CORROSIVE

POISONING
Husin Thamrin dr.,SpPD

Division of Gastro-Entero-Hepatology
Dept. of Internal Medicine – Faculty of Medicine
Airlangga University – Dr Soetomo Teaching Hospital
Jember April 7th
Outlines :
❑ Introduction
❑ Types
❑ Action of Mechanism and complications
❑ Sign and symptoms
❑ Diagnosis
❑ Management
 INTRODUCTION
DEFINITION

▪ Corrosives are a group of chemicals that

have the capacity to cause tissue injury
on contact by a chemical reaction.

▪ Corrosive poisoning is a common

emergency as corrosive agents are
easily available for household use.

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PREVALENCE
▪ The estimated prevalence of corrosive poisoning is 2.5-5%
▪ While the morbidity is above 50%
▪ Mortality is 13%.
▪ 80% percent of corrosive poisoning occurs in children below
five years.
▪ But, adult exposure has more morbidity and mortality due
to significant volume of exposure and possible co-ingestion.

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Types of Corrosive poisons
COMMON CAUSTIC AGENTS

The common caustic agents

include: ▪ Dehydrating agents
▪ Strong acids and alkalis ▪ Halogens and organic
▪ Concentrated weak acids halides
and alkalis ▪ Phenol
▪ Oxidizers (with neutral pH)
▪ Alkylating agents

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 ACID & ALKALI

Acids : The most commonly

abused substance among acids
is hydrochloric acid.

▪ Car battery fluid (sulfuric Alkalis : such as sodium hydroxide

acid)
▪ Descalers (hydrochloric acid)
▪ Metal cleaners (nitric acid)
▪ Rust removers (hydrogen
fluoride)
(NaOH) and potassium hydroxide
(KOH), are also being abused.
▪ Bleach (hypochlorite)
▪ Sodium hydroxide (liquid lye)

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FACTORS DETERMINING CORROSIVENESS

Factors that determine corrosiveness include:

▪ Physical form: Solid/liquid ▪ pH of agent: pH <2 and >11

▪ Duration of contact with are more corrosive
tissue ▪ Food: Presence or absence
▪ Concentration of agent of food in stomach

▪ Quantity of agent ▪ Titratable acid or alkali

reserve

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Mechanism of Action of Corrosive Agents
▪ Acid ingestion: Causes coagulation necrosis
▪ This process includes :
Hydrogen (H+) ions desiccate epithelial cells Producing an eschar
This process leads to edema, erythema, mucosal sloughing,
ulceration and necrosis of tissues

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Mechanism of Action of Corrosive Agents
▪ Alkali ingestion: Causes liquefaction necrosis.
▪ This process includes :
Protein dissolution Collagen destruction Fat saponification
Cell membrane emulsification Submucosal & vascular thrombosis
And cell death

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Pathologic Classification
The pathologic classification of corrosive injuries of the upper
gastrointestinal tract is similar to the classification of thermal skin burns

• is characterized by superficial damage followed by onset of

1st mucous edema and erythema
degree

• is characterized by caustic penetration through the submucosa

2nd into the muscular layer of the organ
degree

• is characterized with perforation of the wall of the esophagus or

3rd stomach
degree

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 Clinical Presentation in Corrosive Poisoning

▪ Clinical presentation of corrosive injuries in the upper GI tract depends on

the physical state, type and quantity of the corrosive substance.
After caustic ingestion, patients complain on :
▪ Painful
▪ Burning mouth and throat
▪ Retrosternal chest and stomach pains
▪ Nausea,
▪ Vomiting, often with bloody content.

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 Clinical Presentation in Corrosive Poisoning

▪ Hypersalivation, difficulty in swallowing with edema, ulceration or whitish

plaques in the oral cavity, palatal mucosa and pharynx
▪ Injuries of the larynx and may cause laryngospasm associated with dyspnea,
tachypnea, dysphonia and aphonia
▪ Aspiration of the corrosive substance may cause endotracheal or bronchial
necrosis with mediastinitis, often leading to fatal outcome
▪ Severe caustic injuries of the stomach may result in perforation of its wall
and development of acute abdomen, which requires emergency surgery

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Laboratory Tests

o Hemogram
o Serum electrolytes: Hypocalcemia can occur with hydrogen fluoride
poisoning.
o Blood grouping and cross-matching
o Renal function tests
o Liver function tests
o Coagulation profile
o Arterial blood gas analysis

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Radiology

Chest X-ray :
▪ Helps in detection of pneumothorax, pneumomediastinum and pleural
effusion.
▪ Air under the diaphragm is suggestive of visceral perforation.

Abdominal X-ray :
▪ Help in the detection of pneumoperitoneum

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Radiology

Contrast studies:
▪ Barium studies have low sensitivity in detecting perforation and high-
risk of aspiration and inflammation.
CT scan:
▪ CT scan of neck/chest/abdomen should be considered if there is a high-
risk of suspicion for perforation despite negative plain X-rays

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Endoscopy

▪ Direct evaluation by endoscopy is useful in grading severity of tissue

injury, planning for nutritional support and long-term management of
strictures.

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Indications for Upper GI endoscopy

▪ Corrosive ingestion by small children

▪ Symptomatic older children and adults
▪ Patients with altered mental status

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Contraindications for upper GI endoscopy

▪ Hemodynamic compromise
▪ Peritonitis and mediastinitis
▪ Mild ingestion (asymptomatic patients with normal oral/upper
airway examination).

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 Endoscopic view of the epiglottis and vocal cords 4 days
after ingestion.

Endoscopic view of the epiglottis and vocal cords 11 days after ingestion. 19
The findings on upper GI endoscopy are based on Zargar’s modified
endoscopic classification of burns due to corrosive ingestion

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ENDOSCOPY KIKENDAL CLASSIFICATION

➢ I GRADE Oedema and erythema of the

mucosa

➢ II A GRADE Haemorrhage, erosions, blisters,

superficial ulcers
➢ II B GRADE Circumferential lesions

➢ III GRADE Deep grey or brownish-black ulcers

➢ IV GRADE Perforation.

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POST CORROSIVE LATE COMPLICATIONS

The most common late complications are :

▪ Esophageal strictures and stenosis
▪ Gastric stenosis of the antrum and pyloris
▪ Esophageal and stomach cancer

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MANAGEMENT OF CORROSIVE POISONING

Early Admission Delayed Admission Late Admission

• Upper GI endoscopy should • Within 72 hours to three • More than three weeks
be performed on Day 1-2. weeks of corrosive of ingestion: Requires
(ideally between 12-24 ingestion: endoscopy and dilatation
hours of ingestion). of stricture
• No endoscopy is
• If endoscopy reveals only indicated.
mild lesions, the patient
can be discharged • Gastrostomy should be
• If severe lesions are found
done if there is severe
on endoscopy, then surgical dysphagia.
gastrostomy is indicated,
which should be followed
by repeat endoscopy and
dilatation after three
weeks.

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Clinical Approach in Management of Corrosive Poisoning
✓ Asymptomatic patient
▪ Minimal corrosive ingestion
and no oropharyngeal
burns on examination
▪ Then the patient requires
only observation in the
Emergency Room
✓ Symptomatic patient
▪ 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
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Clinical Approach in Management of Symptomatic patient

✓ Protection of airway
In the presence of respiratory distress and airway edema,
urgent endotracheal intubation should be done
✓ Hemodynamic status
Hemodynamic correction can be done by replacement
with crystalloid fluids.

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✓ Decontamination
Nasogastric tube should not be inserted since it may cause
esophageal perforation and increase the risk of aspiration
✓ Dilution and neutralization :
- Neutralization is contraindicated
- Emetics are contraindicated because of re-exposition to the
corrosive substance leading to injury exacerbation.
- Activated charcoal is also contraindicated

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STABILIZED PATIENT

Proton
pump
Cortico- Antibio- inhibitors
Nutrition
steroids tics (PPIs) and
H2-
blockers:

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Corticosteroids

▪ While there is no role of systemic steroids in the

management of caustic ingestion, intralesional
steroids can be given

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Antibiotics

▪ Tissue destruction from caustic injury increases the

risk of infection by enteric organisms.
▪ Antibiotics are not recommended prophylactically in
corrosive poisoning.
▪ They are recommended in GI perforation.

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Nutrition

▪ Endoscopic grade of lesions needs to be assessed for planning

nutritional support.
▪ Patients with Grade 1/2a lesions on endoscopy can tolerate oral
feeds,
▪ Grade 2b/3a lesions will need nasoenteral feeding.
▪ Patients with Grade 3b lesions require gastrostomy for enteral
feeding and rarely need total parenteral nutrition (TPN)

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Surgery

Surgical intervention is indicated when there is a:

▪ Complete stenosis that cannot be treated with usual conservative
methods;
▪ Defect of the esophagus or stomach detected with x-ray
examination;
▪ Fistula formation.

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PROGNOSIS

▪ Prognosis in acute corrosive poisonings is variable and depends

on the degree of esophageal and gastric injury as well as on the
general health condition of the patient.
▪ The highest mortality rate has been recorded as a result of
perforation and mediastinitis.

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THANKYOU

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