Advances in the Rehabilitation of the Spinal Cord–Injured Patient

The Orthopaedic Surgeons' Perspective

Brian K. Kwon, MD, PhD, FRCSC; Dan Banaszek, MD, FRCSC; Steven Kirshblum, MD


J Am Acad Orthop Surg. 2019;27(21):e945-e953. 

In This Article

Management of Subacute and Chronic Secondary Complications and Conditions After Spinal Cord Injury

Decision making with regard to which spinal surgery to perform and how urgently are often the simplest aspects of the SCI patient's care. The complexity of the subsequent recovery course and management of multisystem sequelae for both neurologic injury and secondary complications can be far more challenging. Hence, a multidisciplinary team consisting of expertise in nursing, physical therapy, occupational therapy, speech-language pathology, social work, physiatry, and pain management is invaluable, and emphasizes the value in having these patients treated in specialized SCI centers. Previous research has documented decreased hospital length of stay (LOS), a reduction in radiological resources, and reduced febrile days with a multidisciplinary SCI unit.[17] After implementation of a multidisciplinary care, Alizo et al[18] noted reductions in mortality, LOS, nosocomial infection, days spent on a ventilator, and near-significant reduction in Intensive Care Unit LOS. Although the orthopaedic surgeon may not be the one necessarily directing the treatment of the common secondary complications arising from SCI, being aware of them and having a basic approach to their management is essential for the surgeon.

Neuropathic Pain

Although orthopaedic surgeons are most familiar with the management of musculoskeletal/nociceptive pain, patients with SCI frequently suffer neuropathic pain, which is characterized by sensations of allodynia, hyperesthesia, dysesthesia, burning, electrical shooting, and paraesthesia. This is quite distinct from the nociceptive pain present from spinal injury and requires different treatment approaches. Patients with SCI can also develop de novo neuropathic pain in the chronic setting, which should prompt an evaluation for potentially treatable causes such as nerve root or spinal cord compression, tethering, or syringomyelia.

The orthopaedic surgeon is often faced with individuals suffering from neuropathic pain early after their SCI (eg, in central cord injury where this pain can be particularly severe). Treatment interventions for neuropathic pain can be divided into six categories: oral and topical medications, procedural interventions, surgical interventions, physiotherapy including exercise, passive and stimulation therapies, and relaxation and psychotherapy. The CanPain SCI Clinical Practice Guidelines (Table 1) are a useful reference for the clinician.[19] Algorithms for assessing and treating nociceptive and neuropathic pain have also been developed by Siddall and Middleton.[20] A key point to recognize in the management of neuropathic pain is that narcotic medications are relatively ineffective for it. At the lead author's center, the early approach (Figure 1) includes first-line treatment with gabapentin or pregabalin (the latter being considerably more expensive) and nortriptyline, which can be administered through nasogastric tube in cases with restricted oral intake. For burning extremity pain and allodynia, a 4% ketamine/amitriptyline cream provides fast-acting relief. Ketamine and intravenous lidocaine infusions are used for intractable cases.

Figure 1.

Protocol for treatment of acute neuropathic pain exacerbation. BID = twice daily, CI = contraindication, MI = myocardial infarction, PVC = premature ventricular contraction, SCI = spinal cord injury, SNRI = Selective Norepinephrine Reuptake Inhibitor, VTach = ventricular tachycardia, QID = four times daily

Orthostatic Hypotension

The loss of sympathetic tone after SCI in cervical and high-thoracic SCI can result in severe orthostatic hypotension (OH), which has been defined as a decrease in systolic blood pressure (SBP) of 20mmHg, or a diastolic decrease of 10mmHg with change of positioning, regardless of patient symptoms. Because most patients with acute SCI have mean arterial pressure augmented to 85 to 90 mm Hg for the first 7 days, OH tends to be uncommon in this acute time period, but can become a notable impediment to mobilization after this first week of aggressive hemodynamic management ends. Although the disruption in sympathetic tone is the key etiology of OH, it is also important to consider other underlying causes such as hypovolemia, sepsis, and sedative medications, especially when someone who is stable suddenly develops OH or experiences worsened OH.

For the surgeon who is naturally eager to mobilize the patient and therefore can encounter notable challenges associated with OH, the key management considerations are to keep the SBP above 90 mm Hg and to identify contributing causes. Fluid intake is important to prevent dehydration. If intermittent catheterization is used, this should be adjusted accordingly to allow for increased fluid intake. At the lead author's center, patients with documented OH are given a standing order for the short-acting alpha-agonist vasopressor midodrine 5 to 10 mg every 4 to 6 hours as needed during waking hours to maintain SBP above 90 mm Hg, with a maximumdose of 40mg per day. A low dose of fludrocortisone (Florinef) of 0.1 mg/d can also be used to increase sodium retention and blood volume. Patients should be closely monitored for potential adverse effects including hypokalemia, urinary retention, supine hypertension, and paradoxical autonomic dysreflexia (AD).[21] Furthermore, all patients should receive thigh compressive stockings and abdominal garments to avoid LE pooling.

Pressure Injury

Despite greater awareness and improved practices, pressure injury (previously referred to as pressure ulcer) remains the most common with an annual prevalence in the acute setting ranging from 10.2% to 38%.[22] Pressure injury accounts for a disproportionate number of hospitalization days[23] compared with other secondary conditions. Among patients who develop pressure injuries, an estimated 7% to 8% ultimately succumb to related complications.

Pressure injuries can develop very quickly, and one thing the surgeon can proactively do is transfer patients with SCI off of the hard spine boards as soon as possible and—when applicable—clear the C-spine so that the hard transport collars can come off. Inspection for pressure injuries is performed head-to-toe, with photographs taken for treatment response. Sacral, trochanteric, and ischial or intergluteal pressure injuries are seen with prolonged supine, lateral, and seated positioning, respectively.

Hospitals should use a predefined protocol for pressure injury assessment and be cognizant of the potential for individualized equipment based on specific patient risk factors. Primary prevention is geared at frequent repositioning (q2hours), adequate soft-tissue support with patient-specific surface prescriptions (mattresses, wheelchair cushions, commodes, etc), and regular assessment of susceptible areas. The Braden risk assessment tool (Supplemental Digital Content 3, is an invaluable resource in both initial evaluation and monitoring. A systematic review notes that although evidence is limited for optimal timing or frequency of repositioning, avoidance of the 90° lateral position is important due to frequency of trochanteric ulceration.[24] The optimization of nutrition, smoking cessation, and improved diabetic control are also paramount in the healing of pressure ulceration.

Thromboembolic Disease

The risk of deep vein thrombosis (DVT) and pulmonary embolism is markedly increased in the period immediately after SCI. The Consortium for Spinal Cord Medicine clinical practice guidelines (CPG) recommend low-molecular-weight heparin (LMWH) to be initiated as chemoprophylaxis once there is no sign of active bleeding in acute SCI.[25] Although LMWH has been recommended over unfractionated heparin (UH) because of markedly fewer reported cases of pulmonary embolism and DVT associated with LMWH,[26] the comparative efficacy between these two drugs in preventing thromboembolism has been called into question. Recent AO-Spine Guidelines (2017) provide a weak recommendation that either UH or LMWH is a treatment option for acute chemoprophylaxis.[26,27] The use of inferior vena cava filters for patients with contraindications to chemoprophylaxis has also been examined. To date, literature points out that there is currently insufficient evidence to support this practice in patients.[28,29] However, it is acknowledged that treatment decisions in complex patients must be individualized, and certain exceptions may exist.

Treatment for patients with newly diagnosed, established venous thromboembolism after SCI has been anticoagulation, beginning with intravenous UH, followed by the gradual transition to Coumadin for a period of 3 to 6 months.[30]

Respiratory Compromise/Hypoventilation

In the acute evaluation after SCI, the orthopaedic surgeon must be wary of any physical sign of increased work of breathing, such as gasping or diaphragmatic breathing. All patients should be evaluated with baseline arterial blood gases. Adistinction must also be made between respiratory failure that results from diaphragmatic paralysis from very high cervical lesions and the much more common ventilatory failure that results from decreased intercostal muscle activity and poor chest expansion with a rise in CO2. With lower cervical and even high-thoracic SCI, nonfunctional intercostal muscles can lead to rapid decompensation, despite an initially stable presentation.[31] In patients with acute cervical SCI lying supine in a collar, aspiration is also a risk (particularly in the elderly) and may necessitate urgent securing of the airway. For these reasons (especially in cervical SCI where securing of the airway in the presence of an unstable cervical spine can be challenging), the evaluation by critical care specialists or anesthesiologists should take place in the emergency department without delay.

Autonomic Dysreflexia

The term AD refers to a serious and potentially life-threatening complication in patients with cervical or high-thoracic injuries at or above the T6 level, in which there is interruption of modulatory input to the sympathetic preganglionic neurons above the major splanchnic outflow. The most common and worrisome feature is an increase in SBP, defined as ≥20 mm Hg above baseline. A notable rise in BP, if left untreated, can lead to episodes of hypertensive crises placing the patient at risk of hemorrhagic stroke, seizures, or even death.[32] Although previously considered a later complication after SCI, AD can occur in the acute setting as well, and so the surgical team should be aware of this issue.

The most common causes of AD are bladder and bowel distension and these should be ruled out first. Additional causes include venous thromboembolism and infectious etiologies of the abdomen, pelvis, and LEs. Typical symptoms include headache, blurred vision, and sweaty, flushed skin at the level of the head and neck, with an abrupt demarcation to pale and cool skin below the level of injury. Hypertension may be accompanied by mostly tachycardia but occasionally (and classically described) bradycardia.[33]

The Consortium for Spinal Cord Medicine has developed a CPG for the acute management of AD.[34] Prompt identification and management is critical and the patient should first be placed in the seated position. Clothing or constrictive devices should be loosened. The BP should be monitored frequently (usually every 2 to 5 minutes). A survey for instigating causes, beginning with the urinary system, should be initiated. If an indwelling urinary catheter is not in place, the patient should be catheterized. If acute symptoms of AD persist, including a sustained elevated BP, fecal impaction should be suspected. For pharmacologic intervention, an antihypertensive agent with rapid onset and short duration should be used while the causes of AD are being investigated, most especially if the SBP is ≥150 mm Hg. Nitroglycerin ointment (2%), is the most common agent currently used for acute management of AD. Ten mg immediate-release Nifedipine capsules are also commonly used, with the patient instructed to bite down on the capsule and swallow its contents. Hydralazine 10 mg and sublingual captopril 25 have also been used with reported success. The benefit of nitro ointment is that it can be wiped off once the SBP starts to return to baseline. For the other systemic medications, the treatment team will need to monitor for symptomatic hypotension.

Osteoporosis and Fracture

After SCI, rapid bone loss occurs below the level of injury and primarily at load-bearing sites. Bone loss is most rapid in the first 14 months after injury and by 2 to 3 years, 25% to 50% of bone mineral density is lost in the LEs. Continual loss of bone mass then continues, up to 3% per year. The prevalence of fracture below the level of injury in the chronic SCI population is ~25% to 46%;[35] most commonly in persons with complete injuries who are not ambulatory. Fractures are relatively uncommon in the first years after SCI and then increase linearly with time. Most fractures occur while performing normal activities of daily living such as transfers, low impact collisions, falls or even stretching; and present most commonly about the knee including the distal femur and proximal tibia.

For individuals who are ambulatory, management is similar to the non-SCI population. However, in individuals who do not use their LEs for functional mobility, the main goals of treatment are to preserve prefracture function and allow for healing with satisfactory alignment while minimizing complications. Many times, surgery, circumferential casting, and external fixation are not indicated because of low bone mass, recurrent bacteremia, and risk of skin breakdown and osteomyelitis. Nonsurgical treatment using soft padded splints such as a well-padded knee immobilizer for femoral supracondylar, femoral shaft, and proximal tibia fractures or a well-padded ankle immobilizer for distal tibia fractures is commonly recommended. Surgical intervention is generally recommended for fractures that occur in the proximal femur, have rotational deformity, associated severe muscle spasms, poor vascular supply, or will result in unacceptable functional or cosmetic outcomes.

Heterotopic Ossification

Heterotopic ossification (HO) is the formation of extraosseous lamellar bone in soft tissue surrounding peripheral joints located below the level of SCI. Clinically notable HO, which results in a loss of range of motion (ROM) and interferes with function, occurs in 10% to 20% of individuals with SCI, with 5% to 8% progressing to joint ankylosis. In SCI, HO most frequently develops around the hip (anteromedial aspect most commonly), followed by the knee, elbow, and shoulder. Risk factors include the severity of neurologic injury (more frequent occurrence in motor complete injuries), male sex, younger age (although it is less frequent in children and adolescents), as well as the presence of a DVT, spasticity or a pressure injury in close proximity to an involved joint.

Evidence of HO can be detected earliest on the first two phases of the bone scan, which reveals hyperemia and blood pooling; the third phase of the bone scan, which reveals calcification, is positive up to several weeks later. Standard radiographs lag behind the triple phase bone scan by a few weeks and, therefore, are not a sensitive method to identify early HO. Ultrasonography may be positive relatively early in the presentation of HO and has the advantage of being easy to perform, does not require radiation exposure, and was found to have high sensitivity to establish the diagnosis (~90% cases identified at 62 days after injury).[36] Although CT scans may be used to determine the volume of bone for planning surgical resection, it is rarely ordered to establish an early diagnosis.

Treatment of HO includes ROM with gentle stretching, medications (diphosphonates, and NSAIDS,[37] if not otherwise contraindicated); radiation therapy and surgical excision may be considered, if indicated, later in the course. The use of diphosphonates, predominantly etidronate, has been the mainstay of pharmacological treatment. Diphosphonates block the late mineralization phase of bone formation, preventing the conversion of amorphous calcium phosphate to hydroxyapatite, thus serving to decrease the rate of new bone formation but without effect on bone already deposited.[38,39]