CAUSTIC INGESTION ACID FORMULATIONS HOUSEHOLD USES Toilet bowel
CAUSTIC INGESTION
ACID FORMULATIONS HOUSEHOLD USES Toilet bowel cleaners : sulfuric acid, oxalic acid, carbolic acid Hydro chloric acid, Na bisulphate Drain cleaners : Sulfuric acid Antirust compounds : Phosphoric acid, oxalic acid, Hydrochloric acid, sulfuric acid, chromic Gun bluing agents : Selenious acid Soldering fluxes : Zinc chloride, Hydrochloric acid Automobile battery : Sulfuric acid
ALKALI FORMULATIONS Automatic dishwasher – Na metasilicate, detergents Na tripoly. PO 4, Na Carbonate, Clinitest tablets -- Cu sulphate, citric acid, Na hydroxide, Na carbonate Oven cleaners -- Na hydroxide Bleach products – Na hypochlorite, Na carbonate Metal cleaners, paint removers, washing powders
OXIDIZING AGENTS Calcium hypochlorite, hydrogen peroxide, sodium hypochlorite, troclosene sodium and sodium perborate Oxygen may kill bacteria, and damage living tissue.
PATHOPHYSIOLOGY Basic cause for injury by either acid or alkali is altering the ionized state, structure of the molecule and disrupting the covalent bonds Acid causes by hydronium (H +)ions Alkali does injury by hydroxide (OH) ions
PATHOPHYSIOLOGY ACIDS DENATURE PROTEINS COAGULATION NECROSIS COAGULUM & ESCHAR ALKALIS SAPONIFICATION OF FAT SOLUBILISATION OF PROTEINS LIQUIFACTION NECROSIS DEEP PENETRATION PREVENTS DEEP PENETRATION PERFORATION & STRICTURE
CLINICAL FEATURES Acids - Stomach Alkali - Pharynx, hypopharynx, esophagus No correlation between oral injury and internal injury Dysphagia, drooling, vomiting, haemetemesis, pain and melaena Hoarseness, stridor and laryngitis indicate impending airway compromise. Perforation – CV collapse, peritonitis Significant amount of acid ingestion cause metabolic acidosis, hemolysis and renal failure.
PHENOL POISONING Less corrosive Damages kidney, liver and lung edema It can cause metabolic acidosis and cardiac depression Seizures and unconsciousness
GRADING OF INJURY Grade 1 – Superficial mucosal injury Grade 2 A – Transmucosal injury B – Deep isolated lesions Grade 3 – Full thickness transmural necrosis
APPROACH HISTORY EXTERNAL MARKER X– RAY CHEST & ABDOMEN ROUTINE INVESTIGATIONS ABG ENDOSCOPY 1. 12 --24 hrs. may be upto 48 hrs. 2. Determine time to oral feeding and estimation of the risk of stricture& perforation
TREATMENT Secure airway. If there is stridor or not able to visualize vocal cards, go for tracheostomy. I. V. access & fluids Thorough washing of Skin & Eye Dilution with milk or water can be tried in cases of solid or granular alkali not in acid or liquid alkali. Dilution is currently not routinely recommended as they induce emesis, obsucer OGD evaluation and increased luminal pressure causing perforation
TREATMENT ORAL FEEDING 1 st degree – 1 st day 2 A degree – 2 -3 day 2 B & 3 rd degree – Feeding jejunostomy Antibiotics Reserved for documented infection
CORTICOSTERIODS Believed to attenuate the inflammation thereby reducing the stricture formation Some animal studies showed benefits. However, metanalysis in 1991 and 2004 revealed no benefit of steriods and recommends abandonment of this practice.
MEDICAL PITFALLS Failure to evaluate and aggressively manage the airway. Attempting to neutralize the ingested caustic agent with a weak acid or alkaline agent Inducing emesis Assuming that the absence of oropharyngeal burns precludes the presence of significant distal injuries
SPECIFIC TREATMENT Acetic acid – DIC - Cryoprecipitate, FFP Formic acid - 12 th hrly Folinic acid 50 mg. I. V. bolus followed by 1 mg/kg Phosphoric acid PO 4 binders , I. V. glucose, Hydration with normal saline Hydrofluoric acid - I. V. 10% Ca gluconate 10 ml. Then oral Ca tablets 0. 5 gms.
COMPLICATIONS Mediastinitis, pericarditis, pleuritis, tracheoesophageal fistula formation, esophageal-aortic fistula formation, and peritonitis. Delayed perforation - 4 days after an acid exposure Strictures develop 2 -4 weeks postingestion. Gastric outlet obstruction may develop 3 -4 weeks after an acid exposure. Delayed upper GI bleeding may occur in acid burns 3 -4 days after exposure as the eschar sloughs. Long-term risks include squamous cell carcinoma, which occurs in 1 -4 years.
FUTURE TRENDS Focusing on antioxidant treatment like vitamin E to prevent esophageal strictures. Ketotofen (mast cell stabilizer) Phsophatidylcholine which stimulates collagenase activity to prevent excess collagen formation
ETHANOL POISONING Median lethal dose 5 -8 g/kg whiskey-40 -60%; wine- 8 -16%; rum 40 -60% and beer- 3 -7% APPROACH 1. H/o intake & clinical features. 2. Rule out other associated poisonings 3. Look for any injuries like SDH, EDH 4. Ethanol level in all secretions 5. ABG, osmolol gap, anion gap, glucose , electrolytes.
LEVELS & EFFECTS Intoxication or inebriation - 100 -150 mg/dl Loss of muscle coordination - 150 -200 mg/dl Decreased level of consciousness - 200 -300 mg/dl Death - 300 -500 mg/dl
CLINICAL FEATURES CNS: Depression, disinhibition, ataxia, slurred speech, seizures and unconsciousness CVS: Myocardial depression, hypotension, arrhythmias, cardiovascular collapse RS: Depression, aspiration pneumonitis, pul. edema. ABD: Gastritis, pancreatitis, UGI bleeding Metabolic : hypoglycemia, lactic acidosis
TREATMENT 1. 2. 3. 4. 5. 6. 7. Secure airway I. V. access 100 mg. Thiamine I. V. followed by 50 ml. 50% dextrose in comatose pts. Gastric lavage – within 1 hr. Activated charcoal – Coingestants. Alcoholic ketoacidosis – D. N. S. with thiamine and K+ supplements. Hemodialysis
METHANOL Components Anti-freeze Fuel - Gas line & wind shield fluid - Small hobby machines, Camp stoves Solvents - Paint removers, varnishes Canned fuel , Photocopy fluid. Toxic dose – 40 gms. lethal dose
PHARMACOKINETICS After ingestion, peak level 30 -90 mins. 2. Hepatic metabolism 3. Half life is 30 hrs. With ethanol 52 hrs. ADH Methanol Formaldehyde 1. Formic acid H 4 Folate CO 2 + H 2 O
CLINICAL FEATURES 1. 2. 3. 4. 5. 6. Effects begin within 1 hr. of ingestion. FORMIC ACID is the main culprit CNS depression, confusion, altered sensorium, ataxia, seizures and unconsiousness. Blurring of vision, diplopia, alteration of colour perception, dilated pupil and absent pupillary response G. I. & Myocardial depression. Sometimes Parkinsonism after long time due to its predilection for basal ganglia.
DIAGNOSIS Ideal is serum methanol level H/O intake & clinical features ABG , anion gap, osmolol gap, electrolytes, renal function tests, CBC.
TREATMENT GENERAL 1. Induced emesis is not recommended. 2. Secure airway, I. V. access 3. NG suction – 30 mins. 4. p. H < 7. 3, give Na. HCO 3
Na. HCO 3 THERAPY Calculating Requirement (meq) : (15 – HCO 3 level) X Wt. (Kg) X 1 50 % of calculated amount as bolus 50 % in 5% D in 4 hours 8. 4 % solution – 1 meq Na & HCO 3 / ml 7. 5 % solution – 0. 892 meq Na & HCO 3 / ml
ANTIDOTES Alcohol METHANOL FORMALDEHYDE dehydrogenase ETHANOL FOMIPEZOLE FORMIC ACID
INDICATIONS Any one of the following 1. Serum methanol >20 mg/dl 2. Documentation of ingestion and residual osmolar gap >10 mmol 3. Suspected ingestion with 2 of the following : Arterial p. H <7. 3 Serum bicarbonate <20 mmol/l Osmolar gap >10 mmol
DOSE OF ETHANOL Plasma level should be 100 -130 mg/dl. Novice Ch. Alcoholic drinker BOLUS 750 – 1000 mg/kg Maintanance dose 66 mg/kg/hr 154 mg/kg/hr During dialysis 169 mg/kg/hr 257 mg/kg/hr It can be given either 10% I. V. or 40% per oral
MONITORING 1. Respiratory depression – ventilatory support 1. Hypoglycemia – Glucose infusion with thiamine 1. Cardiovascular dysfunction 1. Concurrent use of disulfiram like drugs
FOMIPEZOLE 15 mg/kg I. V. – Loading dose 10 mg/kg I. V. 12 th hrly 4 doses 15 mg/kg I. V. to counteract metabolism Lesser side effects. Costlier Indications to stop 1. Methanol <20 mg/L 2. Normal arterial p. H
COFACTOR THERAPY Alcohol Methanol Formaldehyde dehydrogenase Formic acid H 4 Folate CO 2 + H 2 O Folinic acid 1 mg/kg to max. of 50 mg/kg Folic or folinic acid 50 mg 4 th hrly
DIALYSIS High flux Hemodialysis >Peritoneal dialysis Indications 1. Significant metabolic acidosis p. H <7. 25 -7. 30 2. Abnormalities of vision 3. Deterioration of vital signs despite intensive care 4. Renal failure 5. Electrolyte imbalance 6. Serum methanol >50 mg/dl
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