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Caustic Ingestion: Acid & Alkali Dangers, Treatment, and Complications

Explore the dangers, pathophysiology, treatment, and complications of caustic ingestion involving acids and alkalis. Learn about grading of injuries, medical pitfalls, specific treatments, and future trends.

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Caustic Ingestion: Acid & Alkali Dangers, Treatment, and Complications

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  1. CAUSTIC INGESTION

  2. 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 • INDUSTRIAL USES Above said acids + Hydro fluoric acid

  3. ALKALI FORMULATIONS • Automatic dishwasher – Na metasilicate, detergents Na tripolyPO4, 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

  4. OXIDIZING AGENTS • Calcium hypochlorite, hydrogen peroxide, sodium hypochlorite, troclosene sodium and sodium perborate • Oxygen may kill bacteria, and damage living tissue.

  5. 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

  6. PATHOPHYSIOLOGY ALKALIS SAPONIFICATION OF FAT SOLUBILISATION OF PROTEINS LIQUIFACTION NECROSIS DEEP PENETRATION PERFORATION & STRICTURE ACIDS DENATURE PROTEINS COAGULATION NECROSIS COAGULUM & ESCHAR PREVENTS DEEP PENETRATION

  7. 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 can cause metabolic acidosis, hemolysis and renal failure.

  8. PHENOL POISONING • Less corrosive • Damages kidney, liver and lung edema • It can cause metabolic acidosis and cardiac depression • Seizures and unconsciousness

  9. GRADINGOF INJURY Grade 1 – Superficial mucosal injury Grade 2 A – Transmucosal injury B – Deep isolated lesions Grade 3 – Full thickness transmural necrosis

  10. 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

  11. 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

  12. TREATMENT • ORAL FEEDING 1st degree – 1st day 2A degree – 2-3 day 2B & 3rd degree – Feeding jejunostomy • Antibiotics Reserved for documented infection

  13. 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.

  14. 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

  15. SPECIFIC TREATMENT • Acetic acid – DIC - Cryoprecipitate,FFP • Formic acid - Folinic acid 50 mg. I.V. bolus followed by 1mg/kg 12th hrly • Phosphoric acid - PO4 binders , I.V. glucose, Hydration with normal saline • Hydrofluoric acid - I.V. 10% Ca gluconate 10ml. Then oral Ca tablets 0.5gms.

  16. 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.

  17. 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

  18. ETHANOL POISONING • Median lethal dose 5-8g/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.

  19. 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

  20. 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

  21. TREATMENT Secure airway I.V. access 100mg. Thiamine I.V. followed by 50ml. 50% dextrose in comatose pts. Gastric lavage – within 1 hr. Activated charcoal – Coingestants. Alcoholic ketoacidosis – D.N.S. with thiamine and K+ supplements. Hemodialysis

  22. METHANOL • Components Anti-freeze - Gas line & wind shield fluid Fuel - Small hobby machines, Camp stoves Solvents - Paint removers, varnishes Canned fuel , Photocopy fluid. Toxic dose – 40 gms. lethal dose

  23. PHARMACOKINETICS • After ingestion, peak level 30-90 mins. • Hepatic metabolism • Half life is 30 hrs. With ethanol 52 hrs. ADH Methanol Formaldehyde Formic acid H4 Folate CO2 + H2O

  24. CLINICAL FEATURES 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.

  25. DIAGNOSIS • Ideal is serum methanol level • H/O intake & clinical features • ABG , anion gap, osmolol gap, electrolytes, renal function tests, CBC.

  26. TREATMENT • GENERAL 1. Induced emesis is not recommended. 2. Secure airway, I.V. access 3. NG suction – 30 mins. 4. pH < 7.3, give NaHCO3

  27. NaHCO3 THERAPY Calculating Requirement (meq) : (15 – HCO3 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 & HCO3 / ml 7.5 % solution – 0.892 meq Na & HCO3 / ml

  28. ANTIDOTES METHANOL ETHANOL FOMIPEZOLE FORMALDEHYDE Alcohol dehydrogenase FORMIC ACID

  29. INDICATIONS Any one of the following 1. Serum methanol >20mg/dl 2. Documentation of ingestion and residual osmolar gap >10mmol 3. Suspected ingestion with 2 of the following : Arterial pH <7.3 Serum bicarbonate <20mmol/l Osmolar gap >10mmol

  30. DOSE OF ETHANOL • Plasma level should be 100-130 mg/dl. NoviceCh. Alcoholic drinker BOLUS 750 – 1000 mg/kg Maintanance dose 66mg/kg/hr 154mg/kg/hr During dialysis 169mg/kg/hr 257mg/kg/hr It can be given either 10% I.V. or 40% per oral

  31. MONITORING Respiratory depression – ventilatory support Hypoglycemia – Glucose infusion with thiamine Cardiovascular dysfunction Concurrent use of disulfiram like drugs

  32. FOMIPEZOLE 15 mg/kg I.V. – Loading dose 10 mg/kg I.V. 12th hrly 4 doses 15 mg/kg I.V. to counteract metabolism Lesser side effects . Costlier Indications to stop 1. Methanol <20mg/L 2. Normal arterial pH

  33. COFACTOR THERAPY Folinic acid 1mg/kg to max. of 50mg/kg Folic or folinic acid 50mg 4th hrly Alcohol dehydrogenase Methanol Formaldehyde Formic acid H 4 Folate CO2 + H2O

  34. DIALYSIS • High flux Hemodialysis >Peritoneal dialysis • Indications 1. Significant metabolic acidosis pH <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 >50mg/dl

  35. THANK YOU

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