Neuro Flashcards

1
Q

Clinical evidence of high ICP

A
Vomiting
papilledema
confusion
behavioral changes 
Cushing’s Triad (Bradycardia, HTN, changes in respiratory pattern)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Risks of increased ICP during induction

A
Vomiting
Aspiration 
Changes in Hemodynamic status 
Hypoxia 
Further increase in ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

DDX of Hypotension and Tachycardia intra-op

A

Bleeding
Arrhythmia
Cardiac Ischemia
Venous Air Embolism (VAE)

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

Manifestations of VAE

A
Hypoxemia
Hypercapnea 
Decreased ETCO2
HoTN
Cardiac Dysrhythmia
Cardiovascular collapse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diagnostic Methods for VAE

A

TEE (most sensitive) > Precordial Doppler (Mill-wheel murmur) > PA Catheter > ETN2 > ETCO2

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

Management of VAE

A

Surgeon:

  • Flood the field
  • Control open blood vessels
  • Apply bone wax to exposed bone

Anesthesiologist:

  • Increase FiO2 to 100%
  • Discontinue N2O (if using)
  • Aspirate air from CVP catheter (if placed)
  • Compress neck veins (inc venous pressure)
  • Place operative site below the patients heart (place in Trendelenburg)
  • Place patient in Left Lateral Decubitus (if possible)
  • Support BP w/ fluids and inotropes (Epi!)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Normal vs Elevated ICP levels

A

Nrml: < 15 mmHg

Elevated: >20 mmHg

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

Cerebral Perfusion Pressure Formula

A

CPP = MAP - ICP (or CVP (whichever is greater))

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

Volatile Effects on Brain Physiology

A

Uncouples
CBF: Increase (> 1 MAC)
CMRO2: Decrease

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

Propofol Effect on Brain Physiology

A

Couples
CBF: Decrease
CMRO2: Decrease

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

Etomidate Effect on Brain Physiology

A

Couples
CBF: Decrease
CMRO2: Decrease
- Direct vasoconstrictor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Benzodiazepine Effect on Brain Physiology

A

Couples
CBF: Decrease
CMRO2: Decrease

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

Opioid Effect on Brain Physiology

A

CBF: No effect
CMRO2: No effect

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

Nitrous Effect on Brain Physiology

A

CBF: Increase
CMRO2: Increase

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

Ketamine Effect on Brain Physiology

A

CBF: Increase
CMRO2: Increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment of Increased ICP

A
  1. Positional Therapy
    • Head at 30 degrees
  2. Support Hemodynamics
    • SBP > 110mmHg, MAP > 90mmHg
    • CPP > 70
  3. Analgesia and Sedation
    • Adequate sedation and pain control
    • Propofol can decrease ICP (careful not to lower CPP)
  4. Avoid Hypoxemia (PaO2 < 60)
  5. Hyperventilation (PaCO2 30-35)
  6. Goal Hct greater than 30%
  7. Patient should be normothermic
    • Avoid aggressive rewarming
  8. Osmotic Therapy
    a. Mannitol
    b. Furosemide
    c. Hypertonic saline (NaCl 3% to 5%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Risks of Sitting Position

A
  1. Venous Air Embolism
  2. Hypotension
  3. Hyperflexion of the neck
  4. Peripheral nerve injury
  5. Pneumocephalus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Benefits of Sitting Position

A
  1. Fewer cranial nerve defects
  2. Less potential for brain edema and hemorrhage
  3. Improved ventilation
19
Q

DDx for delayed awakening Neuro patient

A
  1. Bleeding*
  2. Edema*
  3. Tension Pneumocephalus*
  4. Oversedation
  5. Hypercarbia
  6. Hypothermia
20
Q

Pathophysiology of Venous Air Embolism

A

Air bubbles mechanically obstruct pulmonary vasculature leading to hypoxemia and resultant vasoconstriction, V/Q mismatch, increased PAP, and reduced CO

21
Q

Prevention of a VAE

A
  1. Early detection
  2. Minimize elevation of head
  3. Use of bone wax: Minimize open venous channels
  4. Maintain euvolemia
  5. Avoid PEEP/valsalva
22
Q

Cerebral Aneurysm: Hunt and Hess Classificaitons

A
  1. Grade 0: unruptured aneurysm
  2. Grade 1: Asymptomatic or minimal headache and slight nuchal rigidity
  3. Grade 2: Moderate to severe headache, nuchal rigidity, no neurologic deficit other than CN palsy
  4. Grade 3: Drowsiness, confusion, or mild focal deficit
  5. Grade 4: Stupor, moderate to severe hemiparesis, early decerebration, vegetative disturbance
  6. Grade 5: Deep coma, decerebrate rigidity, moribund
23
Q

Cerebral Vasospasm

A
  1. Develops 3-12 days after SAH (peak on day 7-11)
  2. Presents w/ neurologic deterioration and drowsiness
  3. Dx made via angiography, Transcranial Doppler, or clinical progression
  4. Increased ICP and hypovolemia increases likelihood
24
Q

Prophylaxis and Tx of Vasospasm

A
  1. Nimodipine
  2. Triple “H” Therapy: Hypertension, Hypervolemia, Hemodlution
    a. Increase CBF, Increase CPP, improve Cerebral Blood Flow w/ decreased blood viscosity
    b. SBP raised to 160-200 mmHg in clipped aneurysms
    c. Hct decreased to 33%
25
Q

Glasgow Coma Scale

A
Eyes open 
    4 - Spontaneous
    3 - To speech
    2 - To pain
    1 - None
Best Verbal Response 
    5 - Oriented
    4 - Confused
    3 - Inappropriate words
    2 - Incomprehensible sounds
    1 - None
Best Motor Response
    6 - Follows commands
    5 - Localizes to pain
    4 - Withdrawal to pain
    3 - Flexion to pain
    2 - Extension to pain
    1 - None
26
Q

Autonomic Dysreflexia

A
  1. Noxious stimulus below level of Spinal Cord Injury causes a massive reflex sympathetic discharge
  2. Occurs in pts w/ SCI lesion at T6 or above
  3. Usually develops within first 6 months to 1 year after initial SCI
27
Q

Symptoms of Autonomic Dysreflexia

A
  1. Hypertension
  2. Reflex Bradycardia
  3. Headache
  4. Malaise
  5. Piloerection
  6. Sweating and flushing ABOVE level of SCI
28
Q

Treatment of Autonomic Dysreflexia

A
  1. Sit patient up
  2. Identify and remove noxious stimuli
  3. Treat HTN
29
Q

How does chronic HTN effect the cerebral auto-regulation curve?

A

Causes a rightward shift

- requires higher than normal pressure to provide adequate cerebral perfusion

30
Q

Ddx for AMS after Cerebral Aneurysm repair

A
  1. Vasospasm
  2. Hematoma formation
  3. Hydrocephalus
  4. Seizure
  5. Increased cerebral edema
31
Q

‘Triple H’ Therapy for Cerebral Aneurysms

A
  1. Hypertension
  2. Hypervolemia
  3. Hemodilution
32
Q

How do you distinguish between Cerebral Salt Wasting Syndrome (CSWS) and SIADH

A

**Both can cause Hyponatremia
CSWS - Hypovolemic
SIADH - Euvolemic
- Tx: Fluid restriction and Diuresis

33
Q

Ddx for delayed emergence

A
  1. Residual anesthetic, narcotic, and/or sedative drug effect
  2. Hyponatremia
  3. Cerebral Ischemia/Hypoperfusion
  4. Hypoglycemia
  5. Hypothermia
  6. Hypoxia
  7. Hypercarbia
  8. Liver or kidney disease
  9. Medication error
  10. Pseudocholinesterase deficiency
34
Q

Define cerebral autoregulation

A

Myogenic response of vascular smooth muscle of the intracranial cerebral arterioles to dynamically maintain a nearly constant CBF in face of changing CPP
- Normally between MAP of 50 and 150

**Autoregulatory curve shifts to right in uncontrolled HTN

35
Q

What is the relationship of Myasthenia Gravis to Depolarizing and Non-Depolarizing NMBs?

A
Depolarizing NMBs (Sux): Resistant 
Non-Depolarizing NMBs (Roc): Sensitive
36
Q

Factors that help predict post-op ventilator support in Myasthenia Gravis

A
  1. Duration of myasthenia gravis greater than or equal to 6 years
  2. Chronic respiratory disease
  3. Dose of pyridostigmine greater than or equal to 750 mg per day
  4. Vital capacity less than or equal to 2.9 L
37
Q

Criteria to clear a C-Spine

A
  1. No cervical pain or tenderness
  2. No paresthesia or neurologic deficits
  3. Normal mental status
  4. No distracting pain
  5. > 4 years of age

Radiographs

a. ) Negative lateral c-spine showing C1-T1
b. ) An open mouth odontoid view
c. ) lateral plain film

38
Q

Why is LR avoided in Head trauma?

A

Small amount of free water (100ml per liter) could lead to increased brain edema

39
Q

Why is Hyperventilation help only temporarily (24-48hrs) in increased ICP?

A

HCO3 levels in the CSF adjust to compensate for the change in PaCO2

40
Q

Is Hyperventilating recommended in a patient with head trauma?

A

No, unless there was a risk of brain stem herniation

**Risk of exacerbating cerebral ischemia by inducing cerebral vasoconstriction in a patient with lower than normal cerebral blood flow following head trauma

41
Q

What is Spina Bifida Occulta?

A

Failed fusion of neural arch WITHOUT herniation of meninges or neural elements

  • Defect limited to a single vertebra
  • Very common, can be considered a normal variant
42
Q

What is Spina Bifida Cystica?

A

Failed closure of neural arch WITH herniation of merges (meningocele) or meninges and neural elements (Myelomeningocoele) through vertebral defect

43
Q

Is Neuraxial Anesthesia contraindicated for Spina Bifida Occulta or Cystica?

A

No

  • Neuraxial is generally safe
  • Recommend to insert needle remote from site of malformation seen on imaging
  • Patients at higher risk of post dural puncture headache
  • Epidural may be difficult and may be unreliable
  • May need epidural in situ to avoid autonomic hyperreflexia during labor