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SCI - HO & DVT Flashcards

1
Q

How common is post-traumatic syringomyelia in SCI?

A

“8%.
Ref: Review notes – Kathy Craven.

2% per SCIRE
22% at autopsy per SCIRE”

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2
Q

List 5 common symptoms of post-traumatic syringomyelia.

A

“1. Pain (segmental or radicular, aching/burning, worse with valsalva/cough/sneezing, usually in sitting position) - MOST COMMON

  1. DTR loss (ascending) - EARLIEST SIGN
  2. sensory loss - dissociated (loss of P/T at level of syrinx, sparing of V/P), aka ‘suspended sensory loss’ in cape distribution.
  3. Increased or decreased spasticity
  4. Hyperhidrosis
  5. Autonomic dysreflexia
  6. Loss of reflex bladder
  7. Worsening orthostatic hypotension
  8. New Horner’s syndrome
  9. Reduced respiratory drive
  10. Diaphragmatic paralysis
  11. Cranial nerve dysfunction
  12. weakness.
  13. fasciculations.
  14. atrophy.
  15. scoliosis.
  16. sleep apnea (central or obstructive).
  17. impaired CV reflexes.
  18. sudden death.
  19. brainstem symptoms: syringobulbia (diaphragm paralysis, dysphagia, dysphonia, nystagmus).

Ref: SC medicine principles practice textbook pg 502-503; SCIRE – syringomyelia document, Cuccurullo”

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3
Q

“Syrinx:

  1. What is the most common resulting symptom?
  2. What percent of SCI pt have syrinx?”
A

“1. radicular pain, gait ataxia, sensory disturbance, dysesthesias, motor weakness.if progressive sensory loss and increased spasticity
Ref: SCIRE – syringomyelia document pg 2.

  1. two percent (2%); but 22% at autopsy
    Ref: SCIRE – syringomyelia document pg 1.

0.3-3.2% incidence of syrinx in SCI, with mean of 1.3%.
Ref: SPINE Volume 30, Number 10, pp 1206 –1210.”

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4
Q

“List 3 causes of neurologic decline after SCI.

“

A

“1. post-traumatic syringomyelia.
2. tethered spinal cord.
3. peripheral nerve entrapment.
4. myeloradiculopathy (late spinal cord/root compression from degenerative changes or instability).
Ref: SC medicine principles practice textbook pg 832-33.

  1. any neuromuscular disease potentially (motor neuron disease, NMJ disorders, diabetic polyneuropathy, cervical radiculopathy, etc). GL thoughts.
  2. Recurrence of spinal cord tumour. EK thoughts
  3. inadequate spine decompression; review notes.”
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5
Q

What must be ruled out in a SCI patient with fever and normal WBC?

A

“1. heterotopic ossification
2. DVT
Ref: D Hill.”

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6
Q

Define HO, list 4 associated conditions and 4 complications.

A

“Heterotopic ossification is the formation of pathological (lamellar) bone in muscle or soft tissue where it does not usually occur (SCIRE – HO document; ERABI module 11; J Rehabil Med 2005; 37: 129–136).

CONDITIONS:

  1. SCI.
  2. TBI.
  3. soft tissue/MSK trauma.
  4. burns.
  5. post arthroplasty.
  6. post-radiation therapy (rare).

COMPLICATIONS:

  1. pain.
  2. decreased ROM./ankylosis ie joint fussion
  3. pressure ulcers.
  4. neurovascular compression.
  5. increased spasticity.
  6. phlebitis.”
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7
Q

“What percentage of pts with SCI develop HO (heterotopic ossification)?
What percentage of HO is clinically significant?
When does HO usually occur after SCI?”

A

“20-30% develop HO.
10% of those with HO is clinically significant (affects ROM, ADL, mobility).
HO usually occurs within 4 months of SCI.
Ref: Braddom, pg 1335.

13-57% pts with SCI develop HO.
20% of HO is clinically significant, with 8% progressing to join ankylosis.
Within 6 months post SCI, with peak at 2 months.
Ref: Delisa pg 695.”

scire: 3-12 weeks after spinal cord injury. Individuals with SCI typically present with joint and muscle pain, parasthesias and tissue swelling in the involved region, accompanied by a mild fever

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8
Q

name 4 psychiatric, social, or cognitive complications after SCI

A 
"1. depression & suicide.
2. anxiety.
3. social isolation.
4. substance abuse issues.
5. physical/sexual abuse.
6. financial issues.
Ref: Spinal cord medicine principles and practice textbook chapter 65, 66."
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9
Q

What factors increase the likelihood of RTW (return to work) post-SCI?

A

“ENVIRONMENTAL BARRIERS:

  1. able to drive.
  2. job accommodation

NON-MODIFIABLE:

  1. Younger age (declines after 50yo)
  2. Male
  3. Caucasian

PSYCHOSOCIAL FACTORS:

  1. personality.
  2. depression (lack of).
  3. Greater formal pre-injury education

INJURY RELATED FACTORS:

  1. less severe injury.
  2. paraplegia (versus tetraplegia).
  3. longer duration since injury.
  4. AIS D injury
  5. Calendar year after passage of Americans with Disabilities Act
  6. Nonviolent SCI etiology

MODIFIABLE FACTORS:

  1. Married
  2. Employed at time of injury
  3. Greater motivation to return to work
  4. Lower level of social security disability benefits

Ref: Delisa p666; http://www.scireproject.com/case-studies/case-7-mrs-f-l/return-to-work.”

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10
Q

What percentage of SCI individuals return to work?

A

“62% of Canadians with SCI remain unemployed.
Large variation in the world – 20-70%.
Ref: SCIRE http://www.scireproject.com/case-studies/case-7-mrs-f-l/return-to-work “

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11
Q

Name 6 predictors of independent living for pts with an SCI

A 
"1. Marital status.
2. Transportation barriers.
3. Education level.
4. economic disincentives.
5. disability severity (berthed index).
Ref: Arch Phys Med Rehabil. 1984 Feb;65(2):66-73."
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12
Q

Name 4 predictors of discharge to nursing home.

A

“1. ventilator-dependent.
2. older age.
3. tetraplegic with non-useful motor recovery.
4. unmarried.
5. unemployed.
6. medicaid or health maintenance organization (HMO) insurance.
Ref: Delisa pg 666.”

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13
Q

Name 5 changes in bowel function that occur after SCI?

A

“STOMACH:

  1. Delayed gastric emptying
  2. Post-prandial abdominal distension

INTESTINE:

  1. Increased transit time
  2. Decreased bowel/colonic motility (eg. GMCs).
  3. Constipation

SPHINCTER:
1. Loss of sphincter control

GENERAL:
1. Autonomic dysreflexia with Bms

Ref: SCIRE, bowel management; Braddom pg 627.
Notes: UMN vs LMN injury?”

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14
Q

Is it possible to be motor incomplete but sensory complete in terms of ASIA assessment in SCI?

A

“Yes – less than 1% of traumatic SCI will be motor incomplete and sensory complete.
However, usually a transient finding.
Ref: review notes Christine Short.”

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15
Q

Patient (incomplete paraplegia) has an ASIA LEMS (lower extremity motor score) of 10/50 at one week. What percent of patients would be expected to ambulate at one year, if the LEMS (lower extremity motor score) was the same at one month?

A

“LEMS is the total number summation of the grading of L/E muscles on ASIA exam.

LEMS at 1 month predicts community ambulation at 1 year:

a. 1-10: 45%/70%/21% (complete para/incomplete para/incomplete tetra).
b. 11-20: all paras/63% tetras
c. >20/50: ALL patients (para/tetra)

Ref: Spinal Cord Medicine pg 102.
Note: reference has a nice table to help predict ambulation.”

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16
Q

Four control devices for a power wheelchair.

A 
"Control devices can be activated by any reproducible movement of the body (arm, hand, wrist, fingertips or non upper arm movement (head, chin. Tongue, lips, mouth or lower limb).
Proportional control (responds to variable pressure) vs nonproportional control (binary, on/off).
1. Joy stick (t bar handle, knob, long extension handle, mouth stick).
2. Pneumatic controls (Sip and puff).
3. Chin or head pressure controls.
4. Voice activated switch.
5. Toggle switch.
6. myoelectric control switch.
7. Proximity sensing system.
8. Scanning system (eye).
9. Leaf switch .
10. Touch plate (foot).

Ref: Tan p329”

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17
Q

List 4 factors that lead to orthostatic hypotension in SCI.

A 
"1. loss of tonic sympathetic control.
2. altered baroreceptor sensitivity.
3. lack of skeletal muscle pumps.
4. cardiovascular deconditioning.
5. altered salt and water balance.
Ref: http://www.scireproject.com/case-studies/case-9-mrs-m-m/orthostatic-hypotension

MS CBS has orthostatic hypotension”

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18
Q

List 5 cardiovascular concerns in pts with SCI.

A

“1. hypotension (low baseline and orthostatic).
2. bradycardia/cardiac arrest.
3. autonomic dysreflexia.
4. reduced CV fitness, altered exercise capacity.
5. CAD (atypical presentation, silent ischemia).
6. PVD (lack of claudication symptoms, delayed presentations).
7. DVT.
8. drug related effects (succinylcholine-induced cardiac arrest).
Ref: SCI medicine pg 180.”

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19
Q

List 6 non-pharmacological treatments of Orthostatic Hypotension in a SCI pt

A

“LIFESTYLE:

  1. small, frequent meals (less vagal tone).
  2. increased salt (eg. Tablets)/water intake.
  3. adjust activities/therapies to periods of higher BP.
  4. avoid hot baths (vasodilation).
  5. avoid valsalva.
  6. avoid meds that drop BP (diuretics, antidepressants, alpha blockers, narcotics, caffeine).
  7. exercise.

POSITIONS:

  1. elevate head of bed during sleep (reduced nocturnal diuresis).
  2. avoid rapid changes in positioning.
  3. elevate wheelchair leg rests.

EQUIPMENT:
1. abdominal binders/compressive stockings.
2. tilt table, tilt in space wheelchair/recline.
3. FES (functional electrical stimulation) L2, SCIRE.
4. Biofeedback.
Ref: SCI medicine pg 181; Delisa pg 650, 689; http://www.scireproject.com/case-studies/case-9-mrs-m-m/orthostatic-hypotension/non-pharmacological-treatments.”

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20
Q

List 6 pharmacological treatments of orthostatic hypotension in a SCI patient.

A

“1. Mineralocorticoids: fludrocortisone (increased salt/water retention).

  1. sympathomimetics: alpha adrenergics (midodrine is selective, ephedrine is non-selective).
  2. NSAIDS (indomethacin, ibuprofen).
  3. clonidine.
  4. ergot alkaloids (SCIRE – limited evidence for effectiveness).
  5. erythropoietin.
  6. vasopressin analogs (desmopressin).
  7. somatostatin analogs (somatostatin, octreotide).
  8. L-DOPS, L-NAME: precursor to noradrenalin; central acting (SCIRE).

Ref: SCI Medicine pg 181; http://www.scireproject.com/case-studies/case-9-mrs-m-m/orthostatic-hypotension/pharmacological-treatments

SCIRE:

  1. Midodrine (Level 2 - effective)
  2. Fludrocortisone (4 - not effective)
  3. Ergotamine (5 - good with fludrocortisone)
  4. Ephedrine (5 - may prevent)
  5. L-DOPS (5 - with salt)
  6. L-NAME (2 - effective)

"”M FEEL”” good when my blood pressure is higher”

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21
Q

What is the mechanism of action of midodrine in orthostatic hypotension?

A

“1. A selective alpha 1 adrenergic agonist.
2. activates alpha-adrenergic receptors in arteriolar and venous vasculature, increasing vascular tone and blood pressure.

Ref: http://www.scireproject.com/case-studies/case-9-mrs-m-m/orthostatic-hypotension/pharmacological-treatments, SCIRE module”

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22
Q

What is the mechanism of action of fludrocortisone in management of orthostatic hypotension?

A

“1. mineralocorticoid.
2. causes kidneys to retain salt and hence increases water retention and plasma volume.

Ref: http://www.scireproject.com/case-studies/case-9-mrs-m-m/orthostatic-hypotension/pharmacological-treatments”

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23
Q

What is the mechanism of action for ephedrine in orthostatic hypotension?

A

“1. increases cardiac output.
2. induces peripheral vasoconstriction.
Ref: http://www.scireproject.com/case-studies/case-9-mrs-m-m/orthostatic-hypotension/pharmacological-treatments”

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24
Q

“Autonomic Dysreflexia:
4 cardinal symptoms.
List 4 signs.”

A

“HEAD/NECK:

  1. Headache
  2. pupillary constriction (blurred vision) - ?dilated pupils with lesion above T1? (ref: Review notes).
  3. sinus congestion.
  4. seizures.
  5. intracranial hemorrhage.

ABOVE LESION:

  1. sweating.
  2. flushing.

BELOW LESION:

  1. pallor, cool extremities.
  2. piloerection.
  3. bladder/sphincter contraction.
  4. stomach contraction.
  5. erection or penile emission.

CARDIAC:

  1. reflex bradycardia.
  2. cardiac arrhythmias (eg atrial fibrillation).
  3. myocardial infarction.
  4. increased BP >20-40 mmHg above baseline (SCIRE: 20 mmHg above baseline).

OTHER:

  1. pulmonary edema.
  2. malaise.
  3. nausea.
  4. dry, cool pale skin (below lesion).
  5. anxiety.

LIFE THREATENING:

  1. spontaneous intracerebral hemorrhage.
  2. seizure.
  3. retinal hemorrhage.
  4. arrhythmia.
  5. myocardial infarction.
  6. cardiac ischemia.
  7. death.

Ref: Delisa pg 690-91.
Ref: 2003 -CMAJ article.
Ref: Review notes – Kathy Craven.
http://www.scireproject.com/case-studies/case-5-mr-c-m/autonomic-dysreflexia/clinical-features-of-ad

”

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25
Q

List 4 major steps in the pathophysiology of autonomic dysreflexia.

A

“1. strong noxious/non-noxious stimulus (eg. Bladder) travels proximally via spinothalamic and posterior columns below SCI.

  1. massive reflex sympathetic activity from thoracolumbar sympathetics (SNS), causing massive vasoconstriction (splanchnic vasculature) and hypertension (HTN).
  2. brain detects HTN via baroreceptors and CN 9/10.
  3. Brain responds via massive Parasympathetic (PSNS) response:
    a. descending inhibitory impulses to block sympathetic outflow (impaired from SCI).
    b. slowing heart rate via vagus (compensatory bradycardia).

Ref: Review notes – Kathy Craven.”

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26
Q

List 5 potential triggers of autonomic dysreflexia.

A

“1, BLADDER: Infection, Distension, Urinary tract , Urethral distension, Instrumentation, Calculus, outlet obstruction.

  1. GI: Distension, Instrumentation, Infection or inflammation, Ulceration, Reflux, Anorectal Distension, Instrumentation, Hemorrhoids, Anal fissure
  2. DERM: Pressure sore, Ingrown toenail
  3. MSK: Heterotopic ossification, Fracture, Joint dislocation
  4. REPRODUCTIVE: Labour and delivery, Menstruation, Testicular torsion, Ejaculation, Intercourse
  5. HEME: Deep vein thrombosis, Pulmonary embolism
  6. CNS: Syringomyelia
  7. MEDS: Nasal decongestants, Sympathomimetics, Misoprostol
    Ref: CMAJ • OCT. 28, 2003; 169 (9); review notes Kathy Craven.”
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27
Q

List 5 pharmacological treatments for autonomic dysreflexia (HTN).

A

“CARDIAC:
1. nifedipine (Level 2 - may be useful during cystoscopy and other dx/tx procedures)

PROSTAGLANDIN E2 (Blood vessels):

  1. nitrates (nitropaste 2%) (level 5 - no studies shown effectiveness)
  2. captopril (level 4) [?blood vessels -> acts on kidneys]
  3. prazosin alpha-1 selective (level 1 - reduce severity and duration of episodes)

SKIN:
1. phenoxybenzamine (Level 4 - not known)

BLADDER:
1. terazosin (Level 4 - may have positive effects on incontinence and AD)

SCROTUM
1. sildenafil (Level 2 - no effect during ejaculation)

Ref: http://www.scireproject.com/case-studies/case-5-mr-c-m/autonomic-dysreflexia/pharmacological-treatments-ad (this reference categorized meds as above)”

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28
Q

List 4 incomplete SCI syndromes

A 
"1. Central cord Syndrome
2. Brown-Sequard syndrome
3. Anterior cord syndrome
4. Posterior cord syndrome
5. Conus Medullaris syndrome
6. Cauda Equina Syndrome
Ref: Cuccurullo pg 554.

Interestingly, posterior cord syndrome is not listed under the ASIA sheet”

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29
Q

Brown-Séquard syndrome. Name four key clinical features.

A

“C = contralateral, I = ipsilateral.

  1. PAIN and TEMPERATURE impairment below level of lesion (C).
  2. VIBRATION and PROPRIOCEPTION impairment below level of lesion (I).
  3. loss of ALL SENSORY modalities at level of lesion (I).
  4. MOTOR impairment (UMN) at and below level of lesion (I).
  5. FLACCID motor weakness at level of lesion (I).
  6. Can have UMN dysfunction of B/B, however favorable recovery.

Ref: Delisa pg 676.”

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30
Q

2 causes of central cord syndrome

A

“1. Hyperextension injury with cervical spondylosis
Ref: Cuccurullo pg 554.

  1. Syrinx/syringomyelia.
  2. expanding intramedullary mass/tumour
    Ref: 2008 – AAN – spinal cord anatomy, localization, and overview of spinal cord syndromes.
  3. Fracture dislocation
  4. Compression Fracture
    Ref:?”
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31
Q

3 clinical findings of anterior cord syndrome

A

“1. bilateral weakness below lesion.
2. bilateral loss of pain/temperature.
3. preserved vibration/proprioception below lesion.
Ref: Cuccurullo pg 555.”

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32
Q

When does hypercalcemia usually occur post-SCI?

A

“4-8 weeks after spinal cord injury (range 2 weeks-6 months).
More common in: young adolescent males, tetraplegic > paraplegic.
Ref: Cuccurullo pg 585.”

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33
Q

SCI 4 sx’s of hypercalcemia

A 
"1. N/V.
2. anorexia.
3. lethargy.
4. abdominal discomfort.
5. constipation.
6. diffuse MSK pain.
7. polydipsia/polyuria.
Ref: Delisa pg 691.
  1. mental confusion.
    Ref: SCI medicine pg 232; Delisa pg 1262.

Memory aid: Stones, bones, moans, psychic overtones”

34
Q

List 4 possible interventions for treatment of hypercalcemia.

A 
"1. IV fluid hydration (eg. 100-150 cc/hr NS).
2. foley catheter for high volumes.
3. furosemide (once rehydrated).
4. bisphosphonates (Etidronate 30-90 mg IV administration over 4-24 hours).
5. standing (decreases hypercalciuria).
6. calcitonin.
7. glucocorticoids.
Ref: delisa pg 691.
  1. early mobilization.
    Ref: Cuccurullo pg 585.”
35
Q

What are 5 predictors of mortality after SCI injury?

A

“1. Male

  1. Advanced age
  2. Ventilator dependence
  3. Injured by at of violence
  4. High injury level (particularly C4 or above)
  5. Complete injury
  6. Poor self-rated adjustment to disability
  7. Poor community integration
  8. Poor economic status indicators
  9. Having either Medicare or Medicaid third-party sponsorship of care

Ref: Delisa p666”

36
Q

List 5 ways to help prevent SCI.

A

“PRIMARY PREVENTION:

  1. safer automotive design.
  2. mandatory seatbelt legislation.
  3. warnings at diving pools, lakeshores.
  4. drunk driving legislation.

SECONDARY PREVENTION:

  1. minimizing neurologic damage.
  2. preventing death.

Ref: Review notes, Christine Short.”

37
Q

List 3 causes of traumatic spinal cord injuries.

A

“1. MVC (motor vehicle collisions): most common cause.
2. falls.
3. violence.
Ref: Review notes, Christine Short.”

38
Q

“What is the leading cause of death following SCI?
How do causes of death differ for tetra vs paraplegics?
What was the leading cause of death in SCI pts 30 years ago?”

A

“1. Diseases of respiratory system (most commonly, pneumonia).

  1. Heart disease.
  2. Septicemia (associated with pressure ulcers, UTI, respiratory infections).
  3. Cancer (lung, bladder, prostate, colon/rectum).

TETRAPLEGIA: Pneumonia is leading cause.
PARAPLEGIA: Heart disease, septicemia and suicide is leading cause.
ASIA D: Heart disease 24%, pneumonia 11%.

GU disease leading cause of death 30 years ago
Ref: Delisa p 667; Braddom pg 1296.”

39
Q

How long does spinal shock usually last for?

A

“Days to weeks.
Ref: SCI principles and practice, pg 27.

Spinal shock starts immediately – reflexes start to return within 24 hours.
Average – all reflexes return by 2-3 weeks. Some may not return up to 3 months post-injury. Ref: Cuccurullo – pg 554.

In most instances, reflex detrusor activity reappears after 2 to 12 weeks, but in some cases it may not return for as long a 6 to 12 months.
Ref: 1996 – Watanabe, urodynamics of SCI.”

40
Q

Define spinal shock. What are the main symptoms of spinal shock?

A

“Flaccid paralysis and extinction of muscle stretch reflexes below the injury level.
Ref: Delisa p667

The loss or depression of all or most spinal reflex activity below the level of the injury.

Symptoms include flaccid paralysis of muscles, hypotonia, absent myotactic reflexes, bowel reflexes, and bladder reflexes.
SCI principles and practice textbook, pg 27.”

41
Q

What is neurogenic shock?

A

“1. Clinical syndrome of vasodilation, hypotension, decreased peripheral vascular resistance (PVR), decreased preload, and bradycardia.

  1. Caused by unopposed parasympathetic tone from loss of sympathetic innervation from SCI.
  2. any SCI above L1 is at risk of some degree of neurogenic shock (relative loss of SNS).

Ref: SCI medicine pg 118.”

42
Q

Why must there be caution with fluid resuscitation in neurogenic shock? What is the alternative.

A

“1. Risk for neurogenic pulmonary edema.
2. Use vasopressors.

Ref: Delisa p668”

43
Q

What is the Forced Vital Capacity threshold that indicates ventilator compromise, when the patient may require assisted ventilation?

A

“VC less than 1L.

Ref: Delisa p668”

44
Q

What is the incidence of non-contiguous fractures post traumatic SCI injury?

A

“10-40%.

Ref: Delisa p668”

45
Q

Four control devices for a power wheelchair.

A

“1. Improving BLOOD FLOW to spinal cord

  1. Preventing LIPID PEROXIDATION.
  2. FREE RADICAL scavenger
  3. Anti-INFLAMMATORY function
  4. MEMBRANE stabilization.
  5. decrease vasogenic EDEMA.
  6. inhibit ENDORPHIN release from pituitary.

After an SCI, you want to Increase BM (blood flow, membrane stability), and decrease taxes by using E-FILE system.

Ref: Delisa p668; review notes – Christine Short.
NOTE: methylprednisolone less likely to produce neutropenia than other steroids; also crosses cell membranes more rapidly and completely.”

46
Q

How is methylprednisolone given post acute injury?

A

“1. IV Methylprednisolone within 8 hours of injury.

  1. 30 mg/kg IV bolus over 15 min, 45 min pause, then 5.4 mg/kg/h x 23 hours.
  2. length of treatment (varying evidence):
    a. NASCIS 2 (National Acute SCI study 2): continue for 23 hours.
    b. NASCIS 3: length of tx depends on when tx initiated:
    1. < 3 hours post injury: continue for 24 hours.
    2. 3-8 hours post injury: continue for 48 hours.
  3. No benefit of steroids for: > 8 hours post injury, penetrating injuries (increased risk infection).
  4. Complications: sepsis, pneumonia, hyperglycemia, acute corticosteroid myopathy

Ref: Delisa pg 668.
PVA consortium guidelines – no clinical evidence.
SCIRE: no review about acute mgmt of SCI found.
SCI principles and practice textbook: Confirms findings of the NASCIS 3 trial stated above.
Greenberg: highly controversial - study not replicable
- Exclusionary criteria from study: cauda equina, GSW, life-threatening morbidity, pregnancy, narcotic addiction, age < 13 yrs, pt on maintenance steroids”

47
Q

Define spinal instability

A

“White and Panjabi: “The loss of the ability of the spine, under physiologic loads, to maintain its pattern of displacement so that there is no initial or additional neurological deficit, no major deformity, and no incapacitating pain.”

Ref: Delisa p669”

48
Q

List 5 respiratory consequences from SCI.

A

“1. reduced ventilation (hypoxia, reduced exercise intolerance, sleep apnea)
2. reduced cough generation
3. increased risk of pneumonia and atelectasis
4. reduced compliance and compromised lung function with aging
5. reduced strength of voice
6. impaired posture
7. fatigue
Ref: SCIRE chapter on respiratory management after SCI.

  1. increased airway hyper-reactivity.
  2. decreased tidal volume.
  3. decreased response to hypercapnia.
    Ref: SCI medicine pg 159-160.”
49
Q

What are 4 important interventions to provide after an acute SCI? (Secrets)

A

“1. stabilize spine in neutral position (and image entire spine).
2. stabilize hemodynamic status (neurogenic shock) – IV fluids (SBP 95-100, HR 60-100bpm, urine output 30 mL/hr). [or pressors if needed]
3. IV methylprednisolone within 8 hours of injury (ideally within 3).
4. DVT prophylaxis (sequential compression stockings, LMWH within 72 hours).
Ref: Secrets pg 456.

  1. ABCs (obviously).
  2. GI/GU care (ileus prevention, foley).
  3. skin care (prevent pressure ulcers).
    Ref: SCI medicine chapter 7 – acute medical mgmt SCI.”
50
Q

List 5 non-traumatic causes of SCI in patients.

A 
"1. spinal stenosis with myelopathy.
2. neoplasm.
3. MS.
4. transverse myelitis.
5. infection.
6. vascular ischemia.
7. radiation myelopathy.
8. motor neuron disease.
9. syringomyelia.
10. vitamin B12 deficiency.
Ref: Cuccurullo pg 543."
51
Q

What are the two most common causes of non-traumatic spinal cord injuries?

A

“1. spinal stenosis.
2. spinal cord tumours.
Ref: Cuccurullo pg 543.”

52
Q

List two populations at risk for the formation of an epidural abscess?

A

“1. diabetes
2. immunocompromised
Ref: Cuccurullo pg 543

  1. IVDU
  2. CRF
  3. Alcoholism
    Ref: Greenberg p240
    “
53
Q

60yo male presents with localized pain in the region of L2. Labs show increased WBC and ESR. He also has a Hx of diabetes. Give 3 differential diagnosis.

A 
"1. osteomyelitis.
2. discitis.
3. compression fracture.
4. epidural abscess.
Ref: first principles."
54
Q

What is the most common type of odontoid fracture?

A

“Type 2 – through the base of the odontoid at the junction with C2 vertebra.
Treatment: halo vest, but surgery if unstable.
Ref: Cuccurullo pg 545.”

55
Q

What is the rectocolic (anorectal reflex) reflex and what nerve(s) mediate(s) it?

A

“Digital rectal exam (or feces) stretches bowel wall, which causes reflexive peristalsis of colon.

  1. The rectocolic reflex is a pelvic nerve-mediated pathway that produces propulsive colonic peristalsis in response to mechanical distension of the rectum.
  2. Stimulation of the parasympathetic pelvic splanchnic nerve can increase motility of the entire colon.
  3. Colorectal reflex – increase in rectal tone in response to colonic distension.
Pelvic nerve (S2-4, PSNS) - “P for Push”.
Ref: SC medicine principles and practice textbook, pg 341."
56
Q

What is the gastrocolic reflex?

A

“After food is ingested into the stomach, there is increased colonic motor activity. Mediated via vagus (parasympathetics).

Contraction of colon occurring with gastric distension.

Ref: SC medicine principles and practice textbook, pg 492.”

57
Q

What is the vesicoureteral reflux?

A

“VU reflux is when bladder wall hypertrophy occurs resulting in loss of VU angle, which normally prevents reflux back into ureters. Abnormal anatomy causes this reflux, leading to hydronephrosis.

Ref: Cuccurullo pg 570”

58
Q

Other than the rectocolic reflex, describe other reflexes regarding neurogenic bowel.

A

“1. Gastro-colic – colonic peristalsis after gastric distension – mediated by myenteric plexus

  1. Duodeno-colic - colonic peristalsis after duodenal distension
  2. Recto-anal/sphincter – distension of rectum causes internal sphincter to relax – mediated by pelvic (PNS)
  3. Gastro-ileal – ileal peristalsis after gastro distension – push stiff through ileocecal valve
  4. Intrinsic defecation reflex – recto-colonic reflex – intrinsic defecation reflex which is myenteric reflex that results in increased peristalsis secondary to feces in rectum
  5. Recto-colic defecation reflex – distension of rectum results in colonic peristalsis
  6. Vesico-rectal reflex: p641 old Braddom – increased intraabdominal pressure cause external anal sphincter tone – via pudendal nerve
  7. Recto-rectal or colo-colonic reflex – giant migratory reflex – proximal contraction and distal relaxation
  8. Rectal anal inhibitory reflex – once stool enters the rectum, the levator ani can relax, EAS and and, puborectalis muscle and this shortens the anal passage and makes it straight
  9. Holding reflex – contraction of the anal sphincter and puborectalis muscle tighten as feces enters rectum.

Ref:”

59
Q

3 physical exam maneuvers to assess neurological control of the rectum

A

“1. Anal wink - reflexive contraction of the external anal sphincter upon stroking of the skin around the anus – S2,3,4

  1. Bulbocavernosus reflex – mediated by S2,3,4 pudendal afferent and efferent fibers
  2. Anal tone and voluntary contraction – pudendal nerve
  3. Sensation - Pink prick in S4-5, Deep anal pressure

Ref:”

60
Q

What causes “cathartic bowel syndrome”?

A

“Cathartic colon

  • anatomical and physiologic change in colon due to chronic use of stimulant laxatives (> 3x/week x 1 year; other source says requires 15 years or more of laxative use)
  • symptoms: bloating, feeling of fullness, abdo pain, incomplete fecal evacuation
  • x-ray: atonic and redundant colon
  • complications: fluid/electrolyte imbalances, steatorrhea, protein-losing gastrorenteropathy, osteomalacia, vitamin/mineral deficiencies
  • treatment: discontinuation results in partial return of radiographic and functional changes in colon

Note: laxatives include cascara, castor oil, senna, etc.

Ref: www.medscape.com/viewarticle/437034_7; www.learningradiology.com/notes/ginotes/catharticcolonpage.htm”

61
Q

What is a Malone procedure and how does it work?

A

“aka MACE procedure – Malone antegrade continence enema.

MACE operation allows pt to self administer enemas into bowel near the start (ie. At cecum) instead of at the end (anus).

Requires RLQ laparotomy, mobilization of cecum, to bring appendix through abdo wall. Stoma is fabricated by amputating tip to expose the lumen. This opening can be catheterized by the patient.

Normally used in spina bifida, but can be used in SCI.

Ref: SCI medicine principles and practice textbook, pg 344.”

62
Q

“What is the incidence of DVT (deep vein thrombosis) in SCI?

When do most DVTs occur in SCI?”

A

“1. 9-100% (huge variability in studies) – take home point – preventable and treatable cause if potentially severe morbidity/mortality.
2. highest occurrence is within first 2 weeks post-injury.
NOTE: hence guidelines state to start DVT prophylaxis within 72 hours after SCI if no contraindications.

Other DVT numbers:

  1. incidence of fatal PE up to 2% in paraplegics.
  2. prevalence of DVT: 14-100%.

Ref: http://www.scireproject.com/case-studies/case-9-mrs-m-m/venous-thromboembolism”

63
Q

What is DVT treatment in a SCI patient with a long bone fracture

A

“12 weeks UH or LMWH.
2 weeks of compression stockings.

Note: all tx should be individualized to pt.

Ref: PVA guideline – VTE, pg 1.”

64
Q

when should anticoagulation begin after SCI?

A

“Within 72 hours after SCI, provided there is no active bleeding or coagulopathy.

PVA guideline – VTE, pg 1.”

65
Q

What is Well’s Criteria?

A

“In those with suspected DVT, a clinical assessment of probability can be useful to determine which tests to perform. The most studied clinical prediction rule is the Wells score.

When 9 CATS fall into the well, all minus 2 DIE from a DVT.
S3 = Samsung Galaxy S3. I2 = iPhone2

Wells score or criteria: (possible score −2 to 9)

  1. Cancer - active (treatment within last 6 months or palliative): +1 point
  2. Alternative diagnosis at least as likely: −2 points
  3. Tender - localized tenderness along the deep venous system: +1 point
  4. Swollen
    - Swollen unilateral superficial veins (non-varicose, in symptomatic leg): +1 point
    - Calf swelling ≥ 3 cm compared to asymptomatic calf (measured 10 cm below tibial tuberosity): +1 point
    - Swelling of entire leg: +1 point
  5. DVT - previous documented DVT: +1 point
  6. Immobility
    - Paralysis, paresis, or recent cast immobilization of lower extremities: +1 point
    - Recently bedridden ≥ 3 days, or major surgery requiring regional or general anesthetic in the past 12 weeks: +1 point
  7. Edema - unilateral pitting edema (in symptomatic leg): +1 point

Those with score of ≥2 have ≥28% chance of having DVT, those with a lower score have 6% odds. Alternatively, Wells scores can be categorized as high if greater than two, moderate if one or two, and low if less than one, with likelihoods of 53%, 17%, and 5% respectively

Ref: http://en.wikipedia.org/wiki/Deep_vein_thrombosis#Probability”

66
Q

What risk factors predispose SCI patients to DVT?

A 
"1. Virchow's triad (venous stasis, endothelial damage, hypercoagulability).
2. dehydration.
3. administration of blood products.
4. injury to soft tissue and long bones.
5. higher level of injury.
6. complete injury.
7. male > female (5:3).
Ref: review notes Christine Short."
67
Q

what is the appropriate treatment dose of tinzaparin for DVT in SCI?

A

“The approved dose of tinzaparin sodium for the treatment of established DVT with or without PE is 175 anti-factor Xa IU per kilogram of body weight.
Ref: Wikipedia.”

68
Q

What are indications for an IVC filter in an SCI patient?

A

“1. failed anticoagulant prophylaxis

  1. contraindications to anticoagulation (active bleeding in sites that can’t be controlled – CNS, GI, lungs)
  2. high tetras (C2 or 3) motors.
  3. poor cardiopulmonary reserve
  4. thrombus in IVC despite anticoagulant prophylaxis.
  5. high risk of suffering PE or reoccurrence of PE.

Note: IVC filter NOT substitute for thromboprophylaxis. Also can increase risk of DVT, so remove filter should be considered.

SCIRE: L3 evidence that IVC filters significantly reduce risk of PE.

PVA guideline – VTE, pg 1; http://www.scireproject.com/case-studies/case-9-mrs-m-m/venous-thromboembolism/inferior-vena-cava-filter-prevention-of-pe-post-s.”

69
Q

What are the main risk factors in SCI that you would choose to prophylax them for DVT 12 weeks instead of 8?

A

“Demographics

  1. Age > 70
  2. Obesity

PMH

  1. Cancer
  2. Heart failure
  3. Previous thrombosis

SCI-related:

  1. Lower limb fracture
  2. IVC filter

PVA guideline – VTE, pg 1.”

70
Q

If applying compression stockings is delayed past 72 hours post SCI, what should be done before applying them?

A

“US to rule out DVT before applying compression stockings.

PVA guideline – VTE, pg 1.”

71
Q

What is the appropriate DVT prophylaxis regimen in acute spinal cord injury for a C4 ASIA A tetraplegic young male who is otherwise healthy.

A

“Compression boots 2 weeks (SCD – sequential compression devices).
LMWH or UH (monitor aPTT) started within 72 hours (if no bleeding, coagulopathy).
Continue for 8 weeks (uncomplicated complete motor injury) assuming he has no other risk factors (lower limb fractures, hx thrombosis, cancer, CHF, obesity, > 70 yrs old, IVC filter).

PVA guideline – VTE, pg 1.”

72
Q

Define the Neurological Level of Injury, according to ASIA.

A

“Sensory level: most caudal, normally innervated dermatome to both pinprick and light touch sensation.

Motor level: lowest key muscle function that has at least grade 3 (MMT in supine position), providing the key muscle fxns above that level are judged intact (grade 5, MMT).

NLI: most caudal segment of SC with normal sensory and antigravity motor fxn on both sides of the body, provided that there is intact sensory/motor fxn rostrally. Note motor/sensory levels may differ L and R, so the single NLI is the most rostral of these levels.

Ref: Kirshblum, The Journal of Spinal Cord Medicine 2011 VOL.34 NO.6”

73
Q

Define ASIA Impairment Scales A-D.

A

“A: complete – no sensory or motor function preserved in the sacral segments S4-S5.

B: sensory incomplete – sensory but not motor function is preserved below neurological level and incudes the sacral segments S4-S5, AND no motor function is preserved more than three levels below the motor level on either side of the body.

C: motor incomplete – motor fxn preserved below neurological level**, and more than half of the key muscle functions below the single neurological level of injury have a muscle grade <3 (0, 1, or 2).

D: motor incomplete – motor fxn preserved below neurological level**, and at least half (50% or more) of key muscle fxns below NLI have a muscle grade > or = 3 (3, 4, 5).

E: normal – sensation and motor fxn as tested by ISNCSCI graded as normal in ALL segments, and pt had prior deficits. If no SCI, no AIS grade.

Note: C and D: motor incomplete must meet one of two criteria:

  1. voluntary anal contraction
  2. sacral sensory sparing (S4/5 or deep anal pressure) with sparing of motor fxn more than 3 levels below motor level on that side of body (even. Non-key muscle fxns).

Note:
B vs C: use MOTOR LEVEL on each side to distinguish.
C vs D: use the single NLI to distinguish.

Ref: Kirshblum, The Journal of Spinal Cord Medicine 2011 VOL.34 NO.6”

74
Q

Describe the way to test C5 in ASIA exam (grade 0-5).

A

“Biceps Brachii, brachialis.
Grade 3
Patient Position: The shoulder is in neutral rotation, neutral flexion/extension, and adducted. The elbow is fully
extended, with the forearm in full supination. The wrist is in neutral flexion/extension.

Examiner Position: Support the wrist.

Instructions to Patient: “Bend your elbow and try to reach your hand to your nose.”

Action: The patient attempts to move through the full range of motion in elbow flexion.

Grades 4 & 5
Patient Position: The shoulder is in neutral rotation, neutral flexion/extension, and adducted. The elbow is flexed to 90° and the forearm is fully supinated.

Examiner Position: Place a stabilizing hand on the anterior shoulder. Grasp the volar aspect of the wrist and exert a pulling force in the direction of elbow extension.

Instructions to Patient: “Hold your arm. Don’t let me move it.”

Action: The patient resists the examiner’s pull and attempts to maintain the elbow flexed at 90°.

Grade 2
Patient Position: The shoulder is in internal rotation and adducted with the forearm positioned above the abdomen, just below the umbilicus. The elbow is in 30° of flexion. The forearm and wrist are in neutral pronation/supination. Sufficient flexion of the shoulder must be permitted to allow the forearm to
comfortably move over the abdomen.

Examiner Position: Support the arm.
Instructions to Patient: “Bend your elbow and try to bring your hand to your nose.”

Action: The patient attempts to move the elbow through a full range of motion in elbow flexion.

Grades 0 & 1
Patient: The patient is in the grade 2 position with the shoulder in internal rotation and adducted. The palm and ventral forearm are positioned above the abdomen. The elbow is in 30° of flexion. The forearm and wrist are in neutral pronation/supination. Sufficient flexion of the shoulder must be permitted to allow the forearm to comfortably move over the abdomen.

Examiner Position: One hand supports the forearm while the other hand palpates the biceps tendon in the cubital fossa. The belly of the biceps brachii muscle may also be palpated or observed for movement.

Instructions to Patient: “Bend your elbow and try to bring your hand to your nose.”

Action: The patient attempts to move the elbow through a full range of motion in elbow flexion.

Ref: International Standards for the Classification of Spinal Cord Injury Motor Exam Guide 2008.”

75
Q

Describe the way to test C6 in ASIA exam (grade 0-5).

A

“ECRL, ECRB (note: not ECU, which is more C7 or 8).
Grade 3
Patient Position: The shoulder is in neutral rotation, neutral flexion/extension, and adducted. The elbow is fully extended, the forearm is fully pronated, and the wrist flexed.

Examiner Position: One hand supports the distal forearm to allow the wrist to be pre-positioned in sufficient flexion for testing.

Instructions to Patient: “Bend your wrist upwards. Lift your fingers toward the ceiling.”

Action: The patient attempts to extend the wrist through a full range of motion.

Grades 4 & 5
Patient Position: Same as grade 3, except the wrist is fully extended.

Examiner Position: Grasp the distal forearm to stabilize the wrist. Apply pressure across the metacarpals in a downward direction toward flexion and ulnar deviation (since testing ECRL/ECRB, not ECU).

Instructions to Patient: “Hold your wrist up. Don’t let me push it down.”

Action: The patient resists the examiner’s push and attempts to maintain the wrist in the fully extended position.

Grades 0, 1 & 2
Patient Position: Position the patient with the arm resting on the exam table. The shoulder is in neutral flexion/extension, neutral rotation, and adducted. The elbow is fully extended. The forearm is in neutral pronation-supination and the wrist fully flexed. The patient may also be positioned with the shoulder in slight flexion, internal rotation, and adducted, with the patient’s arm above the abdomen. The elbow is flexed to 90° and the forearm is in full supination. The wrist is flexed.

Examiner Position: Support the forearm and ask the patient to bend the wrist backwards into extension. For trace function, palpate the radial wrist extensors just proximal to the wrist, on the radial aspect of the distal forearm. Observe the muscle belly for movement.

Instructions to Patient: “Bend your wrist backwards.”

Action: The patient attempts to extend the wrist though a full range of motion in wrist extension.

Ref: International Standards for the Classification of Spinal Cord Injury Motor Exam Guide June 2008. “

76
Q

What is a common C6 muscle ‘substitution’ you must watch for on ASIA exam?

A

“pt supinating the forearm (eg. C5, biceps), causing wrist extension passively via gravity.

Ref: International Standards for the Classification of Spinal Cord Injury Motor Exam Guide June 2008. “

77
Q

Describe the way to test C7 in ASIA exam (grade 0-5).

A

“C7 Elbow Extensors| Triceps
Grade 3
Patient Position: The shoulder is in neutral rotation, adducted, and 90°of flexion. The elbow is fully flexed with the palm of the hand resting by the ear.

Examiner Position: Support the upper arm.

Instructions to Patient: “Straighten your arm.”

Action: The patient attempts to move through the full range of Elbow extension.

Grades 4 & 5
Patient Position: Same as grade 3, except the elbow is in 45° of flexion.

Examiner Position: Support the upper arm. Grasp the wrist and apply resistance to the distal forearm in the direction of elbow flexion.

Instructions to Patient: “Hold this position. Don’t let me bend your elbow.”

Action: The patient resists the examiner’s pressure and attempts to maintain the position of the elbow in 45° of flexion.

Grade 2
Patient Position: The shoulder is in internal rotation and adducted, with the forearm positioned above the abdomen. The forearm is in neutral pronation/supination. The elbow is fully flexed. When checking Grade 2, sufficient flexion of the shoulder must be permitted to allow the forearm to clear and move over
the chest and abdomen.

Examiner Position: Support the patient’s arm.

Instructions to Patient: “Straighten your arm.”

Action: The patient attempts to move through the full range of elbow extension.

Grades 0 & 1
Patient Position: Maintain the grade 2 position with the shoulder in internal rotation and adduction, and the forearm positioned above the abdomen. The forearm is in neutral pronation/supination and the elbow is in 30° of flexion.

Examiner Position: Support the arm. For trace function, palpate the distal triceps at its insertion on the olecranon. The belly of the triceps muscle may also be palpated and observed for movement.
Instructions to Patient: “Straighten your arm.”

Action: The patient attempts to fully extend the elbow.

Ref: International Standards for the Classification of Spinal Cord Injury Motor Exam Guide June 2008”

78
Q

What are common C7 muscle substitutions one must watch for during the asia exam?

A

“1. ER of shoulder (C5/6, infraspinatus)

  1. quickly flexing/relaxing elbow flexors (C5)
  2. triceps spasticity.

Ref: International Standards for the Classification of Spinal Cord Injury Motor Exam Guide June 2008”

79
Q

Describe the way to test C8 in ASIA exam (grade 0-5).

A

“C8 Long Finger Flexors| FDP
Grade 3
Patient Position: The shoulder is in neutral rotation, neutral flexion-extension, and adduction. The elbow is fully extended with the forearm fully supinated. The wrist is in neutral flexion-extension. The (MCP) and (PIP) are stabilized in extension.

Examiner Position: Using two hands grasp the patient’s hand and stabilize the wrist In neutral. Secure the PIP and MCP joints in extension with both hands while isolating the middle finger for testing. Stabilize the volar aspect of the 3Rd middle phalanx with the thumb of the opposite hand. As an alternate method, 1 hand may be used to stabilize instead of 2. The PIP and MCP joints are stabilized as previously described, with the thumb of the stabilizing hand now securing the middle phalanx.

Instructions to Patient: “Bend the tip of your middle finger.”

Action: The patient attempts to flex the (DIP) joint through the full range of motion in flexion.

Grades 4 & 5
Patient Position: The same as grade 3, except the DIP joint is fully flexed.

Examiner Position: Stabilize the wrist, MCP and PIP joints as in grade 3. Apply pressure with the tip of the finger or thumb against the distal phalanx of the patient’s middle finger.

Instructions to Patient: “Hold the tip of your finger in this bent position. Don’t let me move it.”

Action: The patient attempts to maintain the fully flexed position of the DIP joint, and resist the pressure applied by the examiner in the direction of finger extension.

Grades 0, 1 & 2
Patient Position: The shoulder is in neutral rotation, neutral flexion-extension, and adduction. The elbow is fully extended. The forearm is in neutral pronation-supination and the wrist in neutral flexion-extension. The MCP and PIP joints are stabilized in extension.

Examiner Position: Stabilize the wrist in neutral and the MCP and PIP joints in extension. For trace function, palpate the tendons of the long finger flexors or observe the muscle belly for movement.

Instructions to Patient: “Bend the tip of your middle finger.”

Action: The patient attempts to flex the (DIP) joint through the full range of motion in flexion.

Ref: International Standards for the Classification of Spinal Cord Injury Motor Exam Guide June 2008”

80
Q

what are common C8 muscle substitution?

A

“Grade 1-3: active wrist extension. May cause Involuntary movement of the DIP (tenodesis).

grades 4 and 5, hand intrinsics or the flexor digitorum superficialis.”

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