Neuro Lecture 1

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Neuro Lecture 1
2013-10-06 12:05:16

Neuro Online lecture 1
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  1. The brain constitutes __% of the body weight. But consumes __% of the whole body oxygen uptake and __% of the CO
    The brain constitutes 2% of the body weight. But consumes 20% of the whole body oxygen uptake and 15% of the CO
  2. What defines brain metabolism?
    Metabolism defined by O2 consumption, called cerebral metabolic rate of O2 (CMRO2)
  3. What is the total cerebral blood flow? (__ml/__g of brain tissue/min)
    How do you figure this out?
    • The human brain weighs 1500g and cardiac output is approximately 5000ml/min.
    • 15% of this flow is 750ml goes to brain.
    • So 750ml of blood/1500g brain = 0.5ml/g =50ml/100g brain tissue/min. 
  4. How do you figure out the CMRO2?
    • Whole body oxygen consumption is about 300ml/min and the brain consumes 20% of this (approx. 60ml)
    • So 60ml (O2 the brain consumes) divided by 1500g (weight of the brain) 60/1500 = 0.04ml/100g. 
  5. What population has a higher CMRO2?
  6. CMRO2 is not even, how is it divided in the brain?
    • White matter: area of low metabolism
    • Grey matter: areas of high metabolism
  7. How do we theoretically measure CMRO2?
    • theoretically measure the oxygen consumption of the brain is via the Fick principle.
    • Which would assume the difference between arterial and jugular venous oxygen content reflects brain oxygen consumption
  8. How do we clinically quantify CMRO2
    CMRO2 is quantified non-invasively by an MRI. Metabolically active regions of the brain have different venous O2 saturations than quiet regions and these differences are detectable by MRI.
  9. The brain is adept at meeting increased demand with increased blood flow and the brain is dependent on timely delivery two substrates, what are they?
    Oxygen and glucose (The main substance for energy production is glucose)
  10. We know when oxygen levels are sufficient, glucose is metabolized to pyruvate via the glycolic pathway and ATP is generated. How much ATP is generated from each molecule of glucose? How many ATP are generated without  oxygen?
    • 38 
    • However inabsence of O2, glycolysis proceeds via anaerobic metabolism and in this pathway pyruvate is converted into lactate, but far less ATP is generated, only 2 molecules of ATP are generated for each glucose molecule metabolized. And at this level of ATP production, the brain energy needs are not met.
  11. Why does the brain receive a high blood flow for it's weight?
    Brain has high metabolic rate and that’s why it receives such a high blood flow compared to it’s weight. When metabolic rate increases so does blood flow. So metabolic rate and blood flow are coupled
  12. An increase in either ___ or ___ in the ECF of the brain leads to dilation and increased flow.
    • K+ or H+
    • Other mechanisms that help to couple flow/metabolism are: Ca+, adenosine, iNO, and PGE. 
    • WE also know that high CO2 levels increase the extracellular H+ concentration and therefore increase blood flow.
  13. What happens to the PaCO2 and systemic alkallosis when we hyperventilate our patients? How long does it stay that way vs the CSF pH and the CBF?
    • ↓ PaCO2 continues for at least 18hrs. 
    • Systemic alkalosis continues and stays for 18hrs.
    • The CSF pH and CBF return to normal in 6-8hrs as the concentration of bicarbonate in the CSF is reduced actively, returning the pH to normal.
  14. How does the brain adjust the CSF pH?
    bicarbonate is actively transported out of the brain in order to adjust the CSF pH
  15. What is intracerebral steal syndrome?
    • ↑ CO2 levels, the arterials throughout the brain are maximally dilated, impeding the ability to direct flow to areas of high demand.
    • If there were an ischemic area (ex: if an intracerebral artery were blocked) in the prescence of ↑ CO2, the collateral vessels already maximally dilated, the collateral vessels in area of ischemia would not be able to increase flow.
    • Thus if the CO2 were high, flow would be high and there would be steal from areas that are ischemic and need a higher flow.
  16. What is inverse steal (or the Robin Hood phenomenon)?
    • During focal ischemic events, if the pt is hyperventilated or metabolism is reduced w/thiopental there is overall reduction in CBF but the vessels in the ischemic area would be dilated d/t metabolites and low pH.
    • Thus flow to the ischemic area is maximized .
  17. CBF does autoregulate. In normal pt the CBF does not change as the MAP varies from a MAP of __-____mmHg
    • 50-150mmHg; inside this pressure range, the cerebral vascular resistance adjusts so as to maintain CB
    • Beyond these limits CBF varies directly w/MAP.
  18. What happens if the MAP falls below 50mmHg?
    CBF is reduced and at a pressure of 40mmHg symptoms of cerebral ischemia occur.
  19. What happens to CBF in patients w/HTN?
    • Shift the autoregulation curve to a higher BP, (right shift in the curve)
    • For these pt the  lower limit of autoregulation could well be above 50mmHg. This shift is d/t hypertrophy of the vessel wall.
    • The autoregulation curve may shift back towards normal w/effective anti-HTN treatment
  20. CBF autogreuglation can be abolished by what two things?
    trauma or hypoxia.
  21. How does CO2 effect CBF?
    • CBF increases linearly w/increasing PaCO2 in the range of 20-80mmHg with absolute change of 1-2ml/100g/min for each mmHg change in PaCO2.
    • We can see within physiologic range of CO2 there is a direct correlation between arterial CO2 and CBF
  22. How does O2 effect the CBF?
    • Hypoxemia increases CBF.
    • Hypoxemia is a potent cerebral vasodilator CBF increases markedly below a PaCO2 50mmHg.
    • PAO2 above this (normal range) have little effect on CBF.
  23. What are the two barriers of the CSF?
    The blood brain barrier and the blood CSF barrier.
  24. Describe the blood brain barrier
    • Brain capillary endothelial cells form the BBB.
    • Tight junctions that prevent the passage of substances.
    • The BBB appears to be maintained by glial cells.
    • The BBB impedes the flow of ions and lg molecules (Glucose) but lipid soluble compounds and gases cross the BBB.
    • Volatiles anesthetics easily cross.
    • For those that can not cross, there are carrier mediated processes that allowed them through. For instance, glucose crosses the barrier by a carrier mediated processes. Within this process the glucose can only cross is the concentration in the blood exceeds that in the brain.
  25. How is glucose able to cross the BBB if it is such a large molecule?
    • Carrier mediated processes
    • Only crosses if the concentration in the blood exceeds that in the brain
  26. Why is intra-op hypoglycemia so dangerous?
    • Deficiency of either of the main substrates, glucose or oxygen, causes impairment of neural activity.
    • And w/a patient under GA or deep sedation, hypoglycemia can be difficult to recognize in diabetic, few or no symptoms under GA and a substrate deficiency (glucose) may result in permanent brain damage.
    • Monitor BS levels frequently and if on insulin gtt have glucose running slowly as well
  27. How does the tight junction of the BBB help us to therapeutically pull excess water (Edema) from the brain?
    • Excess fluid or brain edema can be pulled from the brain by giving a large molecule (Mannitol) or an ion (3% NS) that does not cross the BBB.
    • These would exert an osmotic effect drain fluid from the brain. Mannitol is often used in pt w/high intracranial pressure.
  28. The effects of Mannitol or 3% NS to treat brain edema can are dependent on an intact BBB. What may disrupt this?
    The BBB may be disrupted by acute HTN, osmotic shock, disease, tumor, trauma, radiation, and ischemia.
  29. Where is CSF formed?
    primarily formed in the choroid plexus of the cerebral ventricles
  30. What forms the basis of the blood CSF barrier?
    The epithelial cells of the choroid plexus have tight junctions which form the basis of the blood CSF barrier.
  31. What secretes CSF?
    These epithelial cell secrete the CSF.
  32. The CSF volume in the brain is ___ml and it is formed and reabsorbed at a rate of __-__ml/min.
    120ml; 0.3-0.4ml/min
  33. There is complete replacement of CSF volume __-__x/day
  34. How are the Blood/CSF and the BBB similar?
    free movement of water, gases and lipid soluble but requires carrier mediated transported for glucose and ions.
  35. The cranium has a fixed volume. What are the three components within the crainial vault?
    • 1) brain tissue
    • 2) CSF/ECF
    • 3) blood.
    • In some sources these are separated into two diff categories for CSF and ECF.
    • If any of these components increase in volume, the ICP increases.
  36. An increase in volume and ICP has 2 major deleterious effects, what are they?
    • 1) lower the CPP. So as ICP increases, perfusion pressure or blood flow to brain will decreases. If ICP increases greatly, the brain becomes ischemic.
    • 2)An increase in ICP can directly cause brain herniation leading to neurologic damage and death
  37. What is the equation to figure out Cerebral perfusion pressure?
    CPP = MAP –ICP
  38. Small increases in intracranial volume, ICP remains normal. As volume increases further, intracranial compliance decreases and we reach a certain intracranial volume at which the pressure rises rapidly. How is intracranial compliance accomplished? (there are two tways)
    • 1) CSF is moved from the brain to the spinal space
    • 2) venous blood is moved from the cranium to the extracranial veins
  39. There are limits to compliance and once of these limits are exceeded pt may develop marked increases in ICP w/small increases in intracranial volume. Increases in ICP can be caused by the following 3 factors....
    • 1) increased brain tissue volume caused by a tumor or edema
    • 2) increased CSF or ECF volume caused by blockage of CSF circulation or blockage of CSF absorption
    • 3) increased blood volume caused by vasodilation, volatiles, hypercarbia or hypoxia, or by hematoma.
    • *Note the correlation with the 3 components of the cranial vault.
  40. How can we manipulate the cellular (brain tissue) compartment?
    often manipulated by the surgeon (ex: surgical removal of a tumor).
  41. How can we manipulate the fluid compartment (includes ICF and ECF as well as CSF)?
    • manipulated via drainage (ex: surgeon can insert a drain to drain CSF intra-op to manipulate the volume of the CSF or improve surgical exposure)
    • the fluid compartment both ICF and ECF can be decreased by steroids and diuretics.
  42. How can we manipulate the blood compartment?
    • either the arterial or venous side.
    • Arterial side: avoid increases in CBF caused by vasodilation with volatile agents at high doses, avoid vasodilation caused by hypercapnia or hypoxemia.
    • Venous side: elevating the head decreases venous engorgement and improves drainage. Coughing or straining against the ETT causes venous engorgement and worsens venous drainage by increasing intrathoracic pressure
  43. What is the pathophysiology of brain ischemia? (same as the pathophysiology of ischemia anywhere)
    • Main factor causing damage to neurons in ischemic conditions is reduced energy production, lack of oxygen decreases ATP production by 95% for each molecule of glucose.
    • ATP levels fall this low, there is loss of energy dependent homeostatic mechanisms. This causes the ↑ intracellular concentration of Na and Ca+ & ↓ intracellular K.
    • Causes the neurons to depolarize and release excitatory AA (glutamate) the glutamate itself causes further depolarization and allows further Ca+ into the cell.
    • ⇈ intracellular Ca+ level triggers ischemic damage through a # of mechanisms, ↑ the activity of proteases and phospholipases & these ↑ the level of free FA and free radicals. (build up of lactate & H+)
    • Explains why ischemic are acidotic (anaerobic metabolism) and have high K+ levels in their venous blood.
  44. There is primary and secondary brain trauma. Explain each and what we can do to prevent secondary trauma.
    • Primary: direct neuronal damage w/brain trauma.(brain herniation or severed blood vessels in the brain)
    • Secondary: follows the initial insult (much of brain injury in trauma is from this), intracellular Ca+ influx is the trigger for secondary damage.
    • Secondary damage can be reduced w/proper monitoring and treatment. Tx includes reducing ICP, maintaining blood flow, reducing spams, removing blood from the subarachnoid space and using pharm agents to reduce the cascade of events which lead to ischemia.
  45. A 25 year old patient unrestrained passenger in a motor vehicle accidentis admitted to the emergency room. The patient is unresponsive. His right pupil Is fully dilated and his Glascow Coma Scale is 6. You are called to manage the airway.What are the principal steps in evaluating and managing this patient ?
    • Vital signs! Often trauma pt have high BP, catecholamine release and SNS stimulation and high BP unless concomitant injuries. . IMPT to know for brain trauma is possibility of Cushings triad (HTN, bradycardia and irregular respiratory caused by increased ICP).
    • Consider when evaluting VS is factors contributing to poor outcomes in these patients are increased ICP, and sys BP less than 90.
  46. What is Cushing's Triad?
    HTN, ↓HR, & irregular respirations
  47. What is the Glasgow Coma Scale?
    • Way to assess neurologic status and brain dysfunction.
    • Evaluates eye opening, best verbal response and best motor response.
    • Scale ranges from 3-15 points.
    • Score of 6 is very low.
  48. What is minor, moderate and severe njury according to the GCS?
    • 13-15: minor injury
    • 9-12: mod injury
    • Less than 9: severe injury.
  49. A decrease in the GCS of___ or more points indicates catastrophic neurologic deterioration
    3; so even if the score were higher, these patients can rapidly deteriorate
  50. GSC of 6 would describe what type of injury?
    catastrophic neurological injury probably wide spread brain swelling, probably a disruption of BBB.
  51. There are several variation of traumatic intracranial hematomas. List them.
    • Epidural hematoma
    • Subdural hematoma
    • Intercerebral hematoma
  52. What is an epidural hematoma and how would the patient appear?
    • Classic presentation, Pt initially appears lucid but rapidly deteriorates into a coma. 
    • There are almost always skull fx involved and the hematoma occurs between the dura mater and the skull, often in the temporal/parietal region where the skull fx interrupts the middle meningeal artery causing unconsciousness.
    • Then a spasm or clot occurs in the vessel, bleeding stops temporarily and the patient experiences a lucid interval.
    • Over a period of hours the vessel rebleeds and the patient rapidly deteriorates.
    • Emergency hematoma evacuation is necessary.
  53. Describe a subdural hematoma
    • Occurs under the dura mater (between dura and arachnoid)
    • Usually caused by lacerations of the venous sinuses. Usually develops slowly.
    • Subarachnoid is often can’t tell whether the hematoma is subarachnoid or subdural. Subarachnoid is between the dura mater and the arachnoid mater.
    • And again slowly the hematoma caused by the laceration of the venous sinuses
  54. Describe an intracerebral hematoma
    • Collection of blood deep in the brain, usually temporal or frontal lobes.
    • It can be a small petechiae or large collection of blood.
    • These usually can’t be surgically evacuated and are medically managed.
  55. Of the three types of hematomas, which has the best prognosis?
    The epidural hematomas
    • Epidural hematoma.
    • See the disruption of meningeal artery in temporal parietal region.
  56. Why is there a classic lucid interval is seen in 50% of cases with epidural hematomas?
    Fast bleed initially, pt may loose consciousness, spasms, regain consciousness, rebleed, hematoma developing between inner surface of skull and the dura.
  57. Classically a subdural hematoma is caused by sudden head deceleration resulting in lacerated veins. Often there is tearing of superior cerebral veins.
  58. Which is more common, subdural or epidural hematoma?
    Subdural is more common than epidural.
  59. TRUE or FALSE. Subdural hematomas always  cause some degree of brain damage.
  60. When and why should we get a CT scan for hematomas?
    • But all intracranial hematomas are best diagnosed by CT scan.
    • Recommendation is if they’re having loss of consciousness of GCS of less than 15, CT is indicated
  61. Why are subdural and subarachnoid clinically difficult to distinguish?
    Subdural hematoma is often accompanied by subarachnoid hemorrhage so subdural and subarachnoid are difficult clinically to distinguish.
  62. How do we manage a brain injury patient?
    • Manage CO2: intubate and ventilate.Control of CO2 is impt way to control ICP so intubation is necessary
    • Prevent aspiration (GSC of 6 = aspiration risk)
  63. Why is the C spine not cleared by X ray alone?
    • Up to 26% of X-rays of c-spine fail to show a fracture.
    • So c-spine is cleared, (normal) only when the x-ray is normal, the mental status is normal and the patient is asymptomatic.
  64. How do we intubate someone in a C-spine?
    Anterior part of collar is removed, head is stabilized and pt is intubated.
  65. What sedative hypnotics would we use for induction of a patient with a head injury?
    • Propofol or pentothal: ↓ CMOR & vasoconstrict. Benefit in ↓ICP as long as we don't also ↓BP (problem)
    • Induction w/ these meds is reasonable if pt BP is normal or high
  66. Can you use Succinylcholine to intubate a patient with a head injury?
    • Yes, the control of airway and CO2 is primary concern, but you would defasciculate first!
    • Succinylcholine has been shown to increase ICP by increasing muscle activation w/depolarization but this may be attenuated w/a defasciculating dose of a non-depolarizing muscle relaxant.
  67. When would we consider awake fiberoptic intubation for  a patient with a head injury?
    When there is a facial fracture or edema
  68. When should we avoid a nasal intubation in brain injury patients and why?
    • Always avoided in pt w/basilar skull fractures.
    • You can often recognize a pt w/this because there is CSF flowing from nose.
    • If pt has a basilar skull fx, we would avoid putting any tube in nose (ETT or NG) because tube could enter brain
  69. Is hyperventilation routinely used in head injury patients?
    NO, it should be used selectively.
  70. When would we hyperventilate a patient with a brain injury?
    • To lower ICP when there is acute neuro deterioration or when high ICP is refractory to other methods of control
    • In neurosugery we hyperventilate if the surgeon requests to facilitate surgical exposure
  71. How do we decide if we should use an ICP monitor?
    • is based on neuro status and the CT scan.
    • It is widely used to manage intracranial HTN.
  72. A major goal of tx is to maintain CPP of__ or greater.
  73. If the patient has intracranial HTN, how high must we keep the MAP?
    So we know this pt has intracranial HTN (ICP of 20 or higher) we know we need to keep CPP = or greater than 70mmHg so we need to keep the MAP at least 90 in order to keep CPP at least 70.
  74. Why is keeping a MAP 90+ to maintain CPP not a problem in head injury?
    • Usually not a problem at least 90, because trauma pt w/catecholamine release.
    • It can be problem if there are concomitant injuries.
  75. How can head elevation be helpful in head injury?
    Head elevation may help venous outflow and lower ICP.
  76. Describe anesthetic management in acute head injury.
    • FIRST, control of airway &ventilate to PCO2 of low normal.
    • Restore volume of pt who has lost volume d/t concomitant injuries.
    • Maintaining a MAP ≥ 90mmHg
    • Neuro exam
    • If ↑ICP (deteriorating LOC or lateralized findings) then we need to hyperventilate, mannitol therapy, foley, get a head CT.

  77. If there is evidence of elevated ICP by presence of mass effect or shift (lost of cisterns or hematoma on head CT), what do we do?
    need to begin or continue hyperventilaton mannitol or surgery for hematoma and to the ICU.
  78. A 65 patient presents for elective right hip arthroplasty.The patient’s history includes several recent transient ischemic attacks and hypertension. Describe the pathophysiology
    • TIA indicated cerebral vascular disease.
    • Transient impairment of neuro function, no residual effect.
    • So a TIA is a sudden vascular related focal neuro deficit that resolves within 24 hrs.
    • Considered evidence of an impending stroke.
  79. Pt w/TIAs have a __-__% chance of thromboembolic stroke within 5 years and __% of these occur within the 1st year.
    30-40%; 50%
  80. A 65 patient presents for elective right hip arthroplasty.The patient’s history includes several recent transient ischemic attacks and hypertension. How would you further assess this patient?
    • Review the TIA hx.
    • What were the pt symptoms of TIA?
    • Unilateral vision impairment, numbness or weakness of a single extremity or aphasia is suggestive of carotid vascular disease.
    • Whereas bilateral vision impairment, dizziness, ataxia, bilateral weakness or amnesia is suggestive of vertebral basilar disease.
  81. What type of S/S in a TIA are suggestive of a carotid vascular disease?
    Unilateral vision impairment, numbness or weakness of a single extremity or aphasia
  82. What s/s of a TIA are suggestive of a vertebral basilar disease?
    bilateral vision impairment, dizziness, ataxia, bilateral weakness or amnesia
  83. Blood supply to brain is from 2 pairs of vessels. Name them
    the internal carotid arteries and the vertebral arteries
  84. Describe the blood flow to the brain from the two vertebral arteries
    • The two vertebral arteries join to form the basilar artery.
    • These vessels then form the intracranial vessels which are the anterior cerebral artery, middle cerebral artery, posterior cerebral artery, and the circle of Willis.
  85. Occlusion of a single artery results in a predictable neurologic deficit. What happens if there is occlusion of the middle cerebral artery (most common in epidural hematoma)
    There will be contralateral hemiparesis and hemisensory deficit.
  86. Occlusion of a single artery results in a predictable neurologic deficit. What happens if there is occlusion in vertebral or basilar artery?
    • There are more global symptoms.
    • Aphasia, ataxia, bilateral vision impairment.
  87. What study is indicated pre-op for someone w/a TIA?
    • Should not undergo elective surgery w/out non-invasive Doppler flow studies.
    • These patients have co existing CAD and HTN, need eval pre-op.
  88. Most sources say that when the pt gets the Doppler a plaque of greater than __% occlusion is indication for carotid endorectomy.
    These pt w/TIAs have higher risk of post-op stroke, risk is approximately __%.
    60%; 3%
  89. What are our concerns for the patient w/a TIA intraoperatively?
    • Closely manage the BP, remembering the pt w/HTN the cerebral autoregulation curve is right shifted, so need to maintain BP near pt normal values.
    • Hypotension, relative to pt normal BP can result in intracerebral thrombosis and infarction
  90. How long should we wait to perform elective procedures on a patient who had a stroke?
    • Usually elective procedures are postponed at least 6 weeks following a stroke
    • No definite period but there are abnormalities in blood flow and metabolic rate for 2 weeks post stroke.
    • Alterations in CO2 responsiveness and BBB for 4 weeks or greater following stroke. 
  91. How long are there abnormalities in blood flow and metabolic rate post stroke?
    2 weeks
  92. How long are there alterations in CO2 responsiveness and BBB following a stroke?
    4 weeks or more
  93. Use of paretic or paralyzed extremity for monitoring NMB can result in ...........
    • overdosage.
    • Nerve stimulator placed on non paretic side to avoid this.
  94. Avoid succs in pt w/stroke and those w/extensive muscle wasting because...
    risk of hyperkalemia.
  95. Why is there hyperkalemia with Succinylcholine in patients who have had a stroke?
    • up regulation of Ach receptors
    • Ach receptors are over a large portion of the effected muscle and a large portion of receptors bind NMB poorly. 
    • Due to up regulation larger # of Ach receptors, many more ion channels open after administration of succynlcholine which can cause hyperkalemia and cardiac arrest
  96. When does up regulation occur after a stroke or spinal cord injury?
    Occurs 4-7 days following stroke or spinal cord injury.
  97. Clinically we don’t know which have mild or marked. How do we estimate the degree of up regulation
    But since the extrajunction ach receptors are spread of the effected muscle the degree of up regulation may be related to severity of the stroke.
  98. Can we use Succs for the 1st 24 hours after a burn?
    YES.  With burns the up regulation does take 24 hours to occur so can use succs immediately within 1st 24hr post burn.
  99. TRUE or FALSE, up regulation causes resistance to NDMR
  100. List the conditions in which up regulation of nACh receptors occurs.
    • Spinal cord injury
    • Stroke
    • Burns
    • Prolonged immobility
    • Prolonged exposure to neuromuscular blockers
    • Multiple Sclerosis
    • Guillian-Barre syndrome
  101. List the conditions in which down regulation of nACh receptors occurs
    • Myasthenia gravis
    • Anticholinesterase poisoning
    • Organophosphate poisoning
  102. Your next patient is a 75 year old male presenting for a V-Pshunt. He has a non-operable frontal meningioma and new onset of seizures. What two conditions are we dealing with?
    Hydrocephalus and seizures
  103. In hydrocephalus, there is an accumulation of excess CSF. It can be obstructive or non-obstructive. Describe each.
    • Obstruction: obstruction of CSF pathways. Portion of ventricular system is isolated from CSF circulation.
    • Non obstruction: overproduction or inadequate absorption of CSF.
  104. Which is more common, obstructive or non-obstructive hydrocephalus?
  105. Describe how CSF is absorbed into the venous circulation
    • through the villa in the arachnoid membrane of the brain.
    • When the CSF pressure exceeds the pressure in the venous sinuses.
    • The arachnoid villa provided one way flow of CSF from the arachnoid space into the venous system
  106. If either the arachnoid villa or the foramen connecting the ventricles is blocked, pressure builds and hydrocephalus develops. It may be congenital but how can it happen in adults?
    • Neoplastic disease (meningomoma)
    • After trauma (meningitis or subarachnoid hemorrhage)
  107. What is a VP shunt?
    Ventricular peritoneum shunt to remove CSF from the ventricles to the peritoneum
  108. Describe the normal pathway of CSF
    CSF is formed in the choroid plexus of the lateral ventricles→3rd ventricle though the foramen of Monro → along the aquaduct of sylvias into the 4th ventricle→ through 3 small openings ( 2lateral foramen of luschka & the midline forarmen of magendie)→ cisterna magna → reabsorbed from multiple arachnoid villa into venous sinuses → enters the venous blood.
  109. What is the cisterna magna
    large fluid space which is continuous with the arachnoid space which surrounds the brain and spinal cord.
  110. What do we assess for in the patient with hydrocephalus?
    • Assess for s/s of increased ICP (HA, n/v, mental status changes, altered LOC).
    • As ICP continues to rise, symptoms progress to fatigue drowsiness, visual disturbances caused by papil edema (pushing forward of the optic disk).
  111. Why do the s/s of hydrocephalus occur more in the early morning?
    because during sleep the CO2 increases and vasodilation occurs and the limits of compensation are exceeded and ICP rises.
  112. Seizures occurring for the 1st time in adulthood are commonly caused by _______
  113. In addition to the neuro status, we need to evaluate the VS in a patient w/hydrocephalus. What would we expect?
    Usually this person’s BP would be high because in the presence of intracranial HTN we try to preserve CPP by increasing MAP.
  114. For hydrocephalus, besides a neuro exam and VS, a CT scan is also indicated. What will this show?
    • CT will show cerebral edema around the tumor particularly in those tumors with rapid growth.
    • This results from increased permeability of the capillaries in the area of the tumor and the disruption of the BBB.
  115. Describe generalized seizures
    • Generalized seizures involve neurons bilaterally, usually originate from a subcortical or deeper brain focus.
    • In a generalized seizure, consciousness is always impaired or lost.
    • Tonic clonic movement of all 4 extremities
  116. Describe partial seizures
    • Partial seizures, aka focal seizures, involve neurons unilaterally.
    • Tonic clonic movement restricted to a limb
  117. Seizure activity demands a ___% increase in ATP. Cerebral oxygen demand is increased by __%.
    250%; 60%
  118. List everything that could make a seizure likely to occur.
    • Brain tumor
    • Diabetic (hypoglycemic & lack of that important substrate for the brain)
    • Hx of seizures (↑risk for post op seizure)
    • Postoperatively metabolic derangements (hyper or hypo glycemia, acidosis, hypoxia)
    • Local anesthetic toxicity
  119. How do we manage the patient with a seizure risk?
    • Check labs on emergence and intra-operatively more frequently.
    • Early awakening so that neurostatus check is possible.
    • Continue the use of anti-seizure medications to maintain therapeutic levels
  120. What do we need to keep in mind if our patient is on Dilantin?
    Causes enzyme induction and this may speed the metabolism of the anesthetic drugs.
  121. For our patient with seizures, the goal of drug selection is to AVOID EPILEPTOGENIC drugs. Explain what we would or wouldn't choose.
    • Good choices: Barbs, opioids, and benzos. They don’t lower seizure threshold or predispose seizure activity.
    • Bad choices: KETAMINE predispose seizure activity. Methohexital (Brevital) can activate elliptic foci.
    • Volatiles:  all acceptable. Enflurane is the only volatile anesthetic which does evoke seizure activity. N2O is unlikely to increase ICP when used in combination w/a volatile but used alone, N2O does increase CMRO2.
  122. What is the only volatile anesthetic which does evoke seizure activity?
  123. Why is N2O okay to use with another volatile but not alone in a patient w/seizures or brain injury?
    • N2O + volatile = unlikely to increase ICP
    • N2O along = increased CMRO2
  124. It terms of muscle relaxants, what would we avoid in a patient with a seizure disorder?
    There is a metabolite of atracurium and cisatrucurium called laudonosine which does have CNS stimulating effects and could be detrimental.
  125. In a seizure, if LOC occurs, apnea, or resp distress, pt may need to be ventilated. What should we avoid when ventilating this patient?
    hyperventilation, it lowers the seizure threshold.
  126. What types of drugs would we give if our patient was having a seizure?
    administer thiopental, propofol, and midazolam in small increments to lower CMRO2 and midaz would also raise seizure threshold.
  127. Name the complications of a seizure
    • aspiration, hypoxemia, cerebral injury from prolonged hypoxia or prolonged seizure.
    • The patient can become hypotensive or respiratory depression from the anti-convulsant therapy