26.

Approach toPoiGonine ina Child

Razztesh P. Menon

Abstract
Accidental poisoning is a process of uniMentional seF-injury by hvmans.
Infants and toddlers in their devebpmerital slage of exploration and curiosity
are prone to ingesting {usually) poiGOnOUG 8nd non-poisonous (more
common) agents of injury. Optimal management depends on thespecifm
agent involved, severity ot exposure arid tie time ebpsed beMeen expoeue
and presentation. In young intanta, besides history and examination,
toxidromes (symptom constellation) indicate probable agent(s), severity of
exposure and first aid eteps to be adopted. Decontamination of th body (e.g.,
aclivated cfarooel, whole bowel irñgatiou) and specific anidotes (in hospital),
where indialed remain the benchmark of managing this potentially fall
health hazard of childhood curiosity.

Keywords Childhood poisoning; C/iriicaf General principles and evidence

ofinitial care,' La6araf Radiology ofped/afr/c taricology

Poisoning in children Isa global problem. Most ofincidence are accidental

in nature. Occasionally it may be intentional. Infants and toddlers
(especially boys) up to3 years of age are moet curious about their
environment, whereas, older children and pubescent children are most
adventurous and experimenling. These additional behavioral risk factors
make acufe poisoning a very common differential diagnosis of children
wbo present with acute onset of multiorgan system dysfunction with or
withouta history of toxin inhalation/ingestion. Clinical suspicion is aroused
when puzzling complex ofsigns and symptoms" occur in "at-risk° age
group(s). Forced ingestion or intentional poisoning is unusual in chilrlren
and comprises forms ofchild abuse (e.g., water and salr intoxication).'
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 Pediatric Intensive Care Protocols of AIIMS

Initial Evaluation and Stabilization

Pediatric considerations ofacute poisoning includea higher body surface
area to mass ratio, greater susceptibility for dehydration and insensidle
losses. Increased minute ventilation ensuresa higher dose forairborne
toxins by inhalation in toddlers. Higher risk of respiratory fatigue and failure
due to mechanical reasons and physiological sensitivity to hypoxia,
metabolic !oxins, witha lower reser\’e cardiovasctilar, as id-base,
glyagen stores) distinguish children from adults. The majority of pediatric
toxic ingestions are benign; however, 2% result in moderate to severe
damage.'
Airway protection {e.g., endotracheal tube (ET) intubation] should be
anticipated in all children with acute poisoning. Higher adrenergic tone
may result in tachycardia as the lone vital sign abnormality for cardiac
output maintenance. Calcium channel blocker (CCBs)/organophosphate
(OP) pesticides may precipitate circulatory arrest in very small doses.
Hypotension is to be managed with fluids initially. Vasoactive drugs, most
commonIydopamineandepnephñneornorepnephrne,areusedvvhen
hypotension remains fluid unresponsive. Norepinephrine or glucagon is
preferred in hypotension due to beta-blocker or tricyclic antidepressants
(TCA). Developmental pharmacodynamics results in enhanced central
nervous system (GNS) dep ression with clo nidine, codeine ,
dextrometh orphan cough syrups; paradoxical reactions to
benzodiazepines and QTc prolongation with sotalol, etc. Neonates require
other considerations, e.g., carboxyhemoglobin (COHb) concentrations are
higher at 2—5% because carbon monoxide (CO) isa by-product of
protoporphyrin metabolism.' Neonates are also more susceptible to OP
poisoning since their baseline red cell cholinesterase is 50—70% lower.
A quick assessment of mentation, vital signs, and pupils enables
treatment grouping ofthe patient intoa state of physiologic exci'tation (e.g.,
CNS stimulation and increased temperature, pulse, blood pressure, and
respiration); depression (depressed CNS and decreased temperature,
pulse, biood pressure, and respiration); mi'xed physiologic state.
This initial characterization helps to direct initial stabilization eflorts
and providesa clue tothe etiologic agent (including toxidromes— Table 1).
Stabilization follows standard ICU cafe as:
Airway: The airway of children must be monitored carefully. The

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 Approaeh to Poisoning ina Chiid

patency ofthe airway and gag reflex should be evaluated in patients with
depressed mental status. Even when thechild is awake and talking, close
monitoring is needed because hiscondition can deteriorate quickly.
Endotracheal intubation should be performed inall patients in whom the
airway is threatened. If intubation is necessary, cervical spine stabiJization
must be maintained if trauma is suspected.
Breathi'ng. After the airway is adequately secured, the quality of
breathing must be evaluated. Poisoned patients may develop respiratory
failure. Some toxins decrease the respiratory drive, whereas others impair
muscle contraction: still other toxins may directly damage thelung
parenchyma orresult in pulmonary edema. Any otthese mechanisms may
result in hypoxia and/or hypercapnia. Ina symptomatic or rapidly
deteriorating patient, measurement of arterial blood gas should be
obtained, Supplemental oxygenation should be provided to maintain
oxygen saturation >95%.
Circulation: Intoxication by various drugs may cause blood pressure
and heart rate abn0rmalities and/or cardiac conduction disturbances
ranging from minor QT changes toa wide QRS complex form. Blood
pressure measurement anda 12-lead electrocardiogram (ECG) should be
obtained in all patients who present with occult toxic exposure. Continuous
cardiac monitoring is often necessary. The evaluation and management
ofcirculatory compromise in patients with intoxication of unknown or
multiple agents should oocur according to Advanced Cardiovascular Life
Support (ACLS) orPedJatiic Advanced Lite Support (PALS) guidelines.

Identification of the Agent Involved

Most occult toxic exposures in toddlers are with single agent, at horne and
by ingestion. They are easily identifiable and involve medications,
asmetics, cleaning products or personal care items. The general class of
symptom constellation and the common causative agents of such injury
are tabulated below (Table 1).

Assessing the Severity of Exposure

At least one intravenous {IV) line should be established in the stable
patient and Mo large bore lines In the unstable or deterio ating patient.A
naso/orogastric tube must be inserted and the first gastric sample

479
Table 1.Common toxidromes (symptom constellation)‘ and their clinlcal descriptors with common causative agents

Type AvPu/luentai Vitals Pupils Other Examples oftoxic

9tatua Temp/HR/ Manifoatations Agents

Sympatnomimetlc Excitation, TJ/T/Twi¢le Myoria9is Diaphoresis. Ct›caine, amphetamines,

hallucinations, pul6a pressure tremors, thsophylline, caffeine •g
paranola hyper•reflexia,
seizures
Antichalinergic Exfitation, Myoriacis Dry flushed Antihistam‹nes, TCA,
Hal asa hare/dry gs hallucinations, antispasmodics, atropine,
a dorts//ad asa delirium with ilaus, urinary scopolamine, belladonna
beei/mad asa mumbling spaech, retention, alkaloids
hatter/blind asa coma myoclonus.
bai/bowel bladder choreoathetosls,
/oee //te/x lone and picking behavior,
heart rune alone seizures (rare)
e
Agltatlon, Mydrlasis Nystsgmus Phencyclidine, LSO, (e.g..
synesthesia, (usually) MOMA [“Ecstasy"], MDEA)
hallucinations,
depersonalization
Opioid CN34epresson, ñT/T/T Miosis Hyporef]exia, Opioids(e,p„ heroin, 2
noma pulmonary edema, morphine, oxycodone, g
needla marks hydromorphone), W
diphenoxylale
Sedafive-hypnofic CNC depression, J/J/I/I Miosi$ Hyqoreflexia Benzodiazepines,
confusion, stupor, (usually) barbiturates, carisoprodol,
coma alcohols, zolpidem
Table 1. Continued ...

Tyge vitats Pupils Other Examplao ofToxic

Manifestations Agents
RR/BP)

Cholinergic Confusion, coma \/\/\+/tf Miosis Salivation, Organophosphate and

SLUDQE+DUMBELS urinary+ fe0al carbamate Insecticides,
wheezing/diaphotesie’ Incontinence, nicotine, pilocarglne,
bronchorrhea/ diarrhea, GI physostigmine,
bradycardia/miosls cramps, emesis, edrophonium
muscle

seizures
o
Serotonin syndrome Confusion, Mydrlasis Tremor, myoclonue, MAOls alone or with: o
diarrhea, hyper• SSRls, meperidine,
refI6xIa, clonus. dextromathorghar, TCAS,
rigidity diaphoresis, L•tryptophan
flushing, trismus

AVPU Alert, Voice, Paln, Unresponsive; OUMBELS Disrrhea, Urination, Miosic/muscle weakness, Bronchorrhea, Bradycardia, Emasis,
Lacrimation, Salivation/sweating; LSD Lysergic acid dlethylamide; MAOI Mono amine oxida6e inhibitor; MDEA 3,4-methyIenedloxy-
N•ethyjamphetamina; MOMA 3,4- mathylenedloxymethamphetamlne; SLUDGE Salivation, Lac«imlnation, Urinary Incontinence,
Diarrhea, Gastrointestional cramp6, and Emesis; SHRI Selective serotonin reuptake inhibitor; TCA Tricyclic antidepressant;
 Pediatric Intensive Care Protocols of AIIMS

collected. Laboratory tests including blood sugar, blood gas analysis,

lactate, Na , Ca*-, specific drug level (if ingest+d drug known|, plasma
cholinesterase levels in case of organophosphates, are some ofthe
routine tests. Some aspeMs aredetailed below:
• SpO, monitoring. Hypoxemia —Rapid evaluation of oxygenation
should be performed in all patients with altered mental status. This
can be performed witha bedside pulse oximeter and/or arterial blood
gas measurement. which provides additional information about the
patient's ventilation and acid-base status and may, in turn, affect
diagnosis and management. Pulse oximetry does not reflect
oxyh+moglobin saturation in patients with carbon monoxide
poisoning. If carbon monoxide toxicity isa diagnostic consideration,
the carboxyhemog1obin level should be measured by co-oximetry
usinga blood gas sample. Humidified oxygen shou Id be
administered to symptomatic poisoned children with altered mental
status.
• Blood su!9ar. Hypoglycemia — Several drugs cause hypoglycemia;
rapid assessment ofblood giuoose can be performed atthe bedside
witha glucose strip.A concentrated dextrose solution should be
administered if blood glucose is low, or rapid assessment of blood
glucose is not available. The dose fordextrose is 0.25 g/kg
administered intravenously or intraosseously. This is usually
achieved with 2.5 mI/kg of 10% dextrose solution since extravasation
of higher concentrations of glucose will tead to severe tissue
damage.
• Mentation. Opiate intoxication — Administration of naloxone is
indicated in patients who have depressed mental status, diminished
respirations, miotic pupils! or other circumstantial evidence of opiate
intoxication. The dose ofnaloxone varies depending upon theage of
thechild.
• Thiami'ne de ficiency. The administration of thiamine should be
considered in children and adolescents who may be thiamine
deficient because ofchronic disease, malnutrition, eating disorders,
or alcoholism. The notion that thiamine must be given before
dextrose to avoid precipitating Wernickes encephalopathy is largely
unsupported. Uptake ofthiamine into cells is slower than that of
dextrose, and withholding dextrose unti1 the administration of
 Approach to Poisontng ina Child

thiamine is complete may prove detrimental to those with actual

hypoglycemia.
• Osmolar gap. The calculated osmolaliiy is subtracted from measured
osmolality, being <10 mOsm normally. Unmeasured asmoles include
ketones and alcohols. Isopropyl alcohol is the onJy alcohol which
creates an osmolar gap but not an anion gap.

Ouantification of Exposure
Consider the maximum amount of substance that could have been
ingested by oomparing the number oftablets, volume ofliquid remaining,
details on packaging. When children sharea poisonous substance, it is
presumed that each child has taken the maximum amount. Information
about the quantity and timing of ingestion is helpful in making decisions
about decontamination or the use of antidotes. Younger children tend to
ingest small quantities of single agents. In one study of 66 children (age
1.5to 4.5 years), the volume ofa “mouthful” was calculated by subtracting
the volume ofapple juice remaining ina cup after the child had taken one
sipfrom the original volume.* The mean volume ofa mouthful was 9.3 ml
(959• Cl,8 to 11 ml), witha range of 3.5 to 29 ml.Some signs of severe
intoxication are listed in Table 2.

Table 2.Features indicating severe intoxication ina cfiia, need forICU care

• Glasgow coma scale 6; Agitalion requiring restraJn\

• PCO, > 45 mm Hg,hypoxia or respiratory failure (ARDS), and/or endotracheal
intubation
• GBP 80 mm Hg
• Membolic acidosis wilh pH 7.2
• Hyperthermia withT >104”F
• Poisoning wiiha "ioxic time bomb" - Ingested drug packets, sustained-release
preparations bleed foi invasive hemodynamic monitoring; tJeed for whole bowel
irrigation to enhance GI elimination of poison
• feed for emergency hemodialysis. hemoperfusion, hemofiltration
• feed foremergency antidote which requires close monitori+ig (e.g., anTivenom.
digibind, physostigmine, naloxone drip)
• Ischemic chest pain from toxin (e.g.. cocaine. carbon monoxide) MCA or other drug
exposure with QRS >420 ms orOTc > 500 rrrs
SBP Systolic blood pressure; MCA Tricyc{iC antidepressants

The most common 1atal drug ingestions inchildren younger than six
years ofa9e include iron supplements, antidepressants, cardioToxic

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 Pediatric intensive Care Protocols of AIIMS

agents, and salicylates.In addition,a number ofdrugs can be fatal if

ingested bya toddler. even in small amounts. The most common fatal non-
drug ingestions in child ren younger than six years of age incl ude
hydrocarbons, alcohols, cosmetics, cleaning products, and pesticides.

Diagnosis and Management ofa Child with Acute (Occult)

Poisoning°
This isa rapidly evolving and challenging frontier ot emergency an¢i
intensive care. While an exhaustive discussion on the topic is beyond the
scope of thechapter,a thoughtful appraisal ot the basic underlying
principle of managinga child with acute occult toxic exposure is reviewed
here.
A quick and pertinent history exploring the etiology and probable
mechanism ofinjury and its context, relevant to first aid and care of the
poisoned child should be obtained and the medico-legal records updated
(Box 1).
Intervention-clirected examination would be most informative and
efficient especially if the child is mentally depressed or has other vital
signs compromised. The evolution of the toxic stage would also be picked
up by frequent examination of signs.
After the initial diagnostic evaluation and stabilization. other physical
findings should be sought to further definea particular toxic syndrome
(toxidrome), to narrow thepotential etiologies of poisoning (Table 1), and
to evaluate the need forICU care (Table 2).
The dia9• S›• may be assisted by (see Table1 ):
Temperature alterations
• Blood pressure and heart rate alterations
• Respiratory disturbances
• Pupillary findings
• Skin findings
• Neuromuscular abnorrrialities
• Mental status alterations
Characteristic odors (these odors may not be detectable by all
examiners) e.g., Kerosene, pesticides, camphorated oils.

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 Appraach toPoisoning ina Child

Boz 1. Approach toa child with actite (unknown) poisoning

Initial management (reduoe, eliminate continued exposure)

Assessmenl ofgeneral ce'ndition and life support measure

Identif‹caIion of poiso+i leading to appropriate management

Time. royte, duration and oircums\ances (location and intenl) oT exposure

Name8 amouni ofdrug, chemical or ingredient involved
Time otonset, nature are seyeriTy of symptoms and timing of first-aid measures
Detailed family history of diseases and drug Iherap'y

Heart rake, blood pressure, temperature. peripheral perfusion, respiratory rate,

3pecilic pointers- evaluation of pupil, odor ano secretions (Tabh= 3)

Identifying toxidromes (consleI\a\ion of signs and symptoms) tTable 4}
Med legal aspecls (see later)

Other aspects of the physical examination are also reJevant. Nose

bleed may occur in individuals who inhale cocaine or volatile substances.
The Jatter may also cause facial rash, flushing, blisters, ora ring of paint
around the mouth and nose (the "huffer rash"). Wood's light (uJtraviolet)
examination ofthe patient's mouth orclothes may reveal fluorescence if
the patient has ingested antifreeze solution (e.g., ethylene glycol), which
commonly contains fluoresoein dye (added to help in the identlication of
radiator leaks}.6 NeedJe tfaCks sag gest intra ve nou s d rug use.
Oiscrepancies between thephysical examination and the history may
reflect an inaccurate ingestion history,a brief or prolonged time interval
between exposure and physical examination, or intentional poisoning.

Ancillary Studies/Physical/Laboratory Tests

The laboratory evaluation of the child with an unknown ingestion is
performed to detect metaDolic effects of the poison that have both
diagnostic and therapeutic implications. The laboratory evaluation should
include the following:

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