Peds Case 24- 2Y/o W Ams

Front 1

two-year-old with acute onset altered mental status

Back 1

(AEIOU) plus TIPS” causes of altered mental status:

Alcohol, ingested toxins
Epilepsy, encephalitis, endocrine, electrolytes
Infection, insulin
Overdose, opiates, oxygen deprived
Uremia (renal failure)
Trauma, temperature
Insulin, infection
Psychosis
Stroke, shock, space occupying lesions

Front 2

likely from the ddx

Back 2

temperature is only mildly elevated, but tachycardia and hypotension raise concern for infection
Acute onset of altered mental status in a previously healthy child raises suspicion for ingestion, despite parental report
non-accidental trauma

Front 3

unlikely from the ddx

Back 3

not
history of alternating agitation and unresponsiveness is atypical for seizure.
A metabolic disorder would most likely have previous episodes or history of recent illness preceding this episode of altered mental status.
An intracranial mass would most likely present as gradual onset of signs and symptoms

Front 4

possible medication ingestions

Back 4

hypoglycemia at presentation and her great aunt’s history of diabetes strongly suggest an ingestion of an anti-hyperglycemic agent. The great-aunt probably takes a medication like a beta blocker for her hypertension. Older adults can suffer from chronic pain and, in addition to acetaminophen and ibuprofen she could have opioids like codeine in the home. Many adults are treated with antidepressants after the death of a spouse. She could have also been prescribed a sedative-hypnotic medication. She may also be taking antihistamines or decongestants for her allergies.

Front 5

Cholinergic: (organophosphates)

Back 5

Miosis and blurred vision
Increased gastric motility (nausea, vomiting, diarrhea)
Excessive tearing, salivation, sweating and urination
Bronchorrhea and bronchospasm
Muscle twitching and weakness
Bradycardia
Seizures and coma

"SLUDGE": Salivation, Lacrimation, Urination, Defecation, GI mobility, Emesis.

Front 6

Anticholinergic: (diphenhydramine, tricyclic antidepressants)

Back 6

Mydriasis (dilated pupils) "blind as a bat"
Dry skin "dry as a bone"
Red skin (flushed) "red as a beet"
Fever "hot as Hades"
Delirium and seizures "mad as a hatter"
Tachycardia, Urinary Retention, Ileus

Front 7

Sedative-Hypnotic:(benzodiazepines, barbiturates)

Back 7

Blurred vision (miosis or mydriasis)
Hypotension
Apnea and bradycardia
Hypothermia
Sedation, confusion, delirium, coma

Front 8

Opioids: (codeine, morphine, heroin)

Back 8

Miosis (constricted pupils)
Respiratory depression
Bradycardia and hypotension
Hypothermia
Depressed mental status (sedation, confusion, coma)

Front 9

Sympathomimetics: (cocaine, amphetamines, pseudoephedrine)

Back 9

Mydriasis
Fever and diaphoresis
Tachycardia
Agitation and seizures

Front 10

dialated pupils?

Back 10

anticholinergic or sympathomimetics may cause mydriasis, Diphenhydramine is an anticholinergic and pseudoephedrine is a sympathomimetic.

Miosis or constricted pupils= cholinergics and opiods, in this case codeine.

Lorazepam, a benzodiazepine, may cause nystagmus,

Acetaminophen and Aspirin do not cause ocular findings.

Front 11

Ingestions table

Back 11

Front 12

mydriasis, tachycardia, agitation, hypotension and sedation

Back 12

Tricyclic antidepressant
Selective serotonin reuptake inhibitor (SSRI)
Antihistamine
Decongestant
oral hypoglycemic

Front 13

iron presents with

Back 13

severe abdominal symptoms followed by signs of shock.

Front 14

An ingestion of a beta-blocker to treat hypertension causes

Back 14

bradycardia.

Front 15

An ingestion of acetaminophen

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initially presents with minimal symptoms (though gastrointestinal symptoms are not uncommon) followed by symptoms of liver toxicity.

Front 16

An ingestion of aspirin

Back 16

does present with agitation and tachycardia but there is no mydriasis.

Front 17

An ingestion of an opioid or sedative-hypnotic causes

Back 17

sedation and constricted pupils.

Front 18

Tricyclic ingestion

Back 18

Agitation, cardiac manifestations (especially hypotension), dilated pupils and dry, hot skin are classic findings in TCA ingestions

SSRI antidepressants are more commonly prescribed than tricyclic antidepressants, but there is data that older adults tolerate TCAs better and they are more effective for severe depression.

Front 19

SSRI OD

Back 19

SSRI antidepressant requires a significant overdose to cause toxicity. These overdoses cause a serotonin syndrome. The serotonin syndrome presents with

profuse sweaty skin, agitation, fever, mental status changes, diarrhea, myoclonus, hyperreflexia, ataxia and shivering.

Front 20

overdose of a decongestant results in a

Back 20

sympathomimetic toxidrome. This presents with tachycardia and hypertension, as well as agitation, sweating, fever, mydriasis and seizures.

Front 21

Antihistamine ingestions present with

Back 21

anticholinergic effects, much like those in TCA ingestions. TCA ingestions have additional mechanisms that cause unique cardiac manifestations.

Front 22

TCA ingestion mechanism

Back 22

inhibit synaptic reuptake of norepinephrine and serotonin (altered mental status),
antagonize muscarinic acetyl choline receptors (anticholinergic effects),
peripheral alpha receptors (hypotension),
result in sodium channel blockade (dysrhythmias)
block GABA receptors (seizures)

Clinically patients present with an altered mental status, anticholinergic signs and symptoms, hypotension (a hallmark of TCA toxicity), dysthythmias and seizures.

Hypotension stems from direct myocardial depression from sodium channel blockade, and especially peripheral vasodilatation from alpha-1 adrenergic blockade. Refractory hypotension is the most common cause of death from TCA overdose.

Front 23

labs to order for toxicity

Back 23

Continued monitoring serum glucose
Octreotide, a somatostatin analog inhibits insulin release and may be indicated as an antidote in dextrose refractory sulfonylurea overdose.

CBC evidence against infection.

Electrolytes and a blood gas can be used to identify metabolic acidosis/anion gap – characteristic of aspirin/NSAID toxicity.

EKG since tachycardic and tricyclic anti-depressant ingestions can cause serious dysrhythmias. Abnormal levels of Calcium can also affect her heart.

A toxicology screen from the urine or blood should be done to confirm, results not immediately available, but obtain the sample early.

An acetaminophen level should be ordered since acetaminophen toxicity initially presents with minimal symptoms. It is the most common accidental ingestion

LFTs and a urine analysis are of low yield in this case.

Infection is low on the differential; there is no indication for a blood culture or lumbar puncture at this time.

A CT scan of the head is mandatory for a child with altered mental status and agitation, but there is no historical nor clinical evidence for an intracranial mass lesion or increased intracranial pressure. Some physicians would order a head CT but it would have a very low yield. The same can be said for a chest x-ray. Madelyn has no localizing signs on her chest exam.

Front 24

enhance toxin elimination

Back 24

syrup of ipecac, activated charcoal, gastric lavage, cathartics, hemodialysis and hemoperfusion.

Specific agents may have additional methods such as urinary alkalinization for salicylate intoxication.

Front 25

activated charcoal

Back 25

ndicated for ingestions not due to small molecules or heavy metals. It is contraindicated in a patient with a loss of protective airway reflexes due to the risk of aspiration. Elective intubation should be considered for Madelyn. Additional doses of activated charcoal may be indicated due to decreased gastrointestinal motility as a result of the anticholinergic effects of tricyclics. A single dose of a cathartic agent may be given with the initial dose of charcoal.

Front 26

Gastric lavage

Back 26

has not demonstrated consistent clinical benefit.
One adult study demonstrated improved clinical outcomes within one hour of a tricyclic ingestion. It would be technically difficult to a pass a large enough tube in a two-year-old child.

Front 27

Hemodialysis and hemoperfusion

Back 27

not indicated due to the high level of protein binding of tricyclics.

Front 28

Syrup of ipecac

Back 28

contraindicated in our patient due to a risk of aspiration with an altered mental status and potential for serious cardiac side effects and seizures. The AAP recommends that syrup of ipecac not be used as first line therapy for ingestions due to potential side effects.

Front 29

cardiac tox of TCA ingestion

Back 29

Cardiotoxicity primarily responsible for most morbidity and mortality in TCA overdose.
The wide-ranging effects on neurotransmitters and myocardial cells, including the cardiac conduction system, account for the triad of conduction delays, dysrhythmias, and hypotension.
results from TCA effects on the myocardial action potential, direct effects on peripheral vascular tone, and effects mediated by the autonomic nervous system.

Sodium channel blockade affects the His-Purkinje conduction system as well as myocardial cells

= increased PR interval, QRS widening, and QT interval prolongation (the last can predispose to torsades de pointes, although uncommon).
Sinus tachycardia from peripheral muscarinic antagonism and the inhibition of norepinephrine reuptake
wide-complex tachycardia is the characteristic life-threatening dysrhythmias seen with severe TCA toxicity.
In addition to the effects on neurotransmitters and sodium channel blockade, hypoxia, tissue ischemia, and metabolic acidosis may predispose the heart to ventricular tachycardia.
The wide-complex tachycardia seen with TCA toxicity, however, is often not ventricular tachycardia, but sinus tachycardia with a wide QRS / aberrant conduction.
slow, wide-QRS idioventricular rhythm is usually pre-terminal.

QRS duration of >100 msec is associated with an increased risk of serious toxicity, including seizures, coma, hypotension, and dysrhythmias. The terminal 40 msec of the QRS has been touted as an important measurement for risk stratification, but this is not easy to measure. Qualitatively, it is manifested as a negative deflection (terminal S wave) in I and aVL, and a positive deflection (terminal R wave) in aVR. NB: This is not the same as the QRS axis.

(triad = conduction delays, dysrhythmias, and hypotension)

Front 30

management TCA ingestion

Back 30

Continuous cardiac monitoring and serial EKG’s
Most develop major clinical toxicity within several hours of presentation

tx for cardiotoxicity (triad = conduction delays, dysrhythmias, and hypotension)= serum alkalization and sodium loading
indicated for: QRS > 100msec, Rwave in AVR > 3mm, wide complex tachycardias, fluid refractory hypotension and seizures.

serum pH affects protein binding of TCA’s, and metabolic acidosis can depress cardiac function. Hypertonic sodium bicarbonate is given as a 1 mEq/kg bolus initially and every three to five minutes until the QRS narrows and hypotension improves.
target serum pH is 7.50-7.55, and close monitoring of blood gases
Serum alkalization is continued for 12-24 hours after the EKG normalizes, because of the drug’s redistribution from the tissues.

For life-threatening dysrhythmias, lidocaine can be administered.
Class IA antiarrhythmic drugs, which are sodium channel blockers, are contraindicated
Class III antiarrhythmic drugs (which can prolong the QT interval) may also be contraindicated.

For hypotension, beta-adrenergic agonists and dopamine are contraindicated.
Volume expansion, and serum alkalization and sodium loading are the mainstays of therapy, while norepinephrine may be used in refractory situations (0.1-0.2 mcg/kg/min).

Seizures are generally brief. In addition to alkalinization, benzodiazepines, barbiturates or propofol may be used

Phenytoin use is controversial and is usually not indicated due to its potential for cardiac toxicity.