Exam IV: Neuro Diseases Flashcards
CEREBRAL BLOOD FLOW(CBF):
*autoregulated—normally
*___mL/100g brain tissue when CPP ___-___ mmHG
*is about 750 ml/min (___-___% of cardiac output)
50
50-150
15-20%
CBF governed by:
Cerebral metabolic rate-CMRO2
Cerebral Perfusion Pressure-CPP
PaCo2 and O2 tension
Various medications
Intracranial abnormalities
Cerebral Metabolic Rate-CMR
Rate of O2 consumption-3.0-3.8mL O2/100 g brain tissue/min and consumes ____% of total body oxygen
20
Cerebral Metabolic Rate-CMR
Most used to generate ATP for ____ ____ activity
neuronal electrical
Cerebral Metabolic Rate-CMR
*High ____ _____ + low ____ _____ = unconsciousness in 10 sec if perfusion stopped
*If not restored in ___-___ min leads to ATP stores depleted causing cellular injury/death
O2 consumption
O2 reserve
3-8
Cerebral Metabolic Rate-CMR
Decreased by _____ temps, anesth agents
Increased by _____ temps, seizures
lower
higher
CPP =
MAP - ICP (or CVP, whichever is greater)
CPP is normally ___-___ mmHg
60-110
if ICP increases, MAP must _____ to maintain CPP
increase
if MAP falls below 60 mmHg, CPP _______________
cant be maintained
Even with normal MAP, if ICP is ______, CPP (thus CBF) can change
> 30
CPP less than 50 mmHg shows
slowing on EEG
CPP 25-50 mmHg shows
flat EEG
CPP less than 25 mmHg leads to
possible irreversible brain damage
Autoregulation b/t 50-150 mmHG (pressure dep beyond this)
Arterial constriction with ______ BP
Arterial dilation with ______ BP
increased
decreased
Normotensive, if CBF…
___mmHg - ischemia (nausea, dizziness)
___mmHG - vessels max constricted; fluid forced out of vessel causing cerebral edema
35
150
Hypertensive
Autoregulation curve shifted _____
Chronic HTN-lower limit shift _____
right
upward
Auto regulation lost or impaired with:
- intracranial tumors
- vessels around tumor are acidotic
- maximally dilated, now all pressure dependent
- head trauma
- volatile anesthetics
_____ is the most important extrinsic factor
PaCO2
change the PaCO2, change CBF, they are _____ _____
directly proportional
CBF changes approx ___-___ ml/100 g/min per mmHg change in PaCO2.
The change is _____
1-2
immediate
Thought to be b/c of changes in ____ of ____ around walls of arterioles, all compensated after ____-____ hours of hypo or hypercapnia
pH of CSF
24-48
Marked hyerventilation - PaCo2 < 20 shifts the curve to the ____, may have ____ changes
left
EEG
“The ability of hypocapnia to acutely decrease ____, ____, and _____ is fundamental to the practice of clinical neuroanesthesia.”
CBF, CBV, and ICP
CBF not significantly effected by decrease in PaCo2—–until threshold of ____
Below threshold, +cerebral vasodilation and CBF increase; +hyper_____ and +hypo_____ have synergistic effects
50
hypercarbia
hypoxemia
Hypocapnia= ____ _____ with RISKS
FINE LINE
Hypocapnia may be ____ ____ during craniotomy
Impact with TBI or intracranial hemorrhage ____
well tolerated
unclear
CBF changes ___-___% per 1°C
5-7
Hypothermia - decreases ____ & ____
CMR and CBF
Hyperthermia - increases _____ & _____
CMR and CBF
Lower Hct _____ viscosity, but also _____ O2 carrying capacity
decreases
decreases
Increased Hct increases viscosity, decreases _____
CBF
Studies suggest optimal Hct for cerebral O2 delivery = ___%
30
Blood Brain Barrier
unique vessels with junctions between endothelial cells that are nearly _____
fused
BBB is a _____ barrier for brain
lipid
lipid soluble (CO2, O2, H2O, and most anesthetics) move across BBB _____
easily
ionized/large molecular weight have _____ movement across BBB
restricted
BBB is disrupted by:
- severe HTN
- strokes
- trauma
- tumors
- infection
- hypercapnia
- hypoxia
- sustained seizures
(fluid movement now dependent on hydrostatic pressure not osmotic gradient)
CSF major fxn:
protect CNS against trauma
CSF formed by ____ _____ of cerebral ventricles (mostly _____)
choroid plexuses
lateral
CSF produced 2 ways
- ultrafiltration and secretion by the cells of the choroid plexus
- passage of water, electrolytes, and other things across the BBB
- CSF is produced by the ____ ____ in the ventricles
choroid plexuses
- CSF is produced by the choroid plexus in the ventricles
- CSF flows through the _____ _____ from the 3rd to the 4th ventricle
cerebral aqueduct
- CSF is produced by the choroid plexus in the ventricles
- CSF flows through the cerebral aqueduct from the 3rd to the 4th ventricle
- CSF flows into the subarachnoid space by the _____ and _____ _____ also into the spinal canal
lateral and medial aperatures
- CSF is produced by the choroid plexus in the ventricles
- CSF flows through the cerebral aqueduct from the 3rd to the 4th ventricle
- CSF flows into the subarachnoid space by the lateral and medial apertures also into the spinal canal
- CSF removes _____ and provides _____ from within subarachnoid space
waste
bouyancy
- CSF is produced by the choroid plexus in the ventricles
- CSF flows through the cerebral aqueduct from the 3rd to the 4th ventricle
- CSF flows into the subarachnoid space by the lateral and medial apertures also into the spinal canal
- CSF removes waste and provides buoyancy from within subarachnoid space
- Excess CSF will be ______ by the _____ ____ which will drain in tho the ____ _____ sinus
absorbed
arachnoid villi
superior sagittal
Adults: produce ___ mL/hr (500 ml/d) ____ mL is total CSF volume
21
150
LATERAL VENTRICLES
Intraventricular foramina of Monro
3rd Ventricle
Cerebral aqueduct of Sylvius
4th Ventricle
Foramen of Magendie &
Foramina of Luschka
Cisterna Magna
Subarachnoid space
Circulates around the brain & spinal cord
Absorbed into arachnoid granulations
cranial vault is _____
rigid
vault is made up of 3 things
brain - 80%
blood - 12%
CSF - 8%
if one thing in the cranial vault increases, another must ________
decrease
ICP usually ____ mmHg or less - measured in the ____ ventricles or over the cerebral _____
10
lateral
cortex
Monro-Kellie Doctrine:
Any increase in one compartment must be offset by an equal reduction in another to avoid increases in ICP
ICP reduction mechanisms:
- increased CSF absorption
- decreased CSF production
- decrease in total CBV (mostly venous)
- brain stem herniation
normal ICP
5-10 mmHg
mild increase in ICP
20-30 mmHg
moderate increase in ICP
30-40 mmHg
severe increase in ICP
> 40 mmHg
CBV increases ___ ml/100 g of brain per 1 mmHg ↑ PaCo2
.05
Blood pressure effects of CBV dependent on _______ of ______
autoregulation of CBF
if increase in ICP is sustained, can lead to ______
herniation
4 types of herniation
- cingulate gyrus under the falx cerebri (subfalcine herniation)
- uncinate gyrus through the tentorium cerebelli (transtentorial herniation)
- cerebellar tonsils through the foramen magnum
- transcalvarial - any area beneath a defect in the skull
subfalcine herniation leads to compression of anterior cerebral artery causing a _____ ____
midline shift
______ brainstem compression leads to altered consciousness, gaze defects, ocular reflex defect, hemodynamic and resp failure and then _____
transtentorial
death
*If _____ herniation (medial portion of temporal lobe), oculomotor nerve dysfun
uncal
S&S - pupil ______, ptosis, lat deviation of _____ eye and then death
dilatation
affected
S&S - indicates ______ dysfunction—cardio and resp dysfunction and leading to death
medullary
ICP
HA, nausea, vomiting, pupillary dilation, blurred vision (CNII)a, inability to adduct (____) or abduct (____)eye
Focal neurological deficits and unsteady gait
Decreased consciousness, seizures, coma
Cushing’s Triad: irregular _____, _____, _____
CNIII
CNVI
respiration, ↑ BP,↓HR
ICP Dx:
symptoms, CT or MRI, or direct measurement
_______ - helpful to measure, removal of CSF, and CSF sent to lab for analysis
Ventriculostomy
mean ICP should remain below _____
15 mmHg
dramatic increase in ICP leads to ______ and ______ change
hyperventilation and LOC
causes of increased ICP
- Tumor -Due to size, Indirectly b/c of edema in surrounding tissue, Causing obstruction of CSF flow out (tumor in 3rd vent)
- Intracranial hematomas (a lot like tumor)
- Blood in CSF (subarachnoid hemorrhage)
- Infection (meningitis, encephalitis)
- Aqueductal stenosis - congenital narrowing of cerebral aqueduct connecting 3rd and 4th ventricles
- Sz disorder seen in 1/3 of these patients
Decreasing ICP
elevate HOB ___-___ degrees above heart
15-30
Decreasing ICP
head neutral if possible, dont compress _____
jugulars
Decreasing ICP
hyperventilation - maintain PaCO2 ___-____ mmHg, effects diminish in 6-12 hours, rebound increases in ICP can be problematic
30-35
Decreasing ICP
drain _____
CSF
Decreasing ICP
hypo_____
thermia
Decreasing ICP
______ drugs - avoid sig hypovolemia, Mannitol 20% 0.25gm/kg, IV
hyperosmotic
Decreasing ICP
c_______
corticosteroids
Decreasing ICP
cerebral vasoconstrictors - ______, _____
barbs, prop
Decreasing ICP
HTN control - ______, _______, keep MAP _____
labetalol, nicardipine
> 70
Seizure Disorder
Abnormal _____ _____ activity in the brain
___% of population experience seizure in lifetime
Epilepsy-true disorder; recurrent seizures
synchronized electrical
2
underlying mechanisms for seizure disorder: (3)
Loss of inhibitory activity
Enhanced release of excitatory amino acids
Enhanced neuronal firing due to voltage mediated Ca+ current
precipitants to seizures:
- Genetic predisposition (low sz threshold)
- Brain trauma or tumor
- Infection/febrile illness
- Hypoxia
- Drug overdose or withdrawal
- Fatigue/stress
- Methohexital (small doses)
- Ketamine
- Demerol
- Metabolic defects (Na+, hypo: mag, Ca+, or glycemia, alkalosis)
_____ –also called _____
Manifested by motor, sensory, autonomic or psych symptoms
Complex sz - impairment of consciousness
PARTIAL
Focal
GENERALIZED
______ ______ electrical activity—no local onset
May or may NOT have abnormal _____ activity, loss of consciousness, etc
Bilaterally symmetric
motor
Petit Mal - (absence sz) -
transient lapse in consciousness
Grand Mal - (tonic clonic) - ______ common, loss of consciousness followed by clonic and tonic motor activity
most
STATUS EPLEPTICUS: prolonged partial or general sz ______ recovery between attacks; _______ _______
without
MEDICAL EMERGENCY
Seizure Disorder Management
PreOp eval-focus on ____, ____ of sz, and medications
cause, type
Seizure Disorder Management
antiepileptic drugs - ______ ______
Antiepileptic drugs-continue throughout
Seizure Disorder Management
Even partial sz can progress to generalized - major risks assoc with _____, ______, ______
injury, aspiration, hypoxemia
Seizure Disorder Management
PRIORITIES
airway and oxygenation
Seizure Disorder Management
AVOID
- ketamine
- methohexital
- demerol
- atra/cisatracurium (in large doses d/t metabolites)
Seizure Disorder Management
expect hepatic enzyme ______, probably will _____ dose of NMB
induction
increase
Seizure Disorder Management
terminate seizure with:
propofol 50 - 100 mg
dilantin 500 - 1000 mg slowly
benzos - midazolam - 1 - 5 mg
Most common disorder involving motor tracts of extrapyramidal system (controlled by basal ganglia and cerebellum)
parkinsons disease (PD)
PD affects 3% of _____ _____
elderly americans
primary PD
degenerative disorder of substantia nigra; interferes with dopamine pathways to basal ganglia
primary PD onset
after 50
primary PD etiology
unknown
PD hereditary pattern
none
secondary PD
d/t trauma, drugs, infection, toxins (usually reversible)
Parkinson’s Disease-PD
Principle feature: degeneration of ________ pathways (inhibitory) and relative excess of ________ activity (excitatory)
dopaminergic
cholinergic
Parkinson’s Disease-PD
classic signs (cogwheel rigidity)
- ____ _____ tremor - rhythmic, usually at rest, usually disappear with voluntary movement; pill rolling tremor
- _______—1st appears in neck muscles; arm swinging, infrequent blinking
- _______ of facial muscles
- Often oily skin, seborrhea, diaphragmatic spasms, dementia and depression
- Eventually includes muscles of ______ and _____
- Upper airway involvement may _____ airflow
Skeletal muscle
Rigidity
Akinesia
chewing and swallowing
restrict
Tx of PD
Goal is to ↑concentration of ______ in basal ganglia OR to decrease effects of _____
dopamine
ACh
Tx of PD
_______-_______ precursor (Sinemet, Parcopa) - assoc with dyskinesias, confusion, HA, hallucinations
Levodopa-dopamine
Tx of PD
increase myocardial _______
contractility
Tx of PD
_______ hypotension
orthostatic
Tx of PD
Decarboxylase inhibitor - prevents conversion of levodopa to dopamine in _____ to optimize conversion in _____ (Duopa)
periphery
CNS
Tx of PD
anti______
anticholinergics
Surgical Tx of PD
Deep brain stimulation- stimulates various nuclei in _____ ______ to relieve/help with tremor
basal ganglia
Surgical Tx of PD
______ - rigid head frame, MRI, burr hole, electrode advanced
AWAKE
Surgical Tx of PD
______ position (risk of air embolism)
sitting
Surgical Tx of PD
opioids (sparingly) and _______ BEST; diphenhydramine
dexmedetomidine
Surgical Tx of PD
avoid ____ and ____ bc alter recordings of nuclei thus stimulation of appropriate place
propofol and benzos
Surgical Tx of PD
avoid over_____
oversedation
Anesthetic Implications-PD
_____ PD meds perioperatively
continue
Anesthetic Implications-PD
response to NDMR
generally normal
Anesthetic Implications-PD
rare reports of increased ____ with SCh
potassium
Anesthetic Implications-PD
avoid ketamine - _____ response
SNS
Anesthetic Implications-PD
Predisposed to rigidity related to ______
opioids
Anesthetic Implications-PD
avoid dopamine antagonists such as:
- metoclopramide
- phenothiazines (compazine, thorazine)
- butyrophenones (haldol, droperidol)
Most common neurodegenerative dz responsible for 40-80% dementia cases
Alzheimer’s Dz
Alzheimer’s Dz
cause:
unknown
Alzheimer’s Dz
characterized by ____ ____ in intellectual function (____ years). Memory, judgement, decision making, emotional lability.
slow decline
5+
Alzheimer’s Dz
late signs
EPS, apraxias, aphasia
Alzheimer’s Dz
marked _____ atrophy with _____ enlargement
corticol
ventricular
Alzheimer’s Dz
_____ response to many of our drugs along with loss of ____ matter
altered
gray
AD Pathophysiology
Proteins in the neurons become twisted and distorted “_______ triangle”
neurofibrillary
AD Pathophysiology
“Senile plaques” deposit. This disrupts impulse transmission…especially in the _____ ______ and ______
cerebral cortex and hippocampus
Anesthesia Considerations with AD are ________
COMPLICATED
Anesthesia Considerations with AD
New onset of temporary impairment frequent after anesthesia-lasts ___-___ days following
1-3
Anesthesia Considerations with AD
Consent—
must have from someone legally able to provide
Anesthesia Considerations with AD
Central anticholinergics (_____/_____) - add to confusion; use ______ (doesn’t cross BBB) if anticholinergic needed
atropine/scop
glycopyrrolate
Anesthesia Considerations with AD
Many studies have shown neuronal injury and cell death is related to _____ _____—much debate related to GA and elderly and pediatrics
anesthetic agents
Anesthesia Considerations with AD
bottom line
slow, gentle, careful
Anesthesia Considerations with AD
____ contraindications to regional or GA….but consider how you will provide anxiolysis and potential side effects
No
Reversible demyelination at random and multiple sites in the brain and spinal cord
Multiple Sclerosis
Multiple Sclerosis
Much inflammation which eventually causes _____ - gliosis
scarring
Multiple Sclerosis
_______ initiated by a virus??
autoimmune
MS - primarily affects females ___-___ years old 2:1
20-40
MS - unpredictable course of _____/______
attack/remission
MS - 50% require help with walking within ____ years of diagnosis
15
Considerations with MS
____ or ____ can confirm
CSF or MRI
Considerations with MS
remyelination is limited - ____ ____ ____
may not occur
Considerations with MS
Conduction ____ still occur across demyelinated axons, but affected by many things—including _____
CAN
temperature
Considerations with MS
Tx-focused on tx symptoms and stopping disease process
Effect of sx is _____
_____ _____ procedures during exacerbation
unpredictable
NO elective
Considerations with MS
Peripheral nerve blocks ____ - MS is CNS disorder
ok
Considerations with MS
____ _____ problems with GA
no specific
Considerations with MS
if paresis or paralysis - NO ____
sux
Considerations with MS
symptoms may _____ perioperatively - ASSESS
worsen
Neurodegenerative, rapidly progressive of both upper and lower motor neurons
ALS-Amyotrophic Lateral Sclerosis(Lou Gehrig’s Dz)
ALS-Amyotrophic Lateral Sclerosis(Lou Gehrig’s Dz)
No specific known cause—some have ____ _____
Usually present in ____ or _____—muscular weakness, atrophy, fasciculation, spasticity
__-__ years—progresses to all skeletal muscles and vent failure
gene deformity
50’s or 60’s
2-3
ALS-Amyotrophic Lateral Sclerosis(Lou Gehrig’s Dz)
susceptible to _____
anesthesia focus - ____ ____
aspiration
resp care
ALS-Amyotrophic Lateral Sclerosis(Lou Gehrig’s Dz)
no _____ bc of hyperkalemia risk
anectine
Guillain –Barre’ Syndrome
Affects 1-4/100,000
____ onset—paralysis, areflexia, paresthesias
____ _____ paralysis is common
Sudden
Respiratory muscle
Guillain –Barre’ Syndrome
Seems to be immunologic rx against ____ _____ of _____ nerves
Weakness or paralysis starts in the ____ and spreads cephalad over several days
myelin sheath of peripheral
legs
Guillain –Barre’ Syndrome
multiple types (3)
Acute inflammatory dymelinating polyneuropathy-75%
Acute motor axonal neuropathy
Acute motor AND sensory axonal neuropathy
GBS
Peak disability ___-___ days, recovery in weeks to months
Usually follows URI or GI infections
Associated with _____ dz
10-14
Hodgkin’s
GBS
Complication of ____
Some respond to ______
Prognosis is good—although 10% die of complications and 10% have lifelong comps
HIV
plasmapheresis
GBS
ANS is labile +resp insufficiency
No ____
Regional anesthesia is _____
anectine
controversial
GBS Clinical Manifestations
Resp paralysis - 25% require _____ _____
mechanical ventilation
GBS Clinical Manifestations
Autonomic dysfunction is common:
Wide changes in BP
Profuse diaphoresis
Gastroparesis
Tachycardia
Dysrhythmias
GBS Clinical Manifestations
Bulbar involvement-45-75%
_____ _____ weakness
pharyngeal muscle
GBS-Anesthesia Implications
Prepare for and anticipate dysrhythmias and autonomic instability
Hypotension with position change or small blood loss
Exaggerated HTN with laryngoscopy
Anectine is contraindicated
Possible post op ventilation
Regional anesthesia is controversial
Cerebral Vascular Accident (CVA)
Cerebral perfusion is interrupted, depriving brain of ____ and _____
O2 and glucose
Cerebral Vascular Accident (CVA)
creates cycle - cell hypoxia causes edema, edema causes activation of _____ _____ acids, that creates free radicals causing an influx of _____
excitatory amino acids
Ca++
Perioperative Stroke
Overall risk with GA < ____
Risk with GA + hx of CVDz= _____
Mortality rate after intraoperative stroke- ____
.4%
.4-3%
25%
Most common surgery related to CVA (2)
Open heart procedure for valve disease
Surgery on the thoracic aorta
risk factors for CVA
- HTN
- Diabetes
- Cigarette smoking
- Drug abuse
- Age >75
- CADz
- Hyperlipidemia
- Atrial fib
- Heredity
PRIOR STROKE OR Hx of TIA
classification of CVA - _____ or _____
hemorrhagic or ischemic
ischemic CVAs (3)
- thrombotic
- embolic
- global hypoperfusion
CVA-Hemorrhagic
Most common cause is ____ (60-80%)
Other causes: ruptured aneurysm, AV malformation, bleeding into tumor, coag defect
____ usually associated with this type of stroke
HTN
HA
CVA-Thrombotic
Arterial occlusion caused by thrombi in _____ or _____ vessels
Assoc with: atherosclerosis, diabetes, hypercoags, dehydration, arteritis, polycythemia vera, hypertension
Typically evolves over _____ to ____s
carotid or cerebral
minutes to hours
CVA-Embolic
Fragments break from thrombi formed ______ the brain
Associated with atrial fib, endocarditis, valve prosthesis, carotid dz, valvular and aortic surgery
Less common: ____, _____, or _____ emboli
Often lodge in the ____ ____ ____
outside
air, fat, or tumor
middle cerebral artery (MCA)
Thrombotic or Embolic Stroke
IV fibrinolytic tx within ___ ____ of onset of symptoms
3 hours
Thrombotic or Embolic Stroke
Do NOT give ____, ____, or ____ until CAT scan has ruled out an intracranial hemorrhage
ASA, heparin, or tPA
Thrombotic or Embolic Stroke
No fibrinolytic Rx: (4)
- Hx or evidence of bleed
- Known AVM, aneurysm, or neoplasm
- Platelet count <100,ooo or INR >1.7
- Stroke, neurosurgery, or head trauma within the past 3 months
CVA-Anesthetic Implications
____ ____ before discontinuing antiplatelet and anticoags before surgery
Neuro consult
CVA-Anesthetic Implications
Resistance to NMB in ____ ____
paretic limb
CVA-Anesthetic Implications
Monitor TOF in _____ _____
nonparetic limb
CVA-Anesthetic Implications
avoid ____
sux
CVA-Anesthetic Implications
____ may be safer for some procedures (Hip fx)
RA
CVA-Anesthetic Implications
Post CVA, area of infarct:
Loss of ______
Loss of ____ responsiveness
Loss of _____ integrity
autoregulation
CO2
BBB
CVA-Anesthetic Implications
Keep BP slightly higher than normal in the hypertensive patient
*____ ____ in autoreg curve
right shift
Cerebrovascular Dz
Typically have hx of ____ or _____
Risk of stroke ↑ with ____ and _____ of procedure
TIA or stroke
age and type
Cerebrovascular Dz
Asymptomatic ____ _____ —up to 4% in those <40
carotid bruits
Cerebrovascular Dz
Those at greatest risk :
open heart procedures with valvular dz, CADz with ascending aortic atherosclerosis, and diseases of thoracic aorta
Cerebrovascular Dz
All due to _____ (air, clots, debris)
embolism
Cerebrovascular Dz
Non cardiac surgery-risk assoc with _____/_____
hyper/hypotension
CVAs and HTN
- Hemorrhagic stroke due to intercerebral bleed
- Sustained HTN causes BBB breakdown
- Pulse pressures >80 mmHg leads to endothelial injury thus hypoperfusion or embolism
- Blood flow abnormalities-resolve in 2 weeks
- BBB and CO2 responsiveness-takes 4 weeks to heal
- Emergency: hemorrhage, cardiac sources emboli, symptomatic carotid dz
CVAs and HoTN
- watershed infarcts
CVA management
- Neuro and CV eval—no ____ _____ in those with TIA’s that haven’t been evaluated
- Most have comorbidities (HTN, renal dz, diabetes, hyperlipidemia, etc)
- Many on long term ______ or ______ ______
elective surgery
coumadin or antiplatelet therapy
may see CVA pts for:
- Removal of emboli
- CEA
- Endovascular procedures
- Hematoma evac
- Decompressive craniotomy
(Arterial line, have iv vasodilators and β blockers ready)
Spinal Cord Disorders
Numerous types: (5)
- Tumors
- Abscess
- Spinal stenosis
- Fractures (vertebral)
- Degenerative disc disease
SC disorders divided up into ____, _____, _____ and/or _____ issues
cervical, thoracic, lumbar, and/or sacral
Symptoms of SCD
Loss of _____
Weakness or paralysis of extremities
Reflex changes (_____ or _____)
Bladder or bowel incontinence
Back pain
______ spasms
sensation
hyper or hypo
Muscle
SCD - DX by:
DX by MRI/CT, Xray, myelogram
Causes of Spinal Cord Disorders
Trauma (fall, MVA, diving, trampoline, GSW, etc.)
Infection/abscess
Autoimmune disorders
SCD AIs:
- Airway-neutral intubation, possible obstruction/edema, recurrent laryngeal damage
- Positioning issues/injuries
- Cardiovascular issues: reflex bradycardia, arrhythmias, hyper and hypotension
- Respiratory issues-ventilation, ? Paralysis, need for post op ventilation
?pneumonia - Potential loss-blood and CSF
