CAUSES AND PATHOPHYSIOLOGY OF PULMONARY PROBLEMS IN SCI

Click on Respiratory Management Following Spinal Cord Injury for the current clinical practice guideline.

     The causes of pulmonary problems include injury or paralysis of the muscles of inspiration and expiration, which can no longer contract and cause pressure changes in the thoracic and abdominal cavities necessary for inspiration and expiration. Paralysis of the expiratory musculature can result in a decrease in vital capacity of as much as 42% in quadriplegics with lesions below C-4.

     A decrease in blood pressure is correlated with the decrease in breathing capacity (Frisbie, 2005). Injury to the abdominal and chest wall muscles can render the patient unable to produce a forceful cough, which clears normal respiratory secretions and prevents complications, such as pneumonia, atelactasis, and pulmonary edema which can cause respiratory failure and death. Since cough reflex sensitivity is preserved following cervical SCI, ineffective cough results primarily from loss of innervation of the respiratory muscles (Dicpinigaitis, et al 1999).

     Ventilation failure and aspiration often occur in the first five days after injury. Patients with cervical SCI demonstrate significantly disturbed dynamic function of the pharynx and upper esophageal sphincter, an important potential mechanism of aspiration (Neville, et al 2005). Although atelectasis and pneumonia occur most frequently, other complications include bronchitis, tracheitis, upper respiratory infection, and pulmonary embolism (Bergman, et al 1997).

     Patients with high-thoracic SCI also have an increased risk of pneumonia and death. Respiratory complications significantly increase the mortality risk in less severely injured patients. The current findings suggest that high-thoracic SCI patients warrant intensive monitoring and aggressive pulmonary care and attention, similar to that given for patients with cervical SCI (Cotton BA, et al 2005).

     Smoking, persistent wheeze, obesity, and greater maximal inspiratory pressure, in addition to SCI level and completeness, were significant determinants of pulmonary function. In SCI, FEV(1), FVC and FEV(1)/FEV may be less sensitive to factors associated with change in airway size and not reliably detect the severity of airflow obstruction (Jain, et al 2006).

1. The inspiratory muscles are the:
   • Diaphragm (innervated by C3-5), normal contraction of which lifts the thorax and expands the chest, based on the resistance of abdominal contents and mobility of the ribs
   • Scalenes (innervated by C4-8)
   • External intercostals (innervated by T1-11)

2. The expiratory muscles (all innervated by thoracic spinal segments) are the:
   • Internal intercostal muscles, which contribute to inspiration by increasing the anteroposterior diameter at the chest
   • Abdominal muscles, which enable the force of cough and which, together with the abdominal contents, return the diaphragm to a normal resting position

     Complete SCI at any cervical level results in a loss of coordination of the ventilatory musculature. During spinal shock, paralyzed muscles are flaccid and the paralyzed abdominal wall moves outward (instead of contracting to enhance chest wall expansion) which reduces breathing efficiency. Midcervical injuries, for example, can result in vital capacities less than 1500mL and may require ventilatory assistance.

     In C-4 and higher complete SCI, the diaphragm is also paralyzed and lungs cannot be fully inflated. This results in an inability to maintain adequate ventilation for more than a brief period of time and the need for long-term ventilatory assistance for survival.  Ventilator-dependent patients with head and neck control may be able to use some accessory muscles for breathing. Patients with no head or neck control or use of accessory muscles for breathing may also have bulbar involvement, in which case there is also loss of upper airway protection and a high risk for aspiration of pharyngeal and gastric secretions.

     However, a significant number of patients, who initially present with ventilatory compromise due to high cervical SCI, do not require long-term mechanical assistance for survival. The initial drop in vital capacity is frequently followed by an improvement in ventilatory function, due to neurologic recovery, resolution of swelling and posttraumatic inflammation, development of spasticity and recovery of stretch reflexes in the abdominal and intercostal muscles, and use of accessory muscles in the neck and upper chest.