Approach to household substance exposure (pediatrics): Clinical sciences

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Introduction 0:00–0:41

Inhalation or ingestion of various household substances can cause serious morbidity and mortality in the pediatric population.
Increased mobility and frequent hand-to-mouth activity during the toddler and preschool years create the potential for unintentional or exploratory ingestions.
While exposure to some substances like lead cause vague, subacute, or chronic symptoms; ingestion or inhalation of caustic substances, carbon monoxide, organophosphates, or toxic alcohols can cause acute, life-threatening symptoms.
Now, if a pediatric patient presents with a chief concern suggesting a household substance exposure, you should first perform an ABCDE assessment to determine if the patient is unstable or stable.

Unstable Patient 0:41–2:15

If unstable, stabilize the airway, breathing, and circulation; and consider intubation if they demonstrate shallow, ineffective, or absent respirations.
Next, obtain IV access and administer IV fluids. Then, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry.
If needed, provide supplemental oxygen, obtain a point-of-care blood glucose level, and order a 12-lead ECG. Finally, if indicated, consider a surgical consultation or endoscopy.
Here’s your first clinical pearl! Depending on the substance and timing of ingestion, you can consider using a decontamination method to minimize absorption.
While ipecac syrup and gastric lavage are no longer recommended, activated charcoal can be effective if given within one hour of ingestion.
Keep in mind that charcoal does not bind well to liquids or charged molecules like iron; and you should avoid using it for caustic ingestions, since it can obscure visualization during endoscopy.
Always make sure your patient can protect their airway before you give activated charcoal, since it can induce vomiting!
Now that we have discussed unstable patients, let’s return to the ABCDE assessment and look at stable ones. First, obtain a focused history and physical examination.

Stable Patient 2:15–3:12

If your patient is preverbal, or if they present with altered mental status, caregivers or family members can provide details.
For unwitnessed exposures, ask about circumstances surrounding the event, such as the child’s location when they were discovered, and potential hazards in the home or surroundings.
History will reveal either a known or suspected exposure. The patient or their caregiver may report symptoms like headache, nausea, and vomiting; while the exam might reveal vital sign abnormalities, such as bradycardia or tachypnea, as well as altered mental status.
At this point, you should consider a household substance exposure and assess the onset of your patient’s symptoms. Let’s discuss patients with a subacute or chronic onset of vague symptoms.

Lead 3:12–4:22

Here, consider lead poisoning. While many patients are asymptomatic and identified by routine screening, some experience anorexia, abdominal pain, constipation, and developmental delay.
History may reveal risk factors for lead exposure; for example, your patient’s home might have been painted before 1978; or its pipes might have been installed before 1986.
Physical exam findings are often unremarkable, but because chronic lead poisoning can cause anemia, you might notice pallor.
At this point, you should order blood lead levels, and if they’re elevated, diagnose lead poisoning. Here’s a clinical pearl!
While the prevalence of lead exposure has decreased due to government regulations, lead-related morbidity remains a concern among certain populations; like pre-school children, those living in an urban setting, and those from a lower socioeconomic background; so remember to screen for lead exposure during well-child visits.
Alright, let’s switch gears and take a look at patients with acute symptom onset. Here, assess for signs of caustic substance ingestion.

Caustic Substance Ingestion 4:22–5:20

History may reveal a witnessed ingestion of a caustic agent, such as bleach or dishwasher detergent; or the patient may have been found near a spilled bottle of household cleaner.
Affected children frequently present with dysphagia or refusal to swallow; and, if the injury involves the airway, they might also have dyspnea.
The physical exam typically reveals drooling, and you may see oral mucosal burns. Some patients may also have audible stridor or a rash where the agent contacted the skin.
With these findings, consider caustic substance ingestion, and urgently order an endoscopy. If it demonstrates oropharyngeal or esophageal erythema and possibly ulcers, diagnose caustic substance ingestion.
Now, let’s discuss patients without signs of caustic substance ingestion. Here, assess for historical features suggesting carbon monoxide poisoning.

Carbon Monoxide 5:20–6:18

Affected patients typically present with headache, drowsiness, and nausea. However, when it comes to infants, they might act colicky, fussy, or have feeding difficulties.
Symptoms often occur during the winter months, when caregivers are more likely to use wood-burning stoves, kerosene heaters, an old furnace, or indoor fireplaces.
History often reveals multiple individuals in a shared living space with similar symptoms. Keep in mind that because younger children need more oxygen than adults, they might develop symptoms more quickly than adults, too.
If any of these features are present, consider carbon monoxide poisoning, and order a carboxyhemoglobin level. If it’s elevated, diagnose carbon monoxide poisoning.
On the flip side, if you identify no features suggesting carbon monoxide poisoning, assess for signs and symptoms of the cholinergic toxidrome.

Organophosphate 6:18–8:04

To do this, use the mnemonic DUMBBELS, which stands for the muscarinic effects of diarrhea, urinary frequency, miosis, bronchospasm and bronchorrhea, bradycardia, emesis, lacrimation, and salivation.
If any of these are present, consider organophosphate toxicity. History commonly reveals exposure to a known organophosphate, such as an insecticide.
For example, your patient might work on a farm or play in a field that is treated with pesticides. On exam, you may detect an odor of chemicals or garlic.
This clinical picture is highly suggestive of organophosphate toxicity. Here’s a high-yield fact!
Organophosphates are acetylcholinesterase inhibitors, so if you suspect exposure, consider administering atropine, an anticholinergic.
Resolution of symptoms supports the diagnosis of organophosphate toxicity. Let’s follow that up with a clinical pearl!
E-cigarettes and vaping devices contain highly concentrated liquid nicotine, which binds nicotinic acetylcholinesterase receptors and causes effects like muscular fasciculations or paralysis.
Although symptoms of nicotine exposure may mimic those seen in organophosphate exposure, nicotine poisoning does not respond to atropine.
It’s crucial to maintain vigilance around nicotine, since this substance can be fatal, even in very small amounts! Now, let’s look at patients without signs and symptoms of a cholinergic toxidrome.

Toxic Alcohols 8:04–9:45

Here, you can start an evaluation for toxic alcohol poisoning by obtaining labs, including venous blood gas, CMP, serum osmolality, serum ketones, and a urinalysis.
Next, assess the osmolal gap, which represents unmeasured, osmotically active molecules in the blood. Certain substances such as toxic alcohols create an elevated osmolal gap.
To determine the osmolal gap, you’ll need to calculate the serum osmolality. Do this by multiplying the serum sodium by two; then add the serum glucose divided by 18, plus the BUN divided by 2.8.
Then, take the measured serum osmolality from your lab results, and subtract the calculated osmolality to get the osmolal gap.
An elevated osmolal gap of 10 or more is a clue that you might be dealing with a toxic alcohol ingestion. To determine which substance your patient ingested, you’ll also need to look for an elevated anion gap metabolic acidosis.
Your patient has metabolic acidosis if the serum bicarbonate level is below the lower limit of normal. Once you identify metabolic acidosis, you’ll also need to determine the anion gap, which represents unmeasured anions in the blood.
To calculate it, take the serum sodium and subtract the sum of the serum chloride and bicarbonate. An anion gap above 12 milliequivalents per liter is elevated, which means that your patient has an excess of unmeasured anions in the blood.
Now, if your patient has an elevated osmolal gap without metabolic acidosis, consider isopropyl alcohol toxicity. Isopropyl alcohol is commonly found in antiseptics like rubbing alcohol and hand sanitizer, as well as some aftershaves and other cosmetic products.

Isopropyl Alcohol 9:45–10:43

Patients typically present after ingestion with headache, nausea, vomiting, and inebriation. Since both isopropyl alcohol and its metabolite acetone are powerful CNS depressants, the exam commonly reveals stupor.
You may also notice that the breath has a “fruity” odor, from the acetone. When it comes to labs, take a close look at serum and urinary ketones, and check the blood glucose level.
The presence of ketones without acidosis, and normal blood glucose levels, are highly suggestive of isopropyl alcohol toxicity.
Switching gears, let’s look at patients with an elevated anion gap metabolic acidosis. This finding should make you think of methanol or ethylene glycol toxicity.

Methanol and Ethylene Glycol 10:43–12:35

Let’s start with methanol toxicity. In this case, your patient might have ingested windshield washer fluid, an industrial solvent, or “moonshine”.
Patients typically present with nausea, vomiting, and drowsiness, followed by visual disturbances. Exam may reveal retinal edema with hyperemic optic discs.
These findings are highly suggestive of methanol toxicity. In this case, toxicity is mediated by methanol’s neurotoxic metabolites formaldehyde and formic acid, which can cause optic nerve damage and blindness.
Moving on to ethylene glycol toxicity. These patients often present after antifreeze ingestion with nausea, vomiting, and symptoms of inebriation.
Urinalysis may demonstrate calcium oxalate crystals, which are highly suggestive of ethylene glycol toxicity. In this case, ethylene glycol is metabolized to oxalic acid, which precipitates in the kidneys as calcium oxalate and causes variable degrees of renal failure.
Here’s your last clinical pearl! If your patient has an elevated anion gap metabolic acidosis, but you’re not sure what they ingested, you can order blood levels of methanol and ethylene glycol for confirmation.
Keep in mind that results may not be available immediately, so you'll usually need to rely on historical and exam findings to guide acute management.
Alright, as a quick recap… If a patient with suspected household substance exposure has a subacute or chronic onset of vague symptoms, consider lead poisoning.

Review 12:35–13:26

On the other hand, if the onset is acute with signs suggesting a caustic substance ingestion, obtain an endoscopy to confirm the diagnosis.
Otherwise, assess for symptoms of carbon monoxide poisoning, and if present, obtain carboxyhemoglobin levels for confirmation.
Signs and symptoms of a cholinergic toxidrome suggest organophosphate toxicity, while an elevated osmolal gap suggests exposure to a toxic alcohol.
Further assessment for an elevated anion gap metabolic acidosis can differentiate isopropyl alcohol toxicity from methanol or ethylene