Lecture SCI - Secondary Pathologies Flashcards
2° Complications of SCI
Cardiovascular/Respiratory Integumentary Neurological Musculoskeletal Somatosensory GI/GU
Cardiovascular/Respiratory 2° Complications of SCI
6
Cardiac Arrhythmias Orthostatic hypotension Altered thermoregulation Autonomic Dysreflexia DVT/PE Respiratory Dysfn
Integumentary 2° Complications of SCI
Decubitus Ulcers
Neurological 2° Complications of SCI (2)
Spasticity
Syringomyelia
Musculoskeletal 2° Complications of SCI (4)
Osteoporosis
Fractures
Contractures
Heterotopic Ossification
Somatosensory 2° Complications of SCI (2)
Pain
Reflex Sympathetic Dystrophy
GI/GU 2° Complications of SCI
Bowel and Bladder Dysfunction
Altered Sexual Function
What is the single greatest factor leading to increase in hospital stay in patients with a spinal cord injury
Development of Decubitus ulcers
What type of WC would you use for a SCI and why would you not want the other kind
A tilt in space
Would not want a reliciner bc you would start sliding and will create a shear force
Cardiovascular Complications is from
Interruption btw receptor organs & brainstem
Interruption to ANS
Neurogenic Shock
What is the classic triad to neurogenic shock
- Hypotension –
due to loss of sympathetic tone (↓ systemic vascular resistance, & dilation of veins)
Hypovolemia (due to severe hemorrhage, inadequate fluid administration) - Bradycardia - heart less efficient and pumps slower - movement allows the heart to work a bit harder and pump better
- Hypothermia
What is Hypovolemia
Part of the classic triad of neurogenic shock
Due to severe hemorrhage, inadequate fluid administration
(Low volume)
How does orthostatic hypotension happen and what can be done to reduce it
orthostatic hypotension this can happen from supine to sitting bc you have an increase in demand in blood flow to the brain you make them move to make sure they dont pass out - the muscle pump is effective
Why would you use a tilt table?
to progressively help someone while they are sitting up
Graded upright positioning is the PT intervention of choice (i.e. ↑ HOB, recliners, tilt-in-space w/c, tilt table) 🡪 close BP monitoring!
If the tilt table doesn’t work to help orthostatic hypotension what else can be used?
compression garments
Pressure garments (TEDS & abdominal binders) May teach the Valsalva maneuver as preventative measure, but with much caution
How would someone present with Orthostatic hypotension
dizzy, pale and dry skin
Why do cardiac arrhythmias happen and what is the most common type
Also what makes it worse and when would it improve
Due to loss of sympathetic tone & unopposed vagal tone
Most common arrhythmia = Bradycardia
Worsened by stimulation of vagus n. (i.e. during tracheal suction, turning to prone, defecation)
Improves w/in a few weeks as spinal shock resolves
Which nerve is responsible for bradycardia and what does this nerve do
The vagus nerve
It is the longest of the cranial nerves, extending from the brainstem to the abdomen by way of multiple organs including the heart, esophagus, and lungs. Also known as cranial nerve X,the vagus forms part of the involuntary nervous system and commands unconscious body procedures, such as keeping the heart rate constant and controlling food digestion
How does the vagus nerve get stimulated
During tracheal suction, turning to prone, defecation
cardiac arrhythmias are due to
loss of sympathetic tone & unopposed vagal tone
What happens to thermoregulation with a SCI
it becomes altered
↓ thermoregulation below level of lesion
s/p SCI: the connection between the ANS & the cord is interrupted
How would a SCI pt present with altered thermoregulation
The patient will be unable to sweat when warm or shiver when cold below the level of the lesion
How does normal thermoregulation happen
Hypothalamus sends impulses via autonomic pathways to the cord, then through sympathetic outflow to the skin, initiating compensatory reactions to ↑ or ↓ temperature
Why do you have to make sure people are aware of altered thermoregulation
The higher the lesion, the greater the proportion of the body that is unable to maintain safe temperature
What SCI level is at risk for altered thermoregulation?
Above T5
What is altered thermoregulation called above T5?
Poikilothermic
Poikilothermic
Above T5
core temp adapts to temp of environment (can be misinterpreted as febrile)
Someone with altered thermoregulation should do what when they are working out and what should they do when the weather is cold
Should ice after strenuous activity to cool down, or dress warmly in cold weather
Why do we have to be aware of poikilothermic?
When we exercise we increase the temp of the core and the environment. These people get really warm and light headed
What are the 2 things that you worried about when working with a SCI?
Orthostatic hypertension and autonomic dysreflexia
Autonomic Dysreflexia aka, presents as, and what level of injury
Autonomic Hyperreflexia
Affects individuals with lesions >T6 level, where an uncontrolled reflex sympathetic discharge causes:
severe hypertension (>15-20 mmHg ↑ in SBP)
heart rate changes (typically reflexive bradycardia)
severe sweating & flushing
severe headache
piloerection
blurry vision
shivering
How is the treatment of Orthostatic hypertension and autonomic dysreflexia either the same or different?
How we treat them is very different. Orthostatic Hypertension, we would lay them back down and with someone has autonomic dysreflexia you have to keep them sitting up. (this is very important)
What do you have to avoid with autonomic dysreflexia
You want to avoid laying them down as much as possible. because they have Hypertension and a sympathetic reflex that tend to increase as they are lying down
keep them sitting up - avoid laying them down as much as possible, it increases as you lie back down
Signs of orthostatic hypertension:
Dizzy, skin is pallor, they get dry skin - if you see this you would immediately lie them back down (if you know the person well maybe take their BP and see if they adapt)
Signs of autonomic dysreflexia:
red face, HR dec. BP inc. they start sweating, severe HA and etc
Is autonomic dysreflexia serious
Consequences can be severe or even fatal!
Causes of autonomic dysreflexia
Caused by a noxious stimulus below the level of lesion (pt unaware 20 lack of sensation):
Blockage of urine output (kinked catheter or overflowing bag) Impacted bowel Pressure ulcer Ingrown toenail Tight clothing Fracture
Potential complications of autonomic dysreflexia
retinal hemorrhage, SAH, ICH, MI, Sz, death!
How would Autonomic Dysreflexia usually occur?
It occurs do to some restriction in their body. ie: wearing a belt, tight clothing or shoes you have to loosen them
Why do you have to loosen the clothing of someone who has autonomic dysreflexia?
Body is misreading the stimulus as noxious and responding very aggressively
What do you do if patient is going through autonomic dysreflexia
What do you do if patient is going through autonomic dysreflexia
1st thing - sit them up
2nd- look of restriction
3rd- if autonomic dysreflexia continues and BP does not drop it is a medical emergency - you will have to call for help
Autonomic Dysreflexia prevention
Early education of patient & caregivers
Symptom recognition
Immediate interventions
Is risk of PE by level
risk of PE is not by level but rather it is affected by amount of movement you do. that is why it is important to get people moving passively and actively and active assist as much as we can
Prevention & treatment of DVT
Rehab: Early mobilization; compression garments
Medical: Prophylactic Coumadin/Heparin; IVC filters
DVT is more common in
Tetraplegics
Risk factors for a DVT
↓ LE mvt & muscle pump, presence of LE fractures, hypercoagulability
Symptoms of DVT:
Edema
Redness
Tenderness/Pain*
Symptoms of PE: (6)
Dyspnea Tachycardia Hypotension Angina Hemoptysis Fever
What is hemoptysis and what is this a symptom for
coughing up blood
symptom of a PE
Respiratory Complications
of SCI
Pneumonia Aspiration Atelectasis Lung contusions hemopneumothorax (air and blood in the chest cavity) Rib fractures, etc.
Respiratory Complications
and lesion levels
(discuss 3 different levels)
Lesions above C4 -> paralysis of the diaphragm & intercostals ->mechanical ventilation
A lesion between C5-T12 spares the diaphragm, but limits the use of intercostals & respiratory accessory muscles
Complete lesions above T10
-> abdominal weakness & limited expiratory capacity (lack cough)
*This results in a diminished cough & an inability to expectorate lung secretions
Treatments for respiratory dysfunction
DBE, Diaphragmatic breathing
Assisted cough
Incentive Spirometry
Resistive Inspiratory Muscle Trainer – PFlex
What is the single greatest factor leading to ↑ in hospital length of stay and cost
Decubitus Ulcers
Common causes of decubitus ulcers
Poor B&B control can lead to skin maceration & infection
Hypertonia can lead to shearing forces, & in extreme cases, skin contact - movement is not volitional
Trauma, including tape burns
Nutritional deficiencies or comorbid health problems can ↓ healing
Which areas are of risk of a decubitus ulcer
Any WBing part is at risk:
Sacrum, ITs, heels, GTs, malleoli, med/lat knees, elbows, occiput, scapulae, etc.
Best treatment for Pressure ulcers
The best treatment is PREVENTION
Diligent skin care/protection & careful skin inspection
Pressure reliefs: turn every 2 hours in bed; every 15-20 minutes in W/C for a duration of 2 minutes
Power w/c – tilt backwards (do not recline)
Manual w/c – forward lean, sideway lean, triceps push up
If patient unable, caregiver must be taught to perform pressure reliefs
Positioning: Multipodus boots, pillows, specialty beds, prone carts, proper seating/positioning in w/c
Cushions: ROHO, J2 or J2 deep contour, Varilite
W/C setup – seat depth/width, seat to back angle, back height, truncal support, etc.
Mat evaluation – flexible vs. fixed deformities?
Intervention for decubitus ulcers
Intervention
Early on – use of pharmacological agents & wound care, nutritional monitoring, pressure relief
When ulcer is deep to the bone, surgery is warranted 🡪 myocutaneous rotational flap
Clinitron bed post-op, Wound Vac used sometimes
Strict bedside therapy initially with gradual ↑ in time for OOB (half hour/day -> one hour -> 2 hours, etc.)
Prone positioning encouraged
No SBT -> use Beasy Board to prevent shearing
No aggressive ROM -> need MD clearance/orders
Neurological complications of SCI and how is this different from normal
Altered muscle tone
Tone is the resistance of muscles to passive stretch or elongation
Muscle tension at rest
Normal tone is high enough to resist the effects of gravity in posture & movement, yet is low enough to allow free movement
Hypertonia vs. Hypotonia
Hypertonia is:
NOT necessarily velocity dependent
Can be with or without normal voluntary control
Hypotonia is :
A state of decreased muscle tone or flaccidity
What are the 2 types of hypertonia
Spasticity is a velocity-dependent ↑ in resistance to passive movement
The faster the passive movement the stronger the resistance
Measured on the Modified Ashworth Scale
Rigidity is a non-velocity-dependent ↑ in resistance to passive movement
What is spasticity
Lack of inhibition from higher levels causes…
An increase in stretch reflexes (esp. in antigravity muscles)
Exaggerated flexor muscle responses following a noxious stimulus
Explain the difference in spasticity with complete and incomplete lesions
More flexor spasticity in complete lesions
More extensor spasticity in incomplete lesions
Detrimental Aspects of Spasticity
↓ ROM -->Contractures ↑ Pain ↑ Risk of skin breakdown ↓ sitting balance ↓ transfer ability* ↓ bed mobility, dressing, hygiene & self care ADL’s ↓ safety
Can spasticity ever be beneficial
Sometimes spasticity can be beneficial in transfers/functional activities, in maintaining muscle bulk, & increase venous return
Transfer ability can be a positive - if someone has extensor tone they can use it to transfer from sit to stand - not using true strength but using tone
patient dependent
Spasticity Management
PT interventions PROM ↑ WB (tilt table/standing frame) modalities (ice) TENS/Biofeedback serial casting/splinting tone-reducing AFO/foot plate
How does TENs help with spasticity
Example: bicep spasticity - can do PROM to train, can you tens on triceps to help strengthen and straighten out the arm or can put the tens on biceps to over fatigue the muscle - ach gets used up and then the muscle cannot do contraction and it relaxes
Medical treatment of spasticity
Baclofen, klonopin, tizanidine (zanaflex), valium (diazepam), dantrium (dantrolene)
Surgical Treatment of spasticity
IT Baclofen, phenol block, botox (botulinium toxin)
Neurectomy-severing peripheral nerve
Longitudinal myelotomy- severing connections between anterior and posterior horns of SC
Rhizotomy- severing anterior and posterior nerve roots
What is a Rhizotomy
It is a surgery that helps with spasticity
Consists of severing anterior and posterior nerve roots
Syringomyelia aka and what is it
(Posttraumatic Cystic Myelopathy)
It is a cyst of fluid that develops in the SC
Syrinx = A cystic cavitation of the central gray matter of the spinal cord, associated with sensory loss, particularly pain & temp, in UEs
Syringomyelia is associated with
Is associated with late deterioration in function following SCI
Syringomyelia can occur
From 2 months to beyond 20 years post injury
Syringomyelia is likely caused by
Likely caused by blockage of subarachnoid space
Syringomyelia and he valsalva maneuver
Creates a pressure gradient between the ventricular system and the spinal subdural space during Valsalva maneuver
During the maneuver, due to the block, pressure is not distributed to the SA space
Syringomyelia Symptoms
Pain (dull ache, usually ↑ with straining)
Hyperhidrosis above/below level of lesion
Change in tone/spasticity & bladder evacuation
HTN
Neuropathic joints
Orthostasis
Horner’s Syndrome
Diaphragmatic paralysis & CN dmg if high C/S syrinx
Loss of DTRs, dec sensation (pinprick > LT)
Motor weakness
Symptoms may worsen in sitting due to gravity on the cyst
How is a syringomyelia diagnosed and what is the treatment
Diagnosis is by history, then MRI
Treatment is surgical
Laminectomy and drainage
Syringoperitoneal or syringosubarachnoid shunting
Outcomes have been mixed
Some surgeons will not operate if there are only sensory symptoms without motor changes
Musculoskeletal Complications and SCI
Osteoporosis
Osteoporosis and SCI
1) changes in Ca2+ metabolism
↑ reabsorption by osteoclasts leading to osteoporosis and ↑ risk of pathologic fracture
Leads to ↑concentrations of Ca2+ in the urinary system 🡪 renal calculi (stones)
Bone depletion is rapid post SCI
22% loss 3 months post injury, additional 5% loss btw 3rd & 4th months, and at 14 months post ~33% bone depleted
Pattern of depletion: distal to proximal LE’s
2) Due to immobility & disuse from lack of WBing; but…
3) WBing w/o muscle contraction is probably useless, as spasticity appears to prevent this somewhat
Treatment for osteoporosis due to SCI
Treatment to ↑ mm contraction appears to prevent this, thus FES is a reasonable intervention
contractures are due to
Lack of muscle opposition
Hypertonicity
Lack of normal positioning
How does lack of muscle opposition lead to contractures
They get this because one muscle is moving more than the other. ex: C5 injury can move bicep and tricep is very weak. they will have more tone in the bicep
Prevention/Intervention of contractures
Positioning, splinting, ROM, stretching, education of caregiver/patient
Heterotopic Ossification (HO) and SCI pts
~ 50% of SCI patients develop some degree of HO (usually w/in the 1st 4 mo.)
The development of bone is called HO. It can happens pretty quickly and earlier in the spinal cord injury bc earlier they are not moving as much to protect the tissue. It usually happens in the larger joints of the body (like shoulders and hips)
What is HO and where does it occur
Abnormal development of bone below the level of the lesion, usually in soft tissues
Is extraarticular and extracapsular
Occurs adjacent to large joints
Primarily at (anterior) hips and (medial) knees
May also occur at shoulders, elbows and paravertebral area
Predisposing factors of HO
Complete lesions Presence of pressure sores or fractures Hypertonicity Cervical through mid-thoracic lesions Males twice as likely to develop HO
HO occurs when
Connective tissue cells transform to chondroblasts and osteoblasts
After SCI, serum levels of calcium and phosphorus rise with potential for urinary calculi
Early signs of HO
warm, swelling, fever, reduced ROM
Would HO show up on an x-ray
Not really bc the bone is growing, what you want to use is a triple phase bone scan - this will show the areas of growth
How do you prevent HO from happening
Encourage as much ROM esp. early in the stage. So even if someone is in spinal shock we want to move then to create movement, decrease pain and prevent bony osteophytes
Movement will also help prevent the development of contractures
What type of stretching is important when it comes to HO
Low intensity, long duration stretching is important in early care
Aggressive ROM is contraindicated in later stages due to the risk of pathologic fx
At its worst, HO can prevent
Safe & normal sitting posture, transfers; and interfere with preserved ROM & worsen hygiene problems due to B&B issues
Pharmacologic and medical Interventions for HO
Didronel (disodium etidronate)
Some success in preventing ectopic bone formation, but ineffective against mature bone formation; Prevents ossification of the matrix
NSAIDS (ie. indomethacin)
↓ initial matrix formations, but not proven for SCI
Radiation therapy
↓ initial formation of the matrix
Surgical Resection
Pain and pts with SCI
A major problem experienced by those with SCI
Can come from a variety of causes, requiring different interventions Overuse Muscle imbalances Trauma Radicular pain Phantom pain
Interruption of the pathways that are leading to the brain and can cause
Pain
The two types of pain
Nociceptive Pain
Occurs in the innervated body parts (above lesion)
Neuropathic (Neurogenic) Pain
Pain related to injury to the n. roots, SC, or CE
Two types of Neuropathic (Neurogenic) Pain
Radicular: dermatomal distribution pain – burning/tingling, tightness
Central: saddle distribution & LE pain – cutting, burning, piercing, radiating, nagging
RSD stands for and aka
Reflex Sympathetic Dystrophy
Complex Regional Pain Syndrome (CRPS)
Is RSD common with SCI pts
Occurs in a small number of traumatic SCI pts; Likelihood ↑ if SCI is associated with UE injury from a fall or other trauma
(Reflex Sympathetic Dystrophy)
Where does RSD usually occur
Usually in the shoulder
Typified by pain at fingers, hand, shoulder or scapula, but without forearm or elbow pain
How will a pt with RSD present and what is the cause of these changes
(Reflex Sympathetic Dystrophy)
Sympathetic vasomotor changes: red, taut, glossy skin & trophic nail bed changes
What is RSD
You basically get an increase in sensation for no apparent reason
sympathetic nervous system is on a higher alert and it is not really known why
(Reflex Sympathetic Dystrophy)
RSD and movement
The pain leads to a cycle of immobilization & stiffness with demineralization of bone.
That means if you are going to move that arm, what is going to happen → they will not want to move that arm because it is painful
However, one of the best things that have been shown to help RSD is movement esp. rotational movement
if they don’t move the arm this can cause contractures, stiffness, if it is there for a long time they can develop bone growth (bone spurs)
(Reflex Sympathetic Dystrophy)
Treatment for RSD
Steroid injections into the shoulder joint, or sympathetic ganglion blocks followed by swift, but judicious mobilization is the tx of choice
(Reflex Sympathetic Dystrophy)
GI/GU Complications: Neurogenic Bladder, 2 types of urinary syndromes that can occur in SCI
Spastic (aka reflex) bladder – UMN
Flaccid bladder – LMN
With a spastic bladder you get a bunch of small releases
With a flaccid bladder you can not sense the filling and when the bladder cannot hold anymore you release a lot
Spastic Bladder and SCI level
Usually occurs with SCI > T12 level
Flaccid Bladder and SCI level
Occurs with lesions below T12
What is one of the first questions we have to ask our SCI patients?
How is your B/B symptoms and how do you manange it because the successful management of bladder complications is one of the 1° reasons for ↓ morbidity and mortality in people with SCI
It helps limit ulcers and other infections and other secondary complications
if someone has B/B complications a person is less likely to leave the home
Neurogenic bowel, what is it and what are the interventions
Occurs due to loss of neurologic control of the intestinal tract, resulting in the loss of control of defecation
This causes ↓ gastric motility and loss of voluntary control anal sphincters
The result is stool retention
Interventions: digital stimulation, suppositories, enemas, manual disimpaction
Our goal is to put someone on a routine
