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ULY CLINIC
Mhariri:
ULY CLINIC
Imeboreshwa:
19 Februari 2026, 01:55:20
Corrosive compounds poisoning
Corrosive poisoning results from ingestion, inhalation, or contact with strong acids or alkalis that cause chemical burns to tissues. Injury begins immediately after exposure and may progress for hours to days.
Common agents
Alkalis (more dangerous — cause deep liquefaction necrosis)
Sodium hydroxide (drain/oven cleaners)
Potassium hydroxide
Ammonia solutions
Dishwasher detergents
Bleaches (sodium hypochlorite – moderate corrosive)
Acids (cause coagulation necrosis)
Hydrochloric acid
Sulfuric acid
Nitric acid
Toilet cleaners
Battery acid
Disinfectants
Alkalis typically damage the esophagus, while acids more often damage the stomach, but both can injure the entire aerodigestive tract.
2. Mechanism of Injury (Pathophysiology)
Alkali Injury
Liquefaction necrosis
Protein dissolution
Deep tissue penetration
High perforation risk
Acid Injury
Coagulation necrosis
Eschar formation
More superficial but causes gastric perforation
Timeline of injury
Time | Pathology |
Minutes–hours | Tissue necrosis |
24–72 hrs | Maximum inflammation & perforation risk |
1–3 weeks | Ulceration & granulation |
Weeks–months | Fibrosis → strictures |
3. Risk Factors
Children accidental ingestion
Storage in beverage containers
Domestic workers & cleaners
Industrial workers
Suicide attempts
Psychiatric illness
Alcohol intoxication
4. Clinical Features
Symptoms depend on concentration and amount.
A. Oral & Upper Airway
Burning mouth pain
Drooling
Difficulty swallowing (dysphagia)
Painful swallowing (odynophagia)
Hoarseness
Stridor
Oral ulcers
White/black oral burns
Hoarseness = airway injury warning
B. Esophageal
Severe retrosternal pain
Dysphagia
Vomiting
Hematemesis
C. Gastric
Epigastric pain
Abdominal rigidity
Perforation → peritonitis
D. Respiratory
Cough
Wheezing
Respiratory distress
Chemical pneumonitis
E. Systemic
Shock
Metabolic acidosis
Sepsis (late)
5. Diagnostic Criteria
Suspect corrosive poisoning when:
History of ingestion of cleaner/acid/alkali
Drooling + dysphagia
Oral burns
Severe chest or abdominal pain
Absence of oral burns DOES NOT exclude severe injury
6. Investigations
Initial Tests
Full blood count
Urea, electrolytes, creatinine
ABG (metabolic acidosis)
Serum lactate
Imaging
Chest X-ray → mediastinal air
Abdominal X-ray → perforation
CT scan → depth of necrosis (preferred)
Endoscopy (Key Investigation)
Perform within 12–24 hours
Contraindicated if:
Perforation suspected
Severe instability
Endoscopic grading (Zargar Classification)
Grade | Injury |
0 | Normal |
I | Edema/erythema |
IIa | Superficial ulcers |
IIb | Deep ulcers |
III | Necrosis |
7. Management
This is a medical emergency
8. Non-Pharmacological Treatment
Immediate Actions
Remove contaminated clothing
Rinse skin/eyes with water
Keep patient nil per mouth (NPO)
Dilution Therapy
Give small volume water or milk within 30 minutes only
Do NOT exceed small sips
Never attempt neutralization
Airway Management
Oxygen therapy
Early intubation if hoarseness/stridor
Avoid blind nasogastric tube insertion
Surgical Review
Urgent surgical consultation for:
Esophageal rupture
Perforation
Mediastinitis
Peritonitis
Contraindicated
Inducing vomiting
Activated charcoal
Neutralizing agents
Gastric lavage
9. Pharmacological Treatment
Pain Control
IV opioids (morphine titrated)
Acid Suppression
IV proton pump inhibitor (omeprazole/pantoprazole)
Purpose:Reduce secondary injury and promote healing
Antibiotics
Only if:
Perforation
Fever
Sepsis
Grade IIb/III burns
Suggested:
Ceftriaxone + metronidazole
Corticosteroids
Indicated in selected Grade II injuries
Reduce stricture formation(Not recommended in perforation)
Nutrition
Early enteral feeding via guided tube or jejunostomy if severe
10. Monitoring
Observe at least 48–72 hrs
Monitor:
Respiratory status
Signs of perforation
Hemodynamic stability
Ability to swallow
11. Complications
Early
Airway obstruction
Esophageal perforation
Mediastinitis
Peritonitis
Shock
Late
Esophageal stricture (weeks)
Gastric outlet obstruction
Chronic dysphagia
Malnutrition
Esophageal carcinoma (years later)
12. Prognosis
Depends on burn depth:
Grade | Outcome |
I | Excellent recovery |
II | Strictures common |
III | High mortality |
13. Prevention
Do’s
Store chemicals locked
Child-proof containers
Keep original packaging
Read labels carefully
Don’ts
Never store in beverage bottles
Never transfer to food containers
Never leave containers open
Never ingest unknown liquids
References
Ministry of Health, Tanzania. Standard Treatment Guidelines & National Essential Medicines List (STG-NEMLIT). 7th ed. Dodoma: MoH; 2023.
World Health Organization. Guidelines for the prevention and clinical management of chemical poisoning. Geneva: WHO; 2020.
Hoffman RS, Howland MA, Lewin NA, Nelson LS, Goldfrank LR. Goldfrank’s Toxicologic Emergencies. 11th ed. New York: McGraw-Hill; 2019.
Tintinalli JE, Ma OJ, Yealy DM, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. New York: McGraw-Hill; 2020.
Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK. Ingestion of corrosive acids and alkalis: endoscopic classification and prognosis. Gastroenterology. 1991;101(3):657-665.
Contini S, Swarray-Deen A, Scarpignato C. Oesophageal corrosive injuries in children: epidemiology, management and outcome. Int J Pediatr Otorhinolaryngol. 2018;104:146-152.
American College of Gastroenterology. Clinical guideline for caustic ingestion management. Am J Gastroenterol. 2021;116(2):225-248.
