POA: CNS and PNS Disorders – Flashcards
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What are Chiari Malformations?
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A group of disorders consisting of congential displacement of the cerebellum
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What is Chiari I?
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Downward displacement of cerebellar tonsils over cervical spinal cord
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What is Chiari II?
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Downward siplacement of the cerebellar vermis (often associated with meningomyelocele)
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What is Chiari III?
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Extremely rare. Displacement of cerebellum into an occipital encephalocele.
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What are the signs and symptoms of Chiari I and at what age do they appear?
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Can appear at any age. Occiptial headache extending into the shoulders and arms with corresponding cutaneous dysesthesias. Pain is aggravated by coughing or moving the head. Can also have vertigo, ataxia, or syringomyelia.
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What are the signs and symptoms of Chiari II and at what age do they appear?
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Present in infancy Obstructive hydrocephalus plus lower brainstem and CN dysfunction.
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What are the anesthetic implications of Chiari I?
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No spinal taps and caution with RA: could herniate brainstem
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What are the anesthetic implications of Chiari II?
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Increases in ICP Significant interop blood loss
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What is the prognosis for Chiari III patients?
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Can be surgically corrected
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What are the AI for Chiari III?
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Watch airway Watch ICP
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Identify the following condition
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Chiari III
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Identify the following condition:
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Chiari III
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What is Tuberous Sclerosis?
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Proliferation of benign lesions and malformations that occur in all body systems.
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What heart condition is associated with Tuberous Sclerosis?
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WPW (delta wave; re-entry bradycardia)
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What type of brain lesions commonly occur with Tuberous Sclerosis?
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Astrocytomas
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What is the most common benign cardiac tumor associated with Tuberous Sclerosis?
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Cardiac rhabdomyoma (rare)
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What are the anesthetic implications for Tuberous Sclerosis?
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Presence of mental retardation Seizures Upper airway abnormalities Cardiac arrhythmias Impaired renal function Respond normally to inhaled and injected drugs
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What is Von Hippel Landau Disease?
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Characterized by retinal angiomas, hemangioblastomas and CNS (cerebellar) and viscreal tumors. Tumors are usually benign but can put pressure on adjacent structures.
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What condition can occur with Von Hippel Landau that is of particular importance for anesthesia?
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Pheochromocytoma
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What are the three classifications of Neurofibromatosis?
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Classic (von Recklinghousen's disease), acoustic, or segmental
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What skin disorder commonly occurs with Neurofibromatosis?
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Cafe' aulait spots (skin lesions that can occur in deeper peripheral nerves, nerve roots, viscera or blood vessels innervated by the ANS.
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What is the common name for Neurofibromatosis?
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Elephant man's disease
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What characteristics are associated with Neurofibromatosis?
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Cafe' aulet spots, short stature, increased Ca, intellectual impairment (40%)
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What are the AI associated with Neurofibromatosis?
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Difficult airway due to nodules in oropharynx Nodules in oropharynx can bleed Intracranial tumors in 5-10% of patients (need CT to r/o tumors) Kyphoscoliosis and pseudoarthrosis (result in decreased respiratory excursion) --> No RA May have Pheo, thyroid, parathyroid issues May have cervical spine dysfunction
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What considerations should be made for AI for neurofibromatosis with respect to possible cervical spine dysfunction?
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Watch drug interactions (seizure) Variable sensitivity to NMB; can be either sensitive or resistant to Succs Spinal/Epidural anesthesia can cause possible neurofibroma formation in future Epidural is effective method for L&D
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What characterizes Alzheimer's disease?
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Diffuse amyloid-rich senile plaques and neurofibrillary tangles.
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What are the medication interaction AI for Alzheimer's disease?
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Medication interactions (prolongation of succs and relative resistance to other NMBs due to use of cholineseterase inhibitors - Aricept)
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What are the general AI for Alzheimer's disease?
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Patients can be confused/combative Use shorter acting agents --> back to baseline faster
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Although challenging, what are two types of anesthesia that may be best for Alzheimer's patients?
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Regional anesthesia MAC
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What is the pathophysiology for Parkinson's disease?
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Neurodegenerative disorder characterized by loss of dopaminergic fibers in basal ganglia --> regional depletion of dopamine concentration
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What does dopamine normally do within neurons ?
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Inhibits the rate of firing of neurons that control the extrapyramidal motor system.
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What does depletion of dopamine cause in neurons?
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Diminished inhibition of neurons and unopposed stimulation by ACh.
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What are symptoms of Parkinsons?
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Skeletal m. rigidity (proximal muscles of neck first) Loss of arm swings when walking and absence of head rotation when turning the body. Facial immobility (infrequent blinking) Paucity of emotional responses. Tremors (pill rolling); most prominent in resting limbs but tend to diappear during voluntary movement. Seborrhea, oily skin, diaphragmatic spasms, oculogyric crisis Dementia and depression
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What is the triad of Parkinson's disease?
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Skeletal muscle tremor, rigidity, and akinesia
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How is Parkinson's disease treated?
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With dopamine precursor like levadopa combined with a decarboxylase inhibitor --> prevents conversion of levodopa to dopamine periperally and optimizes the amount of levodopa availale to enter the CNS
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What are common side effects of levodopa?
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Dyskinesias Psychiatric disturbances (agitation, halllucinations, mania, and paranoia) Increased myocardial contraction and HR (may reflect increased levels of circulating dopamine from levodopa Orthostatic hypotension (give fluids preop) N;V (from stim of CTZ)
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What other drugs may persons with Parkinson's be on?
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Amantadine --> antiviral agent Selegilene --> type B MAOI (inhibits catabolism of dopamine in CNS and weak inhibitor of Type A (not associated with tyramine)
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When is surgery done for Parkinson's patients?
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Reserved for disabling and medically refractory
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What is DBS?
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Procedure for treatment of Parkinson's that stimulates the subthalamic nuclei to help relieve tremor
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What is Pallidotomy?
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Procedure for treatment of Parkinson's that improves levodopa-induced dyskinesia
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What is fetal tissue transplant used for in treatment of Parkinson's?
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Implant embryonic dopaminergic neurons
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What are the AI for Parkinson's?
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Based on understanding the disease, treatments and medication interactions: Elimination of levodopa and dopamine are short (6-12 hrs) -; do not interrupt treatment or there will be abrupt loss of therapeutic effects. Have the patient take these meds the am of surgery. Call in rep to turn off stimulator if they have one. Low BP and cardiac arrhythmias
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How will drug withdrawal manifest if the Parkinson's patient misses doses of levodopa?
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Skeletal muscle rigidity that interferes with ventilation
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What meds should not be given to Parkinson's patients?
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Any med that antagonizes the effects of dopamine in the basal ganglia: butyrophenones (droperidol, haldol), reglan, phenergan, alfentanil (can lead to acute dystonic rxn due to opioid induced decrease in central dopaminergic transmission, ketamine (questionable d/t exaggerated SNS responses). There are no concerns with NMB's.
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What causes Huntington's disease?
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Premature degenerative disease of the CNS Deficiencies in ACh (and it's synthesizing enzyme choline acetyl transferase) Loss in GABA --> decrease inhibition of dopamine Autosomal dominant --> onset 35-40 y/o
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What are the s/sx of Huntington's?
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Dementia Spastic movements (choreoathetosis) Behavioral changes (depression, aggression, mood swings) Pharyngeal muscle involvement --> aspiration
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How is Huntington's treated?
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Symptomatic --> aimed at decreasing choreiform movements (haldol, butyrophenones for emotional lability) or to interfere with neurotransmitter effect of dopamine via antagonism (haldol) or depletion of dopamine stores (reserpine & tetrabenzine)
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What are the AI implications of Huntingtons?
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Preop sedation with butyrophenones (droperidol/haldol) Watch for aspiration N2O and volatile agents are OK May have decrease plasma cholinesterase (may have prolonged rxn to succs) Sensitive to NDNMBs
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What causes Torticollis?
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Disturbances in the basal ganglia --> spasmodic contraction of nucal muscles --> limb and girdle muscles. Spasm can also affect muscles of vertebral column --> lordosis, scoliosis, impaired ventilation
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What is the treatment for Torticollis?
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Bilateral anterior rizotomy at C1 and C3 with sectioning of the spinal accessory nerve OR selective peripheral denervation of affected cervical musculature.
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What are possible complications of Bil anterior rizotomy?
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Post-op paralysis of the diaphram --> resp. distress.
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What are the AI of Torticollis?
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Spasm of nuchal m. can interfere with maint. of patent upper airway before muscle paralysis. May need awake intubation if chronic skeletal m. spasm has resulted in fixation of cervical vertebrae
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If drug induced Torticollis occurs what drug should be administered?
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Diphenhydramine 25-50 mg IV (benedryl)
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What causes Cruzfeldt-Jakob Disease?
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Caused by prions. Causes accumulation of abnormal protein that acts as a neurotransmitter in the CNS. (Also called Mad Cow disease)
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What are the s/sx of Cruzfeldt-Jakob Disease?
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Rapidly progressive dementia, ataxia, myoclonus, seizures (late sign).
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How is diagnosis of Cruzfeldt-Jakob Disease done?
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Brain biopsy
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What are the AI for Cruzfeldt-Jakob Disease?
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Universal infection precautions (same as with hepatitis or HIV). Double glove, protective glasses, etc. when dealing with CSF. Instruments used for biopsy should be disposable or decontaminated by soaking in sodium hypochlorite or autocaving.
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What causes Multiple Sclerosis (MS)?
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An autoimmune disease affecting CNS in genetically susceptible persons. Combination of inflammation, demyelination, and axonal damage in CNS and formation of demyelinative plaques (no involvement of PNS).
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What happens with MS in pregnant women?
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Relapse rate increases (x 2) esp. in 3rd trimester and in first 3 months postpartum.
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Besides pregnancy, what can trigger an relapse in MS?
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Viral illness
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What is the disease progression for MS?
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Can be chronic and progressive or subacute with relapses and remissions
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What are the s/sx of MS?
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Symptoms depend on the site of demyelination (e.g., optic nerve demyelination --> vision changes)
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If there is no remyelination in the CNS, why to MS patients have remissions?
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Symptoms improve due to correction of transient chemical and physiologic disturbances that have interfered with nerve conduction in the absence of complete demylination.
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What can cause an exacerbation of MS and what can this lead to?
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Increases in temp --> alteration in nerve conduction in regions of demyelination --> seizures (keep normothermic!)
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How is MS diagnosed?
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Immunoglobulin assays, evoked potential testing, signal changes in white matter on MRI.
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How is MS treated?
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Symptom control Corticosteriods for acute relapse (immunomodulatory and anti-inflammatory effects --> restore BBB, decrease edema, may improve axonal conduction. Interferon B: for relapsing/remitting MS
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What are the AI for MS?
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Avoid surgical stress --> can cause exacerbation Avoid Spinals (exacerbations due to neurotoxicity?) Peripheral nerve blocks/epidurals ok Mostly use GA Succs may cause exaggerated release of K (prolonged duration) Resistance to NDNMB has been seen (proliferation of extrajunctional cholinergic receptors like with upper motor neuron lesions) Consider Corticosteriods perioperatively AVOID increases in body temp!! (normothermic)
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What causes poliomyelitis?
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Caused by an enterovirus that infects the reticuloendothelial system and CNS in some patients and targets motor neurons in the brainstem and anterior horn of the spinal cord?
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What are the s/sx of postpolio sequelae?
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Fatigue, muscle weakness, cold intolerance, dysphagia, OSA
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What are the AI for patients with postpolio sequelae?
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RAS often affected --> delayed awakening from anesthetics and sensitivity to anesthetics Severe back pain Severe post-op shivering Increased post-op pain sensitivity Sensitive to NMB Probably not good candidates for outpatient surgery (increased risk of resp muscle weakness and dysphagia --> aspiration)
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What is a seizure?
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Transient, paroxysmal, and synchronous discharge of groups of neurons in the brain
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What are the clinical s/sx of seizure?
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Depends on location and number of neurons involved in seizure discharge and duration. Transient abnormality (like hypoglycemia, hyponatremia, drug toxicity, etc. = single seizure)
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What is epilepsy?
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Recurrent seizures from congenital or acquired factors.
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How are seizures classified?
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Based on LOC and focus of seizure activity.
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For a patient with a seizure history, what lab level should be checked preop?
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Dilantin level (normal is 10-20)
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If doing a resection for epilepsy, how is the seizure area mapped preoperatively?
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MIR and electrocroticography
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How should a seizure be treated?
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Start with one anti-seizure drug to achieve control and increase dose. Combo therapy only when monotherapy fails
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How do anti-seizure drugs generally work?
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Decrease neuronal excitabilty or enhance neuronal inhibition
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Name three common drugs used to treat partial seizure:
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Carbamazine Phenytoin Valproate
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Name common drugs used to treat generalized seizure:
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Carbamazine Phenytoin Valproate + Barbs Gabapentin Lamotrigine
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How are most anti-seizure drugs metabolized and excreted? What is the exception?
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Metabolized: Liver Excreted: Renal Exception is gabapentin (excreted unchanged in kidneys)
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What do carbamazepine, dilantin and barbs all cause with respect to metabolism?
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Enzyme induction (will cause fast metabolism esp NMB) All also cause sedation
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What side effects are common with carbamazepine that has AIs?
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Leukopenia Decreased Na Liver alterations
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What side effects are common with valproate that has AIs?
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Liver failure Pancreatitis Increased bleeding Possible thrombodytopenia Decreased vWF and Factor VIII
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What side effects are common with Dilantin that has AIs?
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Hypotension Arrhythmias Aplastic anemia Stephens Johnson Extravasation!!!! --> signficant vasoconstriction and skin necrosis, compartment syndrome, gangrene
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What drug can be given in substitute for dilantin for IV antiepileptic admin to avoid extravasation effects in Dilantin?
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Phospheytoin
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What lab values should be checked for patients on Carbamazine, Phenytoin or Valproate?
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CBC, Liver Enzymes
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What surgeries are commonly done for seizure?
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Resection of seizure focus Corpus Callostomy Hemispherectomy Temporal Lobectomy
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What is a potential side effect of temporal lobectomy?
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permanent hemiparesis
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What is a more conservative treatment for seizure that is done instead of a temporal lobectomy?
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Implantation of left vagal nerve stimulator
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Why is the left vagal nerve stimulator done instead of the right?
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Right has significant cardiac innervation --> severe bradyarrhythmias
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What is a common side effect of Implantation of left vagal nerve stimulator?
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Hoarseness due to vagal innervation of larynx
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What is status epilepticus?
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A life-threatening condition that manifests as a continuous seizure activity or two or more seizures occurring in sequence without recovery of consciousness between them.
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What is the main treatment goal in status epilepticus?
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Prompt IV access Treatment with anti seizure med Support airway, ventilation, circulation
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What should be first ruled out with sustained seizure?
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Hypoglycemia (give 50 ml D50 with low BS)
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Why shouldn't D50 be given immediately with seizure (before checking BS)?
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Can worsen a brain injury
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What commonly used anesthesia drugs can be used to temporarily halt seizure activity?
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Proprofol or thiopental
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Why shouldn't long term muscle relaxants be given with status epilepticus?
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Because there will be no way to assess whether or not the seizure has stopped
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What lab should be monitored for status epilepticus that will help determine if there is ongoing seizure activity?
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ABGs (metabolic acidosis will occur with ongoing seizure)
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Why do status epilepticus patents sometimes need to be actively cooled?
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Hyperthermia is associated with muscle hyperactivty and increased brain metabolism
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Why should Brevital be avoided in patients with seizure disorders?
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It can activate epileptic foci
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Which drugs can cause eleptiform spikes in patients without a history of seizures but can also suppress epileptiform and epileptic activity?
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Alfenta Ketamine Ethrane forane Sevo
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Which anesthetic has been associated (rarely) with seizure and opisthotonos in patients with seizure disorder?
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Proprofol
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Which NMB have a proconvulsant metabolite?
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Atricurium and cisatricurium
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Which NMB is CNS stimulating?
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Laudanosine
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Do the volatile agents cause seizure?
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Yes, all have produced seizure?
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Which drugs are best to use in seizure disorder patients in anesthesia?
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Barbs Opioids Benzos Iso, des, sevo
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What is syringomyelia?
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A congenital spinal abnormality in which there is a cystic cavitation of the spinal cord.
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What is a communicating syringomyelia?
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There is either only dilatation of the central canal of the cord (hydromyelia) or communication between the abnormal cystic lesions in the spinal cord proper and the CSF spaces.
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What is communicating syringomyelia associated with (other conditions)?
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History of basilar archnoiditis or Chiari malformation
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What is non-communicating syringomyelia?
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Presence of cysts that have no connection to the CSF spaces.
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What is non-communicating syringomyelia associated with?
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History of trauma Neoplasms Archnoiditis
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When do s/sx of syringomyelia occur (age)?
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30's or 40's
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What are the early s/sx of syringomyelia and what is the pathology that causes them?
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Sensory impairment involving pain and temp in the upper extremities --> indicates destruction of pain and temp neuronal pathways that cross within the spinal cord near the central canal.
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What are the later s/sx of syringomyelia and what is the pathology that causes them?
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Skeletal muscle weakness with wasting plus loss of reflexes --> caused by destruction of lower motor neurons
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What is the treatment for syringomyelia?
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No known treatment is effective
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How does tone differ between damage to upper motor neurons versus lower motor neurons?
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Upper: increased tone; clasp-knife rigidity Lower: decreased tone
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How do reflexes differ between damage to upper motor neurons versus lower motor neurons?
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Upper: Increased reflexes below the level of damage; Plantars (toes) upgoing Lowers: decreased reflexes regarding muscles innervated by damaged nerves; Plantars (toes) downgoing
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What are the AI for syringomyelia patients?
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Consider the patient's specific neuro deficits: Thoracic Scoliosis can cause V:Q mismatch Low Motor Neuron disease with muscle wasting --> possibility of hyper K with succs (don't give due to proliferation of receptors) or exaggerated responses to NDNMB
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What is ALS (amyotrophic lateral sclerosis)? Who does it commonly affect (population)?
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A degenerative disease involving lower motor neurons in the anterior horn gray matter and corticospinal tracts (primary descending upper motor neurons). Affects mostly men 40-6- yrs.
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What condition do EMG's of ALS patients resemble?
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Myasthenia gravis
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What are typical s/sx of ALS?
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Muscle atrophy Weakness in skeletal muscles including airway ANS dysfunction --> orthostatic BP and resting tachycardia Emotional lability Leg cramping & Lung CA Death within 6 years
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What are the AI's associated with ALS?
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GA associated with resp depression Watch succs and increased K+ due to lower motor neuron disease Prolonged response to NDNMB (consider use of cisatricurium) Avoid RA
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What is Freidreich's Ataxia?
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An autosomal recessive disorder with degeneration of spinocerebellar and pyramidal tracts.
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What symptoms are common in Freidreich's Ataxia?
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Cardiomyopathy (10-50%) Kyphoscoliosis with steady deterioration of pulmonary function (80%) Ataxia (typical presenting symptom)
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What are the AI for Freidreich's Ataxia?
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Similar to ALS [GA associated with resp depression Avoid RA] x response to NMB normal Additional: Consider negative inotropic effects if cardiomyopathy is present; watch post-op vent failure with kyphoscoliosis
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What are the components of the PNS?
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Autonomic + Somatic
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With problems of the ANS what are some general anesthetic implications?
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Significant hemodynamic changes Abnormal responses to drugs that work on adrenergic receptors
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With problems of the SNS what are some general anesthetic implications?
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Consider choice of muscle relaxants Control of neuropathic pain
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What is Shy-Drager Syndrome?
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A group of disorders with multiple-system atrophy. The hallmark is degeneration and dysfunction of structures important for ANS function
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What are s/sx of Shy-Drager?
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Orthostatic BP Urinary retention bowel dysfunction
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What is the cause of orthostatic hypotension in Shy Drager?
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Plasma NE does not increase with standing or exercise so no increase in HR or vasoconstriction --> syncope
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What are the treatments for Shy-Drager?
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Hypotension meds at home: alpha 1 agonists and alpha 2 antagonists Levodopa for Parkinson-type symptoms
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What should be evaluated preop for Shy-Drager pts?
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Orthostatic BP and beat-to-beat HR variablity
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What are the AI for Shy-Drager pts ?
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Decreased ANS activity --> CV responses to changes in body position, Positive airway pressure and blood loss. Consider negative inotropic effects of anesthetic drugs (avoid) Put in A-line for monitoring Vasopressor effects May need phenylephrine infusion Watch BP with RA - BE VIGILANT Use Vec (a muscle relaxant with less systemic effect) Exaggerated BP response with ketamine
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What can happen in Shy-Drager pts and vasopressor reaction?
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May have exaggerated response to indirect acting vasopressors so use direct acting and use small doses until response is confirmed (can have up regulation of alpha receptors
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What are the s/sx of Guillian-Barre'?
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Sudden onset of skeletal m. weakness or paralysis that starts in legs and goes to the face (most common cause of acute generalized paralysis
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Which motor neurons are affected by Guillian-Barre' and what is caused?
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Lower Motor Neurons --> flaccid paralysis and decreased reflexes.
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What respiratory issues are involved with Guillian-Barre'?
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Respiratory impairment --> trach (don't need NMB)
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What symptoms are caused by ANS dysfunction in Guillian-Barre'?
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Wide fluctuations in BP, sudden diaphroesis, peripheral vasoconstriction, resting tachycardia--> can cause sudden death Increased thromboembolism
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What are the diagnostic criteria for Guillian-Barre'?
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Required for diagnosis: Progressive bilateral weakness in legs and arms Areflexia Strongly supports diagnosis: Progression of symptoms over 2-4 wks Symmetry of symptoms Mild sensory symptoms/signs (definitive sensory level makes diagnosis doubtful) CN involvement (esp. bil facial weakness) Spontaneous recovery 2-4 weeks after progression ceases ANS dysfunction Absence of fever at onset Increased protein concentration in CSF
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What disease occurs in many patients prior to developing Guillian Barre?
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Viral respiratory or GI infections
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What are the treatments for Guillian-Barre?
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Support Ventilation, monitor ABGs ANS dysfunction may require tx of high/low BP Plasma exchange or gamma globulin
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What are the AI for Guillian-Barre'?
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May have profound decrease in BP with position change, blood loss, or + airway pressure Noxious stimuli causes greatly increased BP Use A-line Avoid indirect vasopressors...they are not predictable (use direct) No siccs (nimbex and vec are OK)
