Neuro Flashcards
(43 cards)
1
Q
Clinical evidence of high ICP
A
Vomiting papilledema confusion behavioral changes Cushing’s Triad (Bradycardia, HTN, changes in respiratory pattern)
2
Q
Risks of increased ICP during induction
A
Vomiting Aspiration Changes in Hemodynamic status Hypoxia Further increase in ICP
3
Q
DDX of Hypotension and Tachycardia intra-op
A
Bleeding
Arrhythmia
Cardiac Ischemia
Venous Air Embolism (VAE)
4
Q
Manifestations of VAE
A
Hypoxemia Hypercapnea Decreased ETCO2 HoTN Cardiac Dysrhythmia Cardiovascular collapse
5
Q
Diagnostic Methods for VAE
A
TEE (most sensitive) > Precordial Doppler (Mill-wheel murmur) > PA Catheter > ETN2 > ETCO2
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!)
7
Q
Normal vs Elevated ICP levels
A
Nrml: < 15 mmHg
Elevated: >20 mmHg
8
Q
Cerebral Perfusion Pressure Formula
A
CPP = MAP - ICP (or CVP (whichever is greater))
9
Q
Volatile Effects on Brain Physiology
A
Uncouples
CBF: Increase (> 1 MAC)
CMRO2: Decrease
10
Q
Propofol Effect on Brain Physiology
A
Couples
CBF: Decrease
CMRO2: Decrease
11
Q
Etomidate Effect on Brain Physiology
A
Couples
CBF: Decrease
CMRO2: Decrease
- Direct vasoconstrictor
12
Q
Benzodiazepine Effect on Brain Physiology
A
Couples
CBF: Decrease
CMRO2: Decrease
13
Q
Opioid Effect on Brain Physiology
A
CBF: No effect
CMRO2: No effect
14
Q
Nitrous Effect on Brain Physiology
A
CBF: Increase
CMRO2: Increase
15
Q
Ketamine Effect on Brain Physiology
A
CBF: Increase
CMRO2: Increase
16
Q
Treatment of Increased ICP
A
- Positional Therapy
- Head at 30 degrees
- Support Hemodynamics
- SBP > 110mmHg, MAP > 90mmHg
- CPP > 70
- Analgesia and Sedation
- Adequate sedation and pain control
- Propofol can decrease ICP (careful not to lower CPP)
- Avoid Hypoxemia (PaO2 < 60)
- Hyperventilation (PaCO2 30-35)
- Goal Hct greater than 30%
- Patient should be normothermic
- Avoid aggressive rewarming
- Osmotic Therapy
a. Mannitol
b. Furosemide
c. Hypertonic saline (NaCl 3% to 5%)
17
Q
Risks of Sitting Position
A
- Venous Air Embolism
- Hypotension
- Hyperflexion of the neck
- Peripheral nerve injury
- Pneumocephalus
18
Q
Benefits of Sitting Position
A
- Fewer cranial nerve defects
- Less potential for brain edema and hemorrhage
- Improved ventilation
19
Q
DDx for delayed awakening Neuro patient
A
- Bleeding*
- Edema*
- Tension Pneumocephalus*
- Oversedation
- Hypercarbia
- 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
- Early detection
- Minimize elevation of head
- Use of bone wax: Minimize open venous channels
- Maintain euvolemia
- Avoid PEEP/valsalva
22
Q
Cerebral Aneurysm: Hunt and Hess Classificaitons
A
- Grade 0: unruptured aneurysm
- Grade 1: Asymptomatic or minimal headache and slight nuchal rigidity
- Grade 2: Moderate to severe headache, nuchal rigidity, no neurologic deficit other than CN palsy
- Grade 3: Drowsiness, confusion, or mild focal deficit
- Grade 4: Stupor, moderate to severe hemiparesis, early decerebration, vegetative disturbance
- Grade 5: Deep coma, decerebrate rigidity, moribund
23
Q
Cerebral Vasospasm
A
- Develops 3-12 days after SAH (peak on day 7-11)
- Presents w/ neurologic deterioration and drowsiness
- Dx made via angiography, Transcranial Doppler, or clinical progression
- Increased ICP and hypovolemia increases likelihood
24
Q
Prophylaxis and Tx of Vasospasm
A
- Nimodipine
- 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
Glasgow Coma Scale
```
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
Autonomic Dysreflexia
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
Symptoms of Autonomic Dysreflexia
1. Hypertension
2. Reflex Bradycardia
3. Headache
4. Malaise
5. Piloerection
6. Sweating and flushing ABOVE level of SCI
28
Treatment of Autonomic Dysreflexia
1. Sit patient up
2. Identify and remove noxious stimuli
3. Treat HTN
29
How does chronic HTN effect the cerebral auto-regulation curve?
Causes a rightward shift
| - requires higher than normal pressure to provide adequate cerebral perfusion
30
Ddx for AMS after Cerebral Aneurysm repair
1. Vasospasm
2. Hematoma formation
3. Hydrocephalus
4. Seizure
5. Increased cerebral edema
31
'Triple H' Therapy for Cerebral Aneurysms
1. Hypertension
2. Hypervolemia
3. Hemodilution
32
How do you distinguish between Cerebral Salt Wasting Syndrome (CSWS) and SIADH
**Both can cause Hyponatremia
CSWS - Hypovolemic
SIADH - Euvolemic
- Tx: Fluid restriction and Diuresis
33
Ddx for delayed emergence
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
Define cerebral autoregulation
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
What is the relationship of Myasthenia Gravis to Depolarizing and Non-Depolarizing NMBs?
```
Depolarizing NMBs (Sux): Resistant
Non-Depolarizing NMBs (Roc): Sensitive
```
36
Factors that help predict post-op ventilator support in Myasthenia Gravis
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
Criteria to clear a C-Spine
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
Why is LR avoided in Head trauma?
Small amount of free water (100ml per liter) could lead to increased brain edema
39
Why is Hyperventilation help only temporarily (24-48hrs) in increased ICP?
HCO3 levels in the CSF adjust to compensate for the change in PaCO2
40
Is Hyperventilating recommended in a patient with head trauma?
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
What is Spina Bifida Occulta?
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
What is Spina Bifida Cystica?
Failed closure of neural arch WITH herniation of merges (meningocele) or meninges and neural elements (Myelomeningocoele) through vertebral defect
43
Is Neuraxial Anesthesia contraindicated for Spina Bifida Occulta or Cystica?
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
