Corrosive poisoning by Dr.Ashwin Menon

Otorhinolaryngological aspect of corrosive poisoning.

1. CORROSIVE POISONING DR.ASHWIN MENON

2. 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

3. 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.

4. CLASSIFICATION

5. 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

6. 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.

7. 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

8. MECHANISM OF INJURY

9. ACIDS

10. 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.

11. ALKALIS

12. 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 . Superficial (Superficial to muscularis mucosa ) 1 % Deep - 70-100 %

13. 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

14. C hest radiograph of a child who has ingested a coin-shaped battery

15. SEQUELAE Lead to: Oesophageal burn without perforation Oesophageal burn with perforation Tracheo oesophageal fistula Aorto oesophageal fistula

16. 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

17. LUNG TISSUE

18. RENAL TUBULAR NECROSIS

19. 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

20. 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

21. MANAGEMENT Accurate history defining what and amount of ingestion occurred. ABCs Treat like a burn 3. Evaluate for hoarseness, stridor, drooling, odynophagia, refusal of food.

22. 4. Palpate for subcutaneous air 5. Rigidity and sub sternal chest pain 6. Assess for emesis. -Increased laryngeal/oesophageal exposure MANAGEMENT

23. INVESTIGATIONS 1. Test the pH of the saliva. Neutral pH does NOT mean caustic ingestion did not occur. 2. Labs -CBC -ABG -Urine

24. 3. CXR - Pneumomediastinum -Button battery 4. KUB - Pneumoperitoneum -Button battery 5. CT -Use water soluble contrast . 6. T echnetium 99m– labeled sucralfate study INVESTIGATIONS

25. X ray neck- oesophageal perforation

26. Esophageal rupture with right pneumothorax with midline shift

27. Barium oesophagogram of a perforated esophagus. Arrow shows the extravasation of contrast into the left chest

28. CT scan of a perforated esophagus. Note the air and fluid in the mediastinum.

29. Lesion in the gastric antrum (arrows) demonstrated by x-ray S cintigraphy - Note retention in area of the lesion on both 1-hr and 2-hr images. Uptake in fundus of stomach is also persistent although no pathology existed in this area.

30. ENDOSCOPY

31. When to perform? -Optimally performed 6 - 24 hrs. W hy ? -Because if performed earlier the full extent of the 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

32. 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.

33. 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.

34. Endoscopic view of the epiglottis and vocal cords 4 days after ingestion. Endoscopic view of the epiglottis and vocal cords 11 days after ingestion.

35. 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 .

36. 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 or circumferential ulcers GRADE 3(a)* Small Scattered areas of necrosis GRADE 3(b)* Extensive circumferential necrosis * Lead to Strictures

37. Oesophagoscopy Grade 2A. B Grade 2B of stomach C 3A of stomach D. 3B of stomach

38. FOUR STAGES OF OESOPHAGEAL BURNS

39. VIDEO 1

40. 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. Later Develop into Strictures

41. 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

42. 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 .

43. 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.

44. PHARMACOLOGIC THERAPY CALMS Corticosteroid Antibiotics Lathyrogenic agents - β- aminopropionitrile , N- acetylcysteine , and penicillamine Mitomycin Sucralfate

45. 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 .

46. Other types of stents used are polymeric silicone tubes in the oesophagus. The important type of stents that are available on the market are Polyflex Ultraflex Z stent Bonastent

47. SELF EXPANDING STENT

48. VIDEO 2

49. Mild strictures can be serially dilated in a prograde fashion through an oesophagoscope with filiform dilators.

50. Fluoroscopic guided balloon catheter dilation for acquired strictures has shown little success .

51. VIDEO 3

52. 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).

53. A) Barium swallow shows mid-oesophageal stricture after alkaly ingestion in an adolescent 4 weeks after ingestion and at the beginning 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

54. 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.

55. 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.

56. BILLROTH 1

57. Heineke-Mikulicz Pyloroplasty

58. 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

59. TREAMENT ALGORITHM

60. 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.

61. 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

62. THANK YOU …