General approach to Poisoning and Envenomation Flashcards

Question 1

Q

What types of poisons may children be exposed to?

Answer

A

POISONS

TYPES

Therapeutic drugs
- deliberate or iatrogenic
- e.g.
  - TCAs
  - digoxin (most fatal)
  - Lomotil (diphenoxylate with atropine) - can be toxic at therapeutic doses for some children
recreational drugs e.g. alcohol, solvents
household products
plants (more rarely)
inhalational toxins e.g. chlorine gases (accidents or NAI)
agricultural products e.g. organophosphates, carbamates
corrosives - oesophageal burns and complications

Question 2

Q

What % of children under the age of 5 can open child-resistant containers?

Question 3

Q

What are some risk factors for accidental poisoning?

Answer

A

ACCIDENTAL POISONING

RISK FACTORS

maternal depression
recent change in circumstances e.g. new baby, moving house

Question 4

Q

Which groups of children are most likely to attempt suicide or parasuicide? What interventions do these children need to have? What is parasuicide?

Answer

A

ATTEMPTED

SUICIDE AND PARASUICIDE

parasuicide = apparent attempted suicide without the actual intention of killing oneself
Teens
may be as young as 8-9 yo
need PSYCH and SOCIAL assessment

Question 5

Q

Discuss the primary assessment and resuscitation of poisoning.

Answer

A

POISONING

PRIMARY ASSESSMENT & RESUSCITATION

A
- patency (P/ U on AVPU –> A at risk)
- airway opening manoeuvres + BVM
- adjuncts
- intubation + ventilation
- Challenges
  - corrosive ingestion
  - cardiac arrhythmia e.g. TCA
  - ++ resp secretion e.g. organophosphate
B
- high flow O2 - FM w/ reservoir (resp abnormality, shock, decreased GCS)
- Remember CO2 can accumulate despite normal sats if ventilation is inadequate e.g. poisons that depress respiration => ventilate appropriately (BVM or intermittent PPV if intubated)
- RR increased = methanol, cyanide, carbon monoxide, theophylline, ecstacy, ethylene glycol, amphetamines, salicylates (aspirin) (MCC TH.E GAS)
- RR low = barbiturates, opiates, sedatives, ethanol (BOSE - low like the bass)
- Kussmaul breathing (acidotic sighing respirations) + coma = metabolic acidosis e.g. salicylates, ethylene glycol, ethanol, carbon monoxide (SEEM)
C
- HR
  - increased: phenothiazines, cocaine, theophylline, b-agonists (sympathomimetics), ecstacy, amphetamines, TCAs (PHE.CT BEAT)
  - low: b-blockers, organophosphates, clonidine, digoxin (BL.O.C.D)
- Rhythm
  - Cardiac monitoring IF:
    - HR > 200 bpm (infant)
    - HR > 150 bpm (child)
    - abnormal rhythm
  - Dysrhythmias
    - TCAs = QRS prolongation / VT
    - digoxin
    - quinine
    - antiarrhythmic drugs
  - NB some antiarrhythmic drugs C/I with certain poisons - d/w TOXBASE/ poisons centre
  - Tachyarrhythmia + SHOCK
    - up to 3 synchronous shocks
    - 1-2-2 J
    - attempt asynchronous if broad complex and shock not activated by defib
    - anaesthetise first if conscious
    - NO DC shock in digoxin poisoning
- BP
  - Hypotension/ SHOCK - serious poisoning, different mechanisms
    - = I Can’t Bring The Blood Pressure Back O.P!!!
      - Iron poisoning - GI bleeding
      - Calcium channel blockers
      - Barbiturates - vasodilation
      - TCA
      - Benzo’s
      - Phenothiazines
      - b-blockers
      - Opiates
      - Phenytoin
    - NB avoid inotropes (+ poison causing shock = arrhythmias)
    - Mx: fluid bolus
  - Hypertension - MAOI, ecstacy, cocaine, amphetamines, sympathomimetic agents
- IV/ IO access
  - Bloods
    - baseline incl. FBC, U+E
    - TOXICOLOGY
    - paracetamol + salicylate level
    - gas
    - GLU - BM/ gas + lab
D
- Pupils
  - SMALL
    - Phenothiazines (Remember Pinpoint)
    - Opiates, Organophosphate insecticides - (BOTH O’S - like the tiny little pupils)
  - LARGE =
    - fun stuff e.g. amphetamines, cocaine, cannabis
    - Quite Tremendous And Cute (kawaii eyes) = Quinine, TCAs, Atropine, Carbamazepine
- AVPU / GCS
  - GCS reduced –> trial naloxone if also small pupils
    - opiates
    - sedatives e.g. benzos
    - antihistamines
    - hypoglycaemic agents
- Posture
  - Hypertonia: theophylline, ecstacy, TCA, amphetamines (TH.E.T.A - think of a tough frat boy flexing his muscles)
- Convulsions –> diazepam/ lorazepam/ midazolam
  - hypoglycaemia e.g. ethanol
  - This Patient Only Loves Convulsing
    - TCA poisoning
    - Phenothiazines
    - Organophosphate insecticides
    - Lindane
    - Carbamazepine
E
- Fever/ Hyperthermia:
  - fun stuff: ecstacy, cocaine, amphetamines
  - salicylates. phenothiazines
- Hypothermia: ethanol, barbiturates, phenothiazines
G
- HYPOG
  - 10% GLUCOSE 2 ml/ kg
  - follow with infusion

Question 6

Q

What type of monitoring is needed in cases of poisoning?

Answer

A

MONITORING

POISONING

Neuro: GCS, temp (core)
CVS: HR, BP, ECG
Resp: pulse ox, blood gas
Renal: U+E
Gastro: Blood GLU

Question 7

Q

What assessment must be done at the end of the primary assesment in all cases of poisoning? What information is needed?

Answer

A

LETHALITY ASSESSMENT

assess the potential lethality of the overdose
if the nature of the OD is not known, then assume high potential lethality
NB episods of low lethality often require no Rx
History:
- age & weight
- which substance?
- what dose? (labelling? description?)
- what time? (& time since exposure)
- single dose or staggered?
Use findings from examination and investigations
d/w POISONS CENTRE (complex or life threatening cases)

Question 8

Q

Do the following agents cause metabolic acidosis, an enlarged anion gap, hypokalaemia, hyperkalaemia or a combination?

B-agonists
Carbon monoxide
Digoxin
Ecstacy
Ethanol
Ethylene glycol
Iron
Methanol
Salicylates
Theophylline
TCA’s

Answer

A

CLUES TO THE DIAGNOSIS OF AN UNKNOWN POISON

(SEE IMAGE)

Question 9

Q

What are the principles of drug elimination in overdose?

Answer

A

IF

high potential lethality

OR

exact nature of OD not known

THEN

need to minimise blood conc. of drug

BY

Stopping further absorption
Increasing excretion
Specific antidote (if available)
Active elimination e.g. haemoperfusion, plasmapheresis (rarely used, poisons centre to advise)

Question 10

Q

How does activated charcoal work in cases of poisoning?

Answer

A

POISONING

ACTIVATED CHARCOAL

MOA

large surface area = 1000 m² / gram
give enterally but unpalatable => NGT or lavage tube after gastric washout (NB adding flavouring can decrease its activity)
can bind certain poisonous substances e.g. barbiturates, aspirin, theophylline (BAT)
NB can NOT absorb alcohol/ iron
not systemically absorbed
promotes drug reabsorption back into the bowel –> excreted (& interrupts enterohepatic cycling)
dose = 10 x estimated dose of poison ingested, ~ 25 - 50 g
NB protect the airway esp. if reduced GCS as aspirated charcoal causes lung damage

Question 11

Q

Describe the use of emesis as a management strategy in the treatment of poisoning? Is it still frequently used? In what cases should it be used?

Answer

A

POISONING

EMESIS

ipecacuanha
Dose
- > 2 years = 15 ml with water
- 6 months - 2 years = 10 ml with water
Repeat once after 20 mins if necessary
do NOT use if
- depressed conscious level
- corrosive substance ingested
ONLY use when
- at risk from the poisons ingested
- poisons cannot be bound by activated charcoal
- child will not take charcoal
- present w/i 1 hour of ingestion (only about 30% eliminated even w/i time frame)

Question 12

Q

Is gastric lavage a frequently used tactic in the management of poisoning? Why not? With which drugs in particular should advice re: gastric lavage be sought?

Answer

A

POISONING

GASTRIC LAVAGE

Rarely used
risk outweighs benefit
if IRON or LITHIUM ingested in the previous hour –> d/w NPIS (national poisons information service)

Question 13

Q

At what level of iron poisoning (mg/kg) are the following likely:

Toxicity
Fatality

Answer

A

IRON POISONING

ELEMENTAL IRON

TOXICITY > 20 mg/ kg

FATALITY > 150 mg/ kg

Question 14

Q

What are the symptoms of iron poisoning?

Answer

A

IRON POISONING

SYMPTOMS

D&V
abdominal pain
—>
drowsiness
convulsions
circulatory collapse / shock (gut haemorrhage)

Question 15

Q

Describe the management of iron poisoning.

Answer

A

IRON POISONING

Mx

A
- secure
C
- IV access
- BEWARE haemolysed blood samples - high levels of iron can cause haemolysis
- desferrioxamine PO or IV up to 15 mg/ kg/ hr
  - IMMEDIATELY in
    - shock
    - coma
    - fits
  - IRON level 3 mg/ L at = / > 4 hrs after ingestion AND
    - GI Sx
    - leucocytosis
    - hyperglycaemia
E
- whole bowel irrigation
- AXR can help identify how much iron remains within

Question 16

Q

What are the problems associated with TCA poisoning?

Answer

A

TCA POISONING

Quinidine-like inhibition of fast sodium channels
- BRAIN
- MYOCARDIUM
  - intraventricular conduction delay
  - prolonged QRS ( > 4 little squares = serious)
  - arrhythmias
Anticholinergic effects
- tachycardia
- dilated pupils
- convulsions

Question 17

Q

Describe the emergency management of TCA poisoning.

Answer

A

TCA POISONING

Mx

A
B
- ALKALINISE pH (ideally to 7.5 or at least 7.45) – reduces toxic effects on the heart
  1. hyperventilation
  - PCO2 NOT < 3.33
C
- ALKALINISE pH
  1. sodium bicarbonate 1-2 mmol/ kg
- Hypotension - volume expansion
- Inotropes
  - noradrenaline is 1st choice
  - glucagon
- Antiarrhythmics
  - D/W poisons centre
  - lidocaine or phenytoin
  - do NOT use
    - quinidine
    - procainamide
    - disopyramide
D
- treat convulsions
E
F
G

Question 18

Q

Describe the emergency management of opiate poisoning, indluding methadone. Why is it important to normalise PCO2 before giving an opiate antagonist?

Answer

A

POISONING Mx

OPIATES incl. METHADONE

Stablise ABC
NALOXONE = specific antidote
- 10 mcg/ kg BOLUS
- +/- larger boluses or infusion 5-20 mcg/ hr
- short half life
- relapse often occurs after 20 mins
NORMALISE CO2 BEFORE GIVING !!!
- opioid and adrenergic system inter-related
- hypercapnia + opioid antagonist
  - stimulates sympathetic nervous system
  - sudden rise in adrenaline
    - arrythmias incl. ventricular arrhythmias, asystole
    - flash pulmonary oedema
    - seizures

Question 19

Q

What dose of paracetamol needs to be ingested for toxicity to occur? What does this imply about the method of significant paracetamol poisoning?

Answer

A

PARACETAMOL TOXICITY

> 150 mg/ kg

Can occur with lower doses if hepatic/ renal disease

=> significant paracetamol poisoning is almost always intentional; consider NAI in younger children

Question 20

Q

Describe the emergency management of paracetamol poisoning.

Answer

A

PARACETAMOL POISONING

Mx

ACTIVATED CHARCOAL
- within 1 hour of ingestion
- not with liquid preparations (rapid absorption)
PARACETAMOL LEVEL =/> 4 HOURS POST INGESTION
use a nomogram –>
decide whether IV ACETYLSTEINE is needed
- 300 mg/ kg over 24 hours
- contact a poisons centre

Question 21

Q

Describe the emergency management of salicylate poisoning.

Answer

A

SALICYLATE (ASPIRIN) POISONING

Mx

SALICYLATE LEVEL
- initially 2 hours post
- repeat measurements
- levels will rise sig. in first 6 hours
GAS
- resp. alkalosis
- metabolic acidosis
ALKALINISE
- improves excretion of salicylate
- 1 mmol/ kg sodium bicarbonate over 4 hrs
GASTRIC LAVAGE
- up to 4 hours post ingestion
- aspirin slows gastric emptying
ACTIVATED CHARCOAL
- repeated doses if sustained-release preparation
NB do NOT use forced diuresis
*

Question 22

Q

What commonly used substances contain ethylene glycol? How does its taste make it attractive to children? What clinical appearance does it cause?

Answer

A

ETHYLENE GLYCOL

Cars: Anti-freeze & De-icer fluid

Sweet tasting

Inebriation

Question 23

Q

What is the pathophysiology of ethylene glycol poisoning?

Answer

A

PATHOPHYSIOLOGY

ETHYLENE GLYCOL POISONING

metabolic acidosis (inexplicable ANION GAP)
cellular damage - widespread, esp kidneys

Question 24

Q

Describe the management of ethylene glycol poisoning.

Answer

A

ETHYLENE GLYCOL POISONING

Mx

ETHANOL
- 40% 2.5 ml/ kg = oral loading dose
- aim blood ethanol 100 mg/ dl
- strength of most spirits
- competitive inhibitor of alcohol dehydrogenase
- can block the metabolism of ethylene glycol to poisonous metabolic byproducts
HAEMODIALYSIS +/- FOMEPIZOLE
CO-FACTORS
- THIAMINE
- PYRIDOXINE

Question 25

Q

Describe the pathophysiology of cocaine poisoning.

Answer

A

PATHOPHYSIOLOGY

COCAINE POISONING

Local accumulation of NEUROTRANSMITTERS
- adrenaline
- noradrenaline
- dopamine
- serotonin
Adrenaline & Noradrenaline
- @ myocardium
  - tachycardia
  - increased myocardial oxygen demand
  - reduced diastolic time
  - reduced time for coronary perfusion
- @ Peripheral b-adrenergic receptors
  - vasoconstriction
  - hypertesion
Serotonin
- peripheral 5-HT (hydroxytryptamine) receptors
- coronary artery vasospasm
PLATELET AGGREGATION
SODIUM CHANNEL INHIBITOR
- similar to a type I antiarrhythmic agent
- prolonged QRS
- impaired myocardial contractility
- tachyarrhythmias incl. VT & VF
CORONARY EVENT (in children/ adolescents)
- chest pain
- arrhythmias

Question 26

Q

Describe the emergency management of cocaine poisoning.

Answer

A

COCAINE POISOING

Mx

ACS
- oxygen
- continuous ECG monitor
  - VT
    - DC shock
    - NOT antiarrhythmic drugs (further pro-arrhythmogenic effects)
  - Ventricular arrhythmias
    - consider SODIUM BICARBONATE
    - 0.5 - 1 mmol/ kg
    - counteract sodium channel blockage
- ASPIRIN
- HEPARIN
- NB b-blocker contraindicated
BENZODIAZEPINE e.g. diazepam/ lorazepam
Active cooling for hyperthemia

Question 27

Q

What is MDMA? What dose of MDMA do most ecstacy tablets contain? What is the half-life of ecstacy?

Answer

A

MDMA & Ecstacy

MDMA = 3,4 - methylene dioxy methamphetamine

Most ecstacy tablets contain

30 - 150 mg MDMA

Half life of ecstacy = 8 hours

Question 28

Q

What is the pathophysiology of ecstacy poisoning? What adverse effects can be expected at low and high doses?

Answer

A

ECSTACY

PATHOPHYSIOLOGY

stimulates peripheral and central a- and b- adrenergic receptors
Adverse effects
- MILD at LOW doses
  - General: mild temp elevation
  - Neuro: increased muscle tone, agitation, anxiety
  - CVS: tachycardia
- HIGHER doses
  - Neuro: hypertonia, hyperreflexia, visual disturbance
  - CVS: tachycardia
  - Resp: tachypnoea
- SEVERE
  - General: hypepyrexia
  - Neuro: coma, convulsions, increased muscle tone –> rhadbomyolysis, NMS (neuroleptic malignant syndrome) = deaths after 24 hrs
  - CVS: cardiac dysrrhythmias = early deaths, DIC
  - Renal: metabolic acidosis, acute renal failure

Question 29

Q

Describe the emergency management of ecstacy poisoning.

Answer

A

ECSTACY POISONING

Mx

ACTIVATED CHARCOAL - conscious
DIAZEPAM
- for anxiety
- do NOT give major tranquilisers - can exacerbate Sx
MONITOR
- BP
- Temp > 39
  - ACTIVE COOLING
  - SODIUM DANTROLENE
    - 2-3 mg/ kg
    - over 10 - 15 mins
May need ventilation

Question 30

Q

Name some of the signs and symptoms suggestive of organophosphate poisoning.

Answer

A

ORGANOPHOSPHATE POISONING

SIGNS AND Sx

B: SOB
D: pinpoint pupils
E: salivation, sweating, rhinorrhoea

Question 31

Q

Describe the emergency management of organophosphate poisoning.

Answer

A

ORGANOPHOSPHATE POISONING

Mx

Assess for Sx
- Respiratory
- pinpoint pupils
- salivation
- sweating
NO –> high flow O2 & observe
YES
1. PRALIDOXIME IV
  - 30 mg/ kg over 20 mins
  - –> 8 mg/ kg/ hr
  - max 12g in 24 hrs
2. ATROPINE
  - 20 mcg/ kg
  - can repeat
  - very large doses may be required
  - up to 250 mg

Question 32

Q

What is envenoming caused by?

Answer

A

ENVENOMING

BITES & STINGS

ANIMALS:

Snakes
Spider
Insects e.g. bees, wasps, ants
Jellyfish
Fish
Ticks

Question 33

Q

What is the best management of envenoming and why?

Answer

A

Prevention.

Reversal through the use of antidotes may not resolve all medical problems.

Question 34

Q

What are the symptoms of envenoming the result of?

Answer

A

SYMPTOMS OF ENVENOMING

VENOM - DIRECTLY
ALLERGIC RXN TO VENOM
COMBINATION

Question 35

Q

What are the principles of management of envenoming?

Answer

A

ENVENOMING

MANAGEMENT PRINCIPLES

Remove from danger (esp if venomous animals)
A,B,C,D,E,F,G - RESUS
1. Coagulation factor therapy
2. Sedation
Supportive care to systems affected
Limit uptake of venom (into circulation)
Inactivate venom locally
Antidote/ antivenom - if available
Pain Mx
Local injury sites - treat

Remove from danger (esp if venomous animals)
- ensure it is safe to approach
- avoid further bites/ stings
- some venomous animals can sting repeatedly e.g. jellyfish, other can not e.g. bees
- do not try to catch/ kill the animal, except e.g. removing all ticks in cases of tick paralysis
A,B,C,D,E,F,G - RESUS (see separate note)
Supportive care to systems affected
Limit uptake of venom (into circulation)
- e.g. snakes, funnel web spiders, blue ringed octopus
- PBI first aid = Pressure Bandaging and Immobilisation
  1. broad bandage over the bite site, then over the rest of the limb and over the top of clothing
    - as firm as for a sprain but not so tight as a tourniquet
    - crepe bandage or elasticated
  2. immobilise limb using splint, pt not to move
  3. only discontinue when child is in a hospital capable of giving antivenom
  - limits transport of the venom in the lymphatic system
  - do NOT use for red back spider, ticks, stonefish, jelly fish
Inactivate venom locally
- for jellyfish and fish stings
- box jellyfish
  - inactivate unfired stinging cells on tentactles adherent to the skin
  - flood with vinegar
  - +/- apply coldpack
- other jellyfish, fish and stingrays
  - hot water
  - hot shower immersion at 45 degrees (care to avoid thermal injury)
Antidote/ antivenom - if available
- IgG Ab’s or fractions
- raised in animals against specific venoms
- each one for a particular species/ group of animals
- can neutralise venom but do not reverse damage
- IV usually - more rapid + effective, dilute in 0.9% saline but avoid fluid overload
  - IM - red back spider, stonefish
- Dose depends on quantity of venom injected, not size of pt (same regimen as adults)
- Indications vary based on animal - see separate note
- WHICH antivenom?
  - depends on animal
  - 5 specific snake antivenoms and 1 polyvalent for all types
  - use specific if possible - cost and safety (esp. brown & tiger snake)
  - can use snake venom detection test to aid choice of specific antivenom - NB not diagnostic, -ve does not R/O bite
- BEWARE adverse rxn’s => only use when indicated + make sure adrenaline etc to hand
  - early: rash, fever, anaphylaxis
  - late: serum sickness
Pain Mx / ANALGESIA
- HOT WATER (45 degrees), avoid thermal injury - marine stings
- ANTIVENOM - stonefish, red back spider, +/- box jellyfish
- IV OPIOIDS
- REGIONAL NERVE BLOCK - marine stings
Local injury sites - treat
- all stings and bites can introduce tetanus or other infections
- TETANUS immune status
  - immunisation or booster
  - snakebites - only AFTER acute coagulopathy resolved
- ANTIBIOTICS
  - NOT as routine prophylaxis
  - only in acute infection
- TRAUMA
  - Stingrays
    - laceration of nerves, tendons and blood vessels
    - penetrate abdomen or chest wall
    - direct injury to the heart
    - local tissue damage/ necrosis
  - Wash, debride & control bleeding
  - CAREFUL removal of the sting if near heart - incautious removal can be lethal
- EYES - venom spat into
  - NOT likely to cause envenoming
  - CAN cause
    - intense pain
    - temporary blindness
    - corneal injury
  - Urgent irrigation
  - examine the cornea and treat corneal injury

Question 36

Q

Is enevenoming inevitable after a bite or sting? What kind of factors affect the likelihood of ensuing envenoming after a bite or sting?

Answer

A

ENVENOMING

NOT INEVITABLE - depends on:

Animal
- can often control how much venom injected
- ‘dry’ snake bites which fail to be effective and do not require antivenom
  - NB manage ALL SNAKE BITES as potentially lethal
Child
- Size:
  - smaller –> envenoming more likely as higher concentration of venom
  - chances of severe or lethal envenoming also increase as size decreases
- Clothing: may reduce or prevent injection of venom into skin

Question 37

Q

How do you make the diagnosis of envenoming?

Answer

A

DIAGNOSING ENVENOMING

HISTORY
1. EXPOSURE to a bite/ sting
2. Type of ANIMAL
  - venomous or not
  - prediction of potential risks
  - targeted therapy
EXAMINATION
- evidence of ENVENOMING or ALLERGIC RXN to the bite/ sting
- no history of exposure but UNEXPLAINED
  - Neuro: paralysis, collapse, convulsions
  - MSK: myotoxicity
  - CVS: coagulopathy
  - Renal: renal failure
LABORATORY TESTS
- may be useful in indentifying envenoming e.g. snake bites
- coagulopathy (INR, D-dimer, APTT) & myolysis (CK)

Question 38

Q

With what type of venom are laboratory tests essential for determing the degree of enevnoming? Which tests are these? With which type of venom are laboratory tests NOT helpful in assessing severity?

Answer

A

ASSESSING DEGREE OF ENVENOMING

LABORATORY TESTS

Useful with SNAKE bites
- examination: look for paralytic features
- Test for:
  - Coagulopathy
    - INR
    - APTT (activate partial thromboplastin time)
    - D-dimer
  - Myolysis = CK (creatine kinase)
NOT useful
- spider bites
- tick bites
- marine stings
- insect stings — EXCEPT MASSIVE MULTIPLE

Question 39

Q

Describe the resuscitation and supportive management of envenoming/ envenomation.

Answer

A

ENVENOMING/ ENVENOMATION

RESUS & SUPPORTIVE Mx

= DANGER + ABCDEFG

DANGER
- ensure it is safe to approach
- avoid further bites/ stings
- some venomous animals can sting repeatedly e.g. jellyfish, other can not e.g. bees
- do not try to catch/ kill the animal, except e.g. removing all ticks in cases of tick paralysis
A
- secure - assess frequently
- clear secretions
- may be threatened by
  - reduced GCS
  - bulbar palsy
  - tissues around the airway swollen/ paralysed
- A PARALYSED CHILD MAY BE FULLY CONSCIOUS - ALWAYS ANAESTHETISE BEFORE INTUBATING!!! (Unless GCS is reduced)
B
- Ventilatory support will be needed for:
  - Paralysis
  - Severe muscle spasms
  - Seizures
  - Secretions unmanageable
- Always anaesthetise first as may be fully conscious even if paralysed
- Intubate BEFORE resp. arrest
C
- SHOCK may occur due to
  - cardiac arrhythmia
  - bleeding 2ndary to coagulopathy
  - massive fluid leak into tissues damaged by cytotoxic venoms
- IV access
  - SNAKE BITE - BEWARE coagulopathy - do NOT cannulate / sample from:
    - subclavian
    - femoral
    - jugular
- FLUIDS & ELECTROLYTES
  - avoid fluid overload
  - beware renal/ electrolyte derangement w/ some venoms
- COAGULATION FACTOR Therapy
  - FFP, cryoprecipitate
  - give after anti-venom in cases of sig. active bleeding
  - venom components e.g. snakebite can attack haemostasis system, causing consumptive coagulopathy incl. defibrination
  - anti-venom can neutralise these but it does NOT replace consumed clotting factors - can take hrs to return to safe levels
D
- Pupils
- GCS/ AVPU
  - remember that failure to respond may be due to paralysis and not depressed GCS
- NEURO exam - look for
  - ptosis
  - opthalmoplegia
  - bulbar palsy
- SEDATION
  - bites and stings can cause extreme anxiety
  - consider sedation and anxiolysis esp. for transportation
  - CAUTION in pts at risk of neurotoxic paralysis
E
- full exposure to identify site of bite/ sting
- stings - check areas covered by hair
- tick bites - check scalp & behind ears

Question 40

Q

What are the indications for antivenom use in the following:

Australian snakebites
Funnel web spider bites
Red back spider bites
Stonefish stings
Box jellyfish stings

Answer

A

INDICATIONS FOR ANTIVENOM

Australian snakebites
- systemic envenoming incl.
  - Neuro: collapse, convulsions, paralysis
  - CVS: coagulopathy
  - MSK: myolysis
  - Renal: renal damage
- NOT if ONLY GENERAL Sx
  - headache
  - vomiting
  - abdo pain
Funnel web spider bites
- systemic envenoming
Red back spider bites - controversial
- systemic envenoming
- intractable regional envenoming
Stonefish stings
- sig. local pain
Box jellyfish stings - unclear
- life-threatening envenoming

Question 41

Q

What is the purpose of monitoring in the case of bites and stings? What form does it take?

How long should it go on for in the following:

Dry/ minor bites/ stings
Snakebites
Funnel web spider bites
Red back spider bites
Marine envenoming (in general)
Stingray wounds to the trunk

Answer

A

MONITORING

Purpose = to detect developing envenoming which may not be the case at presentation
What type of monitoring = recurrent
- clinical examination
- blood tests (snakebites)
How long for?

Dry/ minor bites/ stings
- adequate period so envenoming not missed
Snakebites
- at least 12 hrs if NO / MINOR envenoming
- longer in remote areas
- Blood tests @:
  - 1 hr after PBI removed
  - 6 hrs post bite
  - 12 hrs post bite
Funnel web spider bites = BIG BLACK SPIDER
- at least 4 hrs post bite (sig. envenoming will develop within this time frame)
Red back spider bites
- ONLY symptomatic pts
Marine envenoming (in general)
- depends on
  - bite/ sting
  - symptoms
- severe/ life threatening
  - within first hr or less - usually
  - always w/i 4 hrs – EXCEPT
Stingray wounds to the trunk
- may seem fine initially
- observe for a longer period > 4 hrs

Question 42

Q

What are button batteries and what devices may they be found in? What metals anf chemicals do they contain? What type of batteries are the most lethal if ingested?

Answer

A

BUTTON BATTERY INGESTION

Button batteries = small, coin shaped batteries
Used in
- watches
- calculators
- children’s toys
Metals
- mercury
- silver
- lithium
Chemicals
- sodium hydroxide
- potassium hydroxide
Lithium batteries = most fatal

Question 43

Q

Describe the pathophysiology of button battery ingestion and the timeframe in which it occurs.

Answer

A

BUTTON BATTERY INGESTION

PATHOPHYSIOLOGY

not due to leakage

electric current discharged from battery
sodium hydroxide generated
causes liquefaction necrosis of tissues

Timeframe
- if lodged e.g. in oesophagus –> severe burns w/i 2 hrs
- damage continues for days - weeks due to
  - weakened tissues
  - residual alkali

Question 44

Q

What are the complications of button battery ingestion?

Answer

A

BUTTON BATTERY INGESTION

COMPLICATIONS

Perforation
Distillation in adjacent structures e.g. trachea, major vessels
Vocal cord paralysis
Strictures

Question 45

Q

Which age group is most at risk of dying from button battery ingestion?

Question 46

Q

What percentage of children who ingest button batteries have symptoms? What type of symptoms do they have?

Answer

A

BUTTON BATTERY INGESTION

SYMPTOMS

10%

vomiting +/- haematemesis
refusal to take anything orally
increased salivation
dysphagia
airway compromise

Question 47

Q

What investigations should be done in children who have ingested button batteries? What radiological characteristics suggest button battery ingestion?

Answer

A

BUTTON BATTERY INGESTION

INVESTIGATIONS

XR of the entire oesophagus and abdomen
Radiological characteristics
- radiopaque foreign body
- halo effect/ double rim
- lateral XR - step off

Question 48

Q

Describe the management of button battery ingestion.

Answer

A

BUTTON BATTERY INGESTION

Mx

REFER TO SURGEONS as an EMERGENCY for removal if
- in the oesophagus
- in the stomach + ingested alone (w/o magnet) + symptomatic
- still in the stomach after 4 days
- if lodged
REPEAT XR w/i 4 days IF:
- > 15 mm battery AND
- child < 6 yo
- –> if still in the stomach refer for removal
REFER TO MENTAL HEALTH
- consider self-harm in older children

Brainscape's Knowledge GenomeTM

General approach to Poisoning and Envenomation Flashcards

Brainscape's Knowledge Genome^TM