Respiratory Failure In SCI: The Mechanism

Sacramento, CA, 02/04/2016 /SubmitPressRelease123/

Acute respiratory failure is the first medical complication acutely injured people face in the first few days following a catastrophic spinal cord injury (SCI).  Significant pulmonary impairment is a consequence of severe cervical spinal cord injuries and thoracic spinal cord injuries above thoracic level six (T6).  Acute management must begin immediately to reduce the risk and severity of respiratory failure.  There are several mechanisms in SCI that lead to respiratory failure including paralysis of the muscles of inspiration and expiration, increased secretions, and bronchospasm.

 

Paralysis of the muscles of inspiration and expiration causes respiratory insufficiency.  The diaphragm contributes to 65% of inspiration and is supplied by the right and left phrenic nerve that exits the spinal cord at cervical level three, four, and five (C3, 4, and 5).  A complete SCI above C3 will require mechanical ventilation and those between C3 and C4 may require ventilator support depending on the level of completeness of the SCI.

 

The intercostal muscles of the ribs assist with rib elevation during inspiration and are supplied by the spinal nerves from T1 to T11.  With normal inspiration the diaphragm contracts and descends into the abdomen and the chest wall expands via contraction of the intercostal muscles.  Therefore, quadriplegics with a functional diaphragm produces a paradoxical breathing pattern that upon inspiration triggered by the contracting diaphragm that moves the diaphragm down into the abdomen, the chest wall will collapse because of the intercostal muscle paralysis with inspiration rather than expanding.   This paradoxical breathing pattern greatly reduces the lung volumes available to both quadriplegics and upper thoracic paraplegics.

 

Complete quadriplegics must rely on the accessory muscles of inspiration of the neck that are generally reserved to assist neurologically intact persons with breathing in times of vigorous exercise.  A major mechanism of respiratory failure in SCI is fatigue of the diaphragm and neck muscles on post-injury day three and five.

 

The lack of sufficient inflation of the lungs with inspiration produces atelectasis which is the most common complication leading to respiratory failure and pneumonia.  Atelectasis refers to portions of the lung that have no air which is required to keep the various segments of lung inflated so they merely collapse, housing secretions that contribute to the development of pneumonia.

 

Impair expiration from paralyzed muscles lead to an inadequate force to produce an effective cough.  A weak and inadequate cough leads to retained secretions that again contribute to the development of atelectasis and pneumonia that may lead to respiratory failure.  Patients with a SCI above T6 are at significant risk of impaired expiration because of an inadequate cough.

 

The muscles of expiration responsible for coughing are the abdominal muscles, the internal and external obliques, and the pectoralis muscles of the chest.   An effective cough is vital for the spinal cord patient because during expiration the flaccid chest wall simply collapses producing little force that limits the amount of air that can be effectively expelled.

 

Abnormalities of the sympathetic and parasympathetic nervous system contribute to respiratory insufficiency in SCI.   Acutely after a SCI the sympathetic nervous system below the level of injury basically turns off.  The lack of sympathetic nerve supply to the lungs increases secretions up to 40% within the first few hours following SCI.  Increased secretions add to the risk of atelectasis, pneumonia, and acute respiratory failure.

 

The lack of sympathetic nerve supply to the lungs after cervical and upper thoracic SCI contribute to bronchospasms even in patients with no history of asthma.  SCI patients must receive bronchodilators to prevent the resulting bronchoconstriction that produces air trapping, atelectasis, and increases the work of breathing that leads to respiratory failure.

 

Academic Physician Life Care Planners who work with catastrophic case managers understand that SCI are at high risk of respiratory complications and should be transferred to a SCI Model System Hospital as soon as possible.  Respiratory complications are an inevitable complication of those with cervical SCI and those with upper thoracic SCI.  Even at SCI Model System Hospitals up to 85% of persons with C1-C4 injuries and 60% of those with C5-C8 injuries develop respiratory complications.  Paraplegics are also at risk with approximately one-third having complications related to atelectasis and pneumonia.

 

Catastrophic case managers must work to transfers patients to a SCI Model System Hospital.   At these facilities the injured should benefit from a multidisciplinary approach to rehabilitation while they receive ventilator weaning and other specialized care by clinicians and allied health personnel trained in SCI.

 

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2031940/

 

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