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Preventing long term complications of paraplegia. William Desloges, MD Orthopaedic Surgery Department University of Ottawa. Outline. Introduction Complications of paraplegia Pressure Ulcers Pulmonary Complications Osteoporosis and Fractures Urinary Tract Dysfunction

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Preventing long term complications of paraplegia

Preventing long term complications of paraplegia

William Desloges, MD

Orthopaedic Surgery Department

University of Ottawa


  • 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

  • Introduction paraplegia
    Introduction: Paraplegia

    • Causes

    • Spinal cord lesions below T1 level

    • Complete or incomplete

    • Complications

    • Morbidity and mortality

    • Quality of life

    • Multidisciplinary management

    • Orthopaedic Spine Surgeon

    Pressure ulcers regan et al 2009
    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%.

    Pressure ulcers regan et al 20091
    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

    Pressure ulcers prevention strategies
    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)

    Pressure ulcers prevention strategies1
    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)

    Pressure ulcers prevention strategies2
    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

    Osteoporosis and fractures1
    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)

    Osteoporosis and fractures2
    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)

    Osteoporosis and fractures3
    Osteoporosis and Fractures

    (Sheng-Dan et al 2006)

    Osteoporosis and fractures prevention strategies
    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.

    Venous thromboembolic disease1
    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

    Preventing long term complications of paraplegia

    • 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.

    Venous thromboembolic disease2
    Venous Thromboembolic Disease venous thrombotic events

    • 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

    Urinary tract dysfunction
    Urinary Tract Dysfunction venous thrombotic events

    Urinary tract dysfunction1
    Urinary Tract Dysfunction venous thrombotic events

    • 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

    Urinary tract dysfunction2
    Urinary Tract Dysfunction venous thrombotic events

    • 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

    Urinary tract dysfunction3
    Urinary Tract Dysfunction venous thrombotic events

    • 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]

    Urinary tract dysfunction4
    Urinary Tract Dysfunction venous thrombotic events

    • 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.

    Urinary tract dysfunction5
    Urinary Tract Dysfunction venous thrombotic events

    • 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

    Bladder management
    Bladder Management venous thrombotic events

    • 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

    Bladder management1
    Bladder Management venous thrombotic events

    • 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

    Bladder management2
    Bladder Management venous thrombotic events

    • 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

    Bladder management3
    Bladder Management venous thrombotic events

    • 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)

    Shoulder arthropathies
    Shoulder Arthropathies venous thrombotic events

    Shoulder arthropathies1
    Shoulder Arthropathies venous thrombotic events

    • 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

    Shoulder arthropathies2
    Shoulder Arthropathies venous thrombotic events

    • 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)

    Pulmonary complications
    Pulmonary Complications venous thrombotic events

    Pulmonary complications1
    Pulmonary Complications venous thrombotic events

    • 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

    Pulmonary complications2
    Pulmonary Complications venous thrombotic events

    (Schilero et al 2009)

    Pulmonary complications3
    Pulmonary Complications venous thrombotic events

    (Schilero et al 2009)

    Pulmonary complications4
    Pulmonary Complications venous thrombotic events

    • 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.

    Neurogenic heterotopic ossification
    Neurogenic Heterotopic Ossification venous thrombotic events

    Neurogenic heterotopic ossification1
    Neurogenic Heterotopic Ossification venous thrombotic events

    • 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

    Neurogenic heterotopic ossification2
    Neurogenic Heterotopic Ossification venous thrombotic events

    • 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.

    Spasticity venous thrombotic events

    Spasticity venous thrombotic events

    • 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

    Bowel complications
    Bowel complications venous thrombotic events

    Bowel complications1
    Bowel complications venous thrombotic events

    • 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

    Bowel complications2
    Bowel complications venous thrombotic events

    • 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).

    Bowel complications lynch 2001
    Bowel complications venous thrombotic events(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

    Bowel complications lynch 20011
    Bowel complications venous thrombotic events(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

    Bowel complications3
    Bowel complications venous thrombotic events

    • 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

    Neuropathic pain
    Neuropathic pain venous thrombotic events

    • 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

    Cardiovascular complications
    Cardiovascular Complications venous thrombotic events

    • Autonomic dysreflexia:

      • sudden severe elevation in blood pressure

    • Orthostatic hypotension

    • Coronary Diseases

    Literature cited
    Literature Cited venous thrombotic events

    • Aito S, Pieri A, D’Andrea M, Marcelli F, Cominelli E. Primary prevention of deep venous thrombosis and pulmonary embolism in acute spinal cord injured patients. Spinal Cord 2002;40:300-3.

    • Alm M, Saraste H, Norrbrink C.Shoulder pain in persons with thoracic spinal cord injury: prevalence and characteristics. J Rehabil Med. 2008 Apr;40(4):277-83.

    • Coggrave MJ, Rose LS. A specialist seating assessment clinic:changing pressure relief practice. Spinal Cord 2003;41:692-5.

    • Consensus conference on deep venous thrombosis in spinal cord injury: summary and recommendations. Chest 1992;102(Suppl):633S.

    • Consortium for Spinal Cord Medicine. Bladder management for adults with spinal cord injury: a clinical practice guideline for health-care providers. J Spinal Cord Med. 2006;29(5):527-73.

    • BC Craven and AR Morris. Modified Ashworth scale reliability for measurement of lower extremity spasticity among patients with SCI. Spinal Cord (2009), 1–7

    • Dauty M, Perrouin Verbe B, Maugars Y, Dubois C, Mathe JF(2000) Supralesional and sublesional bone mineral density inspinal cord-injured patients. Bone 27:305–309

    • Demirel G, Yilmaz H, Paker N, Onel S (1998) Osteoporosis after spinal cord injury. Spinal Cord 36:822–825

    • Dover H, Pickard W, Swain I, Grundy D. The effectiveness of a pressure clinic in preventing pressure sores. Paraplegia 1992;30: 267-72.

    • Gaber Tarek A.-Z.K. Significant reduction of the risk of venous thromboembolism in all long term immobile patients a few months after the onsetof immobility. Medical Hypotheses (2005) 64, 1173–1176

    • Goemaere S, Van Laere M, De Neve P, Kaufman JM (1994) Bone mineral status in paraplegic patients who do or do not perform standing. Osteoporos Int 4:138–143

    Literature cited1
    Literature Cited venous thrombotic events

    • Gutierrez DD, Thompson L, Kemp B, Mulroy SJ; Physical Therapy Clinical Research Network; Rehabilitation Research and Training Center on Aging-Related Changes in Impairment for Persons Living with Physical Disabilities. The relationship of shoulder pain intensity to quality of life, physical activity, and community participation in persons with paraplegia. J Spinal Cord Med. 2007;30(3):251-5.

    • Henderson JL, Price SH, Brandstater ME, Mandac BR. Efficacy of three measures to relieve pressure in seated persons with spinal cord injury. Arch Phys Med Rehabil 1994;75:535-9.

    • Jami F. Towards a catheter free status in neurogenic bladder dysfunction: a review of bladder management options in spinal cord injury (SCI). Spinal Cord (2001) 39, 355 ± 361.

    • Lippert-Grüner M. Gluteal neuromuscular stimulation in therapy and prophylaxis of recurrent sacral pressure ulcers. Spinal Cord. 2003 Jun;41(6):365-6.

    • Lynch AC, Antony A, Dobbs BR, Frizelle FA. Bowel dysfunction following spinal cord injury. Spinal Cord. 2001 Apr;39(4):193-203.

    • Regan MA, Teasell RW, Wolfe DL, Keast D, Mortenson WB, Aubut JA; Spinal Cord Injury Rehabilitation Evidence Research Team. A systematic review of therapeutic interventions for pressure ulcers after spinal cord injury. Arch Phys Med Rehabil. 2009 Feb;90(2):213-31.

    • Samson G, Cardenas DD. Neurogenic bladder in spinal cord injury. Phys Med Rehabil Clin N Am. 2007 May;18(2):255-74, vi.

    • Sheng-Dan Jiang Æ Li-Yang Dai Æ Lei-Sheng Jiang. Osteoporosis after spinal cord injury. Osteoporos Int (2006) 17: 180–192

    Literature cited2
    Literature Cited venous thrombotic events

    • Shields RK, Cook TM. Lumbar support thickness: effect on seated buttock pressure in individuals with and without spinal cord injury. Phys Ther 1992;72:218-26.

    • Schilero GJ, Spungen AM, Bauman WA, Radulovic M, Lesser M. Pulmonary function and spinal cord injury. Respir Physiol Neurobiol. 2009 May 15;166(3):129-41. Epub 2009 Apr 9.

    • Siddall PJ. Management of neuropathic pain following spinal cord injury: now and in the future. Spinal Cord. 2009 May;47(5):352-9. Epub 2008 Nov 11.

    • Teasell RW, Hsieh JT, Aubut JA, Eng JJ, Krassioukov A, Tu L; Spinal Cord Injury Rehabilitation Evidence Review Research Team. Venous thromboembolism after spinal cord injury. Arch Phys Med Rehabil. 2009 Feb;90(2):232-45.

    • van Kuijk AA, Geurts AC, van Kuppevelt HJ. Neurogenic heterotopic ossification in spinal cord injury. Spinal Cord. 2002 Jul;40(7):313-26.

    • Lisa-Ann Wuermser, MD, Chester H. Ho, MD, Anthony E. Chiodo, MD, Michael M. Priebe, MD, Steven C. Kirshblum, MD, William M. Scelza, MD. Spinal Cord Injury Medicine. 2. Acute Care Management of Traumatic and Nontraumatic Injury. Arch Phys Med Rehabil Vol 88, Suppl 1, March 2007

    • Consensus conference on deep venous thrombosis in spinal cord injury: Summary and recommendations. 1999. Chest102:suppl , p. 6335.