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INTERESTING CASE
ROUNDSAlyssa Morris
Emergency Medicine R3
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Objectives
DDX for toxin induced seizures
DDX for toxin induced status epilepticus
Indications for pyridoxine
Review methylxanthine toxicity
Review MDAC
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CASE
19M took an unknown ingestion and had a seizure.
What is your quick ddx for drugs that cause seizure?
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DDX Drug induced Seizure
OTIS CAMPBELL
O- organophosphates
T- TCAI- Isoniazid, insulinS-
sympathomimetics
C- camphor, cocaine
A- anticholinergic, amphetamines, anticholinergic, antidepressants
M- Methylxanthines
P- PCPB- Benzo w/dE- EtOH w/dL- Lithium,
lidocaineL- lead, lindane
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DDx-Toxin induced Status
INH
Insulin/hypoglycemic agents
TCA
Theophylline
Wellbutrin
CO
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Pyridoxine Indications
INH
Ethylene glycol
Gyromitra Mushrooms
Methylxanthines*
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CASE
19M who ingested 112 caffeine tablets (100mg/tab) who was brought in by friend for intractable nausea and vomiting• Total ingestion >11g (175mg/kg)
O/E: P=131,BP= 164/67, T= 37.6, 02= 98%, agitated, vomiting ++
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CASE
Labs:• APAP/ASA –• CK 14• Na 140, K 2.2, Cl 101, CO2 17, AG:
22• Lactate 8.8• pH 7.23• Caffeine level 429mmol/L
ECG: Sinus tach, no dysrhythmias
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CASE CONT
Continued to be tachy, ++ vomitting, no seizure and no dysrhythmias
Course in ED:• zofran 12mg• Maxeran 10g (still vomiting)• Stemitil 10mg (still vomiting)• MDAC • Central line to replace K+• Zantac 50mg • Ativan 2mg IV x 2
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CASE CONT
Labs in am• CK- 2280• PO4 0.29• K- 3.1• Caffeine level 295mmol/L• Lactate 3.9
Still vomiting and agitated
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CAFFEINE
Methylxanthine Similar to theophylline
Cause release of endogenous catecholamines Stimulates B1 and B2 R
Structural analogue of Adenosine NE and epinephrine release
Inhibit phosphodiesterase (degrades cAMP) Effects like adrenergic stimulation
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PHARMACOKINETICS
Routes: oral, IV, SC, IM, rectal
Oral almost 100% bioavailability
Peak concentration 30-60min
Diffuses readily into total body water and all tissues
Readily crosses BBB
Metabolized by Cytochrome P450 systemActive metabollite is theophylline
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TOXICOKINETICS
Range of toxicity varies greatly
No definite conclusions from serum levels can be drawn
Lethal dose estimated: 150-200mg/kg or 5-10g
Death associated serum levels >80mm0l/L Fatalities <200mmol/L Survivial >400mmol/L
OUR PT: 175mg/kg, serum 429mmol/L
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CLINCIAL EFFECTS
Occur as a result of:1 Adenosine antagonism2 Release of endogenous
catecholamines3 Phosphodiesterase inhibiton
Toxicity affects: GI system Cardiovascular system CNS MSK
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GI
Nausea and protracted emesis
• Severe and difficult to control despite use of multiple anti-emetics
Increase in gastric acid secretion and smooth muscle relaxation
• Gastritis and esophagitis (more common with chronic use)
Transiently elevated liver enzymes
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CARDIOVASCULAR
Tachydysrhythmias Sinus tach SVT MAT Afib PVCs VT
MI
Peripheral vasodilation (wide pulse pressure)
Hypertension or hypotension
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PULMONARY
Stimulates CNS respiratory centre Increased RR Resp Alkalosis
Respiratory failure
Acute lung injury
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CNS
H/AAnxietyAgitationInsomnia
TremorIrritabilityHallucinationsSeizures*
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MSK
Increases intracellular Ca++
Smooth muscle relaxation
Tremor
Fasiculations
Myoclonus
Rhabdomyolysis
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METABOLIC
HypoK Shift into cells from B2 stimulation
HypoMg
HypoPO4
HypoNa
Hyperglycemia
AGMA (lactate)
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MANAGEMENT
Basics: IV, monitored bed
Labs to followextended electrolytesLactateCK
+/- Serum caffeine level
CXR, ECGs
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TREATMENT
MDAC*
Emesis Zofran, maxeran
Dysrhythmias Benzos Esmolol Lidocaine
Rhabdo Fluids and monitor u/o
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TREATMENT
Electrolytes Replace, but careful b/c will become
hyperK when shift back out of cell
Hypotension Fluids Not dopamine
Seizures Benzos Phenobarb Pyridoxine
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MDAC
Definition: more than 2 sequential doses of AC• In many cases, the number of doses
administered is substantially greater
MDAC serves 2 purposes:1 Prevent ongoing absorption of a drug
that persists in the GIT
2 Enhance elimination by either disrupting enterohepatic recirculation or by enteroenteric recirculation
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General Indications
GI decontamination for drug or poison ingestion associated with significant risk of toxicity, where supportive care/antidote alone is insufficient to ensure a satisfactory outcome
The toxin must be able to bind to AC
Must believe that a significant amount of agent is unabsorbed and is amenable to removal
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AACT Position Statement
Position statement states use MDAC only for ingestions of CarbamazepineDapsonePhenobarbitalQuinineTheophylline /Methylxanthines
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Other Drugs
Shown to increase elimination of:DigoxinPhenobarbitalCarbamazepin
ePhenylbutazon
eDapsoneNadolol
TheophyllineSalicylateQuinineCyclosporinePropoxypheneNortriptylineAmitriptyline
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Contraindications
Any contraindication to single-dose activated charcoal • AC known not to adsorb • Airway protective reflexes are
absent or expected to be lost and pt is not intubated
• GI perf (esp caustic ingestion)• Increases severity of injury
(hydrocarbons)• Endoscopy for dx/mx anticipated
Presence of ileus
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Administration
Initial dose• 1g/kg or 10:1 ratio of ACT:toxin, whichever
is >
Repeat dose • 0.25-0.5mg/kg every 1-6hrs
Procedure• Can be administered with cathartic for
the 1st dose only• If pt vomits, repeat the dose• Can use oral, NG or OG route
*Sxn tube before removal to reduce aspiration risk
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SUMMARY
DDX for toxin induced seizures OTIS CAMPBELL
Refractory seizures in toxic ingestion Think about pyridoxine
Caffeine is a methylxanthine Adrenergic stimulation Can get refractory seizures MDAC is indicated