Neurology > Miscellaneous > Flashcards

Miscellaneous Flashcards

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1
Q

What is classification A of the ASIA Impairment Scale?

A

A – Complete: Complete loss of sensory and motor function below neurological level, including sacral segments S4–S5.

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2
Q

What is classification B of the ASIA Impairment Scale?

A

B – Incomplete: Sensory preserved but complete loss of motor function below neurological level, including S4–S5.

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3
Q

What is classification C of the ASIA Impairment Scale?

A

C – Incomplete: Sensory and motor function preserved below neurological level; >50% of key muscles below neurological level have power grade <3.

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4
Q

What is classification D of the ASIA Impairment Scale?

A

D – Incomplete: Sensory and motor function preserved below neurological level; ≥50% of key muscles below neurological level have power grade ≥3.

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5
Q

What is classification E of the ASIA Impairment Scale?

A

E – Normal: Normal sensory and motor function.

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6
Q

What is the definition of neurological level?

A

Neurological level: Most caudal segment of spinal cord with intact sensation and muscle power grade ≥3, provided the segment above has normal sensory and motor function.

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7
Q

What is the incidence of VTE without prophylaxis in SCI?

A

~80% incidence without prophylaxis.

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8
Q

When should VTE prophylaxis be started after trauma?

A

Start ≥72 hours post-trauma if bleeding risk is acceptable.

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9
Q

When should VTE prophylaxis be started after spinal surgery?

A

Start ≥24 hours after spinal surgery if hemostasis achieved.

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10
Q

What is the general timing principle for VTE prophylaxis?

A

Start as soon as safely possible, balancing bleeding risk.

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11
Q

What is the preferred pharmacologic agent for VTE prophylaxis?

A

LMWH is preferred.

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12
Q

Why is LMWH preferred over UFH for VTE prophylaxis?

A

LMWH is preferred because it has better efficacy, once-daily dosing, lower HIT risk, and predictable pharmacokinetics.

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13
Q

What agent should be used if there is a high bleeding risk?

A

UFH if high bleeding risk — short half-life and reversible.

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14
Q

What are the mechanical options for VTE prophylaxis?

A

Intermittent pneumatic compression devices until anticoagulation is safe.

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15
Q

What is the role of an IVC filter in VTE prophylaxis?

A

IVC filter if anticoagulation contraindicated.

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16
Q

What is the duration of VTE prophylaxis?

A

Continue until patient ambulatory or as per guidelines for high-risk patients.

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17
Q

What is a complication of UFH?

A

Monitor for HIT when using UFH.

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18
Q

What is the cause of paralytic ileus in SCI?

A

Due to reduced sympathetic tone.

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19
Q

What is the management of paralytic ileus?

A

Supportive care, nasogastric decompression.

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20
Q

What is the mechanism of constipation and fecal impaction in SCI?

A

Due to unopposed vagal stimulation.

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21
Q

What are the complications of fecal impaction?

A

Can trigger autonomic dysreflexia.

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22
Q

What is the management of bowel dysfunction in SCI?

A

Establish bowel care regimen: stool softeners, stimulant laxatives, manual evacuation if needed.

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23
Q

What is the cause of upper GI bleeding in SCI?

A

Unopposed vagal activity → increased acid secretion.

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24
Q

What is the prevention of stress ulcers in SCI?

A

PPI prophylaxis.

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25
What is the definition of neurogenic shock?
Distributive shock from loss of sympathetic tone.
26
What is the common injury level associated with neurogenic shock?
Typically injury above T6.
27
What is the mechanism of neurogenic shock?
Loss of sympathetic outflow → vasodilation and ↓ preload; unopposed vagal tone → bradycardia.
28
What are the key signs of neurogenic shock?
Hypotension, bradycardia, warm peripheries.
29
What is the cardiac involvement in neurogenic shock?
Loss of sympathetic supply to heart (T1–T4) worsens bradycardia.
30
What is the management of neurogenic shock?
MAP target 85–90 mmHg for 7 days post-injury; fluid resuscitation; vasopressors (noradrenaline); atropine/pacing for bradycardia.
31
What is the definition of autonomic dysreflexia?
Massive sympathetic discharge in response to noxious stimuli below injury.
32
What is the injury level associated with autonomic dysreflexia?
SCI above T6, typically after spinal shock resolves.
33
What are common triggers of autonomic dysreflexia?
Bladder distension, bowel impaction, pressure sores, tight clothes.
34
What is the pathophysiology of autonomic dysreflexia?
Sympathetic surge below injury → vasoconstriction and hypertension; baroreceptor response above lesion → bradycardia, flushing, headache.
35
What are the complications of autonomic dysreflexia?
Retinal haemorrhage, seizures, intracranial bleed, death.
36
What are the signs of autonomic dysreflexia?
Severe hypertension, bradycardia, headache, flushing above lesion, sweating.
37
What are the management steps for autonomic dysreflexia?
Sit upright; remove stimulus; give short-acting antihypertensives (GTN, nifedipine, hydralazine).
38
What urinary problems are associated with renal complications in SCI?
Urinary retention and overflow incontinence due to detrusor/sphincter discoordination.
39
What are the risks associated with renal complications in SCI?
Increased risk of UTI, hydronephrosis, vesicoureteral reflux.
40
What are the management principles for renal complications in SCI?
Early catheterisation; avoid long-term IDC; intermittent self-catheterisation preferred.
41
What are the risk factors for renal calculi in SCI?
Immobilisation hypercalciuria, UTIs, bladder stasis.
42
What is the prevention for renal complications in SCI?
Maintain hydration, avoid long-term IDC, monitor for stones.
43
How does paralysis evolve post-SCI?
Flaccid paralysis initially (spinal shock), then spasticity below level of lesion.
44
What is the management of spasticity in SCI?
Early physiotherapy; oral agents: baclofen, diazepam, tizanidine, dantrolene; intrathecal baclofen pump.
45
What is the management of musculoskeletal pain in SCI?
Address altered posture and contractures with physical therapy and behavioural therapy.
46
What is the cause of pressure sores in SCI?
Immobility and loss of sensation.
47
What are the major consequences of pressure sores?
Increased hospital stay, infection, autonomic dysreflexia, chronic refractory osteomyelitis.
48
What are the prevention and management measures for pressure sores?
Daily skin inspection and moisturiser; good hygiene and perineal care; pressure-relieving mattress; reposition every 2 hours; monitor nutrition; minimise friction/shear; patient/carer education; early referral to wound care/spinal injury team.
49
What are the key elements of psychological support in SCI?
Provide correct information; develop a care plan; involve social worker; communicate prognosis sensitively.
50
What is the effect on lung volumes in high SCI?
Reduced tidal volume, IRV, ERV, VC, TLC; FRC may be unchanged or slightly increased; peak cough flow reduced by 50–80%.
51
What is the cause of diaphragmatic breathing in SCI?
Loss of intercostal and accessory muscles leads to reliance on diaphragm.
52
Why does chest wall compliance reduce in SCI?
Immobility and loss of rib movement decrease chest wall compliance.
53
What is the effect of supine position on VC in SCI?
Supine improves VC by pushing diaphragm into a mechanically advantageous position.
54
What is the spirometry pattern in SCI?
Restrictive pattern.
55
What are the causes of cough impairment in SCI?
Loss of abdominal and intercostal muscles reduces expiratory force, impairing cough.
56
What are the causes of neurogenic shock?
Loss of sympathetic tone from high spinal cord injury.
57
What is the mechanism of hypotension in neurogenic shock?
Peripheral vasodilation → decreased SVR → reduced preload and cardiac output.
58
What is the mechanism of bradycardia in neurogenic shock?
Loss of sympathetic input to heart (T1–T4) with unopposed vagal tone.
59
What is the injury level associated with neurogenic shock?
Typically injuries above T6.
60
What is the postural hypotension mechanism?
Loss of baroreceptor reflexes and vascular tone in lower limbs.
61
What is meant by fixed cardiac output?
Cardiac output fails to increase in response to physiological demand due to absent sympathetic drive.
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