Neuro Anesthesia Part 2 Flashcards

1
Q

Craniotomy

A

Presentation/Diagnosis
* 40 to 60 years of age
* signs and symptoms reflecting increasing ICP (intracranial pressure)
* adult onset seizure disorder
* CT or MRI

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2
Q

Types of tumors & locations

not on test

A
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3
Q

Grading: I & II

A

Grade I
The tumor grows slowly, has cells that look similar to normal cells, and rarely spreads into nearby tissues. It may be possible to remove the entire tumor by surgery.
Grade II
The tumor grows slowly, but may spread into nearby tissue and may become a higher-grade tumor.

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4
Q

Grade III and IV

A

Grade III:
The tumor grows quickly, is likely to spread into nearby tissue, and the tumor cells look very different from normal cells.
Grade IV:
The tumor grows very aggressively, has cells that look very different from normal cells, and is difficult to treat successfully.

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5
Q

Grading…

A

The chance of recovery (prognosis) and choice of treatment depend on the type, grade, and location of the tumor and whether cancer cells remain after surgery and/or have spread to other parts of the brain

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6
Q

Meningioma

A
  • 12-20% of all primary brain tumors
  • the meniges are 3 membranes that cover the brain and spinal cord
  • usually benign, arises from the meninges of the brain and spinal cord
  • most common in middle-aged adults, esp women
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7
Q

Meningioma

A
  • 12-20% of all primary brain tumors
  • the meniges are 3 membranes that cover the brain and spinal cord
  • usually benign, arises from the meninges of the brain and spinal cord
  • most common in middle-aged adults, esp women
  • The M & M rate of meningiomas are difficult to assess accurately.
  • Some are discovered fortuitously when a CT scan or MRI is done for unrelated diseases or conditions.
  • Thus, some patients die with their meningioma and not secondary to it.
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8
Q

Morbidity and Mortality

A

Factors that may predict a higher postoperative morbidity rate:
* patient-related factors
* advanced age
comorbid states: DM/CAD/Altered LOC

Tumor factors
* location / size / vascularity of tumor
* neural involvement
* prior surgery &/or radiotherapy

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9
Q

Sequencing

A

Preoperative Evaluation…
Preparation of Patient: Monitors…
Induction of Anesthesia…
Mayfield pin placement…
Positioning of the patient…
Mannitol, Decadron, I-stat & Glucose …
Maintenance of Anesthesia…
Emergence…

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10
Q

Evidence of intracranial hypertension:

A
  • nausea and vomiting
  • hypertension
  • bradycardia
  • personality change
  • altered level of consciousness
  • altered pattern of breathing
  • papilledema
  • seizures (levels)
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11
Q

MRI - midline shift

A

Midline shift > 5 mm and/or encroachment on CSF cisterns suggest intracranial hypertension
Avoid preop pharmacologic sedation and ventilatory depression

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12
Q

Blood Diversion Phenomenon

A

Inverse Steal/Robin Hood Phenomenon- Vasoconstriction of normal vessels but not in ischemic areas (d/t vaso motor paralysis).
This is one reason we hyperventilate pts. w/ tumors and increased ICP.
Luxury perfusion- BAD-Perfusion in excess of metabolic needs. Vasodilatation to surrounding tissues. AKA
*Circulatory/Cerebral Steal phenomenon- *
localized ischemic areas are already maximally dilated . It you further dilate surrounding vessels, you “steal” blood flow to other areas of the brain away from the ischemic area…

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13
Q

CBF Curve

A
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14
Q

Choice of inhalational agent

A

Inhalational Agents:
decrease CMRO2
> 0.6/1.0 MAC leads to cerebral vasodilation & dose-dependent increases in CBF
vasodilation greatest with: halothane > isoflurane >desflurane >sevoflurane

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15
Q

Nitrous Oxide

A

Effects are generally mild & easily overcome by other agents or changes in CO2 tension…

Combined with other IV agents: N2O has minimal effects on CBF, metabolic rate, & ICP

Controversial…
Adding Nitrous Oxide to a VA, can further increase CBF

When given alone, mild cerebral vasodilatation with the potential to increase ICP

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16
Q

Ketamine

A

Generally increases CMRO2 & CBF
**If **PaCO2 maintained normal in presence of elevated ICP or cerebral trauma, then ketamine does not adversely alter CBF or ICP

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17
Q

Thiopental

A

Four Major Actions on the CNS:
1. Hypnosis
2. Anticonvulsant
3. Decreases CMRO2
4. Decreases CBF due to increased cerebral vascular resistance CBF, and ICP

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18
Q

Propofol

A
  • Decreases CMRO2, CBF, and ICP
  • Excessive hypotension & myocardial depressant effects can compromise CPP
  • decreased MAP leads to decreases CPP
  • Although administration has been associated with dystonic & choreiform movements, it has significant anticonvulsant activity
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19
Q

Etomidate

A

Decreases CMRO2, CBF, and ICP
Decreases CSF production & enhances absorption
Concern over adrenal suppression limits its long term use
Induction: myoclonic movements
Increases EEG activity ONLY in pts. With a history of epilepsy

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20
Q

Opioids

A
  • Opioid induced increases in ICP due to decreased MAP can be avoided simply by controlling MAP during opioid administration.
  • As a result, opioids are unlikely to be an issue during maintenance with respect to brain bulk.
  • Depress ventilation, increasing PaCO2 leading to increases in CBF and ICP
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21
Q

Steroids

A

Dexamethasone (Decadron): Postulated mechanisms of action of corticosteroids in brain tumors include:
1. reduction in vascular permeability (cytotoxic effects of tumors)
2. inhibition of tumor formation
3. decreased CSF production

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22
Q

Acute Post-craniotomy Emesis

A

Occurs in approximately 50% of patients
Appears to be largely prevented by ondansetron 4mg administered near the time of dural closure

This statement is substantiated by research performed at Duke University Medical Center…
*Canadian Journal of Anesthesia. 51:326-341:2004
Evidence-based management of postoperative nausea and vomiting: a review
Journal of Neurosurgical Anesthesiology. 14(2):102-107, April 2002.
A randomized, double-blind comparison of ondansetron versus placebo for prevention of nausea and vomiting after infratentorial craniotomy.*
Anesth Analg 2000;91:358-361
A Randomized, Double-Blinded Comparison of Ondansetron, Droperidol, and Placebo for Prevention of Postoperative Nausea and Vomiting After Supratentorial Craniotomy

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23
Q

Craniotomy-associated Chronic Emesis

A

Little is known about prevalence or treatment…
What we do know is it is Life-threatening…

J Neurosurg 102:547-9, 2005
“Responsiveness of Life-threatening refractory emesis to gabapentin-scopamine therapy following posterior fossa surgery: Case Report”

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24
Q

Monitors

A

Standard plus: arterial line, 2 large bore IV’s
Sitting position/Aneurysm/AVM:
- CVP catheter/long arm
Additional monitoring if PMH warrants

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25
Q

Induction of Anesthesia

A

STP, propofol, or etomidate
Prompt induction without ICP elevation
Muscle relaxant to facilitate endotracheal intubation & mechanical hyperventilation (BEWARE: coughing causes marked increases in ICP)
Succinylcholine does not significantly alter CBF or ICP in patients with neurological injury…

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26
Q

Pressure-Volume (Elastance) Curves

A

Elastance = change in pressure /
change in volume
When intracranial compensatory mechanisms are exhausted, small changes in volume lead to dramatic changes in ICP

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27
Q

Mayfield Pin Placement

A

Goal: Not to have large hemodynamic swings in blood pressure.
Increase with insertion & then decrease after due to the fact you administered a longer acting agent and now there is “down time”…
No one way is “perfect”
Know that your SBP will predictably rise ~40mmhg

Therefore need to lower b/p…
Do NOT let them start until you do this…
AND do NOT lower the b/p UNTIL they have pins in hand ready to go…
What does the evidence reveal & what do I do…

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28
Q

Research related to Mayfield Pin Placement…

A

“The effect of skull-pin insertion on cerebrospinal fluid pressure and cerebral perfusion pressure: influence of sufentanil and fentanyl”
Conclusion:
In anesthetized patients, an intravenous bolus of fentanyl(4.5 mcg/kg) or sufentanil (0.8mcg/kg) prior to skull-pin insertion results in stable values of CSFP, CPP, BP, and HR… The b/p was modified with phenylephrine / atropine were indicated

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29
Q

Pin Placement management

A

Minimum of 4 mcg/kg Fentanyl
Titrate Iso to NO more than 1.0 MAC
Propofol 1mg/kg, titrated to response
Esmolol/Ntg – Only if necessary
Lower SBP by ~40mmg
Consider Lidocaine*
PIN Placement
Lower Iso, Propofol, NTG effects gone…
B/P Normalizes

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30
Q

Positioning for surgery

A

Positioning…100% fio2
Ett/IV can dislodge
monitor vitals closely
can take longer than you think…
Position depends on tumor location
Supratentorial: supine
Infratentorial: prone or sitting (BEWARE: greatly increases risk of **venous air embolism) **

31
Q

Reasons for Mannitol & Importance of “Perfect Timing”

A

Mannitol reduces brain bulk by creating an osmotic gradient across the “intact” blood brain barrier causing water to flux from the extracellular extravascular to intravascular compartments.
There also is evidence that mannitol improves deformability of red blood cells, thereby reducing viscosity promoting increased blood flow.

32
Q

Mannitol

A

Mannitol is best given PRIOR to the time of skin incision (typically 0.5 mg/kg) so the peak effect becomes available upon dural opening.
Additional mannitol may be of value if the brain is still “tight”.

Excessive use of Mannitol with serum osmolalities > 320 mosms may cause renal failure.
Cumulative doses of Mannitol can exacerbate brain edema by leaking it to the brain interstitium.
Adding Lasix is an option.

33
Q

Soooo…What other Adverse Effect Can Mannitol Have???

A
  1. Rebound increase in ICP, if BBB not intact
  2. Pulmonary Edema
  3. Hypovolemia
  4. Hyperkalemia (Transient-seen first)
  5. Transient Hyponatremia & decrease in hgb concentration (acute hemodilution)
    VERY COMMON
34
Q

Why hypoKalemia?

A

I always see Hypokalemia?
Acute increases in osmolaritity are reported to increase K by 0.6meq/L per 10 mOsm/L.
The movement of water out of the cells is accompanied by movement of K out of cells
The latter may be a result of “solvent drag” or the increase in intracellular K that follows cellular dehydration…

If F & E are not repleted with diuresis Hypokalemia ensues…VERY COMMON in neurosurgery…

Refer to Handout related to Mannitol

35
Q

Hypertonic Saline

A

Discussion:
mannitol versus hypertonic saline
pharmacological principles of it use

36
Q

Maint. of anesthesia

A

Maintenance of anesthesia during craniotomy is usually uncomplicated & generic in many respects.

There are two special considerations:
1. In patients with intracranial mass lesions, brain bulk can be a problem, particularly when the dura is being opened.
2. A swollen brain can herniate through the dural defect prohibiting further dural incision…. NOT GOOD!

37
Q

TX cerebral swelling

A
  • mannitol 0.25-1 Gm/kg IV
  • furosemide 0.5-1 mg/kg IV
  • thiopental
  • head up position (not >’er than 10-15 degrees)
  • hyperventilation
  • CSF Drain (Extremely effective)
  • Muscle Relaxants (Muscle activity -”light anesthesia’ contributes to cerebral swelling)
  • Discontinue N2O
38
Q

IV Fluids

A

EBL…Watch the clear plastic pouch
Minimum: 1-3 ml/kg/hr
Glucose NOT recommended
- Discussed previously…
- Hyperglycemia worsens cellular ischemic injury
Isotonic crystalloids
Hetastarch OK / Albumin better

39
Q

Albumin&raquo_space;>

A

Hetastarch decreases platelet aggregation…
“Effect of delayed albumin hemodilution on infarction volume & brain edema after transient middle cerebral artery occlusion in rats”
J Neurosurg 87: 595-601, 1997
Conclusion: Hemodilution with high-concentration albumin decreases focal cerebral ischemic injury

40
Q

Albumin benefits

A

A human protein therefore:
* Binds & inactivates toxic products
* Regulation of plasma interstitial fluid concentrations of endogenous & exogenous administered substances & drugs
* Maintenance of microvascular permeability to proteins
* Scavenging of free radicals & prevention of lipid peroxidation

41
Q

Emergence

A

avoid coughing, straining
thiopental or lidocaine
BEWARE: N2O may cause tension pneumocephalus
delayed return to consciousness or neurologic deterioration: CT or MRI

42
Q

Posterior Fossa Craniotomy

A
43
Q

Infratentorial Crani

A

Brainstem Injury
- Due to retraction, direct surgical trauma, or ischemia
Positioning
- VAE
Pneumocephalus
- Increased likelihood with sitting position
Postural Hypotension

44
Q

Venous Air Embolism

A

**Consider whenever head > 5 cm above heart **
- Air -> RV -> pulmonary circulation
- Decreases pulmonary blood flow
- pulmonary edema, bronchoconstriction, cardiovascular collapse, hypoxemia paradoxical (air) embolism
* cerebral circulations
* via patent foramen ovale (PFO)
* 20-30% of adults have patent foramen ovale

45
Q

Detection of VAE

A

Precordial Doppler ultrasound near right upper sternal border is most sensitive non-invasive monitor (detects 0.25 ml)

trans-esophageal echocardiography is most sensitive, but more invasive and cumbersome then doppler, “mill-wheel” murmur
sudden decrease in ETCO2, increase in ETN2 , increase in PAP’s
hypoxemia, hypotension, dysrhythmias

46
Q

Treatment of VAE

A
  • notify surgeon
  • irrigate operative site with fluid
  • apply occlusive material to bone edges
  • 100% O2, discontinue N2O
  • aspirate air through right atrial catheter (best if tip is at SVC-RA junction)
  • head down position
  • increase CVP, give fluids
  • inotropes, vasopressors may be needed
  • gently compress internal jugular veins
  • BEWARE of PEEP:
  • by reversing RA-LA pressure gradient, may lead to paradoxical air emboli via PFO
  • If the above measures fail, LLD with head slight down in attempt to dislodge air lock
47
Q

Arnold Chiari Malformation

A

A congenital malformation (although there have been some reported cases of an acquired form.)
It is an anomaly in the posterior fossa
A reduction in CSF pathways
A protrusion of the cerebellar tonsils through the bottom of the skull (foramen magnum) into the spinal canal.
The tonsils would normally be round – often become elongated as they protrude down the spinal canal.
Diagnosis can be difficult because not all patients will have the classical sign of deeply herniated tonsils.

48
Q

Categories of Ciari Malformation

A

Type I most common
Characterized by downward displacement by > four millimeters, of the cerebellar tonsils beneath the foramen magnum into the cervical spinal canal.

49
Q

What is the most severe category of chiari malformation?

A

Type I

50
Q

Type 1 common anomalies

A

Compression of the upper part of the spine into the base of the skull with resulting compression of the brainstem.

Bony union of the first level of the spine (C1) to the base of the skull.

Partial bony union of the first and second levels (C1 fusion to C2) of the spine.

51
Q

Surgery for Chiari malformation

A

Local decompression of the overlying bones
Decompression of the bones

Provides more space for the brainstem, spinal cord, and descended cerebellar components.

A tissue graft is often spliced into this opening to provide even more room for the unimpeded passage of CSF.

Removing the back of the foramen magnum and often the back of the first few vertebrae to the point where the cerebellar tonsils end
Monitoring…SSEP/BAER/MEPS
+ Mannitol

52
Q

Transsphenoidal Hypossectomy

A

Using the transsphenoidal route:
Through the nose and across the sphenoid sinus of the face
Result = no noticeable facial scar

53
Q

Transsphenoidal Surgery: Treatment Of Pituitary Tumors

A

In the United States, pituitary tumors represent 10% to 15% of all intracranial tumors diagnosed each year
These benign lesions originate from the cells of the pituitary gland, which is located in the Sella turcica
a rounded, bony structure behind the nose and ethmoid sinus of the face.

54
Q

Pituitary Gland

A

The pituitary gland is sometimes called the “master” gland of the endocrine system, because it controls the functions of the other endocrine glands

The pituitary gland is no larger than a pea, and is located at the base of the brain

The gland is attached to the hypothalumus (a part of the brain that affects the pituitary gland) by nerve fibers.

55
Q

Pituitary Gland Sections

A

The pituitary gland itself consists of three sections:
1. the anterior lobe
2. the intermediate lobe
3. the posterior lobe

56
Q

Anterior Lobe

A

**Growth hormone **
Prolactin - to stimulate milk production after giving birth
ACTH (adrenocorticotropic hormone) - to stimulate the adrenal glands
TSH (thyroid-stimulating hormone) - to stimulate the thyroid gland
FSH (follicle-stimulating hormone) - to stimulate the ovaries and testes
LH (luteinizing hormone) - to stimulate the ovaries or testes

57
Q

Intermediate Lobe

A

Melanocyte-stimulating hormone - to control skin pigmentation

58
Q

Posterior Lobe

A

ADH (antidiuretic hormone) - to increase absorption of water into the bloodby the kidneys
Oxytocin - to contract the uterus during childbirth and stimulate milk production

59
Q

Pituitary Gland and tumor

A

A normal pituitary gland serves the vital function of producing hormones that interact with other parts of the body, such as the thyroid and adrenal glands, to regulate hormonal output

Pituitary tumors can disrupt the output of hormones and are broadly categorized as either secreting or nonsecreting tumors.

60
Q

Types of Pituitary Tumors

A

Secreting tumors cause excess hormone production

The most common type of secreting tumor is the prolactin tumor
* In females, this tumor produces a classic combination of amenorrhea (infertility) and galactorrhea (lactating breasts)
- These symptoms usually cause women to seek medical attention early, so the tumor is often detected while it is still small.

61
Q

Prolactin Tumors

A

Prolactin tumors are less common in males, and are not usually detected until the tumors are larger in size

This is because men tend to ignore the hormonal symptoms which occur as a result of the tumor, including fatigue and lack of sexual interest

Patients with larger tumors that cause visual impairment due to compression of the optic chiasm

62
Q

Secreting Pituitary Tumors

A

Other secreting tumors include the Growth Hormone and the Adrenocorticotropic Hormone (ACTH) types

These tumors stimulate excessive adrenal function and can cause drastic medical issues such as hypertension and diabetes

Most of these tumors are treated surgically, although adjunctive treatment with medication or radiation may be necessary for some in the postoperative period.

63
Q

Pituitary Adenoma

A

Cushing’s syndrome is a debilitating endocrinopathy characterized by excessive cortisol levels in the blood which may be produced from tumors of the pituitary gland, adrenal glands or from tumors or cancer arising elsewhere in the body (ectopic ACTH producing tumors)

Cushing’s disease refers specifically to excessive ACTH secretion by a pituitary adenoma

64
Q

Cushing’s Syndrome / Disease

A

The cause of Cushing’s Syndrome is a pituitary adenoma in over 70% of adults and in approximately 60-70% of children and adolescents

Most pituitary ACTH-secreting adenomas are small in size (microadenomas)

Overall, Cushing’s Disease is relatively rare, affecting 10 to 15 of every million people each year

65
Q

S&S Cushings

A
  • Change in body habitus: weight gain in face (moon face), above the collar bone (supraclavicular) and on back of neck (buffalo hump)
  • Skin changes with easy bruising, purplish stretch marks (stria) and red cheeks (plethora)
  • Excess hair growth (hirsutism) on face, neck, chest, abdomen, and thighs
  • Generalized weakness & fatigue/Wasting of musculature
  • Menstrual disorders in women (amenorrhea)
  • Decreased fertility and/or sex drive (libido)
66
Q

Cushing Syndrome

A

Hypertension
Diabetes mellitus
Depression, mood and behavior disorders

67
Q

Non-secreting Pituitary Tumors

A

Nonsecreting (nonfunctional) tumors are usually large when they are discovered due to the lack of hormonal side effects

People with these tumors don’t realize there is a problem until the tumor begins to compress the optic chiasm, causing visual loss

Patients with nonsecreting tumors usually respond well to surgical treatment, though improvement in visual function is dependent on the length of time vision is impaired prior to the procedure

68
Q

Summary

A

TRANSSPENOIDAL RESECTION for pituitary tumors<10 cm
Surgical approach is underneath the upper lip thru nasal septum and roof of sphenoid sinus to penetrate floor of sella turcica. Surgeon uses a microscope. Pituitary gland sits on top of the sella turcica. Tumors often hormone secreting.

ANTERIOR: ACTH,GH,FSH,LH,PRL

POSTERIOR: ADH (vasopressin)

69
Q

Pituitary Tumor Resection

A

DO NOT treat like other tumors (space occupying lesions)

Normovolemic, normotensive, normocapnic
Do not shrink brain.
A full brain will push tumor down to surgeon-GOOD

70
Q

Major Problems Associated with Transsphenoidal Approach

A

Need for mucosal injection of epi-containing solutions

Accumulation of blood & tissue debris in pharynx & stomach

Risk of hemorrhage from inadvertent entry into the cavernous sinus or internal carotid artery

71
Q

Major problems….

A
  • Cranial nerve damage
  • Pituitary hypofunction
  • Prophylactic Decadron administration
  • Does not effect cortisol levels
  • Diabetes insipitus
  • 40 % chance postoperatively
  • < commonly intraoperatively
  • usually transient, U.O.>1L/hr - give DDAVP
  • Supine & slightly head up predisposes pt to VAE
  • CSF Leak
72
Q

Simplied repair of small CSF leaks with collagen sponge

A
73
Q

Anesthetic Considerations & Monitors

A

VEP may be employed with large tumors that involve the optic nerve
+/- Precordial doppler
2 large bore IV’s
If co-morbidity present, +/- A-line
Many avoid N2O to prevent post op pneumocephalus

Intense muscle paralysis
Intrathecal CSF drain to facilitate surgical exposure
May instill saline…