Household Poisoning

Mahmoud L. Sakr, MD
Professor of Clinical Toxicology
Director of Poison Control Center
Ain Shams University
AIR FRESHENERS
 Formaldehyde: Highly toxic, known carcinogen
 Phenol
AMMONIA
 Very caustic and corrosive
 It is a very volatile chemical, it is very

damaging to your eyes, respiratory tract and

skin.
BLEACH
 It is a strong corrosive. It will irritate or burn
the skin, eyes and respiratory tract. It may
cause pulmonary edema or vomiting and
coma if ingested
DISHWASHER DETERGENTS

 Most products contain chlorine in a dry form

that is highly concentrated
DRAIN CLEANER
OVEN CLEANER
TOILET BOWL CLEANERS

 Corrosive
Batteries
1. Dry cell – Carbon + Heavy metal
2. Wet cell – used for vehicles,
lead and battery acid(H2SO4)
3. Button/Disk battery single cell
batteries used as an energy source for
digital watches, calculators, cameras etc.
4. Contains heavy metals and potassium
oxide solution.
5. If swallowed – majority no symptoms passed
intact with faeces.
6. If impacted in oesophagus – fever, dysphasia,
vomiting and anorexia.
7. Tissue damage cause by flow of electric
current, potentially fatal
Corrosives
 Corrosives
 Pathological effects
Alkalis
They mainly affect the esophagus causing liquefactive
necrosis leading to extensive penetrating lesions
(perforation).

Acids
 They mainly affect the stomach but the

esophagus may also be affected.

 They cause coagulative necrosis forming a

protective eschar of superficial layers thus

preventing deeper penetration.
Stages (phases) and evolution of corrosive
injury
 Inflammation stage and cellular necrosis

( 24 – 48 hours )
 Sloughing stage

◦ Necrotic tissues fall down by 4 – 7 days leaving

ulcers or perforating lesions
 Granulation tissue and collagen deposition
continue for 2 weeks.
 Cicatrisation stage

Dense fibrous tissue is formed in 2 – 4

weeks.
I- Skin
Skin may show burn (chemical burn) of any degree
except second degree

II- Pain
 Severe oropharyngeal, epigastric and retrosternal

burning pain

III- Mouth examination

 Oropharyngeal burns: light grayish to black

lesions
 Edema of tongue, lips, gums pharynx and

epiglottis.
IV- GIT manifestations
 Dysphagia and drooling of saliva (hypersialorrhea)

 Vomiting which is spontaneous and recurrent.

 Hematemesis and or melena

V- Respiratory manifestations
 Repeated cough
 Hoarseness of voice if edema and burns extend to

larynx.
 Stridor due to edema of vocal cords
 Dyspnea and cyanosis in severe cases

 VI- Malnutrition, dehydration and cachexia

They may occur few days after the accident 2ry to dysphagia.
Complications of Corrosives
Acute complications
 Upper respiratory tract obstruction (laryngeal edema-severe stridor).
 GIT hemorrhage (hematemesis or even regurgitation of fresh blood from severe esophageal
corrosion).
 Esophageal and gastric perforation.
 Shock (hemorrhagic, neurogenic or hypovolemic secondary to corrosion impaired feeding
and drinking.
 Septicemia.
 Disseminated intravascular coagulation (DIC).
 Acute pulmonary edema and acute respiratory distress syndrome (ARDS).

Periesophageal complications
 These complications appear by the end of the first week or later. These are due to sloughing of the
devitalized esophageal wall.
 Mediastinitis.
 Tracheoesophageal fistula.
 Pericarditis.
 Pleurisy.

Chronic complications
 Esophageal obstruction secondary to stricture formation.
 Pyloric stenosis.
 Vocal cord edema and airway obstruction secondary to fibrous tissue deposition.
 Malnutrition, dehydration and cachexia.
Investigations
 Complete blood count and coagulation profile:
Monitor hemoglobin for occult blood loss.
Monitor hematocrit to assess hydration status.
Leucocytosis reflects infection or hemorrhage
 Electrolytes
It should be daily measured in patients on Total
Parenteral Nutrition (TPN).
 Renal functions.
 Arterial blood gases (ABG).
 Chest X-Ray to rule out early pneumonia, pleurisy

or mediastinitis.
 Abdominal X-Ray (upright position) to detect any

free air in case of perforation.

 Fiberoptic Endoscopy:
 Endoscopic examination should be done in the

first 24 hours (preferably within the first 6 - 12

h) to assess grades of severity:
Grade II
Grade I Destruction of mucosa Grade III
IIa IIb
Erythema of Discrete ulcers Circumferential Destruction of all
mucosa ulcers layers of the gut
beyond mucosa

 Contraindications of endoscopy:
 Airway obstruction

 Signs of perforation.
Treatment
I- Emergency and first aid measures
 No neutralization no emesis, no gastric lavage, no activated charcoal
and no catharsis.
1- Dilution therapy
 Perforation should be excluded first
 One to two glasses of milk or water only may be

administered to the adult patient within 30 minutes; one

half of this dose may be administered to children.

2- Maintain airway patency and breathing in respiratory

distress
 Oxygen and ventilatory support
 Steroids IV to relieve edema.
 Endotracheal intubation
 Tracheostomy should be performed if vocal cord edema prevents
intubation.
3- Anti-shock measures
 Establish an intravenous line and give IV fluids or blood transfusion

if needed
4- Pain killers
5- Monitor vital signs, and monitor for complications.

II Supportive treatment
1. Total Parenteral Nutrition (TPN) for at least three weeks (grades II
and III).
2. H2 blockers or proton pump inhibitors to minimize acid secretion.
3. Steroids

Indications
 Grade I or II to prevent fibrosis
 Stridor
 Bronchospasm
 Acute pulmonary edema.
Contraindications
 Severe lesions associated with deep perforating lesions (Grade III) and
bleeding.
4. Antibiotics, to guard against infection.
5. Surgical intervention

a. Emergency surgery in
Severe uncontrolled hemorrhage,
Perforation (free air under diaphragm on upright
abdominal X-Ray or mediastinal emphysema on Chest
X-Ray).

b. Elective surgery:
Esophageal bypass surgery (resection anastomosis).
Dilatation of esophageal strictures.
Repair of broncho-esophageal fistula.
Gastrostomy for feeding purposes.
Carbolic Acid (Phenol)
I. Local effects
 Mild corrosive action with local anesthetic effect.
 Skin gangrene if applied for long period.
II. Systemic effects
CNS
 Central depression, confusion and coma.
Respiratory
 Respiratory depression cyanosis, and central respiratory failure.
Heart
 Bradycardia and myocardial depression
Kidney
 Acute toxic glomerulonephritis with oliguria, albuminuria, casts, anuria and renal
failure.
 Urine will be dark green on standing due to oxidation of the excreted metabolites of
phenol (e.g. hydroquinone).
Blood
 Hemolysis leading to hemolytic anemia and jaundice and renal failure
 Methemoglobinemia
Investigations
 Urine analysis for color and evidence of

hemolysis, albuminuria and casts.

 Renal functions: urea, creatinine.
 Methemoglobin level.
 Complete blood count: hemoglobin and RBCs

count
 LDH: Increased in hemolytic crisis
Treatment
I- Emergency measures (ABCD)
II- Elimination
 Skin contamination: wash with water
 Gut decontamination:
Induction of emesis
Gastric lavage
Activated charcoal
III- Symptomatic treatment
 Dialysis in case of renal failure.
 Treatment of methemoglobinemia.
 Treatment of hemolysis.
Oxalic Acid
I- Local corrosive effect
 Pain, vomiting, diarrhea, shock.
II- Systemic effect
1- Hypocalcemia (tetany):
 Tingling and numbness.
 Twitches of the face, extremities & carpopedal spasm.
 Convulsions.
2- Heart: arrhythmias and cardiac arrest.
3- Kidney: dysuria, oxaluria, hematuria, oliguria and anuria.

Investigations
 Electrolytes (calcium and potassium)
 Renal functions (urea and creatinine)
 ECG.
 Urine analysis: calcium oxalate crystals.
Treatment
I- Emergency measures (ABCD)
II- Elimination: Emesis or lavage
III- Antidote
◦ Calcium containing preparations given orally
◦ Calcium gluconate IV slowly
IV- Symptomatic treatment: IV Fluids, dialysis.