drtbalu's important topics in otolaryngology

Caustic injuries to aerodigestive tract

Introduction: Cause for caustic injury to aerodigestive tract is from accidental / suicidal ingestion of caustic agents. Chevalier Jackson in order to prevent accidental ingestion of caustic agents lobbied for special labeling of bottles containing caustic agents. He was instrumental in bringing legislation mandating lower concentrations of certain caustic agents for retail consumption. He was instrumental in bringing the “safe packaging act” which made it mandatory on the part of manufacturers of caustic agents to package them in bottles which had child proof lids. The introduction of liquid based caustic agents has increased the amount of mucosa that could be injured with one swallow versus the damage caused by solid caustic agents.

 Morbidity and mortality from caustic oesophageal burns has decreased during the past century. This is due to improvements in the field of diagnostic imaging, common availability of endoscopes, and development of safe stricture dilatation techniques. Currently mortality rates due to caustic injuries to oesophagus ranges between 20 – 30%. 

Classification of agents responsible for caustic injury to oesophagus:

1. Caustic agents / alkali (pH greater than 7) – Lime, Laundry detergents etc.
2. Corrosives / acids (pH less than 7) – Toilet cleaner, Battery fluid etc.
3. Bleaches (pH approximately 7) – Sodium hypochlorite

This classification is mandated by the fact that the lesions caused by these groups of agents vary histologically. The caustic agents cause liquefaction necrosis on coming into contact with oesophageal mucosa and these patients are more prone for perforating lesions because the disintegration of mucosa causes deep penetrative damage to underlying tissues. Corrosive agents on the other hand cause coagulation necrosis. This process forms coagulum on the mucosa thereby protecting the deeper tissues of oesophagus from further damage. Corrosives very rarely cause perforating lesions. When the corrosive agents reach the stomach the acid pH inside the stomach can heighten the injury. Hence gastric stricture / perforation are common in acid ingestion than alkali ingestion. The unpleasant taste of acid causes the patient to gag early during the process of swallowing causing spill over to occur in the epiglottis causing chemical epiglottitis. This condition should be identified very early and if necessary air way should be secured by performing tracheostomy on the individual. 

 Bleaches have a neutral pH and are mild irritant to the oesophagus. In fact studies have shown that a large proportion of patients who had ingested bleaches have shown no significant morbidity / mortality. These patients need not undergo extensive work up also.

Clinical features:

 Childhood accidental ingestions of caustic agents occur commonly in patients under the age of 5. This infact limits the physician’s ability to obtain accurate history. It should also be borne in mind that all suspected cases should undergo complete examination to rule out oesophageal / gastric damage.  Patients with absent / minimal oral mucosal injuries should also be extensively investigated. 

Indicators of oesophageal injury:

1. Thoraco abdominal pain
2. Tachycardia
3. Hypotension
4. Retrosternal pain
5. Dysphagia

Presence of hoarseness of voice / stridor should warn the physician of laryngeal / tracheal damage.

Diagnostic endoscopy: Should be performed between 24 – 48 hours after injury. This time frame allows injury to manifest itself and instrumentation could be avoided during the period of oesophageal weakness. Endoscopy will help in accurately visualizing the lesions of oesophagus and stomach. 

Endoscopic classification of oesophageal burns:

First degree – Non ulcerative oesophagitis, mild erythema, and mucosal oedema.

Second degree – Whitish exudate, erythema, underlying ulcer extending up to muscularis.

Third degree – Dusky / blackened transmural tissue damage, ulceration extending into peri oesophageal tissue, the oesophageal lumen may be obliterated.

Role of Ba swallow: This is very useful in verifying perforation, evaluation of progressive Dysphagia. This is one sure way of identifying strictures involving oesophagus. 

Treatment:

1. Judicious use of diluting agents like water and milk in large volumes.
2. Fluid intake should be not more than 15 ml /kg body weight. Excessive ingestion of fluids may cause vomiting which is hazardous in these patients.
3. Gastric lavage and induced vomiting are contraindicated in these patients.
4. Administration of neutralizing agents should be condemned as this could lead to more damage due to exothermic reaction.
5. Steroid administration is indicated in patients with grade II oesophagitis. This is aimed to decrease stricture formation. Superficial / Grade I oesophagitis do not progress to stricture formation and hence need not be treated aggressively. Prednisolone is administered in doses of 1-2mg/kg/day. Maximum permissible dose is 60 mg prednisolone per day. This regimen should be continued for 21 days and tapered during a further duration of 2 weeks. 
6. Lathyrogenic agents are known to reduce collagen cross binding and hence have been used to decrease oesophageal strictures. Agents used include Beta aminopropionitrile, acetyl cysteine and penicillamine. 
7. The injured oesophageal wall should be protected against the deleterious effects of gastric acid secretion. Sucralfate has been successfully used in these patients. 
8. Surgery is reserved for grade III injuries only.
9. Strictures any should be dilated

Complications of caustic ingestion:

1. Stricture
2. Oesophageal perforation – Blind passage of naso gastric tube increases the chances of oesophageal perforation
3. Tracheo oesophageal fistula
4. Gastric perforation
5. Mediastinitis
6. Peritonitis
7. Pneumonia
8. Sepsis