| Autonomic Dysreflexia |
Pathophysiology
- Spinal cord injuries T6 and above
- Can begin as early as 2 to 3 weeks after injury
- Secondary to uninhibited or exaggerated sympathetic responses to noxious stimuli below the level of the injury which leads to diffuse vasoconstriction and hypertension.
- A compensatory parasympathetic response produces bradycardia and vasodilation above the level of the lesion, but this is not sufficient to reduce elevated BP.
Clinical manifestations
- Pounding headache, profuse sweating, bradycardia
- Increased blood pressure (SBP 20 > baseline, DBP 10 > baseline)
- Flushing, piloerection, blurred vision, nasal congestion, anxiety, nausea
Possible stimuli
- Bladder distention, UTI, bowel impaction, pressure sores, bone fracture, constrictive clothing/shoes/apparatus
Treatment
- Identification, correction of noxious inciting stimuli
- Sit patient upright
- Remove tight-fitting garments
- Empty bladder (use lidocaine jelly)
- Use lidocaine jelly for bowel impaction
- Bowel impaction (use lidocaine jelly)
Medications: (adjunct only)
- Nitroglycerin paste, Nifedipine, Hydralazine (short-acting anti-hypertensive medications only)
- Use with caution due to risk of rebound hypotension once stimulus removed
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| Respiratory Insufficiency |
Pathophysiology
- C3-C5 injuries associated with:
- Hypoventilation, atelectasis, mucous plugging, and ventilation–perfusion mismatch
- Midthoracic and above injuries associated with:
- Expiratory muscle weakness with ineffective cough and secretion clearance
- Disruption of sympathetic input to the bronchi with increase in bronchial secretion production
Treatment
- Chest physiotherapy, incentive spirometer, cough assist, manually assisted coughing (“quad coughing”)
- Abdominal binder when sitting up
- Early mobilization (If spine stabilized)
- Consider diaphragmatic pacer for patients with C4 and above injury
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| Neuropathic Pain |
Clinical manifestations
- Often described as “pins and needles,” body part “is asleep,” “tight belt” at level of injury, burning, stabbing, or electrical in quality
Treatment
- Antidepressant, antiepileptic, standard analgesic medications are often used in combination. May include:
- Gabapentin
- Trazodone or Amitriptyline
- Opiates
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| Superior Mesenteric Artery Syndrome |
Pathophysiology
- Weight loss leads to loss of the mesenteric fat pad and compression of the duodenum by the superior mesenteric artery
Clinical manifestations:
- Epigastric pain, nausea, eructation, voluminous vomiting, postprandial discomfort, early satiety
Treatment
- Nasogastric decompression and proper positioning (left lateral decubitus, prone, or knee-to-chest position) after eating/feedings
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| Hypercalcemia |
Pathophysiology
- Immobilization stimulates osteoclastic bone resorption which causes calcium loss from the bones and hypercalciuria.
- Hypercalcemia results when the efflux of calcium is massive or when the glomerular filtration rate is reduced.
- Presentation most likely delayed, 4-8 weeks following injury.
High-risk group
- Adolescent and young adult males
- Tetraplegia > Paraplegia
Clinical manifestations
- Fatigue, lethargy, apathy, abdominal pain, constipation, anorexia, nausea, vomiting, polydipsia, polyuria, and dehydration
Treatment
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| Joint Contractures |
Pathophysiology
- Result from reorganization of the collagen tissue matrix that occurs when the muscle lies in the shortened position for an extended period of time
Treatment
- Prevention — positioning, range of motion exercises, splinting
- See specific recommendations from Physical and Occupational Therapy
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| Muscle Spasticity |
Pathophysiology
- Result of loss of inhibition of upper motor neuron function causing development of muscle spasticity below the level of injury
- Not apparent during period of spinal shock
- Tends to be more severe in patients with incomplete lesions
Treatment
- Prevention of exacerbations: range of motion exercises, appropriate positioning, splinting, identification of precipitating factors, and effective bowel, bladder, and skin programs
- Medications if not responsive to conservative treatment and/or interferes with functioning — these include:
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| Scoliosis |
Pathophysiology
- Results from muscle weakness or imbalance with superimposed forces of growth and/or residual vertebral column deformity (caused by the injury or surgical intervention)
- If SCI sustained > 1 year before reaching skeletal maturity the risk of developing is 98%
Treatment
- Close monitoring with frequent radiographs
- Prophylactic thoracolumbar-sacral orthotic (TLSO) bracing — shown to significantly slow the rate of curve progression and delay need for surgery
- Spinal fusion
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| Osteopenia and pathological fractures |
Pathophysiology
- Due to an imbalance between bone formation and bone resorption
- Begins soon after injury and reaches a plateau at 6–12 months
- Predisposes to pathological fractures:
- Common symptoms: swollen extremity with fever
- Most common sites: supracondylar knee, tibial plateau, and femoral neck
Treatment
- Safe handling
- Mobilization
- Medications to consider:
- Vitamin D and calcium supplements
- Bisphosphonates — inhibitors of osteoclastic bone resorption
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| Decubitus Ulcer |
Pathophysiology
- Localized damage to the skin and/or underlying soft tissue that occurs as a result of intense and/or prolonged pressure or pressure in combination with shear, with moisture as a complicating factor
- Typically develop in insensate areas
Treatment
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