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ED Fellowship --> Toxicology > Antidotes > Flashcards

Antidotes Flashcards

1
Q

Discuss indications and contraindications to the use of atropine

A

Indications

  • poisoning by agents that impair AV conduction such as cardiac glycosides, B blocker and Ca blocker
  • Organophosate and carbomate poisoning

Contraindications

  • Closed angle glaucoma
  • Obstructive disease of the GIT
  • Obstructive uropathy
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2
Q

Discuss PD and PK of atropine

A

PD: competitive antagonist of ACh at muscarinic receptors. It reverses excessive parasympathetic stimuation that resutls from inhibition of acetylcholinesterase. Does not act at nicotinic receptors

PK: Poor bioavailability, hepatic metabolism with half life of 2-4 hours. Crosses BBB and placental barries

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3
Q

Discuss administration of atropine and side-effects from excess

A

Bradycardia caused by drug induced AV conduction blockade
-IV bolus of 600mic repeated doses to 1.8mg

Organophoshate and carbamate poisoning

  • IV blolus of 1.2mg with further dsoes every 2-3 minutes doubling the dose each time until drying of resp secretions is ahcieved. HR is not a useful end point as tachy may persist due to nicotinic effects
  • Very large doses can be administered >100mg in severe tox

Excess –> anticholinergic syndrome

Paeds dose initially is 20mic/kg

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4
Q

Discuss calcium as antidote, indications and contraindications

A 
Calcium gluconate (0.22mmol Ca ions/ml)
Calcium cholride (0.68mmol calcium ions/ml)

Indications

  • Calcium channel blockade
  • hydrofluoric acid skin exposure
  • hypocalcaemia of systemic flurosis secondary to ingestion of or extensive skin exposure to hydrofluoric acid
  • Hypocalcaemia secondary to ethylene glycol poisoning
  • iatrogenic hypermagnesaemia
  • hyperkalaemia

Contra

  • Hypercalcaemia
  • Digoxin toxicity
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5
Q

Discuss calcium PD and PK

A

PD: Calcium acts as a physiological antaonist to the effects of hyperkalaemia and hypermagnesaemia on the cardiac conducting system and skeletal muscel. Administration of calcium in hypocalcaemic states restores or maintains ionised calcium at a concentration sufficient to prevent cardiac dysthythmias. In hydrofluroic acid poisoning calcium ions bind to fluride ions and prevent further tissue penetration.
Changes preferred sourec of energey in cardiac tissue to glucose from fatty acids – impairs uptake of glucose due to impaired insuling

PK: 99% of the bodies calcium is concentrated in bones. Of the calcium in plasma about half is ionised and physioogically active while the other half is bound to albumin. Plasma concentration is maintained at close to 2.5 mmol/L by a number of hormonal homeostatic mechanisms

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6
Q

Discuss administration of caclicum

A

Hypocalcaemia/hyperK/HyperMG

  • Administer 10-20ml of 10% calcium gluconate IV over 5-10 minutes or 5-10 mls clacium chloride
  • Cardaic monitoring is essential

Ca blockade

  • 2g (20mls) of calcium chloride or 60mls of gluconate over 5-10 minutes -
  • Repeat the dose every 20 minute up to 3 times until effect is seen

Hydrofloric acid skin exposure
#Topical 2.5% gel
–Minor burns
–For hands palce gel in a glvoe and place the hand in the glove
#local injection of calcium gluconate
-consider if topical application fails
-inject 0.5ml/cm2 intradermally and subcut
-not suitable for finger
-do not inject calcium chloride as this can cause tissue injury
# Bier’s block (foreamr reginal intravenous injection)
-Consider for alrge HF exposure to fingers han or forearm or if gel application to hese regions ahs failed
-insert IV distal in affected arm
-dilute 10mls calcium gluconate in 40mls of normal saline
-inject solution IV with beirs up
-release after 20 minutes
#intraarterial infusion
-insert art line into radial brachial or femoral artery of the affected limb
-dilute 10m of calcium gluconate into 40mls of normals slaine
-infuse over 4 hours

Hydrofloric acid inhalation injury
-give neb 2.5% gluconate solution

END POINTS

  • Hypocalcaemia, hypermag or hyper K normalisation
  • Ca Channel blocker - HD improvement
  • Hydrogluroic acid exposure - resolution of pain

Paeds
- 1ml/kg of calcium gluconate

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7
Q

Discuss HIET, indications and contraindications

A

HIET may allow the heart to overcome the metabolic starvation that results from Ca channel blocker toxicity

Indications:

  • severe Ca channel overdose
  • propanalol overdose

Contraindications
-Nil

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8
Q

Discuss mechanisms of action of HIET

A
  • Increased glucose and lactate uptake by myocardial cells
  • improved myocardial function wihtout increased o2 demand
  • Increased pyruvate dehydrogenase activity thus hastening myocadial lactate oxidation and clear the cystosol of glycotic byproducts that can impair calcium handling and cause diastolic dysfunction

Promotes excitation contraction coupling and contractility because increased glucose availability results in

  • increased SR associated calcium ATPase activity
  • Increased ctyoplasmic calcium concentration
  • enhanced calcium entrance into mitochondira and sarcolemma

HIET is best used adjunctively with catecholamines

  • insulin mediated inotropy is not catecholamine mediated and is not affected by b blockers so addtive effects are likley
  • Although insulin appears to improve contractility it has not chronotropic affect and may cause vasodiliation
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9
Q

Discuss administration of HIET

A

Commence therapy with

  • glucose 25 grams (50ml 50%) IV bolus unless marked hyperglcyaemia >22mmol present
  • short acting insuling 1U/KG bolus to maximally saturate insulin receptors

Continue with

  • Insulin infusion at 0.5 IU/KG/H and titrated every 30 minutes to a max of 5IU/kg/hr
  • dextrose 25g/h infusion to maintain euglycaemia - CVC access may be required to allow concentrated solutions to be used

Monitor

  • glucose- every 2o minutes for first hour then hourly
  • potassium replace only if <2.5mmol and there is a source of K loss - total body stores are not depleted and K will shift back to the extracellular compartment once insulin discontinued
  • Check K hourly during initiation and tiration - 6 houlry once stable

Peak effect usually reached at 1 hour most effective if started early

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10
Q

Discuss intravenous intralipid indications and contraindications

A

Sterile emulsion of soya been oiloil in water used in parenteral nutrition. Novel antidote that requires further study but ay have a role to play in the resus of patients with refractory cardiac instability or arrest due to LA or other lipophil agents

Indication

  • LA induced cardiovascular collapse resistant to standard resus protocols
  • Consider in other toxic caused refractory cardiac instability or arrest ie: TCA, antidepressant, propanolol, Ca channel blockade

Contrindications

  • Inadequate standard resus
  • egg soya or peanut hypersensitivity
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11
Q

Discuss MOA of Intralipid

A

Introduction of an intravascular lipid phase that extracts agent from tissue binding sites, increased myocardial ATP synthesis due to reversal of inhibition of fatty acid delivery to mitochondira and restoration of myocyte funciton by activation of caclium and potassium channels and an increase in intracellular calcium

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12
Q

Discuss admin of intralipid + adverse effects assocaited with its use

A

Give 1-1.5ml/Kg IVLE 20% over 1 minute
Can repeat bolus once or twice at 3-5 minute intervals if required then
-infuse IVLE 0.25ml/kg/min until HD stable
-increase to 0.5ml/kg/minute if hypotension persists
-increasing above 8ml/kg is unlikley to be beneficial

Adverse effect

  • Anaphylaxis
  • pulmonary HTN, Acute lung injury, haematuria, pnacreatitis and hypertriglyceridaemia have been described

Nil data for pregnancy or kids should not be withheld if life threatening situation

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13
Q

Discuss methylene blue its indications and contraindicaitons

A

Treatment of choice for symptomatic drug induced methaemoglobinaemia. It has been proposed as a potential adjunct in the treatment of shock states

Indications

  • symptomatic drug induced methaemoglobinaemia (signs of hypoxaemia with chest pain, dyspnoea or confusion)
  • Consider in asymptmatic patients with methaemoglobin levels >20%
  • Used in refractory anaphylactic and toxic shock states where hypotension persists despite vasopressor administration

Contraindications

  • G6PD deficiency: lack of NADPH in this condition causes methylene blue to be ineffective as it cannot be reduced to leucomethylene blue - haemolysis may also occur
  • renal impairment: dose needs to be reduced
  • methaemoglbinaemia reductase defieincy
  • nitrate induced matehaemoglobinaemia following the treatment of cyanide poisoning
  • hypersensitivity
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14
Q

Discuss mechanism of action of methylene blue

A

Dramatically increases the antural rate of reduction of metHb to haemoglobin. Methylene blue is reduced to leucomethylene blue then reduces MetHb to HB.

Inhibits the nitric oxide synthase and guanyalte cylclase and scavenges endotherial nitric oxide. In shock states it appears to ahve both vasoconstricitve and inotropic effect.

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15
Q

Discuss administration of methylene blue

A
  • Administer 1-2 mg/kg (0.1-0.2 ml/kg of 1% solution) IV slowly over 5 minutes. Follow with a normal saline flush to minimise venous irritation
  • MetHb levels should be measured hourly until a consistent fall is documentede
  • Methaeoglobinaemia usually responds to a single dose howevere a further 1-2mg/kg may be repeated after 30-60 minutes if inadequate response
  • in rare cases such as dapsone poisoning when methaemoglobin formation may continue for days repeat dosing every 6-8 hours may be necessary

END POINTS

  • reoslution of symptoms of hypoxaemia
  • repsonse is confirmed by repeat MetHb estimation
  • Stabilisation of HD parameters

Pulse oximetry reading will be unreliable as Met HB and methylene blue interfere with reading

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16
Q

Discuss adverse effects of methylene blue

A
  • Local pain and irritation commonly occur at the site of administration and extravasation can result in local tissue necrosis
  • Common non-specific adverse effects include headache, dizziness, restlessness nausea vomiting chest discomfort and shortness of breath
  • blue staining of mucous membranes (may mimic cyanosis) and urine
  • Methylene blue may paradoxically cause methaemoglobinaemia when given in high doses (>7mg/kg) secondary to a direct oxidative effect on HB
  • Acute haemolytic anaemia may occur in G6PD deficient individiauls with large doses of methylene blue
17
Q

Discuss NAC indications and contraindications

A

The most widely used sulfhydryl donor in the treatment of paracetamol poisoning. It is almost completley protective against paracetamol induced hepatotoxicity when administered within 8 hours of overdose.

Indications

  • Acute paracetamol overdose
  • repeated supratherapeutic paracetamol ingestion
  • paracetamol induced fulinant hepatic fialure
18
Q

Discuss mechanisms of NAC

A

NAC prevents NAPQI induced hepatotoxciicyt when given within 8 hours of an acute paracetamol overdose. It ameliorates the clinical course of toxicity when given after that time or following repeated supratherapeutic ingestion. Four possible mechainsms contribue to this acution
1) increased glutathione availabiolity
2) direct binding to NAPQI
3) provision of inorganic sulfate
4) reduction of NAPQI back to paracetamol
The antioxidant properties of NAC may offer beneift in a number of other poisoning in which oxidiative stress is an imporatnt toxic mechanism and may also explain its beneficial effects in liver failure

PK
-NAC metabolism is complex with a variety of sulfur contianingn compoungs being prouced. PLasma half life follwoing IV amdinistration is 6 bours and 30% is eliiminated unchanged in the urine

19
Q

Discuss administration of NAC

A

The results of a large retrospective study inidcates that nonallergic anaphylactic reaction during treatment with IV NAC can be reduced using a two bag regime instead of the tradiional three bag

First bag given at 200mg/kg over 4 hours
second bag given at 100mg/kg over 16 hours

20
Q

Discuss Non-allergic anaphylactic reactions seen in NAC

A

Mechanism is non igEmediated histamine release or direct complement activation `

Unlike true anaphylaxis prior exposure to NAC is not needed, nor is continued or future treatment contraindicated

-Incidence of 10-50% including hypotension, flushign rash and angio-oedema

  • These usually occur during or shortly after the intiail dose and can be treated with an oral H1 blocker (loratadine) or promethazine 12.5 mg IV
  • The infusion need only be ceased if the reaction is severe in whcih case it may be restarted as soon as the reaction is settling .

For moderate to severe reactions treat as per anaphylaxis and stop the infusion. Acetylcysteine can then be recommenced once symptoms settle at half rate for 30 minutes and then recommenced as per normal protocol.

21
Q

Discuss indication for Digibind

A

Cardiac glycoside poisoning where there is an imminent threat to life or where the risk assessment such suggest such a risk.

Acute

  • cardiac arrest
  • life threatening dysrhythmia
  • ingested dose >10mg or >4mg child
  • serum dig >15nmol/L
  • serum K >5mmol/L

Chronic

  • Cardiac arrest
  • life threatening dysrhythmia
  • cardiac dysrhythmia or increased automaticity not likely to be tolerated for a prolonged period
  • moderate to severe GIT symptoms
  • any symptoms in presence of impaired renal function
22
Q

Discuss administration and dose of digifab

A

Place the patient in a monitored area where equipment drugs and personnel are available to provide full resus.
Calculate dose required dilute in 100ml of NaCl and admin over 30 minutes

CALCULATION Acute

1) Known
- number of ampoules = ingested dose (mg) x 1.6
2) Unknown
- 5 ampoules if the patient is HD stab
- 10 ampoules if unstable
- 20 amp if arrested
- repeat doses of 5 amp every 30 minutes until reversal of dig toxicity is achieved

Chronic

1) Number of ampoules = (serum dig (ng/ml) x bodyweight) / 100
2) alternatively commence 2 ampoules and observe for response if there is no reversal after 30 minutes repeat dose

OTHER
1) stable 5 ampoules every 30 minutes

Be aware that dig level after treatment may be very high as most serum dig assays measure both free and Fab-bound dig
Hyper K due to dig poisoning is treated with Fab and not IV calcium as dig causes elevation in intracellular myocardial calcium levles.

23
Q

Describe MAO of digi bind

A

40mg of Fab binds 0.5mg of digoxin. Digoxin immune fab binds directly to the free intravascular and interstitial digoxin with much greater affinity than the Na/K ATPase receptor. A concentration gradient is created and intracellular digoxin dissociates from tissues and moves to the intravascular space where binding to immune FAB continues.

24
Q

Discuss adverse drug reaction associated with digifab

A

Rare - very safe drug

  • hypokalaemia
  • allergy
  • exacerbation of underlying cardiac failure
  • loss of rate control of pre-exisiting AF
25
Q

Discuss indication and administration of ethanol

A

Competitively block the formation of toxic metabolites in toxic alcohol ingestion by having higher affinity for the enzyme alcohol dehydrogenase.

Indication

  • Methanol
  • ethylene glycol

ADMIN
-May be administered by the oral NG or IV route to maintain a blood etoh concentration of 22-33

ORAL

  • loading dose 1.8ml/kg of 43% ethanol or 3x40ml shot of vodka for a 70 kg adult - ommit loading dose of ethanol in the already ethanol intoxicated patietn
  • Maintenance 0.2-0.4ml/kg/hr of 43% ethanol or 40ml shot each hour

IV

  • loading of 8ml/kg of 10% etoh
  • Maintenance of 1-2ml/kg/hr of 10%
  • infusion prepared by adding 100mls of 10% to 900mls of 5% dextrose
  • adjust dose to maintain ethanol level
26
Q

Discuss indication, contraindication and dose of flumezanil

A

Indication
-benzo in children with compromised airway and breathing.

Contraindications

  • known siezure disorder
  • known or suspected co-ingestion of pro-convulsant drug
  • known or suspected benzo dependence
  • QRS prolongation on ECG (suggest co-ingestion)

Dose
200mic IV repeated every minute until reversal of sedation

27
Q

Describe administration of fomepizole

A

Loading dose of 15 mg/kg in 100mls of normal saline over 30 moinutes
Maintenance dose of 10mg/kg in 100mls over 30 minutes every 12 hours

28
Q

Discuss administration of naloxone

A

Monitored area. Given an initial dose of 100mic IV or 400 SC or IM- larger initial doses can be used if nil concern for dependence - aiming for resolution of bradypnoea

Doses >400mic are rarely required frollowing heroin overdose but large doses may be needed for partial opioid overdose

Duration is variable and dependent on the absorption and elimination kinetics of the ingested agonost.
If required commence a naloxone infusion at 2/3 the rate of the initial dose required/hour

In the non-opioid dependent indvidual naloxone may be given in sufficient doses to fully achieve and maintain normal mentition.
In the opioid dependent it should be given in a dose sufficient to permit maintenance of an adequate airway and RR

29
Q

Discuss indications, MOA and administration of octreotide

A

INDICATIONS

  • intentional sulfonylurea OD
  • quinine induced hypoglycaemia

MOA: powerfully supresses endogenous insulin release from pancreatic islet cells

ADMIN

  • administer as a bolus 50mic IV
  • commence a continuous infusion at 25mic/hour by diluting 500 mic of octreotide in 500mls of normal asline and runing at 25ml/hour
  • normoglycaemia without glucose supplementation is usually maintained on the octreotide infusion. If it does occur it should be corrected with 50% dextrose and the infusion rate doubled
30
Q

Discuss contraindications and administration of physostigmine

A

Contraindications

  • bradydysrhytmias
  • Intraventicular blocks (QRS >100)
  • AV block
  • Bronchospasm

ADmin
-Administer 0.5-1mg as a slow IV push over 5 minutes and repeat every 10 minutes until the desired clinical effect is observed.

Adverse effects
-Excessive doses can produce seizures (usually seen after rapid admin), bradycardia with variable degree of heart block and bronchospasm, bronchorrhoea, nausea and vomiting and diarrhoea.

31
Q

Discuss indications for sodium bicarb

A

Cardiotoxicity secondary to fast Na channel blockade

  • TCA
  • Bupropion
  • Chloroquine
  • Propanolol
  • Type 1a and 1c antidysrhythmics

Prevention of redistribution of a drug to the CNS
-Severe salicylate poisoning

Immediate correction of profound life threatening metabolic acidosis

  • Cyanide
  • isoniazid
  • Toxic alcohols

Enchanced urinary drug excretion

  • saliculate
  • phenobarb

Increased urinary solubility

  • methotrexate
  • drug induced rhabdo
32
Q

Discuss contraindications of Sodi bic

A 
APO
Hypokalaemia 
metbaolic or resp alkalosis 
poorly controlled CCF
reneal failure 
severe hypernatraemia
33
Q

Discuss MOA of sodi bic

A

Elevation of serum ph
1) improved fast sodium channel function
-Raising the serum ph improves fast sodium channel fucntion and mitigates toxic effects. Any increase from baseline pH is beneficial but the effect is maximal at 7
5-7.55
-the sodium load has a seperate but additive positive effect on the sodium channels
2) alteration of drug distriubtion
-elevation of serum pH can reduce the proportion of drug in un-ionised form- reduce its ability to cross cell membranes and hence reduce the porportion that distributes to tissue compartments (esepcially CNS)
3) immediate correction fo severe life threatening metabolic acidosis
- profound metabolic acidosis has a negative effect on CVS function and my be life threatening at pH approaching 6.7 irrespective of the underlying toxic cause

ALKINISATION of URINE

1) ion trapping and enhanced eliminaition
- an alkaline urinary pH can result in some drugs being predominantly in an ionised form and unable to be reabsorbed across the tubular epithelium
2) Increased solubility
- an alkaline urinary pH promtoes water solubility of some durgs and of myglobin thus prevenint tubular precipitation and seconcary renal injury

34
Q

Discuss Admin of Sodi bic

A

CVS Na fast channels
- Give repeat dose of 2mmol/kg IV until cardiostability is achieved.

Maintenance of serum alk in sever CVS toxicity

  • Should be considered following reuss in the presence of Ventricular dysrhythmias, hypotension or a markedly wide QRS >140
  • Commence an infusion of 150mmol sodi bic diluted in 850ml normal saline running at 250 ml/Hr
  • Check ABGS hourly aiming for ph between 7.5 and 7.55

PREVENTION OF REDISTRIBUTION OF SALICYLATE TO CSN

  • pH must be maintained above 7.4
  • this can be achieved with ventilation in the tubed patient
  • If no intubated give 2mmol/kg

Urinary alkinisation

  • Correct Hypokalaemia if present
  • Give 1-2mmol/kg as a bolus
  • Commence infusion of 150mmol sodium bicarb in 850mls of dextrose at 250ml/hr
  • 20mmol of kcl may be added to maintain K
  • monitor K at least every 4 hours
  • regular dipstick aiming for urinary pH of 7.5

ED Fellowship --> Toxicology (23 decks)

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