Corrosive poisoning results from ingestion, topical exposure or inhalation of compounds that cause tissue injury as a result of chemical

reaction. 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% Of late there has been an increase in the incidence. About 80% of corrosive poisoning occurs in children < 5 yrs. Adult exposure has more mortality & morbidity due to significant volume of exposure & possible co-ingestion.

Alkali (pH>7): hair relaxer, laundry detergents, dishwasher (NaOH) Acids (pH<7): toilet bowl cleaner, battery fluid, and sulfuric acid Bleach (pH7): sodium hypochlorite

P H : Highly corrosive if PH is < 2 or > 11 CONCENTRATION USE: Intended for machinery use- Highly corrosive :Intended for Hand use- Mildly corrosive FORMULATION:Solid - Deep but localized injury :Liquid - Extensive injury AMOUNT INGESTED:> 100 -150ml - Massive poisoning

ACIDS They ppt proteincoag.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 occuring on 3 or 4th day. In the presence of food gastric injuries tend to be less severe and involve the lesser curveand pylorus

ALKALIS They saponify fats & dissolve proteins- liqufactive necrossis & 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. Superficial (Superficial to muscularis mucosa) 1% - Deep - 70-100%

Mucosal sloughing (4~7 days after initial injury)-bacterial invasion, inflammatory response Collagen deposition may not begin until the 2nd week, tensile strength of healing tissue is low during the first 3 weeks Scar retraction begins by the 3rd week, may continue for several months

depend upon type of substance, amount, and physical form of substances solid alkali adheres to mouth and pharynx- maximum damage, relatively sparing esophagus liquid form rapidly through mouth and pharynxgreatest effect on esophagus 10~30% patients with esophageal burns have no oropharyngeal damage 70% patients with oropharyngeal burns do not have significant damage to esophagus Injuries of oropharynx are not a reliable index of damage to esophagus

SYMPTOMS R.S: Dyspnea G.I: Dysphagia, Abd. Pain, Nausea & Vomiting, Haematemesis, Melena SIGNS Stridor, Drooling, Hoarseness, Dysphonia, S.C.Emphysema, Hammans sign,low B.P, Acute Peritonitis SYSTEMIC Anxiety, Agitation, Tacycardia

R.S : Laryngeal Edema SYSTEMIC : Met. Acidosis with anion gap : Meth. Hb - In phenol poisoning : Cardio vascular collapse :Haemolysis with Hyperkalemia : Pul. Edema : Hypovolumic shock : Aspiration :ARDS

Assess the identity, conc. and amount If sample available measure the PH with PH meter ENSURE AIRWAY PATENCY If in resp. distress - immediate ET If no resp. distress - Assess upper airway by direct FOL -If significant injury seen do ECG, ABG, CBC, LFT,RFT , X-RAY CHEST & ABDOMEN

Indication All symptomatic patients All Young Children even if asympt. All Patients who have intentionally ingested

Contraindication Obvious signs of a severe full-thickness esophageal or gastric necrosis with pleural irritation Mediastinal irritation Peritonitis Free air in the abdomen

performed between 24~48 hrs after injury, allowing time to manifest most information wound softening after 2~3 days and lasts up to 2 weeks (avoid endoscopy between days 5~15, increase danger of perforation) endoscope should be advanced until a circumferential 2rd degree burn or 3rd degree burn is seen, attempts to pastincrease risk of perforation

Grade 1: Erythema Grade 2(a): Superficial localized ulcer, Friable Erosion,Haem., Exudate. Grade 2(b)* :2(a) + Localized deep, discrete or circumferential ulcers Grade 3(a)*: Small Scattered areas of necrosis Grade 3(b) *: Extensive circumferential necrosis

CXR: air in mediastinum or under diaphragm (esophageal or gastric perforation) confirm perforation: water-soluble agent (hypaque or gastrograffin) or barium sulfate barium studies: evaluate progressive dysphagia to stricture formation

grade1: permit oral intake and discharge within days grade 2 or 3: nutritional support by parenteral or NG tube (blind passage increases risk of iatrogenic esophageal perforation) Grade 2: NPO 3-5 days Grade 3: NPO >one week

Grade 1: not necessary Grade 2: most effective Grade 3: surgery, risk of perforation Dosage: controversial, recommendation: 1~2 mg/kg/day, 3weeks

Antibiotics: prophylaxis: controversial Recommendation: withhold antibiotics until secondary infection

Intraluminal stent (silicone rubber) may be helpful in selected esophageal injuries patients (grade 2 or 3) long term outcome: unclear

(Endoscopic) dilatation / bougination Surgery :emergent surgery: perforation or shock, acidosis, coagulation disorder with ingested large amount of caustic agentimprove outcome : reconstruction: colon interposition

TO DO
IMM. DILUTION WITH PLAIN WATER 5ml/kg. SECURE AIRWAYPATENCY I.V.FLUIDS PROPHYLACTIC ABS H2 BLOCKERS SUCRALFATE 1gm/6hrs. MONITOR ACID BASE & ELECTROLYTES STATUS

NOT TO DO GASTRIC LAVAGE EMESIS NEUTRILIZATION ACTIVATED CHARCOAL CARBONATED DRINKS

Stricture formation (may contribute to formation of long stricture) Gastric outlet obstruction (less frequently than stricture) Esophageal carcinoma (1000~3000fold increase in the incidence, better prognosis)

Corrosive poison has got the highest mortality than any other poison Alkali are more dangerous Secure airway as soon as possible Endoscopy within 6-24hrs. to assess injury and further management Never forget the dos & donts Steroids controversial, still beneficial