Poisoning in children Dr M A Maleque Molla, FRCP, FRCPCH Conultant Pediatric Intensivist 1 January 25, 2016
Jan 18, 2018
Dr M A Maleque Molla, FRCP, FRCPCH Conultant Pediatric
Intensivist
Poisoning in children Dr M A Maleque Molla, FRCP, FRCPCH Conultant
Pediatric Intensivist January 25, 2016 Case scenario You received a
3 years old childin ER who is breathing hard, not behaving well and
not responding while calling and parent is concerned that child may
have taken some thing. How do you approach the problem? A case
suspected poisoning, the first step is to ascertain whether the
patient is symptomatic or not. In ER patient, priority should be
stabilization of ABC When the patient is stable, Evaluate the child
by history & Physical examination a history should be obtained;
patient age and sex, the time of probable or witnessed toxin
exposure, the type of substance involved, and the method of
exposure (i.e., skincontact, inhalation, or ingestion). Poisoning
Definition: Poisoning refers to an injury that results from being
exposed to an exogenous substance that causes cellular injury or
death*. Poisons can be inhaled, ingested, injected or absorbed.
*WHO Epiodemiology Global rate of poisoning 282.4 / 100,000
population WHO
The global death rate from poisonings 1.8/ 100,000 population
Non-fatal poisoning, more common among children aged 1 to 4 years
Highest rates of fatal poisoning occurs among Children under the
age of one year. Most poisoning occurs at home and common rout of
poisoning is oral Most common agents involved
Over-the-counter preparations: paracetamol, cough/cold remedies,
vitamins and iron tablets, antihistamines and anti-inflammatory
drugs. Prescription medications: Antidepressants, narcotics,
analgesics and illicit drugs. Household products: Bleach,
disinfectants, detergents, cleaning agents, cosmetics, vinegar.
Paraffin/Kerosene. Pesticides:insecticides (Organophosphorus
compound). Poisonous plants. Animal or insect bites: Scorpion
sting, snake bite, Dog. World report on child injury prevention,
WHO 2004 Evaluation of poisoned patient
Priority: Stabilization of the Airway, Breathing,& Circulation
Diagnosis History Patient age and sex, wt. The type of substance
involved, Method of exposure (i.e., skin contact, inhalation, or
ingestion). Assessment of the severity of the exposure Physical
examination Investigations Note: concomitant trauma or illness must
be recognized and addressed prior to initiation of decontamination
History What poison has been taken? How much has been taken?
When the poison has been taken? What are the advarse effect of the
poison? Reliability- Whether any poison has been taken? History
(cont..) What poison has been taken ?: can be identified
from;
Container Illustrated chart How much poison has been taken ?
Calculating the missing amount from the container. In doubt, always
calculate maximum amount of poison that has been consumed. When the
poison has been taken?: Approximatetime elapsed since ingestion or
exposure. History (cont..) What are the adverse effects of the
poison?
Information can get from; From books, internet, pharmacy Poison
Information centers: Tel no. Riyadh # /1999,2003, Jeddah # , Makkah
# , Madinah# History(cont..) Whether any poison have been
ingested?
Any doubt, take that the child has ingested the poison. A history
of medicationused by thefamily members. Poisoning should be
considered forany child, who present with acute onset of; Altered
mental status. Multi organ system dysfunction of unexplained cause.
Respiratory or cardiac compromise. Unexplained metabolic acidosis.
Seizures, or a puzzling clinical picture. Physical examination
Thorough physical examination from head to toe
Evaluation of mental status and vital signs, should be repeated
frequently The diagnosis may be assisted by; Temperature
alterations Blood pressure and heart rate alterations Respiratory
disturbances Pupillary findings Skin findings Neuromuscular
abnormalities Mental status alterations Characteristic odors e.g.
acetone, bitter almond, Garlic In case of unknown poison ingestion,
physical findings should be sought to define a particular toxic
syndrome (toxidrome). Toxidromes Anticholinergics: Atropine,
scopolamine, TCAs, phenothiazines, antihistamines,
antipsychoticmushrooms, Hot as a hare, Blind as bat, dry as a bone,
red as a beet, mad as a hatter CV: tachycardia, hypotension,
hypertension, arrhythmia GI/GU: decreased bowel sounds, urinary
retention Neuro: agitation, hallucinations, coma, extrapyramidal
movements, mydriasis, hyperthermia Toxidromes Cholinergics:
Organophosphates and carbamates
Mascarinic effect Nicotinic effect Diaphoresis/diarrhea Urination
Miosis Brdycardia/bronchospasm Emesis Lacrimation excess Salivation
excess Muscle fasciculation Cramping Weakness (extreme is
diaphragmatic failure) Autonomic hypertension, tachycardia,
pupillary dilation, and pallor Toxidromes Sympathomimetic:
Salbutamol, Amphetamine, Cocain, Ephedrine. Anxiety, Delusion,
Diaphoresis, hyperreflexia, mydriasis, paranoia, seizure
Tachycardia, hypertension, mydriasis, agitation, seizures,
diaphoresis, psychosis, hyperthermia OPIOID; Morphine, hydrocodone,
methadone Hypoventilation, Hypotension, Miosis, Sedation,
Hypothermia, Ileus. Investigations Blood glucose, urea &
Electrolytes
Blood gas & Acid base status Serum osmolality & osmolal
gap, anion gap Quantitativeserum concentration of drugs-
paracetamolsalicylate, Iron Urine analysis;Rabdomyolysis ECG.
Toxicology screens: indicated in children in whom the diagnosis of
poisoning is uncertain. Samples of blood, first voided urine ,
vomitus, and gastric contents should be save for subsequent
analysis. Plain radiographs of the chest & abdomen when
indicated. Management Management of the poisoned child depends
upon
Specific poison(s) involved, Presenting and severity of illness,
Elapsed time between exposure and presentation. Remember the
mainstay of therapy is supportive Management A. General Management
B. Specific Management ABCD
Decontamination: Techniques used to prevent the absorption of the
toxic substance Enhanced elimination: techniques which accelerate
removal of a toxins from the body B. Specific Management Antidote:
a substance which can counteract a form of poisoning 2.
Decontamination Surface decontamination e.g. Organophosphate
poisoning; Removal of the cloths and wash with soap & water
Irrigation ofeyes if affected GI Decontamination: Gastric lavage:
Not used routinely, use onlyselected cases Activated charcoal Whole
bowel irrigation Purgationusing cathartics Decontamination is
notalways warranted and may be contraindicated. Activated
charcoal(AC)
It is an insoluble, non absorbable, fine carbon powder Maximum
benefit, ifadministered within 1 hour of ingestion Dose: g/kg
(maximum 50 to 60 gm), can be repeated at 0.5g/kg Q4-6 hour
Multiple-dose: in case of ingested life-threatening amounts of;
Carbamazepine, Dapsone, Phenoberbital, Quinine, Theophyline Care
must be taken to protect the airway, assess for the presence of
bowel sounds. Activated charcoal(cont..)
Contraindication: Absolute contraindication: Bowel obstruction or
perforation Depressed level of consciousness Ingested non
absorbable acidic or alkaline corrosives e.g. sodium or potassium
hydroxide, or hydrochloric or sulfuric acid. Ingestion
ofhydrocarbonse.g., gasoline, kerosene, liquid furniture polish The
poisons which are not bound by AC e.g. Iron, lead, arsenic. Agents
for which activated charcoal is not recommended
Heavy metals Arsenic Lead Mercury Iron Zinc Cadmium Inorganic ions
Lithium Sodium Calcium Potassium Magnesium Fluoride Iodide Boric
acid Corrosives Acids Alkali Hydrocarbons Alkanes Alkenes Alkyl
halides Aromatic hydrocarbons Alcohols Acetone Ethanol Ethylene
glycol Isopropanol Methanol Essential oils Whole bowel irrigation
(WBI)
It refers to the administration of polyethylene glycol electrolyte
solution (PEG-ES) to induce liquid stool and mechanically flush
pills, tablets, or drug packets from the GI tract. WBI
significantly decreased absorption oftoxic materials Whole bowel
irrigation (WBI)
Indication: Ingestionoflarge amounts of poisons that are not well
bound to AC, sustained-release medications. Contraindications:
Intestinal obstruction, perforation, ileus, or significant GI
bleeding , Persistent vomiting Technique:
Administrationpolyethylene glycol electrolyte solution (PEG-ES)via
nasogastric tube Dose: 20 to 40mL/kgper hour until the rectal
effluent is clear, which takes 4-6 hours. PEG-ES (GoLYTELY) Use of
Cathartics Cathartics accelerate the evacuation by fluid load in
the intestine and stimulating bowel motility. They shouldneverbe
used as the sole method of GI decontamination. Recommended agent:
0.5g/kg(1 to 2mL/kg)of 7 percent Sorbitol(0.9g/mL) 4mL/kgor 250 mL
of Magnesium citratein a 6 percent suspension Sorbitol is not
recommended for use in children younger than one year of age If a
cathartic is used, it should be limited to a single dose in order
to minimize adverse effects Enhance elimination of Poisons
Urinary alkalinization and forced diuresis:eg, salicylates and
Phenobarbital. Hemodialysis: significant ingestion of alcohols,
theophylline, Lithium, Salicylates. Hemoperfusion:Theophylline,
Carbamazepine, valproic acid, procainamide. Exchange transfusion:
arsine or sodium chlorate poisoning Peritoneal dialysis,
Hemofiltration Specific treatment Antidotes Very few poisons have
antidotes.
Information can be found in books or from Poison Information Center
Table. Antidotes for some common toxicant
POISON ANTIDOTE Paracetamol N-Acetylcysteine Anticholinergics
Physiostigmine Lead/Heavy Metals BAL in oil (dimercaprol) Beta
Blockers Glucagon, Cateholamines Carbon Monoxide Oxygen Cyanide
Amyl nitrate, Sodium Nitrate, Sodium Thiosulfate Ethylene Glycol
Dialysis, Fomepizole, Ethanol Iron Desferoxamine Isonazid
Pyridoxine DMSA, BAL, EDTA Methemoglobin Producing agents Methylene
blue Narcotics Narcan Organophosphates Atropine, Pralodixime
Phenothiazines Benadryl Disposition Patient can send home after 4-6
hour of observation if poison is less toxic. Alwaysadmit if
Symptomatic. Ingestion ofiron, tricyclic antidepressant, digoxin
and aspirin. Unconscious child should be admitted in pediatric
intensive care unit. SPECIFIC POISONING Paracetamol Toxic dose:
> 150 mg/kg
Most common ingestion in toddlers, preschoolers and adolescents
Toxic dose: > 150 mg/kg Kinetics dictate that a serum level to
be checked 4 hours after ingestion 4 hour toxic blood level
150ug/dl Apply the level to the management nomogram Rumack-Matthew
nomogram for single acute paracetamol ingestions Paracetamol
Poisoning
Stage I(1/ hours) Malaise, nausea, vomiting, pallor, diaphoresis
Stage II ( hours) Asymptomatic, right upper quadrant pain,
increasing LFTs, PT, PTT & INR Stage III ( hours) Liver
failure,in severe cases renal failure & multi organ failure
Stage IV ( days) Resolution of liver injury & Recovery
Management Activated charcoal 1 gm/kg
Plasma paracetamol level at 4 hours and plot on nomogram
N-Acetylcysteine(NAC),orally: If serum level above the line of
possible hepatotoxicity Ingested > 150 mg/kg & no facilities
to do serum level of paracetamol, Patients with an unknown time of
ingestion beyond 24 hours and a serumconcentration
>10mg/L(66mol/L) Dose of NAC: Loading Dose: 140mg/kg.
Maintenance Dose: 70mg/kg,4 hourly for 17 doses IV: Indicated if
patient is unable to take orally and present within 8-16 hours of
ingestion Dose: (Acetadote) 150 mg/kg over 1hr, followed by 50
mg/kg over 4 hr, followed by 100 mg/kg over 16 hr NAC therapy Is
most effective when initiated within 8 hr of ingestion,
Shown to have benefit even in patients who present in fulminant
hepatic failure There is no benefit before 4 hr post ingestion.
Iron Available preperation Ferrous sulfate -20% elemental
iron
Ferrous gluconate- 12% elemental iron Ferrous fumerate -33%
elemental iron Toxic Dose: Elemental Iron 60 mg/kg potentially life
threatening Clinical features 5 Phases
Phase I (Gastrointestinal): 30 min 6 hours Nausea, Vomiting
correlate with high toxicity, Diarrhea; abdominal pain GI
haemorrhage bloody diarrhea, hematemesis Severe hypotension Phase
II (Latent): hours post ingestion Patient appears better apparent
improvement In severe poising, this stage may be absent. In this
stage, iron accumulates in mitochondria and various organs Clinical
features(cont..)
5 stages Phase III (Shock): 6-72 hours post ingestion;
Hypoglycemia, Metabolic acidosis, Circulatory Failure-Shock Phase
IV (Hepatotoxic): days post ingestion Signs ofhepatic necrosis
raised AST, ALT and direct bilirubin, prolonged PT Renal Failure,
Metabolic Acidosis, Bleeding diathesis, Adult Respiratory Distress
Syndrome Coma Death Phase V: 2-8 weeks after ingestion Signs of
intestinal obstruction due to scarring and pyloric stenosis
Investigation Serum Iron 2-6 hours post ingestion, TIBC
Serum Iron >350gm/dl- mild to moderate toxicity Serum Iron
>500gm/dl- severe toxicity needs urgent intervention Greater
than 1000mcg/dL Significant morbidity and mortality Blood glucose;
Blood glucose >150 mg/dl moderateto severe toxicity CBC,
U&Es LFT, WBC> /cmm- associated with moderate to severe
toxicity Plain x-ray abdomen ABG/VBG Management Supportive care
ABCD Correct dehydration Removal of Iron
Gastric lavage with a large-bore orogastric tube may be indicated
for patients with overdoses of large amounts of iron who have a
large number of visible pills in the stomach on abdominal
radiograph Whole bowel irrigation with colonic solution (colyte,
golytely) if large number of tablets are ingested. No activated
charcoal to be given because it does not bind iron. Repeat x-ray on
abdomen after decontamination. If clumps of tablets can be seen in
x-ray and fail to remove with usual procedures, surgical removal is
indicated in rare cases. Desferoxamine orally promote iron
absorption, so should not be given orally Management Definitive
treatment: Desferoxamine intravenous infusion.
Indications: Serum Iron at 4-8 hours >500g/dl regardless of
symptoms or Serum Iron >350g/dl + moderate to severe symptom
Moderate to severe symptom regardless of serum iron Anion gap
metabolic acidosis Significant no. of pills on abdominal x-Ray
Dose: By IV infusion 15 mg/kg/hour maximum 6 g/24 hours By
intramuscular 90mg/kg/dose 8 hourly maximum 6g/24 hours Duration:
duration of desferoxamine therapy until resolution of clinical
symptoms, usually 24 hour SALICYLATE POISONING Toxic Dose: >150
mg/kg Clinical Manifestation:
Early: nausea vomiting tachypnea, deep sighing respiration,
tinnitus, high temperature, lethargy, and dehydration. Late:
Bleeding tendency, coma. Clinical features Important signs and
laboratory findings:
Phase I: First 12 hours Tachypnea Alkalosis Phase II hours
Tachypnea persist Hypokalemia Paradoxicalaciduria Phase III - 4 to
6 in an infant, or 24 hours in an adolescent or adult Dehydration
5-10% Worsening acidosis Hypokalemia; hyperglycemia/hypoglycemia
Pulmonary edema, pulmonary hemorrhage Cerebral edema Investigations
Plasma Salicylate level no sooner than 6 hours and plot on the
nomogram Urine pH hourly Blood gas Glucose, serum urea electrolytes
and creatinine 6 hourly PT LFT. Nomogram for Salicylate Management
Plasma salicylate levels mg/dl (moderate poisoning), treat and
admit the patient. Plasma salicylate level >65 mg/dl (severe
poisoning), treat and admit in the ICU Decontamination: Activated
charcoal 1 gm/kg. Multiple dose of AC may be needed in severe
poisoning Volume resuscitation: Rehydrate the child and correct
electrolyte specially potassium; Enhance elimination Urine
alkalinization by IV bicarbonate The goal is to achieve a urine pH
>7.5 while maintaining a serum pH 7.55. Hemodialysis
Organophosphate poisoning
Agents: Malathion, Parathion, Diazenon, Chlorothion Clinical
features 1. Mascarinic effect Diaphoresis/diarrhea Urination Miosis
Brdycardia/bronchospasm Emesis Lacrimation excess Salivation excess
2. Nicotinic effect Muscle fasciculation Cramping Weakness (extreme
is diaphragmatic failure) Autonomic : hypertension, tachycardia,
pupillary dilation, and pallor 3. CNS manifestations: Anxiety,
restlessness, tremor, confusion, coma, convulsion Management ABC
Remove cloths and wash the skin with soap and water
Atropine (vagal block) IV mg/kg every 15 minute until complete
atropinization ( dilated pupil, dry mouth tachycardia, fever) then
1-4 hourly for 24 hour Pralidoxime (Protopam, 2-PAM) Regenerates
acetylcholinesterase mg/kg/dose (IM or IV) Repeat in 1-2 hour if
muscle weakness does not relieve Thanks for attention