LEADING ARTICLE 407

Poisoning uptake and reducing hepatic gluconeo-

................................................................................... genesis. In overdose, it can produce
significant gastrointestinal disturbance.

Poisoning in children 5: Rare and In addition to hypoglycaemia, met-

formin can induce a profound lactic
acidosis.7 Serum electrolytes, lactate, and
dangerous poisons bicarbonate should be monitored. Hy-
poglycaemia should be treated with
M Riordan, G Rylance, K Berry intravenous dextrose infusion. Asympto-
matic patients should be observed for 12
...................................................................................
hours.1
Management of children who have ingested β blockers, Acarbose inhibits glucosidases in the
intestine, preventing the digestion and
digoxin, oral hypoglycaemics, organophosphates, carbon absorption of complex carbohydrates.
monoxide, cyanide, isopropanol, ethylene glycol, methanol, Hypoglycaemia is unlikely but diarrhoea
Ecstasy, LSD, cocaine, nicotine, and isoniazid may occur, particularly if patients receive
carbohydrate rich foods following inges-
tion.

I
n the final paper in this series of Treatment in the first instance is with Repaglinide is a newer oral hypogly-
articles on the management of poison- activated charcoal. Repeated doses caemic agent. It acts by stimulating
ing, we deal with exposures to a should be considered.3 Blood pressure insulin release but has a very short dura-
variety of rare, but potentially very and ECG monitoring are required. Elec- tion of action.7 Blood sugar should be
dangerous, toxins. trolytes should be monitored frequently. checked and symptomatic children
Hyperkalaemia should be corrected should receive oral glucose. Effects are
β BLOCKERS using ion exchange resins, glucose and likely to be short lived.
β Blockers competitively antagonise the insulin, or dialysis. Salbutamol and
binding of catecholamines to β receptors. calcium infusions should be avoided ORGANOPHOSPHATES
The effect of specific agents in overdose because of their potential to destabilise Organophosphates are found in insecti-
depends on their receptor specificity, the myocardium. cides, sheep dip, and lice treatments.
lipid solubility, partial agonist activity, Bradyarrhythmias may require treat- They produce irreversible acetylcho-
and dose. ment with atropine or cardiac pacing. linesterase inhibition. Accumulation of
Bradycardia and hypotension are the Tachyarrhythmias may respond to ligno- acetylcholine stimulates muscarinic re-
commonest signs of cardiovascular tox- caine, amiodarone, or phenytoin.1 4 There ceptors at parasympathetic postgangli-
is an increased risk of inducing asystole onic synapses.
icity, but tachycardia and hypertension
with cardioversion and this should be Symptoms of organophosphate poi-
can occur if a partial agonist is con-
used only as a last resort. soning can be delayed for up to 24 hours
sumed. Other signs of cardiovascular
The use of digoxin antibodies should post-exposure. Symptoms, produced by
toxicity include varying degrees of heart
be considered where patients are resist- parasympathetic over stimulation, in-
block, shock, and pulmonary oedema.
ant to supportive treatment or a very clude increased secretions from salivary,
Central effects can occur, particularly
large amount of digoxin has been in- lacrimal, bronchial, and gastrointestinal
with propanolol, and include lethargy,
gested (more than 300 µg/kg). glands, increased peristaltic activity,
hallucinations, and convulsions. Hy-
Plasma digoxin concentrations can be bronchoconstriction, bradycardia and
poglycaemia can also occur.
determined six hours post-ingestion. hypotension, miosis, and loss of visual
Asymptomatic children should receive
The upper end of the therapeutic range is acuity. Urinary and faecal incontinence
activated charcoal. A period of 12 hours
2 µg/l. A blood level above 15 µg/l usually occur secondary to loss of sphincter con-
observation is advisable.1 Symptomatic
indicates severe toxicity. Levels between trol. In severe cases, overwhelming tra-
children require intensive monitoring.
these points should be interpreted with cheobronchial secretions can lead to res-
Hypotension may respond to intra-
caution, as they do not correlate accu- piratory compromise. In large doses,
venous fluids. In resistant cases, intra-
organophosphates produce muscle
venous glucagon (50–150 µg/kg in 5% rately with clinical severity.
stimulation followed by paralysis be-
dextrose) is the treatment of choice. cause of a depolarising block. Hypergly-
High dose glucagon stimulates myocar- ORAL HYPOGLYCAEMICS caemia and glycosuria without ketonu-
dial adenylate cyclase directly, bypassing Sulphonylurea type drugs produce hy- ria may also occur.
β receptors. Isoprenaline or cardiac pac- poglycaemia by depolarising pancreatic While organophosphates can be ab-
ing may be required. Regular estimation β cells and increasing insulin release. sorbed via the skin, symptoms rarely
of blood sugar is essential. Ingestion of a single tablet can produce result from acute exposure. Ingestion
symptomatic hypoglycaemia in children. carries the highest risk of acute toxicity.
DIGOXIN Activated charcoal should be adminis- Asymptomatic children should be ob-
Digoxin is potentially extremely toxic in tered. Asymptomatic children should be served overnight. Symptomatic children
overdose. Children with underlying car- observed overnight as effects can be require careful observation. Mild symp-
diac disease are particularly at risk and delayed for up to 16 hours.5 Symptomatic toms can be treated with supportive
should always receive treatment. Chil- children require intensive monitoring. therapy alone. Patients with cardiorespi-
dren without a history of heart disease Hypoglycaemia should be treated with ratory compromise require intensive
require treatment if they have ingested intravenous dextrose infusion. Resistant care. Atropine, often in very high dosage,
more than 100 µg/kg body weight. hypoglycaemia may respond to sub- acts as an antidote—blocking mus-
The toxic effects of digoxin include cutaneous injection of the somatostatin carinic receptors and preventing the
nausea, vomiting, hypotension, hyperka- analogue, octreotide, which inhibits pan- excessive activity of acetylcholine.
laemia, and a multitude of cardiac creatic insulin release.6 Patients not responding to treatment
arrhythmias.2 Careful monitoring is es- Metformin, a biguanide, acts by in- with atropine should be treated with
sential as patients can deteriorate sud- creasing glucose uptake into the pralidoxime. This drug reactivates inacti-
denly. muscles, inhibiting its gastrointestinal vated acetylcholinesterase. Pralidoxime

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408 LEADING ARTICLE

Table 1 Antidotes for cyanide poisoning

Order Antidote Dose Side effects Comments

1st line Amyl nitrite Crushable perles, vapour inhaled, Methaemoglobinaemia The mechanism of action of amyl nitrite is
either directly or via a bag and Vasodilatation unclear but may relate to its action as a
mask Headache vasodilator

1st line Sodium 412.5 mg/kg (1.65 ml/kg of Nausea Combines with CN to form thiocyanate;
thiosulphate 25% solution), maximum 50ml, Vomiting this is non-toxic and excreted in the urine
give over 10 minutes Muscle cramps
Arthralgia

2nd line Sodium nitrite 0.33 ml/kg of 3% solution, Potentially fatal See amyl nitrite. For moderate to severe
maximum 10 ml, over 4 minutes methaemoglobinaemia, avoid poisoning, do not use as prophylaxis
excessive dose, keep metHb at
about 20%

2nd line Dicobalt EDTA 4 mg/kg over 1 minute, followed In the absence of cyanide, cobalt Chelates cyanide and does not produce
by 50 ml 50% dextrose toxicity can be severe metHb. For moderate to severe poisoning,
Anaphylaxis do not use as prophylaxis

is most effective as an antidote when as high a concentration of inspired both natural, for example, wool and silk;
given within the first 24 hours post- oxygen as circumstances permit should and synthetic, for example, polyurethane
ingestion. be commenced immediately. High con- and polyacrylnitrile. Synthetic polymers
centrations of oxygen hasten the disso- are used extensively in domestic furnish-
CARBON MONOXIDE ciation of COHb. ings. Cyanide and carbon monoxide poi-
Carbon monoxide poisoning accounts The classical sign of “cherry red” lips soning frequently coexist. Symington et
for the largest group of poisoning deaths and nail beds is unusual. Signs of cardio- al found that 4% of those dying in house
among children.8 vascular or neurological toxicity should fires had potentially lethal cyanide
Carbon monoxide (CO) is most fre- be carefully sought. There are often asso- levels.9
quently encountered as a product of ciated injuries, such as burns or smoke Cyanide binds to ferric iron (Fe3+) in
incomplete combustion. The affinity of inhalation. the cytochrome a-a3 complex, inhibiting
haemoglobin for carbon monoxide is 210 Blood should be taken for acid-base its action and blocking the final step in
times its affinity for oxygen. Once bound balance, electrolytes, and muscle en- oxidative phosphorylation. Aerobic me-
to haemoglobin, carbon monoxide disso- zymes. Metabolic acidosis is common tabolism is halted and carbohydrate
ciates very slowly. In addition, the bind- and should not be over corrected, as a metabolism is diverted to the production
ing of a single CO molecule to haemo- mild metabolic acidosis will enhance of lactic acid.
globin increases the strength with which oxygen dissociation in the tissues. Cyanide poisoning requires a high
oxygen molecules are attached, making Wherever possible exposure should be index of suspicion; signs are very hard to
confirmed by direct, end tidal measure- dissect from those of CO poisoning. Car-
oxygen dissociation in the tissues harder.
ment of CO in expired air. Where this is dinal features are the presence of a
The amount of carboxyhaemoglobin
not possible, or practicable, spectropho- profound, refractory acidosis and a mas-
(COHb) formed depends on the concen-
tometric measurement of COHb, from a sively increased anion gap. There may be
tration in inspired air and the duration of
sample of arterial or venous blood, very little difference between venous and
exposure.
should be undertaken. The former test is arterial pO2, termed arteriolisation of
Carbon monoxide dissolved in the
preferable; blood COHb levels exclude
plasma acts as a direct cellular poison in venous blood, because of impaired cellu-
dissolved CO and can underestimate
its own right. Reacting with other haem lar respiration. Patients should be con-
exposure. Measurements of CO are best
proteins, such as mitochondrial cyto- sidered at high risk if they have been
made as soon as possible following
chromes, it disrupts cellular metabolism. exposed to fumes from burning plastics,
exposure; however, the half life of CO is
Patient with up to 20% of haemo- are profoundly unconscious, or have per-
five hours, in patients breathing air, and
globin affected complain of headaches sistent myocardial ischaemia in the
measurements may still be of value after
and nausea. At 20–40% involvement, absence of elevated COHb.
considerable delay.
patients tire and become confused. In- Patients with carbon monoxide poi- Rapid treatment is essential. Blood
volvement of more than 40% haemo- soning that are pregnant, that have any levels are useful in confirming toxicity,
globin results in ataxia, collapse, and neurological signs or symptoms includ- but therapeutic intervention is usually
coma. Cardiac arrhythmias, cerebral ing abnormalities of balance or gait, or necessary before the level is available.
oedema, and acidosis can occur. those with evidence of cardiovascular Patients should receive high concen-
The increased affinity of COHb for abnormalities including abnormal ECGs, trations of inspired oxygen. Mouth to
oxygen means that haemoglobin mol- or myocardial ischaemia/infarction, mouth resucitation must be avoided.
ecules become saturated at very low par- should be discussed with a hyperbaric Specific antidotes should be adminis-
tial pressures of oxygen. Oxygen satura- oxygen centre. Unconscious patients tered as soon as possible (see table 1).
tion monitors are therefore very should undergo early cranial imaging
unreliable in the presence of COHb— and may require aggressive management ISOPROPANOL
saturations of 100% occurring in the to control cerebral oedema. Isopropanol is an alcohol found in some
presence of significant hypoxia. Conven- nail polishes, hairsprays, antifreezes, and
tional blood gas analysers can also be CYANIDE car screen washes. It is also found in
misleading. Cyanide poisoning is most frequently rubbing alcohol, window cleaners, and
Patients considered at risk of carbon encountered following inhalation of tape and CD cleaners.
monoxide poisoning should be removed smoke containing the combustion prod- Isopropanol is absorbed rapidly from
from ongoing exposure. Treatment with ucts of nitrogen containing polymers— the stomach and mucus membranes. It

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LEADING ARTICLE 409

causes gastric irritation, central nervous ethanol therapy, the disadvantages of There is concern over the apparent
system depression, and hypotension which include CNS depression and severe idiosyncratic reactions to Ecstasy.
(which is often refractory). hypoglycaemia.12 Where fomepizole is These effects can occur following doses
Isopropanol is converted to acetone by not available, ethanol remains an alter- that have previously been well tolerated.
the action of alcohol dehydrogenase. native treatment (7.5 ml/kg 10% ethanol Reactions include coma, convulsions,
Acetone is excreted through the lungs in 5% dextrose over 30 minutes, then arrhythmias, malignant hyperthermia,
and kidneys. Ketoacidosis is uncommon 1.65 ml/kg/h of 5% ethanol to keep blood rhabdomyolysis, hypertension, and mul-
in isopropanol poisoning. level at 1–1.5 g/l). Fomepizole should be tiorgan failure.
Asymptomatic children should be en- given every 12 hours (10 mg/kg for four Asymptomatic children should receive
couraged to drink and observed for two doses, then 15 mg/kg) until the plasma activated charcoal if poisoning has oc-
hours. Activated charcoal does not de- ethylene glycol level falls below 200 mg/l. curred within one hour. Blood pressure,
crease absorption. Gastric lavage and Patients require regular measurements temperature, and ECG monitoring are
emesis are unlikely to be effective after of blood gases, renal function, and advisable. Blood levels can be performed
one hour. Both are contraindicated in the plasma calcium. Patients with renal fail- to confirm exposure. In the absence of
presence of central nervous system de- ure or resistant metabolic acidosis will symptoms patients can be discharged
pression. require haemodialysis.13 Fomepizole is after 24 hours observation, provided that
Symptomatic patients require inten- dialysed and the dosage interval should adequate parental supervision is avail-
sive support. Hypotension, secondary to be decreased on dialysis. able. Children with symptoms require a
peripheral vasodilatation, may require minimum of 48 hours observation. Ad-
treatment with intravenous fluids and verse effects, related to psychomotor
inotropes. Haemodialysis is indicated for METHANOL
stimulation or hallucination, require
patients not responding to supportive Methanol is also found in certain anti-
only supportive treatment. These effects
measures or those with a blood isopropa- freezes and windscreen washes. Metha-
usually last for 4–6 hours, but can occur
nol concentration of more than 4 g/l.10 nol is metabolised by alcohol dehydroge-
for up to 48 hours depending on the
Successful treatment of isopropanol poi- nase to formaldehyde, which in turn is
quantity of Ecstasy consumed.
soning has been reported using perito- converted to formate. Toxic effects in-
Patients with signs of cardiac or
neal dialysis.11 This technique does not clude severe abdominal pain, retinal tox-
central nervous system toxicity require
require specialist equipment but may icity, acidosis, convulsions, and coma.
admission to intensive care. Careful
prove ineffective in patients with poor Methanol poisoning can be managed
monitoring of haematological and bio-
peritoneal perfusion caused by refractory in a similar manner to ethylene glycol
chemical parameters is essential. Hyper-
hypotension. poisoning, both ethanol and fomepizole
thermia may respond to simple cooling
inhibiting its metabolism. There are,
ETHYLENE GLYCOL measures but, should these fail, patients
however, a few important differences.
Ethylene glycol is found in certain types should receive dantrolene 1 mg/kg intra-
Severe symptoms of methanol poisoning
of antifreeze, brake fluid, and wind- venously over 10–15 minutes. If there is
tend to occur after hours rather than
screen wash. Ethylene glycol is metabo- no response this dose may be repeated at
minutes. In the absence of symptoms,
lised by alcohol dehydrogenase to a vari- 15 minute intervals to a cumulative
hypocalcaemia, acidosis, or renal dys-
ety of toxic metabolites, including maximum of 10 mg/kg in 24 hours.
function, treatment can be withheld
glycolic and oxalic acid. Toxic effects Hypertension responds to labetalol. Con-
pending the plasma methanol and for-
include convulsions, coma, metabolic vulsions and agitation should be treated
mate concentrations. Methanol has a
acidosis, hypocalcaemia, and renal fail- with benzodiazepines. Chlorpromazine
considerably longer plasma half life than
ure. and haloperidol are best avoided as they
ethylene glycol (43 hours compared with
Ethylene glycol is rapidly absorbed may decrease seizure threshold. Vigorous
18 hours).12 For this reason elective
from the stomach; symptoms can occur fluid replacement is often necessary to
haemodialysis is often necessary, to
within 30 minutes of ingestion, and rehydrate patients, promote a diuresis to
enhance elimination and reduce the
attempts at gastric decontamination are clear myoglobin, and allow for increased
duration of therapy.
likely to be unproductive. insensible losses. However, care is neces-
Methylated spirit does not contain
Asymptomatic children should have sary as self induced water intoxication
sufficient methanol to cause toxicity.
blood taken for plasma ethylene glycol has been described in these patients.
Adverse effects are related to its ethanol
estimation. Blood gases, serum calcium, Fluid therapy should be guided by regu-
content alone.
electrolytes, and renal function should lar blood tests and invasive monitoring.
also be measured. Symptoms of severe
poisoning can occur rapidly and, even in ECSTASY LSD
their absence, treatment is indicated if Ecstasy, 3,4-methylenedioxymetham- Lysergic acid diethylamide (LSD), a 5-HT
ingestion is likely. Ethanol competes phetamine or MDMA, is an ampheta- agonist, is a potent hallucinogen. It is
with ethylene glycol binding at the cata- mine derivative. In common with am- rapidly absorbed and has a short dura-
lytic site of alcohol dehydrogenase. An phetamines, it produces locomotor tion of action. Symptomatic children
oral loading dose of ethanol (2 ml/kg of stimulation, euphoria, excitement, and should be reassured. Gastric decontami-
40% ethanol over 30 minutes; most spir- stereotyped behaviour. In addition, nation is not indicated. Sedation with
its match this criteria) will delay toxic Ecstasy has psychotomimetic effects, phenothiazines should be avoided as
effects until blood results are available. altering perception and mood. The they decrease the threshold for convul-
All children receiving this treatment will mechanism of action of Ecstasy is uncer- sions. In very rare instances, LSD can be
require admission for overnight blood tain but appears to relate to increased associated with malignant hyperther-
sugar estimation and observation. 5-hydroxytryptamine (5-HT) release mia.
Symptomatic children, or those with a accompanied by a decreased 5-HT up- LSD is poorly absorbed through the
plasma ethylene glycol level of more take by nerve terminals.7 skin; “LSD laced” transfer tattoos are an
than 200 mg/l (3.2 mmol/l), should Ecstasy is widely available as a drug of urban myth.
receive intravenous fomepizole (15 abuse. Ecstasy is not addictive as toler-
mg/kg over 30 minutes). Fomepizole is a ance develops rapidly to its positive COCAINE
competitive alcohol dehydrogenase an- effects, while negative effects are exacer- Cocaine is a psychomotor stimulant. It
tagonist. Its use replaces intravenous bated by large doses or frequent use. acts by inhibiting the uptake of

www.archdischild.com
410 LEADING ARTICLE

dopamine, noradrenaline, and 5-HT ISONIAZID Correspondence to: Dr K Berry, Accident and
from synapses. Cocaine is supplied as a Emergency Department, Birmingham Children’s
Isoniazid is widely used in the treatment Hospital, Steelhouse Lane, Birmingham
salt or, more recently, as a free base of tuberculosis. In overdose, isoniazid B4 6NH, UK;
(“crack”). Crack cocaine is favoured by reacts with pyridoxine to form a com- kathleen.berry@bhamchildrens.wmids.nhs.uk
addicts as it can be smoked, producing pound which is rapidly excreted in the
an effect equivalent to intravenous injec- REFERENCES
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