abdomen to enhance expiratory flow and mobilize secretions.4
  2. Postural drainage: if the patient is immobilized, passive positioning techniques using gravity can facilitate the movement of secretions.4
  3. Suction catheter: applies negative pressure at the mouth or tracheostomy site.1
  4. Mechanical insufflation-exsufflation: involves maximal insufflation followed immediately by a decrease in pressure of about 80 cmH2O.4
  5. Bronchoscopy: the most effective method for secretion clearance; reserved for when other methods have been inadequate.4
  6. Bronchodilators: effective adjuncts to prevent atelectasis, decrease sputum production, and stimulate the secretion of surfactant. Beta-2-adrenergic medications improve expiratory pressures which may in turn translate to a more effective cough.15
  7. Mucolytic: medications such as guaifenesin used in combination with adequate oral hydration may thin pulmonary secretions and thereby increase their mobilization.15
  8. Hydration – ensuring sufficient hydration in order to keep secretions thin so they can be expelled. Can be administered by saline, misted air, or heat moisture exchangers.3

Ventilator weaning:

  1. The parameters used to best determine if the patient is ready to be weaned from the ventilator include: values derived from arterial blood gas or capnography, vital capacity, the effectiveness of the cough, and the results of diaphragmatic electromyography.18
  2. Data suggests that cautious implementation of higher ventilator tidal volumes may treat atelectasis and contribute to a reduced time for ventilator weaning.7
  3. Weaning protocols described in the literature for cervical and high thoracic SCI suggest gradually increasing periods of ventilator-free breathing.19
  4. When weaning a patient with a complete cervical SCI, trials are more successful with the patient in a Trendelenburg position. In this position, the diaphragm is higher in the chest secondary to pressure from the abdominal contents. This improves diaphragmatic contraction since the higher the diaphragm is in the chest, the more effective is its contraction.20

Health maintenance:

  1. Recommend annual influenza and regular pneumococcal vaccinations.
  2. Encourage cessation of smoking and avoidance of second-hand smoke.
  3. Perform surveillance for signs of sleep disordered breathing such as polysomnography.3
  4. Encourage use of respiratory muscle training to improve cough reflex and ventilation.3
  5. Consider regular pulmonary function studies to measure vital capacity, end tidal CO2.3

Coordination of care

Care of patients with SCI requires a multidisciplinary team including rehabilitation and pulmonary physicians, respiratory therapists, nurses, physical and occupational therapists, and speech and language pathologists (SLP). For patients requiring assisted ventilation, SLP is particularly important in aiding vocalization.

Patient & family education

Patients and their families must be well educated on the symptoms of respiratory dysfunction and know how to provide prompt assistance.

Emerging/unique interventions

Periodic spirometry (to assess VC, NIF, FEV1, peak cough flow) and polysomnography are recommended to evaluate for changes in pulmonary function and the development of OSA.7

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)

Abdominal binders:

  1. Increase abdominal pressure and place the diaphragm in a more efficient position when upright, helping to increase tidal volume.4
  2. Improve speech in patients with cervical SCI who demonstrate low volume (due to impaired alveolar pressure-generation capability) and short phrases (due to small tidal volume).4

Speech generation:

  1. For ventilator-dependent patients with a tracheostomy, the tracheostomy tube cuff must be deflated for speaking. This often requires a coordinated increase in ventilator-delivered tidal volume to compensate for air loss through the larynx.4
  2. Tracheostomy-ventilation speech is often characterized by short phrases, long pauses, poor voice quality, and variable loudness. Modifying ventilator settings or using a one-way inspiratory valve may improve speech.4

Cutting Edge/Emerging and Unique Concepts and Practice

Cutting edge concepts and practice

Spinal cord stimulator cough assist: An emerging technique that produces vigorous abdominal muscle contraction via direct stimulation of the spinal cord by epidural electrodes.4

The use of ultrasound as a non-invasive, bedside approach to evaluating diaphragm function by measuring  diaphragm thickness on inspiration and expiration.  Diaphragm thickness correlates with the work of breathing during non-invasive ventilation.21-23 Ultrasonography of the diaphragm has been studied on persons with C4–C5 segment SCI revealing that diaphragm thickness and motion are different from healthy controls. Diaphragm ultrasonography was correlated with pulmonary function testing and can be applied to evaluate diaphragm function.12 Additional studies are needed to explore the application of diaphragm ultrasonography in persons with SCI in the acute setting and monitoring diaphragm function after interventions during rehabilitation. 

Emerging and Unique Concepts

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel zoonotic viral pathogen that was detected for the first time in December 2019.24 It has been hypothesized that people with SCI are at increased risk of morbidity and mortality from COVID-19 infections.25, 26 However, others have reported that persons with SCI do not exhibit atypical clinical features or worse clinical course when compared with able-bodied individuals.27 Persons with SCI and COVID-19 infection may exhibit symptoms and present with similar clinical severity than the general able-bodied population.28

Gaps in the Evidence-Based Knowledge

Controversy remains about the optimal volume for ventilation of SCI patients. Further research aimed at determining the incidence of barotrauma and establishing ventilator weaning protocols is needed.


  1. Mourelo Fariña M, Salvador de la Barrera S, Montoto Marqués A, Ferreiro Velasco ME, Galeiras Vázquez R. Update on traumatic acute spinal cord injury. Part 2. Med Intensiva. 2017 Jun – Jul 2017;41(5):306-315. doi:10.1016/j.medin.2016.10.014
  2. Berlowitz DJ, Wadsworth B, Ross J. Respiratory problems and management in people with spinal cord injury. Breathe (Sheff). Dec 2016;12(4):328-340. doi:10.1183/20734735.012616
  3. Reyes MRL, Elmo MJ, Menachem B, Granda SM. A Primary Care Provider’s Guide to Managing Respiratory Health in Subacute and Chronic Spinal Cord Injury. Top Spinal Cord Inj Rehabil. 2020;26(2):116-122. doi:10.46292/sci2602-116
  4. Brown R, DiMarco AF, Hoit JD, Garshick E. Respiratory dysfunction and management in spinal cord injury. Respir Care. Aug 2006;51(8):853-68;discussion 869-70.
  5. Krassioukov A. Autonomic function following cervical spinal cord injury. Respir Physiol Neurobiol. Nov 2009;169(2):157-64. doi:10.1016/j.resp.2009.08.003
  6. Casha S, Christie S. A systematic review of intensive cardiopulmonary management after spinal cord injury. J Neurotrauma. Aug 2011;28(8):1479-95. doi:10.1089/neu.2009.1156
  7. Medicine CfSC. Respiratory management following spinal cord injury: a clinical practice guideline for health-care professionals. J Spinal Cord Med. 2005;28(3):259-93. doi:10.1080/10790268.2005.11753821
  8. Stolzmann KL, Gagnon DR, Brown R, Tun CG, Garshick E. Risk factors for chest illness in chronic spinal cord injury: a prospective study. Am J Phys Med Rehabil. Jul 2010;89(7):576-83. doi:10.1097/PHM.0b013e3181ddca8e
  9. Waddimba AC, Jain NB, Stolzmann K, et al. Predictors of cardiopulmonary hospitalization in chronic spinal cord injury. Arch Phys Med Rehabil. Feb 2009;90(2):193-200. doi:10.1016/j.apmr.2008.07.026
  10. Baydur A, Sassoon C. Respiratory dysfunction in spinal cord disorders. In: Lin V BC, Cardenas D., ed. Spinal cord medicine: Principles and practice. 2nd ed. Demos Medical Publishing; 2010.
  11. Savic G, DeVivo MJ, Frankel HL, Jamous MA, Soni BM, Charlifue S. Causes of death after traumatic spinal cord injury-a 70-year British study. Spinal Cord. Oct 2017;55(10):891-897. doi:10.1038/sc.2017.64
  12. Zhu Z, Li J, Yang D, Du L, Yang M. Ultrasonography of Diaphragm Can Predict Pulmonary Function in Spinal Cord Injury Patients: A Pilot Case-Control Study. Med Sci Monit. Jul 20 2019;25:5369-5374. doi:10.12659/MSM.917992
  13. Como JJ, Sutton ER, McCunn M, et al. Characterizing the need for mechanical ventilation following cervical spinal cord injury with neurologic deficit. J Trauma. Oct 2005;59(4):912-6; discussion 916. doi:10.1097/01.ta.0000187660.03742.a6
  14. Velmahos GC, Toutouzas K, Chan L, et al. Intubation after cervical spinal cord injury: to be done selectively or routinely? Am Surg. Oct 2003;69(10):891-4.
  15. Bryce TH, Vincent., Escalon M. Spinal Cord Injury. Sixth ed. Elsevier; 2021.
  16. DeVivo MJ, Ivie CS. Life expectancy of ventilator-dependent persons with spinal cord injuries. Chest. Jul 1995;108(1):226-32. doi:10.1378/chest.108.1.226
  17. Armitage JM, Pyne A, Williams SJ, Frankel H. Respiratory problems of air travel in patients with spinal cord injuries. BMJ. Jun 1990;300(6738):1498-9. doi:10.1136/bmj.300.6738.1498
  18. Chiodo AE, Scelza W, Forchheimer M. Predictors of ventilator weaning in individuals with high cervical spinal cord injury. J Spinal Cord Med. 2008;31(1):72-7. doi:10.1080/10790268.2008.11753984
  19. Arora S, Flower O, Murray NP, Lee BB. Respiratory care of patients with cervical spinal cord injury: a review. Crit Care Resusc. Mar 2012;14(1):64-73.
  20. Gutierrez CJ, Stevens C, Merritt J, Pope C, Tanasescu M, Curtiss G. Trendelenburg chest optimization prolongs spontaneous breathing trials in ventilator-dependent patients with low cervical spinal cord injury. J Rehabil Res Dev. 2010;47(3):261-72. doi:10.1682/jrrd.2009.07.0099
  21. Matamis D, Soilemezi E, Tsagourias M, et al. Sonographic evaluation of the diaphragm in critically ill patients. Technique and clinical applications. Intensive Care Med. May 2013;39(5):801-10. doi:10.1007/s00134-013-2823-1
  22. Sarwal A, Walker FO, Cartwright MS. Neuromuscular ultrasound for evaluation of the diaphragm. Muscle Nerve. Mar 2013;47(3):319-29. doi:10.1002/mus.23671
  23. Vivier E, Mekontso Dessap A, Dimassi S, et al. Diaphragm ultrasonography to estimate the work of breathing during non-invasive ventilation. Intensive Care Med. May 2012;38(5):796-803. doi:10.1007/s00134-012-2547-7
  24. Wang C, Horby PW, Hayden FG, Gao GF. A novel coronavirus outbreak of global health concern. Lancet. 02 2020;395(10223):470-473. doi:10.1016/S0140-6736(20)30185-9
  25. Korupolu R, Stampas A, Gibbons C, Hernandez Jimenez I, Skelton F, Verduzco-Gutierrez M. COVID-19: Screening and triage challenges in people with disability due to Spinal Cord Injury. Spinal Cord Ser Cases. 05 2020;6(1):35. doi:10.1038/s41394-020-0284-7
  26. López-Dolado E, Gil-Agudo A. Lessons learned from the coronavirus disease 2019 (Covid-19) outbreak in a monographic center for spinal cord injury. Spinal Cord. 05 2020;58(5):517-519. doi:10.1038/s41393-020-0473-z
  27. D’Andrea S, Berardicurti O, Berardicurti A, et al. Clinical features and prognosis of COVID-19 in people with spinal cord injury: a case-control study. Spinal Cord Ser Cases. 08 2020;6(1):69. doi:10.1038/s41394-020-0319-0
  28. Rodríguez-Cola M, Jiménez-Velasco I, Gutiérrez-Henares F, et al. Clinical features of coronavirus disease 2019 (COVID-19) in a cohort of patients with disability due to spinal cord injury. Spinal Cord Ser Cases. 05 2020;6(1):39. doi:10.1038/s41394-020-0288-3

Original Version of the Topic

Deborah A. Crane, MD, MPH. Respiratory impairment with spinal cord injury. 6/7/2013.

Previous Revision(s) of the Topic

Heather Asthagiri, MD, Justin Weppner, DO, Sara Raiser, MD, Justin Albright, MD. Respiratory impairment in SCI. 3/27/2017.

Author Disclosure

Justin Weppner, DO
Nothing to Disclose

Minh Doan, OMS IV
Nothing to Disclose

Ryan Russell, OMS III
Nothing to Disclose