Anesthesia for patients with neurological disorders – Flashcards
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Diseases that affect the neuromuscular junction or muscle tissue
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Myasthenia Gravis Muscular Dystrophy
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Diseases that affect the brain itself
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Parkinson's disease Alzheimer's disease Huntington's disease Cerebral Palsy
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Diseases that affect neurotransmission (demyelination, dennervation)
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Stroke Spinal cord injury Multiple Sclerosis Guilliane Barre
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Describe the pathophysiology of Myasthenia Gravis
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- autoimmune destruction of functional postsynaptic ACh receptors
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Which receptors, pre- or post-junctional, remain normal in myasthenia gravis?
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pre-juncitonal ACh receptors normal
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What percentage is the thymus gland involved in myasthenia gravis?
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75-90%, depending on the source you read
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What antibody is increased in myasthenia gravis?
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IgG
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Describe the clinical presentation of myasthenia gravis
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1. Generalized muscle weakness (improves with rest, worse with repeated muscle movement) 2. Ptosis, diplopia 3. Myocarditis, inflammation produces arrhythmias
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How does myasthenic syndrome differ from myasthenia gravis?
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Improves with repeated muscle movements, worse with rest
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What is the treatment for myasthenia gravis?
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1. Anticholinesterase drugs, pyridostigmine, neostigmine 2. Corticosteroids to decrease autoimmune response 3. Thymectomy for drug-resistant MG 4. Edrophonium test (test dose 1-2 mg edrophonium)
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What is the edrophonium test?
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Give 1-2 mg, if further muscle weakness results, you are in a cholinergic crisis from too much ACh; if symptoms get better, it is a myasthenic crisis
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How should you adjust your dose of paralytic?
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Succinylcholine: reduce the dose in some **anticholinesterase drugs for MG tx may inhibit enzyme that breaks down SCh; patients not on anticholinesterase inhibitors may be resistant to SCh, so will need to increase dose** Non-depolarizers: reduce the dose by 1/2-2/3 **don't need as much drug because not as many receptors to block**
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What is the most common type of muscular dystrophy?
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Duchenne's, or pseudohypertrophic
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What is the genetic inheritance of muscular dystrophy?
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X-linked recessive, mostly in boys
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What age does muscular dystrophy appear?
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2-6 years of age
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What protein causes muscular dystrophy?
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dystrophin is absent; due to defects in this assembly, contraction of the muscle leads to disruption of the outer membrane of the muscle cells and eventual weakening and wasting of the muscle
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How does muscular dystrophy present?
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1. Altered ambulation, progressing to wheelchair, then cardiopulmonary dysfunction 2. Waddling gait, frequent falls (pelvic muscle involvement), then tip toe walking, hypertrophic muscles (fatty deposits) then muscle weakness leading to spine involvement (scoliosis) 3. Elevated plasma creatinine levels due to destruction of muscles 4. Death between 15-25 years old due to pneumonia or heart failure
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What is the treatment for muscular dystrophy?
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There is no cure
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What will succinylcholine potentially cause in muscular dystrophy patients?
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- Exaggerated K release d/t increased permeability of cell membranes - May see cardiac dysrhythmias
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How to dose your non-depolarizers for muscular dystrophy patients
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THey may be more sensitive to them, so decrease dose depending on each patient
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Other anesthetic considerations for muscular dystrophy patients
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1. Increased incidence of malignant hyperthermia (assess for rhabdomyolysis) 2. Weak laryngeal muscles 3. Delayed gastric emptying, decreased motility 4. Exaggerated response to depressant effects of inhaled agents 5. Post-operative pulmonary dysfunction (evaluate PFTs) 6. Cardiac dysfunction (ECHO, assess for heart failure)
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What type of anesthesia is appropriate for muscular dystrophy patients?
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Regional should be used when you can
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Describe the pathophysiology behind parkinson's disease
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Decrease in the amount of dopamine in the substantia nigra located in the basal ganglia. **causes imbalance between dopamine (inhibitory in the CNS) and acetylcholine (excitatory in CNS), so net effect is uncontrolled movement related to unopposed stimulation of ACh; therefore, there is a decreased inhibition of the extrapyramidal NS (lack of fine-tuning movement)
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How does Parkinson's present?
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1. Extrapyramidal SE a. akinesia b. akathesia c. tardive dyskinesia d. dystonia e. torticollis f. oculogyric crisis 2. Muscle rigidity 3. Resting, rhythmic tremor 4. Shuffling gait 5. Autonomic dysfunction 6. Sleep disturbances 7. Depression/dementia
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Treatment goals for parkinson's disease
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1. Goal is to decrease dopamine levels and/or antagonize central ACh levels
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Drugs used to increase dopamine levels via replacement
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1. Carbidopa 2. Levodopa 3. Sinemet (centrally acting, so makes sleepy)
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Drugs used to increase dopamine levels via inhibition of dopamine metabolism
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1. Selegiline
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Drugs that antagonize central ACh effects
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Benzotropine
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Antiviral drug treatment for Parkinson's disease
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Amantadine
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Side effects from drugs used to treat Parkinson's disease
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1. N/V 2. Myocardial irritability 3. Decrease intravascular volume 4. Orthostatic hypotension 5. Sedation, depression
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Other treatment options for Parkinson's disease
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1. Implant dopamine-producing fetal tissue 2. Pallidotomy, Thalamotomy 3. Implantable electrodes into brain to stimulate dopamine production
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Why should you not abruptly discontinue levodopa?
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May worsen muscle rigidity
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What drugs should you avoid in Parkinson's patients?
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Dopamine blockers: butyrophenones (droperidol), phenothiazines (phenergan), metaclopramide
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Can you use anticholinergics to treat tremor for Parkinson's patients?
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Yes! Atropine and benadryl are appropriate choices
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What may occur during induction in terms of hemodyamic changes related to pathophysiology of Parkinson's?
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Hypotension or hypertension s/t volume depletion and catcholamine depletion
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Will your paralytics affect Parkinson's patients?
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No, as they do not cross the blood-brain barrier
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What are Parkinson's patients at risk for during and after anesthesia?
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1. Difficulty with ventilation r/t muscle rigidity 2. Pulmonary aspiration 3. Post-operative delirium cognitive deterioration
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What type of pressor should you use with Parkinson's patients?
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Direct acting pressor such as neosynephrine
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Describe the pathophysiology behind alzheimer's disease
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- neurodegenerative & terminal disease with no cure - fewer nicotinic cholinergic receptors and reduced ACh synthesis - brains contain neuritic plaques and fibrillary changes
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Clinical presentation of Alzheimer's disease
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1. Progressive memory impairment, predominantly early loss of short term memory 2. Language impairment 3. Daily tasks impaired 4. Later symptoms: a. confusion b. anger c. mood swings d. language breakdown e. long-term memory loss f. general withdrawal
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Name some treatment options for Alzheimer's
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1. No cure 2. Supportive 3. Use drugs that increase central ACh levels such as physostigmine
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Anesthetic drugs to avoid in Parkinson's patients
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1. Sedative drugs 2. Centrally acting anticholinergic drugs (glycopyrrolate okay to use) 3. Patients may be taking centrally acting anticholinesterase drugs preoperatively which may influence nondepolarizing muscle relaxants
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What drugs can precipitate or exacerbate dementia?
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High-dose steroids Neuroleptics Benzodiazepines Ketamine Tertiary anticholinergics Opioids H2 blockers Droperidol
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If patient develops delirium post-operatively, what should you rule out first?
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Cerebral hypoxia
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What is the pathophysiology of Huntington's disease
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Mutant huntington results in neuronal cell death in select areas of the brain involved with movement, emotions, cognition, and various types of learning
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Clinical presentation of Huntington's
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1. Delayed appearance until adulthood and progresses over several years 2. Chorea (classic sign) 3. Ataxia 4. Dysarthria 5. Athetosis 6. Psychiatric and cognitive alterations 7. Dysphagia 8. Malnutrition
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What are some of the treatments for Huntington's disease?
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1. Haloperidol to interfere with dopamine transmission 2. Phenothiazines, butyrophenones, thioxanthenes, or heterocyclic antipsychotics to treat psychiatric symptoms 3. Benzodiazepines to treat anxiety
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What can you use pre-operatively to control jerky, choreiform movements?
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Butyrophenones (droperidol or haloperidol)
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What is pseudocholinesterase activity like in Huntington's patients?
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Decreased, so may have increased sensitivity to succinylcholine
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Considerations while taking care of Huntington's patient during anesthesia
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1. May take longer to wake up after GA, at risk for prolonged respiratory depression 2. Maintain normothermia, prevent postoperative shivering
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What anticholinergic should be used if need be for the Huntington's patient?
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Glycopyrrolate
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Is regional anesthesia contraindicated for the Huntington's patient?
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No, but may be difficult because of continuous uncontrollable movements
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Describe the pathophysiology of cerebral palsy
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- Non-progressive disease r/t upper motor neuron dysfunction - Many times related to anoxic or hypoxic cerebral damage in utero or at birth - Also related to atrophy of basal ganglia or white matter
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Clinical presentation of cerebral palsy
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1. Spastic, extrapyramidal, atonic, or mixed 2. May affect only one limb or all limbs 3. Difficulty with speech 4. Seizure disorders 5. Spasticity varies but may cause deformities of joints
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What types of treatments are available for cerebral palsy?
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1. Orthopedic procedures 2. Dorsal rhizotomy (mini laminectomy to dissect out spastic nerve fibers) 3. Botox injections 4. Baclofen pump (GABA potentiator, abrupt withdrawal will send into crisis) 5. Physical, speech, and occupational therapy
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Name some pharmacological treatments for cerebral palsy
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1. Seizure medications 2. Dantrolene 3. Baclofen
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What happens if a CP patient gets hypothermic?
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Makes spasticity worse
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What is the pathophysiology behind stroke and spinal cord injury?
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Dennervation injury: lack of nerve transmission, opposite of innervation
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What specific phenomenon should be prevented with spinal cord injury?
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Autonomic hyperreflexia
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At what transection level does autonomic hyperreflexia occur?
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T5-T6 Can occur anytime post injury, usually after shock phase
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What is autonomic hyperreflexia caused by?
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Distention of bladder or catheterization, impaction of bowel, or any other stimulation below the level of the transection
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Why is there a heightened response to stimuli in autonomic hyperreflexia?
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Because of up-regulation of receptors below the level of the transection; vasodilation occurs above the level of transection as the CNS tries to counteract HTN with PSNS tone but can't communicate with the body below the level of transection
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Signs and symptoms of autonomic hyperreflexia
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1. Severe paroxysmal hypertension (episodic high BP) 2. THrobbing HA 3. Profuse sweating 4. Nasal stuffiness 5. Flushing of the skin above the level of lesion 6. Bradycardia 7. Apprehension and anxiety
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Which types of anesthetic agents are effective in preventing autonomic hyperreflexia?
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GA Spinal anesthetics (epidural anesthesia is not as effective)
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Why are receptors up-regulated in autonomic hyperreflexia?
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There is a lack of response below the lesion because impulses can't get through, so receptors aren't "feeling the love" so they make more receptors to try and compensate
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How to treat HTN in autonomic hyperreflexia
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Direct arterial dilators and alpha blockers (nipride or nitro)
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What type of muscle relaxation should you use for spinal cord injury?
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Non-depolarizers, as succinylcholine may cause increases in K release because of up-regulation of receptors
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How long after the injury is it okay to use succinylcholine?
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Up to 24 hours after injury you can safely use succinylcholine. Should not use after 24 hours and up to 1 year after injury.
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Does pre-treatment with a non-depolarizer attenuate the K release from succinylcholine administration in spinal cord injury?
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No!
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How long does it take for extra-junctional receptors to proliferate post-injury?
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24-48 hours
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If you have an exaggerated response to twitch monitoring in spinal cord injured patients, should you re-dose with paralytics?
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Not necessarily. The response is greater due to up-regulation, so this may lead to overdosing.
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Three types of strokes
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1. Hemorrhagic (avoid driving up pressures) 2. Embolic (bust the clot) 3. Ischemic (drive the pressure up)
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What will twitch monitoring look like in some who has had a stroke?
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It will be decreased in response, so this may lead to underdosing paralytics
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Which side should you place electrodes on for twitch monitoring?
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Unaffected side
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Which way does the autoregulation curve shift for HTN patients?
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RIghtward shift. Maintain levels of BP during case at or near preop baseline
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A decrease in MAP below 10 mm Hg will increase your risk of a stroke by how much?
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4 fold
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Is succinylcholine okay to give to someone who has just had a stroke?
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No because of hyperkalemia. Safe to give within 24 hours of stroke, but should not be give after this and up to 1 year
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What happens if you give a stroke patient non-depolarizers?
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They have an increase response so this may lead to overdosing
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Describe the pathophysiology of multiple sclerosis
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-Scars or plaques on the demyelinated myelin -Autoimmune, attacks CNS leading to demyelination and axonal damage
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Which specific neural cells are damaged in multiple sclerosis?
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Oligodendrocytes: these are the cells responsible for crating and maintaining a fatty layer (myelin sheath) which helps the neurons carry electrical signals
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Are peripheral nerves affected in multiple sclerosis?
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No.
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What diagnostic test will identify demyelinative plaques on the brain or spinal cord?
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MRI
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What are some signs and symptoms of multiple sclerosis?
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1. Optic neuritis 2. Gait disturbances 3. Pain 4. Speech problems 5. Limb paresthesias 6. Weakness 7. Urinary incontinence 8. Ataxia 9. Sexual impotence 10. Spasticity 11. Autonomic insufficiency (be careful sitting pts up) 12. Respiratory muscle weakness 13. Residual symptoms persist during remissions over time
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Treatment for multiple sclerosis
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Amelioration of acute exacerbations, preventing relapse, and relief of symptoms: a. corticosteroids b. interferon c. low-dose methotrexate
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What happens if you give multiple sclerosis patients paralytics?
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SCh may lead to hyperkalemia, exaggerated response Prolonged response to non-depolarizers
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Do epidural and peripheral nerve blocks lead to exacerbations in multiple sclerosis?
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No
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What temperature should you keep multilple sclerosis patients at?
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They like the cold, so don't actively warm patients
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Describe the pathophysiology of Guilliane Barre
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Autoimmune, attacks peripheral nervous system
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When do you see Guilliane Barre? (think infections)
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Campylobacter jejuni Cytomegalovirus Epstien-Barr virus HIV infection
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What is Guilliane Barre characterized by in terms of symptoms?
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Sudden onset of skeletal muscle weakness or paralysis
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How does Guilliane Barre spread throughout the body?
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Starts in legs, then spreads cephalic to involve skeletal muscles of the arms, trunk, and face
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CLinical presentation of Guilliane Barre
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Bilateral facial paralysis Difficulty swallowing Altered ventilation Autonomic dysfunction Pain
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What do Guilliane Barre patients die from?
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Acute respiratory failure Autonomic dysfunction Sepsis Cardiac arrest (rare)
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Name some treatments for Guilliane Barre
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Plasmaphoresis High-dose IV immunoglobulins Immunomodulatory drugs Ventilatory support
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What happens if you give paralytics to Guilliane Barre patients?
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Avoid succinylcholine b/o hyperkalemia risk Sensitive to non-depolarizers so decrease dose
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True or False: Guilliane Barre patients have an exaggerated response to indirect-acting vasopressors
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True
