Neuro Anesthesia Part 2 – Flashcards
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Acute Ischemic Strokes
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-Symptoms evolve over minutes to hours -TIA's sign of impending ischemic stroke -Risk factors: Hypertension, Cigarette smoking, Hyperlipidemia, Diabetes mellitus
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Acute Ischemic Stroke: Management
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-ASA therapy -Thrombolytic drugs -Maintenance of adequate blood pressure, glucose levels, body temp -Rarely cerebellar resection
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Hemorrhagic CVA's
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-4x more likely to cause death than embolic CVA -Deterioration due to increasing cerebral edema and "no flow" patterns -Most commonly results from aneurysm rupture -Risk of rupture depends on size
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Subarachnoid hemorrhage
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-Diagnosis based on clinical symptoms and CT -Symptoms: Worse headache of my life Photophobia Nuccal rigidity Decreased level of consciousness ST-segment depression/T wave inversion/Decreased myocardial contractility -Noncontrast CT required
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Prevent vasospasm
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-calcium channel blockers -statins -triple H therapy: hypertension-R/T loss of autoregulation, hypervolemia-R/T state of hypovolemia and hemodilution
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Complications of SAH
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-Hydrocephalus -Hyponatremia- related to high urine sodium -Hypovolemia-isotonic fluids to normovolemia -Rebleeding/Death
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Subarachnoid Clipping: Induction
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-Induction: maintain "normal" BP, SBP elevation during induction may rupture aneurysm; SBP reduction may cause ischemia -Arterial line*** -CVP- related to diuretic therapy
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Subarachnoid Clipping: Maintenance
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-approx 7% rupture intraop toward late stages of dissection -Appropriate depth* (avoid light anesthesia) -Maintain CPP -Drugs, fluids, blood immediately available -Volatile anesthetics (minus nitrous!!!) -Narcotics -Muscle relaxants -Mild hyperventilation (ETCO2 32-35) -Consistent, Consistent, Consistent -*may need emergent induced hypotension
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Brain relaxation
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-Lumbar CSF drainage -Mild hyperventilation -Loop/osmotic diuretics -Proper positioning -Anti-Seizure drugs -Normovolemia- no glucose containing solutions -Normothermia- elevated temps increase CMRO2 and CBV
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Drug-induced hypotension
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-Traditionally used to decrease transmural pressure across the aneurysm and chance of rupture -Concerned about autoregulation following rupture and risk of global ischemia -Alternatives: regional controlled hypotension...clamping parent artery, Barbiturate suppression
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Emergence
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-Prompt awakening for assessment of neurological status -Short acting antihypertensives as needed (ex. Esmolol) -Lidocaine to suppress airway reflexes -Neuro checks to assess surgical vs. anesthetic causes of delayed emergence
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AVM
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-Abnormal collections of blood vessels -Have multiple direct arterial-venous connections without capillaries -Intramural pressure is less than systemic so rupture not R/T hypertension -Congenital -Present as hemorrhage or new-onset seizures
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AVM: Pre-op
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-Evaluate for evidence of ischemia/increased ICP -Antiepileptic drugs administered -Assess Fluid & Electrolytes following hypertonic contrast material post angiography
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AVM: Induction
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Unlikely to rupture during induction -Art line -Again BP control!!!! -Blunt laryngoscopy response -Muscle relaxants..... Depolarizers vs non??? -Adequate intravenous access- RAPID hemorrhage is very possible CVP catheter** -Consider lumbar CSF drain
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AVM: Maintenance
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-Avoid hypotonic solutions -Avoid glucose containing solutions (raises metabolism) -Administer diuretics -Mild hyperventilation*i.e. prevent cerebral edema which is likely as feeder arteries are ligated and blood flow is directed toward remaining tissue
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AVM: Emergence
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-Most patients emerge and extubate smoothly -Low dose B-blockers/Nipride to control HR -Neuro checks
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Epidural hematoma
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-Tear of middle meningeal artery -75-90% associated with skull fracture -Life threatening emergency
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Subdural hematoma
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-Tear of sagittal veins -Acute or chronic
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Burr holes
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-Rapidly decompress deteriorating brain -Skin flap turned -Small holes drilled through skull to epidural or subdural space
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Burr holes: Anesthesia Management
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-Rapidly control airway: RSI -Induction with propofol or pentothal -Anectine best NMB choice** -Arterial line- no BP swings -Keep deeply paralyzed -GOOD IV access -Adequate depth prior to pinning....if appropriate -Measures to decrease ICP per surgeon....
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Hydrocephalus-Normal Pressure
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-Usually presents as triad: dementia, gait changes, and urinary incontinence -Develops over weeks to months -Thought to be related to impaired CSF absorption from previous insult: trauma, meningitis, SAB etc -LP: normal or low CSF pressure -CT/MRI: enlarged ventricles -Treatment: VP shunt
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Hydrocephalus (Elevated ICP)
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-CSF accumulation that causes ventricular dilation resulting from increased ICP -Congenital or acquired -Imbalance between production and absorption -Common symptoms of elevated ICP: N/V, altered LOC, mydriasis, papilledema, bradycardia, hypertension, breathing pattern changes -Most common cause is impaired circulation/obstruction by structural abnormalities: Stenosis of aqueduct of Sylvius, Tumors, Chiari malformation -Surgical treatment with VP shunt, tumor excision, Chiari repair
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VP shunt: Induction
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-Provide rapid, reliable loss of consciousness....thiopental, propofol -Muscle relaxation....depolarizing vs. non (roc or vec are ideal) -Make sure laryngoscopy reflexes are blunted -Prevent hypo/hypertension -Avoid Ketamine!!
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VP shunt: Maintenance
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-No evidence of superior combination -Profound skeletal muscle relaxation! -Avoid hypervolemia
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VP shunt: Emergence
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-Routine wake-up -Blunt response to endotracheal tube (Lidocaine, Appropriate narcotics)
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Parkinson's disease
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-A neurodegenerative disorder of unknown cause -Increasing age is the single most important risk factor -Loss of dopaminergic fibers from the basal ganglia -Autonomic dysfunction, respiratory obstruction and aspiration pneumonia common
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Parkinson's Disease: Symptoms
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-Triad of symptoms: skeletal muscle tremor, rigidity, akinesia -Muscle rigidity first appears in proximal muscles of neck- loose arm swinging -Tremors are rhythmic, alternating flexion/extension of thumbs and other digits (pill rolling) -Tremors more prominent during rest
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Parkinson's disease: Treatment
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-attempts to increase the concentration of dopamine in the basal ganglia or decrease effects of acetylcholine -Standard: levodopa Dyskinesias, altered myocardial contractility, orthostatic hypotension, N/V -Administered with Carbidopa, MAO-b inhibitors or dopamine receptor agonists to prevent side effects.
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Deep Brain Stimulator
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-Usually implanted in two stages -Stage 1: A rigid head frame is applied, and an MRI taken to coordinate area of surgical approach. Patient is returned to OR, prepped, drapped and a burr hole accomplished for placement of electrodes in sub-thalmic nucleus. Target tissue is stimulated with patient feedback. Leads are sutured in place and burr holes closed.
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Deep Brain Stimulator: Anesthesia Implications
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-Stage 1 -under local/light sedation -Head frame applied in WC/on stretcher -Morning dose of levodopa is omitted so IV starts are challenging; abrupt withdrawal (6-12 hours) can cause skeletal muscle rigidity...ventilation -Small doses of versed, narcotics, dexmedetomidine -Precordial dopplers -Control hypertension- IV Cardene
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Deep Brain Stimulator: Stage 2
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-under general anesthesia -Electrodes are accessed and connected to 1 or 2 generators placed below the clavicle
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Multiple Sclerosis
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-Autoimmune disease affecting the CNS -Genetically associated -Characterized by: Inflammation, Demyelination and Axonal damage in the CNS (not PNS).
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Multiple Sclerosis: Symptoms
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-Symptoms develop over a few days, remain stable a few weeks, then improve -Remission/exacerbations unpredictable -Onset after age 35...slow progression -Symptoms reflect sites of demyelination: Optic nerve: visual disturbance Cerebellum: gait disturbance Spinal Cord: paresthesia , weakness, incontinence
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Treatment of MS: Corticosteroids
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anti-inflammatory effects, help restore blood/brain barrier
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Treatment of MS: Interferon
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limited to patients with rapidly progressing symptoms B/C of cardiac toxicity
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Treatment of MS: Azathioprine
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a purine analogue; depresses cell and humoral mediated immunity
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Treatment of MS: Methotrexate
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inhibits cell and humoral mediated immunity
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Multiple Sclerosis: Management of Anesthesia
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-MUST CONSIDER THE IMPACT OF SURGICAL STRESS!!! -Temperature increases of 1 degree can exacerbate symptoms -Corticosteroid supplementation appropriate -No specific induction, maintenance agents -Probably best to avoid succinylcholine! -Nondepolarizers could increase muscle weakness but resistance to these has been observed
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Myasthenia Gravis
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-Autoimmune disorder caused by a decrease in functional acetylcholine receptors at the NMJ -As many as 80% may be lost -Hallmark symptoms: Weakness/rapid exhaustion of voluntary muscles followed by partial recovery with rest
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Treatment of MG: Anticholinesterase
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-inhibit enzyme responsible for hydrolysis of acetylcholine....more Ach; Pyridostigmine and Neostimine
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Treatment of MG:Immunosuppression
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-indicated when skeletal weakness is not adequately treated with anticholinesterase drugs; very effective but lots of side effects -Steroids, Azathioprine, Cyclophosphamide, Cyclosporin
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Treatment of MG
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-Short term immunotherapy: removes antibodies from circulation by plasmapheresis; temporary effect but useful in preparation for thymectomy -Thymectomy: intended to induce remission; treatment of choice for majority of MG patients. Post of 75% show improvement or remission
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Thymectomy
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-Preoperative: optimize strength and respiratory function PFT's should be included -May be accomplished by median sternotomy or mediastinoscopy -Address postoperative pain issues so postoperative respiratory excursion is optimized
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Myasthenia Gravis: Induction
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-Use short-acting agents to decrease effects of respiratory depression -Consider tracheal intubation without neuromuscular blockade Antibodies result in increased sensitivity to non-depolarizers -Short acting nondepolarizer ideal -1/10-1/20 the usual dose -Sensitivity is increased with concurrent volatile use -Medium acting nondepolarizers best avoided; but care in reversal so as to avoid a cholinergic crisis -Care with other "neuromuscular blocker" (Calcium channel blockers and Diuretics)
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Anticholinesterase drugs impair
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plasma pseudocholinesterase activity.....anectine....but receptors seemingly resistant so Not clinically apparent!
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Myasthenia Gravis: Maintenance
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-Volatile anesthetics: benefit is small amt of muscle relaxation -Little to no opioids -IV tylenol/toradol??
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Myasthenia Gravis: Emergence
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-**Clear evidence of good respiratory function** -Anticipate the need for prolonged ventilation: Patient teaching in preop; If disease present more than 6 years; Associated with COPD; Requiring large doses of pyridostigmine (750mg)
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Guillain-Barre Syndrome
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-Characterized by sudden onset of skeletal muscle weakness or paralysis -Begins in legs and spread cephalad.... -Most serious signs are difficulty swallowing and impaired ventilation -Sensory disturbances precede paralysis -Autonomic nervous system dysfunction prominent!!! -Diagnosis based on clinical symptoms, protein increases in CSF -½ patients develop after UTI or GI infection -Treatment symptomatic
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Guillain-Barre Syndrome: Autonomic dysfunctions
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-BP fluctuations -Sudden profuse diaphoresis -Peripheral vasoconstriction -Resting tachycardia -Orthostatic hypotension -Thromboembolism -Sudden death!!!
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Guillain-Barre Syndrome:Anesthetic Management
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-Strongly consider endotracheal intubation -Correction of autonomic dysfunctions ...hypertension with laryngoscopy...hypotension with positioning/positive airway pressure -Consider arterial line -Avoid succinylcholine!! -Prepare for postop ventilation
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Tumor types
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-Astrocytoma -Glioma -Meningioma -Pituitary tumor -Acoustic neuroma -Metastatic
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Intracranial tumors: Astrocytoma/Gliomas
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-Astrocytes most common neuroglial cells in CNS...many different types of tumor -Gliomas: well differentiated, least aggressive, surgical resection successful for long term prognosis -Glioblastoma: 30% of primary brain tumors; microscopic infiltration of normal brain; resection inadequate; life expectancy weeks
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Intracranial tumors: Meningioma
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-Slow growing, well circumscribed -Benign -Commonly near sagittal sinus or falx cerebri VAE more likely -Receive blood supply from External Carotid Artery* -Surgical resection typical with excellent prognosis; may recur
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Intracranial tumors: Pituitary
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-Arise from cells of Anterior pituitary gland -May occur with tumors of parathyroid and pancreatic islet cells (MEN type I) -Surgically resection curative -Appear as: Microadenomas: hormone secreting and symptoms are related to hormone Macroadenomas: non-hormone secreting and symptoms relate to mass
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Intracranial tumors: Acoustic Neuroma
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-Usually result of benign shwanoma involving CN 8 -Bilateral tumors may occur as part of neurofibromatosis -Symptoms include hearing loss, tinnitus, and disequilibrium -Surgical resection common with auditory evoked potentials -Prognosis is very good; recurrence is common
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Intracranial tumors: Metastatic
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-Originate most often from primary sites in the lung or breast -Most likely diagnosis when more than one lesion if present -Have abnormal angiogenesis: more likely to bleed during resection
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Tumor resection: Pre-op
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-Identify presence/absence of increased ICP: N/V, Altered LOC, Mydriasis/decreased reactivity, Bradycardia, Systemic hypertension, Breathing disturbances -Caution with preoperative sedatives (Hypoventilation...Increased CO2...Increased ICP; Altered LOC difficult to assess
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Tumor resection: Induction
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-Rapid, reliable without increasing ICP...thiopental, etomidate, propofol -Non-depolarizing muscle relaxants -Mild hyperventilation -Adequate depth before laryngoscopy -Avoid abrupt changes in systemic blood pressure
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Tumor resection: Maintenance
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-Combination of drugs -Nitrous oxide is controversial due to potential for venous air embolism -NO spontaneous movements!!! -Avoid peripherally dilating drugs until after dura is opened...nitro, nipride...CBV increases but CPP decreases
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Tumor resection: Fluid therapy during maintenance
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-Avoid glucose solutions -Blood loss probably best replaced with PRBC's -ANY excessive fluid can cause brain edema: goal is toward euvolemia
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Tumor resection: Monitoring during Maintenance
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-Arterial line -Urinary catheter -Temperature -Appropriate intravenous access/CVP -Peripheral nerve stimulation (monitor non-paretic extremity)
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Tumor resection: Emergence
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-Wake-em up! -Blunt response to endotracheal tube (Confirm appropriate airway reflexes)
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Transsphenoidal hypophysectomy
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-Method of choice for resection of pituitary tumors -Performed nasally to avoid complications associated with craniotomies -Otolaryngologist reaches sphenoid sinus (runs along optic nerve and carotid artery), enters sella region. -After tumor resection, CSF leaks controlled with fat or muscle graft; Gelfoam packed into sella to obliterate space; sella floor reconstructed with bone; sphenoid sinus closed
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Transsphenoidal hypophysectomy: Functional tumors (secretory):
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-prolactin...lactation -ACTH...adrenal hyperplasia -growth hormone...acromegaly
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Transsphenoidal hypophysectomy: Pre-op
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-Airway issues: with acromegaly....large tongue, long neck, redundant airway tissue -Cardiovascular issues: HTN, ischemic heart disease, diabetes
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Transsphenoidal hypophysectomy: Maintainence
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-Consider fiberoptic intubation (Consider Oral rae tube) -Standard induction and maintenance drugs -Arterial line -Deliberate oropharyngeal/gastric suction prior to extubation -No nasal cannula postop!! -Complications: VAE, carotid injury
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Venous air embolism
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-Right heart failure -Bronchoconstriction -Cerebral embolism -Coronary artery embolism
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Detection of VAE
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-Doppler ultrasound -TEE -Capnography
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Symptoms of VAE
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-Sudden decrease in PaCO2 -Increase RAP -Hypotension -Tachycardia -Cardiac dysrhythmias -Mill wheel murmur -Cyanosis
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Treatment of VAE
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-Operative site flooded (fluids) -Aspiration of right heart (with CVP) -Nitrous oxide administration discontinued -100% oxygen administered -Inotropic support of BP if needed -B2 agonists if needed
