POISONING- COMMONHOUSEHOLD PRODUCTS

DR. D.Rasika PriyaFIRST YEARMD Pediatrics

Common household poisons:

Hydrocarbon OrganophosphateCamphorMosquito repellantButton battery ingestionDetergentsRat killerInkHair dyes

HYDROCARBON CASE SCENARIO:

21mths old boy ingested an estimated 20 ml of kerosene at 7:00 p.m. on 30/12/2016 and was brought to the hospital 11 /2 hrs post exposure. His mother noticed child was having fast and noisy breathing however did not recall him coughing , vomiting or altered sensorium.• O/E he was sick looking restless , kerosene odour was present on

his breath. His vital signs were B.P=90/60 mm hg pulse=120/min , R/R=62/min, grunting, subcostal retraction positive. Temp 97.6⁰ f no cyanosis spo2=100% with 02. The abdominal, cardiac and pulmonary examination were normal. Chest X-ray taken- normal. He was kept in observation for 12 hrs and was discharged on the next day.

HYDROCARBONS• It constitutes 0.3 to 3.3% of total poisoning.• Accidental – below 5 years • Most common in India – Kerosene

CONTD…• Abundant in modern society.

• Most commonly ingested hydrocarbons - gasoline, lubricating oil, motor oil, mineral spirits, lighter fluid/naphtha, lamp oil, and kerosene.

• Other common sources of hydrocarbons -dry cleaning solutions, paint, spot remover, rubber cement, and solvents.

PATHOPHYSIOLOGY Aspiration of hydrocarbon Inhibit surfactant

Alveolar instability

Early distal air way closure

Ventilation perfusion mismatch Hypoxia

CLINICAL MANIFESTATION• MAINLY- Respiratory : Coughing, choking, tachypnea, grunting,

cyanosis ,Rales, wheezing • Fever -24 to 48 hrs• GIT- vomiting, abdominal pain, bleeding.

• PULMONARY AIR LEAK SYNDROME

DIAGNOSIS• Chest X ray

Significant at 2 to 8 hours after ingestion.Common findings- Fine perihilar opacities, bibasilar infiltrates and atelectasis.

• ABG

• Pulse oximetry

X RAY FINDING

•Findings include airspace disease which may be patchy at the onset but coalesce later, particularly in the lower lobes medially •The pattern is similar to, and may represent in some cases, pulmonary edema •Pneumatoceles may form after the first week

Admission Criteria• Patient has significant respiratory symptoms or an abnormal

chest radiograph.

• Patient has significant CNS depression, severe gastrointestinal symptoms or has ingested a significant amount of Hydrocarbon.

• Observation if respiratory symptoms are worsening or if the chest radiograph is becoming progressively worse.

MANAGEMENT:• Airway – supplemental oxygen• Inducing emesis, gastric lavage, activated charcoal are not indicated in most Hydrocarbon poisonings.• Antibiotics – only when signs of pneumonia/ secondary infections

are evident.COMPLICATIONS:• ASPIRATION PNEUMONITIS• CNS complications- Seizures, encephalopathy.• CVS complications- Arrhythmias

ORGANOPHOSPHOROUS• Less common in children• Less than 1%• Mostly accidental and unintentional.• More common in lower socioeconomic class.• Used in agriculture(crop sprays) and at home as insecticides(rodents, cockroaches etc.)

EXAMPLES: Parathion, DDT, Finis, Baygon and Coopex. Chlorpyrifos (CPF), methyl parathion (MPT), and malathion (MLT) are among the most extensively used organophosphate (OP) pesticides in India.

PATHOPHYSIOLOGY

CLINICAL FEATURES• TOXIC DOSE: 2mg(0.1mg/kg)

• Rapid absorption – skin, lungs, GIT and mucous membrane.

• Sequential triphasic illness follows OP intoxicationo Acute Cholinergic Crisis o Intermediate Syndrome (IMS) o Organophosphate-Induced Delayed Polyneuropathy (OPIDN )

Acute Cholinergic Crisis• Three clinical effects on nerve endings-

o Nicotinic effects at neuromuscular junctions and autonomic ganglia.

o CNS effects ando Muscarinic effects on postganglionic and parasympathetic end

organs.

TIME MECHANISM MANIFESTATIONACUTE(mins to 24 hrs)

Nicotinic Weakness, Fasciculation, Cramps, ParalysisMuscarinic Salivation, Lacrimation, Defecation,

Urination, Gastric cramps, Emesis, Bradycardia, Hypotension,Bronchospasm, Miosis

CNS Anxiety, Convulsion, Restlessness, Respiratory depression

DELAYED(24 hrs- 2 weeks)

Nicotinic Intermediate syndromeMuscarinic Cholinergic- Bradycardia, Miosis, SalivationCNS Coma, Extra pyramidal

SLUDGE/BBB DUMBELS

S = SalivationL = Lacrimation U = Urination D = Defecation G = GI symptoms E = Emesis B = Bronchorrhea B = BronchospasmB= Bradycardia

D = Diarrhea and diaphoresisU = UrinationM = MiosisB = Bronchorrhea, bronchospasm, and BradycardiaE = EmesisL = LacrimationS = Salivation

MUSCARINIC SIGNS OF OP POISONING

INTERMEDIATE SYNDROMEOccurs 24 to 96 hours after the ingestion of an OP compound-approximately 10-40% of patients treated for acute poisoning develop this illness.

• Rapid onset, progression of muscle weakness.

• Increasing respiratory difficulty -anxiety, sweating and use of accessory muscles of respiration.

• If endotracheal intubation and ventilation are not instituted early, cyanosis, coma and death follow rapidly. Paralysis may continue for 2-18 days.

• Proposed mechanisms include persistent inhibition of AChE leading to functional paralysis of neuromuscular transmission, muscle necrosis, and oxidative free radical damage to the receptors.

Organophosphate-induced delayed polyneuropathy (OPIDN)

• 1-3 weeks after acute exposure and an uncertain period following chronic exposure, due to degeneration of long myelinated nerve fibres.

• Mechanism is inhibition of neuropathy target esterase (NTE) enzyme in nervous tissues by certain OP compounds (chloropyriphos).

Symptoms:• Cramping muscle pains in the legs numbness and paraesthesiae in

the distal upper and lower limbs.• Acute weakness of the lower limbs.• Muscle wasting and deformity, such as clawing of the hands, follow.

Sensory loss is variable and is often mild and inconspicuous. Signs:• Physical examination reveals symmetrical flaccid weakness of the

distal muscles, especially in the legs.

• Tendon reflexes are reduced or lost, absent ankle reflexes being a constant feature.

MANAGEMENT• Clinical• Cholinesterase- RBC or Plasma(<50%)• Decontamination.• Check airway, breathing, and circulation.• Left lateral position- to reduce risk of aspiration of stomach

contents. • Gastric lavage- 50-100ml warm NS• Charcoal is limited use.

HISTORY OF ACUTE EXPOSURE-AMOUNT,TIME,ROUTE,TYPE OF COMPOUND

MINOR TOXICITY MAJOR TOXICITY

DECONTAMINATION OBSERVATION:CLINICAL AND ACHE ESTIMATION

ACUTE DETERIORATION

CLINICALLY STABLE FOR 12 HR-DISCHARGE

PSYCHIATRIC REVIEW

MAJOR TOXICITY

AIRWAYBREATHINGCRICULATIONDECONTAMINATION

SPECIFIC MANAGEMENT

MUSCARINIC –ATROPINENICOTINIC – OXIMESSYMPTOMATIC THERAPY

CLINICALLY STABLE-SHIFT TO WARD FROM ICU-12HRS

STABLE 48 HRS-DISCHARGE

WROSENING-TREAT –MAJOR TOXICITY

ATROPINE:Antagonizes the central and muscarinic cholinergic effects and acts by blocking the muscarinic receptors.0.05mg/kg IV every five minutes till the signs of atropinisation appear.

Pralidoxime:• It neutralizes the nicotinic effects of OPC.• 25 to 50mg/kg in normal saline over 30 minutes followed by 10 to

20mg/kg/hr.

CAMPHOR• Lethal dose for children is 0.5-1 gm. and for infants 70mg/Kg.• Clinical effects: rapidly absorbed from Skin/GIT/respiratory tract.

Onset of symptoms within 5-90 minutes Impairment of vision, headache, confusion, vertigo, tremors, jerky movements and seizures.

TREATMENT:Gastric lavage Activated charcoal (15-30 gms)Prevention of further/continuous exposure through skin or from clothes.

MOSQUITO REPELLANT • Synthetic chemicals(DEET[most potent] and PMT) or natural repellants.• DEET o Absorbed through skin and guto Larger amounts- CNS SYMPTOMS- coma, hypotension, abnormal

hypertonic movements, tremors and convulsions within 6 hours.o Eye exposure – irritative conjunctivitiso Skin – dermatitis with erythema, bullous reactions/ urticaria

TREATMENT:• Major ingestion- gastric lavage, activated charcoal, followed by sorbitol or

saline cathartics.• Skin – wash with non irritant soap and water. Topical steroids and oral

antihistamines.• Eye – flushing of eye with copious amount of water.• Seizures – anticonvulsants.

PROGNOSIS: Recovery within 36 hours.

BUTTON BATTERY INGESTION• Nowadays with increasing accessibility of electronic toys and Devices to

children, ingestion of these miniature-sized batteries is on the rise. • 6 months to 3 years.• Removed within 72 hrs.• Delayed will cause erosion and fistulas.• More the time – delayed- more discharge from battery-more the reaction.

• 4 Main types of Button cells – Mercury, Silver, Alkaline manganese, Lithium.Management:Chest and Abdomen X-ray.Nose and Esophagus- remove by endoscopy.Stomach – pass out spontaneously. Daily abdominal radiography. Crossed pylorus – once in 4 days abd X ray.

DIFFERENCE BETWEEN COIN AND BATTERY IN X RAY

DETERGENTS• 3 Main Categories ; nonionic, anionic, cationic.• Nonionic/ anionic- less toxicity, only observation.• Cationic – benzalkonium chloride and citramide - Corrosive effects• Dishwashing powder/ liquids/ tablets are strongly alkaline –

corrosive injury to oral mucosa, lips and tongue.• Abdominal pain, vomiting, hematemesis, melena, esophageal

ulcers, esophageal strictures. • Management – Supportive.

MATCHSTICK POISONING• Components- potassium chlorate, sulphur, gum, glass, red

phosphorus.• Harmless but potassium chlorate - highly reactive and toxic. • On ingestion, leads to rapid oxidative destruction of RBC –

Methemoglobinemia and cyanosis. MANAGEMENT:• Gastric lavage with activated charcoal. Alkaline diuresis or

methylene blue are used. Exchange transfusion/ hemodialysis are done when needed(Methemoglobinemia).

• Hyperbaric oxygen may help. • Symptomatic treatment

RAT KILLER POISONING• The components of rodenticide are usually aluminum

phosphide, zinc phosphide, arsenic,thallium, barium compounds, warfarins and super warfarins group. Super warfarins include bromadiolone, brodifacoum, difenacoum and diaphacinone. Among them commonly used ones are warfarin group.

• PathophysiologyThe anticoagulant effects of warfarins are secondary to inhibition of vitamin K 2,3-epoxide reductase and vitamin K quinone reductase

CLINICAL FEATURES:Hepatic failure and DIC

INVEATIGATION:• Prothrombin time at the time of admission and 48 to 72 hours

after the poisoning helps to assess the coagulation status. APTT, BT and CT. LFT and RFT. CBC in bleeding tendency.

MANAGEMENT:RoutineVitamin K- all rat killer poisoningFFP• Specific antidote for thallium is potassium ferricyano ferrate

(Prussian blue). 250mg/kg/day- 4 divided doses until the concentration of thallium in the urine is less than 0.5mg over 24 hour period

INK• CONTAINS-Dyes, Pigments, Solvents, Water.

• Staining of mucous membrane• GI symptoms

• Observation

HAIR DYES• Main component - paraphenylenediamine (PPD). • Acute poisoning by PPD causes characteristic severe

angioedema of the upper airway accompanied by a swollen, dry, hard, and protruding tongue.

• Systemic intoxication results in multisystem involvement and can cause rhabdomyolysis, acute renal failure (ARF).

• There is no specific antidote for PPD and treatment is mainly supportive.

TAKE HOME MESSAGE

• Poisoning due to household agents - global problem in children. Mainly accidental -< 5 yrs.• Small doses - do not cause toxicity. • Larger doses- Signs of poisoning • The mainstay of management is good supportive care no

specific antidote is available.• Implementation of good safety measures at home will

bring down morbidity and mortality due to poisonings.

THANK U