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Acute Care and Rehab > neuro conditions > Flashcards

neuro conditions Flashcards

1
Q

What are anatomically classified injuries to the PNS

A

Mononeuropathy and Polyneuropathy

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2
Q

What occurs in mononeuropathy

A

Damage to a single nerve or nerve group

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3
Q

What occurs in polyneuropathy

A

Damage occurs to multiple nerves, often symmetrically affecting bilat. of the body

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4
Q

What are etiological classifications for injuries to the PNS

A

Traumatic
Metabolic
Infections / inflammatory
Toxic / chemical

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5
Q

What is an example infection injury to the PNS

A

Infections such as meningitis

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6
Q

What are traumatic injuries to the PNS

A

Injuries caused by external forces and accidents

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7
Q

What are metabolic injuries to the PNS

A

Injuries resulting from systematic conditions such as diabetes, nutritional deficiencies and poisoning

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8
Q

What are infections or inflammatory injuries to the PNS

A

Injuries caused by infections or autoimmune reactions such as meningitis or MS

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9
Q

What are toxic/chemical injuries to the PNS

A

Injuries induced by exposure to toxins or chemicals

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10
Q

What are physiologically classified injuries affecting the PNS

A

Axonopathies
Myelopathies
Vasculopathy

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11
Q

What are axonopathy injuries to the PNS

A

Injuries primarily affecting the axons of the nerves

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12
Q

What are myelopathy injuries of the PNS

A

Injuries affecting the myelin sheath surrounding the nerves, disrupting signal transmissions

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13
Q

What are vasculopathy injuries to the PNS

A

Injuries affecting the blood vessels supplying the nerves, potentially leading to ischaemic conditions

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14
Q

What is the aetiology of Guillian-Barre Syndrome (GBS)

A

Bacterial infection or viral infection
Molecular mimicry can be a probable underlying mechanism

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15
Q

What is the pathophysiology of GBS

A

GBS is an immune-mediated polyradiculoneuropathy with forms including AIDP, ANAN and ASMAN. Each form has unique clinical, pathological and pathophysiological

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16
Q

What is the presentation of GBS

A

Classic GBS is an acute onset ascending sensorimotor neuropathy
Symptoms include (mild to severe)
- Respiratory paralysis
- Autonomic dysfunction

Early diagnosis reduces morbidity and improves prognosis

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17
Q

What are the phases of GBS

A

Acute Phase
Plateau Phase
Recovery Phase

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18
Q

What is involved in the acute phase of GBS

A

Rapid onset of symptoms
Escalates over a period of days or weeks

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19
Q

what occurs in the plateau phase of GBS

A

Stabilisation of symptoms
No further deterioration

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20
Q

What occurs in the recovery phase of GBS

A

Gradual improvement
potential full recovery
May lead to residual deficits

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21
Q

How is GBS diagnosed

A

Based on a combination of medical history, physical exam and tests like CSF examination, electrodiagnostic studies, MRIs, CTs, CT taps

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22
Q

What features are required for diagnosis of GBS

A

Progressive bilateral weakness of arms and legs
Absent or decreased tendon reflexes in affected limbs

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23
Q

What features support diagnosis of GBS

A

progressive phase lasts from days to 4 weeks (usually <2 weeks)
Relative symmetry of symptoms and signs
Relatively mild sensory symptoms and signs (absent in pure motor variant)
Cranial nerve involvement, especially bilateral facial palsy
Autonomic dysfunction
Muscular or radicular back or limb pain
Increased protein level in cerebrospinal fluid (CSF); normal protein levels do not rule out the diagnosis
Electrodiagnostic features of motor or sensorimotor neuropathy (normal electrophysiology in the early stages does not rule out the diagnosis)

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24
Q

What is involved in the acute management of GBS

A

Intravenous immunoglobulin (Ivlg) and plasma exchange are equally effective in treating GBS (only proven effective treatments)

Steroids, plasmapheresis and DVT prophylaxis may also aid

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25
Q

When should GBS patients be admitted to ICU

A

If have one or more:
rapid progression of weakness
severe autonomic or swallowing dysfunction
evolving respiratory distress
EGRIS >4

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26
Q

When should treatment be started for GBS

A

one or more
- inability to walk >10m independently
- Rapid progression of weakness
- severe autonomic or swallowing dysfunction
- respiratory insufficiency

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27
Q

What is involved in monitoring of GBS

A

Regularly assessing muscle strength, respiratory function, swallowing function, autonomic function (BP, HR/rhythm, bladder/bowel control)

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28
Q

What are possible early complications of GBS

A

choking
arrhythmias
infections
DVT
pain
delirium
depression
urinary retention
constipation
corneal ulceration
dietary deficiency
hyponatraemia
pressure ulcers
compression neuropathy
limb contractures

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29
Q

What may occur when a GBS patient clinically deteriorates

A

Suffer from respiratory muscle weakness leading to airway protection loss, ineffective cough, several pulmonary complications

Affects respiratory muscles of 40% of patients and may cause neuromuscular respiratory failure in 25%

30
Q

How is respiratory function measured in GBS patients

A

With bedside pulmonary function
Should also monitor for bulbar paulsy and dysautonomia as these can both impair ability to clear secretions, increasing risk of respiratory failure and pulmonary infections

31
Q

what a laboratory markers of failing respiration?

A

Oxygen saturation less than 92%, pO2 <8kPa, CO2 <6kPa
FVC 30% of FVC from baseline within 24 hours
inconsistent or falling values of FVC at a single test session
A decline in vital capacity by more than 15-20%in the supine position

32
Q

What monitoring is suggested for patients with acute GBS

A

4 hour forced vital capacity (FVC)
4 hourly pulse, BP, SpO2
Check ABGs
(1-2 hourly if FVC <20ml/Kg BW)

33
Q

What are the traumatic causes of spinal cord injuries

A

Car accidents
falls
violence and assaults
sports and recreational injuries
work-related

34
Q

what are non-traumatic causes of spinal cord injuries

A

vascular disorders
infectious diseases
degenerative diseases
neoplasma
developmental disorders
autoimmune disorders
latrogenic causes

35
Q

other causes of spinal cord injuries

A

nutritional deficiencies
radiation

36
Q

describe the cascade of events during a SCI

A

Immediate (seconds):
- haemorrhage
- decreased ATP
- increased lactate

Early acute (hours):
- vasogenic oedema
- ion imbalance
- Release of neurotoxic opioids
- Inflammation
- lipid peroxidation
- glutamate excitotoxicity
- cytotoxic oedema
- free radical formation

Subacute (days/ weeks)
- microglial activation
- macrophage activation
- cellular apoptosis

37
Q

What is involved in acute managment of SCI

A

Spinal surgery:
- Initial evaluation with neurological exam including spinal reflexes
- evaluation of spinal imaging
If scans demonstrate compressive force on spinal cord with incomplete cord injury:
- urgent decompression with or w/out arthrodesis within 24 hrs

If exam beings to show active decline, decompression becomes emergent.

If incomplete injury or other systemic injuries prevent safe operative intervention then patient is admitted to ICU for medical management. Obtain MRI of relevant region without contrast unless contraindicated

38
Q

what is key postoperative or peri-injury management for SCI

A

Early physio
early nutritional support with involvement of nutritional consult service
removal of foley catheter as soon as tolerated
pneumococcus and influenza vaccinations
continued chest physiotherapy daily
continuation of MAP goal >85 5-7 days

39
Q

What occurs post surgery or conservative management decisions

A

chest physio
goals
early mobility as able
preventions of deterioration

40
Q

What are types of spinal cord lesions

A

Tetraplegia
Paraplegia
Complete / incomplete lesions

41
Q

what are possible clinical syndromes post SCI

A

Lateral Syndrome
Anterior syndrome
CES
Posterior syndrome
Conus medullaris syndrome

42
Q

What is used in immediate medical management

A

Surgical stabilisation
Immobilisation and transportation
e.g. aspen collars

43
Q

How can body function and structure be assessed

A

ASIA assessment

44
Q

What are possible respiratory complications post SCI

A

Preserving airways
Breathing
Impaired respiratory capacity
Retained secretiosn
Autonomic function

45
Q

What may be needed if there are issues preserving airways

A

may require invasive or non-invasive ventilation

46
Q

How does breathing complication occur due to SCI

A

Damage to T8 paralyzes intercostal muscles and diaphragm (C3)
Injuries at C5 or above can cause failure leading to intubation
Lower cervical injuries spare the diaphragm but paralyze the intercostals causing chest to draw in during inhalation
- this causes rapid decrease in vital capacity, functional capacity and rapid desaturation

47
Q

How may respiratory capacity be impaired

A

decreased respiratory muscle strength
fatigue
paradoxical chest wall movement > effort breathing
decreased resp capacity
atelectasis
Chest wall rigidity

48
Q

Why may there be increased retained secretions

A

increased secretion production
decreased cough effectiveness

49
Q

What may be associated with autonomic dysfunction

A

increased secretions
Bronchospasm
Pulmonary oedema

50
Q

what is a possible flow of events that may occurs leading to complication in above T6 paralysis?

A

-> lack of abdominal innervation -> weak/absent cough -> sputum retention -> infection risk -> aspiration risk

51
Q

what are possible resources for SCI respiratory management

A

NIV
Cough assist
Manual assisted cough
Secretion management to/ suctioning

52
Q

What may be used to aid in visualisations and turning for the spine

A

Postural allignment
This can be a variety of specialist pillows, splints, elevation, bed types

53
Q

what are possible blood pressure issues whihc may arise

A

Hypotension
Blood pressure instability

54
Q

what is the figure for hypotension

A

hypotension = systolic BP ≤ 110mmHg for men and ≤100 mmHg for females

55
Q

what is orthostatic hypotension (OH)?

A

sustained reduction of systolic BP of at least 20 mmHg or diastolic BP of at least 10 mmHg within 3-min of standing or 60 degree head-up tilt
OH is frequently found in ppl with autonomic dysfunction

56
Q

What are symptoms of OH

A

orthostatic intolerance
- fatigue
- weakness
- light headedness
- dizziness
- blurred vision
- headache

57
Q

What are non-pharmacological options for managing hypotension and OH

A

Exercise
functional electrical stimulation
compression stockings
abdominal binders

58
Q

what is BP instability

A

unpredictable BP changes that can occur frequently but often go unnotives by both pt and clinical

59
Q

What is autonomic dysreflexia (AD)

A

found in adults with SCI at or above T6 that causes elevated systolic BP greater than 20 mmHG above usual base line
Many individuals report few or no symptoms

60
Q

what are possible symptoms of AD

A

Many dont experience symptoms but may be
headache
change in HR
profuse sweating on face, neck and shoulder
piloerection
blurred vision
nasal congestion
feelings of anxiety

61
Q

What is spasticity

A

Exaggeration of stretch reflex caused by hyperexcitability of spinal reflexes in upper motor neuron syndrome

62
Q

How does spasticity occur in SCI

A

Post SCI period of flaccid muscle paralysis and loss of tendon reflexes = spinal shock
lasts 1-3 days to few weeks
this is followed by exaggerated tendon reflexes, increased muscle tone and muscle spasms or spasticity

63
Q

How can spasticity be managed

A

positioning
ROM + stretching and splinting/orthoses
Weight bearing
muscle strengtheningh

64
Q

how does positioning aid spasticity

A

maintenance of muscle length

65
Q

How does ROM and stretching and splinting/orthoses

A

prevention of contractures; long-term stretch; causes temporary reduction in intensity of muscle contraction in reaction to muscle stretch

66
Q

how does weight bearing improve spasticity

A

Prolonged stretch of ankle plantar flexor muscles

67
Q

How does muscle strengthening aid spasticity

A

Emphasis of balance of agonist and antagonist groups of muscles and voluntary control

68
Q

what is the timing of rehabilitation for acute SCI

A

rehab can be offered to patients with acute SCI once medically stable and can tolerate required rehab intensity
any recommendation would be based on indirect evidence or clinical expert opinion

69
Q

what are the goals of acute rehab post SCI

A

increase strength
treat and prevent contractures and muscle changes
improve the performance/function of motor tasks
Improve sensorial integration and sensation

70
Q

What is the role of OT in SCI

A

Sitting ax
w/chair ax
orthosis
functional task and ADL practice
engagement / motivation and social pptcian
adapting environment, support joint decision making

71
Q

what is the role of ns and medicine in SCI

A

weaning from non + invasive ventilation
tracheostomy management
sittining management
pressure sore management
transfers and mobility
spasticity and tone management
respiratory management

72
Q

what is the role of SaLT in SCI care

A

sitting optimisation for sport and E+D
communication
management of trachi : weaning from trache and ventilation, FEES and swallowing

Acute Care and Rehab (8 decks)

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