Neuro (3) Flashcards
What modulated cerebral blood flow?
- Cerebral metabolic rate
- CPP
- PaCO2
- PaO2
- Various drugs/pathology
How is CPP calculated?
MAP-ICP
With autoregulation CBF is approx _____mL/____g brain tissue per minute
50mL/100g brain tissue per minutes
750mL/min
What percent of cardiac output makes up cerebral blood flow?
15%
What makes up the brain and spinal cord compartment?
*Neural tissue
*Blood
*CSF
What is the brain/SC compartment enclosed by?
Dura mater and bone
What is the combined volume of brain tissue, CSF, and intracranial blood?
1200-1500mL
When the intracranial volume is 1200-1500mL what is ICP maintained at?
5-15mmHg
What is the Monro-Kellie Hypothesis?
Any increase in one compartment of intracranial volume (tissue, CSF, blood) MUST be offset by a decrease in another component→ prevents elevated ICP
What happens to homeostatic mechanisms when ICP increases?
Homeostatic mechanisms increase MAP to maintain CPP
What happens if ICP is elevated and homeostatic mechanisms cant keep up to maintain CPP?
Cerebral ischemia occurs
The intracranial vault is considered _____________
Compartmentalized
___________ barriers separate the brain contents
Meningeal
What is the Falx cerebri?
A reflection of dura that separates the 2 cerebral hemispheres
What is the tentorium cerebelli?
Reflection of dura that is rostral to the cerebellum and separates supratentorial and infratentorial spaces
What are herniation syndromes categorized based on?
Region of the brain affected
Can there be increased ICP in just one area of the brain?
Yes, increases in contents of one are can cause regional increases in ICP
extreme cases the contents can herniate into different compartments
What is subfalcine herniation? What structures can be compressed?
Herniation of hemispheric against the flax cerebri
*often compressing branches of the anterior cerebral artery, creating a midline shift
What is transtentorial herniation? What structures are compressed?
Herniation of the supratentorial contents against the tentorium cerebelli
*causes brainstem compression in rostral to caudal direction
What are common S/S of transtentorial herniation?
*AMS
*Ocular reflex defects
*Hemodynamic/resp compromise
*Death
What is uncal herniation?
Subtype of transtentorial herniation wjere uncus herniates over the tentorium cerebelli
What is the uncus?
Medial portion of temporal lobe
What are S/S or uncal herniation?
- Ipsilateral oculomotor nerve dysfxn
- Pupil dilation
- Ptosis
- Lateral deviation of affected eye
- Brainstem compression
- Death
What can cause herniation of cerebellar tonsils? Where do the structures herniate through?
Elevated infratentorial pressure→causes cerebellar structures to herniate through foramen magnum
What are S/S of cerebellar tonsil herniation?
*Meduallary dysfxn
*Cardiorespiratory instability
*Death
Which number is subfalcine herniation?
1
Which number is transtentorial herniation?
2
Which number is cerebellar herniation?
3: Cerebellar contents through foramen magnum
Which number is showing herniation out of the cranial cavity? What can cause this?
4: Caused by trauma
What are causes of increased ICP?
*Tumors
*Intracranial hematomas
*Blood in CSF
*Infections
How do tumors lead to increased ICP?
*D/t size
*indirectly by causing edema in tissue
*obstructing CSF flow
Tumors involving the ____ ventricle commonly cause obstruction of CSF flow
3rd
How does blood in CSF cause increased ICP?
Seen with subarachnoid hemorrhage
*Obstruct CSF reabsorption
*granulation can exacerbate increased ICP
What specific infections commonly lead to increased ICP through development of edema or obstruction of CSF reabsorption?
*Meningitis
*Encephalitis
List methods to decreased ICP:
*Elevate head (encourage jugular venous outflow
*Hyperventilation (lower PaCO2)
*EVD (CSF drainage)
*Hyperosmotic drugs (draw fluid across BBB)
*Diuretics (systemic hypovolemia)
*Corticosteroids (↓ swelling, enhance BBB integrity)
*Propofol: Cerebral vasoconstrictor (↓CMRO/CBF)
*Surgical decompression
What are key take aways from a neuro assessment?
- Know basic path for neuro disorders
- Know pt baseline neuro deficits
- Review imaging/neuro testing
- Review current meds
- Eval potential risk/benefit of anesthetics
- Pre op measures to optimize pt condition
- Clear pre op documentation of factors above and have rationale for chosen anesthetic plan
Which neurological disorders discussed in lecture are genetic?
*Multiple Sclerosis
*Myasthenia Gravis
*Lambert eaton syndrome
*Myasthenia syndrome
*Muscular Dystrophies
*Myotonic dystrophies
_________: progressive, autoimmune demyelination of central nerve fibers
MS
What is the onset for MS? What are risk factors?
20-40y/o onset
Female, 1st deg relative, Epstein Barr Virus, other autoimmune disorders, smoking
What are exacerbation triggers for MS?
*Stress
*Elevated temps
*Postpartum period
What are S/S of MS? What is the cure?
S/S: Motor weakness, sensory disorder, visual impairment, autonomic instability, sx vary d/t site of nerve demylination
Tx: no cure, manage with steroids, immune modulators, targeted antibodies (IVIG)
What are preanesthetic considerations for a patient with MS?
- Assess existing deficits
- PFT
- CBC,BMP,LFT
- Pre op steroids if long term steroid use
- Critical temp management (temp changes can cause exacerbation)
- Avoid SUCCs
What are acceptable anesthetic options for pt with MS?
Ga, regional, peripheral nerve blocks
avoid succs (hyperkalemia, upreg nAch receptors)
What is the pathophys of myasthenia gravis? When is muscle weakness exacerbated?
- Autoimmune antibodies generated against nAch receptors at skeletal muscle end plate
- Effects skeletal muscle (not smooth or cardiac muscle)
*Muscle weakness exacerbated with exercise
______ hyperplasia is common in MG. What can be done to improve symptoms associated with this?
Thymic hyperplasia (10%)
90% pt improvement after thymectomy
What are exacerbation triggers for MG?
- Pain
- Insomnia
- Infection
- Surgery
Treatment for MG:
*Acetylcholinesterase inhibitors→pyridostigmine
*Immunosuppressants
*Steroids
*Plasmapheresis
*IVIG
What are preanesthetic considerations for patients with MG?
- PFTs
- Reduce paralytic dose (avoid prolonged muscle weakness)
- Caution with opioid (resp compromise)
- Pyridostigmine may prolong Succs and ester LAs
- pre op steroids if on long term
- Discuss w/pt about increase risk for post op resp support/vent until fully recovered from anesthesia
Why do we want to check LFTs on some of these patients?
*On immunosuppresant meds that can cause liver function impairment
What labs do we want to pay attention to if a patient is on steroids?
*Glucose and electrolytes
What is the pathophysiology of Eaton-Lambert Syndrome?
Antibodies against VG Ca2+ channels (P type)
* reduce Ca2+ influx into presynaptic cell
* decrease Ach release from presynaptic cell at NMJ
> 60% of Easton Lambert syndrome are associated with _______________.
Small cell lung carcinoma (paraneoplastic syndrome)
What are S/S or eaton-lambert syndrome? What is the treatment?
- Progressive limb-girdle weakness
- dysautonomia
- oculobulbar palsy
- proximal muscle weakness (Improved with repeated use)
TX: 3-4 diaminopyridine (K+ channel blocker), Azathioprine, Acetylcholinesterase inhibitors, steroids, plasmapheresis, IVIG
What are preanesthetic considerations for ELS?
- Know existing deficits
- PFTs
- VERY sensitive to all NMB
- MORE sensitive to ND-NMB than MG pts
- extreme caution of NMB and opioid dosing
- discuss with pt potential for resp support post anesthesia
What is the pathophys of muscular dystrophy?
- Hereditary disorder causing breakdown of dystrophin-glycoprotein complex
- leads to myonecrosis, fibrosis, skeletal muscle membrane permeability
How many types of MD are there? What is the most common and severe?
- 6 types
- Duchenne MD
What patient population is affected by duchenne MD? What is the average lifespan?
- Occurs only in boys (autosomal recessive)
- onset 2-5 y/o
- wheelchair bound by 8-10
- Lifespace 20-25y/o→ cardiopulmonary complications
What are S/S of muscular distrophy?
- Progressive muscle wasting w/o motor/sensory abnormalities
- Kyphoscoliosis
- Long bone fragility
- Respiratory weakness
- Frequent pna
- EKG changes
elevated CK d/t muscle wasting
What are preanesthetic consideration for patient with muscular distrophy?
- CBC,BMP, PFT, CK
- Pre op EKG, echo
- cautious with ND NMBs
*avoid succs and volatiles (exacerbate membrane instability) - MH card with dantrolene available
- regional better than GA (avoids triggers)
What can be triggered by succs and volatiles in patients with muscular dystrophies? What type of anesthetic would be better for these pts?
Hypermetabolic syndrome (similar to MH)
* Can lead to rhabdo, hyperkalemia, vfib, cardiac arrest
Consider low dose roc and TIVA for GA, OR Regional anesthesia
Prolonged contraction after muscle stimulation:
Myotonia
What is the most common for of myotonia? When is the onset?
Myotonic dystrophy→ onset 20-30s
What are S/S of myotonic dystrophy>
*Muscle wasting in face, masseter, hand, pre-tibial muscles
*may also affect pharyngeal, laryngeal, diaphragmatic muscles
*cardiac conduction may be affected (20% have mitral valve prolapse)
What is myotonia congenita?
Mild form of myotonic dystrophy that only involves skeletal muscles
What is central core disease? What are S/S?
*Rare
*core muscle cells lack mitochondrial enzymes
S/s: proximal muscle weakness and scoliosis
All myotonias are triggered by __________ and __________
Stress
Cold temps
What can myotonias be treated with?
*No cure
*S/S management with Quinine, Procainamide, steroids
What are preanesthetic considerations for myotonic dystrophies?
- Know extent of cardiac and pulm abnormalities
- assess heart and breath sounds
- Aspiration risk (GI hypomotility)
- High endocrine abnormalities
- Keep pts warm (avoid flare ups)
- Optimize preop resp status
- avoid succs d/t fasciculations
- caution with opioids (post op resp depression)
- Increased risk for post op weakness
What are the 3 major dementia syndromes?
- Alzheimers (70%)
- Vascular dementia (25%)
- Parkinsons (5%)
Which preop dementia meds may impact anesthetic?
*acetylcholinesterase inhibitors
*MAOIs
*Psych meds
Why might TIVA be better for patients with dementia? Why is regional preferred over GA?
GA with volatiles increases risk for post op delirium
Regional preferred over GA to decrease opioid requirements
What is the cause of Parkinsons? What is the biggest risk factor?
Unknown cause
Advanced age= biggest risk factor
What is pathophys of parkinsons?
- Degeneration of dopaminergic fibers of basal ganglia
- Motor neurons become over stimulated
What is the triad of symptoms associated with parkinsons?
*Skeletal muscle tremor
*Rigidity
*Akinesia
Rhythmic pill-rolling, facial rigidity, slurred speech, difficulty swallowing, respiratory difficulty, depression, demential
What is the treatment for parkinsons?
*Levodopa (crosses BBB)
*Anticholinergics
*MAOIs (inhibit dopamine degradation)
* Deep brain stimulator
What are preanesthetic considerations for parkinsons?
- Assess severity (attn to degree of pulmonary compromise
- Review home meds (interactions with anesthesia)
*labs/PFT - EKG/echo
- aspiration (dysphagia, dementia)
- Continue PO levodopa
- Avoid reglan, phenothiazines, butyrophenones
*Avoid demerol in on MAOI - Disable deep brain stimulator
- use of bipolar cautery if used
Why is PO levodopa continued in preop?
Avoids unstable extreme EPS such as chest wall rigidity
Common symptoms for brain tumors:
- increased ICP
- Papilledema
- Headache
- AMS
- Mobility impairment
- Vomiting
- Autonomic dysfunction
- Seizures
____ are the most common CNS glial cells
Astrocytes
What are the primary brain tumors, and least aggressive astrocytomas? Often found in young adults with new onset seizures
Gliomas
Which brain tumors are mostly benign, good outcomes if resectable, and in children and young adults?
Pilocytic astrocytomas
Which brain tumors are poorly differentiated and usually evolve into glioblastoma multiforme?
Anaplastic astrocytoma
Which brain tumors carry a high mortality, usually require surgical debulking and chemo, and life expectancy is weeks?
Glioblastoma multiforme
Usually benign, arise from dura or arachnoid tissue;
Good prognosis with surgical resection:
Meningiomas
Noncancerous brain tumors, varying subtypes;
transsphenoidal or open craniotomy for removal is usually curative:
Pituitary adenomas
Usually benign schwannomas involving the vestibular component of CN VIII within the auditory canal;
good prognosis w/resection +/- radiation:
Acoustic neuromas
These brain tumors can vary widely in origin and symptoms; outcomes are generally less favorable:
Metastatic carcinomas
Radiation damage may lead to ____ and ___.
lethargy and AMS
- Chemotherapy may also have neurological effects
What are two common medications that patients with brain tumors are on?
- Steroids to minimize cerebral edema (continue them)
- Anticonvulsants
What medication is given to reduce intracranial volume and pressure in brain tumor patients?
Mannitol
In patient’s with brain tumors, ____ ____ may manifest on EKG, labile HR and BPs
Autonomic dysfunction
What diagnostic testing would you consider for patients with a brain tumor?
CBC, BMP (glucose), EKG, CT/MRI
____ is the leading cause of death and disability worldwide
Stroke
Strokes are characterized by sudden neurologic deficits resulting from:
- Ischemia (88% of cases)
- Hemorrhage (12% of cases)
Blood is supplied to the brain from:
- internal carotid arteries
- vertebral arteries
The internal carotid arteries and vertebral arteries from the ___ that provides collateral circulation to multiple areas of the brain
Circle of Willis
Occlusion of a vessel that perfuses a region of brain, causing brain cell necrosis:
Ischemic stroke
Sudden focal vascular neurologic deficit that resolves within 24 hours
Transient ischemic attack
___ of patients who experience a TIA will subsequently suffer a stroke
1/3
If stroke is suspected, a ______ is needed to distinguish ischemic stroke from intracerebral hemorrhage
STAT non-contrast CT
Causes of ischemic stroke are categorized according to the TOAST classification into 5 groups:
- Large artery atherosclerosis (e.g. carotid stenosis)
- Small vessel occlusion (e.g. lacunar stroke)
- Cardioaortic embolic (e.g. emboli from atrial fibrillation)
- Other etiology (e.g. stroke due to hypercoagulable states or vasculopathies)
- Undetermined etiology
What is the initial recommended treatment for an ischemic CVA?
PO aspirin
What is the time window for giving tissue plasminogen activator?
3-4.5 hours post onset
Performed in interventional radiology, allowing for angiographic fluroscopy during administration of thrombolytics or thrombectomy:
Revascularization
Assessment prior to revascularization:
- avoid any delay in treatment
- focus on baseline neuro assessment, ability to safely lay flat, and CV function
- determine whether procedure could be done under sedation or if secure airway necessary
- Patients with ischemic stroke often have CV risk factors and valvular disease that could impact vasoactive drug choices and hemodyamics
What is a hemorrhagic CVA?
Bleeding inside the cranial vault that impairs perfusion of the brain
Hemorrhagic stroke is ___ more likely to cause death than ischemic stroke
4x
What are the two most reliable predictors of outcome for a hemorrhagic CVA?
- Blood volume
- Change in LOC
What does it mean that the cranial nerves are susceptible with MG?
Common Ocular Sx: Diplopia, ptosis
Bulbar involvement: can cause laryngeal weakness (resp insufficiency and aspiration risk)
Conservative treatment of hemorrhagic CVA:
- reduction of ICP
- BP control
- Seizure precautions
- Monitoring
Protocols for cerebrovascular disease:
- New anticoagulant for thrombus = no elective cases w/in 3 months
- Anticoagulants for CVA prophylaxis = consult prescriber to establish protocol
- Close monitoring of coag status
- High risk patients that pause LA anticoags will need SA coags
- If regional is planned, d/c anticoags for sufficient time to safely perform block
Pre-op assessment for cerebrovascular disease:
- Assess orientation, pupils, bilateral grip strength, LE strength
- Ask about headaches, tinnitus, vision/memory loss, bathroom issues
What diagnostic testing would you get for a patient with cerebrovascular disease?
- Imaging = Carotid US, CT/MRI head and neck, echo
- Preop EKG
- CBC, BMP, possible T&C
- Cerebral oximetry is possible
What do aceytlcholinesterase inhibitor drugs prolong?
- Succs
- Ester local anesthetics
Majority of cerebral aneurysms not ____ before rupture
diagnosed
Only ___ of aneurysm patients have symptoms before rupture
1/3
What are symptoms of cerebral aneurysms?
- Headache
- Photophobia
- Confusion
- hemiparesis
- coma
Risk factors for cerebral aneurysms:
- HTN
- Smoking
- Female
- Oral contraceptives
- Cocaine use
Diagnostics for cerebral aneurysms:
- CT/angio
- MRI
- Lumbar puncture w/ CSF analysis if rupture suspected
How soon should interventions be performed for cerebral aneurysms for best outcome?
72 hours
Pre-anesthesia considerations for cerebral aneurysms:
- CT/MRI
- EKG
- Echo
- CBC, BMP, T&C w/ blood available
- BP control, mannitol (to avoid rupture)
- seizure prophylaxis
Surgical treatment for cerebral aneurysms:
- Coiling
- Stenting
- Trapping/bypass (very large aneurysms)
*neurosurgeon may be on standby in case of intra-op rupture/SAH
What causes post-SAH vasospasms?
Free hgb triggers inflammatory mediators which reduce nitric oxide availability and increase endothelin 1, leading to vasoconstriction
When are patients at risk for vasospasms?
3-15 days post SAH
Treatment for post-SAH vasospasms:
Triple H therapy - Hypertension, hypervolemia, hemodilution
What are some interventional treatments for post-SAH vasospasms?
Balloon dilation and direct injection of vasodilators to relieve the spasm
For post-SAH vasospasms, to avoid complications of hypervolemia, ____ is the initial main treatment
hypertension
Pre anesthesia interventions for post-SAH vasospasms:
Same as aneurysm, although normally less invasive –
- CT/MRI
- EKG
- Echo
- CBC, BMP, T&C w/ blood available
- BP control, mannitol
- seizure prophylaxis
Aneurysm grading for prognosis:
*Hunt and Hess classification will gauge the mortality of the patients (won’t have to use this)
What is an arteriovenous malformation?
Arterial to venous connection without intervening capillaries - creates an area of high flow, low resistance shunting
- believed to be congenital
Symptoms of AVM:
Range from mass-effects to hemorrhage
What is the most common location for AVMs?
Supratentorial
Diagnostic testing for AVM:
- angiogram
- MRI
Treatment for AVM:
- Radiation
- Angio-guided embolization
- Surgical resection (higher mortality)
Pre-anesthesia considerations for AVM:
- H&P
- review meds
- imaging
- CBC, BMP, T&C, EKG, echo
- BP control, mannitol?
- Seizure prophylaxis
- CVC or 2 large bore IVs, aline
AVM grading system
Spetzier-Martin: ranges different severities
Congenital brain abnormalities result from defects in the development or structure of the ___
CNS
Are congenital brain abnormalities often hereditary?
Yes
Congenital brain abnormalities may be diffuse or confined to specific ____ ____
Neuronal structures
What is chiari malformation?
Congenital displacement of the cerebellum
Downward displacement of the cerebellum:
Type 1 chiari malformation
Downward displacement of cerebellar vermis, often associated with myelomeningocele
Type 2 Chiari malformation (arnold chiari)
Rare, occipital encephalocele with downward cerebellar displacement
Type 3 chiari malformation
Cerebellar hypoplasia w/o displacement of posterior fossa contents
Type 4 chiari malformation
Symptoms of chiari malformation:
- Headache
- Extending to shoulders/arms
- Visual disturbances
- Ataxia
Treatment for chiari malformation:
Surgical decompression
Pre-anesthesia considerations for chiari malformation:
- Review H&P
- Deficits
- Imaging
- CBC, BMP, T&C
- May hyperventilate to decrease ICP
- Large bore IV x2 or CVC, aline
What is Tuberous Sclerosis?
AKA “bourneville disease
- genetic disease causing benign hematomas, angiofibromas, and other malformations that can occur anywhere in the body
Tuberous sclerosis lesions of the brain include:
Cortical tumors and giant cell astrocytomas
Tuberous sclerosis often involves co-existing tumors of what?
Face, oropharynx, heart, lungs, liver, and kidneys
Presentation for tuberous sclerosis likely includes:
Mental retardation and seizure disorders
Anesthesia considerations for tuberous sclerosis:
Airway compromise, cardiac and/or kidney involvement
What the heck is Von Hippel-Lindau Disease?
Genetic disease process involving formations of benign tumors of the CNS, eyes, adrenals, pancreas and kidneys
Von Hippel-Lindau disease are commonly associated with what?
Pheochromocytoma
- take into account exaggerated HTN
Types of neurofibromatosis:
Type 1 = most common
Type 2
Schwannomatosis (rare)
Anesthesia considerations for neurofibromatosis:
- Account for increased ICP, airway issues, scoliosis, possibility of pheo
What would you want to avoid in patients with neurofibromatosis?
Neuraxial anesthesia due to high likelihood of spinal tumors
What is hydrocephalus?
- Excessive CSF accumulation, causing ↑ICP, leading to ventricular dilatation
- Accumulation of CSF is due to an imbalance btw CSF production and absorption
- Can be congenital or acquired d/t meningitis, tumors,trauma, or stroke
Are symptoms of hydrocephalus acute or chronic?
Can be both
What is the main treatment for hydrocephalus?
Mainly diuretics - furosemide and acetazolamide decrease CSF production
Other treatments for hydrocephalus:
- Diuretics
- Serial lumbar punctures (temporary)
- Majority of cases require surgical treatment (VP shunt or ETV)
What is the difference in a VP shunt and ETV?
VP shunt = drain placed in ventricle of the brain and empties into the peritoneum
ETV (endoscopic third ventriculostomy) = catheter placed into the lateral ventricle that drains into the peritoneal space, right atrium or pleural space (rarely)
VP shunt malformation occurs most frequently in the ___ ___ of placement and have a ___ failure rate
1st year; high
How are traumatic brain injuries categorized?
- “penetrating” or “non-penetrating” depends on breech of dura
- severity categorized by GCS
When does primary injury occur in TBIs?
Occurs at the time of insult
Secondary injuries from TBI:
- Neuroinflammation
- Cerebral edema
- Hypoxia
- Anemia
- Electrolyte imbalances
- Neurogenic shock
Pre-anesthesia considerations for TBI:
- Review co-morbidities,
- degree of injury
- Imaging
- Labs
- Neuro exam
Interventions for TBIs:
- C-spine stabilization, IV access, CVC, aline
- Uncrossmatched blood if no time for T&C
- Refrain from NGT/OGT (potential for basal skull fx)
- Intra-op iSTAT labs, pressors, bicarb, calcium, blood products
What is a seizure?
Transient, paroxysmal, synchronous discharge of neurons in the brain
What transient abnormalities can cause seizure disorders?
- Hypoglycemia
- Hyponatremia
- Hyperthermia
- Intoxication
*in these cases, treating the underlying disease is curative
What is epilepsy?
Recurrent seizures d/t congenital or acquired factors
Antiepileptic drugs decrease ____ excitability/ ___ inhibition
Neuronal; Enhance
Pre-anesthesia considerations for seizure disorder:
Determine source of seizures and how well they are controlled
- want anti-seizure drugs on board before incision
- Review home drugs
- Phenytoin, tegretol, barbiturates are enzyme-inducers (pts on these meds require higher doses of hepatically-cleared medications)
