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58 Cards in this Set
- Front
- Back
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Define Status Epilepticus
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1. Any seizure lasting longer than 30 minutes whether or not consciousness is impaired
2. Recurrent seizures without an intervening period of consciousness |
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What is the status epilepticus cycle?
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1. Seizure activity
2. Increased cerebral metabolic demand 3. Increased cerebral blood flow 4. Relative hypoperfusion 5. Hypoxic cellular injury 6. Ischemic brain damage 7. More seizure activity |
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Relationship of etiology of SE to response
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1. Type I has no structural lesions. It is usually responsive to drug therapy. Etiologies include medication withdrawal, electrolyte/metabolic conditions, alcohol withdrawal and infection.
2. Type II has no structural lesions and is frequently resistant to standard methods of treatment. Etiologies include acute vascular events, drug overdose, anoxic encephalopathies, CNS neoplasms, and trauma. |
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What are the most common causes for precipitation of status in individuals known to have epilepsy?
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1. Drug withdrawal
2. Alcohol abuse 3. Acute infection |
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When patients present in status as the initial manifestation of epilepsy, they have a high proportion of what?
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1. Tumors
2. Post-traumatic lesions of the frontal lobe |
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What are the mechanisms of SE pathogenesis?
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1. Sustained repeated firing of Na channels
2. Excessive Ca conductance 3. Increased excitatory neurotransmitter 4. Loss of control by inhibitory neurotransmitter |
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What body changes are seen during the first 30 minutes of SE?
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1. Increased autonomic activity: hypertension, hyperglycemia, sweating, salivation, and hyperpyrexia
2. Increased cerebral blood flow due to increased metabolic demand |
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What body changes are seen after 30 minutes of SE?
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1. Secondary metabolic changes are seen including lactic acidosis, hypoglycemia, dehydration, rhabdomyolysis, hypotension, and shock
2. Compromised respiration/cardiovascular function 3. Failure of cerebral blood autoregulation with decreased cerebral blood flow, increased intracranial pressure and altered cerebral metabolism |
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What are the goals of treatment of SE?
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1. Terminate electrical and clinical seizure activity within 30 minutes
2. Prevent recurrence of seizures 3. Insure brain oxygenation 4. Correct any precipitating factors (hypoglycemia, electrolytes, fever) 5. Stabilize metabolic balance (correct lactic acidosis, dehydration, shock) |
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Treatment of SE during 0-10 minutes
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1. Start IV infusion with normal saline, containing 50-100 mg thiamine. Give a bolus injection of 50 ml 50% glucose.
2. Give lorazepam 2-4 mg IV at a rate of 2 mg/min. Repeat every 5 minutes until seizures stop. |
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What is thiamine used for in SE?
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it prevents Wernicke's encephalopathy
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Why is lorazepam used in SE instead of diazepam?
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Lorazepam has a longer duration of action centrally than diazepam
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Treatment of SE during 10-30 minutes
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This step is usually skipped.
1. Give IV infusion of phenytoin 20 mg/kg at a rate no faster than 50 mg/min (use 1 gram in 100 ml of NS). 2. Or give IV infusion of fosphenytoin 20 mg/kg at a rate no faster than 150 mg/min. |
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Treatment of SE during 30-60 minutes
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1. Give phenobarbital 20 mg/kg IV given at a rate no faster than 100 mg/min
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Treatment of SE if persistent past 1 hour
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Consider these options: midazolam drip, pentobarbital, IV valproic acid
If these fail, put the patient under with general anesthesia (propofol) |
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Adverse effects of benzodiazepines
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Adverse effects of benzodiazepines include depression of consciousness, respiration, and hypotension. These effects are related to both rate of administration and total dose.
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Adverse effects of phenytoin
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The major adverse effects of phenytoin are heart block, tachycardia, and thrombophlebitis. Other effects include nystagmus, ataxis, sedation, and hypotension. Hypotension and pain at infusion site should be treated by reducing the infusion rate by 10-20 mg/min.
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Adverse effects of fosphenytoin
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Fosphenytoin is more water-soluble than phenytoin, thus requires no organic solvents like phenytoin. It has less tissue irritation and phlebitis. It may also be administered IM and at much higher rates (150 mg/min). Otherwise it has the same side effect profile as phenytoin plus paresthesias and pruritis.
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What are the first considerations in a poisoned patient?
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1. Airway
2. Breathing 3. Circulation |
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Treatment for a patient with altered mental status and suspected poisoning
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Give 100 mg of thiamine and 25-50 grams of glucose IV. If there is no response to the glucose, then give 2-4 mg of naloxone.
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What agents can cause cholinergic syndrome?
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1. Direct cholinergic agents: pilocarpine, bethanecol
2. Cholinesterase inhibitors: organochlorines, organophosphates, carbamates |
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Where does acetylcholine do its work?
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1. ACh is the preganglionic nicotinic, postganglionic nicotinic, and muscarinic neurotransmitter in the parasympathetic system.
2. ACh is a preganglionic nicotinic neurotransmitter in the sympathetic system, but postganglionic norepinephrine dominates as the neurotransmitter. |
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What are the peripheral effects associated with muscarinic and nicotinic receptor stimulation (cholinergic syndrome)?
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1. Muscarinic effects include salivation, lacrimation, urination, diarrhea, emesis, bradycardia, and misosis.
2. Nicotinic effects include weakness, paralysis, pupillary dilation, and respiratory compromise (this is what kills). |
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What are the central effects of cholinergic syndrome?
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Central effects are anxiety, convulsions, coma, areflexia, and altered respiratory patterns.
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Define cholinergic syndrome
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an excess of acetylcholine
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Define antimuscarinic syndrome
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it is the antithesis of cholinergic syndrome
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What are the agents that cause antimuscarinic syndrome?
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atropine
hyoscyamine diphenhydramine tricyclic antidepressants promethazine scopolamine jimson weed mushrooms |
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What are the peripheral and central effects of antimuscarinic syndrome?
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1. Peripheral: thirst, dysphagia, mydriasis, hyperthermia, dry skin, flushing, urinary retention, hypertension, tachycardia (these effects are usually just with very large doses)
2. Central: delirium, hallucinations, lethargy, respiratory failure |
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What agents can cause adrenergic excess?
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1. amphetamines
2. cocaine 3. epinephrine 4. norepinephrine |
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What are the classic symptoms of adrenergic excess?
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Nervousness, tremor, diaphoresis, tachycardia, and hypertension (chronic abusers may have normal HR and BP due to down regulation)
It is very similar to anticholinergic toxicity except sweating, bowel sounds are present, and urinary retention is not normally seen. |
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Describe extrapyramidal syndrome
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Dopamine and acetylcholine act in opposition centrally to smooth out voluntary muscle motion. The system they create is termed the extrapyramidal motor system. An imbalance of either neurotransmitter can lead to adverse muscle movement, but the apparent decrease in dopamine is termed EPS.
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What are the symptoms of EPS?
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Rigidity, tremor, dysphonia, and dysphagia often characterize EPS. In severe cases torticollis, oculogyric crisis, laryngospasm, and opisthotnus may occur.
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What agents can cause EPS?
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Classis agents are phenothiazines and butyrophenones.Strychnine and tetanus can produce similar clinical picture, but toxicologically they are different.
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Describe carboxyhemoglin.
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Carboxyhemoglobin is the most common of the hemoglinopathies. It most often occurs following excessive exposure to atmospheric CO or methylene chloride. Low concentration causes HA, N/V, and malaise. Higher concentrations cause hypoxia, coma, cardiac dysfunction, acidosis, and death.
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Describe methemoglobinemia.
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Methemoglobinemia is a form of hemoglobinopathy. It occurs when the ferrous iron of Hgb is oxidized to the ferric state. Culprits include dapsone, benzocaine, phenazopyridine, and nitrates. High concentrations can lead to hypoxia, cyanosis, coma, acidosis, and death.
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What are the signs and symptoms of opioid poisoning?
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Pinpoint pupils, slurred speech, ataxia, respiratory depression, bradycardia, and hypotension.
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Treatment of opioid overdose.
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A bolus of naloxone will often produce a prompt reversal of symptoms. Higher doses may be needed with a partial agonist or propoxyphene. Large doses of naloxone can and will precipitate withdrawal in an addicted patient.
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Describe metal fume fever and treatment
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Occurs after inhalation of fumes while welding (nickel, zinc, etc). Described as a flu-like syndrome. It is typically self-limiting and usually requires only rest and analgesics.
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What agents can cause serotonin syndrome and what are the typical signs/symptoms?
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SSRIs, SNRIs, and various other antidepressant are common agents. Addition of tramadol and dextromethorphan to a patient's regimen can precipitate this syndrome. Tramadol and SSRIs in combination has been shown to produce seizures in some patients. Patients display altered mental status, muscle spasms, hypertension, and hyperreflexia and should be treated supportively.
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Describe opioid withdrawal.
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In the absence of diaphoresis, lacrimation, and rhinorrhea withdrawal syndrome can mimic anticholinergic syndrome. With exception of neonates, opioid withdrawal is not considered life-threatening. Neonates can seizure during opioid withdrawal and status epilepticus is a real possibility.
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Describe withdrawal of CNS depessants.
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Withdrawal of CNS depressants (alcohol, barbiturates, benzodiazepines) may produce hallucinations, tachycardia, fevers, and seizures. While the rate of fatalities are low, withdrawal from these agents are considered life-threatening.
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Major common signs of toxicity
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1. Cardiac conduction and rhythm problems
2. Metabolic acidosis 3. Altered mental status 4. GI dysfunctions 5. Seizures (3-5 are nonspecific of any specific agent) |
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Which agents can cause a widened QRS complex?
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Sodium channel blockers:
1. tricyclics 2. 1A and 1C antidysrhythmics 3. norpropoxyphene 4. propranolol 5. diphenhydramine |
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What are the agents or abnomalities that can cause metabolic acidosis?
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MUDPILES
M: metformin, methanol U: uremia D: diabetes (DKA) P: paraldehyde, pyrimidine/thymidine NRTIs I: iron, isoniazid L: lactic acidosis (hypoxia) E: ethylene glycol/methanol S: salicylates |
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What labs should we take with a poisoned patient?
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1. electrolytes
2. BUN 3. creatinine 4. INR 5. glucose 6. ABG's 7. PT 8. EKG |
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What drug levels should always be taken on a poisoned patient?
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Always take APAP and salicylate levels. Others to check include lithium, iron, ethanol, theophylline, digoxin, methanol, and ethylene glycol
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What toxic substances can be seen via X-ray?
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CHIPS
C: chloral hydrate H: heavy metals I: iron P: phenothiazines, paradichlorobenzene S: sustained-release preps |
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Decontamination of ocular, skin, and GI
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-ocular decontamination should begin immediately with irrigation at the exposure site
-skin should be rinsed with water or PEG solutions (for petroleum based substances) -GI decomination is controversial; should not be used as punishment |
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Onset of ipecac
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20-30 minutes
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Adverse effects of ipecac
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-protracted vomiting
-aspiration -Mallory-Weiss tears |
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Which agents is ipecac good for?
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1. iron
2. mothballs 3. mushrooms |
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When do we use orogastric lavage?
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-It is reserved for massive ingestions or when activated charcoal is not indicated
-Ideally within 60 minutes of ingestion -Should be followed by charcoal if the substance can be absorbed -Absence of antidote or hemodialysis |
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Contraindications to orogastric lavage
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-substance is too large to pass via the bore
-loss of airway protective relfexes -caustic materials -substance with high aspiration potential -GI bleed or perforation |
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Dose of activated charcoal
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1 gram/kg
Or 25 grams for peds and 50 grams for adults |
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What substances can activated charcoal not bind?
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-Li, Na, Fe, Pb
-hydrocarbons -most alcohols |
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Relative contraindications to activated charcoal
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1. aspiration
2. obstruction 3. caustic ingestion 4. absent bowel sounds |
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When does whole bowel irrigation have the most utility?
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When charcoal will not bind the substance
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Why do we not try to acidify urine?
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Risks outweigh the benefits (increased rhabdomyolysis)
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