PHT 2143C Miami Dade College Spinal Cord Injury Presentation

Spinal Cord Injury Hw L4 L5 S1 p883-887 tables PHT 2143C Rehabilitation Chapter 20 O’Sullivan 7th Edition Spinal Cord Injury • Partial or complete disruption of SC resulting in paralysis, sensory loss, and altered autonomic function and reflex activity • Spinal areas most frequently injured C5, C7, T12, L1 Traumatic causes: MVA, falls, stab and gunshot wounds Non-traumatic causes: (Pathological) disc prolapsed, vascular insult/dysfunction, complications of osteoporosis or rheumatoid arthritis, DJD, neoplasm, abscess, neurological disease (MS, ALS). Demographics Approximately 17,000 new cases annually in the US Between 243,000-347,000 individuals with SCI in the US Men > Women (80% to 20%) Whites more than African Americans, Hispanics and Asians Average age: 42 y/o First peak at 15-29 – Second peak older than 65 y/o Life expectancy has increased over the years Etiology: Can be traumatic and non-traumatic (Trauma is the most frequent cause of injury) • Traumatic Common Causes • MVA • Fall • Violence (GSW) • Sports • Non-Traumatic causes in adults’ result from disease or pathological influence (account for about 38%) • 56% Cervical lesions = tetraplegia • 43% thoracic, lumbar or sacral = paraplegia • Incomplete tetraplegia injuries are most common followed by complete paraplegia, incomplete paraplegia, and complete tetraplegia. Length of stay in acute care has decreased from 24 days (1970) to 11 days (2016). Length of stay in IR has also decreased from 98 days (1970) to 35 days (2016). Anatomy Review Spinal Nerves Exit below corresponding level of spine • Exception is cervical • C1-C7 spinal nerves exit above their corresponding spinal level • C8 exits below spinal level C7 Spinal nerves: 31 pairs • 8 cervical • 12 thoracic • 5 lumbar • 5 sacral • 1 coccygeal • Spinal cord ends about L1-L2 **** • SC tapers into the conus medullaris at lower border of L1 Cauda equina: distal portion of cord as a bundle of nerve roots from L2 to S5- innervates pelvic organs and LE. • VERY IMPORTANT SLIDE TO REMEMBER! Nerve Root Innervation MOTION KEY MUSCLE NERVE ROOT INNERVATION Elbow Flexion Biceps C5 Wrist extension ECRL C6 Elbow Extension Triceps C7 Finger flexion (distal FDS/FDP phalanx) C8 Finger Abduction Lumbricals T1 Hip Flexion Psoas L2 Knee Extension Quadriceps L3 Ankle DF Anterior Tibialis L4 Long Toe Extension EHL L5 Ankle PF Gastroc/Soleus S1 ASIA Scale Page 858 p858 Classification of SCIBroad Functional Categories Tetraplegia = quadriplegia • Cervical lesion • Complete Paralysis of all 4 extremities & trunk • Includes: Respiratory muscles Paraplegia • Complete Thoracic, lumbar, or cauda equina lesion • All or part of the trunk, and LEs paralysis Complete Injuries: The ASIA scale defines a Complete Injury: as having NO sensory and NO Motor function below the neurological level (meaning both, not one or the other) • Including the lowest sacral segments S4 and S5 dermatome. • NO Sacral Sparing. • Sensory and motor of these segments are determined by anal sensation and voluntary anal sphincter contraction Sacral Sparing: determined by sensory function at S4 and S5 dermatome. • The ability to feel deep anal pressure, or voluntary anal sphincter contraction • Big indicator of prognosis • Very important information to know in rehab! Incomplete injuries: ASIA defines an Incomplete Injury: as having sensory and/or motor function below the neurological level. • That includes sensory or motor at S4 and S5 level. • With Presence of sacral sparing! Zones of Preservation: • ASIA defines Partial Zones of Preservation as an individual that has motor and/or sensory function below the neurological level but does not have function at S4 and S5. No sacral Sparing • The areas of intact motor and/or sensory function below the neurological level are termed zones of partial preservation. Designation of SCI level ASIA: American Spinal Injury Association • International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) • Standardized tool to determine severity of injury (motor and sensory loss after SCI) • Neurological level • Most caudal level of SC with normal motor and sensory function on both R & L • Motor Level • Most caudal segment with normal motor function bilaterally • Sensory Level • Most caudal segment with normal sensory function bilaterally Motor Level • The key mm is identified as having intact innervation if it has a MMT of at least 3/5 and the next most rostral key mm exhibits 5/5 • For myotomes that are not clinically testable (C1-C4, T2-L1), and S2-S5) the motor level is defined as the same as the sensory level. Sensory level • The dermatomes are tested using light touch and pinprick on bilateral sides. • Scoring using a 3 point ordinal scale where 0=absent, 1= impaired, 2= normal. ASIA Impairment Scale O’Sullivan p.859 Table 20.1 • A: Complete • No motor or sensory function preserved in the sacral segments S4 or S5 • B: Sensory Incomplete • Sensory but not motor function is preserved below the neurological level and includes the sacral segments S4 and S5 • C: Motor Incomplete • Motor function is preserved below the neurological level, and more than half of the key muscles below the neurological level have a muscle grade of less than 3 • D: Motor Incomplete • Motor function is preserved below the neurological level and at least half of the key muscles below the neurological level have a muscle grade of 3 or more • E: Normal • Motor and sensory function is normal ASIA Impairment Scale Questions • What is sacral sparing? • What are the most common causes of spinal cord injury? • What is the cauda equina? • What is innervated at each level? • What is the ASIA scale? • What is paraplegia and tetraplegia? • How is a complete injury defined? • What are the zones of partial preservation? • How is an incomplete injury defined? • How many spinal nerves are there in each segment? • What spinal level changes from a quadriplegic to a paraplegic? • If a muscle is a 3/5 and all muscles rostral to it are 5/5. What are you defining? • Define the classifications of the ASIA scale SCI Syndromes • Brown-Sequard syndrome • Central Cord Syndrome • Posterior Cord Syndrome • Anterior Cord Syndrome • Cauda Equina Injuries Brown-Sequard Syndrome • Hemi-section of spinal cord • Caused by penetration wounds (gunshot or stab) • Characteristics • Ipsilateral loss of dorsal columns with loss of tactile discrimination, pressure, vibration, and proprioception. • Ipsilateral loss of corticospinal tracts with loss of motor function and spastic paralysis below the level of the lesion • Contralateral loss of spinothalamic tracts with loss of pain and temperature below the level of the lesion This is an UMN lesion Central Cord Syndrome • Most common SCI syndrome • Typical cause • Cervical hyperextension injury • Compressive forces – hemorrhage and edema in central spinal cord • Characteristics • UE involvement > LE involvement • Can walk but may present limitations with UE motion due to distal UE weakness Anterior Cord Syndrome • Typical Cause: • Cervical flexion injury – damage to anterior spinal cord • Compression of the anterior cord from fracture, dislocation, or cervical disc protrusion. • Characteristics: • Loss of pain and temperature (spinothalamic tract damage) • Complete Loss of motor function (corticospinal tract damage) • Preserved: proprioception, discriminative touch*, and vibration Posterior Cord Syndrome • Rare • Characteristics • Loss of posterior columns with preservation of motor function; loss of proprioception • Wide base steppage gait (Ataxic gait) • Intact pain, light touch sensation Cauda Equina Syndrome • LMN lesion • Occurs with injuries below L1 • Flaccid with no reflex activity below the level of the lesion • LE paralysis and paresis is variable depending on the extent of the injury. • Cauda equina lesions are Peripheral injury (LMN) • Have potential to regenerate like peripheral nerve in any other part of the body Clinical Manifestations 1. Spinal Shock • Immediately following SCI there is a period of areflexia that is part of spinal shock. • Characteristics: • Reflexes are depressed or absent • Flaccidity • Loss of sensation • Loss of motor function • Impaired autonomic regulation (hypotension, loss of control of sweating and piloerection) • May last several hours or several weeks. Usually gone within 24 hours. 2.Motor and Sensory Impairments • Complete or partial loss of muscle function below level of lesion • Impaired or absent sensory function below level of lesion • The clinical presentation depends on the specific lesion (level and completeness of the lesion) • ASIA level THIS IS A MEDICAL EMERGENCY! 3. Autonomic Dysreflexia- Skills Check Alert! Pathological autonomic reflex that can be life threatening • More common in patients with SCI above the level of T6 (complete and incomplete) • Can happen below T6 as well. • Caused by a noxious STIMULI (below the level of the lesion) may include: • Bowel and bladder distention/irritation (Caused by a blocked catheter, bladder distention, UTI, Kidney stones, irritation of the bladder or urethra during catheterization or other procedures • Pressure injuries • noxious cutaneous stimuli below the level of the lesion • Kidney malfunction • Electrical stimulation below the level of the lesion • Sexual activity, labor, skeletal fracture below the level of the lesion. • Can be life threatening can lead to subarachnoid hemorrhage, cardiac arrest, seizure and death! Autonomic Dysreflexia- Symptoms Sudden onset- Page 862 • Pounding, excruciating headache • Constricted pupils • Hypertension (**rise in systolic 20-30 mmHg) • Increased spasticity • Nasal congestion • Restlessness • Vasodilation (flushing) above the level of lesion • Bradycardia • Diaphoresis • Vasoconstriction below level of lesion • piloerection • Blurred vision Autonomic Dysreflexia: Intervention • Recognize the symptoms, did you check BP? • Call for help, facility protocol? Some facilities: activate emergency code/911 • If patient is flat, bring him to sitting (to lower BP) at least 45 degrees and loosen any tight clothing or restrictive device (abdominal binder) • Identify noxious stimulus and relieve it (usually bladder) • Survey the patient for causes; begin with urinary system (look for kinks in the Foley tubing, undo clamps) Bladder distention is the primary cause • If the pt. is using an indwelling catheter, check for obstructions and remove any blockage immediately. • If you do not immediately find stimulus, drain bladder (nursing would do intermittent catheterization if no Foley is present) • Pharmacological intervention to lower BP may be required if symptoms do not subside after removing noxious stimuli • Continue to monitor BP • Document and inform the PT (symptoms, stimuli, relief, BP) • Patient education 4. Cardiovascular Impairment: Orthostatic Hypotension- Skills Check Alert! • Decreased in BP (S:20 or more/D:10 or more mmHg) that occurs when a patient assumes an upright position • Caused by disrupted balance between sympathetic and parasympathetic input, lack or decrease in mm contraction, and prolonged time in bed. • Significant in pts with SCI lesions above T6 • Symptoms: • Pallor, nausea, Blurred vision, ringing in the ears, light-headedness, and fainting. • Interventions: • Gradually, slowly progress to upright position to allow CV system adaptation to vertical position • Abdominal binder, compressive stockings • Reverse symptoms by returning to original position • W/C (reclining, elevating) • Tilt table 5. Spastic Hypertonia • Flaccidity during spinal shock then spasticity • More common in patients with cervical level lesions • It is part of UMN syndrome (spasticity, mm spasms, hypertonia, increased DTRs, and clonus) • Emerges below level of lesion • About 50% of pts with SCI report that their spasticity is problematic. • May learn to trigger spasticity to assist with function • If interferes with function, medical management • Oral: muscle relaxants • Intrathecal injections • Baclofen pump • Intramuscular injection of botulinum neurotoxin 6. Impaired Temperature Control • After SCI the hypothalamus can no longer control cutaneous blood flow or level of sweating. • This autonomic dysfunction results in loss of thermoregulation. • Ability to shiver is lost below the level of the injury • Vasoconstriction response does not occur with cold • Hyperthermia due to lack of sympathetic control of sweat glands • Impaired ability to sweat below the level of the lesion affecting normal cooling and causes excessive compensatory diaphoresis above the level of the lesion • Vasodilation response does not occur with heat above the lesion mucho sudor y below the lesion no sudor 7. Respiratory Impairment • C1-C2 level: Phrenic nerve innervation and spontaneous breathing are lost • Ventilator required or Phrenic nerve stimulation • The only mms of respiration are SCM, upper traps, which are the accessory muscles of inspiration. • Expiration is passive • C3-C4 level: partial diaphragm innervation, scalenes, levator scapulae. • Pts may require mechanical ventilation • With recovery and training may be able to breathe on their own but may need part-time ventilatory support (especially C3 level) • C5-C8 level: fully innervated diaphragm, as well as many accessory mms. • Cough is usually weak • Not likely to require a ventilator • Pts with injuries below T10 are likely to have near-normal ventilatory and pulmonary function. (Intercostals – T1-T5 Abdominals T6-T11) 8. Bladder Dysfunction- depends on the level of the injury • Reflexive bladder/bowel (UMN lesion –Above Conus medullaris) above S2 • Spastic bladder • Contracts and reflexively empties in response to a reflex (certain level of filling pressure) • Areflexive bladder/bowel (LMN lesion) S2-S4 • Flaccid bladder • No reflex action of the detrusor muscle Bladder Training • Goals • Control incontinence • Bladder control • Discontinue indwelling catheter if possible • Strategies • Intermittent catheterization • Establish fluid intake pattern • Regular emptying at predictable intervals • Suprapubic tapping- appropriate for reflexive bladder • Suprapubic catheter- surgically inserted 9. Bowel dysfunction • Spastic bowel- Above S2 UMN Lesion • Reflex defecation can occur when the rectum fills with stool. • Flaccid bowel- S2-S4 or Cauda Equina LMN Lesion • Bowel will not reflexively empty • Feces may become impacted • Incontinence may occur (external sphincter is flaccid) • Goal: • Regular pattern of bowel evacuation • Prevent impaction • Bowel program utilizes reflex bowel management strategies • Suppositories • Digital stimulation • Stool softeners • Manual evacuation • Diet • Fluid intake 10. Sexual Dysfunction 465 blue book • People with paralysis report that improved sexual function is the primary factor that would improve their quality of life. • Male/Female response: directly related to the level and completeness of injury • Dependent upon UMN and LMN and complete vs incomplete lesion • UMN lesion (above conus medullaris) vs LMN (conus medullaris & cauda equina) • UMN – reflex arc remains intact therefore the components of sexual arousal are possible due to external stimulation and in men and women (psychogenic response is lost) • LMN- reflex arc is lost therefore a psychogenic responses may be possible through cognitive stimulation. Female: fertility and pregnancy • Fertility and conception is unaffected • Labor and delivery • Impaired respiratory function = complications • Impaired sensation – labor not perceived • Labor may cause dysreflexia • Contractions • Controlled by hormones so paralysis is not an issue • But paralysis affects ability to “bear down” which will prolong labor and increase difficulty • Risk for C-section Secondary Medical Complications: Pressure Sores • Causes: • Unrelieved pressure • Bony prominences • Shearing forces • Contributing factors: • Sensory loss • Inability to change position • Non-compliance with skin care • Spasticity – shearing forces • Moisture – skin maceration (ex: urine, sweat) • Nutrition (low protein, anemia) • Secondary infection • Prevention • Turn every 2 hours • W/C pressure relief • Monitor skin • Pt instruction on skin inspection (mirror) • Education • Positioning is often viewed as bothersome & interfering with lifestyle and sleep – education • Wound Care DVT: Deep Vein Thrombosis Signs • Local swelling • Erythema • Heat Contributing factors • Immobility • Loss of normal “pumping” mechanism with active contraction • Prolonged pressure • Loss of vasomotor tone Intervention: Medical: anticoagulant drug therapy PT placed on hold avoid thrombus to cause emboli Prevention • Early mobilization • Turning to avoid pressure over large vessels • PROM • Support stockings • Positioning for venous return Pain Nociceptive • Common: Shoulder pain and other joints and soft tissues. • Musculoskeletal injuries at the shoulder, wrist, or elbow joints due to overuse or poor posture • Bicep’s tendinitis, RTC tears, impingement, CTS, wrist tendonitis. Neuropathic • Due to injury to the central or peripheral nervous system. • Can be at, below or above the level of the lesion • Allodynia is the experience of pain from a non-painful stimulation of the skin, such as light touch. May occur below the level of the lesion • Radiculopathies Interventions: Medications/TENS/ Massage/Mental imagery/ Biofeedback/ Acupuncture/MeditationNo heating modality What modalities are missing from the list and why? Contributing factors: Contractures • Lack of active muscle contraction • Spasticity • Gravitational forces on flaccid muscles KEY is PREVENTION! • ROM • Positioning • Splinting Heterotopic Ossification: Abnormal bone growth • Abnormal Osteogenesis in non-skeletal tissues, usually near joints, develops 3x normal rate. Resulting in jagged edges. Occurs below the level of the lesion. 3 to 12 weeks post SCI. • Cause: idiopathic • Factors associated include complete injury, trauma, severe spasticity, UTI, and pressure sores trauma, immobilization, muscle spasms, lack of oxygen or inflammation.. • Common in hip and knee joints • Signs • Swelling • Decreased ROM (over short time, 1 day) • Erythema • Localized warmth • Management • Medications • ROM • **Care with PROM: if it is too vigorous it may cause trauma Osteoporosis • Rapid bone mineral loss in the 1st 4-6 mo. Post injury • Prolonged lack of mobility • Prolonged lack of WB Syringomyelia is a disorder in which a cyst forms within the spinal cord. This cyst, called a syrinx, expands and elongates over time, destroying a portion of the spinal cord from its center and expanding outward. References O’Sullivan SB, Schmitz YJ, Fulk GD. (2019). Physical Rehabilitation (7th ed.). Philadelphia, PA: F.A. Davis Company.

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