1. Paediatric Ingestions “A pill can kill”
Jonathan Wills
ED Registrar
16 September 2014

2. Paediatric Ingestions
Most common month
2-3 pills or a mouthful
Think “worst case” scenario
Observation is mainstay
Serious sequelae are rare but some substances can be lethal at small doses...
Usually small amounts are ingested
“Worst case”:
Assume the time of ingestion was the latest time possible
assume all unaccounted for medications were ingested
when more than one child involved; assume that each child ingested all the unaccounted for meds.
The mainstay of treatment is observation before tormenting the child with invasive investigations.

3. “A pill can kill” Calcium channel blockers Propanolol
Dextropropoxyphene (in “paradex”)
TCAs
Chloroquine
Amphetamines
Opioids
Sulphonylureas
Theophylline
1. Calcium channel blockers
eg diltiazem, verapamil
especially dangerous in the high does, slow release preparations (toxicity may be delayed for up to 12 hours)
delayed onset bradycardia, hypotension, conduction defects, refractory shock
2. Sodium channel blockers
propranolol, dextropoxyphene, TCAs, choloroquine.
Propanolol (a betablocker which also has Na channel blocking effects);
causes coma, seizures, VT (due to QRS prolongation), hypoglycaemia
Dextropropoxyphene is an opioid found in “paradex”. In addition to its action on µ receptors, it also has Na channel blocking effects; causes VT because of this.
TCAs such as amitriotyline. Coma, seizures, VT.
Chloroquine (and hydroxychloroquine) malaria prevention; also used in autoimmune disorders such as SLE and RA.
Coma, seizure, cardiovascular collapse.
3. Recreational sympathomimetic drugs such as the amphetamines
Methamphetamine, MDMA (ectasy).
agitation, confusion, hypertension, hyperthermia
4. Opioids
eg methadone, morphine, oxycodone
coma, respiratory depression and arrest
onset may be delayed for slow release morphine (up to 12 hours)
5. Sulphonylureas
stimulate insulin release from pancreatic beta cells
hypoglycaemia
onset may be delayed for up to 8 hours for slow release formulations
6. Theophylline
seizures, SVT.
may be slow release form so toxicity can be delayed up to 12 hours.

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5. Case 1: Johnny 2 year old boy BIB by Auntie
Apparently Grandpa saw him putting white pills in his mouth 30 minutes ago
Unsure what tablets and Grandpa has heaps lying around
No car, no phone to contact Grandpa
Looks well, age appropriate vital signs

6. Case 1: Johnny What do you do? Correct answers may get one of these…
Admit for at least 12 hours observation.
IV access can be deferred until early evidence of toxicity is apparent
Check bedside glucose level:
on presentation
if there is any clinical evidence of hypoglycemia
and at discharge
Monitor the following:
level of consciousness
vital signs (pulse rate, blood pressure and respiratory rate)
early clinical features of hypoglycemia
Perform an ECG and institute cardiac monitoring if there is any abnormality of conscious state or vital signs, or the child appears unwell
Only discharge the patient during the day
Education
safe storage, child resistant latches on cabinets, child resistant lids.

7. Case 2: Jimmy 3 year old BIB parents, 14kg
Ingested of Mum’s Ferrous fumarate tabs (200mg) 30 minutes ago
50mg/kg
He now looks well and has age-appropriate vital signs.
Each of the different iron tablets have different amounts of elemental iron in them. You can work out how much is in each table by the table in the Murray toxicology handbook. For ferrous fumarate you divide the dose by 3 to work out the amount of elemental iron.
So 50mg/kg.

8. Case 2: Jimmy
He looks well and has age appropriate vital signs

9. Case 2: Jimmy How severe? <20mg/kg –– asymptomatic
20-60mg/kg –– GI symptoms only
60-120mg/kg –– potential for systemic toxicity
>120mg/kg –– potentially lethal
20-60mg/kg –– GI symptoms only
corrosive injury to the gastrointestinal mucosa resulting in vomiting, diarrhoea, hemetemesis, melena and fluid losses that may result in hypovolemia.
60-120mg/kg –– potential for systemic toxicity
Although the exact mechanisms are uncertain, iron acts as a cellular toxin targetting the cardiovascular system and the liver, with secondary CNS effects, metabolic acidosis due to hyperlactemia and free proton production from the hydration of free ferric ions, and coagulopathy.
So the typical time course is…
0-6 hours –– vomiting, diarrhoea, hemetemesis, melena, abdominal pain. Significant fluid loseses may lead to hypovolemic shock
6-12 hours –– gastrointestinal symptoms wane and the patient appears to be getting better. During this time iron shifts intracellularly from the circulation
12-48 hours –– Cellular toxicity becomes manifest as vasodilative shock and third-spacing, high anion gap metabolic acidosis (HAGMA) and hepatorenal failure
2-5 days –– acute heaptic failure, although rare mortality is high
2-6 weeks –– chronic sequelae occur in survivors –– cirrhosis and gastrointestinal scarring and strictures

10. Case 2: Jimmy Investigations, consider: Treatment?? Antidote?? BSL ECG
paracetamol level
serum iron >90micromol/L (500mcg/dL) equiv to > 60mg/kg
blood gas
abdo xray
Treatment?? Antidote??
serum iron concentration
peak levels occur 4-6 hours following iron ingestion
after 6 hours iron levels fall due to intracellular shift
levels do not clearly correlate with clinical toxicity, but > 90 micromol/L (500 mcg/dL) is generally considered predictive of systemic toxicity (equivalent to >60mg/kg)
blood gas
the presence of HAGMA is a useful marker of systemic toxicity
in the absence of iron levels a serum bicarbonate level can be used as a surrogate marker
abdominal X-ray — can be used to confirm ingestion
Does anyone know the antidote and its indications??

11. Case 2: Jimmy Fluid resuscitation
Whole bowel irrigation considered for >60mg/kg
Desferroxamine for severe iron toxicity
>90micormol/L at 4-6 hours post ingestion, metabolic acidosis
binds free iron in blood and enhances its elimination in urine 
Can be stopped when clinically stable and serum iron level <60 micromol/L
Iron – like other metals – does not bind to activated charcoal but whole bowel irrigation can be used for abdominal x-ray confirmed ingestions of >60 mg/kg. In potentially lethal ingestions (e.g. >120 mg/kg) surgical or endoscopic removal of iron are options.
Desferroxamine
Indications:
level >90 micromol/L at 4-6 hours post-ingestion
evidence of systemic toxicity
shock
metabolic acidosis
altered mental status
SO PROBABLY WON’T BE NEEDED IN JIMMY.
Administration:
initial infusion rate of 15 mg/kg/h, reduced if hypotension occurs, may be titrated up to 40mg/kg/h in severe toxicity
cardiac monitoring is mandatory
desferrioxamine is is made as a 5 mg/mL solution by reconsituting 500mg in 5 mL sterile water then diluting up to 100 mL with normal saline or 5% glucose.
Adverse effects:
hypersensitivity
hypotension (with rapid or high-dose IV administration)
ARDS (with infusions >24h)
toxic retinopathy
Yersinia sepsis (the ferrioxamine complex is a siderophore that promotes growth)
The infusion can be stopped when the patient is clinically stable and the serum iron level is <60 micromol/L. Ferrioxamine is excreted unchanged in the urine, which classically turns a vin rose colour.

13. Case 3: Jacob
8yo BIBA history of learning difficulties and behavioural disorder
Found unresponsive by parents this morning, Last seen well 8 hours ago.
On Ritalin (methylphenidrate)
Mum has depression on an antidepressive,
Dad uses many recreational drugs. Had house party last night; lots of methamphetamine, ectasy and some prescription benzo’s/opioids

14. Case 3 Jacob: BP 100/50, afebrile, HR 150, RR 26, sat 98% oa, BSL 6.5.
Weight known to be 35 kg.
Vomit in mouth, tolerating OPA from ambulance
GCS 7 (E1V2M4). Pupils 3mm reactive.
Brief to tonic clonic seizure, self terminating.
Any other information??

15. Case 3: Jacob Any guesses on what he might have taken?
Rate of 160 with wide and bizarre ECG complexes. prolonged QRS and prolonged QT intervals.
He had taken 400mg amitriptyline (>10mg/kg)
-RAD
-dominant terminal R wave in aVR
(Poisoning with sodium-channel blocking agents is suggested if:
R wave height > 3mm
R/S ratio > 0.7)
TCAs are noradrenaline and serotonin ruptake inhibitors and GABAa receptor blockers. The toxicity is mainly due to blockade of the fast sodium channels .
With the qrs prolongation we are thinking an agent which causes blockade of the fast sodium channels.
With qt prolongation we would think agents which block potassium efflux, which amitriptyline also does.

16. Case 3: Jacob Intubated Sodium bicarbonate 35mmol (1mmol/kg)
He underwent rapid sequence induction
with thiopentone and suxamethonium and was intubated
and ventilated. He was hyperventilated to keep his ETCO2
between
-thio has a wide dose range (0.25mg/kg-3mg/kg), good for status epilepticus
-sux 1.5-2mg/kg
Given 35 mmol (1 mmol/kg). [Note the Murray toxicology textbook states 2mmol/kg]
of sodium bicarbonate and also received 2 mg midazolam intravenoulsy.
Repeat ECG rate 130, QRS 130ms.
Given further dose sodium bicarb.

17. Case 3: Jacob
Next day normal ECG

18. Thank you.