Corrosive poisoning is a common emergency as corrosive agents are easily available for household use. this ppt. covered the management of corrosive poisoning. Available now.

1. Corrosive poisons
Presented to MSc Toxicology and Forensic science
By:
Asia Alharbi
Asia.g.alharbi@gmail.com

2.  Definition
 Types
 Action of Mechanism and complications
 Sign and symptoms
 Diagnosis
 Management
Outlines :

3. Introduction :
• corrosives are a group of chemicals that have the capacity to cause
tissue injury on contact by a chemical reaction.
• They most commonly affect the gastrointestinal tract (GIT),respiratory
system and eyes.
• corrosive poisons are One of the most challenging situations encountered
in clinical medical practice in humans.

4. Introduction :
• The estimated prevalence of corrosive poisoning is 2.5-5% while the
morbidity is above 50% and the mortality is 13%.
• 80% of corrosive poisoning occurs in children below five years.
• The mean age is 27 years (range 16 - 60 years).
• usually corrosives are ingested in adult by suicidal or for medicinal
purposes.

6. Types of Corrosive
poisons

7. The common caustic agents include:
 Strong acids and alkalis
 Concentrated weak acids and alkalis
 Oxidizers (with neutral pH)
 Alkylating agents
 Dehydrating agents
 Halogens and organic halides
 Phenol

8.  Acids
• Car battery fluid (sulfuric acid)
• Descalers (hydrochloric acid)
• Metal cleaners (nitric acid)
• Rust removers (hydrogen fluoride)
 Alkalis
• Bleach (hypochlorite)
• Sodium hydroxide (liquid lye)

9. Uses of Common Caustic Agents:
1. Hydrochloric acid-metal/toilet bowl cleaner
2. Sulfuric acid-automobile batteries
3. Sodium hydroxide-paint remover/drain cleaner
4. Phenol-antiseptic

10. Car battery fluid (sulfuric acid)
Metal cleaners (nitric acid) Rust removers (hydrogen fluoride)
Bleach (hypochlorite) Sodium hydroxide (liquid lye) Phenol-antiseptic

11. Factors Determining Corrosiveness:
 Physical form: Solid/liquid.
 Duration of contact with tissue.
 Concentration of agent.
 Quantity of agent pH of agent: pH 11 are more corrosive
 Food: Presence or absence of food in stomach
 Titratable acid or alkali reserve (TAR): This quantifies the amount of
neutralizing substance required to bring the pH of a caustic agent
to physiological pH of the tissue.

12. Corrosive substances with a pH of less
than 2 or greater than 12 are highly
corrosive and can cause tissue necrosis

13. A concentrated solution of sodium hydroxide
(22.5% and 30%) can cause perforation of
the esophageal wall, mediastinitis, and fatal
outcome within seconds

14. Action of mechanism

15. Alkali ingestion:
Causes liquefaction necrosis.
protein dissolution collagen destruction fat saponification
cell membrane emulsification submucosal vascular Thrombosis
cell death.

16. Acid ingestion:
Causes coagulation necrosis..
hydrogen (H+)ions desiccate epithelial cells producing an eschar
leads to edema erythema mucosal sloughing ulceration
necrosis of tissues
coagulation necrosis
Both acids and alkalis cause fibrosis
and stricture formation

17. Consequences of
Caustic Injury

18. 1) Necrosis: Occurs within seconds of exposure to caustic agent
2) Ulceration and perforation: Occurs within 24-72 hours of exposure
3) Fibrosis: Occurs within 14-21 days of exposure
4) Stricture: Occurs after weeks to years of exposure
5) Carcinoma formation: Occurs after decades of alkali exposure.

19. Necrosis Ulceration and perforation Fibrosis
Stricture Carcinoma formation(squamous cell)

20. Clinical Presentation in
Corrosive Poisoning

21. GIT
• Excessive salivation
• Severe pain of lips,mouth, throat, chest and abdomen
• Dysphagia and odynophagia
• Epigastric pain and hematemesis
• Symptoms and signs of GI perforation

22. Respiratory system
• Cough
• Dyspnea
• Bronchoconstriction
• Pulmonary edema
• Chemical pneumonitis

23. Eyes and skin
• Pain at the site of exposure
• Burns at the site of exposure
• Erythema and vesicle formation

24. Acute caustic poisonings

25. (Ashish Gautam et al 2013)

26. Case report

28. Diagnosis and Investigations

29. Endoscopy
Direct evaluation by endoscopy is useful in grading severity of tissue
injury . planning for nutritional support and long-term management
of strictures.
Oesophagoscopy
used in case of oesophageal lesions because it’s the best diagnostic
procedure to determine the presence and severity of corrosive

30. Grading

31. Management

32. Early Admission
(Within 48-72 hours of corrosive ingestion)
Upper GI endoscopy should be performed on Day 1-2
• If endoscopy reveals only mild lesions, then the patient
can be discharged and clinical follow-up should be done
at one month.
• If severe lesions are found on endoscopy ,then surgical
gastrostomy is indicated, which should be followed by re
peat endoscopy and dilatation after three weeks

33. Delayed Admission
(Within 72 hours to three weeks of corrosive ingestion)
No endoscopy is indicated. Gastrostomy should be done if there is
severe dysphagia.
Endoscopy and dilatation of stricture (if present) should be done
three weeks after ingestion.

34. Late Admission
(More than three weeks of ingestion)
Requires endoscopy and dilatation of stricture.
• If the procedure is successful, then follow-up endoscopy should be
done at one month.
• If the procedure is unsuccessful, then surgical gastrostomy is
performed, which is followed by retrograde dilatation of stricture
after 10 days of operation.

35. Clinical Approach in Management
of
Corrosive Poisoning

36. Asymptomatic patient:
If there is history of minimal corrosive ingestion and no oropharyngeal
burns on examination, then the patient requires only observation in the
Emergency Room.
Symptomatic patient:
If there is history of ingestion of large volume of corrosive along with
signs like stridor, hoarseness of voice and respiratory distress, then the
patient requires admission in intensive care unit (ICU).

37.  Protection of airway
 Decontamination.
 vital parameters of the patient then dilute the substance with water or milk c
an be done within 60 minutes , After that the further treatment should start.
 Charcoal has no effect.
 Dilution and neutralization: by nasogastric tube lavage generates heat and
 increases the risk of aspiration.
 Stabilized patient: Initial evaluation of a stabilized patient aims to identify the
acute complications of corrosive ingestion.

38. • Corticosteroids: While there is no role of systemic steroids in the management
of caustic ingestion, intralesional steroids can be given.
• Antibiotics: Tissue destruction from caustic injury increases the risk of infection
by enteric organisms.
• Proton pump inhibitors (PPIs) and H2-blockers: Gastroenterologists routinely
recommend PPIs and H2-blockers in caustic ingestion.
• Nutrition.

39. References:
• Review article : Indian Journal of Clinical Practice, Vol. 23, No. 3, August 2012
http://medind.nic.in/iaa/t12/i8/iaat12i8p131.pdf
• Review article :Ingestion of Caustic Substances in ranian Journal of Toxicology
http://ijt.arakmu.ac.ir/article-1-165-en.pdf
• Ashish Gautam et al. JIACM 2013; 14(1): 46-9
file:///C:/Users/hp/Downloads/jact13i1p46%20(1).pdf
• Review Article C.P. LAKSHMI et al 2013 http://archive.nmji.in/archives/Volume-26/Issue-1
/Review-Article.pdf
• SUICIDAL CORROSIVE INGESTION: A CASE REPORT http://www.ejpmr.com/admin/assets
/article_issue/1456712928.pdf
• (Jovancević L, et al. 2008) https://www.ncbi.nlm.nih.gov/m/pubmed/18924590/?i=6&fro
m=/23918323/related
• Taiwo Olugbemiga Adedeji et al. The Pan African Medical Journal - ISSN 1937-8688 htt
p://www.panafrican-med-journal.com/content/article/15/11/full/#ref2