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Neuro Flashcards

1
Q

What volatile anesthetic would you choose for a Neuro case and why?

A

Isoflurane because it causes the greatest drop in CMR

And it facilitates absorption of CSF

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2
Q

What are the dangers of using volatile anesthetic in a Neuro case with suspected ischemia?

A

Volatiles increase CBF by vasodilation, but not in ischemic areas so you could make this worse by circulatory steal

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3
Q

Would you use lidocaine infusion in a Neuro case? Why or why not?

A

I would because lidocaine decreases CBF and may also have neuroprotective effects
It also decreases MAC and opioid requirements –> reduces emergence delirium

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4
Q

What physical exam signs do you look for ICP?

A 
Papilledema
Focal signs
CN deficits
Lethargy
Cognition
Pupil size
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5
Q

How do you treat high ICP.

A

Head of bed up
Steroids if vasogenic edema (not in trauma)
Diuretics - goal of serum osmolality of 300-315 mOsm/L
Moderate hyperventilation (PaCO2 30-33 mmHg)
Anesthetics
Normothermia
Hypertonic saline
EVD

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6
Q

What are the contraindications for using mannitol?

A 
Intracranial aneurysm 
AVM
ICH 
Subdural hematoma
(Until cranium is opened)
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7
Q

What are the potential dangers of using mannitol?

A

Rebound edema
Transient increase in intravascular volume –> pulmonary edema
Rupture of aneurysm/AVM/bridging veins due to abrupt change in transmural wall pressure and expansion of hematoma
Hypotension

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8
Q

What kind of preoperatively tests do you want for craniotomy surgery?

A

CT or MRI - looking for evidence of brain edema, size and location of tumors or aneurysm, midline shift or compression of the ventricles
Labs: glucose level, BMP for electrolytes (SIADH or diuretic therapy), Hct

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9
Q

How will you T this patient with a cranial mass up for surgery?

A

Make sure they get their anticonvulsant and steroid

Correct electrolytes

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10
Q

What other monitors do you want for a craniotomy case?

A

Arterial line - zeroed at external auditory meatus for measurement of CPP at circle of Willis
Central line for fluids, vasopressors and aspiration of catheter in case of VAE
Foley catheter

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11
Q

How will you induce a patient with high ICP?

A

Modest hyperventilation PaCO 30-33
Propofol + lidocaine + fentanyl + rocuronium - modified RSI
Fentanyl to blunt tachycardia response to DL versus esmolol
Propofol for deceased CMR and CBF
Lidocaine for decreased dosages of fentanyl/propofol and decreased CBF
Modified RSI to maintain normocarbia and prevent aspiration

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12
Q

Could you use succinylcholine in a patient with high ICP?

A

Yes, you could because the increase in ICP caused by succinylcholine is transient and failed airway, aspiration, hypoxemia and hypercarbia will be detrimental to this patient and also cause increased ICP

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13
Q

Patient with high ICP is tachycardic and hypertensive after intubation, what do you do?

A

Bolus of propofol (deepen anesthetic)

Beta blockade

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14
Q

How will you maintain a patient with high ICP for craniotomy?

A

TIVA
Or MAC < 0.5 volatile plus IV anesthetics: propofol, lidocaine, remifentanil
Continue hyperventilating (PaCO2 30-35)
IVF - no glucose! Causes increased ischemic brain injury

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15
Q

Why not hyperventilate below PaCO2 of 30?

A

Little to no benefit

Can cause cerebral ischemia and impair oxygen dissociation from hemoglobin

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16
Q

How will you emerge this patient?

A

Want to avoid coughing on tube - lidocaine down ETT
Resume spontaneous breathing
Reverse

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17
Q

What is your differential diagnosis for delayed wakening in a crani case?

A

Drugs: opioid, inhalational, NMB
Stroke
Metabolic derangement: glucose, hypoNa
Pneumocephalus

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18
Q

What monitors would you use for a posterior craniotomy?

A

TEE
Precordial Doppler
Central line with tip at junction of RA and SVC, syringe attached

Other monitors for VAE?
Esophageal stethoscope
PAC (increase in PAP)
Mass spec of nitrogen on the monitor
Drop on ETCO2 or oxygen
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19
Q

Where should CPP be kept in a crani case with increased ICP?

A

70-110

This correlates with a MAP 140-110 for ICP of 30

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20
Q

At the end of a longer spine case a patient wakes up and has visual loss, but no pain? What are you worried about? How did this happen?

A

Intraoperative optic nerve damage

Due to increase orbital venous pressure and decreased perfusion

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21
Q

What are the anesthetic considerations for prone positioning?

A

Airway and facial edema
POVL 2/2 impaired venous drainage
Cortical blindness due to decreased perfusion of the visual cortex
Abdominal compression–> impede venous return, contribute to blood loss thru engorgement of epidural veins!
Femoral artery occlusion –> a vascular necrosis
Genitals, knees, eyes, ENT
Brachial plexus injury

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22
Q

How will you reduce the risk of POVL?

A

Reverse Trendelenburg position
Avoid hypotension
Padding of pressured areas
Neutral head position for draining of head/neck

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23
Q

For an aneurysm case, what kind of monitors do you want?

A

Arterial line - tight BP control to avoid aneurysm rupture
Central line in femoral - cordis for volume resuscitation due to massive blood loss. Femoral to avoid imparing head/neck drainage with subclavian/jugular

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24
Q

How does mannitol work?

A

Osmotic diuresis

Must have intact bbb!

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25
Q

Why keep MAC < 0.5 in intracranial cases?

A

Because levels of volatiles above this cause cerebral vasodilation

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26
Q

Surgeon asks for hypotension during an aneurysm case, how will you do this?

A

I would start a nicardipine drip since it is titratable
Would also bolus propofol to decrease CMRO2
Keep Mac < 0.5

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27
Q

What is diabetes insipid us?

A

Brain is not releasing ADH

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28
Q

What is the treatment of diabetes insipidus?

A

Volume replacement
Vasopressin
Monitor sodium and fluid status

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29
Q

Tell me everything about motor evoked potentials?

A

Assess the lateral corticospinal tract

Minimally affected by IV anesthetics: ketamine, etomidate, opioid, dexmed

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30
Q

What factors effect evoked potentials?

A

Hypoxia
Hypothermia/hyperthermia
Anemia

31
Q

Which evoked potentials are most sensitive to anesthetic?

A

Visual> SSEP > motor > auditory

32
Q

What are the anesthetic goals in TBI?

A 
CPP between 50-70
PaCO2 35-40 (avoid hyperventilation)
Treat ICP greater than 20
Keep Bg below 180
Use anticonvulsants for within 1st week of head injury (phenytoin and carbamazepine have been should to reduce the incidence of early post-traumatic seizures

Do not use albumin or fluid with dextrose
Steroids don’t improve outcome and therefore are not recommended

33
Q

What would you do if a paraplegic patient suddenly became hypertensive and Bradycardic?

A

Ask surgeon to stop stimulation
Deepen anesthetic
Give IV hydralazine, NTG, nitroprusside, magnesium, nicardipine
SL nifedipine if no IV access
Ensure bladder is emptying in Foley
Place arterial line
Monitor patient for sequelae: ICH, stroke, MI, seizure, arrythmia, pulm edema

34
Q

What is the pathophysiology of autonomic hyperreflexia?

A

Unopposed sympathetic efferent flow below the level of the lesion due to lack of inhibitory signals from higher CNS

Activation of ascending spinothalamic and posterior columns causing lower extremity and splanchnic vasoconstriction thru unopposed sympathetic reflex
Reflex Brady

35
Q

When is the risk of succinylcholine induced hyperkalemic arrest highest after a spinal cord injury?

A

Between 4 weeks and 5 months

36
Q

What is the pathophysiology of neurogenic pulmonary edema?

A

Head or cervical injury resulting in sympathetic mediated systemic vasoconstriction –> decreased LV compliance and subsequent pulm edema

37
Q

What are your concerns with a cervical spine injury?

A

Difficult Airway
Loss of diaphragmatic function –> need for vent
Inability to cough/handle secretions/impaired airway reflexes
Aspiration risk due to paralytic ileus
Temperature regulation issues (loss of vasoconstriction below the level of the lesion)
End organ damage : increased ICP, MI,
Arrythmia due to autonomic dysfunction
Positioning difficulty or injury (sacral ulcers)
Stasis –> DVT

38
Q

Would you administer steroids to someone with spinal cord injury? Why or why not?

A

No, due to lack of evidence for benefit.
Also, side effects: infection, GIB, respiratory compromise, death, HTN, fluid retention, hyperglycemia, impaired wound healing and immunosuppression

39
Q

What is spinal shock?

A

Flaccid paralysis
Paralytic ileus
Loss of sensation, reflexes, SNS vasomotor tone, temperature regulation below the level of the injury
Loss of cardiac accelerator fibers - inability to compensate for hypovolemia and decreased SVR

40
Q

What are the symptoms of an anterior cerebral artery stroke?

A

Lower extremity weakness and sensory loss on contralateral side

41
Q

What are deficits from a MCA stroke?

A

Aphasia

Facial and upper and lower extremity weakness and numbness on the contralateral side

42
Q

If you suspect a stroke, what should you do?

A 
1. ABCs! Call for help
Support BP, maintaining MAP > 70 
IV access
2. Mini Neuro exam, check glucose
Get CT/MRI
Consult neurologist
43
Q

In what time frame can you give tPA?

A

Under 4.5 hours

44
Q

What’s included in the work up for stroke?

A

TTE with bubble study
Carotid US
Thrombophilia study
Anti platelet therapy

45
Q

What is the difference between CSW and SIADH?

A

SIADH - euvolemia

CSW - hypovolemia, urine sodium > 100

46
Q

What is the treatment for SIADH?

A

Fluid restriction
Diuresis
Demeclocycline to block ADH in the kidney

47
Q

What is the treatment for CSW?

A

Fluid and electrolyte resuscitation

48
Q

What are the criteria to clear a C-spine?

A
  1. No cervical pain or tenderness
  2. No distracting pain
  3. No paresthesias or Neuro deficits
  4. Normal mental status
  5. Greater than 4 yo

If not met, need C-spine lateral and AP views
T/L spine lateral and AP views
Open mouth Odontoid view

49
Q

Why is a CPP in a TBI patient of 50-70 best?

A

> 70 is associated with higher incidence of ARDS

< 50 is associated with cerebral ischemia

50
Q

Why wouldn’t you use nitrous oxide in a Neuro case with TBI or high ICP?

A
  1. You want patient breathing 100% FiO2
  2. Nitrous oxide causes increase in CBF alone or with other agents
  3. Nitrous oxide is sympathomimetic
  4. Nitrous oxide can cause expansion of air pockets further elevating ICP
51
Q

Which cranial nerve does a blown pupil indicate?

A

Cranial nerve 3 palsy from uncal herniation

52
Q

What is cushing’s triad?

A

Increase in BP due to cerebral ischemia and reflex bradycardia from this systemic increase, plus irregular respiration

53
Q

What are the 3 reasons to give mannitol?

A
  1. Osmotic diuresis, shifting from intracranial compartment to the intravascular compartment
  2. Decreasing the production of CSF
  3. Inducing reflex cerebral vasoconstriction from decreased blood viscosity
54
Q

What are the CV effects of myasthenia gravis?

A 
Mild HTN
Afib
1st degree AV block
Cardiomyopathy
Myocarditis
Dyspnea
Diastolic dysfunction
55
Q

What are some of the symptoms of myasthenia gravis?

A

Diplopia (blurry vision)
Ptosis
Bulbar weakness a difficulty swallowing, dysphagia, dysarthria
Easy fatigued - eyes, face, neck and limbs
Weakness
Dyspnea

56
Q

What are the risk factors for postoperative ventilation?

A
  1. Disease duration of over 6 years
  2. Pyridostigmine dose > 750 mg/day
  3. Vital capacity < 2.9 L or 4 ml/kg
  4. Concomitant pulmonary disease
  5. PIP < -25 H2O
  6. NIF < - 20
57
Q

How could you tell the difference between cholinergic crisis and myasthenia crisis?

A 
Pupil size
Muscle fasciculations (cholinergic)
Edrophonium test (if gets better = MG)
58
Q

What are the signs and symptoms of cholinergic crisis?

A 
Salivation
Miosis
N/V
Urinary urgency/frequency 
Muscle fasciculations
Bradycardia
59
Q

What would you use EMG for in a spine surgery

A

Monitoring peripheral nerves to prevent nerve root injury during pedicel screw placement

60
Q

Where do you place a Precordial Doppler?

A

Right of the sternum between 2-4 ribs

61
Q

What’s the optimum position for central line for VAE?

A

2 cm below the SVC-atrial junction

62
Q

With pituitary resection, what is the patient at risk for?

A

Massive hemorrhage from cavernous sinus and internal carotid artery

63
Q

Is PEEP recommended in the treatment of VAE?

A

Can be helpful to increase venous pressure at the surgical site, but it is not as effective as jugular venous occlusion

Can shift atrial pressures and cause paradoxical embolism in a patient with PFO

64
Q

How do you diagnose diabetes insipidus?

A

Urine specific gravity less than 1.005
Rising sodium
Urine osmolality increases with admin of exogenous ADH

No hyperglycemia

65
Q

What is the differential for polyuria?

A

Hyperglycemia
Diuretic use
Mobilization of third space
Diabetes insipidus

66
Q

How do you treat DI?

A

Replace loss with hypoosmolar fluid at equal rate to hourly maintenance requirements + 2/3 UOP
Desmopressin if require >350 ml/HR of replacement

67
Q

What is the blood supply to the spinal cord?

A

Two posterior spinal arteries supply posterior 1/3 (sensory)
1 anterior spinal artery supply anterior 2/3 (motor) from vertebral and basilar arteries.
6-8 radicular arteries feed anterior spinal artery
Artery of Adamkiewicz = major supplier to anterior lower 2/3 cord.

68
Q

What is the artery of Adamkiewicz usually located?

A

T9-12 (60%)

Otherwise anywhere from T5-L5

69
Q

How would you assess for residual heparin effects?

A

Heparin-protamine titration assay or ACT

70
Q

Why is lasix better than mannitol?

A

Because mannitol causes a transient increase in ICP by shifting volume intravascularly
Have to have an intact BBB with mannitol

71
Q

How can you tell the difference between brain stem ischemia and VAE?

A

Difference in ETCO2
High CVP or PA pressures in VAE
Should be hypercarbia in brain stem ischemia due to Hypoventilation in inadequately relaxed patient

72
Q

What are the absolute contraindications to tPA?

A

uncontrolled HTN with SBP > 185, DBP > 110
Serious head trauma or stroke within last 3 months
Coagulopathy or TCP
Acute ICH
Therapeutic LMWH w/in 24h
Factor Xa inhibitors, direct thrombin inhibitors
Hypoglycemia < 50
Hyperglycemia > 400

73
Q

What are the relative contraindications to tPa?

A 
Advanced age (>80)
Severe stroke and coma
Recent major surgery 
Arterial puncture of a non compressible vessel within the last 7 days
Recent GI Gu bleed
Recent MI (3 months)
Seizure at onset
Presence of neoplasm, AVM, aneurysm
74
Q

Why isn’t hyperventilation a long term treatment option for increased ICP.

A

Because ions will move into the CSF in 6-12 hours to normalize the ph and thereby decrease vasoconstriction effects

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