Seizures Flashcards

Question

IRON TOXICITY

Answer 1

IRON TOXICITY -due to direct corrosive effects on mucosal tissue and cellular dysfunction -an elemental iron dose of: 20mg/kg: abdominal pain, diarrhea, vomiting 60mg/kg may be fatal INITIAL PERIOD (0-6hours): severe gastritis, vomiting tachycardia, hypotension QUIESCENT PERIOD (up to 12hours) deceptive improvement, patient may appear stabilized subtle signs of hypotension RECURRENT PERIOD (12-48 hrs) multiorgan failure, GI bleeding, lethargy, vasomotor collapse, pulmonary edema, hepatorenal failure, hypoglycemia and acidosis LATE PERIOD (2-6 weeks) INITIAL MANAGEMENT *Ask for amount of elemental iron ingested, time ingested and other substances ingested *collect 10ml blood for total serum iron (TSI) 3-5 hours post ingestion and send sample of gastric aspirate *May request for stool exam with occult blood and plain abdominal radiograph *manage specific problems: cerebral edema, decreased PT, hypovolemic shock, metabolic derangements, renal failure, seizures

Answer 2

ISONIAZID TOXICITY -Clinical effects occur 30mins to 2hrs seizure dose: 80-120 mg/kg Triad of toxicity: seizure, coma, metabolic acidosis Severe overdose: seizures and LOC Signs: hyperpyrexia, tachycardia, dilated pupils, dysarthria, hyperreflexia, hypotension, coma MANAGEMENT: *Insert NGT and do gastric lavage with activated charcoal (1g/kg) to make a slurry *To enhance excretion, five alkalinization therapy with NaHCO3 at 1meq/kg IV every 6 hours until urine PH ≥7.5

Answer 3

KEROSENE TOXICITY -leading cause of accidental ingestion in children ≤6yo -may be absorbed in the GIT (optimal), through inhalation or via skin -can depress the CNS and lead to hypoxia Nausea, vomiting, diarreah, cough, mucous membrane irritation, DOB CNS symptoms: initially may be excited but seizures may follow Signs: respi distress, cyanosis, tachycardia, abdominal tenderness, perianal burns, altered sensorium MANAGEMENT *remove clothes and do decontamination procedures *Give O2 via nasal cannula *do not induce emesis *no benefit with using activated charcoal *specific problems: gastritis, seizures, aspiration pneumonia

Answer 4

ORGANOPHOSPHATE TOXICITY -Organophosphates inhibit the action of cholinesterase, the enzyme that breaks down acetylcholine to acetic acid and choline -can be absorbed through inhalation, ingestion and dermal contact -its toxic effects may appear as early as 10 minutes to as late as 2 hours post-exposure MUSCARINIC (MILD): malaise, vomiting, diarrhea, sweating, pain, salivation, miosis MUSCARINIC AND NICOTINIC (MODERATE): mild symptoms plus: dyspnea, decreased muscle strength, bronchospasm, muscle fasciculations, motor incoordination, impairment of speech, bradycardia, involuntary defacation/urination MUSCARINIC, NICOTINIC and CNS (severe): moderate symptoms plus: Respiratory paralysis, extreme hyper secretion, coma, cyanosis, hypotension, paralysis, behavioral changes, seizures MANAGEMENT: *If poison absorbed dermally, inhaled or ingested then vomited, provide O2, remove clothing and do sponge bath using alkaline soap *If poison ingested: insert NGT and do gastric lavage with activated charcoal (1g/kg to make a slurry) *Phenytoin for cases of malathion, parathion, or dichlorvos poisoining *Pralidoxime chloride *Atropine *Manage other problems: acidosis, pulmonary congestion and seizures

Answer 5

BENZODIAZEPINE TOXICITY -effects are mediated mainly by binding with GABA receptors -most significant finding of overdose: CNS depression -other findings: slurred speech, incoordination and ataxia Symptoms: Slurred speech, dizziness, increased sleepiness Signs: changes in sensorium (may be intermittent), hypothermia, bronchial hypersecretion, ataxia,nystagmus, dysarthria, weakness, aggressive behavior MANAGEMENT: *If within 1 hr of ingestion, insert NGT and do gastric lavage with activated charcoal at 1g/kg to make a slurry *Flumazenil (0.01mg/kg) if with respiratory depression (may be repeated at 1-2 minute intervals up to a total dose of 1mg) *specific problems: hypoxia, hypotension, respiratory acidosis

Answer 6

Cholinergic syndrome - “SLUDGE” o Salivation, Lacrimation, Urination, Diarrhea + Diaphoresis, GI upset, Emesis - “DUMBBELLS” o Diarrhea, Urination, Miosis, Bradycardia, Bronchospasm, Emesis, Lacrimation, Limp, Salivation/Sweating

Answer 7

- Enduring predisposition to generate seizures - >2 uprovoked seizures occurring in a time frame of >24h - 2 or more independent sz that are unprovoked Breakthrough seizure – already treated with antiepileptic drugs but has achieved low drug levels. Sz recurrence in a person with epilepsy who has had a sustained period of sz freedom. - Causes: noncompliance to AED, sleep deprivation, severe emotional stress, menstrual-related, infection, metabolic - Tx: load with appropriate antiepileptic medication Seizure type – primary determinant of type of Rx px is likely to respond to Epilepsy syndrome – determines prognosis

Answer 8

Pathophysiology Etiology – any pathology that disrupts neural function and connectivity. Often leads to epileptogenesis Epileptogenesis – ID which part of the brain turns epileptic - Kindling: repeated electrical stimulation of selected areas initially causes no apparent changes but with repeated stimulation cause epilepsy Epileptic state of increased excitability – seen in all pxs regardless of etiology - In a sz focus, neurons develop a stereotypic synchronized response called paroxysmal depolarization shift - When after hyper-polarization is disrupted, the inhibitory surrounding is lost, and neurons fire at the same rate and time resulting in a sz focus Seizure related neuronal injury – neuronal injury on MRI - May be transient/permanent - May include apoptosis and necrosis of neurons

Answer 9

CM Common Epilepsy syndromes 1. Benign Rolandic epilepsy – benign childhood epilepsy with centrotemporal spikes - Usually begins 3-13yo - Single nocturnal sz with clonic movt of the mouth and gurgling, inability to speak, preserved consciousness and comprehension - Sz resolve by 16yo - Altered consciousness, postictal confusion, and aura rare - EEG: typical broad-based centrotemporal spikes that are markedly inc in freq in drowsiness and sleep - MRI normal 2. Temporal lobe epilepsy – 70% of partial sz - Many w/ prior febrile sz or head trauma - Prodrome: lethargy - Oral or motor automatisms, altered consciousness, head and eye deviation, contralateral twitching, or tonic-clonic movts, posturing 3. Absence seizures – sudden cessation of motor activity or speech with a blank facial expression and flickering of the eyelids - Uncommon <5yo. Usually starts at 5-8yo - Never associated with an aura, rarely persists for >30sec - Not assoc with postictal state - Patients do not lose body tone and usually resume activity after sz - Hyperventilation of 3-5min can precipitate sz - EEG: 3 Hz spike-and-slow-wave discharges 4. Generalized tonic-clonic – most common generalized motor sz - Can be primary (bilateral) or secondarily generalized - Starts with LOC or sudden cry - Tonic phase: jaw snaps ff by 10-15s or longer of tonic spasms, apnea, cyanosis - Clonic phase: 1-2 min of rhythmic gen contractions - Postictal state: vomiting, confusion, somnolence, intense headache 5. Myoclonic – repetitive sz of brief, often symmetric muscular contractions with loss of body tone and falling or slumping forward 6. Infantile spasms – West syndrome - Begins at 4-8 mos - Brief symmetric contractions of neck, trunk, extremities - EEG: hypsarrhythmia

Answer 10

Dx: 1. EEG 2. CT/MRI

Answer 11

Mgt Refer to Neurology 1. Benign Rolandic epilepsy - Oxcarbazepine, carbamazepine, levetiracetam, valproic acid 2. Focal sz – oxcarbazepine, carbamazepine 3. Absence – ethosuximide: as effective as valproic acid but less toxic (most common initial drug) - Valproic acid, lamotrigine (less effective) 4. Juvenile myoclonic epilepsy – levetiracetam, topiramate, valproic acid 5. Infantile spasms – ACTH, CS, vigabatrin 6. Epilepsy with GTC sz only – levetiracetam, lamotrigine, topiramate, valproic acid

Answer 12

- Continuous sz lasting for at least 30min, or a series of sz with no regaining of consciousness between sz - Medical emergency! International League Against Epilepsy (ILAE) definition (2015): - Condition resulting from: 1. The failure of the mechanisms responsible for sz termination OR 2. Initiation of mechanisms w/c lead to abnormally prolonged sz (after time point t1) - Long term consequences (after time point t2): neuronal death, neuronal injury, alteration of neuronal networks, depending on type and duration of sz Mechanism - Failure of desensitization of AMPA glutamate receptors leading to increased excitability - Reduction of GABA-mediated inhibition --> BZDs are less effective the longer the sz episode

Answer 13

Type of SE Operational Dimension 1 Time (t1) when a sz is likely to be prolonged Operational dimension 2 Time (t2) when a sz may cause long-term consequences Tonic-clonic SE Operational Dimension 1 Time (t1) when a sz is likely to be prolonged: 5 min 30 min Focal SE with impaired consciousness Operational Dimension 1 Time (t1) when a sz is likely to be prolonged10 min Operational dimension 2 Time (t2) when a sz may cause long-term consequences>60 min Absence SE Operational Dimension 1 Time (t1) when a sz is likely to be prolonged10-15min Operational dimension 2 Time (t2) when a sz may cause long-term consequences unknown

Answer 14

Dx 1. Serum glu, Na, Ca, Mg 2. CBC 3. Basic metabolic panel 4. CT scan – r/o organic pathology 5. Continuous EEG – ID type (gen/focal), monitor tx 6. BCS, spinal CSF C/S 7. Toxic screen 8. Tests for inborn errors of metabolism

Answer 15

Mgt Goal of tx is to stop EEG sz activity before reducing tx (complete flattening of EEG). Long term consequences start to ensue after 30 min of generalized convulsive status epilepticus And after 60 minutes of focal motor status epilepticus with impaired awareness.

Brainscape's Knowledge GenomeTM

Seizures Flashcards

Brainscape's Knowledge Genome^TM