corrosive poisoning by dr.ashwin menon
TRANSCRIPT
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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 …