Post on 11-Jan-2017
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CORROSIVE POISONING
DR.ASHWIN MENON
• 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
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.
CLASSIFICATION
THREE TYPES
ACIDSALKALIS
(Most dangerous)
OXIDANTS
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
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.
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
MECHANISM OF INJURY
ACIDS
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.
ALKALIS
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%
• 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
Chest radiograph of a child who has ingested a coin-shaped battery
SEQUELAE
• Lead to:– Oesophageal burn without perforation– Oesophageal burn with perforation– Tracheo oesophageal fistula– Aorto oesophageal fistula
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
LUNG TISSUE
RENAL TUBULAR NECROSIS
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
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
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.
4. Palpate for subcutaneous air
5. Rigidity and sub sternal chest pain
6. Assess for emesis. -Increased laryngeal/oesophageal exposure
MANAGEMENT
INVESTIGATIONS
1. Test the pH of the saliva. Neutral pH does NOT mean caustic ingestion did not occur.
2. Labs -CBC -ABG -Urine
3. CXR -Pneumomediastinum -Button battery4. KUB -Pneumoperitoneum -Button battery5. CT -Use water soluble contrast.6. Technetium 99m–labeled sucralfate study
INVESTIGATIONS
X ray neck- oesophageal perforation
Esophageal rupture with right pneumothorax with midline shift
Barium oesophagogram of a perforated esophagus. Arrow shows the extravasation of contrast into the left chest
CT scan of a perforated esophagus. Note the air andfluid in the mediastinum.
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.
ENDOSCOPY
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
• 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.
• 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.
Endoscopic view of the epiglottis and vocal cords 4 days after ingestion.
Endoscopic view of the epiglottis and vocal cords 11 days after ingestion.
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.
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
OesophagoscopyA. Grade 2A. B Grade 2B of stomach B. C 3A of stomach D. 3B of stomach
FOUR STAGES OF OESOPHAGEAL BURNS
VIDEO 1
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
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
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.
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.
PHARMACOLOGIC THERAPY
CALMS
Corticosteroid
Antibiotics
Lathyrogenic agents-β-aminopropionitrile, N-acetylcysteine, and penicillamineMitomycin
Sucralfate
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.
• 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
SELF EXPANDING STENT
VIDEO 2
• Mild strictures can be serially dilated in a prograde fashion through an oesophagoscope with filiform dilators.
• Fluoroscopic guided balloon catheter dilation for acquired strictures has shown little success.
VIDEO 3
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).
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
• 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.
• 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.
BILLROTH 1
Heineke-Mikulicz Pyloroplasty
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
TREA
MEN
T AL
GORI
THM
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.
• 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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