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AP III Oral Exam > Neuro > Flashcards

Neuro Flashcards

1
Q

Describe the function of the circle of willis, as well as the major vasculature that supplies and creates the circle of willis.

What is the venous drainage system of the brain?

A
  • Functions as a shunt, providing collateral flow when there is a regional disruption of blood flow
    • Limited because there’s lots of variation in anatomy
  • Miller emphasizes that a lot of people have complete CoW but lots of variation (figure B)
    • Consider that CoW is not complete in everyone
  • 4 major arteries supply CoW
    • L Internal carotid & R internal carotid⇒ anterior portion CoW
    • L and R vertebral artery ⇒ basilar artery (posterior portion) ⇒allows for nice circle of flow with intact CoW
      • If blockage at any point (ie internal carotid) there’s some hope of collateral flow to that region of the brain
  • Venous drainage is predictable
    • Superficial cortical veins ⇒supply pia mater, superficial cortical layer
    • Deeper cortical veins⇒ drain deeper structures of brain
      • Ultimately drain into major sinuses (superior sagittal sinus, inferior sinus, vein of galan)
        • All drain into jugular vein
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2
Q

Describe the spinal cord blood supply.

A
  • Not as well collateralized as brain
  • Anterior spinal artery comes off of vertebral arteries
    • Lots of flow from radicular arteries
      • 6-8 other radicular arteries that help supply SC (including Artery of Adamkiewicz)
    • Some regions of SC are well perfused (cervical/thoracolumbar area) other areas are more tenuous
      • Artery of Adamkiewicz (T11/T12) really important for 2/3 of blood flow to inferior SC (supplies T8 to conus medullaris)
        • Interruption of artery can cause major ischemic damage
  • Anterior 2/3 cord by anterior spinal artery with very little collateralization
    • Interrupted= big trouble
    • Primarily motor function
    • Anterior side also covers lateral so can see combo of sensory/motor issues when
  • Posterior 1/3 SC has 2 arteries provides more opportunities for collateral flow
    • Slightly less at risk for ischemic damage
    • Primarily sensory
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4
Q

What is ICP? What determines ICP?

A
  • Normal pressure 8-12 mmHg (B8th= 7-15 mmHg)
  • ICP by convention means supratentorial CSF pressure measured in the lateral ventricles or over the cerebral cortex and is usually 10mmHg or less. Rigid cranial vault fixed volume
    • In lateral recumbent position lumbar CSF approximates supratentorial pressure
  • 2 problems with increased ICP
    • 1) decreased CPP to the point that the brain becomes ischemic
    • 2)herniation across the meninges, down the spinal canal, or through an opening in the skull
  • ICP components are:
    • Brain (cellular and ICF) (80%= 1400ml)
      • Cells impacted by sugeon, anesthesia world we don’t control cell size
      • Can control ICF with diuretics, steroids
      • The cellular compartment (neurons, glia and ICF).
        • compartment is in the hands of the surgeon.
        • However, when the brain is bulging into the surgical field at the conclusion of evacuation of an extradural hematoma, the clinician should ask whether a subdural or extradural hematoma is present on the contralateral side that warrants either immediate bur holes or immediate postprocedure radiologic evaluation.
      • The fluid compartment. This compartment can be addressed with steroids and diuretics.
    • Blood (arterial and venous)(12% 150ml)
      • Limitation to how much we can impact this because it’s only 12% of volume
      • Decrease cerebral blood flow or improve venous drainage
      • This is the compartment is the most amenable to rapid alteration. The blood compartment should be considered two separate components: venous and arterial.
    • CSF (8%= 150ml)
      • 8% in someone with no hydrocephalus
      • Can control with venticulostomy/lumbar drain
      • Remove CSF and augment control
      • There is no pharmacologic manipulation of the size of the CSF space
        • The only relevant means for manipulating the size of this compartment is by drainage
          • A tight surgical field can sometimes be improved by passage of a brain into a lateral ventricle to drain CSF.
            • relevant in both supratentorial and infratentorial procedures when poor conditions in the posterior fossa are thought to be the result of downward pressure by the contents of the supratentorial space
        • Lumbar CSF drainage can be used to improve surgical exposure in situations with no substantial hazard of uncal or transforamen magnum herniation.
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5
Q

What is intracranial elastance? What determines intracranial elastance? Compensatory mechanisms?

A

Determined by the change in ICP after a change in intracranial volume – compensatory mechanisms include:

  1. Initial displacement of CSF from cranial to spinal compartment
  2. Increased CSF absorption
  3. Decreased CSF production
  4. Decreased CBV (primarily venous)
  • Healthy patients can tolerate change on ICP curve well. (Bottom left of curve normally)
    • Intracranial pressure-volume relationship.
    • The horizontal portion of the curve indicates that initially there is some compensation with expanding intracranial lesion
      • is accomplished largely by displacement of cerebrospinal fluid (CSF) and venous blood from the intracranial to the extracranial spaces
      • once compensation exhausted, small changes causes large increase in ICP with r/f herniation or decreased CPP resulting in ischemia
  • Someone with swelling, edema, hematoma, can reach point where small change in volume makes a big change in ICP.
    • Think of where do we think pt is on curve
      • Avoid hypoventilation, maintain CPP, mannitol, CSF diversion, cerebral vasoconstricting anesthetics, decompressive craniectomy
    • Completely awake, no signs increase ICP, no nausea A&OX3 no pupillary changes⇒ may be able to tolerate
    • If patient confused, throwing up, cushing triad, ICP issues,⇒ avoid ANY increase in volume, be very conservative with which anesthetics are chosen
  • If ICP gets close to MAP⇒too much resistant to perfusion and CPP will drop to unacceptable levels and won’t get glucose/O2 to brain and then you start to worry about herniation
  • Elastance is change pressure/change volume. Compliance is change in volume/change in pressure.
    • Used interchangeably in texts
    • Compliance varies locally in diff areas of brain
      • Affected by arterial BP and PCO2
        • Autoregulation kicks in with hypotension (vasodilation- increase CBV) or hypertension (vasoconstriction- decrease CBV)
        • CBV increases 0.05mL/100g of brain per every 1 mmHg increase PaCO2
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7
Q

Whe is the relationship between cerebral blood flow and cerebral blood volume?

A
  • Parallel but not 1:1 relationship
  • We care about flow because it influences total cerebral blood volume
    • CBV = 5ml/100 gm of brain tissue
    • VA increase CBF even if cerebral blood volume doesn’t increase
    • Think of arterial and venous drainage/tone
  • Consider not only arterial flow (and tone) but also venous drainage (and tone)
    • Obstruction to outflow (position, PP vent with high PIP)
    • Positioning makes big impact on ICP and impacts CBV significantly
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8
Q

Describe how neuronal activity (metabolism) influences local CBF?

A
  • “Flow-metabolism coupling”
    • Metabolic by-products (glial, neuronal, vascular)
      • H ions, adenosine, prostaglandin, lactate, glutamate can influence local blood flow
      • Ie glutamate stimulates NMDA receptor (on neurons), Ca enters cell, Ca stimulates NO production, NO is major vasodilator.
        • Ca can also create arachidonic acid⇒ PG ⇒major vasodilator
      • Different substances couple metabolism with vascular tone and blood flow
    • Multiple signaling pathways involved
  • CBF to localized brain regions change up to 100-150% within seconds in response to local neuronal activity changes (sensory input/arousal)
  • Barash 8th
    • vasoconstrictive forces= catecholamines, ionic calcium, endothelin, and thromboxane.
    • Dilators= B2 agonists, nitric oxide, adenosine, prostaglandins, .
    • Other mediators – acetylcholine, bradykinin, serotonin, substance P, dopamine.

pic:

  • Figure 11-4.. From Miller 9th description below:
  • Cerebral flow-metabolism coupling. Synaptic activity leads to glutamate release, activation of glutamatergic receptors, and calcium entry in neurons. This results in a release of arachidonic acid (AA), prostaglandins (PGs), and nitric oxide (NO). Adenosine and lactate are generated from metabolic activity. These factors all lead to vascular dilation. Glutamate also activates metabotropic glutamate receptors (mGluR) in astrocytes, causing intracellular calcium entry, phospholipase A 2 (PLA 2 ) activation, release of AA and epoxyeicosatrienoic (EET) acid and prostaglandin E 2 (PGE 2 ). The latter two AA metabolites contribute to dilation. By contrast, AA can also be metabolized to 20-hydroxyl-eicosatetraenoic acid (20-HETE) in vascular smooth muscle. 20-HETE is a potent vascular constrictor. cGMP, Cyclic guanosine monophosphate; eNOS, endothelial nitric oxide synthase; NMDAR, N-methyl d -aspartate glutamate receptor; nNOS, neuronal nitric oxide synthase.
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11
Q

What is CPP?

A
  • MAP – ICP (or CVP whichever is greater)
  • Normal is 80-100mmHg
    • When ICPs are higher, augment (increase) MAP to help CPP
  • Cardiac output also appears to influence CBF (appears to be linear relationship)
    • particularly in hypovolemia
      • when patient hypovolemicà get huge impact in CBF (19:26)
    • Decrease in CO by 30% resulted in a 10% decrease in CBF in several recent Doppler studies
      • Improvement in CBF with increase CO observed in acute storke, SAH induced vasospasm, and sepsis
      • However, not a uniform relationship b/w CO-CBF. Depends on pathophys at hand. No improvement in CBF with increase in CO with traumatic head injury, neuro surgery, cardiac surgery
      • Does appear CO influences CBF when circulating volume is reduced and in shock states.
  • Normal ICP is 10mmhg so CPP usually determined by MAP MM615
  • Miller 9th 302The conventional view of cerebral hemodynamics is that perfusion pressure (MAP or CPP) is the primary determinant of CBF and that the influence of cardiac output is lim- ited.
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12
Q

What is cerebral blood flow? Normal? Important factors impacting CBF during anesthesia?

A
  • Normal Adult 45-55ml/100g/min =750ml/mi
    • Global blood Flow
    • Gray matter(cortical) has lots of electrophys activity (80mL/100g/min)
    • White matter (subcortical- myelinated) 20mL/100g/min
    • Infants 40ml/100g/min
    • Children 95ml/kg/min
    • Spinal cord gray matter (60ml/100g/min) and white matter (20ml/kg/min)
  • Blood flow closely linked with metabolism
    • Making fist, motor cortex will get more blood flow
    • Reading, occipital blood flow will increase
    • Wherever you have activity going in brain, will see more blood flow
      • Regional CBF parallels metabolic activity and can vary from 10-300ml/100g/min (MM615).

Important factors impacting CBF during anesthesia

  1. Anesthetic Agents
  2. Level of arousal (stimulation & pain)
  3. Metabolic by-products
  4. Blood Viscosity
  5. Temperature
  6. Concentration of CO2 and H+ ions
  7. O2
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13
Q

What happens to cerebral blood flow with increase PaCO2 and H ions?

A
  • CO2 + H20 = carbonic acid
    • More aerobic metabolism⇒ more CO2⇒ more H ions from dissociation
  • Carbonic acid disassociates into H+
    • H+ ions cause “almost” proportional vasodilation of cerebral vessels
      • Thought that vasodilation increases blood flow to carry away H, reduce chance for CO2 narcosis
  • Other acidic metabolic substances can also increase CBF (lactic acid, pyruvic acid, etc.)
  • Each 1 mmHg change in PaCO2 between 20-80mmHg
    • CBF changes approximately 1-2ml/100g/min
      • Double CO2 20⇒ 40 then will double CBF
      • Hyperventilate 50⇒ 25, ½ CBF
        • Use in short term in anesthesia when we turn on VA since we expect increase CBF with VA
    • Below 20mmg- tissue hypoxia reflexive dilation
      • Don’t want to go below 20 mmHg⇒ extreme tissue hypoxia
      • Typically don’t go below 30 mmHg when hypoventilating. Don’t want extreme value. Causes more harm than good
  • Effect lasts ~ 6-8 hrs and then in will return to normal despite maintenance of altered CO2 levels (bicarb transport)
  1. Effect useful in anesthesia for short periods with VA
  2. Critical to recognize if a patient with ICP alterations has been hyperventilated for extended period - why?
    - need to maintain same level of ventilation/don’t’ make major change quickly because it can cause some major problems
    * The benefit of increased CBF with increased H ion is a compensatory mechanism to prevent CO2 narcosis - that increased H ion concentration greatly depresses neuronal activity and increased CBF carries away the increased CO2 ( H ions) and therefore helps maintain a constant H ion conc. and a normal constant level of neuronal activity
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14
Q

What is normal brain metabolism?

A
  • Only 2% of total body mass, 15% of total body metabolism and cardiac output
    • Gets huge percent CBF based on size
  • Cerebral Metabolic Rate (CMRO<u>2</u>)
    • 3.5ml/100g/min = 50ml/min of O2
  • Pediatric patients higher CMRO2 = 5.2ml/100g/min (mean age 6 yr)
    • One of the reasons why kids desaturate so quickly on induction
  • Metabolism used to maintain normal K/Na to pump against gradient after AP
    • 60% of O2 used to maintain normal EP activity, 40% used to maintain healthy cell membrane
  • Brain not capable of much anaerobic metabolism (high metabolism coupled with low local glycogen and oxygen stores)
  • Brain glucose consumption 5 mg/100g/min
    • 25% of total body glucose consumption
  • Use barbituates, propofol etc to get EP activity down to suppression levels and drop metabolic need
    • Anesthetics can’t reduce into basal cerebral maintenance metabolism (last 40% of CMRO2- mainly accounts for Na-K ATPase pump to restore intracellular gradients)
    • Anesthetics only help reduce CRMO2 to a certain point
  • Reason for this is because brain does not work well on only anaerobic metabolism. Anaerobic can’t keep up with needs for brain
    • Only 2 minutes of glucose in brain at time, why LOC occurs with 5-10 seconds loss of blood flow
      • In absence of O2, brain resorts to anaerobic metabolism where only 2 units ATP produced for each molecule of glucose
    • Glucose utilization not dependent on insulin
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15
Q

What is the relationship between CBF and O2 concentration?

A
  • Except for cases of intense brain activity, O2 utilization by brain tissue remains within narrow range ( a few % points around 3.5mlO2/100gm brain tissue)
  • If PO2 of brain tissue drops below 30mmHg (35-45mm Hg normal) or PaO2 drops below 50-60mmHg CBF increases dramatically
    • PaO2 doesn’t really have significant impact until in ischmic territory (Pao2 <50) then will see dramatic increase in CBF
    • See hail mary with cerebral blood vessels dilating to get as much O2 delivered as possible
    • CBF not really changed until you fall below 60mmHg that is the same level where there is a rapid reduction in oxyhemoglobin saturation. See an inverse linear relationship with O2 sat and CBF. Deoxyhemoglobin plays a central role here by causing the release of NO and its metabolites as well as ATP.
  • Slight vasoconstriction >350 mmHg

Slide notes:

  • Thus, the oxygen mechanism for local regulation of cerebral blood flow is a very important protective response against diminished cerebral neuronalactivity and therefore, against derangement of mental capability.
  • At 3-8 minutes ATP stores are depleted and irreversible cellular injury begins to occur. The Hippocampus and cerebellum appear most sensitive to hypoxic injury MM616.
  • Neurons have a very high metabolic rate using more energy than other cells – 2% body mass, 20% total body O2 consumption. N10
  • Hypoxia induced K+ATP channel opening= hyperpolarization and vasodilation. The response to hypoxia is synergistic with the hyperemia produced by hypercapnia and acidosis. This hypoxic driven increase in CBF appears to be controlled at least in part by the rostral ventrolateral medulla - O2 sensor within the brain.
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16
Q

What is cerebral autoregulation of CBF and arterial BP?

A
  • CBF auto-regulated between MAP of 60-150mmHG
    • Barash8th 60-160 mmHg; some individuals lower limit <60mmHg others >80 mmHg
      • New edition of miller challenges this.
      • For purposes of boards/OR still assume autoregulation 6-150
    • Miller 9th emphasizes this is an oversimplification of “complex regulation”
  • Cerebral vasculature adjusts to changes in CPP/MAP after 1-3 minutes
  • Varies between individuals: HTN will shift auto-regulatory range to higher minimum values and maximums of 180-200mmHg
  • Above the upper limit = BBB disruption, cerebral edema, cerebral hemorrhage
    • Pressure dependent situation
    • Can burst smaller vessels and end up with hemorrhage
  • Below the upper limit= ischemia
  • Mechanism of reflex still controversial. Thought to be myogenic in nature (more stretch ⇒ dilation, less stretch ⇒ constriction) probably a little simplistic
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17
Q

Describe the relationship between BP, hypercapnia, and CBF autoregulation?

A
  • Point of 2 graphs, CO2 responsiveness can be influenced by blood pressure
  • Red⇒ linear relationship with CO2 and CBF is true with normotension
    • Patients that are hypotensive, will see curve for CO2 flattening.
      • Not as much influence of CO2 with hypotension
    • In extreme hypotension, CO2 doesn’t have any impact on CBF and not much CBF to begin with
  • If flip the other way, if patient has normal CO2 autoreg in typical range (60-150)
    • When hypercapnic, will see loss of autoregulation and be impaired
    • CO2 on lower end, will see plateau of autoregulation extended.
      • More consistent CBF across larger range of MAPs with hypocapnia
        • Why we like to hyperventilate too, get more cerebral autoregulation

Pic:

A, Relationship between cerebral blood flow (CBF) and partial pressure of carbon dioxide (Paco2).

  • CBF increases linearly with increases in arterial Paco2.
    • Below a Paco2 of 25 mm Hg, further reduction in CBF is limited.
    • Similarly, the increase in CBF above a Paco2 of approximately 75 to 80 mm Hg is also attenuated.
  • The cerebrovascular responsiveness to Paco2 is influenced significantly by blood pressure.
    • With moderate hypotension (mean arterial pressure [MAP] reduction of <33%), the cerebrovascular responsiveness to changes in Paco2 is attenuated sig- nificantly.
    • With severe hypotension (MAP reduction of approximately 66%), CO2 responsiveness is abolished.
  • B, The effect of Paco2 variation on cerebral autoregulation.
    • Hypercarbia induces cerebral vasodilation and, consequently, the autoregulatory response to hypertension is less effective.
    • By contrast, hypocapnia results in greater CBF autoregulation over a wider MAP variation.
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18
Q

What is the impact of temperature on CBF?

A
  • CBF changes 6-7% per 1 degree C change
  • Hypothermia decreasesCBF and CMRO2
    • Why people can drown in cold temperatures and come back neurologically intact
  • Hyperthermia opposite effect
  • Clinical evidence does NOT currently support the use of hypothermia <35 degrees C without CP bypass
    • It is beneficial following cardiac arrest
    • It might be beneficial in high risk patients with temporary focal ischemia (need more research)
      • Research saw increase in infection, influence coagulation, and decreased cardiac function
      • For now, keep above 35 Celsius and avoid hyperthermia
  • Temperature can influence basal metabolic rate of brain (unlike anesthetics, which only influence EP activity)
  • At 37 C, CRMO2 is 3.3mL/100g/min function and 2.2 integrity. With decrease to 27 celsius, see function decrease to 1.4 mL/100gm/min AND integrity decrease to 0.9mL/100gm/min
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20
Q

What factors influence cerebral blood flow?

A
  • Autoregulations 50-150 not reliable in every clinical situation. Very complex
  • ABP,⇒ myogenic autoregulation
  • CO ⇒ impacts CV function
  • Neurogenic control can influence autoregulation
  • Metabolic activity⇒neurovascular coupling
    • Increase H, PG, adenosine, will see enhanved CBF
  • CO2 levels, parallel relationship in vascular reactivity AND Extreme hypoxia will see change in CBF⇒ vascular reactivity
  • In healthy patients, autoregulatory range was pretty narrow and other factors impacted CBF
    • One study with 48 patients
    • In future, autoregulation pressure may be redefined. For now, 50-150
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22
Q

Relationship between blood viscosity and CBF?

A
  • Decrease in HCT will increase CBF but decrease O2 carrying capacity of the blood
  • Severe polycythemia can reduce CBF
    • Might consider intervention ~ Hct of 55%
  • Hct 33-45% probably no significant change in CBF
  • By optimal Hct – best CBF with maintenance of adequate O2 carrying capacity.
  • In theory probably most useful to have decreased viscosity with focal ischemia where max vasodilation already has occurred. Early studies have not shown this optimal hct to really improve outcome with acute ischemic stroke however- probably only true clinical relevance is to avoid polycythemia.
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23
Q

What are the regions of focal ischemia? What is global versus focal ischemia?

A

Focal ischemia there are three regions

  1. No blood flow – same as global ischemia
  2. Penumbra – receives collateral flow only partially ischemic, marginal blood flow may be <15ml/100g/min)
    1. CBF 6-15 mL/100g/min
    2. With someone with focal ischemia, think of what can you do to save penumbra
    3. Optimize blood flow to penumbra
  3. Normal perfusion
  • Global – total circulatory or respiratory arrest (cardiac arrest, drowning, asphyxia, etc.)
  • Focal – embolic, hemorrhagic and atherosclerotic strokes, or trauma. In the penumbra if further injury can be limited and normal flow is rapidly restored these areas may recover completely. MM623
    • Impacts specific region of brain
    • Withinfocal, have 3 areas
  • If the insult is maintained for a prolonged period the neurons in the penumbra will die. More neurons in the penumbra will survive if collateral blood flow is increased with such mechanisms as inverse steal (why TPL is useful in focal not global ischemia). Preventing secondary ischemia is the key following focal brain injury. Intracranial blood can cause free radical formation using the iron from Hgb.
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24
Q

What the cerebral pathophysology of ischemia?

A
  • Oxidative phosphorylation is blocked – ATP production falls 95%
    • Needed to maintain ionic gradients
      • Can’t reestablish Na/K levels
    • Needed to maintain cellular integrity
  • ATP-dependent pumps fail – intracellular Ca and Na increase, K decreases – neurons depolarize excessively
    • Water rushes into the cell down osmotic gradient leading to neuronal edema (necrotic death)
  • Glutamate is released as cells die– more Ca enters
    • Apoptotic death
    • Positive feedback cascade ensues
    • Glutamate stimulates AMPA, NMDA, metabatropic glutamate increases intracelular Na and Ca.
      • Increased intracelular Ca is what signals apoptosis/cell death
      • With cell damage, release more glutamate, which impacts other cells locally
  • Intracellular Ca increases because ATP-dependent pumps fail, increased intracellular Na and release of the excitatory neurotransmitter glutamate.
  • High Ca levels increases damage via proteases and phospholipases (free fatty acids and free radicals damage the cell membranes, DNA, mitochondria, etc. )
  • Lactate and Hydrogen build up (pH drops)
  • No ATP available to repair damaged DNA proteins/lipids
  • Arachidonic acid is produced in excess is converted to thromboxane (intense vasoconstriction), prostaglandins, and leukotrienes (edema)
  • Reperfusion of previously ischemic regions can increase damage secondary to free radical generation and inflammatory mediator infiltration
    • Can cause lesions to expand
    • Interest on research side to stop process of excitotoxicity (too much glutamate, Ca, activity etc)
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25
Q

What are the various types of herniation?

A
  • 4 common types
  1. Subfalcine (cingulate gyrus)- asymmetric expansion of cerebral hemisphere displaces the cingulate gyrus under the falx cerebri
    1. Compressions of anterior cerebral artery (supplies primary motor/sensory cortex)
    2. Subfalcine (cingulate gyrus) – asymmetric expansion of cerebral hemisphere displaces the cingulate gyrus under the falx cerebri (strong process which descends vertically in the longitudinal fissure between the cerebral hemispheres). Pts at risk for compression of anterior cerebral artery with ischemia of primary motor and/or sensory cortex with weakness and sensory deficits in the leg.
  2. Transtentorial (uncal)- medial temporal lobe compressed against tentorium cerebelli
    1. Compress posterior cerebral artery leading to pupillary dilation, ocular paralysis, visual deficits
    2. Transtentorial- medial temporal lobe compressed against tentorium cerebelli. With progressive temporal lobe displacement 3rd cranial nerve and PSNS fibers compressed = pupillary dilation and occular paralysis on the side of the lesion. Also posterior cerebral artery is often compressed resulting in ischemia of the visual cortex which is supplied by this vessel.
  3. Tonsillar - displacement of cerebellar tonsils through the foramen magnum
    1. Compression of vasoactive/respiratory centers, not compatible with life
    2. Tonsillar – displacement of cerebellar tonsils through the foramen magnum. Life threatening – causes brain stem compression with disruption of vital respiratory centers in the medulla oblongata. Often the patient gets secondary hemorrhages in the midbrain and pons most likely a result of kinking of penetrating branches of basilar artery with resultant necrosis and hemorrhage during displacement of the brainstem.
  4. Transcalvarial -through a skull defect
    1. Fracture in skull with herniation through defect
    2. Also happens in surgery with skull/dura mater open. Make sure patient completely relaxd and no Valsalva in surgery
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26
Q

What is the flow of CSF?

A
  • Fluid from lateral ventricles passes through intraventricular foramina (of Munro) to the third ventricle additional fluid is added
  • then it flows downward along the aqueduct of Sylvius into the fourth ventricle, more fluid is added and then it passes out of the fourth ventricle through three small openings
  • two lateral foramina of Luschka, and a midline foramen of Magendie entering the cisterna magna ( a large fluid space that lies behind the medulla and beneath the cerebellum) which is continuous with the subarachnoid space
  • lateral ventricle-→ Intraventricular foramina of Munro⇒ third ventricle⇒ aqueduct of sylvius⇒ fourth ventricle⇒ two lateral foramina of lushcka or midline foramen of Magendie
  • Each ventricle adds more CSF to the flow
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29
Q

Anesthetic impact on CSF production?

A
  • Increased during sleep (and during anesthesia)
  • Increased by desflurane and enflurane
    • Could make theoretical case against des in hydrocephalus
  • Decreased by halothane and etomidate
  • No change isoflurane and fentanyl

* Info derived from animal data- may or may not be true in humans

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30
Q

What factos affect absorption of CSF?

A
  • Decreased by halothane and enflurane
    • Enflurane definitely worse choice in someone with hydrocephalus (get increased production of CSF and decreased absorption)
  • No change desflurane
  • Increased by isoflurane, fentanyl, and etomidate

* Info derived from animal data

  • So enflurane is clearly the less desirable agent compared to the others from a CSF dynamics perspective.
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31
Q

What is the blood brain barrier? What can cross the BBB?

A
  • Fenestrations between endothelial cells in brain 1/8th size of fenestrations in other areas
    • Protect brain from foreign substances
  • Exists in tissue capillary membranes in all areas of the brain parenchyma excepthypothalamus, pituitary, and area postrema
    • Need hypothalamus/pituitary to be exposed to osm, electrolyte, etc
    • Area postrema important in N/V important for body to recognize poison
  • Movement across BBB depends on size, charge, lipid solubility, and degree of protein binding in the blood
    • Small size, no charge, lipid soluble, low protein binding gets across BBB
    • Permeable: H20, C20, O2, lipid soluble substances (anesthetics, ETOH)
    • Slightly permeable: Na, Cl, K, Ca, Mg
      • Take longer to get accross
    • Impermeable: polar molecules, plasma proteins, glucose (facilitated diffusion only), non-lipid soluble large organic molecules (mannitol)
  • Substances needed by brain that do not cross BBB are transported across capillary endothelial cells by carrier mediated process – active or passive (facilitated diffusion). Glucose is example of facilitated diffusion can only move molecules of glucose in if concentration in blood is higher than in the brain
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32
Q

What causes disruption in BBB?

A
  • Anesthetics might/might not directly breech BBB. However…
    • They may produce conditions that lead to a breech
      • Ie extremes in BP
      • They may have different effect in a brain with disrupted BBB
  • Disruptions:
    • severe HTN
    • tumors
    • CHI (closed head injury)
    • stroke
    • nfection
    • marked hypercapnia
    • hypoxia
    • prolonged seizures
    • osmotic shock
    • irradiation
  • BBB disruption: movement dependent on hydrostatic rather than osmotic pressure
    • May cause anesthetics to have more access/different effect on brain
    • Patient with disrupted BBB can be more sensitive to HTN causing edema
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33
Q

What effect do volatile anesthetics have on cerebral hemodynamics?

A
  • Dose related, reversible alterations in CBF, CMR & electro-physiologic activity
    • Decreases CMR
    • Direct vasodilatory effect of cerebral vascular smooth muscle
      • If have tight cerebral vault, then this increase in blood flow can be detrimental
  • Effect on ICP depends on
    • CSF dynamics,
    • CBV,
    • PaCO2,
    • surgical stimulation,
    • other drugs administered &
    • baseline compliance
  • Dose dependent impairment of auto-regulation
    • Sevoflurane appears to impair autoregulation the least
  • Typically in normal physiology, CBF and CMRO directly related
  • Carbohydrate metabolism decreases while energy stores (ATP, adenosine diphosphate,and phosphocreatine) increase. Effects of specific agents are complicated by other factors such as other drugs, surgical stimulation, intracranial compliance, BP, PaCO2. (ex. Hypocapnia or TPL blunts increased CBF, ICP seen with ketamine and VA). MM619-20.
  • When producing an isoelectric EEG Isoflurane and sevoflurane the relative reductions in the CMR and CBF are more intense in the neocortex than in other areas of the cerebrum.
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34
Q

Relationship between volatile anesthetics, CBF and CRMO?

A
  • Direct vascular smooth muscle dilation (↑ CBF)
  • ↓ CMR (↓ CBF) (d/t flow metabolism coupling)
    • huge clarification in miller ch 11 pg 311. this is due to the naturally occur flow-metabolism relationship,. because CMR decreases, you will get a decrease in CBF until higher doses of VA are administered
  • “Luxury Perfusion” Dose related
    • 0.5 MAC CMR reduction is predominate ↓ ; not much change CBF (miller says may be small decrease c/t awake state)
    • 1.0 MAC CMR decrease & vasodilation in balance no change CBF (3:38)
      • Sevo and Des may actually still decrease CBF at 1.0 MAC depending on which study you look at
    • >1.0 MAC vasodilation dominate ↑ CBF
  • Decouple is older terminology because amount of uncoupling depends on dose of VA
  • All studies in healthy volunteers. Never comfortable running 1 MAC VA. Generally stick to 0.5 MAC or less
  • If assessment of patient makes you think they won’t tolerate any increase in CBF, then stick to 0.5 MAC or less
  • Uncoupling probably too strong a term if you are talking about a lower dose VA as the drop in CMR can have a favorable impact on CBF and CBV – in addition the two still seem to be coupled (although the ratio changes) even at larger doses. Difficult to interepret some of these results because most studies use normal brains and not diseased brains (I.e. our neuro patients).
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35
Q

What is the effect of VA on CMR?

A
  • All agents = dose dependent ↓ CMR (except nitrous oxide)
  • Order of CMR ↓
    • Halothane< Enflurane< Desflurane < Isoflurane < Sevoflurane
      • With Sevo, Iso and Des max EEG reduction at 1.5-2.0 MAC = max CMR reduction
  • i.e. sevo reduces CMR the most and is theoretically superior for reducing CMR.. Desflurane and Sevoflurane are about the same as Iso and Enflurane.
  • Unlike hypothermia, there is no further decrease in CMR after the EEG goes isoelectric.
  • VA CMR reduction is not uniform throughout the brain – isoflurane reduces mostly in the neocortex.
  • Exception with enflurane – if enflurane precipitates sz then CMR will increase. MM619-21
  • Table 27-5 is important pg B754. Isoflurane’s metabolic effect which reduces CBF competes with its direct vasodilatory action to limit the net increase in CBF with this agent. Enflurane causes sz type discharges especially with hypocapnia and auditory stim can increase CMR and CBF by 50%. Des advantage over iso faster onset and recovery. However, has shown to increase ICP more in patients with altered intracranial compliance and it causes sympathetic hyperactivity. Sevo has demonstrated cerebral protection during incomplete ischemia in rats. Thus, Sevo and Iso agents of choice in neuroanesthesia
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36
Q

Relationship between VA and CBF/CBV?

A
  • Order of vasodilating potency:
    • halothane >> enflurane > isoflurane = desflurane > sevoflurane
      • sevo is best choice in pt with impaired neuro hemodynamics
      • halothane vasodilates the most, sevo the least
  • Agent and dose dependent ⇑
    • CBF 20% (isoflurane)-200%(halothane)
      • Desflurane & Sevoflurane may actually ⇓ CBF in some areas of the brain
  • Studies difficult to interpret because CBF doesn’t ⇑ uniformly throughout different brain regions
  • Would not want high dose prop and VA in someone with high ICP. Stick with just prop
  • CBV⇑ 10-12% and this is the factor that is most important when considering ICP
  • Effect depends on baseline CMR reduction
    • If CMR already reduced by another drug (propofol) the VA vasodilating potency will be more dramatic and could negatively impact ICP.
  • Response of cerebral vasculature to CO2 retained (in normal brain)
    • Hyperventilation can blunt the increased CBF/ICP with isoflurane or sevoflurane even if initiated after the VA is started ( >1.5 MAC this effect is abolished)
  • Volatile agents when used at anesthetic concentrations increase CBV (compared with propofol)
    • should be used with caution in patients with mass occupying lesions/elevated ICP
      • → any chance of ICP increase, stick to TIVA
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37
Q

What is the impact of VA on autoregulation?

A
  • All VA impair autoregulation → Dose dependent effect
    • Ex: Increasing dose → BP dependence on cerebral BF more narrow
      • **high dose= no autoregulation
      • Importance of MAP > 50-60 w/ VA to maintain CPP
  • Note left shift= less protection with HTN (worry about cerebral edema, etc)

In preliminary studies it appears sevo preserves autoregulation the most of all the volatile agents.

Looking at the graph above - what is the clinical significance? HTN during DVL, emergence, etc. maybe less protection from HTN related BBB disruption and/or hemorrhage.

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39
Q

What is circulatory steal phenomenon in neuro?

A
  • Possible when anesthetics are used in patients with focal ischemia
    • Focal= stroke, tumor, brain injury
  • VA increase CBF in normal areas, however ischemic areas are already maximally dilated
  • Thus, blood is redistributed from ischemic to normal areas
  • Also termed “uncoupling” of CMR and CBF. VA’s alter this relationship and increase CBF when CMR is decreasing also known as “luxury perfusion” . This might be a useful effect if you are using isoflurane for controlled hypotension for example.
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40
Q

What is the effect of IV anesthetic agents on CMR or CBF?

A
  • General trend → maintain coupling between metabolism and blood flow
  • CMR decrease
  • CBF decrease
    • Exception: Ketamine (both increase)
  • Range of effects:
    • Dramatic:
      • Propofol
      • Etomidate
      • Thiopental
    • Intermediate:
      • Dexmedetomidine
      • Benzos
    • Mild:
      • Opioids
        *
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42
Q

What are some cerebral protective agents?

A
  • Calcium Channel Blockers:
    • Nimodipine- reduces frequency of vasospasm subsequent to subarachnoid hemorrhage and may improve outcome.
      • Otherwise, unclear if beneficial (thought that reducing Ca would decrease cell death → not proven)
  • Steroids:
    • reducing edema associated with tumors (not useful in most other neurosurgical contexts – potentially harmful)
  • Diuretics: (Mannitol, Furosemide)
    • reduce volume of brain’s ICF and ECF compartments
  • Anticonvulsants:
    • any acute irritation of the cortical surface, head injury, SAH, cortical incisions and irritation of the brain surface by retractors has the potential to result in seizures
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43
Q

Effect of neuromuscular blockers on cerebral hemodynamics?

A
  • No direct actions
  • Side-effects may be problematic
  • Avoid histamine releasing (cerebral vasodilation – ICP ↑and HoTN– CPP↓)
    • Atracurium
    • Mivacurium
  • Succinylcholine:
    • ↑ ICP ~ 5mmHg
      • offset with other drugs (propofol) and baseline decreased LOC - not contraindicated in emergency
  • Pancuronium:
    • tachycardia
    • HTN
  • Avoid light anesthesia, hypercapnia, & hypoxemia
  • *Sugammadex has not been evaluated
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44
Q

Vasodilators effect on cerebrla hemodynamics?

A
  • i.e. NTP, NTG, hydralazine, adenosine, calcium channel blockers
  • Response to most is cerebral vasodilation and increased CBF (dose dependent)
    • Maintains CBF in face of decrease MAP
  • Despite reductions in BP, CPP often remains the same or increases as does ICP
  • when hypotension is induced with a cerebral vasodilator, CBF is maintained at lower MAP values than when induced by either hem- orrhage or a noncerebral vasodilator. In contrast to direct vasodilators, the ACE inhibitor enalapril does not have any significant effect on CBF. L-type calcium channels highly expressed on cerebral vessels. ACE and ARBs do not impact resting BF and autoregulation is maintained
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45
Q

Effect of barbituates on neuro hemodynamics?

A
  1. Hypnosis
  2. Depression of CMR 30% induction dose
  3. Reduction of CBF 30% induction dose (increased cerebral vascular resistance)
  4. Anticonvulsant activity (one exception)
    1. Methohexital promotes seizure activity
  5. Robin Hood/Reverse Steal Phenomenon
    1. Thiopental preserves blood flow to ischemic areas
      1. Vasoconstrict normal brain and maintain dilation ischemic
      2. Direct blood flow from healthy to diseased brain (robin hood/reverse steal)
  6. Facilitate CSF absorption
46
Q

What are key considerations for anesthesia during/after a cerebral ischemic event?

A
  • Adequate anesthesia (no agents conclusively protective)
  • Prevent seizures
  • Normocapnia and normoglycemia
    • Hypocapnia only beneficial short term and can cause reflexive vasodilation if <20
  • Avoid hyperoxia
    • Not conclusive if it’s a problem, but some evidence it can increase production of oxygen free radicals and cause inflammatory damage
    • O2 doesn’t have huge impact on cerebral hemodynamics, so just better to avoid hyperoxia
  • CPP at least 60mmHg; MAP 70-80mmhg or 30% of baseline
  • Hypothermia (prevent hyperthermia!)
    • 32-34 degree C for 24 hours following global ischemia with cardiac arrest improves outcome
    • Lg. studies of hypothermic patients 1) undergoing aneurysm repair under anesthesia 2) trauma patients demonstrated no benefit
    • Studies on-going in stroke patients
    • Re-warm slowly….
      • Don’t want them to shiver and increase CMR
  • Volatile agents, propofol, TPL all have been shown to be cerebral protective. Higher incidence of thrombocytopenia, bradycardia, ventricular ectopy, hypotension and infection are common
  • Barash 8th mentions that long-term cooling after TBI up to 5 days shows promise while short term cooling 24-48 hours not helpful.
47
Q

Key considerations with supine positoning in neuro anesthesia?

A
  • Horizontal supine almost no perfusion gradient exists between the heart and arteries in the head
  • Pressures change by 2 mmHg for each 2.5cm that a given point varies in vertical height above or below the heart
    • May keep transducer at external auditory meatus to measure pressure in brain
    • Head 25 cm higher than heart, then 20 mmHg diff in MAP
  • Head neutral or rotated for frontal, temporal, or parietal access
  • Extremes of head rotation can obstruct jugular venous drainage consider a shoulder roll
  • The head is neutral for bifrontal craniotomies and transsphenoidal approaches to the pituitary
  • Adjusting the operating table to a chaise lounge (lawn chair) position (flexion, pillows under the knees, slight reverse Trendelenburg) promotes cerebral venous drainage and decreases back strain
48
Q

Positoning considerations for prone procedure for neuroanesthesia?

A
  • Uses:
    • Spinal cord, occipital lobe, craniosynostosis, and posterior fossa procedures
  • Cervical spine and posterior fossa procedures
    • require neck flexion
    • reverse Trendelenburg
    • elevation of the legs
  • Head positioned in a pin head holder (applied before the turn), a horseshoe headrest, or a disposable foam headrest
  • This orientation serves to bring the surgical field to a horizontal position. Awake tracheal intubation and prone positioning can be used in patients with an unstable cervical spine-unchanged neurologic status confirmed before anesthesia induction
  • Important to place chest rolls to prevent:
    • abdominal compression
    • resultant decreased diaphragmatic excursion
    • obstruction of aorta and IVC
      • translate pressure in other areas and increase bleeding
  • Head/neck neutral –
    • turning can obstruct arterial perfusion and venous drainage
      • → increased ICP decreased CPP
  • Considerations:
    • Head below heart level → venous congestion of the face/neck/head occur
    • Head above heart level → air entrapment in open veins possible
    • No pressure on breast/genitals, arms < 90 deg, iliac crest, knees, heels, etc padded, ETT well secured
49
Q

Considerations for sitting position? Benefits?

A
  • Semi Recumbent rather than sitting.
    • Legs kept high w/ pillow to promote venous return → enhance CV stability
    • Pin holder apparatus
      • A: correct → quickly lower head (in case of emergency, VAE etc)
      • B: incorrect → cannot lower HOB w/o causing severe damage or moving to diff location
  • Access to posterior fossa - midline structures (the floor of the fourth ventricle, the pontomedullary junction, and the vermis)
  • Multiple complications possible, often avoided
  • Number of complications often related to experience level of team
  • Benefits of Sitting position:
    • provides excellent surgical exposure
    • facilitates venous and CSF drainage.
    • Better ventilation and easier access to the chest airway ETT and extremities.
    • Facial and conjuctival edema is reduced.
51
Q

What are some hemodynamic impacts of sitting position

A

Sitting Position and Hemodynamics

  • Measuring and maintaining perfusion pressure at level of the surgical field
    • Transducer placement: level of Circle of Willis (tragus of ear)
  • NIBP - must correct for hydrostatic difference between the arm and the operative field
    • Ex: A column of water 32 cm high exerts a pressure of 25 mm Hg
  • Consider PA catheter if CAD or valvular heart disease
    • Typically place central line in case of VAE in sitting position

Sitting Position and Circulatory Stability

  • Changes r/t sitting position:
  • Atrial filling pressures: decrease (left > right)
  • Sympathetic tone: increases
    • SVR increase 30-60%
    • PVR increase 50-100%
  • Parasympathetic tone: decreases
  • RAAS activated
    • Fluid and electrolytes are retained by the kidneys
    • Intrathoracic blood volume: decrease 500ml
    • Renal BF: decrease 30-75%
  • CO: decrease 20-40%
  • SV: decrease 50%
  • HR: increases 30%
  • CBF: decrease 20%
  • Treatment of HoTN:
    • pressor administration
    • aggressive pre-positioning hydration
    • elastic bandages to legs
    • slow movement
  • Evaluate the patient’s ability to tolerate reduced cardiac index, increased SVR
  • Healthy patients:
    • CPP minimum value= 60 mmHg
  • Higher CPP
    • elderly, hypertensive, cerebral vascular disease , cervical spinal stenosis or sustained retractor pressure to brain or spinal cord
52
Q

What are some complications of the sitting position?

A
  • Head flexion
    • limited to by placing 2 fingers between mandible and sternum
  • Macroglossia - swelling of pharyngeal structures
    • including soft palate, posterior wall, pharynx, and base of the tongue, has been observed
    • Caution: AW swelling → AW compromise
      • Avoid foreign bodies (oral AW)
  • Quadraplegia or Paraplegia
    • Head flexion causing cervical spine cord strain or compression of vertebral arteries
  • Pneumocephalus
    • Caution w/ N2O
  • Venous Air Embolism
    • Head above level of heart
  • Paradoxical Air Embolism
    • Ex: PFO, right to left shunt
53
Q

What is the rate of occurence of VAE? High risk procedures? VAE sources?

A
  • Rate of occurrence depends on:
    • Procedure
      • Higher risk: near venous sinuses
    • Patient position
      • Risk: Sx site above level of heart
        • May occur when operative field is elevated 5 cm or more above the right atrial level.
    • Method of detection used (sensitivity of monitor)
      • Ex: Posterior fossa sx
        • w/ doppler → 40% detection in sitting
        • transesophageal ECHO → 76% detection
  • High risk of VAE: Posterior fossa, upper c-spine procedures, and supratentorial procedures
    • (ex. parasagittal or meningiomas near sagittal sinus, craniosynostosis procedures- premature fusion of head bones)
  • VAE sources:
    • emissary and cervical epidural veins
    • major cerebral venous sinuses (transverse, sigmoid, posterior half of sagittal sinus)
      • Problem → non-collapsible bc of dural attachments (suck air in if left exposed)
    • Pins
      • Important to remove pins AFTER head lowered at end of case
54
Q

What are various means to monitor for VAEs? Most sensitive detector?

A
  • Precordial Doppler and ETCO2 monitoring
    • current standard of care
  • TEE
    • more sensitive to VAE than precordial Doppler
    • offers advantage of identifying right-to-left shunting of air
      • detects low volumes of air
      • Cons: risk of esophageal perforation
  • Expired N2 concentrations
    • very small unless large VAE thus lack sensitivity

VAE sensitivity monitors

  • T-ECHO- very sensitive
    • Detect before any compromise (ideal)
    • TEE is more sensitive to VAE than precordial Doppler) and offers the advantage of identifying right-to-left shunting of air. However, its safety during prolonged use (especially with pronounced neck flexion) is not well established.
  • Doppler- standard of care
    • Detect before compromise
      • Technique: placed parasternal (R or L side- better R) between 4th and 6th intercostal spaces
        • Better R → more likely to have R atrial air
  • ETCO2- see greatly dampened
    • Modest physiologic change by ETCO2 dampen
    • Use WITH doppler as standard of care
  • CO/CVP
    • Clinically apparent changes
55
Q

What is the pathophysiology behind VAE?

A
  • intense vasoconstriction in pulmonary circulation (secondary to mechanical obstruction and hypoxic vasoconstriction) which results in:
    • VQ mismatch
    • interstitial pulmonary edema
    • reduced cardiac output as pulmonary vascular resistance increases.
  • Air may also pass directly through the pulmonary circulation or through right to left cardiac shunts (PFO 20-30% population) to the coronary and cerebral circulation when right atrial pressure exceeds left atrial pressure.
    • In sitting position 50% of patients right atrial pressure exceeds left atrial pressure – risk PAE (paradoxical air embolism) is 5-10%. Avoid in patients with a known PFO.
57
Q

Management of VAE?

A
  • Prevent further air entry
  1. Notify surgeon (flood or pack surgical field)     
  2. Jugular compression    
  3. Lower head
    1. Stop more air from entering
  • Treat the intravascular air     
  1. Aspirate via a right heart catheter
  2. Discontinue N2O     
  3. FIO2: 1.0 (max)   
  4. Pressors/inotropes/CPR
58
Q

Preoperative evaluation for neuro surgery?

A
  • Underlying medical conditions
    • Ex: Patent Foramen ovale- specific for sitting position/high risk VAE (sx near dural sinus)
  • Procedure length and position
  • Question optimized for surgery
    • Ex: subarachnoid hem, trauma pts → on mannitol, 3% NS, blood products
  • Negotiate hemodynamic/ventilation & position goals with surgeon
  • Determine need for:
    • Abx
    • Steroids- only for tumors (normalize edema ring → improve outcomes)
    • Diuretics
      • Bolus mannitol/3% NS prior to start
    • Anticonvulsants- Prophylactic admin
      • Common w/ trauma (brain exposed to blood)/brain tumors
        • Ex: phenytoin, phenobarb
  • Carefully assess fluid and electrolyte status – correct pre-op
    • Glucose levels: 90-180 mg/dL in diabetic patients
    • Avoid changes in Na+ > 3-4 mEq/L per hour (central pontine myelinolysis)
    • Plt count >100,000mm3
59
Q

Considerations for neuro assssment?

A

where are they on compliance curve?

  • Level of consciousness
    • Awake/alert → can tolerate extra volume
  • ICP
    • Headache
    • Nausea
    • Papilledema
    • pupil size
    • respiratory pattern
      • any ICP issues → TIVA (propofol) approach
      • avoid hypoventilation/CO2 increase
  • Neurological deficits
    • Ex: look at brain – is it bulging?
  • MRI or CT results
  • Location of lesion
  • Surgeon’s impression of intracranial compliance and VAE risk
  • Supratentorial disease= ICP mgmt. problems
  • Infratentorial lesions = mass effects on vital brain stem structures w/ elevated ICP d/t obstructive hydrocephalus
  • ICP derangements can be identified radiologically – “slit ventricles” or shift in midline brain structures of more than 5mm – advanced pathology
60
Q

What are some sudden and severe complications in interventional neuroradiology?

A
  1. Hemorrhagic –
    • Protamine
      • Dose: 1 mg per 100 units heparin admin
    • Controlled HoTN
      • Deepen anesthetic
      • Esmolol
      • NTG
      • NTP
  2. Occlusive – device (coil/balloon) deployed to unintended area → worry of ischemic damage distal to occlusion
    • Deliberate HTN – enhance collateral flow through CoW.
      • BP > 30-40% baseline or until neurologic symptoms resolve
        • Phenylephrine
        • Dopamine
    • Direct thrombolysis
  3. Anaphylaxis
    • Contrast media = anaphylaxis risk
      • Admin Epi
      • 3rd spacing → have fluids available
61
Q

Overall goals for treatment in interventional neuroradiology?

A
  • Overall treatment → Neuroprotective measures
    • Hyperventilate – decrease ICP
      • ETCO2 26-30 mmHg
    • Rapid fluid admin – for hemorrhagic
    • Diuretic admin
      • Mannitol 0.5 g/kg
    • Anticonvulsants
      • Phenytoin
      • Phenobarb
    • induce Hypothermia (33-34 deg C)
    • EEG suppression- TPL coma (burst suppression)
      • reduce CMRO2 → preserve marginally perfused cells
        • Ensuring O2 going to maintenance of cell integrity
    • HOB 15 deg and neutral
  • Make sure you have access to all of these agents in the event of an emergency because rapid response will be required. Hypothermia to 33-34 degrees C B6th767
  • For deliberate hypertension consider phenyephrine or dopamine – get BP 30-40% > than baseline or until neurologic symptoms resolve. For controlled hypotension consider esmolol, NTG or NTP. Dose of protamine is 1mg for each 100U heparin given. Head up 15 degrees and neutral, PaCO2 around 28-30mmHg, give 0.5g/kg mannitol, rapid IV infusion, phenytoin and phenobarbital, TPL coma (burst suppression), temp 33-34C.
62
Q

What are supratentorial tumors? symptoms?

A

Pathophysiology

  • Supratentorial – located ABOVE tentorium
    • Tentorium: process of dura mater between cerebrum and cerebellum supporting the occipital lobes (cerebellum and occipital lobe)
    • Most common for craniotomy
    • Ex:
      • Meningiomas-
        • large size
        • difficult location
        • highly vascular → considerable BL
          • surgically challenging → lengthy procedure
        • Necrotic hemorrhagic core
        • Wide border of brain edema
          • increased bulk
          • increased impaired autoreg area
      • Gliomas (oligodendrogliomas, astrocytomas)
        • Easy access location
        • Less vascular – less bleeding risk
        • Hard to get clear margins → often reoccur (often “Debulking procedures”)
      • Metastatic lesions (breast, melanoma, lung, kidney)
      • Chronic subdural hematomas-
        • Space occupying lesions → displace other structures (specific symptoms or HA or Sz)
  • Symptoms:
    • ICP problems. Small changes in BP= big changes CBF/ICP
    • appear when compensatory mechanisms exhausted by growing lesion
63
Q

Considerations for supratentorial tumors

A
  • Consider tumor location & size (blood loss & surgical position)
    • Locations:
      • Hypothalamus: SNS disturbance, altered LOC, temp, fluid reg, DI, cerebral salt wasting syndrome
      • Dural sinus: concern for VAE
        • Low risk except lesions encroaching on sagittal sinus
    • Size: Ability to displace structures
      • → ICP increase risk → CPP/herniation issues**
        • Generally: tumors = vascular
          • Necrotic hemorrhagic core
          • Wide border of brain edema (ischemic penumbra)
            • increased bulk
            • increased impaired autoreg area → maintain CPP
        • Tx: Steriods 24-48 hrs prior
          • stabilize edema ring
          • stabilize BBB
  • VAE risk:
    • Low, except lesions encroaching on sagittal sinus
  • Small changes in BP = big changes CBF/ICP
    • Impaired autoregulation area near tumor
  • Bilateral Subfrontal approach (retraction/irritation frontal lobes) - “frontal lobey”
    • Consequence of frontal lobe retraction →
      • delayed emergence
      • disinhibition
      • both (delayed emergence & disinhibition)
    • Considerations:
      • reduced IV anesthetic drugs (lower midaz/opioids)
        • to ensure whether its cognitive irritation or too much sedative
64
Q

Anesthesia considerations for craniotomy for supratentorial, intracrnail tumors?

A
  • Control ICP (*top priority*)
    • Institute measures before open dura → then visually assess
  • Diuretics
    • Mannitol: 0.25-1.5 g/kg
    • 3% NS: 50-100 ml/hr
      • hourly Na+ checks → don’t change levels too fast
  • Corticosteroids
    • Dexamethasone: 10 mg q6hrs (48 hrs before and during case)
  • Hyperventilation
    • Goal: PaCO2 ~ 25- 30 mmHg
    • AVOID: PaCO2 < 25 mmHg → too much vasoconstriction (ischemic brain)
      • Aline → obtain CO2 gradient (assume 5 mmHg gradient in ABG and ETCO2)
  • Optimize hemodynamics
    • CPP adequate
  • Normovolemia
    • Avoid hyposmolar fluids
      • Ex:
        • Plasma = 295
        • LR = 273 mOsm/L (hyposmolar)
          • AVOID
        • *NS= 308 (hyperosmolar)
          • Hyperchloremic metabolic acidosis
        • *Plasmalyte/Normosol = 294 (isosmolar) <<< ideal choice
  • Normal blood glucose
    • Hyperglycemic → promotes anerobic metabolism → increase brain damage
  • Improve venous return (positioning)
    • HOB elevated 10-15 deg (adequate venous drainage)
    • Avoid PEEP
  • TPL, propofol
    • Parallel dec in CMRO2 & CBF
  • Mild hypothermia
    • Keep paralyzed → Prevent shivering
    • Rewarm slowly
  • Prevent coughing and bucking → could herniate through craniotomy
    • deep anesthesia
    • muscle relaxants
65
Q

Induction considerations for supratentorial intracranial tumor?

A
  • Place A line pre/post
    • Transducer at external auditory meatus (pressure perfusing CoW)
  • Optimize ICP
    • Caution w/ sedatives (hypoventilation)
  • Deep induction (avoid ICP change)
    • Lidocaine 1.5 mg/kg
    • Fentanyl 3-5 mcg/kg
      • Liberal → most pain @ case beginning (incision, bone flap, dura)
        • No pain receptors on brain → little surgical pain
    • Propofol 2 mg/kg
      • Small bolus right before intubation too (0.5 mg/kg)
66
Q

Maintenance of supratentorial intracranial tumors

A
  • VA < 0.5 MAC
    • 1 MAC: Vasodilates → ↑ CBV (ok if brain looks ok)
  • Propofol drip 150 mcg/kg/min
  • Propofol 0.5-1 mg/kg
    • Pin placement → pain
      • Opioids
      • Esmolol
  • ABG – early
    • See CO2 gradient
  • Mannitol 1 g/kg
  • Dura open
67
Q

Emergence supratentorial intracranial tumor

A
  • smooth
    • NO REVERSAL until pins out/head dressing on
    • Avoid → ↑ risk hemorrhage/edema
      • Shivering
      • Pain
      • Bucking
      • HTN
    • LTA
    • Precedex
      • Caution w/ HoTN
  • Overall:
    • Drugs easily titratable/adjust!
68
Q

What is an infratentorial/posteiror fossa intracranial tumor? Symptoms?

A
  • BELOW tentorium
    • Small space
    • Structures of posterior fossa include: → when interrupted cause MAJOR problems
      • Medulla
      • Pons
      • Cerebellum
      • Major motor/sensory pathways
      • Primary resp/CV centers
      • Lower cranial nerve nuclei
        • Ex: Significant CV responses***
          • HTN
          • HoTN
          • Bradycardia
          • Tachycardia
  • Other symptoms:
    • Preop dysphagia
    • laryngeal dysfunction
    • respiratory abnormalities
    • chronic aspiration
  • More common in children (ex: medulloblastoma, pilocytic astrocytoma, ependymoma, brainstem glioma)
  • In Adults: acoustic neuromas, metastases, meningiomas, and hemangioblastomas
70
Q

Positioning and monitoring for infratentorial tumor?

A
  • Positioning:
    • Sitting, lateral, prone, park bench, or three quarters prone position (keep in mind CV effects and complications
      • Quadriplegia
      • Macroglossia
      • Pneumocephalus
      • VAE (incidence 39% in sitting position)
      • PAE
  • ECG- alterations rate, rhythm
  • Arterial line (CPP and brain stem alterations)
  • BAEP/SSEP may be monitored
    • TIVA (propofol) → wont interrupt monitors
  • MEP or Electromyographic monitoring of facial nerve
    • Need at least ~2/4 twitches on TOF at least
71
Q

Induction considerations for infratentorial tumor?

A
  • Tumor detection → compression of vital areas
    • Baseline AW patency issues
    • CV
    • Dysphagia
    • Chronic aspiration
      • *RSI
      • *Resolve pulmonary infection 1st
72
Q

Maintenance/emergence consideratiosn for infratentorial/posterior fossa tumor?

A
  • Maintenance:
    • Positioning
      • Sitting/HOB elevated →
        • central line/CVP cath
        • Doppler
        • ETCO2 detection
    • Monitor Aline → surgical interventions affecting rhythm
  • Emergence: → ICU for >24 hrs
    • Issues:
      • Edema
      • Hemorrhage
      • Obstruction hydrocephalus
      • CV/Resp changes
      • LOC changes (any signs need to come back for decompression)
    • Extubation:
      • Awake/alert
      • Ready to reintubate if needed
  • Choose anesthetics with cardiovascular performance in mid.
73
Q

Posterior fossa tumor monitoring?

A
  • Good communication w/ surgeon!! → very small surgical space
  • Warning signs of damage to adjacent cranial nerve nuclei & respiratory centers:
    • Bradycardia & hypotension
    • Tachycardia & hypertension
    • Bradycardia & hypertension
    • Ventricular dysrhythmias
      • Communicate!! Represent damage to pons/lower medulla
        • don’t treat dysrhythmias but talk with surgeon!
  • Dissection on floor of 4th ventricle
    • Possibility of injury to cranial nerve nuclei & swelling
      • Even small swelling has large consequence since sx area small
        • CN dysfunction IX, X, XII
    • Consequences: → extubate? Go to ICU for monitoring
      • upper airway patency loss
      • cranial nerve function loss
      • respiratory drive loss
74
Q

What are functioning vs non-functioning tumors?

A
  • 1. NONFUNCTIONING
    • diagnosed when large and causing symptoms by impinging on adjacent structures (ICP issues)
      • ex: chromophobe adenomas, craniopharyngiomas, meningiomas
        • s/s: ICP, HA, visual changes, cranial nerve palsies
  • 2. FUNCTIONING
    • diagnosed when small symptoms related to production of an excess of 1 or more anterior pituitary hormones
      • ex: prolactinomas followed by GH and ACTH – secreting adenomas
        • s/s:
          • Prolactinomas: amenorrhea, impotence
          • GH:
            • Before puberty → gigantism
            • After puberty → acromegaly
          • ACTH: cushings dx (excessive cortisol) from bilateral adrenal hyperplasia
75
Q

Preop assessment of pituitary tumors

A
  1. Panhypopituitarism?
    1. Tumor compressing gland → not secreting enough hormone
      1. Tx: Correct hypocortisolism & hyponatremia; hypothyroid, etc.
      2. Can rupture and be emergency
  2. Acromegaly?
    1. Evaluate airway, cardiac function (arrhythmias and hypertrophic cardiomyopathy)
      1. AW enlargement: Enlarged tongue, narrow glottis, hypertrophied nasal turbs, mandible enlargement, glottic stenosis
        1. Tx: fiberoptic intubation → diff AW d/t growth
          1. ½ size smaller ETT d/t glottic stenosis
      2. CV enlargement:
        1. Hypertrophic cardiomyopathy
        2. Arrythmias
  3. Cushing’s Disease?
    1. Evaluate- CV workup
      1. DM
      2. OSA
      3. hyperaldosteronism (hypokalemia and metabolic alkalosis)
      4. HTN
      5. CHF
      6. obesity
  • Know size and location of tumor
    • Ex: functioning/nonfx
      • Pituitary microadenomas = no mass effect (fxing type → no ICP issue)
      • Pituitary tumors w/suprasellar involvement- nonfxing
        • Larger → evaluate for ↑ ICP
  • Clear dexamethasone with surgeon –
    • false positive for post-surgical hypopituitary function
  • Visual exam
    • assess optic nerve integrity
  • Transsphenoidal
    • nasal culture → ABX
  • SIADH with sellar tumors (low sodium with fluid overload) → preop correction
    • Tx: Demeclocycline (tetracycline)
      • inhibits ADH activity at renal tubules (see on med list)
76
Q

Anesthetic considerations for pituitary tumor?

A
  • Monitors –
    • standard +/- arterial line (working around carotids/venous sinuses)
  • Position
    • Supine
    • VAE precautions (doppler + right atrial line) if >15 degree surgical site-heart gradient
  • Pharyngeal pack
    • Placed by surgeon → document pack removed after sx
  • ETT
    • RAE
    • secured lower jaw
    • opposite site surgeon dominant hand
  • Transcranial Approach:
    • > ICP mgt VS transsphenoidal
    • Brain retraction → brain irritation risk (sz, DI, blood loss)
  • Transsphenoidal Approach: incision under upper lip, through nasal septum
    • Better M&M
    • High risk:
      • CSF leak
      • Meningitis
    • LA: 4 % cocaine & 2 % lido w/epi infiltrated èwatch dysrhythmias
      • Cocaine: inhibits NE reuptake → vasoconstriction/analgesia
  • CO2 management – depends on surgical goals
    • Ex: Hypocapnia → minimize brain volume → minimize arachnoid bulge degree into sella
    • Ex: Hypercapnia: larger tumor w/ suprasellar extension = normal/increased CO2 → deliver lesion into sella for excision
  • VEP monitoring – MOST sensitive to VA
    • Optic nerve and chiasm
  • C-Arm Fluoroscopy
    • head & hands inaccessible after drape
      • Peripheral Nerve Stim on LE
      • IVs and Aline working well after tucking
      • Check compression of C Arm on body (nerve damage)
77
Q

What are some considerationg for emergence following pituitary surgery?

A
  • Smooth emergence - especially if CSF space has been opened
    • Issues → Meningitis r/t CSF leak!!
      • Valsalva maneuvers (coughing/vomiting) may contribute to reopening of a CSF leak and worsen the risk for subsequent meningitis
  • Suction well
    • AW cleared of debris, including formed clots
    • Packs removed
  • Visual acuity should be assessed pre-extubation
  • Nose packed – remind patient to breath through mouth
  • fully awake extubation
    • LTA
    • Propofol bolus

notes:

  • Smooth emergence, especially if the CSF space has been opened (and resealed with fibrin glue or by packing the sphenoid sinus with fat or muscle). Valsalva maneuvers, as with coughing or vomiting, may contribute to reopening of a CSF leak and worsen the risk for subsequent meningitis. Inspect the pharynx with a laryngoscope. The airway should be cleared of debris, including formed clots. allows one to more confidently extubate promptly at the first signs of reactivity to the endotracheal tube.
  • The chosen anesthetic technique should permit gross visual acuity exam before pt. extubated. If visual acuity is worse then may need emergent decompressive surgery.
78
Q

What are some complications of pituitary surgery?

A
  • CSF Leak/Rhinorrhea – meningitis (transsphenoidal*)
  • Damage to Surrounding Structures-
    • CN 3-6
    • cavernous sinus
    • internal carotid
    • hypothalamus
    • optic nerve
    • Optic chiasm
  • Pituitary/Adrenal Axis Malfunction – dexamethasone followed by prednisone for 5 days post-op or until testing clears pt.

Pituitary Surgery: Complications- Diabetes Insipidus

  1. Development: 12-48 hrs postop
    1. rarely arises intraoperatively
  2. Diagnosis:
    1. Polyuria: 2-15 L/day
    2. rising serum osmolality: > 300mOs/kg
    3. specific gravity: < 1.005
  3. Treatment:
    1. 1/2NSD5W = Hourly maintenance fluids plus 2/3 previous hour’s urine output.
      1. (or hourly urine output minus 50 mL plus maintenance)
    2. Hourly requirement > 350-400 mL → add desmopressin (synthetic ADH)
      1. DDAVP: 0.5-1.0 uG IV/SQ
  • One of the important surgical considerations is the avoidance, when possible, of opening the arachnoid membrane. Postoperative CSF leaks can be persistent and are associated with a considerable risk of meningitis. In situations in which one is concerned that a persistent CSF leak may occur, some surgeons will place a lumbar CSF drain to maintain CSF decompression in the early postoperative period.
79
Q

Interentions with intracranial aneurysms/SAH?

Risks? Grading?

A
  • Discovered pre-rupture:
    • *elective endovascular coiling (favored approach)
    • surgical clipping used
  • Subarachnoid hemorrhage
    • CoW aneurysm rupture:
      • 1/3 functional survivors
      • 1/3 die before hospital
      • 1/3 vegetative state
    • Operative clipping versus the endovascular approach in IR
  • Risks: 50’s (peak risk), female, HTN
  • Aneurysmal SAH surgical risk and outcome predicted via grading systems
    • World Fed. of Neurosurgeons – 1-5 based on GCS and Motor Deficit
      • 1-2: less severe (more favorable in outcome)
      • 4-5: severe
    • Hunt and Hess (clinical symptoms)
    • Fisher Grade (radiologic bleeding)
80
Q

Symptoms of intracranial aneurysm/sah? Diagnostic?

A
  • Symptoms:
    • N/V
    • severe HA
    • stiff neck
    • photophobia
    • LOC
      • Blood + subarachnoid space = abrupt increase ICP
      • Pressure increasing → SNS response → increase catecholamines
        • HTN
        • dysrhythmias
  • Dx: CT scan, angiography = size and location
    • Small < 10 mm
      • > 6 mm require treatment
    • Large 10-24 mm
    • Giant > 24 mm
81
Q

ECG changes associated with SAH?

A

Canyon T waves

  • Hemorrhage → body recognizes threat → catecholamine surge
    • NE/Epi → Heart exposed → dysrhythmias
      • Canyon T Waves – dips in T waves
  • Other common changes
    1. ST depression or elevation
    2. T wave flattening
    3. U waves
    4. Prolonged QT
    5. Dysrhythmia
  • w/in 10 days resolves
  • Increase CV enzymes
83
Q

What are some complications of intracranial aneurysms/SAH?

A
  • Intracranial HTN
    • Emergency ventriculostomy
    • Diuretics- 3% NS/Mannitol
    • Intubation (higher grades 3-5)
      • LOC issues
    • Hyperventilation
      • Prevent herniation short term (> 6 hrs → Bicarb tx to brain to normalize pH)
  • Hydrocephalus
    • Obstructive- hematoma blocking flow through ventricular system or Hgb clogs arachnoid villi preventing flow out
      • V/P shunt placement
  • Rebleeding
    • Most common cause of death in hospitalized SAH patients
    • Risk: Spontaneous rebleed
      • 1st 24 hrs = 4% risk
      • > 24 hrs = 1.5%/day
        • 19% over 2 weeks
  • Cerebral Vasospasm
    • Max risk days 3 to 14 post-rupture
      • Highest risk: 7 -10 day (avoid sx these days → worst outcomes)
    • Mechanism unknown. – structural and pathologic changes have been demonstrated in the vessel wall. Removal of extravasated blood decreases the occurrence and severity of ischemic deficits. Oxyhemoglobin thought to be the blood component responsible for vasospasm
      • Theory: Exposure of cerebral vessels to blood promotes vasospasms
        • Remove blood to decrease risk
    • Symptoms: 30% symptomatic (occurs in 70% of pt)
      • HA, increase BP, confusion, lethargy, focal motor speech impairment
        *
84
Q

What is typical surgical managmenet of intracranial aneurysms?

A
  • Contemporary management = early (
  • Ideally to OR w/in 18-24 hours
  • If early intervention not feasible: surgery delayed 10-14 days (beyond max risk vasospasm period)
    • Ex: days 4-12 after SAH
  • Early intervention pros:
    • decrease risk of rebleed
    • decrease risk of vasospasm
    • better tolerance of vasospasm treatment if needed
    • less bedrest
  • Early intervention cons:
    • more hydrocephalus/edema
    • more ICP issues
    • clot poorly organized
85
Q

Diagnosis of cerebral vasospasm? Treatment?

A
  1. Diagnosis: angiography/transcranial doppler
    • HA
    • HTN
    • Confusion
    • Lethargy
    • Focal motor/speech deficits
    • Coma
  2. Nimodipine (CCB): standard prophylactic therapy
    • Improved long-term outcomes
  3. “Triple H Therapy”- less popular
    • Hemodilution
    • HTN (increase SBP 20-30mmHg)- phenylephrine
    • Hypervolemia (traditionally hypervolemia thought to help, now moving towards euvolemia and HTN as mgmt)
    • Euvolemia
      1. → more likely to bleed tho
      2. HTN and euvolemia more recent preference for therapy
  4. Cerebral balloon angioplasty or intra-arterial vasodilators (verapamil, nicardipine. Milrinone, papaverine, etc.)
  5. Promising new approaches –
    • PDE (cilostazol): platelet inhibitor and vasodilator: small Jan 2013 non-blinded trial
      1. Findings: decrease vasospasm and delayed cerebral infarction
    • TXA- Crash 3 Trial just published October 14th 2019 highly favorable
      1. – will probably become standard of care in TBI
    • Fibrinolytics- increase incidence of ischemic symptoms and hydrocephalus
      1. Miller 9th → don’t cite any convincing studies
    • Endothelin A receptor antagonist- Improved mortality did not improve long term functional outcomes
    • Magnesium- large randomized trial did not show a benefit
    • Statins - meta-analysis not significant…. larger trial failed to demonstrate significant reduced incidence of cerebral ischemia and death
86
Q

Preop considerations intracranial aneurysms/SAH

A
  • Note severity, acuteness, stage of SAH
    • Grade 1-2 bleed → favorable outcome
    • >3 bleed → intubated, LOC
  • Surgery Timing
    • Difficulty swallowing? Pneumonia/DVT risk?
  • ICP status
  • Assess for hypothalamic dysfunction and sympathetic over-activity
    • CoW near hypothalamus → rupture → SNS overactivity, temp regulation issues, EKG changes, endocrine/electrolyte imbalances
  • Assess Fluid Status:
    • SIADH - too much ADH →
      • intravascular volume expansion
      • low Na
        • tx: Volume restriction
    • Cerebral salt wasting syndrome
      • contracted intravascular volume
        • hyponatremia after SAH is more likely to be consequence of cerebral salt-wasting syndrome d/t release of a natriuretic peptide by the brain (similar ot hear)
        • triad of hyponatremia, volume contraction, and high urine sodium concentration
      • Pt excrete Na (low Na) → water follows Na → dehydration
        • Tx: Fluid replacement
87
Q

What are the major anesthetic goals for management of intracranial aneurysm/SAH?

A
  1. Acute HTN = risk of rerupture = often FATAL
    • Risky times:
      1. Intubation
      2. Mayfield pins
      3. surgical stimulation
    • Keep DEEP and tx HTN
      1. Preinduction aline
  2. Brain relaxation facilitates surgical access
    • Measures reducing ICP:
      1. ETCO2 25-30, PaCO2 ~30
      2. mannitol prior to opening dura – 1 g/kg
      3. TIVA
      4. Avoid VA > 0.5 MAC
  3. High-normal MAP
    • → prevent critical reduction of CBF to ischemic penumbra around SAH
      1. Ex: allow lower during critical periods but after want high/normal
  4. Tight MAP control as surgeon clips aneurysm and/or controls bleeding from a ruptured aneurysm
    • Promote collateral flow
    • Lower BP ex: Propofol 1 mg/kg to deepen
      1. dec CMRO2 to burst suppression level
      2. reserving all O2 to cellular integrity
    • MAX safe clamp time (during “trapping”) = 14 minutes (@ nml temp and BP)
      1. > 30 min → 100% brain damage incidence

Be prepared: Major intraoperative complication = hemorrhage!!!!

88
Q

Consideratiosn during surgical clipping of the aneurysm?

A
  • Adenosine 0.3-0.4 mg/kg
    • temporarily halt circulation while a permanent clip is placed on the aneurysm
      • have fib pads
  • Burst suppression w/
    • Propofol 1-2 mg/kg (w/ phenylephrine → reduce CMRO and support CPP) or
    • VA
  • Temporary occlusion - < 14 minutes
  • Mannitol
    • Additional 1g/kg 15 minutes before temporary occlusion
    • might have CBF enhancing effect during periods of CBF reduction
  • SSEP and MEP – monitoring ischemic changes
    • Communicate propofol bolus
  • IF a rupture occurs…. Preparation must occur before the episode of bleeding- immediate control of MAP 40-50 mmHg range may be required
  1. Deep isoflurane VS adenosine VS sodium nitroprusside infusion prepared before induction
  2. Normovolemia prior to bleeding episode essential
    1. Don’t aggressively fluid load before aneurysm clip
  • After hemorrhage – once temporary clips have been applied normal BP is desirable. If the surgeon is unable to temporarily occlude the bleeding aneurysm and blood loss is not excessive can lower MAP to 50mmHg or lower to assist the surgeon to gain control of the bleed. Judgment call – if blood loss is excessive fluid resuscitation must be accomplished before using drugs to lower BP
89
Q

What is important to remember about autoregulation around ischemic penumbra?

A

(i.e. be careful with controlled hypotension!)

  • Ischemic penumbra – no autoregulation
    • Pressure passive
      • Ex: MAP 50 → low CBF
      • Want high/normal MAP to get CBF close to 50 (requires much higher MAP)

Normal and absent autoregulation curves. The “absent” curve indicates a pressure-passive condition in which cerebral blood flow (CBF) varies in proportion to cerebral perfusion pressure. This curve is drawn to indicate subnormal CBF values during normotension as have been shown to occur immediately after both head injury and subarachnoid hemorrhage. The potential for modest hypotension to cause ischemia is apparent.

91
Q

Monitor and induction consideration for intracranial aneurysm/SAH?

A
  • Monitors:
    • SSEPS – impact anesthetics
    • Aline- REQUIRED
    • CVP (higher grades) – 10-12 mmHg
  • Induction: how prevent rebleeding? Minimize ICP changes!
    • Agents suppressing intubation response (need deep!)
      • Lido 1.5-2 mg/kg
      • Esmolol – prevent rebleeding at only induction
        • Labetalol (long 1/2L and after this want high/N MAP)
      • Propofol* high dose
      • Etomidate (poor EF)
      • Opioid
92
Q

Maintenance and emergency concerns for intracranial aneurysms?

A
  • Maintenance:
    • Deep for pins, scalp incision, turning bone flap, clipping (dec CMRO + robust BP to promote collateral BF)
    • *SEVO –
      • Des- catecholamine surge (HTN)
    • Burst suppresion during clipping/aneurysm exposure 1-2mg/kg propfol + 100-150 mcg/kg/min + vasopressor to maintain CPP
    • Mild hypothermia – completely relaxed and rewarmed after
      • (32-34degrees C)
    • Prior to dura opening:
      • Hyperventilate
      • Mannitol
      • Antisz med
  • Emergence:
    • Grade 1-2: Extubate
    • Higher grade: remain intubated
93
Q

What is the patho behind head injuries? review of gcs?

A
  • Patho: 2 Injuries
  • Primary injury – we have no control
    • biomechanical effect of force applied to skull and brain (milliseconds)
  • Secondary injury (goal = prevention)
    • Excitotoxicity- glutamate
    • Ischemic penumbra- optimize chance of neurons here survive
      • Patho: Ischemia, brain swelling, edema, intracranial hemorrhage, increased ICP, herniation (minutes to hours)
    • Aggravating factors: → secondary injury worse
      • Hypoxia
      • Hypercarbia
      • Hypotension**- max CPP
        • hypoxia + hypotension significantly worse > 90% patients severe outcome or death
      • Anemia
      • Hyperglycemia
      • Seizures
      • Infection
        • 40% will have another life-threatening injury

Glasgow Coma Scale – defines neurologic function impairment

  • Eyes open – Never (1)-spontaneous (4)
  • Best Verbal Response None (1) – oriented (5)
  • Best Motor Response None (1) - obeys commands (6)
  • Mortality closely related to initial score
  • Scores < 8 = considered severe
    • require intubation and controlled ventilation for ICP & airway control
95
Q

What is involved with inline stabilization during intubation?

A
  • 3 person job
    • # 1- hold manual c-spine stabilization against bed (no flexion)
      • No sniffing position
    • # 2- laryngoscopist
    • # 3- cricoid pressure to prevent aspiration
96
Q

COnsiderations for airway mgmt with head trauma?

A
  • Airway management → ICP is not the only priority! (ABC’s)
  1. Full stomach
    1. Succs- increases ICP but don’t want aspirating
      1. Succs + propofol suppresses response anyway
  2. Cervical spine stability?
    1. R/o w/ CT scan
  3. Airway injury?
    1. blood + structural injury (larynx, cricoarytenoid cartilage, etc.) 
  4. Skull base fracture
    1. avoid nasal ETT
  5. Volume status?
    1. Large blood loss examples:
      1. Lacerated liver
      2. Long bone fracture
  6. Uncooperative/combative
  7. Hypoxemia
  8. ICP
    1. Keep sight of the ABCs of resuscitation: securing the airway, guaranteeing gas exchange, and stabilizing the circulation are higher initial priorities than control of ICP is. Do not risk losing the airway or causing severe hypotension for the sake of preventing coughing on the tube or brief hypertension with intubation.
98
Q

Considerations for anesthetic mgmt of head trauma fro BP? temperature? ventilation? fluids?

A
  • Blood Pressure
    • Hypotension and ischemia are devastating to injured brain
    • Exact target BP controversial
    • CPP 60-70 mmHg
      • 2007 guidelines Brain Trauma Foundation
    • “maintain CPP at or just above 60 mmHg 1st 2-3 days” M9th1893
  • Hypothermia
    • 3 Recent large clinical trials show no benefit
  • Hyperventilation (Brain Trauma Foundation recommendations)
    • Routine use discouraged (especially 1st 24 hrs)
      • ischemic brain = Harmful → decreases CBF
    • May use for acute ICP management, herniation prevention, minimizing retractor pressure, improve surgical access
    • If used → recommend brain tissue PO2 monitoring
  • Fluids – maintain intravascular volume
    • Prevent reduced serum osmolarity and colloid oncotic pressure
      • Prevent brain edema
    • Check labs –
      • cumulative pre-op mannitol
      • fluid therapy impact
    • Products:
      • 0.9% saline
      • 5% albumin
      • Blood products/plasmalyte/normosol > LR (hypoosmolar)
        • NS- hyperchloremic metabolic acidosis, electrolyte imbalances
99
Q

Anesthetic mgmt for head injury in regards to coagulopathy? hyperdyanmic circulatory response? cushing’s triad?

A
  • Coagulopathy
    • Brain tissue thromboplastin release → lead to DIC
      • Assess coags
      • Order products appropriately
  • Hyperdynamic Circulatory Response
    • Massive catecholamine surge (Epi) after head injury
      • → Tachycardia, HTN, increased CO, arrhythmia, CHF (prior CV impairment)
    • Tx:
      • Labetalol
      • esmolol
  • Cushing’s Triad – Need ICP reduction
    • Symptoms:
      • BP high → trying to enhance CPP
      • HR low → baroreceptors bring HR down
      • Irregular breathing
        • HERNIATION!!
    • Tx:
      • Diuretics
      • HOB 30 degrees
      • Barbiturates (more so propofol now)
      • PaCO2 30-35mmHg
      • ventricular drainage
      • consider mild hypothermia ~ 34-35 degrees C (controversial)
  • Multi-center large trial of hypothermia reduction within 8 hours of injury showed no benefit – question is….. If they are cooled sooner within 4 hrs is there potential for improved outcome? Study underway to evaluate.
100
Q

Use of TXA in head injury?

A
  • GOOD in head injury
    • TXA safe w/in 3 hrs of injury
    • Reduced brain injury death
      • ADMINISTER!!
101
Q

Montior, induction, maintenance, emergence for anesthesia for head trauma?

A
  • Monitors
    • Aline- pre/post?
    • Priority is to get cranim open as rapidly as possible
      • Never delay crani after IV accesss achieved
  • Induction
    • HoTN issue but also don’t want extra bleeding from HTN (similar to SAH)
      • Maintain normotension
      • Virtually any induction agent except ketamine can be used
  • Maintenance:
    • ICP issues → TIVA superior (CMRO dec and CBF maintained)
      • VA causes dilation at 1 MAC→ dec CBF
        • Keep < 0.5 MAC
  • Emergence:
    • Swelling peaks w/in 1st 3 days
      • Leave intubated past that period
102
Q

Management for various head injuries?

A

Decompressive craniectomy/craniotomy performed for:

  • depressed skull fractures
    • OR < 24 hrs to prevent infection/meningitis
    • Bony fragments and penetrating objects should only be removed in OR (potential for tamponading a lacerated vessel or dural sinus)
  • midline shift- herniation impending
  • vassal cistern compression
  • refractory ICP increases
  • Evacuation of hematomas:
    • Subdural-
      • Intracranial HTN- common w/ acute (symptoms w/in 72 hours) subdural hematoma → require major therapy to control edema and ICP before during and after evacuation
    • Epidural- middle meningeal arteries → EMERGENCY
      • Symptoms: Bleed → temporary LOC → vasospasm/clotting occurs → wakes up → lucid interval → then rapid deteriorates!
        • minimal deficits to unconsciousness and signs of mass lesion (hemiparesis, unilateral decerebration, pupil changes), lucid period
      • Management: O.R. ASAP for decompression!
    • Intracerebral
      • Anesthetic approach similar for all three:
        • Maximize BP
        • Control ICP

AP III Oral Exam (5 decks)

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