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PassPMR - 01 Stroke > Chapter 4 - Stroke Complications > Flashcards

Chapter 4 - Stroke Complications Flashcards

1
Q

Prevention (Prophylaxis) of Post-Stroke Seizures? Yes or No? 🔑

A

Routine prophylaxis for patients with ischemic or hemorrhagic stroke is not recommended

There is no evidence that prophylactic anticonvulsive treatment is beneficial post stroke.

Braddom 6th Edition Chapter 44 Stroke pg962

Stroke Rehabilitation Clinician Handbook 2020 Model 6 pg40

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2
Q

Classification of post stroke seizure 🔑

A
  1. At stroke onset 39%
  2. Early after stroke (1–2 weeks) 57%
  3. Late after stroke (>2 weeks) 88% → higher probability of recurrence

Majority of seizures were generalized, tonic-clonic

Cuccurollo 4th Edition Chapter 1 Stroke pg47

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3
Q

List 3 risk factors for late seizures post Stroke 🔑🔑 EXAM

A

EARLY SEIZURE

  1. Younger Age
  2. Cortical Stroke
  3. Large Stroke
  4. Hemorrhagic strokes
  5. Greater Disability

LATE SEIZURE

  1. Large Stroke
  2. Cortical Stroke
  3. Early-onset seizures

Stroke Rehabilitation Clinician Handbook 2020 Module 6 pg39

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4
Q

Treatment of Post-Stroke Seizures 🔑🔑 EXAM Treatment of Status Epilepticus Post Stroke 🔑🔑

A

Seizure

  1. Phenytoin
  2. Carbamazepine [Tegretol] (partial seizures)
  3. Valproic acid [Valproate] (generalized seizures)
  4. Levetiracetam [Keppra]

Status Epilepticus

Benzodiazepines

  • Lorazepam [Ativan] and Diazepam [Valium] given intravenously
  • Midazolam 10 mg given by the buccal

Cuccurollo 4th Edition Chapter 2 TBI pg76

Stroke Rehabilitation Clinician Handbook 2020 Module 6 pg39

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5
Q

Driving and Post-Stroke Seizures 🔑🔑 OSCE Q

A

Patient will need to be seizure-free for at least 6 months, on stable treatment and assessed by a neurologist conducting the EEG before they can drive again.

Stroke Rehabilitation Clinician Handbook 2020 Model 6 pg41

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6
Q

Post-Stroke Fatigue. 🔑 What medications have been shown to be of benefit from the available evidence? 1 mark What are possible non-pharmacologic strategies? 2 marks

A

PHARMACOLOGICAL

  1. Dopaminergic: Amantadine, Methylphenidate

NON-PHARMACOLOGICAL

  1. Cognitive Therapy
  2. Graded Activity Training
  3. Proper sleep hygiene
  4. Energy conservation methods
  5. Pacing activities
  6. Rest just before therapy sessions

https://www.strokebestpractices.ca/recommendations/mood-cognition-and-fatigue-following-stroke/post-stroke-fatigue

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7
Q

List 4 Risk Factors for Depression post stroke 🔑

A

RISK FACTORS

  1. Female gender
  2. Significant impairment in ADLs
  3. Nonfluent aphasia
  4. Cognitive impairment
  5. Lack of social supports
  6. Prior psychiatric history specially depression
  7. High stroke severity National Institutes of Health Stroke Scale (NIHSS)

Cuccurollo 4th Edition Chapter 1 Stroke pg46

Stroke Rehabilitation Clinician Handbook 2020 Module 7

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8
Q

Management of post stroke depression. 2 pharmacological & 2 non-pharmacological 🔑🔑

A

NON-PHARMACOLOGICAL

  1. Cognitive behavioral therapy (CBT)
  2. Physical exercise
  3. Repetitive transcranial magnetic stimulation (rTMS)
  4. Deep brain stimulation
  5. Music
  6. Mindfulness
  7. Motivational interviewing.
  8. Deep breathing
  9. Meditation
  10. Visualization

PHARMACOLOGICAL

SSRI: Fluoxetine (Prozac), Escitalopram (Cipralex) 5-10mg

Avoid in hemorrhagic stroke, it may worsen the bleeding.

TCA

GENERAL GUIDE FOR MEDICATIONS

  • If the person’s mood has not improved 2-4 weeks after initiating treatment, assess patient compliance with medication regime. If compliant, then consider increasing the dosage, adding an additional medication, or changing to another antidepressant.
  • If a good response is achieved, treatment should be continued for a minimum of six to 12 months.

Cuccurollo 4th Edition Chapter 1 Stroke pg46

Stroke Rehabilitation Clinician Handbook 2020 Module 7

https://www.strokebestpractices.ca/recommendations/mood-cognition-and-fatigue-following-stroke/post-stroke-depression

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9
Q

List 2 Screening tools for depression

A
  1. Patient Health Questionnaire (PHQ)-9
  2. Hospital Anxiety and Depression Scale (HADS)
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10
Q

What do you call decline in cognitive function after stroke? Treatment?

A

Vascular cognitive impairment (VCI)

Range of cognitive deficits due to the impact of cerebrovascular disease, including stroke.

Vascular Dementia

Second most common cause of dementia after Alzheimer’s disease.

Treatment

Acetylcholinesterase inhibitor: Donepezil (Aricept) 5-10mg

Although there is strong evidence that Donepezil is effective in vascular dementia; several meta-analyses have not recommended these drugs for Mild Cognitive Impairment which is what is most common post stroke

Stroke Rehabilitation Clinician Handbook 2020 Model 5 pg6

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10
Q

Clock-Drawing Test 🔑🔑 What is the scale? What does it measure? What are its limitations?

A

What is it?

  • Patient draw a clock, place the numbers on the clock in their proper positioning and then place the arms of the clock at a requested time.

Measurement

  • Quick assessment of visuospatial and praxis abilities
  • May detect deficits in both attention and executive dysfunction

Influenced by

  1. Increasing age
  2. Reduced education
  3. Depression

Stroke Rehabilitation Clinician Handbook 2020 Model 5 pg14

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11
Q

Mini-Mental State Examination 🔑🔑 What does it measure? What are its limitations?

A

💡 ORARL.C: Orientation - Registration - Attention - Recall - Language - Construction (17-24)

MMSE consists of 11 simple questions or tasks, typically grouped into 7 cognitive domains: orientation to time, orientation to place, registration of three words, attention and calculation, recall of three words, language and visual construction.

Score

Total score of 30

Levels of impairment: none (24-30), mild (18-24) and severe (0-17)

Limitation

Lack of sensitivity in identifying small changes in cognitive impairment.

Stroke Rehabilitation Clinician Handbook 2020 Model 5 pg15

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12
Q

List 8 causes of shoulder pain post stroke. 🔑🔑 EXAM

A

SOFT TISSUE:

  1. adhesive capsulitis.
  2. impingement syndrome.
  3. rotator cuff injury.
  4. bicipital tendinopathy.
  5. soft tissue contracture.
  6. myofascial pain.

BONY:

  1. GH subluxation/dislocation.
  2. humeral fracture.
  3. AVN.
  4. osteoarthritis.
  5. Heterotopic ossification.

NEURO:

  1. CRPS type 1.
  2. brachial plexopathy.
  3. axillary neuropathy.
  4. suprascapular neuropathy.
  5. spasticity.
  6. central thalamic pain.

OTHER:

  1. tumour.
  2. referred pain (neck, visceral, intra-abdominal).

Ref: Braddom pg 1200; EBRSR module 11 pg 5.

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13
Q

Summary of Management of Shoulder Pain post stroke🔑🔑

A

HEMIPLEGIC SHOULDER PAIN (MSK)

  1. Physiotherapy: Gentle stretching and mobilization techniques goal to increase external rotation and abduction
  2. Taping of the affected shoulder has been shown to reduce pain
  3. Oral medications: ibuprofen or narcotics
  4. Injections of botulinum toxin into the subscapularis and pectoralis muscles
  5. Subacromial corticosteroid injections (rotator cuff or bursa pathology)

CRPS

  • Diagnosis based on Budapest Criteria +/- Triple phase bone scan
  1. Oral corticosteroids, starting at 30 – 50 mg daily for 3 - 5 days, and then tapering doses over 1 – 2 weeks
  2. Active or passive range of motion exercises can be used to prevent CRPS
  3. Sympathetic block is resisted cases

CENTRAL PAIN

  1. First-line: Anticonvulsant (such as gabapentin or pregabalin)
  2. Second-line: Tricyclic antidepressant (amitriptyline) or an SNRI (duloxetine)

https://www.strokebestpractices.ca/recommendations/stroke-rehabilitation/management-of-shoulder-pain-complex-regional-pain-syndrome-crps-following-stroke

https://www.strokebestpractices.ca/recommendations/stroke-rehabilitation/rehabilitation-to-improve-central-pain

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14
Q

List 4 local complications in shoulder with person with hemiplegia

A
  1. Subluxation
  2. Spasticity
  3. Contracture
  4. Adhesive Capsulitis
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15
Q

What is the definition of shoulder subluxation?🔑
List 2 Clinical manifestations of shoulder subluxation in stroke patient?🔑

A

Definitions

Changes in the mechanical integrity of the glenohumeral joint that results in an incomplete dislocation, due to intact joint capsule, where articulating surfaces of the glenoid fossa and humeral head remain in contact.

Stroke Rehabilitation Clinician Handbook 2020 Model 4 pg48

Presentation

  1. Palpable gap between the acromion and humeral head
  2. Decrease in arm external rotation
  3. Shoulder pain (Conflicting evidence)

Cuccurollo 4th Edition Chapter 1 Stroke pg33

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16
Q

Case of stroke. Would you use sling for the shoulder? And why? 🔑🔑

A

Advantages:

  1. Supporting flaccid hemiplegic arm to limit traction during standing or transferring
  2. Protecting the arm from accidents during ambulation
  3. Reduce upper limb edema

Disadvantages:

  1. Discourage arm use
  2. Encourage flexor synergies
  3. Inhibit arm swing
  4. Contracture formation
  5. Decrease body image causing the patient to further avoid using that arm

http://www.ebrsr.com/sites/default/files/C_Motor_Recovery_(PR).pdf

17
Q

List 3 possible etiologies of shoulder subluxation 🔑🔑

A
  1. Supraspinatus muscle is flaccid during the initial phase of hemiplegia. The weight of the unsupported arm can cause the humeral head to sublux downward in the glenoid fossa.
  2. Decreased trapezius tone the scapula rotates and humeral head subluxes from the glenoid fossa
  3. Rotator cuff flaccidity

Cuccurollo 4th Edition Chapter 1 Stroke pg33

Stroke Rehabilitation Clinician Handbook 2020 Model 4 pg48

18
Q

What is the most effective initial treatment for post-stroke shoulder subluxation? 4 marks 🔑🔑

A
  1. EDUCATION about joint protection strategies for patient and caregiver
  2. PHYSIOTHERAPY
    • Gentle stretching and mobilization techniques (increasing external rotation and abduction)
    • Active range of motion should be increased gradually
    • Taping of the affected shoulder has been shown to reduce pain
    • Avoid beyond 90 degrees of flexion/abd
    • Avoid over-head pullies
  3. OCCUPATIONAL THERAPY
    • Lap tray at rest
    • Arm through or sling during ambulation
  4. MODALITIES: Functional electrical stimulation
  5. MEDS: Oral NSAID (ibuprofen)

Cuccurollo 4th Edition Chapter 1 Stroke pg33

Stroke recovery and rehab textbook pg 518-519; first principles.

https://www.strokebestpractices.ca/recommendations/stroke-rehabilitation/management-of-shoulder-pain-complex-regional-pain-syndrome-crps-following-stroke

19
Q

List 3 x-ray views for assessing shoulder subluxation

A
  1. AP: Glenohumeral joint space
  2. Scapular Y: Anterior and posterior dislocation
  3. Axillary: Anterior and posterior dislocation

https://www.orthobullets.com/shoulder-and-elbow/3038/shoulder-imaging

20
Q

What benefit is there for the use of FES in hemiplegic shoulder pain and shoulder subluxation? (Functional electrical stimulation).🔑🔑

A
  1. FES does not reduce hemiplegic shoulder pain (strong evidence).
  2. FES does prevent shoulder subluxation (strong evidence).

EBRSR executive summary pg 20.

21
Q

Incidence of hemiplegic shoulder pain in regards of spasticity in stroke?

A

Higher incidence of shoulder pain in spastic (85%) than in flaccid (18%) hemiplegia.

Stroke Rehabilitation Clinician Handbook 2020 Model 4 pg50

22
Q

Spasticity affection in shoulder mechanics? What is the last motion to be recovered? 🔑🔑

A

In spasticity shoulder likely to be in internal and adduction position:

  • Shoulder external rotation
  • Shoulder abduction beyond 90 degrees.

Last areas of shoulder function to recover:

  • Internal rotators of the shoulder

Stroke Rehabilitation Clinician Handbook 2020 Model 4 pg50

23
Q

List 4 Muscles that contribute to spastic internal rotation/adduction of the shoulder 🔑🔑

A
  1. Subscapularis
  2. Pectoralis major
  3. Teres major
  4. Latissimus dorsi

Stroke Rehabilitation Clinician Handbook 2020 Model 4 pg50

24
Q

Bicipital tendonitis, list 2 clinical findings 🔑🔑

A
  1. Tenderness in anterior shoulder
  2. Positive Yargason’s and speed test
25
Q

Pathophysiology of Thalamic/Central Pain States Post Stroke (CPSP) 🔑
Signs of Thalamic or central pain.🔑

A

Damage to spino-thalamic pathway (from its name “Thalamic pain”)

→ impaired pain and temperature

  1. Hyperalgesia: Increased pain response to a normally painful stimulus
  2. Allodynia: Abnormally unpleasant somatosensory experience, often poorly localized, elucidated by normally non-nociceptive stimuli
  3. Dysesthesia: Unpleasant sensations, either spontaneous or evoked

Intact lemniscal pathway

→ Touch, 2-point discrimination and vibration are normal

Stroke Rehabilitation Clinician Handbook 2020 Model 6 pg42-43

PMR Secrets Chapter 54 Stroke Rehab pg452

26
Q

Treatment of Central Pain Post Stroke 🔑🔑

A

FIRST-LINE TREATMENT

  • Anticonvulsant (such as gabapentin or pregabalin)

SECOND-LINE TREATMENT

  1. Tricyclic antidepressant (e.g., amitriptyline)
  2. SNRI (particularly duloxetine)

https://www.strokebestpractices.ca/recommendations/stroke-rehabilitation/rehabilitation-to-improve-central-pain

27
Q

Present a differential diagnosis for the patient with a tender and swollen limb 🔑🔑

A

💡 Skin - Nerve - Artery - Vein - Muscle - Bone - Joint

  1. Cellulitis
  2. Peripheral neuropathy
  3. CRPS
  4. Angioedema
  5. Deep venous thrombosis
  6. Compartment syndrome
  7. Osteomyelitis
  8. Fracture
  9. Inflammatory arthritis
  10. Malignancy

Rheumatology Secrets 4th Edition Chapter 65 CRPS pg514 q12

28
Q

30 years old man present with a left hand pain happened 6 months ago after a door closed on his forearm. He presented with a right hand shiny skin and decreased hair growth, the area very tender to touch. 🔑🔑
What do you think the presumptive diagnosis? 1 mark
How many type of this condition are and explain?

A

Complex Regional Pain Syndrome:

Spontaneous and continuing pain, allodynia, or hyperalgesia occurs, is not limited to the territory of a single peripheral nerve, and is disproportionate to the inciting event.

Type 1:

A syndrome that develops after an initiating noxious event (injury, surgery, or infarction) or a cause of immobilization.

Type 2:

Causalgia, syndrome that develops after a nerve injury.

Rheumatology Secrets Chapter 65

29
Q

List 6 Risk factors for DVT 🔑🔑

A
  1. OCP
  2. Immobility
  3. Obesity
  4. Pregnancy
  5. Malignancy
  6. Coagulopathy
  7. Trauma
  8. Surgery
30
Q

Mention 4 risk factors for DVT in ABI patient.

A
  1. Age > 40
  2. Presence of clotting disorder
  3. Severe Injury
  4. Bone Fracture
  5. Prolonged immobilization > Cast
31
Q

List 4 signs of DVT. When do you raise suspicion? 🔑🔑

A
  1. Pitting Edema
  2. Tenderness
  3. Swelling >3cm compared to asymptomatic leg
  4. Dilated superficial veins
  5. Paresis
  6. Recent decrease in activity > 3 days

Stroke Rehabilitation Clinician Handbook 2020 Model 6 pg27

32
Q

What is currently the gold-standard assessment to confirm a diagnosis of DVT? PE? 🔑🔑

A

DVT

  1. Magnetic resonance venography

New gold standard, sensitivity of 94.7% and a specificity of 100%

  1. Doppler ultrasonography
  2. Contrast venography

Used to be gold standard, sensitivity 70-100%, and specificity from 60-88%)

X-ray venograms are invasive they are typically only used now when an ultrasound yields negative results

PE

  1. Computed tomography pulmonary angiogram. (CTPA)
  2. Pulmonary Ventilation (V) and Perfusion (Q) Scan (pregnant women)

Cuccurollo 4th Edition Chapter 2 TBI pg87

ERABI Module 8 pg15

33
Q

Recently admitted patient with hemiparesis post stroke. Patient is on LMWH (Clexane) as prophylactic anticoagulation. When do you consider stopping Clexane? 🔑🔑

A

It is common practice to use ambulation of 150 ft (45 meter) as the threshold to discontinue prophylactic anticoagulation.

In PMR hospital we have parallel bar which measure 10 meter for full cycle x 5 = 50 meter.

Braddom 6th Edition Chapter 44 Stroke pg963

34
Q

Mention 2 prophylactic measure for DVT in stroke patient. 🔑

A
  1. Low molecular weight heparin (LMWH)
  2. Intermittent pneumatic compression

Braddom 6th Edition Chapter 44 Stroke pg963

35
Q

Treatment of Venous Thromboembolism

A
  1. Heparin Therapy
    1. LMHW 5000 IU S/C q8h
    2. Clexane 40mg/0.4ml S/C OD
    3. Paradexa 150mg PO BID
    4. Xarelto 15mg PO BID 3 weeks → 20mg PO BID
  2. Warfarin INR 2-3
  3. Compression stockings (pneumatic)
36
Q

List 3 DVT prophylaxis in TBI. DVT treatment in ABI and duration 🔑

A

Prophylaxis

  1. Intermittent pneumatic compression
  2. Low-molecular-weight heparin (LMWH): Clexane
  3. Inferior vena cava (IVC) filter

Treatment

  • First initiated with intravenous (IV) heparin
  • Warfarin takes about 5 days to achieve full anticoagulation (INR above 2).
  • During the first few days of warfarin therapy, patients are prothrombotic due to a decrease in protein C and S (natural anticoagulants) before thrombin levels diminish significantly.
  • Anticoagulation continues for 3 to 6 months.
  • IVC filter placed when anticoagulation is contraindicated.

Cuccurollo 4th Edition Chapter 2 TBI pg88

37
Q

Indication of IVC as PE prophylactic in SCI.

A
  1. Failed anticoagulant prophylaxis
  2. Contraindications to anticoagulation (active bleeding in sites that can’t be controlled – CNS, GI, lungs)
  3. Poor cardiopulmonary reserve

Cuccurollo 4th Edition Chapter 7 SCI pg597

38
Q

Treatment of DVT in any case.

A
  1. Pneumatic compression devices
  2. Clexane (LMWH)
    • Until discharge from rehabilitation
    • If documented proximal DVT, treatment continued for 6 months
    • May be stopped if patient walks 50 meter daily (parallel bar 10m x 5 rounds)
  3. Inferior vena cava (IVC) filter
39
Q

Predisposing factors for DVT 🔑 & Late DVT complications

A

Predisposing Factors

  1. Older age
  2. Virchow’s triad: Venous stasis/intimal injury/hypercoagulability
  3. Immobility
  4. Malignancy
  5. History of previous DVT
  6. LE fractures
  7. Obesity
  8. Diabetes
  9. Arterial vascular disease

Late DVT Complications

  1. Distal venous HTN: Residual obstruction of outflow—incompetent valve
  2. Swelling
  3. Spasticity
  4. Chronic pain (postthrombotic syndrome)
  5. Autonomic dysreflexia

Cuccurollo 4th Edition Chapter 7 SCI pg595-596

PassPMR - 01 Stroke (6 decks)

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