The mainstay of ICU treatment of SCI is supportive for respiratory and cardiac systems and preventative for infections and DVTs.
Cervical cord injury is often associated with changes in respiratory patterns that are important to be aware of and can impact on ventilatory strategy. High-level cervical lesions result in the recruitment of accessory muscles with inspiration resulting in expansion of the upper rib cage with concomitant ascending diaphragm. This results in a paradoxical breathing pattern, reduction in all lung volumes (except residual volumes) but increased pulmonary and chest wall compliance and work of breathing.33 Lower cervical lesions may result in less ventilatory difficulties but a significant inability to clear secretions. As a result, this population is at significant risk for developing aspiration pneumonia.
The main goals of respiratory management are to provide aggressive pulmonary hygiene, routine bronchodilator therapy, and aggressive attempts at ventilator weaning. Attempting intermittent ventilation with high tidal volumes (10 to 15 mL/kg), sighs, or adequate positive end-expiratory pressure (PEEP) may reduce the incidence and complications related to atelectasis.
Hemodynamic instability is common after SCI. Lesions involving the cervical and upper thoracic cord result in sympathetic denervation, resulting in arteriolar vasodilation, venous pooling, bradycardia, and reduced myocardial contractility. The end result of this is a shock state that is characterized by hypotension, low systemic vascular resistance, and sinus bradycardia. However, given the impairment in myocardial contractility, hypotension cannot be overcome just with volume resuscitation and often requires additional vasopressor and/or inotropic agents. Some practitioners advocate for augmentation of MAP to maintain an adequate "cord perfusion pressure" greater than 60 mm Hg, although there is no reliable method to measure cord pressure and no clinical data support this practice.34
SCI patients have a very high incidence of DVT, and while all agree this type of patient population should receive early prophylaxis, the regimen varies among institutions with regard to timing, dosing, and duration of pharmacologic intervention, as well as to the use of inferior IVC filters (see above). In general, there is no advantage to either subcutaneous low-molecular-weight heparin or heparin.35
Infectious complications are the leading cause for morbidity and mortality after SCI.36 This may be due to a combination of acquired immunodeficiency from the injury itself as well as frequent use of high-dose steroids.37 For reasons outlined above, this patient population is at very high risk for developing respiratory infections. Urinary tract infection risk is elevated due to neurologic dysfunction resulting in incontinence, high bladder pressures, and reflux. There should be a low threshold for investigating for GI tract infections in patients with persistent fever given the inability of patients to mount symptoms.