Emergency department 11/10/17 Pediatric Ingestions Emergency department 11/10/17

Case 1: 18 month old girl brought the ER by ambulance after grandmother was unable to wake her up from a long nap. No concurrent illness On exam: Shallow breathing, moans and withdraws in response to pain, does not open her eyes. Rest of physical exam is normal. No fever. No evidence of trauma. Based on this initial assessment : what should you do next?

Initial plan of action : 1. Airway – compromised? 2. Cardiac leads, EKG stat 3. Glucose level 4. Labs: routine ? Grandmother states that the patient was found with her pill box earlier in the day. Grandmother does not have the box with her and does not recall the medications she is taking.

What next? Which medications could be fatal in a small dose ? - Opioids - sedatives - cardiac drugs - hypoglycemic agents Do you give activated charcoal or not?

CASE 2 3 year old is referred to ER by his pediatrician Child came to the parents holding his throat and saying he had swallowed something. Unsure what it was. Soon after, refused to eat. Afebrile with normal vital signs and no respiratory distress. Oropharynx and lung exam are clear What, if any, imaging is recommended? Is a surgical consult indicated Can he be safely discharged home?

Case 3 15 year old adolescent girl is brought to the ER for possible suicide attempt. Patient reports taking an entire bottle of ‘pain pills’ An old bottle of acetaminophen with hydrocodone is now empty. She took the medications 4 hours ago She is tearful and tired but rest of exam and vitals are within normal Are there any specific drug levels that should be checked ? Should u give naloxone or NAC? When can the patient be medically cleared for transfer to a psychiatric facility?

Medicines known for high risk of fatality Antiarrhythmics: block cardiac function Anti-malarials: chloroquine, hydroxychloroquine and quinine act as class 1A antiarrhythmics to block sodium channels and also cause Respiratory and CNS depression Anti-psychotics: Some possess sodium channel blockade properties and many can result in CNS depression and hypotension Betablockers: Bradycardia, hyperkalemia, hypotension, CNS depression Calcium channel blockers: Bradycardia, hypotension, hyperglycemia Camphor: GI symptoms, altered mental status, seizure

Medicines known for high risk of fatality Clonidine : alpha 2 receptor agonist: transient hypertension then bradycardia and hypotension, respiratory and CNS depression Opioids: Severe respiratory and CNS depression Methyl salicylate: Highly concentrated salicylates can cause respiratory alkalosis and metabolic acidosis Sulfonylureas : hypoglycemia Tricyclic antidepressants block sodium channels and also have anticholinergic properties

Pearls to remember: BK VIRUS : BETA blockers HYPERKALEMIA Calcium gluconate: Calcium channel blockers, hyperglycemia

TOXIDROMES TO REMEMBER Cholinergic Anticholinergic Bradycardia with hypotension Hyperglycemia Hypoglycemia Opioid Sedation Seizure Sympathomimetic Serotonin

Rapid recall : Peripheral nervous system :  Autonomic nervous system (regulates involuntary processes including digestion and breathing)  Somatic nervous system (transmits signals from the central nervous system and external stimuli to skeletal muscle and also mediates hearing, sight, and touch) Autonomic nervous system: Sympathetic and parasympathetic

Rapid review Cholinergic drugs produce the same effects as acetylcholine. Acetylcholine is the most common neurohormone of the parasympathetic nervous system, the part of the peripheral nervous system responsible for the every day work of the body. While the sympathetic nervous system acts during times of excitation, the parasympathetic system deals with everyday activities such as salivation, digestion, and muscle relaxation.

Cholinergic effects The effects of the cholinergic drugs are to produce the same effects as stimulation of the parasympathetic nervous system. These effects include slowing of the heartbeat, increases in normal secretions including the digestive acids of the stomach, saliva and tears.

Cholinergic toxidrome The possible adverse effects of cholinergic drugs are: slow heart beat, possibly leading to cardiac arrest. muscle weakness, muscle cramps, and muscle pain convulsions weak breathing, inability to breath increased stomach acid and saliva nausea and vomiting dizziness, drowsiness, and headache

Examples of cholinergic drugs/uses Not commonly used as a drug Organophosphates Carbamates Anticholinesterase inhibitors

Anticholinergic Toxidrome : opposite of cholinergic toxidrome ! Hyperpyrexia* Mydriasis Tachycardia Dry skin* Ileus Urinary retention Altered mental status

Anticholinergic drugs or toxins Antihistamines Carbamazepine Cyclobenzaprine Jimson weed Tricyclic antidepressants *Anticholinergic : MydriAsis*

Opioid toxidrome Miosis Hypothermia Hypotension Respiratory depression Ileus Causes: Natural opioids: morphine and derivatives synthetic opioids eg fentanyl Semisynthetic opioids eg hydromorphone, hydrocodone Methadone Buprenorphine

Bradycardia with hypotension Beta blockers Calcium channel blockers Clonidine Digoxin

Hyperglycemia Alpha agonists Beta agonists Calcium channel blockers Colchicine Methylxanthines

Sedation Anticonvulsants Antipsychotics Barbiturates Benzodiazepines Ethanol Opioids

Seizures Anticholinergic agents Buproprion Hypoglycemic agents Isoniazid Sympathomimetic drugs

Sympathomimetic toxidrome Hyperpyrexia Mydriasis Tachycardia Hypertension Diaphoresis Altered mental status Seizures Causes: amphetamines, cocaine, ephedrine, phenethylamines, Bath salts

Serotonin Syndrome Potentially life-threatening condition associated with increased serotonergic activity in the central nervous system (CNS). Therapeutic medication use Inadvertent interactions between drugs Intentional self-poisoning. Clinical findings often include mental status changes, autonomic hyperactivity, and neuromuscular abnormalities.

Serotonin Syndrome

Drugs implicated in Serotonin Syndrome SSRIs : Citalopram, escitalopram, fluoxetine, paroxetine, sertraline SNRIs: Desvenlafaxine, duloxetine, venlafaxine Buproprion St John’s Wort Metoclopramide Lithium

Serotonin Syndrome- Hunter criteria Clinical diagnosis Includes ingestion of a serotonergic drug and one of: - Spontaneous clonus - Inducible clonus and agitation or diaphoresis - Tremor and Hyperreflexia - Hypertonia - Temperature >38C and ocular clonus or inducible clonus

Serotonin Syndrome : clinical features Hyperthermia Agitation Slow, continuous, horizontal eye movements (referred to as ocular clonus) Dilated pupils Tremor Akathisia : restlessness Deep tendon hyperreflexia (common) Deep tendon hyperreflexia (common) Inducible or spontaneous muscle clonus (common) Muscle rigidity Bilateral Babinski signs Dry mucus membranes Flushed skin and diaphoresis Increased bowel sounds  

Serotonin Syndrome

Anticholinergic vs Serotonin Syndrome

Altered mental status or not Things to remember : Pupils Diaphoresis Altered mental status or not Temperature

Initial stabilization PALS algorithm: airway, breathing circulation History: allergies, medications, past medical history, events before presentation Focused history for ingestion: name, strength, formulation, quantity and time of ingestion Initial testing: blood glucose, EKG - blood gas: equivocal impact - pregnancy testing in adolescent females

Physical exam Vital signs including temperature Tachycardia: sympathomimetic/anticholinergic Bradycardia: beta blocker, calcium channel blocker, digoxin, clonidine Respiratory rate: increased in salicylates, decreased in narcotics or sedatives Skin: hot, dry or sweaty, petechiae, bruising Mouth : caustic substances Pupils Tremulousness: hypoglycemia, hypocalcemia, lithium ingestion Seizures: electrolyte derangement, buproprion, isoniazid, antihistamine, antiepileptic drugs.

Diagnostic studies: ANION GAP (Na – Cl – HCO3) ANION GAP with ill appearing child, suspected ingestion M : methanol, metformin U: Uremia D: diabetic ketoacidosis P: propylene glycol, paraldehyde I : Isoniazid, iron L: lactate E: ethylene glycol S: salicylate

Acetaminophen and salicylate levels Diagnostic studies EKG Acetaminophen and salicylate levels Radiographic studies Urine tox screens

Diagnostic studies Acetaminophen: 4 hours later or immediately on admission if time of ingestion unknown Salicylate: Generally symptomatic so usefulness is low. However symptoms can be masked If opioids also ingested Can have nonspecific symptoms so recommend testing if unsure of ingestion Ethanol levels: may be helpful in obtundation Iron levels: may help

EKG Screening for unknown ingestions Digoxin: first degree heart block, sagging ST segment, hyperkalemia Tachycardia Widened QRS interval: Anti arrythmics that block fast sodium channels Prolonged QTc interval: Anti arrythmics that block potassium efflux channels TCAs have both sodium and potassium blockage properties : tachycardia, QRS widening, QTc prolongation Low sensitivity, specificity and not clinically useful in studies done on pediatric ingestion

Radiographic studies Strongly radio opaque medications: ferrous sulfate, calcium carbonate, potassium chloride, foreign bodies with lead Useful most in distinguishing coins from button batteries: AP radiograph with double rim or step off on lateral film.

Ingested button battery with double rim

Urine toxicology screen Know what the hospital screen offers and limitations to screening

The End!