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140 Cards in this Set
- Front
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What are the three major blood vessels that supply the brain?
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1) Two INTERNAL CAROTID ARTERIES: branch off from the common carotid arteries and bifurcate into the anterior and the middle cerebral artery in the brain. These also branch into the opthalamic artery.
2) Two VERTEBRAL ARTERIES: branch from the subclavian arteries at the posterior aspect of the neck. In the brain they fuse into the basilar artery, which becomes the posterior cerebral artery. 3) The CIRCLE OF WILLIS: Provides backup circulation to the brain via the posterior communicating arteries. ...interconnects all of the arteries that supply the brain. |
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The internal carotid arteries are _______ circulation and branch into the _______ cerebral arteries.
The vertebral arteries are _______ circulation and branch into the _____ cerebral arteries. |
The internal carotid arteries are ANTERIOR circulation and branch into the ANTERIOR AND MIDDLE cerebral arteries.
The vertebral arteries are POSTERIOR circulation and branch into the POSTERIOR cerebral arteries. |
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According to the MONROE-KELLIE DOCTRINE,
What are the 3 major factor involved in ICP control (due to a fixed intracranial volume)? |
Blood Volume
CSF Brain Tissue |
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Cervical – __ vertebrae
Thoracic – __ vertebrae Lumbar – __ vertebrae Sacral – __ vertebrae |
Cervical – 7 vertebrae
Thoracic – 12 vertebrae Lumbar – 5 vertebrae Sacral – 5 vertebrae |
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Anterior Spinal Cord Supply
Arises from ________ arteries Supplies ________ of the cord What artery(ies) make up this? |
Anterior Spinal Cord Supply
Arises from vertebral arteries Supplies anterior 2/3 of cord Artery of Adamkiewicz (T7 -T12) - Lower thoracic and lumbar region of the spinal cord. |
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Posterior Spinal Cord Supply
Includes what artery(ies)? Arises from _______ arteries Receive contribution from _______arteries |
Posterior Spinal Cord Supply
2 posterior spinal arteries Arise from vertebral arteries Receive contribution from radicular arteries Supply the posterior 1/3 of the spinal cord |
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What determines the metabolic rate of the brain?
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The Rate of Depolarizations in the brain.
You can control this with medication. |
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How does the metabolic rate of the brain relate to cerebral blood flow?
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They directly related.
Increased metabolism (rate of depolarizations) will increase CBF d/t VD from local sources. |
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How will hypothermia affect ICP?
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Hypothermia will slow down CBF (decr metabolic rate.)
This will decrease ICP. |
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Normal CSF volume is ____ mL.
Normal CSF production is _____mL per day. |
Normal CSF volume is 150 mL.
Normal CSF production is 500 mL per day. |
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CSF is produced by the ______ ______ in the lateral ventricles. It then travels through the ___ and ___ ventricles and ends up ____(where?)______.
It's function there is _____, _____, _____, and _____. CSF is then absorbed in the ___________. |
CSF is produced by the CHOROID PLEXUS in the LATERAL VENTRICLES. It then travels through the 3rd and 4th ventricles and ends up in the SUBARACHNOID SPACE and in spaces around the brain. It's function there is to provide a CUSHION, REGULATE PH AND ELECTROLYTES, WASTE DISPOSAL, AND DELIVER NUTRIENTS. CSF is then absorbed in the DURAL VENOUS SINUSES.
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What are the 4 functions of CSF?
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Cushioning
Regulating pH and electrolytes Waste disposal Delivering nutrients |
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T/F
Small changes in BLood volume, brain tissue, or CSF can cause large changes in ICP! |
False.
Small changes can be accomodated. Large increases = increased ICP. |
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A normal ICP is less than ___ mmHg.
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15 mmHg.
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When do you treat increased ICP in a CHI pt?
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When it is > 20 mmHg.
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N/V during hydrocephalus is due to
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Increased ICP
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With increased ICP due to a brain hemmorage, what will happen to the brain?
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Increased blood volume will push the brain down onto and into the ventricles. The brain will herniate. This can be lethal.
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Explain how ICP increases with increased intracranial mass.
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It starts out moderately increasing, but as intracranial mass increases more and more it increases exponentially.
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If you have a pt who has a dramatic increase in ICP...what does that tell you?
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There is a dramatic increase in intracranial mass...do something ASAP or brain will be crushed.
This could be due to tumors, swelling in the brain or hemmorrage. |
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What are some things that Increase cerebral blood flow?
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Stimulation
Arousal Mild Hyperthermia Elevated CO2 (does not affect metabolism) Decreased PaO2 < 50 mmHg). Anemia These are all due to Increased metabolism except for CO2 and low PaO2, and anemia which are local factors for VD. |
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What are some things that Decrease cerebral blood flow?
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Sedatives
Hypnotics Hypothermia Decreased CO2 These are all due to decreased metabolism except for CO2, which is a local VDr. |
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The brain has a __% increase in CBF for every ___mmHg increase in CO2.
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The brain has a 3% increase in CBF for every 1 mmHg increase in CO2.
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How does anemia increase CBF?
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Decreased O2 supply to the brain causes VD (part of the brains autoregulatory effects).
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How can hypothermia protect the brain?
Are there any restriction on it? |
Mild to moderate hypothermia decreases metabolic rate, this decreases CBF and ICP.
Hypothermia as a cerebral protective mechanism is ONLY effective if it is induced BEFORE the cerebral ischemia occurs. Examples of hypothermic procedures: Thoracic Aortic Dissection: Cool the pt down to 14 deg celcius. |
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What are the benefits of hyperventilation for neuro pts? What is the goal PaCO2?
What is the downside to hyperventilating a pt to decrease ICP? What risk can it impose? What is another limitation to this technique? |
Hyperventilation causes cerebral vasoconstriction. This
---> Relaxes the brain ---> Facilitates surgical conditions ---> Beneficial in pvting brain herniation with TBI or cerebral edema in EARLY resuscitation efforts. Goal is to keep arterial CO2 = 35-40 mmHg. (So current literature says you want normocapnia, not hypocapnia). RISKS/LIMITATIONS: ---> However, vasocontriction can decrease blood flow and can CAUSE cerebral ischemia. This poses a huge risk with trauma pts...who are already at risk for ischema d/t hemmorage. ---> After 24 hrs, hyperventilation to decrease ICP is no longer effective. (ACUTE TX ONLY). |
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Describe how PaO2 changes will change cerebral blood flow.
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Initially decreases in PaO2 mildly increase CBF.
But once PaO2 < 50 mmHg, CBF increases dramatically. |
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Define autoregulation of the brain.
What is the normal MAP range in which the brain can autoregulate? |
The brain maintains a constant CBF/ CPP despite moderate changes in MAP via changes in cerebrovascular resistance.
The brain can autoregulate MAP values b/n 60 and 150 mmHg (that's alot!) |
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What is the pressurehead for blood flow to the brain?
Ie, what do you regulate to control perfusion to the brain? |
MAP!!!
CPP = MAP - ICP. |
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Normal Cerebral Perfusion Pressure (CPP) is?
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50 mmHg
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If you don't have an ICP monitor in your pt, how can you calculate CPP?
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For a pt with NO HEAD INJURY, assume a normal ICP of 15 mmHg. Then use the formula: CPP = MAP- ICP.
If you patient has a HEAD INJURY: ---> Insert a central line and subs. ICP with CVP: CPP = MAP - CVP, OR... ---> Assume a really high ICP, Increase MAP to compensate just in case. |
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How does HTN affect the MAP autoregulation range of the brain?
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Shifts it to the right...you need a higher map to get the same effect.
Normal is 60-150 mmHg. HTN makes it like 80-170mmHg or more. This means the pt can have cerebral ischemia at higher pressures. |
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What happens when you have a super high MAP outside the brain's autoregulatory range?
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Hyperemia in the brain!!!
Increased ICP. Hemmoragic Stroke!!! Brain Herniation. Rebleeding of clipped aneurysms, carotic endarterectomies, etc. |
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How do the volatile gases affect CBF?
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Sevoflurane:
---> Low Doses: Decrease CBF ---> High Doses: Unchange or Increased. Isoflurane/ Desflurane: ---> CBF is unchanged or increased. --->(Due to the extreme VD, decr MAP the brain VD's to compensate..but volatiles decrease metabolism so this decreases CBF a little...ends up unchanged). Very High Doses of Volatiles can ABOLISH autoregulation. (Must watch MAP!!) |
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How do Thiopenthal and Propofol affect CBF?
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CBF is decreased due to sedation and decreased metabolism w/o the extreme systemic VD of volatiles.
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How does Ketamine affect CBF?
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Ketamine increases CBF and ICP!!!
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What problems Interrupt CBF?
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* Trauma with edema
* Depressed skull fractures * Spine fractures (affect CSF drainage). * Diffuse injury to neurons * Disruption of vasculature (ischemia or hemorrhage) * Mass lesions/tumors * Hemorrhage (anywhere) * Hydrocephalus |
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What are the two types of Hydrocephalus and how is it treated?
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Hydrocephalus increased CSF in the brain and spinal cord d/t an imbalance b/n production and drainage.
COMMUNICATION HYDROCEPHALUS: Communicating hydrocephalus, also known as non-obstructive hydrocephalus, is caused by impaired cerebrospinal fluid resorption in the absence of any CSF-flow obstruction between the ventricles and subarachnoid space. It has been theorized that this is due to functional impairment of the arachnoidal granulations (also called arachnoid granulations or Pacchioni's granulations), which are located along the superior sagittal sinus and is the site of cerebrospinal fluid resorption back into the venous system. OBSTRUCTIVE HYDROCEPHALUS: A problem with the flow of CSF (blockage). * Infants under 1 year old: Drain the CSF from the anterior fontanelle (which has not closed). * Adults: Place a VP Shunt, which takes CSF from the brain ventricles to the peritoneal cavity where it can be absorbed. |
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T/F
BIS monitors are useful in monitoring for cerebral ischemia. |
FALSE
BIS monitors are EEG's that monitor the depth of anesthesia. 40-60 for anesthesia |
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What lines would you need in someone who has a subdural hematoma and is about to have a craniotomy.
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2 Large Bore IV's and an art line.
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What happens when the brain loses it's continuous supply of glucose and O2 via blood flow?
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You pass out.
The brain shuts down non-vital function to lower the cerebral metabolic rate. This is in an effort to prevent anaerobic metabolism and lactic acid buildup in the brain. |
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Explain the damage that reperfusion can have on the brain once it has had ischemia.
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The absence of oxygen and nutrients from blood during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than restoration of normal function.
---> An upregulation of NO synthase during ischemia leads to an excess of NO during reperfusion. ---> Toxic oxygen species: In prolonged ischemia hypoxanthine is formed as breakdown product of ATP metabolism. The enzyme xanthine dehydrogenase acts in reverse, that is as a xanthine oxidase as a result of the higher availability of oxygen. This oxidation results in molecular oxygen being converted into highly reactive superoxide and hydroxyl radicals. ---> Releases excitotoxic amino acids ---> These potent, reactive radials and superoxides calls tissue damage and inflammation....leading to celllular apoptosis. |
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Mild Hypothermia is __- __ degrees Celcius.
What are it's benefits? Limitations? |
Mild (33-35 degrees Celsius)
BENEFITS: ---> Decreases cerebral metabolism ---> Decreases the immune and inflammatory response to ischemia (that can cause damage with reperfusion). ---> Studies show improved outcomes LIMITATION: ---> Hypothermia must be induced BEFORE the insult occurs. ---> In cases of occlusive diseases, hypothermia will have no benefit. (most cases of cerebral ischemia are occlusive diseases so that is not good). |
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Profound Hypothermia is < ___degrees Celcius.
What are it's benefits? Limitations? |
Profound (<32 degrees Celsius)
BENEFITS: ---> Neuroprotective d/t decr CMR ---> Used in Circulatory arrest (<20 degrees for <30 minutes) ---> Decreases cerebral activity and energy requirements This is why people found in cold water, etc have been resusitated. LIMITATION: ---> Occlusive ischemia and ischemia that occurs before hypotermia can be induced. |
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For circulatory arrest cases, in which the blood flow to the brain will be stopped, what are the hypothermia requirements?
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< 20 degrees celcius for < 30 minutes!!!
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What is an important preop assessment before spinal or cranial surgery on a patient?
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Check motor/ muscle strength.
Any preexisting motor weakness must be checked and documented before and after spinal or cranial surgery. If you find preexisting motor weakness, DON'T USE SUCCS because upregulation of nicotinic receptors can lead to hyperkalemia with succs. |
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A glascow coma scale ranges from __ to ___.
__ means brain death. |
A glascow coma scale ranges from _3 to 15.
3 means brain death. |
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What important preop assessment before neurosurgery should be checked BEFORE giveing any meds?
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The glascow coma scale
AND Test for motor strength. |
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What FIVE things must you avoid during induction of a pt for neurosurgery?
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HOTN - can cause cerebral ischemia
HTN - can cause hyperemia and exagerrate cerebral hemmorages. (give meds to blunt SNS response to DL. ANECTINE: in pts with increased ICP, motor/ muscle weakness, hyperkalemia (use roc instead). APNEA - will increase PaCO2 and VD the brain, causing increased ICP! This is bad!. Avoid apnea on induction. |
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When can you use Succ for intubation for neurosurgery?
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When the patient is normokalemic and has an absence of muscle weakness.
And when the pt does not have increased ICP...the fasciculation from Succ can increase ICP!! |
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Airway of choice for spinal and neurosurgery is...
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ETT
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Explain in-line neck stabilization during induction.
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For trauma pts...always assume a cervical spine fracture unless proof of the contrary. Must keep C-spine alignment to pvt spinal cord injury.
For induction, you will need another person holding the neck in alignment while you DL. C-collar will have ot be opened on the front. A GRade 1 view will turn into a grade 2,3. A grade 2 view will turn into a grade 3,4. You will need a glideoscope by the bed. Anticipate a difficult airway. May need an awake fiberoptic intubation.Make sure you numb them really well to pvt bucking, will increase the risk of spinal cord injury. RSI with cricoid. |
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Maintenance of neuroanesthesia is most often what type of technique?
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Balanced
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Considerations in maintenance of neuroanesthesia.
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Type of monitoring available
Brain relaxation to decrease O2 demands. Desired level of anesthesia at procedure end. Consider neurological eval at the end of the procedure. |
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When is hyperventilation to decrease ICP contraindicated??
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Pts with traumatic brain injuries (are already at risk for ischemia).
24 hours after initial hyperventilation was started..it's no longer effective. |
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What are goal PaCO2 levels during neurosx?
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35-40 mmHg.
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List the requirements for fluid management intraop for neurosurgery.
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-> EUVOLEMIA WITH ISOTONIC SOLUTIONS (Normal Saline).
* To maintain cerebral perfusion pressure at 50-70 mmHg, (CPP = MAP-ICP) aim for euvolemia or slight hypervolemia ...avoid HOTN but also DO NOT FLUID OVERLOAD. Aggressive resuscitation will cause hyperemia. * Water movement from the intravascular space is dependent on osmotic pressure. So if you maintain a higher serum tonicity with isotonic fluids, you will not have water movement and will maintain euvolemia. * Avoid LR, which is a hypotonic fluid and will cause water movement OUT of the blood. |
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How does mannitol/ osmotrol work and what is important about it's management?
Dose? |
Mannitol is a large molecule sugar used as an osmotic diuretic. It pulls water out of the body tissue and into the blood. It can be used to tx cerebral edema.
DOSE: 0.25 - 1 g/kg BENEFITS: ---> Decreases the viscosity of the blood by putting fluid in it. This is good for microcirculation to tissues. ---> Decreases CSF production...this is good for decreasing ICP. (combine with furosemide for an added effect). MUST MONITOR Na LEVELS!!! Large movement of water into the blood can cause dilitional hyponatremia. |
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T/F
Colloids are more beneficial to the management of euvolemia in neurosurgery. |
FALSE
Colloids have no proven advantage over ISOTONIC crystalloids. |
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Hetastarch (Hespan) is a _______ fluid. It's maximum dose is ____ mL/kg/day OR ___ liter(s) per day. Large doses of hespan can cause _________ and __________.
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Hetastarch (Hespan) is a colloid fluid. It's maximum dose is 20 mL/kg/day OR 1 liter per day. Large doses of hespan can cause decreased plt function and coagulopathies.
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Although the lower limit for Hgb is undefined, do not go below ___Hgb or ___Hct on ANY neuro-case without tranfusing..
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Although the lower limit for Hgb is undefined, do not go below 7.0 Hgb or 21% Hct on ANY neuro-case.
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The decision to tranfuse during neuro sx depends on
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1) Hgb/ HCt levels (tranfuse if lower than 7 Hgb or 21% Hct.
2) The presence of cerebral ischemia 3) The rate of blood loss. |
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Your sx is over, your patient is to have a cerebral angiography after leaving the OR...how do you proceed with emergence?
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LEAVE INTUBATED AND SEDATED.
This procedure has the risk of loss of airway, extubation now is contraindicated. |
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Your neurosurgery case if over, before you begin emergence, what do you need to have on hand? What other considerations must you make?
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A hyperdynamic state with emergence can cause dramatic hemodynamic changes. Coughing and bucking can occur. You want to avoid this to prevent increased ICP (this pt just had brain sx!). The drug you give will depend on it's duration of action and how long you anticipate the HTN to last...whether it is just due to emergence (esmolol) or if it has been trending up (ie...will be long term) (CCB, metoprolol).
Have the following on hand to control BP and HR: * Esmolol * CCB * Nitroglycerin/ Nipride * Lidocaine IV - to pvt coughing/ bucking ...you basically want something to drop their BP for the amt of time it will be elevated. Be cautious with using fentanyl...you don't want to oversedate your pt. * You can also drip lidocaine down the sides of the ETT. |
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You pt just had spinal surgery. During emergence, what types of problems might you anticipate seeing?
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Pt has been in prone position for a long time:
*Facial Edema *Pulmonary Edema *Airway Edema - check for a cuff leak before deflating and extubating to assure no airway edema. * Hypoxemia * Hemodynamic instability |
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Your neurosurgery case is over and your pt is going straight to the PACU. During emergence, your pt is prone to hemodynamic changes that will increase ICP....should you or should you not give fentanyl to help?
What is your goal for emergence? |
Goal is to extubate ASAP so that neuro exams can be performed ASAP!
GIVE FENTANYL MINIMAL DOSE ONLY. To much fentanyl will sedate them and the pt needs to be awake in the PACU for followup neuro exams. |
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What happens with a coup, contra coup injury?
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The skull is hit on the front of the head. Brain hits the front of the head, bounces off and hits the back of the head. You get bleeding on top of the head and brainstem swelling and tearing.
Fracture to the front of the head...initial hit spot. |
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Secondary brain injury due to
Inflammation Superoxide production Excitotoxic amino acid release and apooptosis is usually due to.... |
Reperfusion injury.
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T/F you can pvt further injury after a reperfusion injury with hypothermia.
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False.
Once you have received a reperfusion injury you cannot pvt the brain damage from occuring. |
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How can you treat a brain injury as an anesthetist?
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Ventilation, Oxygenation, and Perfusion.
Airway Breathing Prevent hypercapnia: will increase ICP, bleeding, etc. Prevent hypoxemia: don't hyperventilate too much...VC to the brain. |
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What are some indications that would make you intubate your neuro pt asap
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Decreased level of consciousness
Risk for aspiration Concern for hypoxia Concern for hypercarbia Diagnostic studies |
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Thiopenthal...what is the induction dose and what are the effects on the brain?
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DOSE: 3-6 mg/kg
BRAIN: Decr CMR, CBF, ICP d/t sedation. This drug can exacerbate HOTN!!! |
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Propofol...what is the induction dose and what are the effects on the brain?
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DOSE: 1-2 mg/kg
BRAIN: Decr CMR, CBF, ICP d/t sedation. This drug can exacerbate HOTN!!! |
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Amidate (Etomidate)...what is the induction dose and what are the effects on the brain?
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DOSE: 0.2-0.3 mg/kg
BRAIN: Decr CMR, CBF, ICP d/t sedation. Etomidate is cardiac stable. Good to use for pts who are already HOTNsive. |
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Lidocaine...what is the induction dose and what are the effects on the brain?
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DOSE: 1.5 mg/kg
BRAIN: Decr ICP d/t no coughing/ bucking. Can blunt the SNS response to laryngoscopy |
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What is the only NMR approved for RSI's?
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Rocuronium
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How can muscle relaxants affect ICP?
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Decrease ICP by preventing coughing, bucking, etc.
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What are the benefits and the downsides to using Roc?
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BENEFITS: No fasciculations that can increase ICP like with Succs. No hyperkalemia with muscularly weak patients like with succs.
DOWNSIDES: Long duration - 25 min. If you can't get the pt intubated, spont. resp will not return for 20-30 min. You have establish some type of airway ASAP. Roc also has a slightly slower onset. |
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You recieve a trauma with a confirmed head injury that has had hemmoraging.
T/F you plan for an aggressive fluid resuscitation with blood, IVF, etc. |
FALSE
Aggressive fluid resuscitation will TBI should be avoided...it can cause hyperemia and increased ICP...restore just enough to get adequate circulation to the brain. |
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ICP catheter to measure ICP is placed where?
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At the trachus of the ear.
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Fluid resuscitation in a neuro or TBI pt is a balance b/n what two variables?
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Pvt cerebral edema
vs Maintain organ perfusion. |
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When you visit a pt pre or post op with an ICP monitor in ...what do you need to find out?
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Need to know how much CSF they are pulling out and what color it is …if blood tinged….you don’t know if this is a new change or not unless you find out what it has been looking like. Need to know preop and post op ICP levels and neuro levels (glascow coma scale) to tell if you caused any problems in surgery.
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GLASCOW COMA SCALE
Mild Head Injury = Moderate Head Injury = Severe Head Injury= Brain Dead = |
Mild Head Injury = 13-15
Moderate Head Injury = 9-12 Severe Head Injury ≤ 8 |
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Unilateral & dilated pupil =
Bilateral pupil dilation = |
Unilateral & dilated pupil = brainstem compression
Bilateral pupil dilation = close to herniation = very poor prognosis |
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When using mannitol...what you your goal serum osmolarity?
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Serum osmolarity < 320 mOsmo
IF the serum osmolarity was any higher, it would pull too much fluid out of the brain...this would be bad. |
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What is Hypertonic Saline/ HS -Dextran and when is it used?
SIDE EFFECTS? |
Hypertonic Saline/HS-Dextran
Treats intracranial HTN refractory to Mannitol. Establishes gradient for H2O to move from brain into intravascular space. Lacks severe electrolyte disturbances vs. Mannitol Bolus or infusion. (Infusion needs to go thru a CENTRAL LINE!!!!). Taper infusion the to pvt dilutional hyponatremia, edema. SIDE EFFECTS: Hypokalemia (not K sparing). Coagulopathies with too much dextran. Hyponatremia and edema with sudden turn off (no taper. ) |
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You have a pt with a TBI. Suddenly you start seeing bradycardia, irregular respiratory pattern, and HTN. What should you do??
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Hyperventilate the pt ASAP to decrease ICP!! This is Cushing's Triad. The pt is herniating.
Goal PaCO2 is 35-40 mmHg. |
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What are some signs of brain herniation?
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Bradycardia
Irregular respirations HTN This is called cushing's triad. Also: Pupil Dilation (bilateral). |
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You have a pt with long term cerebral edema/increased ICP and have been treating them with barbituates to decrease ICP but they are not helping...what can you do now?
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...Well you could try mannitol or Hypertonic Saline with Dextran...
BUT ICP that is refractory to barbituates has a POOR PROGNOSIS!!! |
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What pts are candidates for barbituate therapy?
What is a risk? |
Hemodynamically stable pts (causes HOTN) that are fluid resuscitated.
Risks: HOTN |
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What are the signs of propol infusion syndrome?
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Causes a mitochondrial disorder:
Rhabdomylosis Metabolic Acidosis Renal failure. |
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Ways to reduce brain water to reduce ICP (increase CPP)
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1. Mannitol
2. Hypertonie Saline iwth dextran 3. Furosemide |
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Ways to remove CSF as a means to reduce ICP
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1. External ventricular drain
2. Lumbar Drain 3. Hypertonic fluid |
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Ways to decrease CBV as a means to reduce ICP
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1. Head up position
2. Neutral neck position (won't suppress vessels). 3. Metabolic suppression (propofol or a barb) 4. Mild/moderate hyperventilation |
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Ways to elevate MAP to increase CPP.
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1. Adequate intravascular volume resusucitation
2. Vasopressors |
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Your in the preop holding area and your TBI trauma pt is wiggling around laying in the fetal position. He's complaining of a major headache. What do you do to bring down ICP?
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Elevate head, put neck in neutral alignment. Sedate with prop or a barb. Mildly hyperventilate.
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Complex spinal cases have increased risk of ...
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bleeding due to closeness of vessels to spinal cord.
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The spinal cord enters the spine via the _____ ______. It ends at ___ in adults and at ___ in peds/neonates.
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The spinal cord enters the spine via the foramen magnum. It ends at L1 in adults and at L3 in peds/neonates.
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The artery of adamkiewicz supplies blood to what area of the spinal cord?
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T7-T12
lower thoracic and sacral area (anterior artery). blockage can cause LE paralysis. |
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What are the ascending pathways that are stimulated for evoked potential monitoring?
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SSEP
BAEP (brain auditory) VEP (visual) |
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What is the descending pathway that is stimulated for evoked potential monitoring?
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Motor evoked potentials.
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Magnitude of change in the oscillating variable with each oscillation within an oscillating system.
Strength of signal. = |
Amplitude
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The time between exposure to a pathogen, chemical or radiation, and when symptoms first become apparent.
Time delay between signal and response = |
Latency
Shown as the # after the P or N (polarity). (in milliseconds). Also correllates with how far along the graph the deflection occurs. |
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The direction of wave deflection in an evoked potenital waveform is the..
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Polarity
N = negative deflection P = positive deflection |
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SSEP- Somatosensory Evoked Potentials.
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Signal detectable on EEG. Get repetitive signals and average them. Signal generated in time lock fashion to sensory input
BENEFITS * May be used in many surgeries (Craniotomies, Carotid) * Very useful in spine surgery * Paralytics are okay. DOWNSIDES * Has to have intact neural pathway…if you don’t it will transmit to muscle or to other tissues. * Dose dependent depression with volatile anesthetics. * ISCHEMIA is the biggest cause of loss of SSEP. Causes a decreased amplitude and increased latency. Signs of spinal/nerve ischemia: ---> > 50% decr in amplitude ---> > 10% increase in latency If then occurs then you immediately assure that you have a normotensive pt and that you didn't recently deepen the anesthetic. * Another cause is movement..paralytics are okay as long as you are not also monitoring MEPs. * To pvt spinal ischemia maintain oxygenation and ventilation. Monitor H&H's. |
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What are the 3 most common nerves stimulated by SSEP?
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Ulnar Nerve
Median Nerve Posterior tibial Nerve |
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SSEP's are decribed by ...
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Polarity
Latency and Amplitude. |
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What is the range of PaCO2 in which you have a linear rise in CBF with increased PaCO2?
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25-65 mmHg
Anything before or after this and it changes exponentially. |
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What are signs of spinal/ nerve ischemia during SSEP monitoring?
What do you do? |
> 50% decrease in amplitude.
> 10% increase in latency. Assure normotension and that anesthetic is not too deep. Get an H&H. Oxygenate and ventilate. |
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Brain-Auditory Evoked Potentials
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Standardized sound placed to 8th cranial nerve (VESTIBULAR COCHLEAR NERVE).
MOA: A series of peaks generated: The latency of each peak has significance with respect to integrity of different parts of auditory pathway. USE: --->Acoustic neuroma surgery ---> Can be used with any surgery around the BRAINSTEM BENEFITS: --> not affected by anesthetics!!! YAY! |
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Visual Evoked Potential Monitoring.
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Light Stimulation of the Retina
* Goggles that emit LED lights worn by patient * Monitor integrity of optic nerve DOWNSIDES: ---> Signals difficult to record consistently when under anesthesia (especially when prone). ---> Research still ongoing ---> Dose dependent depression with volatile anesthetics. |
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Motor Evoked Potential Monitoring
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Monitors DESCENDING Pathways.
* Complements SSEP (esp in spine surgery). * Larger amplititude than SSEP (stronger). * Major muscles monitored: ---> THENAR EMINENCE: Thumb muscle ---> ABDUCTOR HALLUCIS: medial border of the foot. Nerve is the PLANTAR NERVE. *AMPLITUDE is the ONLY thing you can use to monitor for ischemia. MOA: A stimulus is applied in a transcranial fashion over the motor cortex. Deflection is detected by electrodes in the muscle belly ( the middle of the muscle). BENEFITS: ---> Greater amplitude than SSEP (stronger). This allows them to overshadow the spontaneous EEG, so they are not mixed in with background waves like w/ SSEP. This mean you don't have to use as much stimulation. (Don't have to take an avg). DOWNSIDES: ---> Paralytics are contrainidicated. ---> These can cause pt movement during the procedure. (A bite block is a MUST!!) ---> Latency is unreliable to tell you of ischemia. ---> Dose dependent depression by volatile anesthetics |
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Complex spinal procedures should have what type of monitoring?
Are paralytics okay. |
SSEP AND MEP.
Paralytics are contraindicated due to MEP. Use roc or succs for intubation. |
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Ketamine...how does it effect EP's?
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No effect or increase amplitude
Ketamine gtts are good. (Good for pain control d/t analgesic effects. Do not affect amplitude) |
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Narcotics...how does it effect EP's?
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Mild reduction in amplitude
Allows consistent monitoring Remi and sufentanyl drips |
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Benzo's...how does it effect EP's?
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DECREASED AMPLITUDE!!!
LIttle effect on latency. |
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Muscle Relaxants...how does it effect EP's?
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No significant effect on evoked potentials. :)
Helps suppress artifact from muscle activity - good! If complete blockade, then suppress evoked muscle response (do not use with motor evoked potentials)!!!!! |
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Tell me all the factors that make Spinal Anesthesia the "Perfect Storm"
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*More complex
* Longer cases - blood loss/ fluid status issues. Compression, eye inj. more common d/t prone position. * Multilevel fusions * Combined anterior/posterior approaches: mx position surgeries inc risk of extubation, loss of lines, incr risk of infection. (Anterior approach has increased risk of infection and post-op pulmonary complications d/t big belly incision. * Staged procedures: incr pt's tolerance to anesthesia. * Increasing age * Increasing comorbidities (obesity, etc) * More sophisticated monitoring (can also be a bad thing b/c dependent on monitoring give surgeons a false sense of security…try more risky techniques). |
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Differentiate b/n primary and secondary spinal cord injury.
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PRIMARY INJURY:
The injury itself: typically involved damage to bones and ligaments * CAUSES: ---> Traumatic injury to spinal cord, ---> Compression ---> Hemorrhage ---> Vasospasm Unstable injury puts neural elements at risk. SECONDARY INJURY Ischemic event Mediated through cascade of events CAUSES: --->induction of nitric oxide synthase --->release of excitotoxic amino acids --->cellular influx of calcium --->oxidative stress ---> lipid peroxidation May be exacerbated by hypotension |
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Central Cord Injuries
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Damage the central spinal cord:
* Cervical spine lesion VIA HEMORRHAGE following trauma. * Greater paresis in upper extremities (weak arms). * Bladder Dysfunction * Variable loss of sensory below lesion |
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Anterior Cord Syndrome
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Disruption of blood flow through anterior spinal arteries
AFFECTS: ---> Loss of motor below the lesion. --->Variable effects on sensation --->Pain and temperature sensation lost NOT AFFECTED: --->Proprioception intact |
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Brown Sequard Syndrome
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Interruption of HALF of the spinal column
CAUSE: Typically penetrating trauma EFFECTS: ---> Loss of motor and touch IPSILATERALLY ---> Loss of pain and temperature CONTRALATERALLY |
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Cauda Equina Syndrome
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Injury below level of caudal end of cord (typically below L2)
CAUSE: Perineal anesthesia EFFECTS: --->Urinary retention ---> Fecal incontinence --->Lower extremity weakness |
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American Spinal Injury Association Classification for Spinal Injury
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CLASS A: Complete cord injury
----> Loss of motor AND sensation in sacral roots S4 and S5 CLASS B: Incomplete cord injury ---> Loss of motor ONLY below lesion including S4 and S5. CLASS C: Incomplete cord injury ---> Sensory intact. ---> motor function intact below the level of injury, but with strength less than 3 in hald of the major muscle groups. CLASS D: Incomplete cord injury ---> Sensory intact ---> Motor intact. Strength of 3 or more in at least HALF of the major muscle groups. CLASS E: No cord injury. |
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Your trauma pt has a SCI. You give fluids to maintain euvolemia but BP is still too low...what should you do?
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Don't give anymore fluids!!
Support BP with pressors and inotropes. |
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HIgh level SCI's have what effects on the pt?
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Sympathectomy and VD....BP will tank.
Support with fluids and pressors. |
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When you restore fluids in a traumatic SCI pt, should you use crystalloids or colloids?
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Crystalloids and blood if needed.
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What are the benefits of methylprednisone for an SCI and what is the time in which you can give it?
SE? |
Must be given w/n 24 hours of the SCI!!! or it has no effect. Studies show that it improves motor function by preventing inflamation and further injury.
SE: hyperglycemia. Make sure you are monitoring BG levels. |
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A trauma pt comes in that was found in a ditch with a confirmed SCI. No one knows how long he layed there. Should you give steroids?
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No...they will have no effect.
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The goal for surgery to correct an SCI is within __ hours of the injury.
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The goal for surgery to correct an SCI is within 24 hours of the injury.
Need to hurry up and decompress neural structures and stabilize the spinal cord. |
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A SCI trauma pt comes in and needs emergency sx to decompress neural structures.
The pt currently is experiencing ARDS. What should you do? |
Delay sx until pt is hemodynamically stable.
You 24 hrs to get the sx done. |
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Induction with an SCI
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ETT if not received prior to OR
? C-spine cleared…no unless told otherwise. HALO or cervical collar: use a glideoscope to intubate RSI vs. Standard induction: RSI for traumas. SI might be okay for a spinal case with NPO pt. ? Awake fiberoptic intubation: use aggressive local block to pvt bucking. |
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What kind of venous access and monitoring do you need for an SCI decompression surgery?
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Significant risk of blood loss
Arterial line needed Large bore IV’s vs. CVL (16g’s and 14g’s) Pulmonary artery catheters…will need to insert a central line with an introducer if you think they will need a PA catheter. |
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Indications for a central line
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Difficult sticks
CVP monitoring Giving pressors that will cause local tissue damage. |
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Prone Position
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Pad pressure points: Eyes, ears, nose, breasts, genitalia, knees, toes
REVERSE TRENDELENBURG facilitates venous drainage from head (reduce congestion and intraocular pressure) Padding does not compress neck Check and document the pressure points and eyes, etc every 15 min. Don't overload pt with fluid. |
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AUTONOMIC HYPERREFLEXIA
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Chronic spinal cord lesions ABOVE T7
CAUSE: Occurs when stimulated BELOW level of lesion. EFFECTS: ---> Severe HTN and reflex bradycardia ---->Intense vasoconstriction BELOW lesion level ---->Vasodilatation ABOVE lesion |
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Can you use Succs on a stroke pt....
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depends on how fresh the stroke is...1st 48 hours and you can.
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Post op vision loss is most commonly due to
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Ischemia
Ischemic optic neuropathy (ION). |
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What are the causes of Ischemic Optic Neuropathy ION?
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--->Blood loss
--->HOTN --->Long duration cases (d/t increased IOP and occlusion of vessels) --->Multifactorial including vasculature of individual (pts who are HTN, diabetic, CAD, etc increase the risk). |
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If your pt has ION what do you do?
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Get an opthamology consult ASAP. The sooner the tx the sooner it can resolve.
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How can you prevent ION?
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*Keep pt euvolemic.
* Don’t fluid overload b/c will increase IOP. * Make sure nothing is on the eyes. Avoid HOTN. * Use the reverse trendelenburg position. * Monitor VEP. * Stage complex spinal cases. |
