4 - SCI Complications Flashcards
What are 4 important interventions to provide after an acute SCI? π
π‘ Think about acute spine trauma and immobility measures.
- Stabilize spine in neutral position (and image entire spine).
- Stabilize hemodynamic status (neurogenic shock) β IV fluids or vasopressors
- IV methylprednisolone within 8 hours of injury (ideally within 3).
- DVT prophylaxis (LMWH within 72 hours).
- GI/GU care (ileus prevention, foley).
- Skin care (prevent pressure ulcers).
Ref: Secrets pg 456.
Ref: SCI medicine chapter 7 β acute medical mgmt SCI.
List 3 causes of neurologic decline / sudden deterioration after SCI. ππ EXAM
- Post-traumatic syringomyelia.
- Tethered spinal cord.
- Peripheral nerve entrapment.
- Myeloradiculopathy (late spinal cord/root compression from degenerative changes or instability).
Ref: SC medicine principles practice textbook pg 832-33.
Define spinal shock.
What are the main symptoms of spinal shock?
Duration? ππ
Spinal Shock
Temporary loss or depression of all spinal reflex activity below the level of the lesion
Symptoms
- Sensory loss
- Flaccid & hyporeflexic weakenss
- Autonomic βBBSHβ
- Hypoactive Bowel, Bladder
- Hypothermia, No piloerection, No sweating.
- Bradycardia, hypotension
Duration
Spinal shock usually lasts for days or weeks after spinal cord injury and the average duration is 4 to 12 weeks
Cuccurollo 4th Edition Chapter 7 SCI pg556
DeLisa 5th Edition Chapter 27 SCI Rehab pg667
Four-Phase Model of Spinal Shock, Duration/Phases of Spinal Shock ππ
Phase 1: Areflexia (0 to 24 Hours)
Phase 2: return of planter reflex, then BCR and anal wink. (1-3 Days)
Phase 3: Early hyper-reflexia (3 weeks to 3 months)
Phase 4: Spasticity and hyper-reflexia (1 to 12 months)
Braddom 5th Edition Chapter 49 SCI pg1054
Cuccurollo 4th edition Chapter 7 SCI pg557
Reflexes Returning After Spinal Shock Which one is the first? what is the clinical correlation for each one?
1- Delayed plantar response
First to return after spinal shock
Correlation with complete injuries & poor prognosis for lower extremity (LE) recovery.
2- Bulbocavernosus reflex (BCR)
Return within 24 hours
Reflex innervation of S2βS4 (bowel and bladder) is present
If not present by 24 hours, LMN injury may be suspected
3- Perianal sphincter reflex (anal wink)
Perianal stimulation causes contraction of the anal sphincter
Similar clinical correlation with BCR.
Cuccurollo 4th Edition Chapter 7 SCI pg556-557
Spinal vs neurogenic shock.
What are the main symptoms of spinal shock? Duration? ππ
Cuccurollo 4th Edition Chapter 7 SCI pg556
DeLisa 5th Edition Chapter 27 SCI Rehab pg667
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6218357/
Ref: SCI medicine pg 118.
Reflexes Returning After Spinal Shock
Which one is the first?
What is the clinical correlation for each one?
π‘ Return of reflexes indicated resolution of spinal shock, unless there is LMN injury or misdiagnosis.
1- Delayed plantar response
First to return after spinal shock
Correlation with complete injuries & poor prognosis for lower extremity (LE) recovery.
2- Bulbocavernosus reflex (BCR)
Return within 24 hours
Reflex innervation of S2βS4 (bowel and bladder) is present
If not present by 24 hours, LMN injury may be suspected
3- Perianal sphincter reflex (anal wink)
Perianal stimulation causes contraction of the anal sphincter
Similar clinical correlation with BCR.
Cuccurollo 4th Edition Chapter 7 SCI pg556-557
Non-Pharmacological Interventions for Spasticity in SCI
π‘ Active exercise interventions such as hydrotherapy, FES-assisted cycling and walking and robot-assisted exercise may produce short-term reductions in spasticity.
- Passive Movement or Stretching (i.e. Prolonged Standing)
- Electrical passive pedaling systems
- Robot-Assisted Movement [Level 1b]
- Functional Electrical Stimulation [Level 4] β short term only
- Tilt Table Standing [Level 4]
- Body Weight Support Treadmill Training [Level 4]
- Segway device for dynamic standing [Level 4]
- Hydrotherapy [Level 4] β not more effective than conventional rehabilitation alone
- Taping [Level 1b] β short-term effects of decreasing spasticity
- TENS [Level1a] β may last for up to 24 hours
- Massage [Level 4] β effect lasting no longer than a few minutes, good for warmup
- Cryotherapy [Level 4] β reduce muscle spasticity for up to 1 hour
- Extracorporal Shock Wave Therapy [Level 4] β need 3+ sessions
- Repetitive Transcranial Magnetic Stimulation [Level 1a] β short-term effect
https://scireproject.com/wp-content/uploads/spasticity-following-a-SCI-version-6.0.compressed.pdf
To simplfy physiotherapy plan of thoughs
- Passive therapy: Stretch, Tilting Table
- Active therapy: Cycling, Hydrotherapy
- Assisted Devices: FES, Robotic, Treadmill, Orthosis
Pharmacological Interventions for Spasticity in SCI
1- Oral Baclofen Level 1a evidence
GABA-B agonist
Starting 5mg three times daily up to 80-100mg in 4 divided doses
Oral baclofen is inferior to botulinumtoxin A injection and oral tolperisone by 6 weeks of spasticity treatment in people with SCI.
2- Intrahtecal Baclofen Level 1a evidence
GABA-B agonist
Up to 100mcg/daily
Good for spasticity, but not functional outcome.
3- Tizanidine (Sirdalud) Level 1a evidence
Ξ±2-adrenergic agonist
Effective dose 12-16mg in three divided doses
Starting 2mg 2-3 times daily and increase every 3-7 days
4- Clonidine (Catapres) Level 1b evidence
Ξ±2-adrenergic agonist
0.02 mg/day and systematically increased to an optimal level (0.05-0.25mg/day).
5- Botulinum toxin (BTX) Level 1b evidence
Good for focal muscle spasticity, but not quality of life
More Details
https://scireproject.com/wp-content/uploads/spasticity-following-a-SCI-version-6.0.compressed.pdf
What is the definition of deafferentation pain? π
List 2 clinical features of deafferentation pain after SCI.
Another Q: What are the sources of pain in SCI patient?
1- Central or Neurogenic Dysesthetic Pain
Central pain
Pain that is initiated by a primary lesion within the CNS.
Deafferentation pain
Type of pain that results from complete or partial interruption of afferent nerve impulses. Result from lesions that interrupt the spinothalamic pathways
Causes
- CNS (such as thalamic pain, brainstem infarction with bulbar pain)
- PNS (such as peripheral nerve injury, trigeminal neuropathic pain)
- Post-herpetic neuralgia: pain post shingles (viral skin infection)
- Central pain (pain after CNS injury)
- Phantom limb pain
- At or below the level of the lesion
- Burning, aching and/or tingling sensation
- Sensory loss (pain and temperature sensation)
- Abnormal sensory phenomena (allodynia, hyperalgesia, dysesthesias, hyperpathia).
2- Musculoskeletal or Mechanical Pain
Clinical features
- At or above the level of the lesion
- Nociceptive pain: from bone, ligaments, muscle, skin, other organs
C5 ASIA B developed burning pain in arms and hand one month after injury.
What is your most likely diagnosis?
Investigations to support your diagnosis?
Three classes of medications to treat.
DIAGNOSIS
- Deafferentation pain
INVESTIGATIONS
- EMG to rule out CTS
- MRI to rule out cervical radiculopathy
NON-PHARMACOLOGICAL
- Physical therapy [L1b-L2]
- Transcutaneous electrical nerve stimulation [L1b]
- Exercise [L1b-L2]
- Manual Therapy [L2] Osteopathy [L1b]
- Electrostimulation acupuncture [L1a-L2]
- Cognitive-behavioral pain management programs [L1b-L2]
PHARMACOLOGICAL
- ANTICONVULSANTS
- Gabapentin or pregabalin [L1]
- Lamotrigine for incomplete [L2]
- ANTIDEPRESSENT
- TCA, Amitriptyline [L1 Evidence]
- SSRI, Citalopram
- ANESTHETIC
- Subarachnoid lidocaine, IV ketamine [L1]
- Capsaicin [L4]
https://scireproject.com/wp-content/uploads/pain_management_FINAL_7.0-1.pdf
Ref: CMAJ 2006 β neuropathic pain a guide for the clinician; 2009 β pain after SCI β a review, Cardenas.
Explain Autonomic Dysreflexia (AD).
Why it happens in SCI above T6? π
List 4 major steps in the pathophysiology of autonomic dysreflexia.
Autonomic innervation of the GI tract
- Sympathetics T5-L2
- Parasympatheticsβ CN X and S2-S4
Splanchnic vessels innervation
- Innervated at T5-L2, constrict and raise the BP in response to stimulus
- Body canβt send parasympathetic signals to oppose it.
Pathophysiology
- Strong noxious/non-noxious stimulus (eg. Bladder) travels proximally via spinothalamic and posterior columns below SCI. (1-2)
- Massive reflex sympathetic activity from thoracolumbar sympathetics (SNS), causing massive vasoconstriction (splanchnic vasculature) and hypertension (HTN). (3-5)
- Brain detects HTN via baroreceptors and CN 9/10. (6)
- Brain responds via massive Parasympathetic (PSNS) response (7A-7B)
- Descending inhibitory impulses to block sympathetic outflow (impaired from SCI).
- Slowing heart rate via vagus (compensatory bradycardia).
Ref: Review notes β Kathy Craven.
List 8 Common Causes for Autonomic Dysreflexia (AD) ππ (OSCE Q) Risk factors for AD ππ
Risk Factors for AD
- High SCI level
- Previous AD episode
- Bowel and bladder dysfunction
- Urinary cathertrization
- Anticholenergic medications β s/e urinary retention and constipation
- Altered skin integrity
My Answer, just look for common causes of AD.
List 6 Signs and symptoms & 4 complications of Autonomic Dysreflexia ππ
MAIN SYMPTOMS
- Sudden rise in blood pressure of 20 to 30 mmHg above the personβs normal systolic blood pressure
ABOVE LESION
- Pounding or throbbing headache
- Blurred vision, Seeing spots
- Sinus congestion
- Widened (dilated) pupils
- Cardiac arrhythmias, atrial fibrillation
- Difficulty breathing or a feeling of chest tightness
- Profuse sweating
- Flushing
- Piloerection
BELOW LESION
- Dry and pale skin due to vasoconstriction
- Increased number and severity of muscle spasms
COMPLICATIONS
- Cerebral vascular accident (CVA)
- Subarachnoid hemorrhage (SAH)
- Intracerebral hemorrhage.
- Myocardial infarction (MI)
- Retinal hemorrhage
- Seizure
- Death
Cuccurollo 4th Edition Chapter 7 SCI pg564 Table 7-8
https://scireproject.com/wp-content/uploads/AD-Chapter-Mar-26-18-FINAL.pdf
Management and prevention of Autonomic Dysreflexia (AD) ππ (OSCE Q)
a. What are your initial 2 actions before doing a body survey?
b. How often do you monitor BP during this acute episode?
c. The BP is still elevated. What are the next 2 systems to check and what precautions do you need to take? ππ
SITTING
- Sit patient upright (the first aspect of treatment)
- Loosen all tight fitting clothing and devices.
BP MANAGEMENT
- Check blood pressure, and re-check every 2-5 minutes
- Nifedipine (Adalat, Procardia, Fast Acting CCB)
- 10mg sublingually or chew and swallow (1st line)
- Nitrates (Nitroglycerine)
- 0.3 to 0.6 mg sublingually or 0.2 to 0.4 mg/hr patch
- Nitropaste 0.5 inch up to 2 inches
- Captopril (Fast Acting ACE)
- 25mg sublingual
- Prazosin (Minipress)
- 0.5-1mg TID
- Seek medical attention if there is no reduction in blood pressure
STIMULUS
- Bladder: catheter, obstruction, change folyβs with Lidocaine application
- Bowel: constipation, hemorrhoid, anal fissure, PR with Lidocaine
- Skin: pressure ulcer, cellulitis, ingrown nail
- Others: Cardiorespiratory - MSK
PREVENTION
- Clonidine [Catapres]: Ξ±β-adrenergic agonist
- Spinal anesthesia prior to labour or diagnostic procedure
- Lidocaine with bowel and bladder care
SCIRE Guideline - Autonomic Dysreflexia
Cuccurollo 4th Edition Chapter 7 SCI pg564 Table 7-8
https://scireproject.com/wp-content/uploads/AD-Chapter-Mar-26-18-FINAL.pdf
Define poikilothermia. How to manage?
Poikilothermia
- Inability to regulate core body temperature
- People with SCI tend to have a higher body temperature in warm environments and a lower temperature in cold environments.
Brief explanation of heat regulation.
- Heat and cold signals are normally carried by afferent nerves to the hypothalamus
- Increase in core temperature, sympathetic inhibition occurs with vasodilation and sweating
- Decrease in core temperature causes a sympathetic stimulus, with vasoconstriction and shivering.
Cold environment
- Appropriate clothing should be worn
Hot environment
- Strenuous exercise to be avoided.
- Use cool, moist compresses to lower temperature
Distinguish Autonomic Dysreflexia (AD) from Preeclampsia ππ EXAM 2019 How to prevent AD in during labour?
Autonomic dysreflexia:
- Severe headache and increased BP occur in synchrony with uterine contractions.
- BP and symptoms normalize during relaxation of the uterus
Preeclampsia
- High BP is more persistent in an individual with preeclampsia.
- Renal insufficiency, Proteinuria (>300 mg)
- Elevated LFT
- Thrombocytopenia
Treatment
- Epidural anesthesia extending to T10 level
- Continue for at least 12 hours after the delivery or until AD resolves.
Cuccurollo 4th Edition Chapter 7 SCI pg 580
Define Orthostatic Hypotension ππ
Orthostatic Hypotension
- Decrease of 20 mm Hg in systolic and/or 10 mm Hg in diastolic blood pressure within 3 minutes in an upright position with or without postural symptoms.
Pathophysiology
- Upright position causes decrease in blood pressure (BP)
- Itβs triggered by tilting the patient upright to >60 degrees
- Aortic and carotid baroreceptors sense decrease in BP
- Lack of sympathetic outflow lead to impaired peripheral vasoconstriction
- Orthostasis lessens with time due to development of spinal postural reflexes which allow for vasoconstriction
Sympathetic Innervation
- T1βL2 outflow, which is activated in stressful situations to raise heart rate and blood pressure and to cause vasoconstriction to certain organs.
Cuccurollo 4th Editio Chapter 7 SCI pg563
Braddom 6th Edition Chapter 49 SCI pg1082 & Chapter 45 pg997
List 4 predisposing factors for Orthostatic Hypotension . π
- Changes to the autonomic nervous system (main reason)
- Cardiovascular deconditioning
- Low blood volume and salt levels in the blood
- Loss of muscle activity in the legs and trunk after SCI
- Medications side effects (baclofen, antihypertensives)
- Eating large meals (blood pooling into GI system)
- Exercise (in people with high level SCI have poikilothermia)
SCIRE Orthostatic hypotension - patient information
List 4 Sign and symptoms of Orthostatic Hypotension π
Signs
- Hypotension: Loss of sympathetic tone β decreased preload
- Tachycardia: Aortic & carotid baroreceptors respond to hypotension
Symptoms
- Lightheaded
- Dizziness
- Syncope
- Nausea
- Pallor
Cuccurollo 4th Editio Chpater 7 SCI pg563
Newly admitted SCI patient, after taking history and examining the patient, you noticed that he is having orthostatic hypotension. How would you manage?
List 6 NON-pharmacologic treatments of Orthostatic Hypotension in a SCI pt
Non-Pharmacological
- Gradual reposition, not to make fast adjustments
- Tilting Table or Recliner wheelchair
- Elastic stocking/abdominal binder
- Increase fluid intake
- Avoid heat
- Avoid large meals, eat small frequent meals
- Avoid unnecessary antihypertensive medications
- Avoid straining while defecation, use high fiber diet with stool softeners
Pharmacological
- Salt tablets 1 g four times a day
- Alpha-1 adrenergic agonist (Midodrine) 2.5-10mg TID β avoid in peripheral vascular disease
- Fludrocortisone (Mineralocorticoid) 0.1 mg OD up to QID β kidneys to retain salt and increases water retention and plasma volume
- Ergotamine
- Ephedrine (increases cardiac output and vasoconstriction)
- L-DOPS
DeLisa 5th Edition Chapter 26 Parkinson Disease pg650
Cuccurollo 4th Edition Chapter 7 SCI pg563-564 Table 7-8
SCIRE
Name 4 psychiatric, social, or cognitive complications after SCI
- Depression
- Suicide (young patients)
- Anxiety
- Social isolation
- Substance abuse (alcohol most common)
- Physical/sexual abuse
- Financial issues (high complete injury, unemployment)
Ref: Spinal cord medicine principles and practice textbook chapter 65, 66.
List the clinical features of depression post-SCI. π
π‘ DSM-5 criteria for major depressive disorder
At least 5 of the following symptoms have to have been present during the same 2-week period (and at least 1 of the symptoms must be diminished interest/pleasure or depressed mood:
- Depressed mood: For children and adolescents, this can also be an irritable mood
- Diminished interest or loss of pleasure in almost all activities (anhedonia)
- Significant weight change or appetite disturbance: For children, this can be failure to achieve expected weight gain
- Sleep disturbance (insomnia or hypersomnia)
- Psychomotor agitation or retardation
- Fatigue or loss of energy
- Feelings of worthlessness
- Diminished ability to think or concentrate; indecisiveness
- Recurrent thoughts of death, recurrent suicidal ideation without a specific plan, or a suicide attempt or specific plan for committing suicide
- The symptoms cause significant distress or impairment in social, occupational or other important areas of functioning.
- The symptoms are not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition.
List the clinical features of depression post-SCI. π
DSM-5 criteria for major depressive disorder
At least 5 of the following symptoms have to have been present during the same 2-week period (and at least 1 of the symptoms must be diminished interest/pleasure or depressed mood:
- Depressed mood: For children and adolescents, this can also be an irritable mood
- Diminished interest or loss of pleasure in almost all activities (anhedonia)
- Significant weight change or appetite disturbance: For children, this can be failure to achieve expected weight gain
- Sleep disturbance (insomnia or hypersomnia)
- Psychomotor agitation or retardation
- Fatigue or loss of energy
- Feelings of worthlessness
- Diminished ability to think or concentrate; indecisiveness
- Recurrent thoughts of death, recurrent suicidal ideation without a specific plan, or a suicide attempt or specific plan for committing suicide
- The symptoms cause significant distress or impairment in social, occupational or other important areas of functioning.
- The symptoms are not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition.
4 pre-morbid & 4 post-morbid factors predisposing to suicide in SCI.
List 4 risk factors for cardio-vascular diseases (CVD) in SCI patient. What is your preventive management?
π‘ Think of typical patient: immobility - obese - DM - smocks - poor diet
Risk Factors
- Tetraplegics and neurologically complete injuries
- Physical inactivity
- Increased obesity and visceral adipose tissue
- Higher prevalence of insulin resistance, diabetes, metabolic syndrome
- Decreased fat free mass
- Increased rate of smoking
- Low high-density lipoprotein (HDL)
- High total cholesterol and low-density lipoprotein (LDL)
Management
- Smoking cessation
- Modify diet
- Weight loss
- Increase activity levels: Exercise 3. per week (FES of arm ergometry)
- Pharmacotherapy used if HTN, hyperglycemia, and dyslipidemia do not respond to the previous actions
Cuccurollo 4th Edition Chapter 7 SCI pg589
How does the SCI level affect respiratory system? ππ
Functional outcome (Respiratory ability) based on SCI level ππ
Respiratory Innervation
- Diaphragm (innervated by C3βC5) is the major muscle of inspiration contributing approximately 65% to the vital capacity (VC).
- Abdominal muscles including the rectus abdominus, transversus abdominus, internal and external obliques (T4βL2 from nipple to umbilicus)
- Internal intercostal (II) muscles of the lower rib cage (T6βT12 lower ribs).
C3βC4
- Impaired diaphragm and all abdominal muscles
- Leading to respiratory failure
- Require ventilation & clearance aid (nebulization, suction and chest physiotherapy)
Above C8
- Intact diaphragm
- Loss of all abdominal and intercostal muscles
- Able to inhale partially (in supine position) with passive exhalation
- Impairing forceful expiration or cough.
- Require clearance aid (nebulization, suction and chest physiotherapy)
T1 through T5
- Intact diaphragm
- Impairment of all abdominal muscles
- Able to inhale partially (in supine position) with passive exhalation
- Impairing forceful expiration or cough.
- Require clearance aid (nebulization, suction and chest physiotherapy)
T5 through T12
- Intact diaphragm and partial abdominal muscles
- Able to inhale and exhale
- Impairing forceful expiration or cough.
- Require clearance aid (nebulization, suction and chest physiotherapy)
Cuccurollo 4th Edition Chapter 7 SCI pg589-590
A 17-year-old, newly SCl-injured, muscular man with C6 incomplete tetraplegic complains of lethargy and abdominal cramping.
What could it be?
What is your management?ππ
Diagnosis
- Immobilization hypercalcemia
- Appears 4 to 8 weeks after SCI
- 2 weeks to 6 months post-injury
Presentation
π‘ βpainful bones, renal stones, abdominal groans, and psychic moans,β
- BONE: Fatigue, Lethargy
- STONES: Polyuria, Polydipsia, Dehydration
- ABDOMEN: Constipation, Nausea & Vomiting
- PSYCH: Psychosis
Investigations
- Measurement of the total serum calcium adjusted for the total protein
- Serum ionized calcium (accurate test)
Treatment
- Early mobilization
- IV fluid hydration (eg. 100-150 cc/hr NS)
- Furosemide (Lasix) Once rehydrated
- Calcitonin can be used in resistant cases
- Bisphosphonates (Etidronate 30-90 mg IV administration over 4-24 hours)
Cuccurollo 4th Edition Chapter 7 SCI pg587
PMR Secrets 3rd Edition Chapter 55 SCI pg464
DeLisa 5th Edition Chapter 27 SCI pg691
PMR Secrets 3rd Edition Chapter 55 SCI pg464
What are 3 common causes of secondary hyperparathyroidism in SCI patients?
π‘ Why we have low calcium?
- low calcium intake
- reduced exposure to sunlight
- renal failure (not activating vitamin D)
SCI principles and practice textbook, pg 232
Patient complain of chronic back pain post SCI.
Charcot spine
- Progressive destructive arthropathy (vertebral joint degeneration)
- Occurrs after loss of neuroprotective sensation and proprioceptive reflexes causing insensate joint destruction
Presentation
- Chronic pain
- Autonomic dysreflexia
PMR Secrets 3rd Edition Chapter 55 pg 464 Q24
Risk factor of fractures in SCI π
π‘ Most common site of fracture is the supracondylar region of the femur
- Prior fragility fracture
- High alcohol intake
- Female gender
- Body mass index (BMI) <19
- Paraplegia
- Motor complete SCI
- Family history of fracture
Cuccurollo 4th edition Chapter 7 SCI pg588
