Injury Scenario

Posted in Mechanism of Injury on April 27, 2008 by Brian

http://www.maitrise-orthop.comBrian Smith is a 19 y.o. male. On February 28, 2008 he was riding his Honda Rebel 250 on his way from work to meet friends at Central Park. Brian was riding on 1st avenue, when at the intersection of 34th street, a taxi turned into his path. Brian was thrown from his motorbike as a result of colliding into the taxi’s left passenger door. Brian was riding at a speed of 40 mph at the time of the collision, and he was thrown into the air 100 feet, landing across the intersection with his head hitting the ground first. Brian suffered a flexion injury to his cervical spine, causing a compression injury to the anterior and middle aspects of the vertebral column.

Brian was found lying on the ground, unable to move. Two good samaritans, untrained in medical first aid, picked him up and moved him to the sidewalk. As they were carrying him, his unsupported head and neck shifted into a hyperextended position. Radiographs revealed a teardrop fracture, accompanied by a sagitally-oriented fracture of the C5 vertebral body. Brian received care within a few minutes of the accident due to the proximity to NYU hospital. However, the fact that he was initially transferred improperly resulted in a posterior displacement of C5 bony fragments into the neural canal (i.e., the teardrop fragment remained attached to the anterior longitudinal ligament while the rest of the vertebral body fragments were posteriorly displaced into the neural canal). The end result was anatomical transection of the spinal cord at the level of C6.

photo credit: Tear drop fracture of C5 http://www.maitrise-orthop.com

Pathophysiology of Spinal Cord Injury

Posted in SCI Physiology on April 27, 2008 by Brian

The pathophysiology of Brian’s spinal cord injury is complex, with multi-system involvement over a prolonged period of time. The systems- including the nervous, vascular, and immune- all play a vital role in healing the site of injury. However, their healing responses can/will simultaneously exacerbate the damage and long-term dysfunction. The reaction cascade by all three systems, which starts immediately following trauma to the spinal cord, is divided into three phases: acute, secondary, and chronic (CSCI, 2005).

The acute phase, initiated within the first seconds of Brian’s injury, was marked by systemic and local involvement. On the systemic level, the body reacted with a brief period of hypertension, followed by a prolonged phase of hypotension. Hypovolemia, with subsequent vasospasm and release of vasocontrictive substances, resulted from mechanical trauma to the blood supply in the cord (net effect of ischemia). The ischemia ultimately caused necrosis of neuronal cell bodies and isolated spinal shock (click here to read more about our description of spinal shock)- a temporary state of spinal cord hypoexcitability/loss of function within 2-24 hours post-injury. Brian still has full innervation of the diaphragm (CSCI, 2005).

The secondary phase likely began minutes after trauma, and lasted for weeks. This phase was marked by the formation of free radicals, an onset of immune system responses, and apoptotic cell death. Click here to read more of our detailed information of the secondary phase (CSCI, 2005).

The chronic phase begins within a months, and lasts for years. Brian experience more changes both on a microlevel and macrolevel. Click here to read more of our detailed information on the chronic phase (CSCI, 2005).

Neurophysiology of C5 Spinal Cord Injury

Posted in SCI Physiology on April 27, 2008 by Brian

Brian has suffered from a myriad of neurological complications as a result of his C5 complete spinal cord lesion. Brian’s injury is classified as complete tetraplegia. This signifies that Brian has lost all motor and sensory function at and below the level of the lesion, including as far distal as the last sacral segment of the cord at S5. The spinal cord- connected to the brain via afferent and efferent sensory and motor pathways- has lost its essential connection to the brain from the level of the lesion distally. When the brain fails to receive sensory signals traveling up the main tracts of the dorsal and anterolateral columns, a person is unable to perceive sensation. In addition, all motor outputs, which are normally integrated, modified, and directed down the motor tracts (lateral corticospinal, ventral corticospinal, rubrospinal, vestibulospinal, lateral and medial reticulospinals) by the brain, fail.

While Brian’s injury is classified as complete, he has a zone of partial preservation, or slight recovery one level below C5 innvervation (at C6, 1/5 in MMT) .  At C6, the cord demonstrates signs of a lower motor neuron lesion (flaccidity, diaschesis) because of the disruption in the reflex arc. C7-S5 is termed the “isolated cord”. The isolated cord exhibits signs of an upper motor neuron lesion, with involuntary hyperreflexia, hypertonicity, and loss of voluntary motor control. Brian has lost sensation from C6-below, becoming anesthetic to light or crude touch, pain, temperature, vibration and proprioception.

Another neurophysiological complication, as a result of Brian’s tetraplegia, is an impediment of the autonomic nervous system’s regulatory abilities. In Brian’s case, most of his parasympathetic fibers maintain their connection to the brain except for the sacral segments, but his entire sympathetic chain will operate independently from the cortex. As a result, anything that stimulates the sympathetic chain can exacerbate its sensitivity and cause autonomic dysreflexia. The parasympathetic fibers originating from the cranial nerves will attempt to regulate the autonomic dysreflexia (hypertension) by decreasing the heart rate and blood pressure (apparelyzed.com, 2008). This lack of synchronization between the two opposing systems will also cause problems with thermoregulation, orthostatic hypotension, and loss of voluntary bladder, bowel, and sexual control.

Spasticity

Posted in SCI Physiology on April 27, 2008 by Brian

For the initial 48 hours post-injury, Brian presented with flaccidity and hypotonicity. During re-evaluation, he also presented with motor signs of spasticity and hypertonicity. Over time, the spasticity can increase and physical therapy management must occur promptly to prevent discomfort and maintain ROM. Our initial physical therapy treatment intervention for spasticity focused on two types of exacerbating stimuli: first, we aimed to eliminate any sources of nervous system irritation (primarily pressure sores, and including UTI, emotional lability, tight clothing, bowel and bladder distention). The second course of action wasdirected at eliminating any factors (intrinsic and extrinsic nociceptive stimuli from bladder/colon/rectum distention, or infection) responsible for lowering the stretch reflex threshold. Range of motion exercises should be taught to Brian’s caretaker for long-term intervention.

The following were used as effective interventions to reduce Brian’s spasticity (Krasilovsky, 2007):

  1. Watsu in a tepid pool for relaxation.
  2. Utilization of postural reflexes.
  3. Rood techniques: slow, applied pressure at the tendon insertions of hypertonic muscles.

Bladder, Bowel and Sexual Function

Posted in Bladder, Bowel and Sexual Function on April 27, 2008 by Brian

The autonomic nervous system’s severance from the brain in high level tetraplegic patients disrupts normal function of the bowel, bladder and sexual function. With high level injuries such as Brian’s, the bladder and the external sphincter muscle are no longer voluntarily controlled, while the kidneys, ureters and urethra remain involuntarily intact. For injuries above T12, the bladder will be termed “automatic”, or spastic/reflexive. Brian’s spastic bladder voids at any point in time due to the micturition reflex stimulus. He is incapable of receiving the signal from his brain that his bladder is full, and is no longer able to voluntarily prevent his bladder from voiding.

The conservative management program that Brian interchangeably uses to regularly collect the urine from his bladder is either an indwelling catheter or an external condom catheter. He is dependent on others for management of the program. This program will prevent infection (a major medical concern with SCI patients, who can have autonomic dysreflexia) and facilitate voiding without embarrassment (University of Alabama at Birmingham, 2001).

Similar to the bladder, the bowel is reflexive as well. A reflexive bowel is characterized by tone of both the internal and external anal sphincter, and evacuates with the defecation reflex. However, a C5 patient lacks awareness that the bowel is full and ready for passage, and cannot volitionally evacuate. Brian’s bowel program consists of use of a stool softener, followed by insertion of a suppository and rectal digital stimulation. Fluids and high fiber diets are important. Brian is dependent on others for help in emptying his bowels, which is necessary to do on a regularly scheduled basis each day (Umphred, 2001; University of Alabama at Birmingham, 2001).

Sexual issues are rightfully a major concern for all spinal cord injured patients. Brian experiences involuntary reflex erections (from S2-S4), which are short in duration and responsive to stimulation, rather than psychogenic erections, which require emotion and signals from the brain. Abnormal ejaculation and sperm count make it difficult for men with Brian’s level of injury to fertilize a female egg, but there are treatments such as penile vibratory stimulation and medication for erectile dysfunction. Psychological and sexual counseling are fundamental components of therapy (Umphred, 2001; University of Alabama at Birmingham, 2001).

Acute Evaluation

Posted in Evaluation on April 27, 2008 by Brian

C5 – ASIA A

Subjective

♂ pt. arrived to facility in a Halo 3/1/08 s/p spinal fusion 1 wk. ago. Pt. states that he underwent immediate medical intervention after sustaining a C4 flexion teardrop fracture. There was severe ligamentous disruption and posterior dislocation. Pt states that injury was caused by falling from his motorcycle. Pt. is a 19 y.o. Landscaper, from New Jersey. Parents state that Pt. suffers from depression and substance abuse. Hx. of a previous fibula/tibia fx. due to motorcycle accident in 2004. Current Medications: Seroxat 30 mg for depression, anti-embolytics for edema. Parents state that the Pt.’s overall health is good.

Objective

MMT: 3/5 deltoids (per Halo precautions, will be re-evaluated with Halo removal for full strength), 5/5 R elbow flexors, 5/5 L elbow flexors, 1/5 R wrist extensors, 1/5 L wrist extensors , absent bilat. elbow extensors, absent bilat. finger flexors, absent bilat. finger abductors, absent bilat. hip flexors, absent bilat. knee extensors, absent bilat. ankle dorsiflexors, absent bilat. long toe extensors, absent bilat. ankle plantar flexors. Pt. is w/o sacral sparing.

Neurological evaluation: Pt. is sensitive to both pinprick and light touch in all key sensory points up to and including C5. Below this sensation is absent. Patient’s position sense from C5 and above could not be tested due to Halo restrictions and precautions. Below C5, position sense was absent. Pt. presented with areflexia below C5.

Range of Motion: Bilat. ROM included: hip flexion 0-75°, elbow flexion 0-120°, UE horizontal adduction 0-5°; R long finger flexion 0-85°, L long finger flexion 0-80°; bilat: long finger extension not tested (to preserve tenodesis), knee flexion 0-130°, df 0-20°. No contractures noted.

Functional Abilities: To be assessed in re-eval: bed and mat skills, transfers, w/c skills, instruction of others.

Skin Integrity: Skin inspected each time the patient is turned. Redness over bony prominences disappears within 30 minutes. No evidence of skin breakdown. Edema noted bilat. LE. (+) TEDS. Pt. and family educated on how to reposition patient q 2 hours. Pt. and family re-educated on proper hygiene at the Halo pin sites and of the skin underlying the vest.

Cognitive: A + O x 3

Respiratory: Vital Capacity 30% of normal. Impaired forceful exhalation. Some capacity for cough. Decreased chest expansion, normal epigastric rise. BP 90/60. HR 60.

Equipment: Pt. lacks needed equipment. Arrangement for equipment purchase will be made. Talk to family about ordering options for:

  1. Feeding – sling, universal cuff, plate guard.
  2. Self care – bath mat, non slip surface in the bath, soap and shampoo dispensers, long handled comb, toilet transfer aids, bath transfer aids (commode), catheter and catheter aids (loops and straps for leg bag), and suppository.
  3. Dressing – trapeze, loose clothing (1-2 sizes bigger), no buttons, extensions to zippers.
  4. Beasy™ board/notched transfer board, bed mobility aids.
  5. See Home Modifications.

Assessment

Pt. is not expected to be functionally ambulatory. Due to the fact that this patient has diaphragmatic innervation, his vital capacity will improve with stabilization, breathing exercises, chest expansion, and accessory muscle breathing. Pt. demonstrates adequate deltoid and bicep strength, as well as ROM in shoulders and elbow to prepare for rolling and transfers. Diagnosis: Practice Pattern 5H: Impaired Motor Function, Peripheral Nerve Integrity, and Sensory Integrity Associated With Nonprogressive Disorders of the Spinal Cord.

Plan

Will see Pt. BID @ B/S. Will train Pt. and family in respiratory hygiene, ROM, bed mobility, skin integrity and strengthening. Educate Pt. on avoiding trunk motion, hip flexion > 90° and shoulder flexion> 90°.

Expected Outcomes:

Short Term Goals

Respiratory:

  1. Pt. will be able to achieve a VC of 40-60%. Improve VC with positioning, trunk supports, abdominal binder. Improve chest expansion for posture and strengthen accessory respiratory muscles.
  2. Pt. will be able to phonate 6-8 syllables per breath.
  3. Pt. and family will be educated on how to assist with bronchial hygiene/assisted cough 3-4 times per day.
  4. Pt. will learn facilatory breathing techniques with accessory respiratory musculature.

ROM:

  1. Pt. will maintain full ROM in all UE joints for proper self-care, posture, and eating.
  2. Improve shoulder extension by 5° to prepare Pt. to hook arms behind push handles.
  3. Pt. will maintain at least neutral extension at hip to prepare for prone lying and prone mat activities.
  4. Hamstrings ROM 90° to prepare for mat mobility, sitting ability, and transfers.
  5. DF to neutral to prevent skin breakdown at metatarsal heads and toes.

Strength:

  1. Improve strength by 1 Grade in MMT for periscapular muscles, horizontal shoulder adductors, and elbow flexors to prepare for transfers, bed mobility, and ADL.
  2. Build strength of scapular adductors, shoulder flexors and elbow flexors for future w/c mobility.
  3. Pt. will tolerate upright sitting without skin compromise in tilt in space wheelchair for 10 minutes.

Skin:

  1. Pt on Roto-rest to avoid skin breakdown.
  2. Family will demonstrate padding/ positioning.
  3. Pt. will inspect skin BID.

Re-Evaluation

Posted in Evaluation on April 27, 2008 by Brian

Re-evaluation:

Subjective

Pt.’s Halo removed 2 wks ago. Pt. states he isn’t getting better fast enough. Would like to have more hours of therapy. Anxious to gain strength, range, and musculature. States that he would like to be independent in UE dressing and feeding. Inspects skin BID. Performs weight shift q 15 mins. Surgeon consulted about Pt.’s readiness for new activities. Med: Diazepam, Seroxat.

Objective

MMT: 5/5 deltoids, 5/5 R elbow flexors, 5/5 L elbow flexors, 1/5 R wrist extensors, 1/5 L wrist extensors, absent bilat elbow extensors, absent bilat. finger flexors, absent bilat. finger abductors, absent bilat. hip flexors, absent bilat. knee extensors, absent bilat. ankle dorsiflexors, absent bilat.long toe extensors, absent bilat. ankle plantar flexors. Pt. is w/o sacral sparing. Involuntary muscle contraction noted in R knee extensors. Pt. was not able to contract and relax knee extensors on command.

Neurological Evaluation: Pt. is sensitive to both pinprick and light touch in all key sensory points up to and including C5. Below this, sensation is absent. Position sense at C5 and above intact. Below C5, position sense absent.

ROM: Spasm elicited by tactile stimulation, in addition to Grade 3 spasticity in R LE . Bilat. tested: hip flexion 0-100°, elbow flexion 0-140°, UE horizontal adduction 0-5°; R long finger flexion 0-85°, L long finger flexion 0-80°; bilat: long finger extension not tested to preserve tenodesis; L knee flexion 0-140°, df 0-20°

Skin Integrity: Skin inspected each time the patient is turned. No edema noted. No discoloration. Redness over bony prominences disappears within 30 minutes. No evidence of skin breakdown. Pt. and family educated on how to reposition patient q 2 hrs.

Cardiovascular: Abdominal binder used to help increase VC. VC 55% in supine with abdominal support- 45% without support. BP 110/60; HR 70. Pt. and family have been educated on coughing techniques.

Cognition: A + O x 3. Pt. appears anxious.

Home Environment: Ramp has been built in entrance to home, door knobs have been replaced with large door handles, family hired a contractor to change toilet height to the level of the w/c, and lower sink height. Grab bars installed around the toilet and in the shower. Bathtub will be converted into roll in shower with no shower doors. See home modifications .

Assessment

The functional potential for this patient includes min-mod. assist. bed skills, max. assist. transfers, independent manual and power w/c, and independent pressure relief using power tilt. The Pt. is not expected to be functionally ambulatory. Pt. demonstrates adequate deltoid and bicep strength, as well as ROM in shoulders and elbow to practice rolling and transfers. Diagnosis: Practice Pattern 5H: Impaired Motor Function, Peripheral Nerve Integrity, and Sensory Integrity Associated With Nonprogressive Disorders of the Spinal Cord.

  1. Pt. able to sit upright for with UE support.
  2. Pt. demonstrates weight-shifting ability.
  3. ROM and VC have improved.

Plan:

Interventions

  1. Joint mobilizations and PROM PRN.
  2. Evaluate family’s ability to perform PROM and position Pt. / prolonged stretching for spasticity.
  3. PNF with pulley system setup for UE sidelying.
  4. Sling suspension in quadruped alternating UE.
  5. Power and manual w/c skills: seating, forward/backward propulsion, tilting, turns, positioning, terrain.
  6. Evaluate Pt.’s ability to problem solve independently.
  7. Watsu for UE and cardiovascular endurance.

Short Term Goals

Bed mobility:

  1. Pt. will demonstrate rolling R to L, L to R.
  2. Pt. will demonstrate rolling prone to supine and supine to prone, with MD clearance.
  3. Supine to sit mod. assist. with leg management, with MD clearance.
  4. Instruct family, nursing staff and OT about bed mobility, positioning, and safety.

Long Term Goals

Transfers:

  1. Instruct Pt. and family on positioning of w/c prior to transfer (casters forward, locked wheels, arm rest lifted, leg rest swing out).
  2. Instruct Pt. and family on bed to chair airplane transfer, max. assist. horizontal transfer.
  3. Instruct Pt. and family on transfers to bed, toilet, bath, car, floor.
  4. Assist Pt. in problem-solving.

Grooming: (referral to OT for dressing, bathing and additional grooming) Click here for adaptive device page.

  1. Set up washing face and shaving.
  2. Set up comb hair.
  3. Set up oral care.

Power and manual w/c mobility prior to discharge:

  1. Negotiate smooth surfaces, ramps, rough terrain, curbs.
  2. Negotiate doorways, elevators.
  3. Create trunk stability in w/c.
  4. Usage, removal, and manipulation of wheelchair parts.
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