Caustic Ingestions

Introduction

There are more than 200,000 caustic ingestions reported each year in the United States.  Of these caustic ingestions, 80% occur in children less than six years old

Most ingestions in this age group are accidental and tend to be ingestions of small amounts; however there have been some reports of caustic ingestions due to child abuse. 

The severity of tissue damage depends on the duration of contact with the caustic agent, the amount ingested, which substance is involved, its pH, concentration and whether it is a solid or liquid.

 

Alkaline and Acidic Ingestions

 Acids and bases cause injury to tissues through different mechanisms.  Ingestions of alkaline substances cause tissue damage by liquefactive necrosis.  This involves saponification of fats, denaturation of proteins, and disruption of cellular membranes, allowing the alkaline substance to diffuse into deeper layers of the mucosa.  Small vessel thrombosis and heat production also occur. 

Agents with a pH greater than 11 cause the most damage.  In liquid form, bases are tasteless and denser than water which results in more distal injuries to the esophagus. 

Examples of alkaline substances are

  • Oven cleaners
  • Liquid drain cleaner
  • Disk batteries
  • Hair straighteners/relaxers
  • Household cleaners
  • Dishwasher detergents.

Of note, household bleach has a low concentration and neutral pH.  Because of this, esophageal burns are rare and those that do occur tend to be mild and do not require treatment.

Acids of pH less than 2 are very damaging to tissue.  Unlike alkalis, they tend to taste badly and are irritating.  This results in choking and gagging which may lead to aspiration of the caustic material and airway compromise. 

Acids cause tissue damage through coagulative necrosis that forms an eschar.  The eschar is thought to prevent acids from penetrating as deep into tissue as alkaline substances do.  While the eschar may partially protect the esophagus from deep burns, acid tends to pool in the antrum of the stomach, potentially leading to gastric perforation or pyloric obstruction. 

coagulative necrosis_1.jpg
Coagulative necrosis of mucosa (upper) and submucosa (lower). Note the relatively preserved contour of mucosal glands with loss of individual nuclei.  http://pathology.class.kmu.edu.tw/ch01/Slide6.htm

 

Examples of common acidic substances are:

  • Toilet bowl cleaners
  • Swimming pool cleaners
  • Rust removers

 

Following the initial necrosis caused by ingestion of either acidic or alkaline substances, destruction of tissue continues due to inflammation and vascular thromboses for several days. 

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Injury to the larynx and epiglottis after the ingestion of alkaline material.
Evaluation and Management of Caustic Injuries from Ingestion of Acid or Alkaline Substances.  K Park. Clin Endosc. 2014 Jul;47(4):301-307

After 2-4 days, granulation tissue begins to form.  During this time, the tissue is weak and vulnerable to perforation.  Collagen deposition and fibrogenesis occur 2-3 weeks after the initial injury.

 

Presentation and Clinical Findings

The clinical features of caustic ingestions vary greatly and may even be absent.  The most common symptom is dysphagia which can occur even in the absence of severe esophageal injury. 

Patients may have burns on the lips, mouth, and oropharynx; however the presence or absence of these injuries does not correlate with the presence of injury to the stomach or esophagus. 

Patients can also present with drooling, retrosternal or abdominal pain, nausea, vomiting, hematemesis, and odynophagia.  If upper airway injury is present, patients may exhibit stridor, hoarseness, nasal flaring and retractions.

 

Diagnostic Workup and Initial Treatment

It is important to gather as much information about the specific agent ingested as well as the time, nature of the exposure and duration of contact. 

Information on caustic agents can be obtained by looking at Material Safety Data Sheets and consulting with the local poison control center.

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Click on the Poison Help Logo ABOVE to visit the Illinois Poison Center.

Physical exam is imperative, though it is important to remember that exam findings often do not correlate with severity of injury.  Signs of impending airway obstruction (stridor, dysphonia, respiratory distress, tachypnea) necessitate intubation, preferably fiberoptic-assisted intubation to avoid risk of soft tissue perforation. 

Signs of severe injury include altered mental status, peritoneal signs (evidence of viscous perforation), hypotension and shock.

 

Initial evaluation includes:

  • NPO status with IV fluids
  • Labs:  CBC, BMP, and ABG levels as well as urinalysis to provide baseline values and as indications of systemic toxicity.
  • Type and cross may be indicated if patients have signs of viscous perforation. 
  • In the case of hydrofluoric acid ingestion (found in some rust removers), calcium levels should be monitored closely. 
  • Chest and abdominal X-rays are taken to look for pneumomediastinum, pleural effusions, aspiration pneumonitis, pneumoperitoneum, and/or a disk battery. 
  • In the case of disk batteries lodged in the esophagus, immediate removal is required.

It is essential to document the presence or absence of esophageal or gastric injury following a caustic ingestion in children, even if children are asymptomatic and lack oral burns as these are poor predictors of tissue damage (note that this is different than asymptomatic adults with low risk exposure who may be discharged after observation for 2-4 hours). 

An exception to this is children who ingested household bleach often do not require endoscopy due to the very low likelihood of tissue damage.  The presence and extent of injury is documented using flexible endoscopy. Endoscopic ultrasonography has been demonstrated to more accurately show the depth of lesions and may be used more widely in the future to aid in diagnosis and treatment. 

Endoscopy should be performed within the first 12-48 hours following ingestion as endoscopy occurring more than 48 hours after ingestion increases the risk of perforation of the weakened tissue.

Tissue damage is graded on a scale of 0 to 3 with 0 being normal mucosa.  Grade 1 involves injury limited to edema and erythema of the mucosa. Grade 2A burns are transmucosal, linear ulcerations and necrotic tissue with whitish plaques and/or hemorrhages. Grade 2B burns have Grade 2A findings but are circumferential.  Grade 3 burns are transmural and involve ulceration and necrosis and even perforation.  Circumferential burns are most likely to lead to stricture formation

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A high esophageal stricture (arrow) following caustic ingestion.
www.radiologyassistant.nl

For any burn grade 2B or 3, it is recommended to place a nasogastric (NG) tube under direct endoscopic visualization. This helps stent open the injured area, hopefully preventing future stricture formation and is a means to provide nutrition during the healing phase.  Additionally, NG tube suction may be beneficial in treating large volume liquid acid ingestions to help minimize damage to the stomach and small intestine.

It is imperative not to induce emesis as vomiting may lead to additional esophageal injury and even perforation.  Gastric lavage is also contraindicated due to risk of esophageal perforation and tracheal aspiration of stomach contents.  Neutralization should never be attempted because the neutralization reaction is exothermic, potentially further exacerbating tissue damage.  It is also not recommended to attempt dilution of ingested material.  Any attempts greater than 30 minutes after ingestion are unlikely to be beneficial and there is a risk of inducing emesis with this technique.  In addition, the amount of liquid required to neutralize a caustic agent is often too large to be a practical therapy.

Corticosteroids were once thought to be helpful in preventing stricture formation following circumferential burns.  However, numerous studies have found that steroids do not protect against the development of esophageal strictures and may even be harmful.

Though corticosteroids are not a recommended treatment, administration of a third-generation cephalosporin or ampicillin/sulbactam is indicated if there is evidence of perforation.  Narcotics are beneficial in reducing pain associated with caustic ingestions.

 

Long-term Treatment and Prognosis

Any patient with a Grade 2 burn or higher should be followed up with an upper GI (UGI) series 2-3 weeks after ingestion.  Patients with 0 to Grade 1 burns should have a UGI series 3-6 weeks after ingestion or earlier if dysphagia develops.  Such contrast studies are not performed at the time of ingestion as they are not a reliable means of detecting acute injury or predicting stricture formation. 

Strictures can form as early as 2-4 weeks after ingestion and are the most common complication of caustic ingestions.  Esophageal stricture occurs in up to 50% of all documented esophageal burns and in 70-100% of circumferential burns.  Strictures tend to occur at sites of anatomic narrowing of the esophagus (e.g. at the esophageal hiatus). 80% of patients with strictures will develop obstructive symptoms within 2 months. 

Strictures that are confirmed with UGI series are treated with esophageal dilation, typically with balloon dilators in children.  Though dilation may provide temporary improvement in symptoms, most patients require repeat dilations.  Recent evidence has suggested that mitomycin C, a fibroblast proliferation inhibitor, may reduce the need for repeat dilations in children.  Progressive obstruction may require esophagectomy.

Other possible complications that arise from caustic ingestions are perforation of the esophagus which can lead to tracheoesophageal fistula formation, mediastinis, pneumonia and sepsis.  Perforation of the stomach or duodenum can also occur.  Gastric outlet obstruction may develop 3-4 weeks following acid exposure.  If the larynx suffered severe burns, tracheostomy may be required.

 Transmural burns (Grade 3) of the esophagus have a 20% mortality rate.  Additionally, injury and stricture formation increase the risk of squamous cell carcinoma of the esophagus by a factor of 1000.  1-4% of all patients with significant damage from caustic ingestions develop carcinoma within 40 years of exposure.  This carries a poor prognosis with a 40% survival rate at 1 year and only a 13% survival rate at 5 years.

 

References

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  2.  Turner A., Robinson P. (2005) Respiratory and gastrointestinal complications of caustic ingestion in children. Emerg Med J 2005;22:359-361  
  3. Elshabrawi M, A-Kader HH (2011) Caustic ingestion in children. Expert Rev Gastroenterol Hepatol 5(5):637-45.
  4. Kay M, Wyllie R (2009) Caustic ingestions in children. Curr Opin Pediatr 21(5):651-4.
  5. Lupa M, Magne J, Guarisco JL, Amedee R (2009) Update on the diagnosis and treatment of caustic ingestion. Ochsner J 9(2):54-9.
  6. Gun F., Abbasoglu L., Celik A., Salman F. (2007) Early and Late Term Management in Caustic Ingestion in Children:
    A 16-year Experience.
    Acta chir belg, 107, 49-52
  7. Pace F, Antinori S, Repici A (2009) What is new in esophageal injury (infection, drug-induced, caustic, stricture, perforation)? Curr Opin Gastroenterol 25(4):372-9.
  8. Pelclová D, Navrátil T (2005) Do corticosteroids prevent oesophageal stricture after corrosive ingestion? Toxicol Rev 24(2):125-9.
  9. Poley JW, Steyerberg EW, Kuipers EJ, Dees J, Hartmans R, Tilanus HW, Siersema PD (2004) Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy. Gastrointest Endosc 60(3):372-7.