Preop Neruo Eval (1) Flashcards
Three identified risk factors for preoperative stroke:
History of stroke or TIA
Advanced age
Pre-existing renal disease
Independent Predictors of Perioperative Stroke (12)
~ Atrial fibrillation
~ Valvular cardiac disease
~ Heart failure
~ Diabetes mellitus
~ Female gender
~ MI within 6 months
~ Prior cardiac intervention
~ Current dialysis
~ Acute renal failure (acute or chronic disease)
~ COPD
~ Current smoker
~ Hemiplegia
Chads Vas score
~ Congestive heart failure/LV dysfunction (1)
~ Hypertension (1)
~ Age >75 (2)
~ Diabetes Mellitus (1)
~ Stroke/TIA/ Thromboembolism (2)
~ Vascular disease (1)
~ Age 65-74 (1)
~ Sex (female) (1)
Chads Vas Scoring =
Adjusted stroke rate (% per year) with 95% confidence interval
0 = 1.9 (1.2-3.0)
1 = 2.8 (2.0-3.8)
2 = 4.0 (3.1-5.1)
3 = 5.9 (4.6 -7.3)
4 = 8.5 (6.3-11.1)
5 = 12.5 (8.2-17.5)
6 = 18.2 (10.5-27.4)
Bruits associated with symptomatic carotid disease need?
Further workup (carotid arteriography is the gold standard but ultrasound is faster and less invasive)
Aneurysms and AVMs
Usually found incidentally - 3.2% incidence worldwide, only 0.25% rupture
Myasthenia Gravis
Autoimmune disease - body attacks post synaptic nicotinic ACh receptors. Causes muscular weakness.
What drugs should be avoided or used with care in Myasthenia Gravis?
Paralytics.
What drugs are used to treat Myasthenia Gravis?
~ Pyridostigmine (anticholinesterase / cholinesterase inhibitor)
~ Corticosteroids
~ Immunosuppressives
~ With severe bulbar and respiratory compromise, IV Immunoglobulin (IVIG) or plasmapheresis preferred
Clinical manifestations of Myasthenia Gravis
Ocular
~ Diplopia
~ Ptosis
~ Ophthalmoplegia
Respiratory
~ Breathlessness
~ Weak Breathing
~ Respiratory Failure
Bulbar
~ Fatiguable chewing
~ Dysarthria
~ Dysphagia
Limbs, Neck
~ Dropped Head
~ Proximal > distal
~ Arms> legs
Myasthenia Gravis surgical treatment
Thymectomy: Removal of the thymus (thought to interfere with the production of autoantibodies) (tumor of thymus, called thymoma)
Myasthenia Gravis history exam:
clinical features of MG
disease severity
duration
medications
recent exacerbations
Myasthenia Gravis medecation recommendations
Pyridostigmine can be held if agreed upon by providers but is not recommended. Avoid premedication with sedatives or opioids because of CNS depressive effects.
Myasthenia Gravis Anesthesia Technique
Nerve blocks when possible. Caution in nerve blocks that could effect the phrenic nerve: diaphragmatic paralysis
Myasthenia Gravis steroids
If patients take long term steroids be aware a stress dose of steroid may be needed
Myasthenia Gravis, muscle relaxant approach
~ Depolarizing agents (succinylcholine) have unpredictable responses
~ Non-depoarizing agents are preferred with dose reduced by 1/3 to 1/2
Myasthenia Gravis other medications to avoid (NMB potential):
Certain antibiotic
Beta-blockers
Calcium Channel Blockers
Botox
Lithium
Magnesium
Verapamil
Myasthenia vs Cholinergic crisis!
Myasthenia crisis - exacerbation of disease - increased weakness and respiratory distress - treated with additional dose of NMB reversal
Cholinergic crisis: excess ACh at NMJ - increased weakness and respiratory distress, bronchospasm, sialorrhea, diarrhea, bronchorrhea
small dose of edrophonium to help distinguish one from the other
Cholinergic crisis (too much ACh)
Increased cholinergic activity
secretions increased
Bradycardia
Pupils constricted
Weak muscular tone and fasciculations
Edrophonium (Tensilon) test: Symptoms Exaggerated
Myasthenia Crisis (Not enough ACh)
Decreased cholinergic activity
secretions normal
tachycardia
pupils normal or dilated
weak muscular tone
Edrophonium (Tension) test: Relieves Symptoms
Leventhal criteria: Predictive scoring system for the need for postoperative ventilation in Myasthenia Gravis patients
1: Duration of disease for 6 years or longer
2: Chronic comorbid pulmonary disease
3: Pyridostigmine dose >750mg/d
4: VC <2.9L
5: Other indicators include preoperative use of steroids, and previous episode of respiratory failure
Myasthenia Gravis in neonates
~ Temporary due to transplacental transfer
~ Usually lasts a few weeks
~ Infants are floppy at birth, poor sucking, muscle tone, and respiratory effort
~ ICU obs with respiratory support and IV feedings
~ Short-term treatment with AChEIs possibly required
~ Infants of mothers who have taken corticosteroids should be monitored for adrenal inefficiencies during newborn period
Eaton-Lambert Syndrom is:
An auto immune disease in which antibodies are directed at voltage gated calcium channels in the presynaptic nerve terminals.
Eaton-Lambert Syndrom is most commonly associated with:
Small cell lung cancer
Eaton-Lambert Syndrom: muscle weakness is most significant when?
In the morning and improves as the day progresses
Eaton-Lambert Syndrom temperature considerations:
Avoid hypothermia as this may exacerbate condition
Myasthenia gravis vs Eaton-Lambert Syndrom (antibodies)
~ MG = Antibody against nAChR
~ LES = Antibody against voltage-gated Ca2+ channel
Myasthenia gravis vs Eaton-Lambert Syndrom (Tumor association)
MG = Associated with Thymic Tumor (Thymoma)
LES = Associated with Small cell lung cancer
Myasthenia gravis vs Eaton-Lambert Syndrom (Muscle weakness)
MG = Weakness worsens with prolonged exercise
LES = Weakness improves with prolonged exercise
Myasthenia gravis vs Eaton-Lambert Syndrom (DTRs)
MG = Normal DTRs
LES = Decreased or absent DTRs
Myasthenia gravis vs Eaton-Lambert Syndrom (Nerve stimulation)
MG = With repeated nerve stimulation, there is decremental response
LES = With repeated nerve stimulation, there is increased response
Eaton-Lambert Syndrom pre-anesthesia considerations
~ Evaluate lung function to assess post-op complication
~ PTs sensitive to depolarizing and non depolarizing NMB
~ Consider MAC or regional anesthesia if possible to avoid NMB
Amyotrophic Lateral Sclerosis (ALS, Lou Gehrig Disease) is:
A progressive incurable disease of degradation, dysfunction and eventual paralysis of upper and lower motor neurons
Amyotrophic Lateral Sclerosis (ALS, Lou Gehrig Disease) approximate survival time:
3-5 years after dx. Death results from ventilatory failure due to neuromuscular weakness
Amyotrophic Lateral Sclerosis (ALS, Lou Gehrig Disease) airway assessment
Possible masseter spasticity, muscular laxity leading to TMG dislocation
Muscular Dystrophies: which is most common
Duchenne muscular dystrophy is most common with an occurrence of 1:3500 births
What are Muscular Dystrophies:
X linked chromosome disease (can come from mom or dad). results for lack of dystrophin which helps anchor muscle cells to the extracellular matrix.
Muscular Dystrophies: progression
Muscle fibers inadequately tethered, these fibers are then replaced with fibrous connective tissue leading to pseudohypertrophy (false enlargement from abnormal tissue, not muscle as in hypertrophy).
Muscular Dystrophies: appear when
In childhood, with progressive wasting and weakness usually of the proximal muscles. Typically becomes fatal by late adolescent from respiratory or cardiac failure.
Muscular Dystrophies: Becker’s muscular dystrophy mechanism
In Becker’s muscular dystrophy, the dystrophin protein is only partially absent. Symptoms are less severe.
Muscular Dystrophies: Duchenne details
~ Most common type
~ Begins between ages 2 and 3
~ Affects lower limbs first
~ Impacts heart and respiratory muscles later on
Muscular Dystrophies: Becker’s details
~ Appears between ages 5 and 15
~ Has slower progression than DMD
~ Affects hips and pelvic area first
~ Causes muscle weakness in the heart for most
~ Partial absence of dystrophin
Muscular Dystrophies: Limb-Girdle details
~ Starts in either adulthood or childhood
~ Creates muscle weakness and atrophy in hips and shoulders
~ LGMD’s progression is dependent on the age of onset
Muscular Dystrophies: Pre-Op considerations
~ Possible need for cardiology consultation due to presence of cardiac conduction abnormalities
~ Increased risk for preoperative complications including rhabdomyolysis, hyperkalemia, malignant hyperthermia, and cardiac arrest
~ Restrictive lung disease is present in DMD
Guillain Barre Syndrome: what is it?
~ Immune-mediated polyneuropathy that often follows a viral or bacterial illness within the preceding 4+6 weeks
Guillain Barre Syndrome: progression
~ Generally weakness ascending from the legs and is symmetrical
~ Rapidly progressing respiratory muscle weakness may result in intubation and ventilation
Guillain Barre Syndrome: Acute inflammatory demyelinating polyradiculoneuropathy (AIDP)
Most common for in North America and Europe. Most common sign is muscle weakness that starts in lower part of body and spreads upward
Guillain Barre Syndrome: Miller Fisher syndrom (MFS)
Paralysis starts in the eyes. Also associated with unsteady gait. Less common in the U.S. but more common in Asia
Guillain Barre Syndrome: Acute motor axonal neuropathy (AMAN) and Acute motor-sensory axonal neuropathy (AMSAN)
Less common in the U.S. but AMAN and AMSAN are more frequent in China, Japan, and Mexico
Cerebral Palsy: what is it?
~ A group of chronic non-progressive disorders of motor development and posture
~ Caused by damage to a developing immature brain
~ Manifestation is variable
~ Aspiration due to bulbar muscle impairment and epilepsy are common
Cerebral Palsy: Clinical Classification Spastic
Spastic (70%)
~ Quadriplegia (27%)
~ Diplegia - paralysis affecting symmetrical parts of the body (21%)
~Hemiplegia - partial or complete paralysis on one side of the body (21%)
Cerebral Palsy: Ataxic
Ataxic (10%)
~ Intention tremor and head tremor, loss of balance
Cerebral Palsy: Dyskinetic
Dyskinetic (10%)
~ Dystonia - involuntary muscle contractions that cause repetitive or twisting movements
~ Athetosis - slow involuntary and continuous writhing movements in the muscles of limbs, face, neck, tongue, and trunk
~ Chorea - movement disorder that causes involuntary, irregular, and unpredictable muscle movements
Cerebral Palsy: Mixed
Mixed (10%)
~ Spasticity and athetoid movement
Parkinsons Disease: What is it?
Without dopamine stimulation / inhibition from Substantia Nigra of the GABA sites in Striatum, unopposed Glutamate stimulation in Subthalamic Nucleus leads to GABA inhibition of Thalamic control of voluntary motor movement
Parkinsons Disease: Classic Triad
Rigidity, Bradykinesia, Resting tremor
Parkinsons Disease: Pharmacotherapy
Designed to restore dopaminergic acitivity in the dopamine-deplete striatum
Parkinsons Disease: Carbidopa-levodopa
Carbidopa-levodopa (Sinemet) replaces dopamine
Parkinsons Disease: Dopamine agonists
Dopamine agonists (pramipexole, lisuride, ropinirole) Stimulate dopaminergic receptors
Parkinsons Disease: COMT inhibitors and MAO-B inhibitors
COMT inhibitors (entacapone, tolcapone, and opicapone) and MAO-B inhibitors (selegiline) inhibit dopamine metabolism
Parkinsons Disease: NMDA inhibitors
NMDA inhibitors (amantadine) weak glutamate antagonist. Limits severity of levodopa-induced dyskinesias
Parkinsons Disease: Deep brain stimulation
Deep Brain Stimulation (DBS) of sub thalamic nucleus is effective for all major movement symptoms of Parkinson’s disease (tremor, bradykinesia, rigidity, and problems with walking and balance)
Parkinsons Disease: specific patient med history
Obtain detailed medication history and exact dosing schedule. Have pt bring home anti-PD meds as they may not be formulary (to avoid missed doses and abrupt interruption)
Parkinsons Disease: surgery timing
Schedule surgery early in the morning to minimize missed / delayed doses of anti-PD meds, preserve sleep-wake cycle, and resume mobility on DOS whenever possible
Parkinsons Disease: MRI
Asssess MRI safety of deep brain stimulator ahead of time incase MRI is needed
Parkinsons Disease: morning of medecations
Have patients take morning anti-PD medications morning of surgery unless contraindicated (Levodopa may be given 20-30 min prior to induction and resumed post-op in the PACU as soon as the patient is awake).
Parkinsons Disease: prolonged fasting and orthostatic hypotension
Plan surgery to minimize fasting while still considering risk of aspiration
Parkinsons Disease: MAOIs and inhibition of phenylpiperidine narcotic metabolism
Avoid meperidine, fentanyl, indirect-acting sympathomimetics
Parkinsons Disease: Worsening of extrapyramidal effects
Avoid dopaminergic antagonists (haloperidol, droperidol, metoclopramide come to mind)
Parkinsons Disease: pre-existing DBS may be damaged with electrocautery use
Turn off DBS prior to surgery if electrocautery to be used. Request bipolar cautery
Parkinsons Disease: Increased risk post-op pulmonary complications
Preoperative spirometry training. Coordination with physical therapy / Rehab services
Seizures: mode of presentation for
intracranial tumors
Seizures: Medications in the perioperative period
Continue anti epileptic medications throughout the perioperative period.
~ One exception: patients requiring intraoperative electroencephalography (EEG) monitoring and localization
Seizures: Antiepileptic drugs Mechanism of Action
Inhibit depolarization of neurons by:
~ Inhibition of excitatory neurotransmission (Glutamate)
~ Enhancement of inhibitory neurotransmission (GABA)
~ Blockage of voltage-gated positive current (Na+) and (Ca2+) channels
~ Increase outward positive current (k+)
***Most alos induce hepatic enzymes altering the pharmacokinetics of your anesthetic agents (don’t last as long)
Seizures: History
frequency of seizure, type, last seizure occurrence, postictal phase, history of status epileptics, home anti seizure medications regimen and any adverse effects, compliance with antiseizure medications
Seizures: Labs
Obtain CBC and CMP blood levels of anti-seizure medications not required unless concerned about toxicity or non-adherence (surgery and anesthesia can significantly alter serum levels of anti seizure medications)
Seizures: medications prior to surgery
~ Morning of surgery, allow P.O. anti seizure meds with small sips of water
~ If patient is strict NPO or having intestinal surgery: give parenteral formulation of anti-seizure medication
Seizures: and pregnancy
Assess pregnancy status in women of child-bearing age to guide the choice of anti-seizure medication. Keppra probably the safest
Good things to remember:
~ The major cause of death in patients with NM disorders is respiratory insufficiency
~ extent of general muscle weakness does not necessarily correlate with the severity of respiratory muscle involvement
~ Cardiovascular involvement may manifest as autonomic dysfunction in patients with neuropathic disorders
~ Clinical signs of autonomic dysfunction include: orthostatic hypotension and resting tachycardia
~ Presence of these clinical signs may indicate profound hemodynamic instability requiring invasive monitoring to manage intravascular volume status and myocardial contractility
~ Severity of skeletal muscle involvement does not necessarily correlate with severity of cardiac involvement
