Otorhinolaryngological aspect of corrosive poisoning.

2. CORROSIVE POISONING
DR.ASHWIN MENON

3. • 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

4. 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.

5. CLASSIFICATION
THREE
TYPES
ACIDS
ALKALIS
(Most
dangerous)
OXIDANTS

6. 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

7. 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.

8. 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

9. MECHANISM OF INJURY

10. ACIDS

11. 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.

13. ALKALIS

14. 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%

15. • 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

16. Chest radiograph of a
child who has ingested a
coin-shaped battery

17. SEQUELAE
• Lead to:
– Oesophageal burn without perforation
– Oesophageal burn with perforation
– Tracheo oesophageal fistula
– Aorto oesophageal fistula

18. 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

19. LUNG TISSUE

20. RENAL TUBULAR NECROSIS

22. 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

24. 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

26. 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.

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

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

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

30. X ray neck- oesophageal perforation

31. Esophageal rupture with right pneumothorax with
midline shift

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

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

34. Lesion in the gastric
antrum (arrows)
demonstrated by x-ray
Scintigraphy - 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.

35. ENDOSCOPY

36.  When to perform?
-Optimally performed 6 - 24 hrs.
 Why?
-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

37. • 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.

38. • 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.

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

40. 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.

41. 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

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

43. FOUR STAGES OF OESOPHAGEAL BURNS

44. VIDEO 1

45. 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

47. 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

48. 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.

49. 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.

50. PHARMACOLOGIC
THERAPY
C
A
L
M
S
Corticosteroid
Antibiotics
Lathyrogenic agents-β-aminopropionitrile, N-
acetylcysteine, and penicillamine
Mitomycin
Sucralfate

51. 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.

52. • Other types of stents used are polymeric silicone
tubes in the oesophagus.
• The important type of stents that are available on the
market are
1. Polyflex
2. Ultraflex
3. Z stent
4. Bonastent

53. SELF EXPANDING STENT

56. VIDEO 2

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

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

59. VIDEO 3

60. 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).

63. 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

64. • 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.

66. • 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.

67. BILLROTH 1

68. Heineke-Mikulicz Pyloroplasty

69. 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

70. TREAMENTALGORITHM

71. 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.

72. • 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

73. THANK YOU …