Approach to medication exposure (pediatrics): Clinical sciences

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Introduction 0:00–0:34

Medication exposure includes the ingestion, inhalation, or topical absorption of prescription or over the counter medications.
Many medications pose a serious risk to the pediatric population, either through unintentional exposure, often among infants and children, or intentional ingestion seen in adolescents.
Using clinical manifestations, medication exposures can be roughly categorized into those that cause tachycardia and those that cause bradycardia.
Now, if a pediatric patient presents with a chief concern suggesting medication exposure, you should first perform an ABCDE assessment to determine if the patient is stable or unstable.

Unstable Patient 0:34–2:31

If unstable, stabilize the airway, breathing, and circulation. You may need to consider intubation if the patient is apneic or has shallow, ineffective respirations.
This is especially important in children with altered mental status. Next, obtain IV access and give IV fluids.
Don't forget to put your patient on continuous vital sign monitoring, including BP, heart rate, and pulse oximetry. If needed, provide supplemental oxygen, measure glucose, and obtain an ECG.
You should also consider administering naloxone if there is any concern for opioid ingestion. Time for some clinical pearls.
At this point, you might find clues to the causative medication. For example, ECG might reveal a widened QRS complex, or even life-threatening arrhythmias, which points to tricyclic antidepressant toxicity.
Alternatively, you might find a prolonged corrected QT interval, in which case, you should think of selective serotonin reuptake inhibitor, or SSRI toxicity.
Now, 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, let's go back to the ABCDE assessment and look at the stable patients. Start with a focused history and physical examination.

Stable Patient 2:31–3:21

Since obtaining a history directly from these patients might be difficult due to age or the effects of the medication on the patient's mental status, consider involving a caregiver or friend.
History may include a witnessed ingestion, or the patient may have been found with a medication bottle. Meanwhile, the physical exam may reveal an altered mental status.
At this point, you should consider medication exposure. And obtain a urine drug screen, APAP, or acetaminophen concentration, and salicylate concentration.
Additionally, order a VBG, CMP, and ECG. Next, assess the patient's cardiovascular status.
OK, let's start by looking at patients with tachycardia. Here, you can next assess for tinnitus and hyperpnia.

Tachycardia/Salicylate 3:21–4:59

If present, consider salicylate exposure. History may include a known aspirin or salicylate ingestion and vomiting.
Physical examination will be notable for increased respiratory rate and depth of breathing, and low BP. At higher doses, you might find altered mental status and seizures.
Lab findings will typically reveal evidence of a respiratory alkalosis on VBG including an elevated pH and decreased PCO2.
However, keep in mind that salicylate toxicity can cause both respiratory alkalosis and metabolic acidosis, which might cancel each other out.
So the pH ends up being normal. Additionally, if labs reveal an elevated salicylate concentration, you can diagnose salicylate ingestion.
Here's a clinical pearl. Salicylate toxicity initially causes rapid, shallow breathing in the form of tachypnia, which results in respiratory alkalosis.
As the salicylate metabolizes into lactate and the lactate levels rise, metabolic acidosis develops. To compensate, the patient will hyperventilate with rapid deep breaths.
If no intervention occurs, the patient may progress into respiratory failure, and the high anion gap metabolic acidosis will become the primary metabolic disorder.
Now, when hyperpnia and tinnitus are absent, you can assess for a toxidrome. First, let's look at a patient with an anticholinergic toxidrome, which occurs when a medication exposure blocks activity in the muscarinic acetylcholine receptors.

Toxidromes/TCA 4:59–6:41

They may experience the combination of madriasis, altered mental status, erythematous, hot and dry skin, decreased bowel sounds and constipation, urinary retention, and tachycardia.
You can remember all these signs and symptoms using the saying, blind as a bat, mad as a hatter, red as a beet, hot as a hair, dry as a bone, the bowel and the bladder lose their tone and the heart runs alone.
Additionally, you can also distinguish anticholinergic toxidrome from other toxodromes, because these patients will likely have normal reflexes.
OK, if this toxodrome is present, consider tricyclic antidepressant or TCA ingestion. Patients may have a history that includes a known TCA ingestion.
In addition to the toxodrome findings, physical examination may reveal signs of CNS depression, like slurred speech, somnolence, or confusion, as well as seizures.
Additionally, ECG often reveals a widened QRS complex. Don't forget that life-threatening arrhythmias can also occur.
It can be helpful to think of TCA toxicity as the three C's, which are coma, convulsions, and cardiotoxicity. At this point, obtain a serum TCA level.
If it's elevated, diagnose TCA ingestion. Let's move on to patients with serotonin syndrome toxidrome.

SSRI 6:41–8:22

These patients will experience diaphoresis, increased bowel sounds, and diarrhea, and hyperreflexia. At this point, you should consider selective serotonin reuptake inhibitor or SSRI toxicity.
The history may include a known SSRI ingestion, like with an intentional overdose in an adolescent. Physical examination may reveal additional serotonin syndrome findings, like autonomic instability, fever, sedation, though the patient may be agitated or restless early in the course of illness, or in a less severe case, tremors, muscle rigidity, and clonus.
The ECG will likely reveal a prolonged corrected QT interval. These findings are consistent with SSRI toxicity.
Time for a clinical pearl. Any medication that increases serotonin levels can lead to serotonin syndrome.
Other common classes of medications include serotonin and norepinephrine reuptake inhibitors, or SNRIs for short, and monoamine oxidase inhibitors, or MAOIs.
While serotonin syndrome can potentially occur with taking a single medication, the combination of any two increases the risk.
Keep in mind that the finding of QT prolongation is not part of serotonin syndrome, but rather, a separate finding that can be seen with both SSRI's and SNRI's, but typically, not with MAOI's.
All right, let's back up and look at patients who have bradycardia. In the case of bradycardia, assess for respiratory depression, including shallow or slowed breathing.

Bradycardia 8:22–9:01

If present, consider opioid or clonidine exposure. Opioids act on the mu receptor, while clonidine is an alpha-two adrenergic receptor agonist.
These receptors share some similar functions, creating comparable signs and symptoms. To distinguish between opioid and clonidine exposures, assess for hypothermia, or an initial presentation of hypertension, followed by hypotension.
If present, consider clonidine exposure. The patient's history may reveal a known clonidine ingestion, while the physical exam could include signs of CNS depression and meiosis.

Clonidine 9:01–9:16

With these findings, diagnose clonidine ingestion. On the flip side, if hypothermia and initial hypertension are absent, consider opioid exposure.

Opioid 9:16–9:37

History may include a known opioid exposure, while physical exam can reveal signs of CNS depression and meiosis. If the urine drug screen is positive for opioids, diagnose opioid ingestion.
Now, if respiratory depression is absent, assess for abdominal pain. If present, consider iron and acetaminophen exposures.

Iron 9:37–11:15

Starting with iron, patients might report a known ingestion of iron, and initially experience vomiting and diarrhea, which can be bloody.
As the patient enters the 2nd stage of the clinical course, these symptoms may resolve before returning during stage 3. At this time, physical exam may reveal hypotension, and labs typically reveal a high anion gap metabolic acidosis.
In the fourth stage, labs will include an elevated AST and ALT. Keep in mind that there are 5 total stages to iron toxicity, and patients may move through these stages rapidly, or even skip stages.
With these findings, consider iron ingestion and obtain a serum iron concentration. If elevated, you have confirmed the diagnosis.
Here's a clinical pearl. If an abdominal X-ray was obtained during the workup, iron tablets may be seen on the radiograph, though not all formulations are radio opaque.
Let's follow that up with a high yield fact. An easy way to recall the causes of a high anion gap metabolic acidosis is to use the mnemonic mud piles, which stands for methanol, uremia, diabetic ketoacidosis, peraldehyde, and propylene glycol, iron and isoniazid, lactic acid, ethylene glycol, and salicylate.
Next up is acetaminophen exposure. History might include a possible known ingestion of acetaminophen, as well as malaise, nausea, and vomiting.

Acetaminophen 11:15–12:11

Keep in mind that nausea and vomiting without abdominal pain may be the primary symptoms. Physical examination might include pallor and right upper quadrant tenderness on palpation, as well as tachycardia and altered mental status.
CMP might reveal elevated AST and ALT. If the APAP concentration is elevated, diagnose acetaminophen ingestion.
Here's another high yield fact, timing of the APAPP concentration is important. The Rumak Matthew nommogram helps predict the potential for hepatotoxicity.
To use this nommogram, obtain a level 4 hours after the ingestion, or as soon as possible after 4 hours. Lastly, if abdominal pain is absent, you should assess the patient's glucose level.

Beta Blocker 12:11–12:35

First, let's look at patients with hypoglycemia. Here, the history may include a known beta-blocker ingestion, while the physical exam might demonstrate hypotension and altered mental status.
The ECG might show an AV block. These findings are consistent with beta-blocker ingestion.
Now, when it comes to hyperglycemia, history may include a known ingestion of a calcium channel blocker. The physical exam might be significant for hypotension, and the ECG could reveal an AV block.

Calcium Channel Blockers 12:35–12:54

In this case, diagnose calcium channel blocker ingestion. All right.
It's a quick recap. When a pediatric patient presents with the chief concern suggesting a medication exposure, obtain a focused history and physical exam, as well as a urine drug screen, APAP and salicylate concentration, VBG, CMP and ECG.

Review 12:54–13:45

If a patient with tachycardia has tinnitus or hyperpnia, consider salicylate ingestion. Otherwise, assess tachycardic patients for toxodrome and consider TCA and SSRI ingestions.
Patients with bradycardia and respiratory depression should make you think of either clonidine or opioid exposure, while bradycardia with abdominal pain points toward iron or acetaminophen ingestion.
Finally, for other patients with bradycardia, assess glucose level to differentiate between beta-blocker and calcium channel blocker exposure.