Corrosive poisoning by Dr.Ashwin Menon

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Transcript of Corrosive poisoning by Dr.Ashwin Menon

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CORROSIVE POISONING

DR.ASHWIN MENON

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• An average home contains a dozen different cleaning products. These are responsible for a large number of accidental and intentional poisoning.

• Incidence :- 2.5 - 5%• Mortality :- 13%• Morbidity :- > 50%• About 80% of corrosive poisoning occurs in children < 5

yrs.

INTRODUCTION

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INTRODUCTION

• The route of entry of corrosive substances in the body is:

– ingestion– inhalation (rarely)

• Adult exposure has more mortality & morbidity due to significant volume of exposure & possible co-ingestion.

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CLASSIFICATION

THREE TYPES

ACIDSALKALIS

(Most dangerous)

OXIDANTS

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FACTORS DETERMINING CORROSIVENESS

Factors that determine corrosiveness include:

• Physical form: Solid/liquid

• Duration of contact with tissue

• Concentration of agent

• Quantity of agent > 100 -150ml - Massive poisoning

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FACTORS DETERMINING CORROSIVENESS

• pH of agent: pH <2 and >11 are morevcorrosive

• 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.

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EXAMPLES

ACIDS

• SULPHURIC ACID - CAR BATTERIES• NITRIC ACID – METAL CLEANERS• HYDROCHLORIC ACID & ACETIC ACID -DESCALERS• PHENOL & BORIC ACID -DISINFECTANT• HYDROFLUORIC & OXALIC ACID – RUST REMOVERS

ALKALIS

• AMMONIA – HOUSE HOLD CLEANERS & LAUNDARY DETERGENTS• BLEACH – DISINFECTANT• SODIUM HYDROXIDE - DRAIN CLEANERS

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MECHANISM OF INJURY

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ACIDS

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ACIDS

• They ppt protein → Coag.→ Necrosis • Coagulum forms a barrier and limits further damage.• Sq. epithelium of pharynx and oesophagus are resistant

to acids.• Stomach (Antrum) is the most commonly involved

organ.• Most common complication is perforation occurring on

3 or 4th day.• In the presence of food gastric injuries tend to be less

severe and involve the lesser curve and pylorus.

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ALKALIS

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ALKALIS

• They saponify fats & dissolve proteins → liquifactive necrosis & rapid injury.

• Sq. epithelium of pharynx and oesophagus (lower half) are the most commonly affected parts.

• Most common complication is stricture - 2 to 4 weeks.– Development of stricture depends on the depth of the burns.

o Superficial (Superficial to muscularis mucosa) 1%o Deep - 70-100%

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• Disk shaped batteries are easily swallowed but if they get lodged in the oesophagus, they cause injury by – – Leakage of alkali : direct caustic injury– Absorption of toxic substances– Pressure necrosis– Electrical discharge → Mucosal burns

ALKALIS

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Chest radiograph of a child who has ingested a coin-shaped battery

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SEQUELAE

• Lead to:– Oesophageal burn without perforation– Oesophageal burn with perforation– Tracheo oesophageal fistula– Aorto oesophageal fistula

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HISTOPATHOLOGIC EVENTS ASSOCIATED WITH 10% SODIUM HYDROXIDE BURN OF

OESOPHAGEAL MUCOSA

• Oedema of submucosa• Inflammation of submucosa with thrombosis• Sloughing of the superficial layers• Necrosis of the muscular layer• Fibrosis of the deep layers• Delayed re-epithelialization

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LUNG TISSUE

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RENAL TUBULAR NECROSIS

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CLINICAL FEATURES

GIT

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

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Respiratory system• Cough• Dyspnea• Bronchoconstriction• Pulmonary oedema• Chemical pneumonitis

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

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MANAGEMENT

1. Accurate history defining what and amount of ingestion occurred.

2. ABCs– Treat like a burn

3. Evaluate for hoarseness, stridor, drooling, odynophagia, refusal of food.

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4. Palpate for subcutaneous air

5. Rigidity and sub sternal chest pain

6. Assess for emesis. -Increased laryngeal/oesophageal exposure

MANAGEMENT

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INVESTIGATIONS

1. Test the pH of the saliva. Neutral pH does NOT mean caustic ingestion did not occur.

2. Labs -CBC -ABG -Urine

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3. CXR -Pneumomediastinum -Button battery4. KUB -Pneumoperitoneum -Button battery5. CT -Use water soluble contrast.6. Technetium 99m–labeled sucralfate study

INVESTIGATIONS

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X ray neck- oesophageal perforation

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Esophageal rupture with right pneumothorax with midline shift

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Barium oesophagogram of a perforated esophagus. Arrow shows the extravasation of contrast into the left chest

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CT scan of a perforated esophagus. Note the air andfluid in the mediastinum.

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Lesion in the gastric antrum (arrows) demonstrated by x-ray

Scintigraphy - Note retention inarea of the lesion on both 1-hr and 2-hr images.

Uptake in fundus of stomach is also persistent although no pathologyexisted in this area.

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ENDOSCOPY

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When to perform?-Optimally performed 6 - 24 hrs.

Why?-Because if performed earlier the full extent ofthe injury may not be apparent.-If performed later the risk of the perforation is high (especially with rigid endoscopy)

• First assess the cricopharynx and then larynx If burns are noted prophylactic ET.

ENDOSCOPY

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• Where Oesophagoscopy should not be performed?

– haemodynamically unstable patients.– evidence of GI perforation.– Patients with significant airway oedema.

• If the patient presents >48 hours after initial ingestion, barium swallow may be considered instead of Oesophagoscopy.

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• Anatomical areas of narrowing oftentimes receive the most damage-

-Cricopharyngeal area (UE)-Aortic arch-LES-Antrum/body of stomach

• These are also the most common sites of stricture formation.

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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.

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ENDOSCOPIC GRADING-KIKENDALL 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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ENDOSCOPIC GRADING -ZARGAR’S CLASSIFICATION

GRADE 1 Erythema

GRADE 2(a) Superficial localized ulcer, Friable Erosion,Haemorrhage, Exudate.

GRADE 2(b)* 2(a) + Localized deep, discrete orcircumferential ulcers

GRADE 3(a)* Small Scattered areas of necrosis

GRADE 3(b)* Extensive circumferential necrosis

* Lead to Strictures

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OesophagoscopyA. Grade 2A. B Grade 2B of stomach B. C 3A of stomach D. 3B of stomach

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FOUR STAGES OF OESOPHAGEAL BURNS

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VIDEO 1

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CINE - OESOPHAGOGRAPHY• Detects motility disorders

• Atonic rigid oesophagus• Atonic dilated oesophagus • Abnormal un co-ordinated contractions

*Cine Oesophagram is a video version of Barium Swallow.

LaterDevelop intoStrictures

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TREATMENT

TO DO:

IMM. DILUTION WITH PLAIN WATER 5ml/kg.

SECURE AIRWAY I.V.FLUID PROPHYLACTIC AB’S H2 BLOCKERS SUCRALFATE 1gm/6hrs. MONITOR ACID BASE & ELECTROLYTES

STATUS.

NOT TO DO:

GASTRIC LAVAGE EMESIS NEUTRILIZATION ACTIVATED

CHARCOAL CARBONATED DRINKS

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WHY – NOT TO DO?

GASTRIC LAVAGE : Risk of perforation(Immediate lavage within 1-2 hrs. after large

volume of ingestion is beneficial)

EMESIS : Leads to new exposure and risk of aspiration.NEUTRILIZATION : Leads to heat production more

injury.

ACTIVATED CHARCOAL : Obscures endoscopic view.

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STEROIDS?

Role of steroids controversial.• Animal studies have proven to be beneficial, but human evidence lacking.

Local injection of TRIAMCINOLONE is also beneficial.• Steroids definitely have a role in preventing laryngeal oedema.

- Prednisolone 1 - 2mg/kg/6 hrly. for 2 weeks.- Contraindicated if perforation.

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PHARMACOLOGIC THERAPY

CALMS

Corticosteroid

Antibiotics

Lathyrogenic agents-β-aminopropionitrile, N-acetylcysteine, and penicillamineMitomycin

Sucralfate

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MECHANICAL THERAPY

• The simplest mechanical method for maintaining a lumen in a third degree oesophageal burn is to place a nasogastric tube at the time of initial endoscopy.

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• Other types of stents used are polymeric silicone tubes in the oesophagus.

• The important type of stents that are available on the market are1. Polyflex2. Ultraflex3. Z stent4. Bonastent

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SELF EXPANDING STENT

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VIDEO 2

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• Mild strictures can be serially dilated in a prograde fashion through an oesophagoscope with filiform dilators.

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• Fluoroscopic guided balloon catheter dilation for acquired strictures has shown little success.

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VIDEO 3

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ENDOSCOPIC LUMEN RESTORATION (ELR)

• Multiple strictures are managed most safely with retrograde dilators, popularized by Tucker.

• ELR is best accomplished by a multidisciplinary approach including an experienced gastroenterologist/endoscopist, an otolaryngologist, and a swallowing therapist (speech pathologist).

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A) Barium swallow shows mid-oesophageal stricture afteralkaly ingestion in an adolescent 4 weeks after ingestion and at thebeginning of retrograde dilations.

B) Same patient 5 years later, after 4 years of repetitive dilations; the patient has a stable stricture and is generally non symptomatic.

A B

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• Esophageal replacement with gastric tubes, right colon, transverse colon, or descending colon has been described.

• The right colon has been reported to be the most useful conduit.

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• Gastric outlet obstruction as a complication of acid ingestion is well known.

• Presenting symptoms include – frequent non-bilious emesis– secondary marked weight loss.

Treatment is surgical and includes -Gastro-jejunostomy or Billroth I for complete

obstruction -The Finney or Heineke Mikulicz pyloroplasty for partial obstruction.

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BILLROTH 1

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Heineke-Mikulicz Pyloroplasty

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ORAL FEEDING, WHEN TO START?

GRADE-1 INJURIES ON ENDOSCOPY- DAY 1

GRADE-2 INJURIES ON ENDOSCOPY- LIQUID FOODS AFTER 48-72 Hrs.

GRADE-3 INJURIES- NIL ORAL- FEEDING JEJUNOSTOMY /TPM

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TREA

MEN

T AL

GORI

THM

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CONCLUSION

• With corrosive poisoning the injury ranges from minimal mucosal erythema to frank transmural necrosis of the oesophagus and stomach with viscous perforation.

• Full length oesophageal endoscopy is the most accurate initial method of examination, and is indicated after any ingestion of a strong liquid alkali.

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• Oesophageal stricture formation is the chief long-term complication with a potential devastating impact on quality of life. Although repetitive stricture dilations are the mainstay of management, prevention or reduction in the severity of this complication is promising.

CONCLUSION

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THANK YOU …