Advanced Neurophysiology And Neurosurgery

Question 1

How does acute hypoglycemia lead to global brain injury? Which cells are most likely to be injured? Acute hypoglycemia vs starvation:

Answer 1

Acute, sustained hypoglycaemia produces brain injury in a pattern similar to that of global hypoxia, in that the entire brain is affected, and those cells that are most metabolically active are the most likely to have the greatest injury

Question 2

25 year old man following traumatic brain injury (TBI) has a measured intracranial pressure (ICP) of 28 cc H20 through an external ventricular drain (EVD), and mean arterial pressure (MAP) of 60. The EVD has been draining 12 cc of cerebral spinal fluid (CSF) an hour and is set to drain above a pressure of 20 cm H20. Which of the following is the next most important step in this patient’s management:

A. Decrease the level of the drain to 15 cm H20
B. Apply intermittent suction to the EVD
C. Flush the EVD with 20 cc of warm saline
D. Start a phenylephrine drip
E. Measure a CVP

Answer 2

An EVD can be placed both to measure the ICP as well as drain fluid. When the ICP is greater than the EVD ‘pop-off’ pressure, CSF fluid is drained. In cases of rapid ICP increases, the CSF cannot drain as quickly as ICP increases. Other causes of an ICP being elevated with EVD in place include insufficient amount of CSF, restrictions on how much CSF can be drained per hour, and a kinked or obstructed (including misplaced) catheter. Flushing 20 cc of saline into the ventricle with high ICPs is dangerous as it may further increase ICP. Applying suction to an EVD is idiotic, hopefully for obvious reasons. Decreasing the ‘pop-off’ of the EVD to 15 cm H20 will not help as the ICP is already greater than the level of the drain. Lowering the CVP would only help if it were greater than CSF, and there is no indication in the stem that the CVP would be greater than 28 cm H20 (which would likely be an error anyway if it read that high). Phenylephrine will raise the MAP to increase perfusion (MAP – ICP).

Question 3

What is the formula for CPP?

Answer 3

Cerebral perfusion pressure (CPP) = MAP – ICP

Question 4

Which of the following conditions would blood flow to the brain expect to rise to the greatest extent in an otherwise healthy patient:

A. MAP of 100 mm Hg
B. MAP of 180 mm Hg
C. PaCO2 75 mm Hg
D. PaO2 of 20 mm Hg
E. 50% decrease in viscosity

Answer 4

D: PaO2 of 20 mm Hg

Cerebral vascular resistance decreased with hypercarbia and hypoxia and is autoregulated from approximately 50-60 mmHg to 150-160 mm Hg. In autoregulation, increases in MAP do not result in increased flow, because vascular resistance proportionately increases to ‘match’ the MAP up to a MAP of 160 mm Hg. Recall Ohm’s law, where Flow = MAP / Resistance; therefore a proportional increase of resistance in the setting of increasing MAP will essentially cancel each other out. Above a MAP of 160 mm Hg, cerebral vascular resistance can no longer increase to restrict pressure dependent increases in flow. In general, very high MAPs will not increase flow as much as moderately bad hypercarbia or hypoxia (which vasodilate the cerebral vasculature). Cerebral vascular resistance (and therefore flow) increases nearly in a linear inverse fashion with increased PaCO2. As PaCO2 rises above 80, the curve starts to flatten and above 120 or so very little further increases are possible with increased PaCO2. Oxygen has little effect on cerebral blood flow until PaO2 drops below (about) 50, at which point in rises exponentially. Therefore, a very low PaO2 such as 25 will produce extremely high cerebral blood flow. Viscosity has very little effect of cerebral blood flow as it is only a minor contributory to cerebral vascular resistance.

Question 5

Which of the following would likely be associated with the highest cerebral blood flows: (ABG: pH/ PaO2/ PaCO2):

A. 7.30/ 65 / 63
B. 7.15 / 350 / 75
C. 7.05/ 65/ 40
D. 6.95 / 60 / 65

Answer 5

B: 7.15 / 350 / 75

As discussed above, both hypoxia and hypercarbia can affect cerebral blood flow. Normal and even moderately low PaO2 have almost no effect on blood flow as compared to very high oxygen tensions. Only when hypoxia is severe (< 50) does cerebral blood flow start to rapidly climb. Also, as stated above, cerebral blood flow increases almost linearly with PaCO2 from 20 to 80. Therefore since answer B had the highest PaCO2, one would expect that patient to have the highest blood flow. The mechanism appears to be CO2 crossing into the CSF, causing an acidosis. This is why even though answers C & D have lower pH’s (due to either pure or mixed metabolic acidosis), the blood flow is lower (since donated H+ from acids in the plasma do not cross the blood brain barrier (BBB) into the CSF

Question 6

What does coupling mean?

Answer 6

Cerebral blood flow to oxygen consumption

Question 7

Volatile agents-coupled or uncoupled?

Answer 7

Volatile agents uncouple flow CBF and CMRO2 in that oxygen consumption decreases and flow (and therefore oxygen delivery) increases.

Question 8

Opioids and coupling:

Ketamine and coupling?

Answer 8

Fentanyl and opioids have rather minor effects on both CBF and CMRO2; and ketamine (depending on the source) increases CBF with minor changes, if any, in CMRO2.

Question 9

Normal CMRO2 and CBF:

Answer 9

A normal CMRO2 of 3.5 ml/ 100g/ min and a cerebral blood flow of 50 ml/ 100g/ min are probably worth knowing for the boards

Question 10

Which of the following would NOT be expected to disrupt the blood brain barrier (BBB):

A. Extreme hypercapnea
B. Extreme hypertension
C. Extreme hyperglycaemia
D. Extreme hypoxia
E. Sustained seizures

Answer 10

C: Extreme hyperglycaemia
Extremes of hypercapnea & hypoxia, sustained seizures, tumors, strokes, infection, and trauma can lead to disruption of the BBB. Even extreme and prolonged levels of hyperglycaemia, such as seen with hyperosmolar coma, will have an intact BBB.

Question 11

What does the BBB prevent from going through? What does it let in?

Answer 11

The BBB slows, or in some cases, prevents the entry of larger, charged, or hydrophilic compounds into the brain. Water, CO2, and lipophilic molecules cross easily.

Question 12

How many times a day does the entire CSF volume replace itself?

Answer 12

About three times a day

Question 13

Which of the following is NOT a normal compensatory mechanism to decrease intracranial pressure (ICP) in the setting of intracranial hypertension:

A. Displacement of the cerebellar tonsil below the foramen magnum
B. Displacement of intracranial CSF below the foramen magnum
C. Increased CSF absorption at the arachnoid granulations
D. Decreased CSF production at the choroids plexus
E. Decreased intracranial venous blood volume

Answer 13

: A: Displacement of the cerebellar tonsil below the foramen magnum

Displacing the cerebellar tonsil below foramen magnum is referred to as herniation and is uniformly fatal. The other answers are normal compensatory mechanisms so that answer A is avoided.

Question 14

Which of the following processes are most likely to be occurring with an ICP of 30:

A. Cerebral perfusion pressure (CPP) decreases, leading to brain ischaemia and swelling, further increasing the ICP
B. CPP decreases, leading to brain ischaemia and shrinking, lowering the ICP

Optimal MAP?
Normal ICP 5-15

Answer 14

A: Cerebral perfusion pressure (CPP) decreases, leading to brain ischaemia and swelling, further increasing the ICP

CPP = MAP – ICP. If ICP increases, then CPP decreases, making answers D & E wrong. With decreased CPP, comes decreased blood flow, and therefore decreased oxygen delivery leading to ischaemia. Ischaemia results in cellular breakdown, inability to extrude sodium, and swelling, increasing brain mass and therefore ICP. As ICP increases further, CPP continues to decrease, and the process continues to worsen and worsen. This is why it is essential that MAP be raised when dealing with high ICPs, even though the intracranial blood volume may rise a bit. Decreased heart rate is part of the Cushing response, along with hypertension with a widened pulse pressure and irregular breathing, often with periods of apnea. The Cushing response (reflex) is secondary to increased ICP, not lowered CPP.

Finding the optimal MAP, or CPP, is a complicated discussion and we won’t get into the specifics, needless to say picking a value of 60 mm Hg to apply to everyone may be insufficient for some and more than needed for others. The basic thing you should take away are two important points. First, at CPPs that are too low, ICP will increase via additional edema secondary to the hypo perfusion (tissue hypoxia). At CPPs that are to high the ICP will increase simply due to hyperaemia (one of the three components of intracranial mass - brain and CSF being the other two). Therefore, the optimum CPP is not too low and not too high, and 60 mm Hg works well for most people so we typically pick that. Second, hyperaemic intracranial hypertension is always better than oligaemic intracranial hypertension. At least in the former the brain is getting oxygen.

Question 15

Cushing’s is a response to what?

Answer 15

Increased ICP

Question 16

How does mannitol work? Why can pulmonary edema and heart failure result? After mannitol treatment, what can happen? How can giving mannitol expand hematomas?how can aneurysms rupture with mannitol? Electrolyte abnormalities with mannitol?

Answer 16

Mannitol increases serum osmolality, therefore drawing intracellular and interstitial water into the intravascular space and out into the urine (as mannitol passes freely through the glomerulus but is not reabsorbed).
By decreasing brain swelling, haematomas that are being tamponaded by the swollen brain tissue can expand.
Cerebral aneurysms can rupture when transmural pressures increase (Transmural pressure = MAP – (either ICP or CVP), either by increasing MAP or decreasing ICP (as with mannitol). As an osmotic diuretic, loss of electrolytes are common resulting in hypokalaemia.

Question 17

How are propofol’s effects on CMRO2 and CBF similar to thiopental?

Answer 17

Both propofol and barbiturates powerfully decrease CMRO2 and CBF.

Question 18

Reverse steal, or Robin Hood phenomenon, is where:

Answer 18

In reverse steal, normal brain vasculature vasoconstricts due to some stimulus such as anesthetics (barbiturates, propofol, etomidate, benzodiazepines) or hypocarbia, while ischaemic brain vasculature is unable to respond. Therefore, blood is preferentially directed away from oxygen rich brain (normal) to oxygen poor brain (ischaemic

Question 19

In a patient with elevated ICP, the role of opioids are to:

Answer 19

A: Blunt the sympathetic surge from intubation

Opioids have very little effects on ICP, CSF production, CBF, or CMRO2. Opioids, in general, have minor effects in increasing CSF absorption, but the primary role of these drugs are to decrease hypertension and increased intracranial blood volume during stimulations, as with intubation.

Question 20

Which of the following is the most to least SENSITIVE monitor for intraoperative VAE

Answer 20

> Doppler > PA pressure changes > ETN2

TEE is most sensitive and can detect very small bubbles. Precordial Doppler requires at least 0.25 cc of air for detection. PA pressure changes and ETN2 increases require far larger volumes of air. A popular estimate is it requires about 300 cc of air to prove lethal for an average adult.

Question 21

VAE-position, what. Am you be doing? Why no PEEP onVAE?

Answer 21

The correct answer is: C: Change the position from sitting to left lateral decubitus reverse-trendelenberg position

After diagnosing a VAE, the surgeon should be notified to flood the field with saline and bone wax, nitrous oxide should be stopped (so the VAE does not expand) and 100% oxygen begun, and the patient should be repositioned so the head and heart are at least at the same level. Change the position from sitting to left lateral decubitus reverse-trendelenberg position is partially correct that an obstructing (air-lock) bubble of air at the right outflow tract might be moved away towards the right ventricular apex in the left lateral position, but only when in Trendelenberg, not Reverse-Trendelenberg. Application of prolonged positive pressure to the thorax can increase superior vena cava venous pressures to stop or slow the entrainment of air. Compression of the jugular veins is an attempt to accomplish the same goal. In the setting of cardiovascular instability, fluids, pressors, and chest compressions might be helpful, with the latter theoretically disrupting a large air lock. Hyperbaric oxygen therapy and aspiration of air from the central line might also be helpful; at least theoretically. On the boards, PEEP is probably contraindicated, as it may lead to increased right heart pressures and a paradoxical VAE through an ASD or VSD and ultimately stroke.

Question 22

EKG and central line

Answer 22

biphasic p-wave indicated a mid atrial position of the catheter, and supposedly pulling back one centimeter (not sonometer, don’t be that guy…and, no, thats not how its pronounced in England either) from here puts it at the SVC/ right atrial positio

Question 23

What causes aneurysmal rupture?

Why do you want to wait u til the cranial vault is opened?

Answer 23

Rupture results when the transmural pressure increases above a threshold. Since transmural pressure = MAP –ICP, a decrease in ICP (as with hyperventilation and mannitol) or CVP can increase this pressure as well as increased MAPs.
After the cranial vault is opened, ICP drops to 0, and transmural pressure = MAP. At this time MAP can be dropped, but a MAP of 40 (answer E) would likely lead to hypoperfusion of critical organs including normal brain. The concern with giving ICP lowering measures prior to cranial vault opening is that the ICP is unknown and MAP needs to be maintained to avoid ischaemia; leading to the possibility of an increased transmural pressure and aneurysm rupture before the vault is opened (leading to rapidly increasing ICP).

Question 24

Tell me about the 2 general strategies in clipping an aneurysm:

Answer 24

The traditional approach is placing the clips directly beside the aneurysm. In this case, a low MAP is associated with a decreased chance of bleeding, and it is even reasonable to induce hypotension with propofol, thiopental, nicardipine, nipride, or other drugs just prior to the clip placement. Even administration of adenosine to temporarily stop cardiac output is a reasonable option in some cases. The second strategy is to place a temporary clip on feeding vessel(s) so that the blood flow at the aneurysm is decreased (or even absent). In this case, induced hypertension may be needed to maintain perfusion pressure in collateral distributions to the feeding artery.

Question 25

SAH and the following:
12 lead ECG shows diffuse and scattered ST segment changes, inverted T waves, and U waves. Telemetery demonstrated two short runs of non-sustained ventricular tachycardia. Electrolytes, creatinine, complete blood count, and ABG on room air are all within normal limits. She has a headache, nuchal rigidity, drowsy, and mildly confused.

Question 1/3: Regarding her cardiac status, what should be done over the next 8 hours in preparation for surgery:

Answer 25

Troponin check and echocardiogram

SAH is associated with numerous ECG changes of unknown etiology. In most cases it is assumed that ECG changes are a result of associated sympathetic stimulation induced by the SAH itself as well as increased ICP

Question 26

Hunt and Hess score:

Answer 26

Grade Clinical Symptoms Mortality*
0 Unruptured aneurysm
1 Minimal HA, mild nuchal rigidity 5%
2 Mod-severe HA, nuchal rigidity, no neuro deficit 10%
3 Above + drowsiness, confusion, or mild deficit 30%
4 Stupor, hemiparesis, mild decerebration 50%
5 Comatose, decerebrate rigidity 70%

Question 27

What’s Cushing’s response?

Answer 27

bradycardia, hypertension, and irregular breathing).

Question 28

Cerebral vasospasm after SAH

Answer 28

The incidence of vasospasm is around 15%, peaks at one week, and rarely occurs after two weeks. Its incidence generally parallels the amount of subarachnoid blood. The reason for this is that it is thought that the oxyhaemoglobin in subarachnoid space leads to free radical production causing decreased NO production in endothelial cells. Makes sense that more blood equals more vasospasm then.

Question 29

Which of the following is the best method for monitoring for cerebral vasospasm:
A. Frequent neurochecks
B. Transcranial doppler
C. Frequent neurochecks and transcranial doppler combined
D. Daily cerebral angiogram
E. Daily head CT

Triple “H”

Answer 29

C: Frequent neurochecks and transcranial doppler combined

Neither neurochecks or transcranial Doppler is very sensitive or specific for absolute diagnosis of vasospasm, but combined they are a good monitor
Diagnosed vasopspasm can be treated medically or with interventions. Hypertension, hypervolaemia, and haemodilution (HHH-therapy, or Triple H therapy) is useful in both prevention and treatment.

Question 30

Wedge pressures and CVP in triple H therapy: hemodilution and HCT as well as pressures

Answer 30

in general, wedge pressures should be titrated to around 8-14 or CVP > 8, haemodilution to a HCT of around 30, and systolic blood pressures as high as 160 prior to clipping, and even as high as 200 after clipping.

Question 31

1 Lucid interval following head trauma, lenticular appearance on CT
2 Associated with old age, crescent shape on CT expanding past skull sutures
3 Red blood cells in CSF
4 Diffuse bleeding into an area of cerebral contusion
A Intracerebral haematoma
B Epidural Haematoma
C Subarachnoid Haematoma
D Subdural Haematoma

Explain!

Answer 31

The correct answer is: B: 1 = B; 2= D; 3 = C; 4 =A

Intracerebral haematomas are associated with TBI and disruption of blood brain barrier (BBB) leading to diffuse bleeding and cerebral oedema. Epidural haematomas are typically from arterial injuries associated with head trauma, classically the middle meningeal artery, have a lenticular appearance on CT that does not cross the sutures of the skull, and sometimes has a lucid interval. Subdural haematomas are more common in elderly patients (due to bridging veins). They can be acute, chronic, and pretty much ubiquitous in the setting of TBI. Subarachnoid haematoma is very common in TBI, somewhat diffuse, usually apparent on CT, but can be confirmed on lumbar puncture with RBCs in the CSF.

Question 32

TBI and brain auto regulation:
What about CO2 responsiveness? Mannitol vs hypertonic saline?
ICPs associated with herniation?

Answer 32

Patients with TBI typically lose the ability for autoregulation, making brain perfusion essentially pressure dependent. This is, again, why cerebral perfusion pressure (CPP) is so critical in these patients. CO2 responsiveness, in general, is preserved explaining why hyperventilation is used (to lower ICP) and is dangerous (cerebral ischaemia from increased cerebral vasculature resistance). Both mannitol and hypertonic saline can decrease cerebral oedema and neither have been proven beyond a reasonable doubt to be better than the other. Mannitol can lead to electrolyte deficiencies and hypertonic saline can lead to hypernatraemia (shocking, I know). Pulmonary oedema is common with TBI, both cardiogenic, neurogenic, and non-cardiogenic (ARDS is a type of non-cardiogenic). It appears that high CPPs (above 70) may be risk factors for increased ARDS. ICPs > 30-40 are associated with much higher risk of herniation. Generally ICPs under 25 are far less dangerous.

Question 33

What is neurogenic pulmonary edema-like it’s a combo of what?

Answer 33

True neurogenic pulmonary oedema is a combination of both cardiogenic and noncardiogenic pulmonary oedema. The cardiogenic portion is from catecholamine release causing left ventricular dysfunction, therefore raising LVEDP. The non-cardiogenic portion is very much like ARDS in that it is characterized by capillary leak syndrome from an unknown mechanism.

Question 34

70 kg patient with traumatic brain injury (TBI) has a serum sodium of 154 and nearly 200 cc of urine an hour. Treatment for this condition is:

A. Bed rest
B. DDAVP
C. Vasopressin
D. Fluid restriction
E. Salt tablets

Answer 34

B: DDAVP

The patient has diabetes insipitus (DI) and in neurogenic causes (such as this) is due to lack of ADH secretion and is treated with ADH. ADH is a vasopressin analogue, but with less hypertensive effects (which is why vasopressin is not as good of a choice).

Question 35

Hyponatremia in the setting of TBI can be what two things? Differences? Treatment?

Answer 35

Hyponatraemia in the setting of TBI can be either SIADH (syndrome of inappropriate ADH secretion) or cerebral salt wasting syndrome. Fluid restriction and possibly salt tabs are used with SIADH. These patients are classically euvolaemic. Cerebral salt wasting also presents with worsening hyponatraemia, poorly responsive to fluid restriction and can often be hypovolaemic from fluid losses.

Question 36

What is spinal shock? Complete vs incomplete? How to treat?

Answer 36

The patient has spinal shock from a high cervical injury following intubation. Spinal cord injury is categorized as complete or incomplete. Incomplete injury means that some (or even all) the function (motor, sensation, etc) below the injury is intact. If the patient can voluntarily contract the anal sphincter or feel pinprick around the anus, it is incomplete. Complete injury rarely is recoverable. Loss of sympathetics (T1-L2) result in unopposed vagal stimulation, resulting in bradycardia and poor venous tone. Fluid resuscitation is key for these patients, as early after the injury vagal tone is high (as would sympathetic tone be as well if it were intact). Pressors are often needed, and epinephrine, dopamine, or norepinepherine would be a better choice than phenylephrine in most cases, especially in unopposed vagal mediated bradycardia. Answer D, diuresis, would be helpful if the patient was hypervolaemic, which he is not. Balloon pump would be useful if the problem was low systolic function. High dose steroids treat the secondary injury of a spinal cord trauma, which is essentially the swelling after the trauma.

Question 37

Which of the following treatments have the greatest effect on outcome in the setting of spinal cord injury:

A. 5.4 mg / kg/ hr of methylprednisolone
B. Titration of MAP to 85-90 mm Hg with fluid and pressors
C. Titration of MAP to 50-60 mm HG with nicardipine or nipride
D. Therapeutic hypothermia

Answer 37

B: Titration of MAP to 85-90 mm Hg with fluid and pressors

Question 38

In what type of patient would a nasally placed endotracheal tube be contraindicated:

A. Absolutely any basilar skull fracture
B. Absolutely any Le Fort I fracture
C. Any fracture involving the cribiform plate
D. Comminuted jaw fracture

Answer 38

The correct answer is: C: Any fracture involving the cribiform plate

One should be very careful before placing nasal ETTs with basal and Le Fort fractures as an intracranial ETT placement is possible. Interruption of the cribiform plate makes this much more likely as it provides a direct pathway from the nasopharynx to the cranial vault.

Question 39

Which of the following has the LOWEST likelihood of resulting in unstable cervical spine injury:

A. Cervical burst fracture of the vertebral body
B. Isolated fracture of the C1 anterior arch
C. Alar ligament and/or tectorial membrane rupture
D. Burst fracture of the C1 ring (Jefferson fracture)
E. Type II dens fracture

Answer 39

The correct answer is: B: Isolated fracture of the C1 anterior arch

This is a hard question, and it is not reviewed in the standard anesthesia review books. However, understanding what constitutes a stable and unstable neck is part of what separates the technician from the consultant. In general isolated fractures of C1 and the occipital condyles (answer B) (get out your old anatomy book if you have to, do NOT passively read!) in general are stable fractures and are not the type that result in a paralyzed patient after intubation. A burst fracture of C1; however, is a different story. With this fracture, both the anterior and posterior arches of C1 are broken (away from) the main body, and it leads to instability even with intact ligaments. This is usually treated with a halo. Any cervical burst fracture (answer A), should probably be assumed unstable as bone fragments may disrupt the ligaments or enter the spinal column until a CT or MRI has definitively ruled out injury. Ligament injury (answer C) is perhaps the most dangerous (for intubation) as subluxation and alanto-occipital dislocation is very possible. The boards would not ask you which ligaments are most important, but you have the answer: alar and tectorial, although they are all important. Dens fractures are in general less dangerous than they sound, but all types of fractures (I – tip of dens; II – base of dens; III – into the body of axis (C2)) are unquestionably unstable.