Respiratory complications are the most significant cause of morbidity and mortality in SCI patients. The level and amount of respiratory complications depend on the SCI injury level (Berlowitz et al., 2016). SCI can lead to respiratory dysfunction, which includes insufficiency of respiratory muscles, reduction in vital capacity, ineffective cough, decreased lung and chest wall compliance, and excess oxygen cost of breathing. It has been found that SCI patients have a high prevalence of sleep-related respiratory disorders, particularly obstructive sleep apnea syndrome, which can adversely affect the quality of life. Up to 45% of SCI patients have a sleep disorder (Berlowitz et al., 2016); Sezer et al., 2015).
Along with respiratory complications, cardiovascular complications are common as well. Common cardiovascular complications in SCI are orthostatic hypotension, autonomic dysreflexia, impaired cardiovascular reflexes, reduced transmission of cardiac pain, loss of cardiac reflex acceleration, cardiac atrophy with tetraplegia due to loss of left ventricular mass, and pseudo-myocardial infarction (Sezer et al., 2015; Yarar-Fisher et al., 2017).
The loss of genitourinary and gastrointestinal function in non-traumatic SCI is common for patients who have had a chronic injury. SCI is recognized to cause bladder dysfunction, often referred to as neurogenic bladder (Tate et al., 2016). Incontinence, renal impairment, urinary tract infection, stones, and poor quality of life are complications of neurogenic bladder (Taweel et al., 2015). Many patients with a neurogenic bladder will require management to ensure low-pressure reservoir function of the bladder, complete emptying, and dryness (Taweel et al., 2015; Gater, 2020; Braaf et al., 2017).
Along with neurogenic bladder, neurogenic bowel is also a complication of non-traumatic SCI. Neurogenic bowel occurs when there is a colon dysfunction due to a lack of nervous control (White et al., 2019). Nearly 40% of patients with an SCI will experience neurogenic bowel, affecting the quality of life and social activities (White et al., 2019; Emmanuel, 2019).
One of the most common complications of non-traumatic SCI is spasticity. Spasticity is characterized by hypertonus, increased intermittent or sustained involuntary somatic reflexes (hyperreflexia), clonus, and painful muscle spasms (McKay et al., 2018). The pathogenesis of spasticity in SCI patients is unclear but a significant burden source (Sezer et al., 2015; Abel & Rupp, 2015; Finnerup, 2017).
As imagined, chronic pain is frequently associated with a non-traumatic SCI. At least 80% of patients with an SCI experience some form of pain (Hagen & Rekand, 2015). Two forms of pain are most common after an SCI. Neuropathic pain can occur anywhere near the level of injury. Neuropathic pain above the level may arise from complex regional pain syndromes. After SCI, chronic musculoskeletal pain, a type of nociceptive pain, may occur with gait, abnormal posture, and overuse of the arm and shoulder (Hagen & Rekand, 2015).
A significant secondary complication of non-traumatic SCI is pressure ulcers. Pressure ulcers become localized injuries to an area of the skin and/or underlying tissue and can be life-threatening (Bhattacharya & Mishra, 2015). Pressure ulcers are usually located in the ischium (31%), trochanters (26%), and sacrum (18%), and occasionally the heel (Sezer et al., 2015).
The last well-known complication of SCI is osteoporosis. Low bone mass with deterioration of the skeletal structure characterizes osteoporosis. Those with an SCI are predisposed to disuse osteopenia from prolonged immobilization and overall decreased mobility and independent functional capabilities. The first two weeks after the initial injury or SCI is recognized as the most vulnerable period for decreased bone formation (Soleyman-Jahi et al., 2018).
)
