Neuro Flashcards
(152 cards)
1
Q
Where is CSF made?
A
In the ependymal cells of the choroid plexus in the lateral ventricles.
- The choroid plexus is essentially the blood-brain barrier. It is only one cell thick and prone to hemorrhage.
- Normally, 20-30mL/hr of CSF is made.
*About 500mL of CSF is made every day and reabsorbed into superior saggital sinus via the arachnoid granulations.
2
Q
Name some of the functions of the CSF:
A
- Transports nutrients, chemical messengers and waste products.
- Supports and cushions the brain.
- Interchanges with interstitial fluid of the brain.
- Surrounds all exposed surfaces of the CNS.
3
Q
What is normal ICP?
A
5-15mm/Hg
Anything above 20mm/Hg is considered for treatment.
4
Q
Basic functions of the cerebellum…
A
Coordination of voluntary movement
Balance/equilibrium
Muscle tone
5
Q
Basic functions of the basal ganglia
A
Controls movement, even blinking. Because we are always moving, the BG has a high metabolic demand. Therefore, it functions poorly in hypoxic states.
Parkinson’s effects the BG.
6
Q
What is the tentorium?
A
- A prominent fold in the dura mater that separates the upper brain (supratentorium) from the lower brain (infatentorium) at the level of the cerebellar/occipital interface.
- The only communication between the infa and supra is the channel that connects the third and fourth ventricle.
7
Q
Basic functions and cranial nerves of the Pons…
A
Reticular Activating System (RAS)
Contains CNs IV, V, VI, VII and VIII
Dysfunction occurs in infratentorial herniation due to proximity to cerebellar tonsils.
8
Q
Basic functions and cranial nerves of the medulla oblongata…
A
Regulates autonomic functions such as HR, BP and digestion.
Contains CNs IX, X, XI and XII, and the respiratory center.
9
Q
CN I
A
Olfactory
Transmits sense of smell from nose to brain
10
Q
CN II
A
Optic nerve
Transmits visual information from retina to occiput via the midbrain.
Communicates directly with CN III. A bright light is sensed by CN II, then both pupils should constrict in response to stimuli from CN III.
Located in midbrain
11
Q
CN III
A
Oculomotor
Eye movement, pupillary constriction, upper eyelid move’t
Located in midbrain
Will be affected by supratentorium ICP since it will be compressed by the uncus (uncal herniation).
12
Q
CN IV
A
Trochlear
Allows eye to look down and inward
Located in anterior, superior pons
13
Q
CN V
A
Trigeminal Has three branches at different levels of the face (V1 ophthalmic, V2 maxillary, V3 mandibular) that sense facial stimulation. Mastication Assessed via corneal reflex Located in superior, anterior pons
14
Q
CN VI
A
Abducens
Allows eye to turn outward
15
Q
CN VII
A
Facial
Facial muscle movement
Assessed via corneal reflex
Located in mid pons
16
Q
CN VIII
A
Vestibulochlear/Accoustic
Transmits sounds and equilibrium information from the inner ear to the brain.
Assessed via doll’s eye test.
Located in inferior pons
17
Q
CN IX
A
Glossopharyngeal
Muscle control of pharynx (assists with swallowing)
Gag reflex
Located in superior medulla.
Will be compressed by cerebellar tonsils in cases of infratentorium pathology.
18
Q
CN X
A
Vagus
- Sensory innervation of pharynx, larynx, thoracic and abdominal viscera, heart, GI tract and tongue.
- Motor innervation to pharyngeal and laryngeal muscles.
- Provides parasympathetic innervation to the thoracic and abdominal viscera including the heart, GI tract and most abdominal organs.
- Gag and cough reflex
- Loacated in superior medulla, just above the respiratory center.
19
Q
CN XI
A
Accessory/Spinal Accessory
- Cranial branch controls muscles of soft palate and pharynx.
- Spinal branch controls trapezius and SCMs.
20
Q
CN XII
A
Hypoglossal
Innervation muscles of tongue
21
Q
Trace right side cerebral blood flow from LV to brain…
A
Anterior
Aorta -> brachiocephalic -> right common carotid -> internal carotid -> circle of Willis -> MCA/AComm/ACA
Posterior
Aorta->brachiocephalic -> right vertebral artery-> basilar -> PCA/PComm
22
Q
Trace left sided cerebral blood flow…
A
Anterior
Aorta -> left common carotid -> left internal carotid -> circle of Willis -> MCA/AComm/ACA
Posterior
Aorta->left subclavian -> left vertebral -> basilar -> PCA/PComm
23
Q
The internal carotid arteries account for approximately how much of the cerebral blood flow?
A
40% each.
The vertebral arteries account for 10% each.
24
Q
What lobes does the MCA supply and what does its stroke syndrome look like?
A
Stems from the Circle of Willis. It is the largest of the cerebral arteries and is the one most often associated with CVAs. It feeds the temporal, parietal and some of the frontal lobes.
Of the cortical homunculus, it supplies the face and arms.
Facial droop, arm hemiparesis
Global aphasia - trunk of L MCA
Broca’s aphasia - anterior branch of L MCA
Wernicke’s aphasia - posterior branch of L MCA
25
List the vessels that stem from the Circle of Willis
MCAs
PCAs
ACAs
26
If collateral circulation exists, how long can a penumbra remain salvageable for?
6-8 hours
27
What percentage of CVAs are ischemic?
87%
(70% thrombotic [clot forms at site], 30% embolic [clot travels from elsewhere and lodges in vessel])
*The remaining 13% of CVAs are hemorrhagic
28
There are three types of aneurysms (fusifor, saccular and berry). What is the most common type?
Berry
(Berry shaped aneurysm at bifurcation)
*The ACommA is a common site for berry aneurysms and SAH.
29
How can you tell the difference between a CVA and a focal hemi-seizure?
- A person having a CVA will have a left sided lesion that causes right side deficits but will a have left sided gaze. (Looking toward the lesion).
- A focal seizure from the left brain could also have a right side deficits, but will have a right sided gaze along with it (looking away from the stimulus).
30
What type of strokes are associated with sudden onset dizziness, gaze palsy, nystagmus, N/V, ataxia, gait disturbance and incontinence?
Cerebellar CVAs.
They are generally severe and associated with high rates of mortality due to compression of the medulla.
31
Full occlusion of the basilar artery can result in what syndrome?
Locked In Syndrome (total muscle paralysis).
The basilar artery supplies the brainstem with 100% of its CBrDO2.
32
If someone has face, arm and leg hemiparesis, what is the most likely cause of the CVA?
It will likely be a deep tissue site in the internal capsule. Another possible source is carotid artery occlusion.
33
What lobe(s) does the ACA supply and what would its stroke syndrome look like?
Frontal lobe.
It includes the leg of the cortical homunculus.
Dysarthria, dysphasia, urinary incontinence.
Leg/shoulder hemiparesis > arm/hand/face hemiparesis
34
What lobe(s) does the PCA supply?
Occiput
| Vision loss will occur if occluded.
35
What lobe(s) does the basilar artery supply?
It supplies 100% of the brainstem and RAS.
Occlusion will result in CN dysfunction, seizures and locked in syndrome.
*Seizures with CN dysfunction (facial palsies, occulomotor dysfunction, abnormal V/S) is a vestibular-basilar stroke until proven otherwise.
36
Where does CSF leave the CNS?
At the superior sagittal sinus at the top of the brain. If ICP rises, CSF is forced out but the fluid is still in the cranial vault since it needs to descend down the venous system.
37
Key features of uncal herniation...
- Ipsilateral pupillary dilation to site of insult
| - Contralateral hemiparesis
38
Myp's step by step (superior to inferior brainstem) cranial nerve exam...
- Open eyes, assess symmetry and size (midbrain CN II, III)
- Constriction x 2 pupils in response to light (midbrain CN II, III)
- Corneal reflex - eyes should blink (superior pons; middle pons CN V, VII)
- Doll's eyes test - if no c-spine (inferior pons CN VIII)
- Gag reflex (superior medulla CN IX)
- Cough reflex (superior medulla CN X)
- Respiratory drive (middle medulla)
39
Post cardiac arrest, the patient is demonstrating roving eyes. What is this indicative of?
CN III, IV, VI are functioning and receiving input from the cortex.
40
When reporting on a neuro patient, what are three things that are important to communicate?
1. Confounders such as sedation, hypothermia
2. Brainstem reflexes, including any apneic periods
3. GCS, especially motor exam
41
Score a GCS - M6
- Obeys commands. Can look right/left, stick out tongue and give a thumbs up or wiggle fingers/toes. Squeezing the hands is a primitively response so avoid assessing it.
- Indicates cortex is intact.
42
Score a GCS - M5
- Place arms at pt's side and provide a pain stimulus (trap squeeze, supraorbital pressure). Pt's contralateral arm must move across midline.
- Indicates cortex is intact, but dysfunctional.
43
Score a GCS - M4
Withdraws
- Place pt's hands on abdo and provide constant fingernail stimuli. Pt's hand must curl and pull away.
- Indicates severe cortical dysfunction.
44
Score a GCS - M3
Abnormal Flexion
- Place pt's hands on abdo and provide constant pressure to fingernail. Pt's hand must supranate and bicep will flex.
- Indicates deep brain damage and cortex is fucked.
45
Score a GCS - M2
Abnormal Extension
- Place pt's hands on abdo and apply constant fingernail pressure. Pt's arms must fully extend with flexed triceps and hands rotated outwards. Feet will point down.
- Indicates brainstem pathology.
46
List the five reflexes and associated spinal roots
```
Bicep - C5
Brachioradialus - C6
Tricep - C7
Knee - L4
Achilles - S1
Grade on a scale of absent->normal->brisk.
```
47
The plantar reflex is a upper motor neurone sign. If the toes point up, is it a good thing or a bad thing?
Bad thing. Toes should point down.
48
What's the difference between dysarthria and dysphasia?
Dysarthria can still comprehend and produce writing. Dysarthia means your tongue isn't working due to loss of brain input. Dysphasia means your brain is fucked and make you no words good.
49
Is monitoring pupillary response a solid clinical finding for cerebellar pathology?
No. CN II and III are located in the superior portion of the midbrain and will not be effected in the case of cerebellar ICP increases.
50
Describe the Monro-Kellie Doctrine:
The cranial vault is made up of 80% parenchyma, 10% CSF and 10% arteries and veins. If the mass of one increases, there must be a reduction in one or two of the other. Since veins and CSF are the only low pressure compartment, fluid must shift out of these compartment.
51
What is the approximate volume of the cranial vault and its contents?
1600mL
Parenchyma: 1300mL
Vessels: 150mL
CSF: 150mL
52
What is the intracranial compliance curve?
In regards to the Monro-Kellie doctrine, intracranial compliance worsens as pathological mass increases. CSF and venous blood are shunted out of the cranium as ICP is driven upwards. The curve eventually plateaus when the parenchyma starts to herniate.
53
List the three waves in an ICP waveform:
P1: arterial pulsation (gets smaller with ICP increase)
P2: venous/parenchymal bulk (gets larger with ICP increase)
P3: closure of the aortic valve
54
How does mannitol work? How is it different from HTS?
Osmolar diuretic. It draws fluid out of brain parenchymal cells, thus reducing the volume of parenchyma. The extra fluid is then diuresed by the kidneys. It is a volume contractor whereas HTS is a volume expander and a better agent in hypovolemic states.
55
How much will elevation HOB and loosening collars reduce ICP by?
HOB: 5-10mmHg
Collar: 5-10mmHg
56
How does appropriate sedation facilitate a reduction in ICP?
Decreases cellular metabolism which decreases CBF via flow-metabolic coupling.
57
How much change in ICP does one mmHg of PaCO2 affect?
Every 1 mmHg of PaCO2 will change CBF by 2-3%. Since there is only 150mL of intracranial blood, small changes in PaCO2 can drastically affect CBF.
Target PaCO2 to 35-40mmHg
58
When using mannitol, how much fluid do you put back in?
Measure urinary output and replace fluid (normal saline) at a 1:1 ratio.
59
What is the caveat to using 3% HTS?
It has an osmolarity of 512mmol. If urine osmolarity is greater, it won't work. Use 5% HTS if you can get it.
HTS is incompatible with almost all drugs so it must go through it's own IV line. It is not contraindicated for I/O.
60
How much does one degree of temperature change affect CBF?
20%.
If patient's are hyperthermic, it is likely due to hypothalamic dysfunction. Acetaminophen won't work well, so actively cool the patient instead.
61
Does ketamine increase ICP?
Dr. Sekhon: "No, that's garbage."
Dr. E. Vu: "Who cares about transient increases, anyways?"
62
4 indications for anticonvulsant therapy in TBI:
1. Hx of seizure with TBI
2. Temporal lobe pathology
3. Compressed skull fracture
4. Penetrating trauma
63
What is a common sequelae of common drugs used to treat TBI?
Mannitol, propofol and phenytoin all can cause hypotension. If SBP drops < 90 just once, you increase mortality by 50%.
64
What is the cerebral oxygen delivery equation?
CBrDO2 = CBF x arterial oxygen content
Arterial oxygen content = (1.34 x Hgb x SaO2) + (0.003 x PaO2)
*The brain takes up only 2% of body weight, but accounts for 25% of cardiac output. This is because is cannot store oxygen or glucose like other cells can. This is an important consideration for preventing secondary injury.
65
A MAP < 50 is considered __________ and blood vessels are _______
Cerebral ischemia
Constricted
*Chronic HTN shifts this to the right.
66
A MAP > 150 is considered ________ and blood vessels are ________
Cerebral hyperemia
| Dilated (engorged and loss of autoregulation)
67
Four factors that affect cerebral flow regulation:
Temperature
Level of consciousness/sedation
PaCO2
Autoregulation
68
Best to worst vasopressors when treating TBI
1. Levophed
2. Phenylephrine (activates CNS alpha receptors)
3. Vasopressin (can make cerebral edema worse by changing serum Na+ levels)
69
If you learned one thing from Myp's lecture, it should be this... What's the initial care bundle for brain injury?
1. MAP > 80, SBP < 140-160 (SBP more important in bleeds)
2. Normal temp
3. PaCO2 35-40
4. PaO2 80-100
5. Hgb > 90
6. HOB 30, loosen collars/ties
7. Optimize platelets/INR
8. Propofol/fentanyl to RASS -4
70
What is the target PaO2 for TBI?
80-100mmHg
71
Where is the RAS located?
In the posterior Pons, close to the cerebellar tonsils.
72
You hear a patient has cerebellar pathology, what should you prepare for?
Grab the patient and GTFO! This pt is headed straight to NSx.
Interventions en route.
Keep confounders as light as possible.
*Generally, a good prognosis since cerebellum is such a hypo metabolic organ in the first place.
73
Define TBI:
It's a made up disease, more of a syndrome. Defined as blunt traumatic injury to the brain with an unconfounded GCS of less than or equal to 8.
74
Key features of subdural bleed:
- Under the dura mater, above the arachnoid
- Involves large bridging veins
- Almost always results from trauma
- Crescent shaped on CT
- May have adjacent parenchymal edema prone to secondary injury.
75
Key features of epidural bleed:
- Between the dura mater and the skull, lentiform shape
- Involves arteries so bleeding is rapidly dangerous
- Brain parenchyma is usually spared so prognosis is good as long as surgical intervention is PROMPT!!
- Hx often indicates an initial normal exam, followed 1-6 hours later by rapid deterioration.
76
Key features of subarachnoid hemorrhage:
- Small veins, but small space to bleed into. No mass effect unless obstructive hydrocephalus.
- Lines the brain, optic nerves, ventricles, cisterns.
- Blood outside of the brain is extremely irritating and causes abnormal signal transduction.
- Won't increase ICP by itself.
77
Key features of diffuse axonal injury:
- Rotational and shear forces applied to neurons and microvasculature.
- No mass effect, but diffuse micro-bleeds throughout cerebrum.
- Requires optimal CBrDO2.
- Don't rebleed so take time to ensure optimize CBrDO2 (good MAP, Hgb, PaCO2, PaO2, Na+)
78
Key features of cerebral contusion:
- Usually occurs in frontal lobes, but often with SDH or SAH as well.
- Associated with high ICPs. Mannitol and HTS are very effective with these bleeds since they shrink the parenchyma.
- Hemorrhage + surrounding edema leads to large mass effect.
- Keep PaO2 > 150mmHg
79
Key features of TBI management:
```
A-line MAP > 80, NIBP SBP < 160 (or 140 for epidural)
PaCO2 35-40
PaO2 80-100
Hgb > 90, INR 1.0, Platelets 150-350
Na+ > 140, < 150
Temp 36.0-37.5
Seizure prophylaxis (depressed skull, temporal lobe, penetrating, Sz)
Propofol, with fentanyl if required.
HOB 30, loosen ties/collars
```
80
What do you look for when measuring optic nerve sheath diameter?
- The nerve is surrounded by the meninges. When ICP is pushed out of the ventricles, it goes to compliant areas. It engorges the meninges around the optic nerve and causes diameter to widen.
- It is measured 3mm behind globe. Larger than 5.8mm is indicative of an ICP of 20mmHg.
- Invalid in the setting of hydrocephalus, EVD, SAH or bone plate off.
81
Key symptoms of SAH?
Photophobia
Sudden onset severe H/A
Nuchal rigidity (causes non-inflammatory meningitis)
Consider bacterial meningitis if patient has a fever and wear PPE.
82
WFNS (World Federal association of Neurosurgeons) score for SAH:
1. GCS 15, no motor deficits
2. GCS 13-14, no motor deficits
3. GCS 13-14, motor deficits in limbs
4. GCS 7-12
5. GCS 3-6
83
Modified CT Fischer score for SAH:
1. Thin (<1mm) edema, no IVH
2. Thin (<1mm) edema, IVH positive
3. Thick (>1mm) edema, no IVH
4. Thick (>1mm) edema, IVH positive
84
Aneurysmal SAH Management
- Keep MAP > 70 and SBP < 140. Rebleeding is lethal! Use labetalol and/or nimodipine infusion.
- Check QTc, optimize Mg++ (>1.0) and K+, watch for Taketsubo.
- Monitor Na+ (SIADH, CSW, DI)
- Continue statins if pre-existing
- Consider vasospasm after 3 days post SAH onset.
- Correct any anticoagulation!
85
Discuss rebleeding prevention in the setting of SAH:
- 85% of SAH are aneurysms. A clot will form, but if rebleeding occurs, it is usually lethal.
- Maintain SBP < 140
- Use labetalol infusion proactively.
- 60mg Nimodipine q. H4
- Statins
- MgSO4
86
Discuss seizure prophylaxis in the setting of SAH:
-Only provide anticonvulsant therapy if there is visible tonic-clonic activity.
87
What arrhythmias are common in the setting of SAH?
- SAH prolongs QTc for some reason or another. Therefore, it can produce Torsades de Pointes
- Keep Mg++ levels greater than 1.0.
- Give 5g infusion of Mg2+ over 20 minutes. Added benefits include smooth muscle relaxation and increased seizure threshold.
- Also monitor K+.
88
How does hydrocephalus form in the setting of SAH?
Blood forms in the lateral ventricles and coagulates above the channel to the third ventricle. CSF is still being produced, but it can't go anywhere so ventricles swell and expand. This will increase ICP and possibly even cause uncal herniation.
89
Cardiogenic shock in the setting of SAH? Say whaaaat?!
-SAH irritates the brain and interferes with neuronal activity. This sometimes causes a catecholamine storm. The distal blood vessels (apical) in the heart are small, watershed vessels most affected by alpha agonism. Blood flow declines, stuns the LV apex and a Taketsubo cardiomyopathy forms. I know, fucked, right?!
90
Okay, we talked about Taketsubo in SAH, now you're telling me Na+ levels can go screwy too!! Explain yo'self! Tell me about cerebral salt wasting (CSW).
-Hypothalamus irritation can spit out a bunch of atrial naturetic peptide (ANP). ANP causes Na+ and H2O to be dumped out of the kidney's collecting tubules causing polyuria and hyponatremia. Treat with fluid resuscitation, HTS 3%, mineralcorticoids.
91
What about syndrome of inappropriate ADH (SIADH)? How is that connected to SAH?
Hypothalamus irritation causes ADH secretion. ADH causes H2O to be pulled out of the collecting tubule causing hypervolemia and a relative hyponatremia. Indicated by lack of urine output and low serum Na+ levels in SAH.
Treat with HTS 3%.
92
Whoa, whoa, whoa! SAH can cause hyponatremia through SIADH or CSW... Now you say it can cause hypernatremia as well?! GFY!
- Diabetes Insipidus
- ADH production stops completely causing kidneys to flush super dilute urine out of the collecting ducts. Massive polyuria with low urine osmolarity. Serum Na+ rises instead.
- Tx with DDAVP or vasopressin and replace urine output with a 1:1 ratio.
93
Is vasospasm a problem with SAH?
| Hint: yes, it is
- Bleeding on outside of vessel walls breaks down into heme. Heme scavenges NO so vessels constrict. This reduces CBF and increases CPP, resulting in increased risk of re-bleeding.
- Treat prophylactically with Nimodipine and statins. Consider milrionone for its cerebral vasodilative properties. Eurovolemia, hemodilution, electrolyte correction and augmented BP to keep MAP > 90 are also recommended.
- It's generally not a problem until day 3 post SAH and is worst between day 8-11.
94
When transporting a patient with an EVD, what are some considerations?
- If transporting open, discuss pitch of aircraft with pilots. It will effect levelling of EVD and drainage. Helicopters usually fly 5 degrees nose down.
- Make diagram of what each position of the valve does so you're not relying on memory when you need to shut it off.
- Make sure it is leveled to tragus of ear.
- Check height of EVD vs height of aircraft door. Use thin mattress.
- Shut it off for unloading and loading since the pt won't be level.
- Use whole runway for take-off. Avoid turbulence.
- Monitor exit site. Do not let that thing pop out of the skull!
95
Define 1. status epileticus (SE), 2. refractory status epileticus (RSE) and 3. super refractory status epileticus (SRSE):
1. SE is a continuous seizure for > 5 min, or multiple seizures with no return to baseline.
2. SE that is refractory to 1 x AED and 1 x IV agent.
3. SE that is refractory to 1 x AED and 2 x IV agents.
96
Causes of seizures (DIMS)
Drugs: Withdrawal from benzos/EtOH/AEDs, stimulants, antipsychotics, TCAs, wellbutrin.
Infection: Meningitis, encephalitis
Metabolic: Hyponatremia, hypoglycaemia, hypomagnesia, liver failure, kidney failure, eclampsia.
Structural: Hemorrhages, CA
97
First, second, third line and other treatments for status epileticus:
1.) 0.1-0.2mg/kg midazolam with 20mg/kg of phenytoin or kepra 500-1000mg PO. Phenytoin contraindicated in tox.
...wait 5 min
2.) Propofol infusion at 10-80mcg/kg/min or midazolam infusion at 10mg/hr.
...wait 5 min
3.) Ketamine (1-2mg/kg) or barbiturates
Other: 5g of Mg++, verapamil
Paralyze patient if you have. You stop the physical seizure but the brain is still getting fucked up.
98
In status epileticus, what happens to GABA receptors with repeated dosing of GABA agonists?
They get saturated and down regulate themselves into the cell.
NMDA receptors don't have the same property, hence ketamine can be considered as a third line agent for status epileticus.
99
Locate the major motor fibres and their spinal roots in the upper spinal cord:
```
C5 - Deltoids (patient can lift arms)
C6 - Biceps
C7 - Triceps
C8 - Hands
T1 - Finger splaying
```
100
List the major motor fibres and their spinal roots in the lower spinal cord:
```
L4: Knee extension
L5: Dorsi-Flexion of the foot
S1: Plantar Flexion
S2: Hamstring
S2-4: Genitals, rectal tone
```
101
ASIA Scoring:
A: vertebral #, no sensory/motor/anal tone
B: vertebral #, preserved sensation, anal tone in tact
C: vertebral #, abnormal sensation, weak motor
D: vertebral #, abnormal sensation, preserved motor
E: vertebral damage, no neurological deficits
102
Which ASIA scores must be transported to VGH?
A, B, C and D
| Not E
103
Rule of thumb... What level of C-spine injury do you intubate?
C5, and above. If the patient can't use their biceps, they get plastic. Bi's to fly!
104
What spinal roots provide sympathetic innervation of the heart?
T1-T5. Any injury above this site will leave the heart exposed to parasympathetic innervation only. That means no beta agonism (inotropy, chronotropy) and no alpha agonism (vessel dilation and loss of preload)
105
Treatment for neurogenic shock:
- Put at least 2L of crystalloid to make up for the vessel dilation in the legs.
- First agent is dopamine, second is levophed. Avoid phenylephrine since it constricts carotids, stimulates baroreceptors and leads to more unopposed parasympathetic activity (bradycardia).
- Low g-force take off.
- Target MAP to > 85
106
What is Guillain-Barre Syndrome?
-A preceding infection creates antibodies that go onto attack neurons. They attack long fibres first, hence initial symptoms are parethesias in the toes/fingers. As the antibodies chew through the myelin sheaths, paresthesias turn into paralysis and symptoms creep centrally. When respiratory muscles are affected, it can create type II respiratory failure.
107
Hallmark features of GBS:
- Ascending paresthesia/paralysis
- Blunted reflexes
- History of infection
- Autonomic swings
108
At what point would you consider intubating a neuromuscular disease?
- Tachypnea with a normal/high PaCO2 = shallow tidal volume
- Vital capacity < 20mL/kg IBW
- Significant accessory muscle use
- Significant oropharyngeal secretions
109
What is myasthenia gravis?
Thymus starts making random ACh antibodies that interfere with synaptic cleft transmission at muscular fibres. Nerves remain intact so no paresthesia, just muscle weakness.
110
When treating a patient with a history of mysthenia gravis, what is one important consideration?
There are a ton of drugs that trigger and/or worsen a myasthenia crisis!
111
Embolic CVAs form in one of two ways. Where are they?
- Carotid atherosclerosis
- Cardioembolic (AF, PFO, veg, atrial myxoma, transmural apical MI involving the LAD with an EF < 20% that forms 2/52 post STEMI)
112
Timeframe for thombolysis and mechanical thrombecotmy post symptom onset:
tPa: 4.5 hours
Thrombecotmy: 6 hours
*Neurologist must assess CT if patient woke up with symptoms.
113
SBP goals for patients with ischemic CVA:
Thrombolysis attempted: SBP < 180
| No tPa: SBP < 220
114
Treatment for ischemic CVA:
Lay patient supine (can increase collateral CBF by 10%)
Provide 1L of N/S
Increase PaO2 100mmHg
115
What is the trifecta of bacterial meningitis symptoms?
Fever
Neuro symptoms (DLOC/headache/photophobia/seizure)
Nuchal rigidity
116
Are the four agents (strep pneumo., H. flu, neisseria meningiditis, listeria) that cause bacterial meningitis airborne or droplet spread?
Mostly airborne. Don't take any chances. Wear PPE and warn the pilots. Tape down HME filters and clamp the tube.
117
What is encephalitis?
Inflammation of the brain parenchyma. Caused by numerous agents. HSV is an agent we can treat for (acyclovir 10mg/kg).
Symptoms include personality changes, DLOC and seizures.
Airborne infection so wear PPE, warn pilots and clamp tube/filters.
118
What conditions can cause bilateral pinpoint pupils?
Opioid overdose
Pons bleed
Cholinergic overdose
119
Signs of increased ICP:
- Basal cistern effacement is often the first sign
(1. Intrapenduncular cistern 2. quadrigeminal cistern 3. prepontine cistern 4. fourth ventricle)
- Loss of sulci (grey/white) differentation
- Midline shift > 5mm (observe pineal gland)
- Ventricle collapse
- ONSD > 5mm
- Ipsilateral blown pupil, contralateral deficits, posturing, Cushing's
- Grainy, poorly contrasted CT is a sign of possible brain death.
120
Common complications of aneurysmal SAH:
- Rebleeding
- Vasospasm
- Cerebral ischemia
- Obstructive hydrocephalus and increased ICP
- Seizures
- Cardiac complications
- Electrolyte imbalances
- Non cardiogenic pulmonary edema
121
Is a MAP goal of 65 good enough when treating patients with elevated ICP?
No. Remember that CPP = MAP - ICP.
CPPs > 70 mmHg are often required to prevent cerebral infarction in the setting of elevated ICP.
122
Rebleeding treatment consideration for aneurysmal SAH patients with a delayed time to definitive care:
TXA
123
You're transporting an aneurysmal SAH for clipping/coiling when all of a sudden, they deteriorate. Do you hit them with triple H therapy (hypertension, hyperemia, hemodilution)?
No. Triple H therapy for vasospasm can only be initiated once the aneurysm has been occluded.
124
What's the new triple H therapy for aneurysmal SAH vasospasm?
- Modest hemodilution
- Induced HTN (phenyl, levophed, dopamine -> dobutamine)
- Euvolemia
125
In the setting of transporting an unsecured SAH aneurysm, how do you tell the difference between vasospasm and rebleeding in a sedated patient?
You don't. Vasospasm is unlikely to occur in < 72 hours, but regardless, re-bleeding is way worse and should be treated as such until proven otherwise. Keep SBP < 140. Avoid triple H therapy.
126
Doses for HTS and Mannitol:
```
HTS:
-Elevated ICP: 3cc/kg
-Herniation: 5cc/kg
Mannitol
-Elevated ICP: 0.25-0.5g/kg
-Herniation: 1g/kg
```
127
In TBI, what's worse and why? Hypotension caused by propofol infusion or just hypotension?
Just hypotension. Propofol lowers cerebral metabolism so ischemia is better tolerated.
128
State some factors that go into deciding whether to use HTS3 or mannitol:
HTS is often the agent of choice. It's a volume expander so it works well in polytrauma. Mannitol could be used as a frontline agent if it's an isolated TBI, especially in the setting of acidosis < 7.20.
* Nothing else can run in with HTS.
* Mannitol requires a filter set.
129
BP goals for unsecured aneurysmal SAH:
SBP < 140
130
BP goals for ischemic CVA:
Pre/post lysis: SBP < 180
| No lysis: SBP < 220
131
BP goals for hemorrhagic CVA:
Awake, follows commands: SBP < 140
| Comatose: SBP < 180, MAP > 80
132
5 herniation syndromes
- External/transcranial
- Uncal
- Tonsilar (2 x pinpoint/DLOC)
- Central (2 x pinpoint/DLOC)
- Subfalcine
133
Possible complications of prophylactic HTS-3:
- Neurons rapidly adapt to increased tonicity.
- Once sodium starts to decline, patients are at risk for rebound edema.
- May cause volume overload, pulmonary edema, AKI and/or hyperchloremic metabolic acidosis.
134
Discuss ctyotoxic edema:
- Often the result of global hypoxia
- Loss of oxygen to the cell reduces ATP production.
- Ion pumps that rely on ATP fail, specifically Na+ builds up in cell.
- Water follows Na+ into cell and causes edema and cellular dysfunction.
- Often shows up as a fuzzy or grainy CT image.
135
Discuss vasogenic edema:
- Often, there's been an insult to the blood vessel that initiates the inflammatory cascade.
- Vessel walls become more permeable and leak oncotic agents into interstitium. Compresses cellular parenchyma and causes dysfunction.
- Often shows up as hypoechoic substance surrounding a lesion on CT.
136
Treatment considerations when you see cytotoxic vs vasogenic edema on head CT:
-Cytoxic edema is best resolved by improving CBF (PaO2, osmolar therapy, PaCO2) while vasogenic edema is best resolved by reducing contents seeping out of the vasculature (SBP < 140).
137
Key signs of cauda equina syndrome:
- Saddle paralysis
- Fecal incontinence
- Urinary bladder retention
- Bilateral leg weakness
138
How do you test the corneal reflex and what does it test?
-Brush a piece of soft, clean tissue against the patient's iris (not sclera). It tests CN V (sensation) and CN VII (motor response).
139
Meningitis, by itself, doesn't cause DLOC. What is it called when it does, and how do you assess for it?
- Meningoenephalitis
- Nuchal rigidity still occurs, as long as they're not on NBRAs
- Assess for fever and perform an LP
* LP with elevated neutrophils and low glucose = bacterial
* LP with elevated lymphocytes = viral
* Pupura = Neisseria
140
Meningitis treatment:
- Ceftriaxone 2g b.i.d.
- Vancomycin 20mg/kg bolus, then 1g b.i.d.
* Ampicillin 2g q. 4h if immunocompromised
* Meropenem 2g t.i.d. + Vancomycin if PCN Ax
Dexamethasone
141
A common complication of TBI is DI. What drug and dose can you administer when U/O reaches > 300ml/hr?
0.03u/min of Vasopressin
Caution: Your Na+ levels are going to be fucking screwy!!
Also consider DDAVP
142
Hypertension often occurs transiently in TBI. If you give labetalol or hydralazine, those drugs can stay in the system long after the patient starts to crash and then those hypotensive agents are detrimental. This is an easy one. What can you use to bring the BP down instead?
Propofol. Just higher doses than you're using for your RASS goal.
143
Differentiate between CSW, SIADH and DI:
- CSW: Hyponatremia, increased UO, Tx HTS/Fluticasone
- SIADH: Hyponatremia, decreased UO, Tx HTS
- DI: Hypernatremia, increased UO/osmolarity, increased Cr, Tx DDAVP (high BP) or vasopressin (low BP)
144
When transporting an elevated ICP patient, what's one value that needs to be correlated before you transport?
Delta CO2 at time of ABG
CO2 has such a rapid and heavy effect on ICP, it must be targeted appropriately!
145
Spikes in ICP during transport are most often contributed to...
Changes in PaCO2
Also, temperature.
Not so much with sedation levels.
146
What atypical agent could be considered for combative head injuries that will likely have limited effects on hemodynamics?
Haldol
147
When targeting ICP reduction, what three compartments of the Monro-Kellie doctrine must you look at, and therapies for each?
1. Parenchyma (HTS, mannitol)
2. Blood (PaCO2, BP, HOB30, collars/ties, OG, PEEP < 12, temperature, sedation)
3. CSF (EVD)
148
Calculate CPP
CPP = MAP - ICP
If ICP climbs, then increases in MAP are the only way to maintain CPP > 70.
149
Hunt and Hess a MoFo!
1. Asymptomatic, or minor H/A or nuchal rigidity.
2. Moderate to severe H/A, nuchal rigidity, no deficits but CN palsies are possible.
3. Drowsiness/stupor, mild focal deficit.
4. Stupor, moderate-severe hemiparesis.
5. Coma, decerbate posturing.
158
What's the equation for CBrDO2?
CBrDO2 = CBF x CaO2
```
CBF = CPP - CVR
(CPP = MAP - ICP)
```
CaO2 = (Hgb x 1.34 x SaO2) + (PaO2 x 0.003)
159
IBCC approach to status epilepticus:
- ABCs (give O2)
- 0.1mg/kg Ativan IV
- Check Na+ and BG
- Kepra or Dilantin (for non-tox)
- Intubate using both ketamine and Propofol with a half dose of Roc.
- High dose propofol infusion (50-200mcg/kg/min)
Be aggressive. GABA receptors internalize after a few minutes of seizure activity so be aggressive with benzos.
160
Are benzos effective for status epilepticus management later in the seizure?
No. As the seizure progresses, GABA receptors get internalized into the cell. Hit them early in the seizure with 0.1mg/kg ativan or midazolam and then move to agents like ketamine. Between ketamine (NMDA) and benzos (GABA), you really soak the brain with cerebral depressants.
