Approach
Children may present in one of two ways. Some children are asymptomatic on presentation and present because they have claimed or are suspected to have taken an overdose or ingested a poison. Other children present with symptoms of acute poisoning. These may include non-specific findings such as altered mental status, seizures, or abnormal vital signs. There may be historical clues such as time to seek care, patterns of behaviour, and type of ingestion that may lead a practitioner to suspect intentional rather than unintentional poisoning.
An overdose or poison ingestion in a child is a clinical diagnosis supported by laboratory findings. In accidental ingestions, it is often possible to use targeted investigations if the identity of the ingested substance is known, or if the range of possible ingested substances is narrow. However, if the identity of the substance is not known, or the ingestion was deliberate, testing should be broad in order to identify all ingested substances. Toxicologists and laboratory experts have developed a list of recommended diagnostic tests that should be available to healthcare workers treating a poisoned child. These specific tests should be performed in all patients to identify the ingested toxins.[33]
Household or medication ingestion
The main aim of the history is to establish how and when the ingestion occurred and to establish, if possible, the identity of the ingested substance. Accidental ingestions tend to occur in children <6 years old who are exploring their environment, whereas deliberate ingestions tend to occur in older children and adolescents. Despite a general lack of evidence regarding the effectiveness of cough and cold medications, they remain in widespread use and intentional and unintentional poisonings are common. Fortunately, death in unintentional cough and cold medication poisoning in children is uncommon.[34] On the other hand, one study found that paediatric fatalities associated with cough and cold medicine, when they did occur, involved young children (<2 years old) and the administration by the carer was deliberate with non-therapeutic intent.[35]
Immobile children: in children who are immobile and not yet creeping, crawling, or walking, the ingestion is usually an accidental medication error by a carer. The carer is usually aware of the error.
Toddlers: medications that look like sweets or familiar objects may be ingested when the carer is distracted for a brief period. In this situation, the ingestion is often witnessed. Children may also ingest objects found in a family member's handbag, behind the couch, or in other places in the home. Older children can climb and find medications that are put up high, or accidentally ingest substances that have been placed in their non-original containers (e.g., chemicals in soft-drinks bottles). Medical help is usually sought immediately if the ingestion was witnessed, involved a chemical ingestant (that causes crying and typical physical clues), or the child was found with the bottle or a pill in their mouth. Otherwise, the child may not present until the carer notices a change in the child's behaviour or other symptoms.
Older children: ingestions tend to be deliberate, usually as a cry for help, and the child will tell a friend or supervisory adult. Girls are more likely than boys to consider self-harm.[11] The substance is usually easier to identify from the history and is most likely to be a medication that is either present in the house or can be easily purchased without a prescription. A readily available chemical in the garage, attic, or store may also be ingested. If the child does not tell anyone about their poison ingestion or overdose, he/she may not present until symptoms appear, which may be presumed to be due to other illnesses (e.g., paracetamol overdose presenting with nausea and vomiting).
It is important to obtain a full list of medications that are in the house, or have been in the house previously, as well as any other chemicals to which the child may have had access.
Poisoning can be associated with fabricated or induced illness. Intentional poisoning of this kind should be suspected when large quantities of a substance have been ingested, if the child is intoxicated, or if there is no history or a history of ingestion of small amounts of poison inconsistent with the clinical presentation. The most common agents of intentional poisoning include drugs prescribed for family members (e.g., anticonvulsants, antidepressants, salt, iron, laxatives, emetics, insulin, or recreational drugs). Frequent presentations with purported 'accidental' ingestion should raise the suspicion of child neglect due to poor supervision or lack of safety provision in the home.
Paediatric patients with all non-accidental ingestions, or any suspicion of cough or cold/antipyretic/analgesic accidental ingestion, should have a paracetamol and salicylate level check, as the child may be asymptomatic on initial presentation.
Toxic plant or mushroom ingestion
Plant or mushroom ingestions usually cause nausea, vomiting, and diarrhoea, but some plants may be deadly. Examples of deadly plants include the autumn crocus (colchicine), mayapple (podophyllotoxin), water and poison hemlock (cicutoxin and coniine), monkshood (aconitine), and foxglove (digitalis). Podophyllotoxin and colchicine present initially with nausea, vomiting, and diarrhoea, but may progress to bone marrow failure and changes in mental status with seizures, coma, and death. Cicutoxin is an excitatory neurotoxin that causes seizures, and coniine can cause respiratory failure. Aconitine and digitalis can cause lethal cardiac arrhythmias. There are several potentially lethal mushrooms that may resemble other non-toxic mushrooms. The onset of symptoms is delayed for some types of mushroom. If plant or mushroom ingestion is suspected, discussion with a specialist (e.g., a medical toxicologist) or a regional poison control centre can help with the identification of the plant or mushroom and subsequent management.
Substance misuse
Children ingesting medication to get 'high' are usually older and of the age where peer pressure is significant. Features of the history that prompt suspicion include:
A child who comes home late, has been partying, or is with friends that parents do not know or parents are uncomfortable with; there may have been a recent sudden change in friends
A recent deterioration in school work
Forgetfulness or secretive behaviour
Absent-minded behaviour on returning home, somnolence, or hallucinations
Talking about substances that are unknown to the parent or 'pharm parties', 'trail mix', or 'bowl parties'.
The major drug of misuse in this population is ethanol, but other substances may also be used. Medications that children use to attain an altered state include, but are not limited to, benzodiazepines such as alprazolam, opioids such as hydrocodone or oxycodone, amfetamine and methylphenidate, and over-the-counter cough and cold preparations such as dextromethorphan, diphenhydramine, and pseudoephedrine. There are several illicit substances such as marijuana or cannabinoid receptor antagonists ('spice'), metamfetamine and serotonergic amfetamines (MDMA, MDA, 2C-I, 25i-NBOMe), 'bath salts' (hallucinogenic amfetamine derivatives of methcathinone such as MDPV and methylone), and opioids that children may also abuse. They may also inhale halogenated hydrocarbons (e.g., Dust-off), or organic solvents through methods described as 'huffing', 'sniffing', or 'bagging'.
Assessment of symptoms and signs
A child who has ingested a medication or substance may be asymptomatic with a normal physical examination if they present early or if they ingested a small amount. Other children present with symptoms and signs of acute poisoning. Non-specific symptoms include nausea, vomiting, diarrhoea, fever, and rash. In more severe poisonings, patients present with altered mental status or seizures. Chemical ingestions (usually due to cleaning products) may leave physical clues such as staining of the oropharynx or clothing, odours, or burns of the mouth. Stridor may be present in severe cases. A toxic ingestion should always be considered in any child presenting with unexplained seizures or an acute change in mental status. Patients require a full examination, including a neurological examination, and measurement of vital signs to search for clues as to the underlying cause.
The combination of abnormal vital signs and physical findings is termed a toxic syndrome or toxidrome, each of which is characteristic of a particular poisoning. The most common toxidromes include:
Sympathomimetic: metabolic overdrive with hypertension, tachycardia, tachypnoea, hyperthermia, agitation, seizures, and mydriasis. The presence of this toxidrome suggests ingestion of alpha agonists, beta agonists, amfetamines/psychostimulants, tricyclic antidepressants, or monoamine oxidase inhibitors (MAOIs).
Antimuscarinic: hypertension (not as marked as sympathomimetic), tachycardia, hyperthermia, mydriasis, flushed red skin, urinary retention, absent bowel sounds, loss of sweating, agitation to sedation, and seizures. Suggests ingestion of an antimuscarinic agent such as diphenhydramine.
Opioid: miosis, bradypnoea and hypopnoea, absent bowel sounds, and coma. Bradycardia and hypotension may also be present. These symptoms suggest ingestion of any opioid. Examples include codeine, heroin, morphine, pethidine, tramadol, fentanyl, dextromethorphan, hydrocodone, oxycodone, buprenorphine, and methadone.
Sedative-hypnotic: coma or depressed mental status with relatively normal vital signs. Patient tends to be poikilothermic and becomes mildly hypothermic. These symptoms suggest ingestion of a benzodiazepine or barbiturate.
Cholinergic: features are predominantly due to muscarinic stimulation, with increased secretions (oral, bronchial, tears, vomiting, diarrhoea), bradycardia, hypotension, small pupils, and mental status changes. However, nicotinic stimulation may also occur, producing tachycardia, hypertension, respiratory depression and paralysis, muscle fasciculations, or seizures. Some children may not show many muscarinic findings but be floppy and limp with an altered mental status. These symptoms suggest anticholinesterase toxicity (e.g., organophosphate poisoning).
Toxidromes are useful if the poisoning is caused predominantly by a single agent. However, with multiple drug ingestion, a constellation of symptoms are present, which are more complex and difficult to diagnose, and symptoms must then be assessed individually. Key symptoms and signs that provide clues as to the diagnosis include:
Hypotension with bradycardia: suggests poisoning with beta-blockers, calcium-channel blockers, alpha-2 agonists, or digoxin. Calcium-channel blockers produce peripheral vasodilation and warm extremities, whereas beta-blockers produce peripheral vasoconstriction with cold extremities.
Hypertension with hyperthermia: suggests poisoning with sympathomimetics or antimuscarinics.
Hypoventilation: suggests poisoning with opioids or alpha-2 agonists.
Hyperventilation: suggests poisoning with salicylates, uncouplers of oxidative phosphorylation (e.g., cyanide or iron), or substances that cause a metabolic acidosis (e.g., salicylates, iron, or toxic alcohols). Changes in respiratory rate and depth that suggest salicylate intoxication are often subtle and easily missed.
Hyperreflexia and myoclonus: suggest serotonin syndrome. Causative agents include antidepressants (selective serotonin-reuptake inhibitors [SSRIs], venlafaxine, clomipramine, imipramine), opioids (pethidine, tramadol, fentanyl, dextromethorphan), MAOIs, amfetamines, lithium, and tryptophan.
Muscle rigidity: suggests poisoning with phenothiazines, atypical antipsychotics, antiemetics, or Parkinson's disease medications. Neuroleptic malignant syndrome may be seen in severe cases.
Nystagmus: suggests poisoning with dextromethorphan, ethanol, MAOIs, or SSRIs.
Ataxia: suggests poisoning with any sedative hypnotics, antipsychotics, or anticonvulsants.
Reduced vision or blindness: suggests poisoning with methanol, quinine, chloroquine, or hydroxychloroquine.
Reduced hearing or tinnitus: suggests poisoning with salicylates, loop diuretics, aminoglycosides, opioids, vancomycin, quinine, hydroxychloroquine, and chloroquine.
Reddened skin discoloration: suggests cyanide poisoning.
Seizures: may be caused by a range of drugs, including sympathomimetics, antimuscarinics, antidepressants, cholinergics (including cholinesterase inhibitors), propranolol, theophylline, or some opioids such as tramadol or pethidine.
Jaundice: a late sign of paracetamol toxicity. May also be present in obstructive jaundice due to therapeutic use of antibiotics or oral contraceptives.
Symptoms and signs of hypoglycaemia: these include nausea, confusion, tremor, sweating, palpitations, and hunger, and may indicate poisoning with sulfonylureas.
Initial investigations
Serum electrolytes
This may reveal a range of abnormalities. Hypokalaemia suggests ingestion of sympathomimetics or barium salts, and is frequently accompanied by hypomagnesaemia. Hyperkalaemia suggests ingestion of digoxin or fluoride-based cleaning products. Hyponatraemia suggests use of the amfetamine MDMA. Hypocalcaemia suggests fluoride toxicity or ethylene glycol.
Urea and creatinine
Acute kidney injury can occur either due to overdoses that are directly nephrotoxic or as a result of rhabdomyolysis from prolonged seizures, hypotension, or acidosis. Those assays that use the Jaffe reaction to determine creatinine can have a falsely elevated creatinine in the presence of ketones.
Fingerprick and serum glucose
Hypoglycaemia suggests poisoning with sulfonylureas or beta-blockers, or severe salicylate poisoning. Hyperglycaemia suggests calcium-channel blocker or theophylline poisoning.
Arterial blood gas (ABG)
May reveal a metabolic acidosis (seen in salicylate, toxic alcohol, or iron poisoning due to direct effects on metabolism, or in sympathomimetic or theophylline poisoning due to end-organ ischaemia), hypoxaemia from hypoventilation (seen in opioid or clonidine poisoning), or a respiratory alkalosis (seen in salicylate poisoning before the onset of metabolic acidosis).
Serum lactate
Elevated in metabolic acidosis produced by agents that interfere with aerobic metabolism or produce ischaemia.
Acetone or ketone levels
Ketone formation is seen with starvation and may be seen with an overnight fast, especially if glycogen stores are low. It is also seen in salicylate poisoning and chronic abuse of alcohol in children.
Serum creatine kinase
Elevated creatine kinase indicates rhabdomyolysis, which may be due to prolonged seizures, hypotension, or acidosis.
Urinalysis
Haem without red blood cells suggests rhabdomyolysis. Calcium oxalate crystals suggest ethylene glycol poisoning. Phenol produces a brownish coloration of the urine.
International normalised ratio (INR)
An increased INR suggests poisoning with warfarin, another coumarin rodenticide, or a hepatotoxin (e.g., paracetamol).
Liver function tests (LFTs)
These are primarily used to monitor the progression of hepatotoxicity. Abnormal LFTs indicate ingestion of a hepatotoxin, usually paracetamol. Results should be interpreted in the context of the INR. Improving LFTs in the face of a rising INR and rising total bilirubin suggest fulminant hepatic necrosis.
Pregnancy test
It is important to be aware of the presence of pregnancy when treating a toxic ingestion, as the treatment threshold for certain poisonings may be lower. Treatment of the mother is usually sufficient to treat the fetus and takes precedence in therapy.
ECG
Should be performed to detect signs of poisoning by a cardioactive substance. Characteristic findings suggest specific ingestions. Certain ST-T changes and rhythms are consistent with digoxin poisoning. An R-wave in aVR and an S wave in I and aVL are early signs of a sodium channel blockade, which progress to widening of the QRS complex. QT prolongation suggests potassium-channel blockers (antipsychotic, methadone and other opioids, arsenic), calcium-channel blockers, or changes in the electrolytes such as hypocalcaemia, hypokalaemia, and hypomagnesaemia. Bradycardia suggests alpha-2 agonists, calcium-channel blockers, beta-blockers, digoxin, or cholinergics.
Abdominal x-ray
May be helpful to diagnose ingestion of foreign bodies or radio-opaque medications (iron, heavy metals, some chlorinated hydrocarbons, enteric coated tablets, phenothiazines).
Chest x-ray
A chest x-ray may be needed for signs of aspiration or non-cardiogenic pulmonary oedema.
Specific diagnostic tests
Paracetamol levels
Should be performed in all patients 4 hours after the time of the suspected ingestion. The level of serum paracetamol relative to the time of ingestion will determine the need for subsequent treatment. The graph used to assess serum levels varies between countries, and physicians should consult the local paracetamol overdose protocols.
In the UK, a treatment graph that covers normal and high-risk patients is used, whereas in the US, the Rumack-Matthew nomogram is widely used, and a similar guideline is used in Australia and New Zealand.[36][37]
The diagnosis of paracetamol toxicity based on the paracetamol treatment graphs is reserved for single acute ingestions of paracetamol occurring within the past 24 hours. It cannot be used before 4 hours or after 24 hours.
The following cases should be discussed with a regional poison centre or a paediatric toxicologist: children with repeated supratherapeutic ingestion of paracetamol; repeated ingestion over time; co-ingestion with drugs that alter gastric motility, such as opioids or antimuscarinic medications; co-ingestion with ethanol; ingestion of sustained-release paracetamol products; ingestions occurring 24 hours or more before presentation; or cases in which the time of ingestion is unknown. Nomograms such as the Rumack-Matthew nomogram cannot be used in these circumstances.
Salicylate levels
Should be performed in all patients with an intentional overdose, due to the ubiquity and fatality of these ingestions. A positive result is seen in acute salicylate poisoning, but a negative result may be seen in sub-acute or chronic poisoning. For this reason, the diagnosis should be based both on clinical features and on laboratory findings, including the results of ABG analysis.
Urine drug screen
A urine drug screen should be performed in all children with a deliberate or suspected ingestion. However, the limitations of these tests need to be appreciated. A screen may cover ingested, injected, and inhaled drugs. A range of screening assays are available, which typically cover varying numbers of commonly misused substances, such as amfetamines, cocaine, phencyclidine (PCP), cannabinoids, and opioids. If a category is reported (e.g., opioids), it is important to inquire which specific substances (e.g., opium, codeine, heroin, morphine) are actually detected as some specific compounds may be excluded. Additional testing can be ordered if needed for any substances of interest that are not covered by a given urine drug screen.
The tests are usually immunoassays that screen for a group of substances within a class of medications, and therefore may identify false positives (e.g., the cough suppressant dextromethorphan can give a false positive on the PCP assay). Conversely, a negative result does not exclude the presence of the drug. It can mean that the particular screen used does not detect the drug, the drug has been metabolised to a form that the assay cannot detect, or the drug is present at a level below the limit of detection. The results should be interpreted in the context of clinical findings and may identify the need for a social services evaluation. A confirmatory test such as gas chromatography–mass spectrometry should be considered in cases that may result in legal action against either the parents or the patient.
Ethanol levels
Should be considered in older children suspected of substance misuse. Any detectable level of ethanol using serum alcohol levels is diagnostic. There are situations that may cause a false positive with a breathalyser.
Serum methanol or ethylene glycol levels
Should be measured if clinical symptoms suggest these poisonings or if there is an anion gap on the ABG that is not explained by lactate or ketones. Ethylene glycol levels should also be measured if calcium oxalate crystals are found on urine examination. Consider treatment with fomepizole or dialysis empirically if the lab work will take more than 4 hours or if the patient’s condition requires it.
Serum digoxin level
Should be considered if digoxin toxicity is suspected based on the clinical features, presence of hyperkalaemia, or ECG findings.
Serum anticonvulsant levels
Should be considered if toxicity due to phenobarbital, phenytoin, valproate, or carbamazepine is suspected.
Serum iron levels
Should be considered if iron toxicity is suspected.
Other tests
Specific tests for rarer ingestions may include serum lithium and theophylline, and whole blood heavy metal levels. Measurement of cholinesterase activity is considered useful but not essential. In addition, comprehensive urine drug testing may be considered as a confirmatory test. These tests are generally designed to test for several hundred medications using a sensitive and specific method, but they are time-consuming and results may not be immediately available. The results should be interpreted in the context of the clinical features. If specialised laboratory testing is considered, a medical toxicologist or poison control centre should be contacted for guidance.[Figure caption and citation for the preceding image starts]: Paracetamol treatment graph. This consists of a normal treatment line, which connects 1.32 mmol/L (200 mg/L) at 4 hours and 0.04 mmol/L (6.25 mg/L) at 24 hours, and a high-risk treatment line for those at increased risk of liver damage, which connects the points at 50% of the plasma paracetamol concentrations of the normal line. Patients should be treated if their plasma paracetamol concentration is above their appropriate treatment lineWith permission of Professor P.A. Routledge, Therapeutics and Toxicology Centre, Cardiff University [Citation ends].
Therapeutic trial of relevant antidote
In cases of severe poisoning with clinical features of a particular ingestant, a therapeutic trial of the relevant antidote can be used to establish the diagnosis. This should be done in consultation with an expert experienced in the management of poisoning in children or a poison control centre.
Naloxone: this should be given if features of the opioid toxidrome are present and there is evidence of respiratory depression; a positive response may be diagnostic of opioid ingestion, but may sometimes be seen in clonidine ingestion. Do not give if the patient is intubated.
Sodium bicarbonate: this should be given if the QRS interval on ECG is prolonged in combination with clinical features of sodium-channel blocker poisoning. A narrowing of the QRS is diagnostic of sodium-channel blocker toxicity. It can also be considered if there are symptoms of salicylate poisoning, which should improve. Expert consultation for these patients is recommended.
Atropine and pralidoxime: should be given if there are features of the cholinergic toxidrome in consultation with an expert experienced in the management of poisoning in children. Improvement in symptoms suggests cholinesterase inhibitor poisoning.
Flumazenil: may be considered if there are clinical features of the sedative-hypnotic toxidrome in patients who are not chronically taking benzodiazepines and withdrawal is not a concern. This should be given in consultation with an expert experienced in the management of poisoning in children. Improvement in symptoms suggests benzodiazepine poisoning.
Octreotide: this may be considered if there is hypoglycaemia suspected to be due to sulfonylurea toxicity or massive insulin injection. This should be given in consultation with an expert experienced in the management of poisoning in children. A positive response is highly suggestive of either sulfonylurea ingestion or massive insulin injection.
Physostigmine: may be considered when there is evidence of peripheral and central antimuscarinic features in appropriate patients. Expert consultation before using physostigmine for these patients is recommended as its use in some poisonings (e.g., tricyclic antidepressants) may be contraindicated.
Online diagnostic information
A number of online resources are available that provide information on the diagnosis of a wide range of known poisonings:
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