POISONING
CLINICAL APPROACH TO A CHILD WITH
SUSPECTED POISONING.
• The initial approach includes stabilisation and rapid assesement of
airway ,breathing and circulation.
• After initial assesement and stabilization of vital signs,general
physical and neurological examination is done.
• Physical examination may reveals clues to identify potential
poisonous agents.
signs Probable poisoning effects / agents
pallor hemolysis
cyanosis methemoglobinemia
icterus Hepatotoxicity , hemolysis
Acidotic breathing Alocohols , salicylates
Tachycardia or Sympathomimetic and anticholinergic agents
tachyarrhythmia
Bradycardia or Digitalis and cholinergic agents.
bradyarrhythmia
TOXIDROMES
• A particular poison produces a constellation of features involving
various organ systems , known as toxidromes .
• Toxidromes can confirm the likely diagnosis.
COMMON POISONINGS
[Link]
• Hydrocarbon ingestion accounts for ~5% of accidental poisonings and ~ 25% of deaths realated to
ingestion in children in <5 years globally.
• HCs are inappropriately stored in unlabelled containers or drinking glasses and are often attractive in
colour or pleasant smelling like furniture polishes.
• Categorised into : aliphatic (kerosene) ,aromatic (benzenes),halogens (carbon tetrachloride) and mixed
compounds.
• Aromatic and halogen compounds have predominant effect on CNS.
• Aliphatic HCs have a risk of aspiration and pulmonary symtoms.
• Most imp manifestation of HC toxicity is aspiration pneumonitis cia inactivation of type ii pneumocytes
and resultant surfactant deficiency.
• Risk of causing aspiration pneumonitis by HC is inversely proptotional to its viscosity and directly
propotional to its volatility.
• Compounds with high volatility ,low viscosity and low surface tension like kerosene ,gasoline,naphtha
likely to be aspirated and cause severe lung injury.
CLINICAL AND LABORATORY
MANIFESTATIONS.
• Respiratory system- develop early (within 6 hours) due to aspiration during
ingestion or following vomiting.
-May vary from mild cough and respiratory distress to
ARDS and respiratory failure.
-chest xray- may be normal initially or show infilterates ,
pleural effusion , ARDS and pneumatocoeles
• CVS- dysarrhythemias seen with aromatic HC abuse.
• CNS – restlessness drowsiness seizures and coma due to hypoxia and acidosis.
• fever and leukoctosis are common and do not necessarily imply bacterial
superinfections.
TREATMENT
• Mainly supportive
• Gastric lavage or induction of emesis – not recommended due to risk
of aspiration.
HC Ingestion
Symptomatic
Normal cxr Asymptomatic (wheezing, altered
sensorium ,tachypne
Observe for 6 a)
Abnormal cxr
hours
Discharge if Admit : O2,iv fluids , beta
asymptomatic Admit and agonists.
observe, ,monitor respiratory and
discharge if neurologic status.
asymptomatic No steroids or pro[phylactic
Lead poisoning
Sources
• 1 Main source of environmental source of lead is gasoline although
drinking water from lead pipes
• 2 chewing lead paints on toys
Clinical features[plumbism]
• Occurs in three ways
• 1 inhalation
• 2 ingestion
• 3 skin
• Abdominal colic , constipation, loss of appetite
• Blue lines on gum
• Anemia
• Wrist drop, foot drop
• Insomnia
• Headache
• Mental confusion
• Delerium
MANAGEMENT
• PREVENTIVE MEASURES
• 1 SUBSTITUTION
• 2 ISOLATION
• 3 LOCAL EXHAUST VENTILATION
• 4 PERSONAL PROTECTION
• 5 GOOD HOUSE KEEPING
• 6PERSONAL HYGIEN
• 7 HEALTH EDUCATION
• 8 PERIODIC MEDICAL EXAMINATION OF WORKERS
• 9 MEDICAL MANAGEMENT
• A. SALINE PURGATIVE
• B. D PENICILAMINE
PARACETAMOL
POISONING
INTRODUCTION
• It is widely used as antipyretic and analgesic
• Most common cause of acute liver failure in western
world
Mechanism
• By formation of highly reactive metabolite NAPQI LEADS
TO depletion of gluthathion stores
CLINICAL MANIFESTATIONS
• STAGE TIME AFTER INGESTION CHARACTERISTICS
• 1. 12-24HRS asymptomatic,nausea and vomiting
• 2. 24-48 hrs resolution of earlier symptoms ,elevated liver
• enzymes
• 3. 3-5 days anorexia,nausea,vomiting multiorgan
• dysfunction
• 4. 4-14 days recovery phase with resolution of clinical
symptoms and improvement
MANAGEMENT
• N-acetyl cysteine –precursor of glutathione synthesis reduces
incidence of hepatotoxicity
Organophosphorus
poisoning
introduction
• Organophosphorus and carbamates are commonly used pesticide and
a common cause fof poisoning in developing nations.
Mechanism of action
• Inactivting acetylcholinesterase resulting in excess of nicotinic and
musacarinic activity in the peripheral and central nervous systems.
Clinical features
• D-Diarrhoea
• U-Urination
• M-miosis
• B-bronchospasm
• B-bradycardia
• E-emesis
• L-lacrimation
• S-salivation
treatment
• [Link]-Airway,breathing,circulation.
• Provide 100% oxygen and mechanical ventilation
• 2. IV fluids and ATROPINE[0.02 mg /kg/dose] as bolus
• Pralidoxime PAM 25mg/kg IV over 20-30 minutes then infusion at 10-
20 mg /kg/hr in saline
• Repeat atropine [0.05 mg/kg/dose] after 5 min if no improvement
after first dose
