Preventing long term complications of paraplegia

1. Preventing long term complications of paraplegia William Desloges, MD Orthopaedic Surgery Department University of Ottawa

2. Outline • Introduction • Complications of paraplegia • Pressure Ulcers • Pulmonary Complications • Osteoporosis and Fractures • Urinary Tract Dysfunction • Neurogenic Heterotopic Ossification • Spasticity • Venous thrombosis • Upper extremity arthropathies • Bowel Complications • Cardiovascular Diseases • Neuropathic/Spinal cord pain • Conclusion

3. Introduction: Paraplegia • Causes • Spinal cord lesions below T1 level • Complete or incomplete • Complications • Morbidity and mortality • Quality of life • Multidisciplinary management • Orthopaedic Spine Surgeon

4. Pressure Ulcers

5. Pressure Ulcers (Regan et al 2009) • The cost of accelerated wound treatment to heal a stage III ulcer in a community- dwelling paraplegic over a 3 months period has been estimated at $27,632 Cdn. • Among patients with SCIs, annual incidence rates of pressure ulcer range from 20-31%, and the prevalence rates from 10.2% to 30%.

6. Pressure Ulcers (Regan et al 2009) • Risk factors: • Limitations in activity and mobility • Injury completeness • Moisture from bowel and/or urinary incontinence • Lack of sensation • Muscle atrophy • Nutritional status

7. Pressure Ulcers Prevention Strategies • Pressure relief practices: • On average, it takes ~ 2 minutes of pressure relief to raise the transcutaneous oxygen tension to normal levels (Coggrave et al 2003) • Effective pressure relieving techniques for paraplegic patients unable to perform manual weight shift include (Henderson et al 1994) • Forward leaning position: 78% reduction in ischial tuberosity pressure as compared to neutral sitting position • 65° tipped back position: 47% reduction in ischial tuberosity pressure as compared to neutral sitting position • Leaning side to side • Doing a pressure relief lift for > 2 minutes • Neuromuscular Electrical Stimulation: • (Level 4 evidence) Electrical stimulation increases regional blood flow thereby assisting in prevention of pressure ulcers (Regan et al 2009)

8. Pressure Ulcers Prevention Strategies • Wheelchair Cushion • Materials: static (gel, foam, water) vs dynamic (air-filled bladders) • Shape • Temperature effects: Higher temperatures increase tissue susceptibility (Foam) • Specialized pressure mapping assessment to account for interindividual differences in pressure contact areas • Lumbar Support • Varying lumbar support thickness was found to have negligible effect on reducing seated buttock pressures at the Ischial Tuberosity (Shields et al 1992)

9. Pressure Ulcers Prevention Strategies • Seating Clinics and Education • Have been shown to reduce the incidence of pressure ulcers when incorporated in rehabilitation programs (Dover 1992) • Emphasize personal responsibility for skin care, make recommendation for appropriate seating system, and give on going feedback to patients

10. Osteoporosis and Fractures

11. Osteoporosis and Fractures • In paraplegia, osteoporosis affects the pelvis and lower extremities; sublesional topography of demineralization • Radiological evidence of decreased bone mineral density and content can be detected in paralyzed limbs as early as 6 weeks post Spinal cord injury (Sheng-Dan et al 2006) • Cancellous bone is more affected than cortical bone • In the lower extremities, the trabecular metaphysical-epiphyseal areas of the proximal tibia and distal femur are most affected (Sheng-Dan et al 2006) • The paraplegic fracture: supracondylar femur fracture • Demirel et al. (1998) found a significant difference in bone mineral density when comparing patients with complete and incomplete lesions • Reduction in bone mineral density was found to be less in SCI patients with spasticity (Sheng-Dan et al 2006)

12. Osteoporosis and Fractures • Age at the time of injury and duration since injury have been shown to affect bone mineral density • It is controversial as to whether or not a steady state in bone mineral density is achieved post SCI • Minor increase in BMD was observed in the humerus of paraplegic patients 1 year post injury (Dauty 2000) • Bone mass of the vertebral column is generally spared; rare to see compression fracture of vertebrae • Completeness of SCI is the single most important risk factor for pathological fractures among all modifiable and nonmodifiable risk factors. (Sheng-Dan et al 2006)

13. Osteoporosis and Fractures (Sheng-Dan et al 2006)

14. Osteoporosis and Fractures: Prevention Strategies • Intensive exercise regime: • Contributed to preservation of upper extremity bone loss, but did not affect lower extremity bone loss in quadraplegics • Goemare et al. (1994) reported that standing may prevent bone loss in the region of the femoral shaft but not at the proximal hip • Pharmacological (Sheng-Dan et al 2006): • Calcium and Vitamin D supplementation does not prevent osteoporosis after SCI • Calcitonin has been shown to counteract early bone loss following SCI • RCTs using bisphosphonates have shown promising results in prevention of decreased mineral bone density in paraplegic patients; further studies required using higher doses.

15. Venous Thromboembolic Disease

16. Venous Thromboembolic Disease • The incidence of DVT has been reported to range between 9% and 90% in acute spinal cord injured patients (Aito et al. 2002) • Virchow’s triad: hypercoagulability, stasis, and intimal (venous inner wall) injury

17. Strong evidence supporting the use of LMWH in reducing venous thrombotic events • The use of heparin 5000 units sc Bid is no more effective than placebo as prophylaxis against DVT post-SCI. • Using a higher dose of unfractionated heparin than 5000 units Bid was found to be an effective DVT prophylactic, although it increased bleeding complications • Limited evidence to support nonpharmacological treatments such as sequential pneumatic compression devices or gradient elastic stockings • Given its predictability, dose-dependent plasma levels, long half-life, its low tendency to induce thrombocytopenia and reduced bleeding for a given antithrombotic effect, LMWH is the preferred prophylactic agent.

18. Venous Thromboembolic Disease • Consensus is to discontinue prophylactic anticoagulants after 4 months as the risk of venous thromboembolism drops dramatically after 3–4 months (Gaber 2005). • Hypothesis (Gaber 2005): • Muscular spasticity • Arterial atrophy and reduced blood flow to the paralyzed lower limbs • Monitor patient for clinical signs and symptoms of venous thromboembolic disease since risk higher than normal population

19. Urinary Tract Dysfunction

20. Urinary Tract Dysfunction • Anatomy: • Internal sphincter: • junction of the bladder neck and proximal urethra • Functional sphincter: progressive increase in tone with bladder filling • Autonomic control: sympathetic alpha-receptors • External sphincter: • Somatic innervation (pudental n. S2-4) • In males, is at the level of the membraneous urethra

21. Urinary Tract Dysfunction • Physiology: • Bladder contraction: • Parasympathetic efferent via pelvic nerves from sacral cord at S2-4 • Outlet resistance and Storage • Preganglionic Sympathetic efferent originate at T11-L2, then travel through the sympathetic paravertebral ganglia • Postganglionic fibers in the hypogastric nerves activate alpha- and beta-adrenergic receptors within the bladder and urethra • Beta-receptors: produce smooth muscle relaxation of the bladder wall • Alpha-receptors: high density at the internal sphincter and prostatic urethra increases outlet resistance

22. Urinary Tract Dysfunction • Voiding Centers • Sacral Micturation Center: Afferent impulses provide info regarding bladder fullness. Reflexive parasympathetic impulses to the bladder cause bladder contraction • Pontine MicturationCenter: coordinates external sphincter relaxation when the bladder contracts (Detrusor Sphincter Dyssynergia) • Cerebral cortex: voluntary inhibition of the sacral micturation center [Suprasacral SCI=involuntary (uninhibited) bladder contraction]

23. Urinary Tract Dysfunction • Voiding Dysfunctions: • Suprasacral Spinal Cord Lesions • Initial period of spinal shok resulting in detrusor areflexia • Uninhibited bladder contractions • Detrusor-external sphincter dyssynergia: Occurs in 96% of individuals with suprasacral lesions • Autonomic dysreflexia (T6 or above): exaggerated response to noxious stimuli that provokes uninhibited bladder contractions and sphincter dyssynergia • Sacral Lesions • Detrusor areflexia: result in highly compliant acontractile bladder • Normal or underactive external sphincter resulting in dyssynergy or coordination, respectively.

24. Urinary Tract Dysfunction • The majority of patients with SCI have voiding dysfunction (Consortium for Spinal Cord Medicine 2006) • Renal diseases were the main cause of mortality in spinal cord injured patients prior to the WWII and the Korean war (Jamie 2001) • Management goals for prevention of urogenic complications (Samson 2007) • Ensure social continence for reintegration into community • Allow low-pressure storage and efficient bladder emptying at low detrusor pressures • Avoid stretch injury from repeated overdistension • Prevent upper and lower urinary tracts complications from high intravesical pressures • Prevent recurrent urinary tract infections

25. Bladder Management • Management method used is based on urodynamic studies • Acute management: indwelling catheter followed by clean intermittent catherization • Longterm management depends on many factors, including the level and completeness of injury, amount of hand function, sex, and motivation. • Clean intermittent catheterization (CIC): • considered the best and safest long-term bladder management method (Samson 2007) • Indwelling catheter: • For patients with limited hand function or lack of motivation to perform CIC. • Increased risk for urinary tract infections; urethral diverticula; urethral strictures; urethritis; traumatic hypospadias; bladder calculi; small, low compliance, high-pressure bladder; and bladder cancer • Crede and Valsalva maneuvers (Samson 2007): • Useful in areflexic bladders with impaired detrusor contraction • Works by increasing intraabdominal pressure or applying direct suprapubic pressure. May be time consuming. • May exacerbate haemorrhoids, hernias, vesico-ureteric reflux and dyssynergia

26. Bladder Management • Reflex voiding: • Consist of suprapubic tapping to stimulate the bladder • Useful in patients with Suprasacral lesions with intact sacral reflex arc, in the absence of dyssynergy • May require requires transurethral sphincterotomy • Pharmacological management: • Anticholinergic agents to prevent detrusor overactivity in patients practicing CIC • Intravesical therapy (Samson 2007) • Injection of botulin toxin in the detrusor musculature • Length of action between 16-36 weeks • Effect: suppression of bladder overactivity, increase in cystometric and maximum bladder capacity, decrease in voiding pressure, and elimination of urinary incontinence that may be associated with detrusor overactivity • Injection into the external urethral sphincter is also used to treat neurogenic detrusor-sphincter dyssynergia

27. Bladder Management • Condom catheter: • used for incontinence in males to promote dry perineum • Surgical management: • When primary bladder management methods fail • Electrical stimulation and posterior sacral root rhizotomy • Augmentation cystoplasty, cutaneous conduits, and urinary diversions • Transurethral sphincterotomy: for bladder outlet obstruction and Detrusor Sphincter Dyssynergia

28. Bladder Management • Complications of neurogenic bladder • chronic urinary tract infections, bladder diverticulae, bladder stones, urethral trauma leading to penile fistulae or strictures, perineal decubiti, bladder cancer, vesicoureteral reflux, hydronephrosis, pyelonephritis, and renal failure • It is not recommended to give prophylactic antibiotics or to treat asymptomatic bacteriuria (Samson 2007)

29. Shoulder Arthropathies

30. Shoulder Arthropathies • Prevalence of shoulder pain in paraplegic individual has been reported to be between 30% and 70% (Alm 2008) • In paraplegic patients, the shoulder becomes weight bearing and is overused • The use of manual wheelchair contributes to the high incidence of shoulder arthropathies due to the significant stability and mobility demands it places on the shoulder • Neuromuscular fatigue leads to decreased stability and superior displacement of the humeral head • Common pathologies include: • Chronic inflammation (especially supraspinatus) • Impingement syndrome • Bursitis • Rotator cuff tears • Bicipital tendinitis • Glenohumeral and acromioclavicular arthritis • Peripheral neuropathies (carpal tunnel syndrome) are also common

31. Shoulder Arthropathies • Gutierrez et al. (2007) demonstrated that paraplegic patients with higher levels of shoulder pain reported lower subjective quality of life and physical activity scores • Interventions: • Designing ergonomic ways for patients to transfer • Wheelchair biomechanics (power) • Physiotherapy to enhance shoulder stability • Core body support for patients with high thoracic paraplegia • Medical management • Surgical management (cuff repair, subacromial debridement, shoulder arthroplasty)

32. Pulmonary Complications

33. Pulmonary Complications • Leading cause of mortality in the first year following SCI (Wuermser et al. 2007) • Primary contributors: • Difficulty handling secretions • Atelectasis • Hypoventilation • Weak or paralyzed abdominal muscles preclude an effective cough. • Vital capacity declines in high paraplegia from respiratory muscle weakness, can lead to a restrictive ventilatory deficit

34. Pulmonary Complications (Schilero et al 2009)

35. Pulmonary Complications (Schilero et al 2009)

36. Pulmonary Complications • Recent findings suggest that expiratory muscle training, electrical stimulation of expiratory muscles and administration of a long acting Beta2-agonist (salmeterol) improve physiological parameters and cough. (Schilero et al 2009) • Prompt treatment of infectious pulmonary diseases is required.

37. Neurogenic Heterotopic Ossification

38. Neurogenic Heterotopic Ossification • Incidence ranges from 10% to 53% • Generally manifests 1 to 6 months post-injury but may develop several years after SCI • Occurs below the level of SCI most commonly affecting the hips • Common clinical findings: • Decreased ROM, peri-articular swelling, erythema, and warmth, pain (in patients with sensory sparing), low grade fever, spasticity • NHO originates in connective tissues • Factors associated with NHO (van Kuijk et al. 2002): • Completeness of SCI, presence of pressure sores, UTI (immunogenic), DVT, severe spasticity and trauma

39. Neurogenic Heterotopic Ossification • Primary prevention: • Controlling contributing factors: pressure sores, trauma, UTI, and DVTs. • Gentle ROM exercises to prevent ankylosis; avoid rigorous exercise which can induce microtrauma • Early identification and appropriate treatment • No controlled trials exist on the prophylactic use of NSAID, diphosphonates, and irradiation in the prevention of heterotopic ossification in SCI patients.

40. Spasticity

41. Spasticity • Part of the upper motor neuron syndrome • Commonly affects antigravity muscles; in the lower limbs, the extensors are most often affected. • Amongst patients with chronic SCI, 65–78% report symptoms of spasticity; and 37% of them require treatment. (Craven 2009) • Mainstays of treatment • Avoiding triggers: UTIs, constipation, bladder distention • Therapy: hot or cold application, stretching, positioning and splinting to prevent contracture • Pharmacological treatment: A recent review has supported the efficacy of baclofen, tizanidine, clonidine, cyproheptadine, gabapentine and L-threonin, in reducing spasticity following SCI (Crave 2009) • Neurosurgical procedure

42. Bowel complications

43. Bowel complications • Continence is maintained by the resting tone and reflex activity of the internal anal sphincter, external anal sphincter and muscles of the pelvic floor • Reflex contraction of the external anal sphincter complex on coughing and valsalva prevents incontinence • Rectal distension triggers the rectoanal inhibitory reflex, where the internal anal sphincter relaxes. In this situation, voluntary contraction of the external anal sphincter is required to retain continence • Enteric nervous system (intrinsic) coordinate gut motility • Extrinsic nervous system modulates the activity of the enteric nervous system and coordinate gut activity to systemic demands

44. Bowel complications • Parasympathetic activity through the pelvic nerves (pelvic plexus S2-4) causes smooth muscle contraction, which promotes gut motility. It also leads to internal anal sphincter relaxation • Sympathetics (T9-10) are inhibitory and function to decrease blood flow and slow motility by relaxing the colonic wall to increase compliance • The sympathetic effect is excitatory, and tonic discharge maintains IAS closure • The external anal sphincter is a striated muscle innvervated from the sacral cord via the pudendal nerves (S2-S4).

45. Bowel complications (Lynch 2001) • supraconal injury: • results in loss of conscious sphincter control • Anorectal dyssynergy: Spastic EAS • Manual stimulation: rectoanal inhibitory reflex (result in relaxation of IAS, EAS, and triggers peristalsis) • Manual evacuation: If unable to relax EAS

46. Bowel complications (Lynch 2001) • Cauda equina injuries • EAS and pelvic muscles become flaccid (loss sympathetic tone and voluntary contraction) • Loss of parasympathetic control and reflex innervation to IAS result in decreased resting anal tone • Valsalva results in incontinence when rectum full • LMN injury from a lesion affecting the conus, cauda equina or pelvic nerves results in interruption of the parasympathetic supply to the colon and reduced spinal cord-mediated reflex peristalsis. • Lesions above T1 result in delayed mouth-to-caecum time • Patients with thoracic spine injury show abnormal response to increasing intestinal volumes which suggests that the CNS is necessary to modulate colonic motility • The lack of compliance leads to functional obstruction, increased transit times, and abdominal distension, bloating and discomfort

47. Bowel complications • Colorectal dysfunction is a common problem affecting approximately 80% of patients. • Important long term implications for quality of life • Complications: obstruction, diverticulosis, bloating, incontinence, psychosocial • Bowel care regimen: bowel evacuation to prevent incontinence or impaction • Dietary manipulation: water and fibers to promote transit and soft stools • Stool softeners: prevents constipation and potential for autonomic dysreflexia • Prokinetic agents • Enemas • Digital stimulation: triggers rectoanal inhibitory reflex (relax IAS). Usefull in patients with UMN lesions. • Manual removal: LMN lesions and Anorectal dyssynergy • Colostomy

48. Neuropathic pain • Prevelance of pain in patients with SCI is around 65-85%, 1/3 of which have severe pain (Siddall 2009) • Poor prognosis • Pharmacological (pain clinic) • Surgical

49. Cardiovascular Complications • Autonomic dysreflexia: • sudden severe elevation in blood pressure • Orthostatic hypotension • Coronary Diseases

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