Spinal cord injury rehabilitation

Spinal cord injury rehabilitation management discussed in detail in this presentation.

1. Spinal cord injury Rehabilitation Dr Harshanand Popalwar MBBS, MD, DNB, MNAMS, PGDHM, FDFM Specialist -PMR Department of Physical Medicine and Rehabilitation Safdarjung Hospital, New Delhi

2. Historical Aspects For thousands of years, injury to the spinal cord was synonymous with death, either instantly or after a period of great suffering The Edwin Smith Surgical Papyrus, written by an Egyptian physician almost 5000 years ago, vividly describes the symptoms of neurologically complete injury to the cervical spinal cord—that is, paralysis and sensory loss in the arms and legs, urinary incontinence, and priapism

3. approximately 400 bc , Hippocrates described paraplegia caused by injury or disease as being associated with paralysis, bladder and bowel dysfunction, and pressure ulcers

4. During the nineteenth century, treatment of SCI continued to be conservative and without much hope for survival. In 1805, Lord Nelson, the Admiral of the British Fleet, received a gunshot wound to his thoracic spine during the battle of Trafalgar, causing paraplegia.

5. Nelson spoke with his ship’s surgeon, Mr. Beatty, and described his loss of power of motion and feeling below the chest, and then expressed his view that he would have but a short time to live. The surgeon’s reply was, “My lord, unhappily for our Country, nothing can be done for you.” Within a few hours Lord Nelson was dead.

6. In 1881 the twentieth president of the United States, James A. Garfield, was shot in the spine, causing a neurologically incomplete conus–cauda equina lesion, but even with such a lesion he was dead within 3 months

7. During the early part of the twentieth century, there was little progress made in the management of SCI, and most persons with SCI died within weeks or months. Harvey Cushing observed that during World War I, 80% of all U.S. soldiers with SCI died within 2 weeks

8. During the 1930s and 1940s, management of SCI finally started to change. During the late 1930s, Dr. Donald Munro at Boston City Hospital developed a dedicated unit for comprehensive care of persons with SCI, and by 1943, he was able to demonstrate significant drops in both morbidity and mortality, primarily by focusing on better bladder management.

9. A few years later, in Great Britain during World War II, it was decided to congregate all casualties with SCI in special units that were supervised by an experienced physician. These units were to be sufficiently staffed by nurses and therapists, housed in facilities with rehabilitation workshops, and organized to provide resettlement and aftercare services.

10. Dr. Ludwig Guttmann was placed in charge of such a unit at Stoke Mandeville, where he introduced comprehensive care and interdisciplinary rehabilitation for persons with SCI, a program that was widely modeled around the world

11. Incidence and Prevalence of SCI The annual incidence of traumatic SCI requiring hospitalization in the United States is approximately 40 new cases per million population. Almost all studies show that the incidence of SCI is lowest for persons younger than 15 years and highest for persons 16 to 30 years of age. After the age of 30, there is a consistent decline in incidence

12. More than 80% of all SCI occurs in males, a figure that has remained essentially constant for more than 30 years in the United States Although India is the second most populous country in the world, to date no demographic data are available for SCI.

13. Causes of Spinal Cord Injury vehicular crashes (42.1%), falls (26.7%), violence (15.1%), sports (7.6%). In recent years, there has been a gradual decline in SCIs related to vehicular crashes and sports, whereas those relating to falls have increased.

14. Neurologic Level and Extent of Neurologic Deficit According to the National SCI Database, tetraplegia is more common than paraplegia (50.5% vs. 44.1%). These are subdivided into the following neurologic categories: incomplete tetraplegia (30.1%), complete tetraplegia (20.4%), complete paraplegia (25.6%), and Incomplete paraplegia (18.5%). Recent trends show an increase in incomplete tetraplegia and a slight reduction in complete paraplegia.

15. Mathur N 1,  jain S 1,  kumar N 1,  srivastava A 1,  purohit N 1,  patni A 1. Spinal cord injury: scenario in an indian state. Spinal cord.  2015 may;53(5):349-52. Doi : 10.1038/sc.2014.153. Epub 2014 sep 16.

16. Length of Stay, Rehospitalization , and Discharge Destination The average length of stay for patients with SCI has declined dramatically over the years, according to the National SCI Database. This is true for both acute and rehabilitation hospitalizations, from 25 acute days in 1974 to 12 days in 2008, and from 115 rehabilitation days to 37 days.

17. Life Expectancy and Causes of Death Life expectancy for persons with SCI has increased steadily for many decades but still remains below that of able bodied individuals. The mortality rate is highest during the first postinjury year, at 6.3%, but declines significantly thereafter.

18. Diseases of the respiratory system, especially pneumonia, are the leading cause of death both during the first post injury year and during subsequent years. The second most common cause of death, “other heart disease,” is thought to reflect deaths that are apparently caused by heart attacks in younger persons without apparent underlying heart or vascular disease and cardiac dysrhythmia

19. Pathophysiology of Acute Spinal Cord Injury The Primary injury

20. Pathophysiology of Acute Spinal Cord Injury The secondary injury cascade is a term that refers to a series of biochemical processes that occur after an SCI, and that tend to cause further neuronal damage beyond the mechanical damage caused at the moment of impact. Ischemia of the gray matter at the site of injury occurs almost immediately after SCI. This ischemia appears to result from vasoconstriction of blood vessels supplying the cord, and is mediated by the rapid release of various vasoactive substances such as serotonin, thromboxanes , platelet-activating factor, peptidoleukotrienes , and opioid peptides after SCI

21. Ischemia is followed by the development of edema at the site of injury. At a cellular level, there is a marked rise in intraneuronal calcium concentrations. Intracellular calcium facilitates the activation of phospholipases A2 and C, which leads ultimately to the production of free radicals and free fatty acid metabolites, which cause damage to local cell membranes

22. Microhemorrhages appear in the central gray matter at the site of impact. Iron in this hemorrhaged blood catalyzes the peroxidation of lipids, leading to further tissue damage as well as catalyzing the further production of oxygen free radicals

23. Initially, neutrophils migrate to the site of injury, where they can contribute to cellular injury by producing lysosomal enzymes and oxygen radicals. These are followed by macrophages that phagocytose cell debris

24. Spinal Mechanics and Stability There is no universally accepted definition of spinal stability. White and Panjabi467 defined clinical instability as “the loss of the ability of the spine under physiologic loads to maintain relationships between vertebrae in such a way that there is not initial damage or subsequent irritation to the spinal cord or nerve roots and, in addition, there is no development of incapacitating deformity or pain due to structural changes.”

25. The anterior column is composed of the anterior longitudinal ligament, the anterior two thirds of the vertebral body, and the anterior two thirds of the annulus fibrosis or disk.

26. The middle column is composed of the posterior one third of the vertebral body, the posterior one third of the annulus fibrosis, and the posterior longitudinal ligament.

27. The posterior column is composed of the pedicles, facet joints, laminae , supraspinous ligament, interspinous ligament, facet joint capsule, and ligamentum flavum

28. When the integrity of the middle and either the anterior or the posterior column is affected, the spine is likely to be unstable

29. C–SPINE FLEXION/HYPEREXTENSION INJURIES Flexion Injuries Compression Fractures Mechanism: cervical flexion with axial loading • C5 is the most common compression fracture of the cervical spine. • Force ruptures the plates of the vertebra, and shatters the body. Wedge-shaped appearing vertebra on x-ray • May involve injury to the nerve root and/or cord itself. • Fragments may project into spinal canal.

30. Unilateral Facet Joint Dislocations • Mechanism: flexion-rotation injury • Vertebral body < 50% displaced on x-ray • Unstable if the posterior ligament is disrupted. • Narrowing of the spinal canal and neural foramen • C5–C6 most common level • Also note that flexion and rotation injuries may disrupt the intervertebral disc, facet joints, and interspinous ligaments with little or no fracture of the vertebrae. • If spinal cord injury results, it is more likely to be an incomplete injury

31. Bilateral Facet Joint Dislocations • Mechanism: flexion injury • Vertebral body > 50% displaced on x-ray, causing significant narrowing of the spinal canal • Unstable with disruption of the PLL • Most common level is C5–C6 because of increased movement in this area. • Injury more likely to be neurologically complete

32. Hyperextension Injuries • Can be caused by acceleration-deceleration injuries, • Soft tissue injury may not be seen on radiologic studies. • Hyperextension injury of the C-spine in the elderly may result in a central cord syndrome. • C4–C5 is the most commonly affected level.

33. NONTRAUMATIC (NT) SCI • NT-SCI includes etiologies, such as spinal stenosis with myelopathy , spinal cord compression from a neoplasm, multiple sclerosis (MS), transverse myelitis , infection (viral, bacterial, fungal, parasitic), vascular ischemia, radiation myelopathy , motor neuron diseases, syringomyelia , vitamin B12 deficiency, and others. • Spinal stenosis and spinal cord tumors are the most common causes of NT-SCI presenting for inpatient rehabilitation in the United States .

34. Spinal cord tumors – Can be primary or metastatic, intradural , or extradural . The majority of spinal cord tumors are metastatic in origin, and 95% of these are extradural . – Approximately 70% of spinal metastasis occurs in the thoracic spine , with clinical presentation of pain, typically worse at night, and when the patient is in the supine position. – The most common sources of secondary tumors are the lung, breast, and prostate . The most common primary tumors are ependymoma and astrocytomas

35. FRACTURES OF THE SPINE Cervical Region • Jefferson Fracture (C1 Burst Fracture) – Burst fracture of the C1 ring. Usually a stable fracture with no neurological findings – Mechanism: axial loading causing fractures of anterior and posterior parts of the atlas ( ie , football spearing) – Treatment: rigid orthosis ( ie , Halo vest) if it is a stable fracture. If it is unstable, will require surgery.

36. Hangman Fracture (C2 Burst Fracture) Usually bilateral from an abrupt deceleration injury ( eg , MVC with head hitting windshield) – Most often stable with only transient neurological findings – Treatment: external orthoisis (halo is first line treatment). Unstable fracture will require surgery.

37. Odontoid ( Dens ) Fracture – Type I: fracture through the tip of dens. No treatment usually required. – Type II (most common): fracture through the base of odontoid at junction with the C2 vertebra. Usually treated with a Halo vest, but surgery may be required if unstable. – Type III: fracture extends from base of odontoid into the body of the C2 vertebra proper. Usually treated with a Halo vest

38. Thoracolumbar Region • Chance Fracture Transverse fracture of thoracic or lumbar spine from posterior – to anterior through the spinous process, pedicles, and vertebral body – Usually affects T12, L1, L2 levels – Previously was most commonly seen in patients wearing lap seat belts. Now typically due to falls/crush injury with acute hyperflexion of the thorax. – Tend to be stable fractures and are seldom associated with n neurological compromise unless a significant amount of translation occurs

39. Vertebral Body Compression Fracture (Anterior Wedge Fracture) – Most commonly caused by axial compression with or without flexion: vertebrae body height is reduced—may cause thoracic kyphosis (Dowager hump) – Spontaneous vertebral compression fractures are stable injuries—ligaments remain intact.

40. Classification of Spinal Cord Injury The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) provides a procedure for classifying an SCI. A complete injury is defined within the ISNCSCI as an injury in which there is the lack of any sensory or motor function in the lowest sacral segment; this includes sensation deep within the anus, sensation at the anal mucocutaneous junction, or a voluntary contraction of the external anal sphincter. An incomplete injury is defined as an injury in which there is at least partial sensory or motor function in the lowest sacral segment

41. The sensory portion of the neurologic examination includes the testing of a key point for absent, impaired, or normal sensation in each of the 28 dermatomes on each side of the body for both light touch and pinprick. The motor portion of theneurologic examination includes the testing of a key muscle function for strength on a 6-point scale for each of 10 myotomes on each side of the body), as well as testing for contraction of the external anal sphincter

42. Myotomes testing C 5 C6 C7 C8 T1 L 2 L3 L4 L5 S1

43. ASIA impairment scale

44. “Will I walk again?” “Will I regain use of my hands?” “Will I regain control of my bowel and bladder?”

45. Neurologic Recovery in Complete Tetraplegia Only 2% to 3% of persons initially classified as having an AIS of A convert to AIS D by 1 year Overall, between 30% and 80% of persons with motor complete tetraplegia recover a single motor level, meaning gaining functional motor strength at that level, within 1 year of injury A muscle with grade 1 or 2 strength at 1 week has a 70% to 80% chance of reaching grade 3 by 1 year.

46. Neurologic Recovery and Ambulation in Incomplete Tetraplegia Maynard et al reported that 87% of persons with motor incomplete tetraplegia initially were walking by 1 year, whereas 47% of persons with sensory incomplete, but motor complete, tetraplegia were walking by 1 year.

47. Persons with preservation of pinprick sensation near the anus have a greater than 70% chance of regaining ambulatory ability, while persons who have spared light touch sensation only in the same region are unlikely to regain ambulatory ability

48. Neurologic Recovery and Ambulation in Paraplegia Among persons with complete paraplegia, about 75% retain the same NLI at 1 year that they had at 1 month postinjury , 20% gain a single level, and 7% gain two neurologic levels. Persons with T1–T8 complete paraplegia do not recover lower limb voluntary movement. However, 15% of persons with complete paraplegia between T9 and T11, and 55% of persons with paraplegia at T12 and below, recover some lower limb function

49. Persons with incomplete paraplegia have the best prognosis for ambulation among all the groups of persons with traumatic SCI. 80% of individuals with incomplete paraplegia regain functional hip flexion and knee extension within 1 year of injury, making both indoor and community-based ambulation possible

50. Management 1. accident site management 2. primary care 3. care at tertiary care hospital

51. Principle of ABC Airway Breathing Circulation

52. Evacuation and immobilization

53. I mmobilization

54. Transfer from accident site

55. RETREIVAL FROM WATER OF A SUSPECTED CERVICAL SPINE INJURY

56. Cont…The Role of MRI We suggest that MRI be performed in adult patients with acute SCI prior to surgical intervention, when feasible, to facilitate improved clinical decision-making. (Grade: Weak Recommendation; Very Low Evidence We suggest that MRI should be performed in adult patients in the acute period following SCI, before or after surgical intervention, to improve prediction of neurologic outcome. (Grade: Weak Recommendation; Low Evidence)

57. Diagnostics Plain films Lateral, A/P, odontoid; C-T-L spines May be used for rapid identification of gross deformity CT Scan Comprehensive, cervical through sacral Demonstrates degree of compression and cord canal impingement MRI Scan Demonstrates ligamentous, spinal cord injury

58. Cervical Spine Clearance Occiput to T1 need to be cleared ER, Neurosurgery or Orthopedics physician If the patient Is awake and oriented Has no distracting injuries Has no drugs on board Has no neck pain Is neurologically intact then the c-spine can be cleared clinically, without any need for XRays CT and/or MRI is necessary if the patient is comatose or has neck pain Subluxation >3.5mm is usually unstable

59. Cervical Traction Gardner-Wells tongs Provides temporary stability of the cervical spine Contraindicated in unstable hyperextension injuries Weight depends on the level (usually 5lb/level, start with 3lb/level, do not exceed 10lb/level) Cervical collar can be removed while patient is in traction Pin care: clean q shift with appropriate solution, then apply povidone-iodine ointment Take XRays at regular intervals and after every move from bed

60. Gardner-Wells tongs

61. Surgical Decompression and/or Fusion Indications Decompression of the neural elements (spinal cord/nerves) Stabilization of the bony elements (spine) Timing Emergent Incomplete lesions with progressive neurologic deficit Elective Complete lesions (3-7 days post injury) Central cord syndrome (2-3 weeks post injury)

62. Minerva vest and halo-vest

63. McQuillan, K., Von Rueden, K., Hartsock, R., Flynn, M., & Whalen, E. (eds.). (2002). Trauma Nursing: From Resuscitation Through Rehabilitation. Philadelphia: W. B. Saunders Company. Reprinted with permission.

64. Fractures-Dislocations Atlanto-occipital dissociation Complete injury; death Atlanto-axial dislocation Complete injury; death Jumped, Jump-locked facets Require reduction; may impinge on cord; unstable due to ligamentous injury

65. Fractures-Dislocations Facet fractures High incidence of cord injury in cervical spine Odontoid (dens) fractures Rarely cord injury

66. Fractures-Dislocations

67. SCIWORA Spinal Cord Injury without Radiographic Abnormality Most frequently children Dislocation occurs with spontaneous relocation Cord injury evident Radiographs negative

68. Management Airway C1-4 injuries require definitive airway Injuries below C4 may also require airway due to Work of breathing Weak thoracic musculature Breathing Adequacy of respirations SpO2 Tidal volume Effort Pattern

69. Management Circulation Neurogenic shock Injuries above T6 Hypotension Bradycardia –treat symptomatic only Warm and dry Poikilothermic – keep warm Fluid resuscitation Identify and control any source of bleeding Supplement with vasopressors

70. Neurogenic Shock Injury to T6 and above Loss of sympathetic innervation Increase in venous capacitance Bradycardia Decrease in venous return Hypotension Decreased cardiac output Decreased tissue perfusion

71. Management Urine output Urinary retention Atonic bladder Foley Initially avoid intermittent catheterization High urine output from resuscitation fluids

72. Management Deficit Spinal shock Flaccid paralysis Absence of cutaneous and/or proprioceptive sensation Loss of autonomic function Cessation of all reflex activity below the site of injury Identify level of injury

73. Management Pain Frequent physical and verbal contact Explain all procedures to patient Patient-family contact as soon as possible Appropriate short-acting pain medication and sedatives

74. Management Communication Blink board Adapted call bell system Avoid clicking, provide a better option Speech and occupational therapy Prism glasses Setting limits/boundaries for behavior

75. Management Special Treatment Hypothermia Recommends 33 o C intravascular cooling Rapid application, Monitor closely Anecdotal papers High dose methylprednisolone No longer considered standard of care

76. Management Rotational bed therapy Maintain alignment and traction Prevent respiratory complications of immobility

77. Management Surgical Determined by Degree of deficit, location of injury, instability, cord impingement Anterior vs. posterior decompression/ both Emergent Reserved for neurologic deterioration when evidence of cord compression is present

78. Decompression and pedical screw fixation

79. Rehabilitation of SCI

80. Team Approach

81. Physical skill training

82. ROM exercises

83. Upper limb strengthening

84. Mat activities

85. Tilt table

86. Transfer training

87. Standing in parallel bar

88. Weight shift in parallel bar

89. Gait training in parallel bar

90. Gait training with walker

91. Gait training with elbow crutches

92. Spinal Cord Injury Education

93. Adjustment to disability

94. Secondary conditions post SCI Pulmonary complications Pulmonary complications, including atelectasis , pneumonia, respiratory failure, pleural complications, and pulmonary embolism (PE), are the leading causes of death for persons with SCI in all years after SCI. They accounted for 37% of all deaths during the first year after SCI, and 21% of the deaths beyond the first year

95. Atelectasis is the most common respiratory complication in people with SCI and can predispose to pneumonia, pleural effusion, and empyema

96. management Secretion clearance CPAP Mechanical insufflator-exsufflator Bronchodilators

97. Vascular system DVT Persons with SCI are prone to stasis of the venous circulation, hypercoagulability of the blood, and intimal vascular injuries. These risk factors for development of deep vein thrombosis (DVT) are known as Virchow’s triad. Stasis is a direct result of the loss of the muscle-pumping action of the lower limbs and peripheral vasodilatation. Hypercoagulability is caused by release of procoagulant factors after injury, whereas intimal injury can occur from trauma.

98. Management Low molecular wight heparin Warfarine IVC filters DVT prevention pumps ROM ex.

99. Cardiovascular and Autonomic System Persons who have SCI, both paraplegia and tetraplegia , often lead sedentary lives, resulting in poor physical fitness and an increased risk for untoward cardiovascular events. Persons with SCI, both those with paraplegia and tetraplegia , have a high prevalence of asymptomatic coronary artery disease as detected by thallium stress testing

100. Treatment Daily exercise Lifestyle modification Dietary modification

101. Autonomic dysfunction The autonomic nervous system is under supraspinal control, and therefore its function is disturbed by SCI. The autonomic nervous system normally controls visceral functions and maintains internal homeostasis through its nerve supply to smooth muscles, cardiac muscle, and glands

102. After SCI, autonomic reflex function is generally retained, but in those with high-level SCI, this is without supraspinal control .

103. Orthostatic hypotension Immediately after SCI, there is a complete loss of sympathetic tone, resulting in neurogenic (“spinal”) shock with hypotension, bradycardia , and hypothermia. The hypotension occurs as a result of systemic loss of vascular resistance, accumulation of blood within the venous system, reduced venous return to the heart, and decreased cardiac output

104. Over the course of time, the sympathetic reflex activity returns, with normalization of blood pressure. Supraspinal control continues to be absent in those individuals with high-level and neurologically complete SCI, however, and they continue to be prone to orthostatic hypotension.

105. SCI leads to disruption of the descending spinal cardiovascular pathways, resulting in sympathetic hypoactivity and unopposed prevalence of the intact vagal parasympathetic control. 18  Sympathetic hypoactivity results in low resting blood pressure , loss of regular adaptability of blood pressure, and disturbed reflex control

106. Orthostatic hypotension is defined by The Consensus Committee of the American Autonomic Society and the American Academy of Neurology (1996) as a decrease in systolic blood pressure of 20 mmHg or more , or in diastolic blood pressure of 10 mmHg or more , upon the assumption of an upright posture from a supine position, regardless of whether symptoms occur.

107. Mechanisms underlying orthostatic hypotension in SCI

108. management Management of orthostatic hypotension includes application of elastic stockings and abdominal binders, adequate hydration, gradually progressive daily head-up tilt , and at times, administration of salt tablets, midodrine , or fludrocortisone

109. Autonomic Dysreflexia AD is a syndrome that affects persons with SCI at the T6 level or above, which is above the major splanchnic outflow. It is caused by a noxious stimulus below the injury level, which elicits a sudden reflex sympathetic activity, uninhibited by supraspinal centers , resulting in profound vasoconstriction and other autonomic responses

110. The symptoms of AD are somewhat variable but include a pounding headache; systolic and diastolic hypertension; profuse sweating and cutaneous vasodilatation with flushing of the face, neck, and shoulders; nasal congestion; pupillary dilatation; and bradycardia . The hypertension can be profound and result in cerebral hemorrhage and even death

111. Patho -physiology of Autonomic dysrefelexia Strong Sensory stimulus (noxious/non noxious) Exaggerated Sympathetic response   Vasoconstriction below level of injury ( splanchnic and peripheral vessels)   Baroreceptors response to hypertension   Parasympathetic response through vagus nerve   Bradycardia , vasodilatation above level of injury   Absen transmission of inhibitory signals due to spinal cord injury

112. management Recognition of symptoms and identification of the precipitating stimulus are paramount. The patient should be sat up, constrictive clothing and garments should be loosened, the blood pressure monitored every 2 to 5 minutes, and evacuation of the bladder done promptly to ensure continuous drainage of urine. If symptoms are not relieved by these measures, fecal impaction should be suspected and, if present, resolved.

113. Local anesthetic agents should be used during any manipulations of the urinary tract or rectum. If hypertension is present, fast-acting antihypertensive agents shouldbe administered, usually nitroglycerin or nifedipine . After resolution of the AD episode, the person’s symptoms and blood pressure should be monitored for at least 2 hours.

114. Other issues in management of SCI Bladder management Bowel management Pressure ulcer management Sexual rehabilitation Vocational rehabilitation …….To be discussed in other presentations!

115. To conclude…! Spinal cord injury person can live normal life with proper rehab management. Interdisciplinary integrated team approach for complete rehab of Spinal cord injury person is must. Physical Medicine and Rehabilitation specialists trained in Rehabilitation of SCI are key person for this !

116. Thank You !