Approach to medication exposure (pediatrics): Clinical sciences

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.

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 blood pressure, 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 arrythmias, 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. 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.

Okay, let’s start by looking at patients with tachycardia.

Here, you can next assess for tinnitus and hyperpnea. 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 blood pressure. 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 tachypnea, 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 hyperpnea 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 at the muscarinic acetylcholine receptors.

They may experience the combination of mydriasis; 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 hare, dry as a bone, the bowel and bladder lose their tone, and the heart runs alone.”

Additionally, you can also distinguish anticholinergic toxidrome from other toxidromes because these patients will likely have normal reflexes.

Okay, if this toxidrome is present, consider tricyclic antidepressant, or TCA, ingestion.

patients may have a history that includes a known TCA ingestion.

In addition to the toxidrome 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 arrythmias can also occur. It can be helpful to think of TCA toxicity as the 3 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. 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.