Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuromuscular System Evaluation and Management > Lecture SCI - Secondary Pathologies > Flashcards

Lecture SCI - Secondary Pathologies Flashcards

1
Q

2° Complications of SCI

A 
Cardiovascular/Respiratory
Integumentary
Neurological
Musculoskeletal
Somatosensory
GI/GU
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cardiovascular/Respiratory 2° Complications of SCI

6

A 
Cardiac Arrhythmias
Orthostatic hypotension
Altered thermoregulation
Autonomic Dysreflexia
DVT/PE
Respiratory Dysfn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Integumentary 2° Complications of SCI

A

Decubitus Ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Neurological 2° Complications of SCI (2)

A

Spasticity

Syringomyelia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Musculoskeletal 2° Complications of SCI (4)

A

Osteoporosis
Fractures
Contractures
Heterotopic Ossification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Somatosensory 2° Complications of SCI (2)

A

Pain

Reflex Sympathetic Dystrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

GI/GU 2° Complications of SCI

A

Bowel and Bladder Dysfunction

Altered Sexual Function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the single greatest factor leading to increase in hospital stay in patients with a spinal cord injury

A

Development of Decubitus ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What type of WC would you use for a SCI and why would you not want the other kind

A

A tilt in space

Would not want a reliciner bc you would start sliding and will create a shear force

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cardiovascular Complications is from

A

Interruption btw receptor organs & brainstem

Interruption to ANS

Neurogenic Shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the classic triad to neurogenic shock

A
  1. Hypotension –
    due to loss of sympathetic tone (↓ systemic vascular resistance, & dilation of veins)
    Hypovolemia (due to severe hemorrhage, inadequate fluid administration)
  2. Bradycardia - heart less efficient and pumps slower - movement allows the heart to work a bit harder and pump better
  3. Hypothermia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Hypovolemia

A

Part of the classic triad of neurogenic shock

Due to severe hemorrhage, inadequate fluid administration

(Low volume)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does orthostatic hypotension happen and what can be done to reduce it

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why would you use a tilt table?

A

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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

If the tilt table doesn’t work to help orthostatic hypotension what else can be used?

A

compression garments

Pressure garments (TEDS & abdominal binders)
May teach the Valsalva maneuver as preventative measure, but with much caution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How would someone present with Orthostatic hypotension

A

dizzy, pale and dry skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why do cardiac arrhythmias happen and what is the most common type
Also what makes it worse and when would it improve

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which nerve is responsible for bradycardia and what does this nerve do

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does the vagus nerve get stimulated

A

During tracheal suction, turning to prone, defecation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

cardiac arrhythmias are due to

A

loss of sympathetic tone & unopposed vagal tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What happens to thermoregulation with a SCI

A

it becomes altered

↓ thermoregulation below level of lesion

s/p SCI: the connection between the ANS & the cord is interrupted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How would a SCI pt present with altered thermoregulation

A

The patient will be unable to sweat when warm or shiver when cold below the level of the lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does normal thermoregulation happen

A

Hypothalamus sends impulses via autonomic pathways to the cord, then through sympathetic outflow to the skin, initiating compensatory reactions to ↑ or ↓ temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why do you have to make sure people are aware of altered thermoregulation

A

The higher the lesion, the greater the proportion of the body that is unable to maintain safe temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What SCI level is at risk for altered thermoregulation?

A

Above T5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is altered thermoregulation called above T5?

A

Poikilothermic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Poikilothermic

A

Above T5

core temp adapts to temp of environment (can be misinterpreted as febrile)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Someone with altered thermoregulation should do what when they are working out and what should they do when the weather is cold

A

Should ice after strenuous activity to cool down, or dress warmly in cold weather

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Why do we have to be aware of poikilothermic?

A

When we exercise we increase the temp of the core and the environment. These people get really warm and light headed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the 2 things that you worried about when working with a SCI?

A

Orthostatic hypertension and autonomic dysreflexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Autonomic Dysreflexia aka, presents as, and what level of injury

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How is the treatment of Orthostatic hypertension and autonomic dysreflexia either the same or different?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What do you have to avoid with autonomic dysreflexia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Signs of orthostatic hypertension:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Signs of autonomic dysreflexia:

A

red face, HR dec. BP inc. they start sweating, severe HA and etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Is autonomic dysreflexia serious

A

Consequences can be severe or even fatal!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Causes of autonomic dysreflexia

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Potential complications of autonomic dysreflexia

A

retinal hemorrhage, SAH, ICH, MI, Sz, death!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How would Autonomic Dysreflexia usually occur?

A

It occurs do to some restriction in their body. ie: wearing a belt, tight clothing or shoes you have to loosen them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Why do you have to loosen the clothing of someone who has autonomic dysreflexia?

A

Body is misreading the stimulus as noxious and responding very aggressively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What do you do if patient is going through autonomic dysreflexia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Autonomic Dysreflexia prevention

A

Early education of patient & caregivers

Symptom recognition

Immediate interventions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Is risk of PE by level

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Prevention & treatment of DVT

A

Rehab: Early mobilization; compression garments
Medical: Prophylactic Coumadin/Heparin; IVC filters

45
Q

DVT is more common in

A

Tetraplegics

46
Q

Risk factors for a DVT

A

↓ LE mvt & muscle pump, presence of LE fractures, hypercoagulability

47
Q

Symptoms of DVT:

A

Edema
Redness
Tenderness/Pain*

48
Q

Symptoms of PE: (6)

A 
Dyspnea
Tachycardia
Hypotension
Angina
Hemoptysis 
Fever
49
Q

What is hemoptysis and what is this a symptom for

A

coughing up blood

symptom of a PE

50
Q

Respiratory Complications

of SCI

A 
Pneumonia
Aspiration
Atelectasis
Lung contusions hemopneumothorax (air and blood in the chest cavity) 
Rib fractures, etc.
51
Q

Respiratory Complications
and lesion levels

(discuss 3 different levels)

A

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

52
Q

Treatments for respiratory dysfunction

A

DBE, Diaphragmatic breathing
Assisted cough
Incentive Spirometry
Resistive Inspiratory Muscle Trainer – PFlex

53
Q

What is the single greatest factor leading to ↑ in hospital length of stay and cost

A

Decubitus Ulcers

54
Q

Common causes of decubitus ulcers

A

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

55
Q

Which areas are of risk of a decubitus ulcer

A

Any WBing part is at risk:

Sacrum, ITs, heels, GTs, malleoli, med/lat knees, elbows, occiput, scapulae, etc.

56
Q

Best treatment for Pressure ulcers

A

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?

57
Q

Intervention for decubitus ulcers

A

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

58
Q

Neurological complications of SCI and how is this different from normal

A

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

59
Q

Hypertonia vs. Hypotonia

A

Hypertonia is:
NOT necessarily velocity dependent
Can be with or without normal voluntary control

Hypotonia is :
A state of decreased muscle tone or flaccidity

60
Q

What are the 2 types of hypertonia

A

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

61
Q

What is spasticity

A

Lack of inhibition from higher levels causes…

An increase in stretch reflexes (esp. in antigravity muscles)
Exaggerated flexor muscle responses following a noxious stimulus

62
Q

Explain the difference in spasticity with complete and incomplete lesions

A

More flexor spasticity in complete lesions

More extensor spasticity in incomplete lesions

63
Q

Detrimental Aspects of Spasticity

A 
↓ ROM -->Contractures 
↑ Pain
↑ Risk of skin breakdown
↓ sitting balance
↓ transfer ability*
↓ bed mobility, dressing, hygiene & self care ADL’s 
↓ safety
64
Q

Can spasticity ever be beneficial

A

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

65
Q

Spasticity Management

A 
PT interventions 
PROM 
↑ WB (tilt table/standing frame) 
modalities (ice)
TENS/Biofeedback
serial casting/splinting 
tone-reducing AFO/foot plate
66
Q

How does TENs help with spasticity

A

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

67
Q

Medical treatment of spasticity

A

Baclofen, klonopin, tizanidine (zanaflex), valium (diazepam), dantrium (dantrolene)

68
Q

Surgical Treatment of spasticity

A

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

69
Q

What is a Rhizotomy

A

It is a surgery that helps with spasticity

Consists of severing anterior and posterior nerve roots

70
Q

Syringomyelia aka and what is it

A

(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

71
Q

Syringomyelia is associated with

A

Is associated with late deterioration in function following SCI

72
Q

Syringomyelia can occur

A

From 2 months to beyond 20 years post injury

73
Q

Syringomyelia is likely caused by

A

Likely caused by blockage of subarachnoid space

74
Q

Syringomyelia and he valsalva maneuver

A

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

75
Q

Syringomyelia Symptoms

A

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

76
Q

How is a syringomyelia diagnosed and what is the treatment

A

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

77
Q

Musculoskeletal Complications and SCI

A

Osteoporosis

78
Q

Osteoporosis and SCI

A

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

79
Q

Treatment for osteoporosis due to SCI

A

Treatment to ↑ mm contraction appears to prevent this, thus FES is a reasonable intervention

80
Q

contractures are due to

A

Lack of muscle opposition
Hypertonicity
Lack of normal positioning

81
Q

How does lack of muscle opposition lead to contractures

A

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

82
Q

Prevention/Intervention of contractures

A

Positioning, splinting, ROM, stretching, education of caregiver/patient

83
Q 
Heterotopic Ossification (HO)
and SCI pts
A

~ 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)

84
Q

What is HO and where does it occur

A

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

85
Q

Predisposing factors of HO

A 
Complete lesions
Presence of pressure sores or fractures
Hypertonicity
Cervical through mid-thoracic lesions
Males twice as likely to develop HO
86
Q

HO occurs when

A

Connective tissue cells transform to chondroblasts and osteoblasts

After SCI, serum levels of calcium and phosphorus rise with potential for urinary calculi

87
Q

Early signs of HO

A

warm, swelling, fever, reduced ROM

88
Q

Would HO show up on an x-ray

A

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

89
Q

How do you prevent HO from happening

A

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

90
Q

What type of stretching is important when it comes to HO

A

Low intensity, long duration stretching is important in early care
Aggressive ROM is contraindicated in later stages due to the risk of pathologic fx

91
Q

At its worst, HO can prevent

A

Safe & normal sitting posture, transfers; and interfere with preserved ROM & worsen hygiene problems due to B&B issues

92
Q

Pharmacologic and medical Interventions for HO

A

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

93
Q

Pain and pts with SCI

A

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
94
Q

Interruption of the pathways that are leading to the brain and can cause

A

Pain

95
Q

The two types of pain

A

Nociceptive Pain
Occurs in the innervated body parts (above lesion)

Neuropathic (Neurogenic) Pain
Pain related to injury to the n. roots, SC, or CE

96
Q

Two types of Neuropathic (Neurogenic) Pain

A

Radicular: dermatomal distribution pain – burning/tingling, tightness

Central: saddle distribution & LE pain – cutting, burning, piercing, radiating, nagging

97
Q

RSD stands for and aka

A

Reflex Sympathetic Dystrophy

Complex Regional Pain Syndrome (CRPS)

98
Q

Is RSD common with SCI pts

A

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)

99
Q

Where does RSD usually occur

A

Usually in the shoulder

Typified by pain at fingers, hand, shoulder or scapula, but without forearm or elbow pain

100
Q

How will a pt with RSD present and what is the cause of these changes

A

(Reflex Sympathetic Dystrophy)

Sympathetic vasomotor changes: red, taut, glossy skin & trophic nail bed changes

101
Q

What is RSD

A

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)

102
Q

RSD and movement

A

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)

103
Q

Treatment for RSD

A

Steroid injections into the shoulder joint, or sympathetic ganglion blocks followed by swift, but judicious mobilization is the tx of choice

(Reflex Sympathetic Dystrophy)

104
Q

GI/GU Complications: Neurogenic Bladder, 2 types of urinary syndromes that can occur in SCI

A

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

105
Q

Spastic Bladder and SCI level

A

Usually occurs with SCI > T12 level

106
Q

Flaccid Bladder and SCI level

A

Occurs with lesions below T12

107
Q

What is one of the first questions we have to ask our SCI patients?

A

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

108
Q

Neurogenic bowel, what is it and what are the interventions

A

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

Neuromuscular System Evaluation and Management (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions