Shane Pahlavan, M.D.

Disclaimer: The information contained within the Grand Rounds Archive is intended for use by physicians and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No warranties, either express or implied, are made with respect to accuracy, completeness or timeliness of this material. This material does not necessarily reflect the current or past opinions of the faculty of Baylor College of Medicine and should not be used as a basis for diagnosis or treatment, and is not a substitute for professional consultation and/or peer-reviewed medical literature.

A 15-year-old male with a previous diagnosis of mild mental retardation. He presented to Texas Children’s Hospital Emergency Room status post reported caustic ingestion. He reportedly drank industrial strength cleaning detergent his mother brought home from work in a plastic cup. His mother reported immediate onset of drooling and emesis at that time. He did require supplemental oxygen on transportation to the Emergency Room.

Past medical history: Significant for the mild mental retardation as well as fatty liver disease.
Surgeries: No surgeries.
Medication: Risperdal.
Allergies: No allergies.
Family History: Significant for his mother also with mild MR
Social History: Denies any tobacco, alcohol, or drugs.
Physical Examination: He was afebrile. His vitals were stable on admission. He did have heart rate of 120 and respiratory rate of 36. His O2 saturations are 96% on two liters nasal cannula. Generally: He was alert. He was in mild distress with noted drooling. He had a hoarse muffled voice. Oral cavity and oropharynx exam revealed diffuse erythema and edema with ulcerations on the tongue as well as the lips. On flexible fiberoptic scope exam, he did have diffuse erythema of the epiglottis and both false vocal cords. This was partially obstructing visualization of the true cords. His lungs were coarse bilaterally.
Initial Laboratory Work: Hemoglobin 13.6, he did have slightly elevated white blood cell count at 18.71. He did get an ABG at that time, it showed a pH of 7.4, Co2 of 42, bicarbonate is 25 with a 0.6 creatinine. On chest x-ray, there was noted thickening of the epiglottis as well as the paravertebral soft tissues.

He was taken to the operative room immediately for direct laryngoscopy and bronchoscopy in conjunction with the Gastroenterology service for EGD. Here are pictures from the initial operative trip. Note the edematous epiglottis as well as arytenoids and false vocal cords. It is difficult to assess the true cords secondary to supraglottic edema and inflammation. Here are the true cords where he did have some evidence of edema anteriorly. It was decided at that time to go ahead and intubate the patient in the operating room for airway protection. An NG tube was placed as well at the time under direct visualization. This was done after the GI service performed an EGD, which revealed circumferential grade II esophageal mucosal burns. After the OR he was transferred to the pediatric intensive care unit and he was kept NPO. He was started on Prednisone as well as ampicillin and omeprazole twice daily. Subsequently, he returned to the operating room on post operative day #2 for repeat direct laryngoscopy and bronchoscopy. You can see here from the second trip to the OR, two days later, some improvement in the epiglottic edema. The vocal cords have resolved edema anteriorly. It was decided at that time to go ahead and extubate the patient and monitor him closely in the Intensive Care Unit. He did well postoperatively from the second direct laryngoscopy and bronchoscopy. On post operative day #4, barium swallow was done which, at that time, showed no strictures or leaks. Two weeks later on post operative day #14, the GI service performed an upper GI, which did reveal some distal esophageal narrowing.

I will start my discussion with a background, historical perspective on caustic ingestion, and pathophysiology behind the injury to the esophageal mucosa. I will come back to the clinical presentation of our patient and I have broken down the management into three distinct phases: initial assessment in the ER, secondary management, and late management of complications.

There was significant concern toward the end of the 19th century and beginning of the 20th century when lye products became available for domestic use. There was an increase in reported accidental ingestion by children, which led to serious upper airway digestive and esophageal injuries at that time. Chevalier Jackson as previously mentioned became a pioneer again toxic congestion during this time. This subsequently led to the Federal Toxic Act of 1927, which mandated basic labeling of toxic substances. Furthermore, in 1953, the Poisoning Control Center was developed, and it provided a central source of information about product contents, toxicity, and treatment support. Later in 1970, the Poison Prevention Accident Act was introduced, which required these toxic products to be labeled and packaged in childproof containers.

Despite these precautions, there are still a reported 5,000-15,000 cases per year. Ingestion does affect two basic groups in bimodal distribution. The first group is the pediatric population such as the patient in our case presentation with accidental ingestion. The other group includes the adolescent to adult age group from related suicide attempts. In the latter groups, the adolescent and adults, it is oftentimes much worse because of the actual amount of toxin ingestion.

Pathophysiology of esophageal mucosal injury relates back to an organic chemistry review. The lower the pH or pKa signify the stronger the acid. These strong acids actually accept a proton or hydrogen and cause necrosis of the esophageal mucosa. Subsequently, a high pH or high pKa denote a strong base, which actually will give off the hydrogen and hydronium ion. This will cause necrosis as well. So, caustics produce a tissue injury by altering ionized state in breakdown of covalent bonds in esophageal epithelium. In aqueous solutions, the hydronium ion (H+) produces the principle toxic effects for acids, whereas the hydroxide ion (OH-) produces such effects for bases. This is just a chart describing that the lower the pH and pKa the stronger the acid and the higher pH and pKa that higher the basic content. So, pH and pKa is less than 2 are considered strong acids and pH and pKa greater than 12 are considered strong bases. This is important in evaluating the patient in the Emergency Room to understand how likely there will be an associated esophageal injury as it can oftentimes change management. For example, with bleach ingestion it has a pH of 7, so these patients can be observed overnight and do not necessarily require a trip to the operating room or intubation.

Severity of tissue injury takes into account many variables. After considering the pH and pKa, it is important to ask about the concentration. In this specific case presentation, this patient had ingested industrial strength laundry detergent which is much higher concentration of sodium hydroxide compared to over-the-counter of laundry detergent. The duration of contact is also important to consider in your history including the physical form of the substance ingested. Liquid products tend to cause more distal injury; whereas solid products tend to cause more proximal injury inside the oral cavity and not necessarily distally in the esophagus or the stomach.

Alkaline ingestion is estimated at 68% of cases of caustic ingestion. These are just a few common household examples: Drano, ammonia, Clinitest tablets, laundry detergents, and dishwasher detergents. The pathophysiologic mechanism behind alkaline ingestion includes liquefactive necrosis after contact with mucosa resulting in deep penetration with full-thickness burns. Tissue edema occurs immediately and can persist for 48 hours, eventually progressing to airway obstruction. Oftentimes, these patients will need to be intubated as our case presentation. Tissue injury occurs in 3 distinct phases:

  • Burn: necrosis, thrombosis and saponification with PMN and bacterial infiltration in the 1st 48 hours
  • Reparative: Approximately 5 days after ingestion with granulation, reepithelialization and fibroblast infiltration
  • Scar: Starts between 2-3 weeks

Over time, tissue related will be replaced by necrotic tissue. The first stage is the burn phase, which is where we see necrosis with microthrombosis resulting in neutrophil and bacterial infiltration in the first 48 hours. This is one theory behind why it is important to start these patients on antibiotics early. The repetitive phase is approximately five days of congestion with granulation, reepithelialization, and fibroblast infiltration. The scar develops between 2-3 weeks later when there is concern for esophageal stricture formation. So, over the next 2-4 weeks, the scar tissue thickens and causes strictures. The incidence of stricture formation is primarily dependent upon the depth of the burn. It is important to get our Gastroenterology colleagues to assist us in cases such as this. Superficial burns result in strictures in less than 15% of cases. On the contrary, full-thickness burns result in strictures in nearly 100% of cases. Severe burns also may be associated with esophageal perforation.

Some common household examples or products implicated in acid ingestion include: toilet bowl cleaners, swimming pool cleaners, drain cleaners, rust removers, and automotive battery liquid. The pathophysiologic mechanism of injury to the esophagus is a little bit different with acids. This causes injury by coagulative necrosis with the formation of an eschar or coagulant. The eschar tends to limit the penetration of the acidic substance and helps to prevent full-thickness burns.

The clinical presentation in the pediatric population is most commonly suffering ingestion when they are unsupervised by their parents. So, our history can sometimes be difficult because the parents may have not been present. It is important to try to obtain as much history as possible including brand name of the product, type of product, and amount of ingestion. It is also very helpful if the parents are able to bring the container with them to the Emergency Room. It is important to get the Poison Control Center involved as they can give quite a bit of information very rapidly on toxicity and antidotes for specific substances.

When the patient presents in Emergency Room, the most common symptoms you see are dyspnea, odynophagia, drooling, and hoarseness. Stridor can oftentimes be a precursor to a pending airway obstruction. Other symptoms include refusal of food, nausea with vomiting, substernal chest pain, abdominal pain and guarding. These are a little more concerning for a perforation that develops either in the esophagus or stomach. One important note in reference to oral cavity or oropharyngeal pain and burns is that 20% of patients with oral injury can still have esophageal injury. There is no predicted value of oropharyngeal burns and injury to esophageal. So, a lot of these patients can have no evidence of oral burns and actually have very severe esophageal burns. It is important to fully examine these patients and they may require endoscopy.

In the initial assessment, the first thing is always to stabilize the airway and maintain the circulatory system. Gather the history of the substance ingested and contacting either the Poison Control Center or Toxicology Center. Next, perform a secondary survey with a complete head and neck exam including fiberoptic laryngoscopy if the patient is stable. Now you have seen the patient in ER and the question is whether or not to induce emesis but this will potentially re-expose the esophagus, pharynx, mouth, and larynx to the caustic agent and worsen damage. So, should we then gastric lavage these patients? Some studies have shown that giving either water or milk at a maximum 15 ml/kg can dilute the substance ingested. However, distending the stomach could induce emesis, so be very cautious with diluting these agents. It has been shown to potentially limit the severity of injury. Do you want to neutralize these ingestions? This will potentially create a large exothermic reaction and worsen the burn that has already occurred by neutralizing either a strong acid or strong base. This creates a weak acid or weak base in this exothermic reaction can have a considerably worse injury. Most patients should get radiography with the literature suggesting at least a chest x-ray and a KUB to rule out any esophageal or gastric perforation. A contrast esophogram is usually not considered to be helpful in early stages, however. Laboratory tests in the Emergency Room have usually already been ordered. There have been many studies that show that laboratory tests show no consistent predicted value of gastric or esophageal injury. I do think it is important to go ahead and get at least an arterial blood gas to make sure these is no metabolic component of the injury.

Secondary management includes surgical intervention if perforation is suspected based on a free air seen on CXR or a KUB. When to perform endoscopy has been studied extensively. There is no reliable sign or symptom that actually predicts the extent of esophageal injury based on the oral cavity or oropharyngeal exam. Endoscopy timing is crucial and should be done between 24 to 48 hours. Endoscopies in this setting are not indicated before 12 hours after ingestion as the exam will underestimate the damage. If performed too early, the patient may have a negative exam and actually have significant injury to the esophagus. It is performed greater than 48 hours, endoscopy is thought to increase iatrogenic injury with subsequent perforation. After 48 hours, there is structural weakness in the esophageal wall and it increases the chance of complication.

Staging of esophageal burns has changed throughout the literature with different descriptions offered by multiple authors. The first-degree burns involve erythema and edema of the mucosa. Second-degree burns involve mucosal and submucosal or transmucosal with blood ulceration. Third-degree burns are full-thickness burns with the muscular involvement that form a circumferential exudate.

Steroid administration is thought to reduce the inflammatory response and decrease the risk of perforation and stricture formation. It should be initiated within 24 to 48 hours for full benefit. The dose is controversial but usually between 1 or 2 mg/kg/day is generally recommended. Steroids are primarily indicated for patients with grade II injury based on esophageal exam or EGD. Grade I injury only has about a 1% chance of developing an esophageal stricture, so steroids are not recommended for grade I injury. Steroid administration in grade III injury or full-thickness injury is thought to be contraindicative because of an increased risk of perforation and potential to mask signs of perforation.

Anderson et al in NEJM in 1991 studied the effect of steroids in patients status post caustic ingestion. This was an 18-year randomized perspective study with 60 children treated with or without steroids at a dose of 2 mg/kg/day of prednisone. They performed repeat endoscopies to monitor for the development of strictures. Strictures developed in 10 of 31 in steroid group and 11 of 29 in the controls. Their conclusion was that of no benefit to the use of the steroids.

Bautista et al in 1996, did a similar study but in this study used an animal model. He used cotton swabs of sodium hydroxide and placed on the esophageal mucosa of 30 rabbits and they were randomized to a control group, dexamethasone group and then a prednisone group. After three weeks, the rabbits were sacrificed and results were significant for decreased stricture formation in only in the dexamethasone group. So, his conclusion was that rapid post-injury dexamethasone significantly reduces frequency and severity of strictures.

Antibiotic use is controversial but I.V. ampicillin or clindamycin are most commonly given. Human studies have failed to show any benefit. However, in theory there should be a role in reducing bacterial count in alkaline ingestion to prevent transmigration of bacteria and also reducing the risk of mediastinitis or peritonitis in full-thickness burns.

Esophageal stenting has been a component of the treatment of caustic ingestion for many years. Some texts would recommend a silastic stent or NG tube. Esophageal rest is important in minimizing any further irritation and allow for reepithelialization. Lathyrogens have been used to reduce crosslinking of collagen and potentially reduce stricture formation. Common used lathyrogens include N-acetylcysteine and penicillin. Anti-reflux management is usually started with twice a day dosing of a proton pump inhibitor. Sucralfate in the elixir form has been shown to help protect the mucosa by providing a barrier to further injury.

Late management includes following these patients for delayed development of esophageal strictures using a periodic contrast esophagoscopy and esophageal dilations can be initiated. Esophageal cancer surveillance is also an important component to late management. Patients with a history of caustic ingestion have an increased risk of esophageal cancer, reportedly between 1,000 to 10,000 times higher. There is an average 15 to 40-year latency period between injury and development of esophageal cancer. Some articles actually recommend annual barium swallows in patients that have grade III injuries or severe esophageal stricture.

In summary, this is a treatment algorithm of caustic ingestion. Symptomatic patients will need esophagoscopy in 24-48 hours. With asymptomatic patients or bleach ingestion, observation is good option to monitor for the development of symptoms.

Our patient subsequently developed esophageal strictures of the mid and distal esophagus. He underwent balloon dilation prior to discharge and multiple dilations as an outpatient. He continues to tolerate a pureed diet and supplements with 4-6 cans of Ensure per day. He is not able to tolerate a regular diet at this point. He has had no further sequelae from his laryngeal injury.

In conclusion, as with most accidents, prevention is the best form of the treatment. Unfortunately, sometimes we cannot protect our patients from themselves. There is no reliable relationship between physical examination and aerodigestive tract injury. Alkali agents cause liquefactive necrosis, which allows for deeper penetration of injury. These are more concerning than acidic agents that cause coagulative necrosis, which is protective and limits the injury to underlying tissue. Endoscopy is the gold standard for diagnosis in patients presenting within 48 hours of ingestion. Barium swallow should be done in patients presenting after 48 hours as endoscopy generally considered contraindicated for risk of perforation. Patients with esophageal burns need to be followed throughout their lifetime for stricture formation as well as increased risk of esophageal cancer.

Case Presentation

J.S. is a 15 year old male with a history of mental retardation presented to TCH ER status post alkaline ingestion. He reportedly drank industrial strength cleaning detergent that his mother had brought home from her work in a plastic cup. His mother reported immediate onset of drooling and emesis. He did require supplemental oxygen on transport by ambulance.

He was taken to the operating room for direct laryngoscopy and bronchoscopy in conjunction with Gastroenterology for EGD. Laryngoscopy revealed an edematous epiglottis, arytenoids, and false vocal cords. Patient was intubated for airway protection and a nasogastric tube was placed under direct visualization. EGD revealed near circumferential Grade 2B esophageal mucosal burns. The patient was transferred to the PICU for close monitoring. He was kept NPO and Prednisone 2mg/kg/day, Ampicillin 1 gram IV q8 hours, and Omeprazole BID were started.

He returned to the OR on POD#2 for repeat direct laryngoscopy and bronchoscopy which revealed mild epiglottic edema with normal vocal folds. He was extubated in the operating room and tolerated extubation without adverse event. On POD#4 barium swallow revealed no strictures or leaks. On POD#14 Upper GI revealed distal esophageal narrowing. He underwent balloon dilation prior to discharge home and was maintained on a pureed diet. Patient was subsequently developed significant esophageal strictures of the mid and distal esophagus. He has undergone and multiple dilations as an outpatient (last being 3/25/08). He continues to tolerate a pureed diet and supplements with 4-6 Ensure cans per day. He has had no further sequelae from his laryngeal injury.

Bibliography

Alford BR, Harris HH. Chemical burns of the mouth, pharynx, and esophagus. Ann Otol Rhinol Laryngol 1959:68:122-128.

Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J Med 1990;323:637-640.

Baskin D, Urganci N, Abbasoglu L, Alkim C, Yalcin M, Karadag C, Sever N. A standardized protocol for the acute management of corrosive ingestion in children. Pediatr Surg Int 2004;20:824-828.

Bautista C, Estevez M, Varela C, Villanueva J, Tojo S, Cadranel S. A retrospective analysis of ingestion of caustic substances by children. Ten year statistics in Galicia. Eur J Pediatr 1997;156:410-414.

Cardona JC, Daly JF. Current management of corrosive esophagitis: an evaluation of results in 239 cases. Ann Otol Rhinol Laryngol 1971;80:521-527.

Cheng YJ, Kao EL. Arterial blood gas analysis in acute caustic ingestion injuries. Surg Today 2003;33:483-485.

de Jong AL, Macdonald R, Ein S, Forte V, Turner A. Corrosive esophagitis in children: A 30-year review. Int J Pediatr Otorhinolaryngol 2001;57:203-211.

Di Costanzo J, Noirclerc M, Jouglard J, Escoffier JM, Cano N, Martin J, Gauthier A. New therapeutic approach to corrosive burns of the upper gastrointestinal tract. Gut 1980;21:370-375.

Friedman EM. Caustic ingestion and foreign bodies in the aerodigestive tract. In: Bailey BJ, editor. Head & Neck Surgery-Otolaryngology, 3 rd edition. Philadelphia: Lippincott; 2001. pp 925-932.

Friedman EM. Caustic ingestions and foreign bodies in the aerodigestive tract of children. Pediatr Clin North Am 1989;36:1403-1410.

Friedman EM. Caustic ingestion and foreign body aspiration: an overlooked form of child abuse. Ann Otol Rhinol Laryngol 1987;6:709-712.

Friedman EM, Lovejoy FH. The emergency management of caustic ingestions. Emerg Med Clin North Am 1984;2:77-86.

Harley EH, Collins MD. Liquid household bleach ingestion in children: A retrospective review. Laryngoscope 1997;107:122-125.

Holinger LD. Caustic ingestion, esophageal injury and stricture. In : Holinger LD, Lusk RP, Green CG, editors. Pediatric Laryngology and Bronchoesophagology. Philadelphia: Lippincott-Raven; 1997. pp 295-303.

Hugh TB, Kelly MD. Corrosive ingestion and the surgeon. J Am Coll Surg 1999;189:508-522.

Isolauri J, Markkula H. Lye ingestion and carcinoma of the esophagus. Acta Chir Scand 1989;155:269-271.

Jackson C. Esophageal stenosis following the swallowing of caustic alkalis. JAMA 1921;77:22-23.

Kay M, Wyllie R. Caustic ingestions and the role of endoscopy. J Pediatr Gastroenterol Nutr 2001;32:8-10.

Lamireau T, Rebouissoux L, Denis D, Lancelin F, Vergnes P, Fayon M. Accidental caustic ingestion in children: is endoscopy always mandatory? J Pediatr Gastroenterol Nutr 2001;33:81-84.

Lemke T, Wang R. Emergency department observation for toxicologic exposures. Emerg Med Clin North Am 2001;19:155-167.

Miller KA, Dudgeon DL. Caustic esophageal injuries and perforations. Operative Pediatric Surgery. McGraw-Hill: New York 2003; pp 341-347.

Tilanus HW, Siersema PD. Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy. Gastrointest Endosc 2004;60:372-377.

Turner A, Robinson P. Respiratory and gastrointestinal complications of caustic ingestion in children. Emerg Med J 2005;22:359-361.

Ulman I, Mutaf O. A critique of systemic steroids in the management of caustic esophageal burns in children. Eur J Pediatr Surg 1998;8:71-74.

Wijburg FA, Heymans HS, Urbanus NA. Caustic esophageal lesions in childhood: prevention of stricture formation. J Pediatr Surg 1989;24:171-173.