Toxicology Flashcards
Resus RSI DEAD
ABC, seizures, glucose, temp
Risk assessment - drug, dose, time, current clinical status (does picture fit), patient factors (comorbidities, weight)
Supportive care (fast hugs in bed please - fluids, analgesia/antiemetics, sedation, thromboprophylaxis, head up, ulcer prophylaxis, glucose control, skin/eye care, IDC, NGT, bowel care, environment, de-escalation, psychosocial support)
Investigations (ECG, paracetamol, others)
Decontamination - charcoal, whole bowel, endoscopy
Enhanced elimination - multi dose activated charcoal, urinary alkalinisation, dialysis
Antidotes
Disposition
When to NOT use charcoal
Later than 2-4 hours
Risk of aspiration
Alcohols
Hydrocarbons
Metals
Corrosives
Indications for whole bowel irrigation and how is it performed
Iron > 60mg/kg
Slow release potassium > 2.5mmol/kg
Lead
Arsenic
Life threatening slow release verapamil/diltiazem
Body packers
Dilute 8 sachets of movicol (or 2sachets of glycoprep C) in 2L of water and given 20-30ml/kg (1.5L) in the first hour (within 4hrs of ingestion) followed by 20-30ml/kg/hr (1L/hr) until diarrhea runs clear
Has risk of ileus, bowel obstruction and perforation
Indications for multi dose activated charcoal and how does it work
Carbamazapine
Colchicine
Phenytoin
Barbiturates (Phenobarbitone)
Theophylline
Quinine
Dapsone
Conisdered in Massive modified release paracetamol
Interrupts entero-hepatic circulation (requires biliary excretion leading to charcoal absorption in the small intestine)
GI dialysis - drug passing down concentration gradient across gut mucosa from intravascular to intraluminal space where it is absorbed by activated charcoal. Only for small molecules, lipid soluble with low protein binding and low VD
How is MDAC administered and what are the complications
1g/kg (50g) stat followed by 0.5g/kg (25g) every 2hrs
Need aspirate NG and to ensure bowel sounds prior to each dose
Rarely used past 6hrs
COMPLICATIONS
Vomiting +/- aspiration
Charcoal bezoar formation, BO and perforation is rare
Corneal abrasion
Constipation
Distraction from resus and other supportive care
Which toxins are able to be dialyzed (apart from AEIOU)
Toxic alcohols
Salicylate
Lithium
Metformin
Antiepileptics (Carbamazepine, Valproate, barbituates etc)
Potassium
Paraquat and herbicides
Theophylline
How do you perform urinary alkalinization
Alkaline urine pH promotes ionisation of highly acidic drugs preventing reabsorption in renal tubules and promotes excretion
Needs drug to be filtered at glomerulus, have small VD and be a weak acid
Salicylates and phenobarbitone
1-2mmol/kg (1 bottle =100mmol) sodium bicarb bolus and infusion of 150mmol NaHCO3 in 1L 5%glucose running at 166ml/hr
Will need 2hrly VBG and EUCs with strict K replacement to maintain K 3.5 - 4
Aim urinary pH>7.5 and UO 1-2ml/kg/hr
How and when to give sodium bicarbonate
- Cardiotoxicity due sodium channel blockade (propranolol, TCAs, chloroquine, quinine, bupropion)
- Urinary alkalisation (salicylates, phenobarbital)
- profound acidosis (cyanide, toxic alcohol, isoniazid)
CI - APO, hypoK, severe hyperNa, renal failure
Adverse effects - alkalosis (keep pH < 7.6), hyper Na, hyper osmolarity, hypoK, local tissue irritation, fluid overload
2mmol/kg bolus initially
In cardiotoxicity can repeat 5 mins until stable
Infusion 100mmol in 1000mls at 250ml/hr guided by ABG and ECG
What are the management steps of toxicological hyperthermia
Cold IVF (4deg C) up to 20ml/kg (aim UO 1-2ml/kg/hr)
IV benzos to treat agitation and suppress shivering
- Diazepam 0.02mg/kg (2mg) q5min
- Midaz 0.01mg/kg (1mg) q5min
- Aim pt calm and relaxed
Ice to groin and axilla
Tepid sponging and fanning
Cooling mats and blankets
Antidotes if available
Severe hyperthermia (>41) or refractory consider
- Intubation and paralysis
- Immersion ice bath
Hemodialysis, ECMO, cooling catheter
Avoid restraints and antipyretics
1 pill can kill in toddler
Amphetamines
Beta bloackers - propanolol
CCB - Diltiazem/verapamil (15mg/kg fatal)
Chloroquine (20mg/kg)
Diabetics - Sulfonylureas (0.1mg/kg)
Depression - TCA (15mg/kg)
Opiates - Oxycodone, morphine, methadone
Theophylline
1 sip can kill in toddler
Organophosphates
Paraquat
Hydrocarbons
Toxic alcohols
Eucalyptus oil, camphor (50mg/kg fatal)
Naphthalene (1 mothball = methaehmoglobinaemia and haemolysis)
Caustic agents - ammonia, boric acid, hydrofluoric acid
Toxicological causes of delirium
Alcohol intoxication
Alcohol withdrawal
Serotonin syndrome - (SSRIs, SNRIs, TCAs, lithium, tramadol, fentanyl, MDMA)
Neuroleptic malignant syndrome - (haloperidol, metoclopramide, prochlorperazine)
Sympathamomietic syndrome - (amphetamine, cocaine, theophylline)
Anticholinergic syndrome - parkinson drugs, TCAs, antipsychotics, carbamazepine, oxybutynin
Cannabis
Hallucinogens
Salicylate OD
Theophylline OD
Atypical antipsychotic OD
Drugs that cause QT prolongation and its management
Delay cardiac repolarisation, most commonly potassium channel blockade but also in hypokalemia, hypocalcemia and hypomagnesemia.
Risk of Torsdes de points
Manage electrolytes
Torsades use Magnesium 0.2mmol/kg (8mmol) over 10 minutes then 0.12mmol/kg/hr (2-3mmol/hr) over 12-24hrs)
Keep HR >90, isoprenaline 0.1microg/kg (20microg) ever 2-3 minutes
What drugs cause sodium channel blockade
Wide QRS and tall R wave in aVR
Tricyclics with anticholinergic syndrome
Bupropion with seizures
Carbamazepine with antimuscarinic
Cocaine with high and fast toxidrome
Propanolol with low and slow toxidrome
Quinin with cinchonism (tinnitus hearing loss)
Hydroxychloroquine with antimalarial toxidrome (hyopK and altered LOC)
LA toxicity
Drugs that cause QRS widening and its management
Most commonly due to sodium channel blockade
1-2mmol/kg (100mmol) of NaHCO3 every 3-5 minutes aiming serum pH 7.45-7.55 (MAX 6mmol/kg)
+ Hyperventilation aim pCO2 30-35
Expect to need to replace potassium after
Defib unlikely to be successful
Lignocaine 1.5mg/kg (100mg) third line once pH>7.5
Differentials of the hot and confused patient
Meningoencephalitis
Systemic sepsis
Heat stroke
Thyrotoxicosis
Phaeochromocytoma
Anticholinergic syndrome
Serotonin syndrome
Neuroleptic malignant syndrome
Sympathomimetic syndrome
Alcohol withdrawal
Methylxanthine toxicity
Salicylate toxicity
Malignant hyperthermia
Neuroleptic malignant syndrome - causes, risk, diagnostic criteria, presentation and management
Caused by dopamine antagonist drug administration (antipsychotics but more common with high potency drugs like haloperidol or depots) or withdrawal from dopaminergic drugs (parkinson medications, bromocriptine)
Also prochlorperazine, metoclopramide etc
RISKS
Start, change, addition of drug increases risk
Young, male, dehydration, comorbid, organic brain disorder, genetic increases risk
DIAGNOSTIC CRITERIA
Slow onset over days, weeks to resolve
Major criteria (must have all 3)
- Exposure to dopamine antagonist drug
- Severe muscle rigidity
- hyperthermia
At least 2 minor criteria
- tachycardia, HTN, diaphoresis, labile BP
- Raised serum CK (>3xULN), leucocytosis
- Dysphagia, tremor
- Altered LOC, mutism, incontinence
Classic tetrad
- extrapyramidal : lead pipe rigidity, brady/akinesia, dystonia, dysphagia, tremor
- Temp dysregulation (>39)
- Autonomic effects: tachycardia, hypertension, labile BP, diaphoresis, tachypnea
- CNS effects: Drowsiness, confusion, coma, mutism, incontinence
Discontinue causative drugs
Supportive, cooling (cold IVF, ice packs, cooling blankets) , clonidine/GTN for HTN, ETT
Bromocriptine (dopamine agonist) - 2.5mg PO/NG Q8hr for severe or prolonged NMS (titrated to hyperthermia and rigiditiy)
Dantrolene 1mg IV to relax muscle rigidity and heat production can be considered
Serotonin syndrome - causes, risk, presentation, diagnostic criteria and management
SSRIs, SNRIs, TCAs, MAOIs, lithium, amphetamines, methadone, tramadol, St Johns Wort, methylene blue, hallucinogens
Venlafaxine asssociated with highest mortality
Start, change, addition, OD increases risk
More rapid onset over hours and resolve over 24hrs
CNS - apprehension, anxiety, seizure, coma
Autonomic - HTN, tachycardia, hyperthermia, sweating, mydriasis, flushing, diarrhoea
Neuromuscular excitation - clonus (sustained, ocular/ankle), hyperreflexia, increased tone, rigidity, tremor
Hunter diagnostic criteria help confirm diagnosis of moderate to severe serotonergic toxidrome (sensitivity 84% specificity 97%)
Taken serotonergic drug AND 1 of the following
- spontaneous clonus
- inducible clonus plus agitation or sweating
- ocular clonus plus agitation of sweating
- tremor plus hyperreflexia
- hypertonia plus temp >38 and inducible or ocular clonus
Supportive (self resolves within 12-24hrs)
Charcoal and hydration
Diazepam first line (0.2mg/kg, not more then 120mg in 24hrs)
Cyproheptadine 12mg second line, 8mg TDS for drugs with longer half life/modified release (fluoxetine and tramadol)
ETT if temp > 39.5
What are the differences between NMS and SS
NMS occurs within 1-2 weeks while SS more rapid (over hours)
NMS severe muscle rigidity, hyporeflexia and rhadbo while SS hyperreflexia, clonus, hyperactive bowel sounds/diarrhoea
NMS more frequently associated with multiorgan failure
NMS is idiosyncratic reaction after prolonged exposure to neuroleptics or after withdrawal of dopamine receptor agonist
NMS - mutism/confusion SS - apprehension/anxiety
NMS - lead pipe rigidity and hyporeflexia SS - cogwheel rigidity, hyperreflexia and clonus
NMS - hypoactive bowel sounds SS - hyperactive bowel sounds and diarrhea
Anticholinergic syndrome- causes, presentation, diagnostic criteria and management
Pure anticholinergic - atropine, benzatropine, oxybutynin, hyoscine (buscopan)
Mixed syndromes with anticholinergic -
Antiparkinson, antihistamine, TCAs, antipsychotics, carbamazepine,
Plants
Brugmansia (angels trumpet), Datura (Jimsonweed or thorn apple), Belladona/nightshade, Duboisia (corkwood)
Central - agitated delirium, picking, visual hallucinations, mumbling, slurred speech, fluctuating mental state, tremor, myoclonus, seizures, coma
Peripheral - tachycardia, dry mouth, dry skin, mydriasis, flushing, urinary retention, reduced bowel sounds, hyperthermia (blind as a bat…)
Supportive
Charcoal if possible
Benzo’s. Can use droperidol if not antipsychotic overdose
Adequate hydration, IDC
Antidote
Physostigmine if not responding to benzos and moderate to severe delirium - 0.5mg (0.01mg/kg) over 5 minutes every 15 minutes. Max 2mg over 60 minutes
Short acting and may need repeat dose
Contraindicated if bradycardia, bronchospasm, heart block as it is a cholinesterase inhibitor
Cholinergic syndrome- causes, presentation, diagnostic criteria and management
Acetylcholine agonists - acetylcholine, pilocarpine, nicotine, mushrooms (amanita, clitocybe and inocybe)
Acetylcholinesterase inhibitors - oraganophosphates, carbamates, chemical warfare, donepezil, neostigmine
CNS - agitation, seizures, coma
Muscarinic (DUMBBELLS) - diarrhea, diaphoresis, urination, miosis, bronchospasm, bronchorrhea, bradycardia, emesis, lacrimation, lethargy, salivation
Nicotinic - HTN, tachycardia, resp muscle weakness/paralysis, fasciculations, diaphoresis
Killer B’s - bronchospasm, bronchorrhea, bradycardia, breathing bad (resp muscle paralysis)
Early ETT (resp muscle weakness, secretions, coma)
Avoid succinylcholine
Hydration (lots of secretions)
Atropine 1.2g (50microg/kg) IV 2-3 mins doubling dose then infusion to stop bronchospasm/bronchorrhea and bradycardia (end points are HR>80, SBP>80 and clear chest)
Pralidoxime 2g (25mg/kg) or 8mg/kg/hr in organophosphate
Over atropinisation (Anticholinergic effects)
- Confusion
- Pyrexia
- Absent bowel sounds
Methaemoglobinaemia - causes, presentation and management
Consider when Sats 85-90% and cyanosis but normal paO2 on gas
Blood samples chocolate brown
Iron in oxidized form (ferrous to useless ferric) in Hb so not able to carry O2 (left shift of O2-Hb dissociation curve) causing functional anemia and impaired O2 delivery to tissues
CAUSES
Nitrites and nitrates (well water, preserved food, GTN, amyl nitrite)
LA - prilocaine, lidocaine
Herbicides (paraquat), pesticides, fertilizers
Chloroquine
Sulfonamides and dapsone can cause sulfhaemoglobinemia and require multiple doses of methylene blue
10-20% Slate grey cyanosis
20 - 30% Headache, tachycardia
30 - 50% Drowsiness, confusion, tachypnoea
50 - 70% Coma, seizures, arrhythmia, metabolic acidosis
>70% lethal
Methylene Blue if symptomatic with level>20% or asymptomatic but >25%
1-2mg/kg IV over 3-5 minutes. Can rpt after 30 minutes if still high or symptomatic
Alternatives include ascorbic acid, exchange transfusion or hyperbaric oxygen
Amanita Phalloides - signs, symptoms, prognosis, management
High source of cyclopeptides
1 mushroom cap can cause fulminant liver failure and death while other mushrooms need more then 10
Typically, asymptomatic for 6-18hrs. GI symptoms: Abdo pain, N/V, watery diarrhoea
Dehydration/AKI/electrolyte derangement/metabolic acidosis from above
Mildly elevated LFTs in first 24hrs
Over next 1-7 days: progressive liver failure, coagulopathy, multiorgan failure (mortality 10-30%)
> 7 days: complete resolution over weeks to months OR chronic hepatitis
POOR PROGNOSTIC FACTORS:
- Worse prognosis with earlier onset symptoms
- lactate >5 or progressive rise in context of hepatitis
- Rising ALT (may take up to 24hrs)
- AKI with acute liver injury
- Rising INR 3 days post ingestion or INR>6 on day 4
Onset of diarrhea 6-10hrs or INR>6 from day 4 indicate possible need for liver transplant
MANAGEMENT
Amatoxin has significant enterohepatic recycling, benefits from charcoal and MDAC even if presenting after 2days from ingestion
Antidote silibinin 5mg/kg over 1hr
then 20mg/kg/24hrs for 4 days
or benpen 3g (60mg/kg) q4hrly
or rifampacin
+
NAC 200mg/kg over 4hrs and 100mg/kg over 16hrs fro hepatoprotection
Methanol - toxic dose, symptoms and investigations.
Home brew, paints, varnishes, rocket and race car fuel, solvents/cleaners, embalming fluid, windshield wiper fluid
Metabolised to formaldehyde and then to formic acid (neurotoxic to retina and optic nerves) by ALDH
Ingestion > 0.1ml/kg signficiant toxicity in children
30g (30ml of 100%) will cause coma and blindness
Effects at 12-24 hours
CNS depression - Intoxicated, coma, seizure later due to acidosis
Retinal toxicity - blurred vision, scotomata, papilloedema, loss of light reflex, blindness
Cardio - hypotension secondary to acidosis
HAGMA (low pH best predictor of severe toxicity)
High osmolar gap (Serum osmo - 2xNa+Ur+Glucose+1.2xETOH>10)
NORMAL CALCIUM (low in ethylene glycol)
Normal renal function and no urinary calcium oxalate crystals (found in ethylene glycol
Brain imaging (CT/MRI): bilateral putamen necrosis, basal ganglia haemorrhages and necrosis of the caudate nucleus with atrophy of the optic chiasma and lesions in the occipital cortex and subcortical white matter.
Ethylene glycol
Antifreeze, radiator coolant, brake fluid, degreasing agents, foam stabilizers, metal cleaners
Metabolized to glycolaldehyde and then via ALDH glycolic acid. Then oxalic and glycoxylic acid. Oxalic acid combines with serum calcium and deposits in renal tubules leagding to ARF as well hypocalcemia (QT prolongation and ventricular arrhythmia)
Ingestion > 1ml/kg fatal
CNS depression
- intoxicatClincial
- Coma and seizures (secondary to acidosis)
GI - N/V and abdo pain
Cardio - hypotension secondary to acidosis (12-24hrs)
ARF, oligouria, flank pain (24-72hrs)
HAGMA (high anion gap best predictor of severe toxicity)
High osmolar gap (Serum osmo - 2xNa+Ur+Glucose+1.2xETOH>10)
HypoCa
Calcium oxalate crystals in urine
Lactate gap (glycolate interfering with POC lactate and artificially raising)
Treatment methanol/ethylene glycol
IVF and correct hyperK
No role for charcoal (too rapidly aborbed)
NaHCO3 for severe acidosis
Ethanol and fomepizole inhibit ADH and prevent toxic metabolites
Fomepizole has easier dosing regime and better side effect profile but costs more
Ethanol worsens sedation and agitation leading to higher rates of intubation and ICU admissions but more readily available
Should be commenced in any pt
- confirmed ingested toxic dose of methanol or ethylene glycol toxic dose
- unexplained metabolic acidosis
- High osmolar gap
ETHANOL
- Needs ETOH level prior
- IV or NG
- Aim ETOH level 22-44mmol/L and continue until methanol/ethylene glycol <20mg/dL (6.24 mmol/L for methanol, 3.23 mmol/L for ethylene glycol).
- Ethanol 10% 6ml/kg loading dose (if not already intoxicated)
Then Ethanol 10% 1-2ml/kg/hr (100ml/hr) thereafter.
- If dialysis then double
0.6g/kg followed by 0.1g/kg/hr (10g/hr) if using spirits
Alcohol volume= (required ethanol g)/(alcohol concentration %) x 100
FOMEPIZOLE
- 15mg/kg IV loading
then 10mg/kg q12hrly
- Give q4hrly if dialysis
continue until methanol/ethylene glycol <20mg/dL (6.24 mmol/L for methanol, 3.23 mmol/L for ethylene glycol)
DIALYSIS (intermittent hemodialysis preferred)
- Confirmed toxic dose ingestion
- Metabolic acidosis
- AKI
- Serum level > 50 mg/dL (15.6 mmol//L for methanol, 8.07 mmol/L for ethylene glycol)
EXTRA
Folate for methanol
- calcium folinate/folic acid 50mg IV QID
Vit B in Ethylene Glyco
- Pyridoxine (B6) 50mg IV QID or thiamine (B1) 100mg IV QID
Isopropanolol
Surgical spirits - disinfectant, solvents, window cleaners
4ml/kg can cause coma
Supportive as per ETOH intoxication
Only toxic alcohol that causes ketosis without acidosis
Beta blockers - risk assessment and clinical presentation
RISK FOR TOXICITY
- Propranolol (coma, seizures, Na channel blocker) and sotalol (QT prolongation) most toxic
- Children 1 dose can be toxic
- 1g propanolol can be toxic
- Modified release (metoprolol only)
- Older Age
- Medical conditions (heart disease, cirrhosis)
- Co-ingestion with other cardiovascular drugs (CCB, diogxin, ACE etc)
CLINICAL - within 1-2 hrs
Cardiovascular
- Hypotension due to myocardial depression and bradycardia
- Sinus brady most common arrhythmia and PR prolongation earliest sign of toxicity
- 1st/2nd/3rd HB, junctional brady, ventricular brady and asystole in severe
- QRS widening in propranolol
- QT prolongation in sotalol
CNS
- Seizures, delirium and coma in lipophilic betablockers (propanolol)
Resp
- Bronchospasm and APO
Metabolic
- Hypo/hyperglycemia (interferes in gluconeogenesis and glycolysis but uncommon in adults)
- HyperK
Beta blocker toxicity management
Charcoal as soon as possible for severe overdose
Otherwise 2hrs in IR adn 4hrs in MR
Early intubation in refractory cardiovascular instability or decreased LOC with pretreatment of Atropine 600microg to prevent vagal mediated bradycardia during laryngoscopy
Hypotension with IVF first line
- TTE can be helpful in determining cardiogenic shock vs vasodilatory shock
Bradycardia with hypotension
- 1st line: Atropine 600microg q15min
- 2nd line: Adrenalin 10-20microg (0.1microg/kg) q3min followed by infusion 0.1microg/kg/min
- Isoprenaline 20microg (0.1microg/kg) q3min followed by infusion can also be used for bradycardia but may worsen hypotension
IN VASOPLEGIC SHOCK
Norad 0.05-0.5microg/kg/hr second line vasopressor
IN CARDIOGENIC REFRACTORY SHOCK
High dose insulin euglycemic therapy
1unit/kg actrapid with 50ml 50%glucose (2.5ml/kg of 10%)
Followed by
1unit/kg/hr (MAX 10unit/kg/hr) with 50% glucose 20ml/hr or 10% 100ml/hr (10g/hr)
- 2.5ml/kg/hr of 10% in children
Aim BSL 4-5 and check every 30min
K replacement and aim K 4-4.5. Check every 2-4hrs
Intralipid controversial but can be considered if still refractory
- 20% 1.5ml/kg bolus q5min for 2-3 doses if in asystole otherwise infusion 0.25ml/kg/min for 30-60minutes
Hemodialysis only effective in sotalol and atenolol
VA ECMO if available but not after intralipids as clots circuit. Evidence in cardiogenic shock but no vasoplegic shock
Sodium Bicab 1-2mmol/kg q3minutely (6mmol/kg) if refractory hypotension or cardiac arrest as acidosis decreases effectiveness of inotropes OR in Na channel blockade
QT prolongation management
Seizures
- Glucose first line (intracellularly deplete despite normal BSL)
- benzos second line
Glucagon no longer recommended as short half life and dose required quickly exhausts hospital supply
Who should be admitted for beta blocker overdose
Any symptomatic pts with
- large ingestions
- delibrate ingestions
- unintentional ingestions >2x daily dose
Otherwise medically cleared if asymptomatic and normal ECG after
- 6hrs in IR
- 12hrs in MR
Calcium channel blocker OD features
Most concerning are diltiazem and verapamil
2-3x normal dose (10 tabs, > 15ml/kg) toxic
Can be immediate release - first 2-4 hours or delayed 4-16 up to 24 hours
Bradycardia, 1-3 HB, hypotension, ACS, CVA, ischaemic gut, hyperglycaemia, lactic acidosis, shock, seizures
Calcium channel OD treatment
- Charcoal (up to 4 hours slow release)
- Expect bradycardia and hypotension - IVF, pacing (rather than drugs), adrenaline, ECMO/bypass
- High dose insulin glucose therapy
Calcium glutinate 10-20mls 10% IV repeated with monitoring of Ca levels
Acute digoxin OD features
Drugs, toad toxin, oleanders
10 x daily dose toxic, lethal > 10mg (4mg children)
GI early - n+v, abdo pain
CVS later 8-12 hours - bradycardia, slow AF, HB, increased automaticity, bigeminy, SVT, VT, hypotension
CNS - leathery, confusion, seizure
Dig levels at 4 hours
< 1 therapeutic
2-3.2 potentially toxic
> 3.2 toxic
Often hyperkalaemia - poor sign if > 5.5 early
ECG - reverse tick ST depression lateral leads, shortened QTc
Acute digoxin OD treatment
- Cardiac arrest - 20 amps digibind
- Life threatening arrhythmia, refractory hypotension, refractory hyperK, significantly symptomatic then give digibind
- dose digibind vials = ingested dose in mgx0.8x2
- if unknown start 2-5
- atropine 0.6mg, pacing
- arrhythmia - magnesium, lignocaine
- hyperK - insulin/dextrose, bicarb NOT calcium
Chronic digoxin toxicity
Usually intercurrent illness (sepsis, NSAIDs etc) so renal impairment and delayed elimination
GI upset, bradycardia, syncope
Lower levels than acute cause problems
- bradycardia alone with level 2.5 50% toxic
- GI alone with level 2.5 60% toxic
- bradycardia and GI level 2.5 90%
- automaticity + others level 2.5 100%
- cardiac arrest 5 amps
- digibind 1-2 amps
What are the toxic effect of antiepileptic overdose and some potential toxic doses in pediatrics
CNS toxicity is main effect (if absent unlikely to develop significant toxicity)
- Horizontal and vertical nystagmus
- Ataxia
- Dysarthria
- Dose dependent decreased GCS (drowsiness to coma)
- Resp depression
- Seizures
GI - N/V
Cardio
- Hypotension
- Tachy/bradycardia
- Cardiotoxic effects (Na channel blockade and QRS prolongation particularly in carbamazepine and lamotrigine)
Consider serum drug concentration for carbamazepine, phenobarbitol, phenytoin and valproate
Management:
Intubation
IVF and management of QRS prolongation
Charcoal (even if delayed)
MDAC (carbamazepaine, phenytoin and barbiturate)
Dialysis (barbiturates, carbamazepine, lamotrigine and valproate)
Which snake bites are associated with Venom induced consumptive coagulopathy and describe its pathophysiology
Brown (pseudonaja), Taipan (Oxyuranus), Tiger (Notechis), Hoplocephalus species, and Rough scaled snakes (Tropidechis) always cause VICC in significant envenoming.
Not present in Death Adders, Sea Snakes or Black snakes but black snakes have anticoagulant in its venom and can cause mild to mod elevation in APPT and INR. Fibrinogen and D Dimer typically normal
In VICC, Prothrombin activators in venom lead to consumption of major coagulation factors including fibrinogen, factor V and factor VIII.
Which snake bites cause Neurotoxicity
Taipan (Oxyuranus) and Death Adders (Acanthophis) commonly cause neurotoxicity with death adders having slower onset over hours.
Tiger and Sea Snake can also cause it uncommonly with Tiger being slower onset over hours
Brown can rarely cause it
Not present in Black snakes
