Caustic Ingestion (Cleaning Products)

Caustic agents are acidic or alkaline substances that damage tissues severely if ingested. Alkali ingestion typically damages the esophagus via liquefactive necrosis, whereas acids cause more severe gastric injury leading to coagulative necrosis. Ingestion of large volumes and high concentrations of caustic agents can lead to severe and extensive injuries. Additionally, aspiration affects the laryngeal and tracheobronchial structures. Signs and symptoms include oral pain, burns, dysphagia, vomiting, and abdominal pain. Severe injuries can present with shock, abdominal rigidity, respiratory distress, and/or altered mental status. Diagnosis is based on laboratory tests, abdominal and chest imaging, and endoscopy within 24 hours (if without contraindications) to determine the extent of damage. Management involves stabilizing the cardiorespiratory status, decontamination, and supportive therapy. Severe injury may require surgery.

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Overview

Introduction

Caustics and corrosives cause tissue injury by a chemical reaction.

Injury by alkaline chemicals is overall more toxic than that caused by acidic substances:

  • Alkaline substances:
    • Most common
    •  Include sodium or potassium hydroxide (“lye”) present in drain cleaners, household cleaning products, and disc batteries
  • Acidic substances include concentrated hydrochloric, sulfuric, and phosphoric acids present in toilet-bowl cleaners and battery fluids.

Caustic ingestion:

  • Usually accidental in children
  • Usually intentional in adults
  • Associated with psychiatric illnesses

Epidemiology

  • In the United States, cleaning substances account for > 190,000 exposures annually.
  • 80% of ingestion of caustic substances noted in children < 5 years of age
  • Occupational exposures are often more severe because industrial products are more concentrated than household products.

Etiology

Common acid-containing products:

  • Toilet-bowl cleaners
  • Rust-removal products
  • Metal-cleaning products
  • Cement-cleaning products
  • Drain cleaners
  • Automotive battery liquid

Common alkali-containing products:

  • Drain cleaners
  • Ammonia-containing cleaning supplies
  • Swimming-pool cleaners
  • Oven cleaners
  • Automatic dishwasher detergents
  • Hair relaxers
  • Bleach
  • Cement

Pathophysiology

Tissue injury occurs by changing the ionized state and structure of molecules, thereby disrupting the covalent bonds.

Alkaline ingestion

  • The hydroxide ion (OH-) in alkaline substances is responsible for toxicity.
  • Accepts a proton in aqueous solutions and causes a chemical reaction → liquefactive necrosis:
    • Saponification of fats 
    • Solubilization of proteins
    • Disruption of cellular membranes and emulsification → cell death 
  • Effects:
    • Full-thickness burn/penetrating injury:
      • Occurs within seconds of ingestion and lasts 3–4 days
      • Leads to perforation and mediastinitis in severe cases
    • Vascular thrombosis and mucosal inflammation → focal or extensive sloughing and ulceration
    • Progressive thinning of esophagus from sloughing, and development of fibrosis over 2 weeks
    • Process of re-epithelialization can take up to 3 months.
  • Partial neutralization of the ingested alkali by gastric acidity results in generally decreased stomach injuries.
  • Specific injury with disk batteries (button batteries):
    • Can adhere to the esophageal or gastric mucosa
    • Adherence leads to perforation due to prolonged contact with extruded chemicals (sodium hydroxide or potassium hydroxide) and residual electrical discharge.

Acid ingestion

  • Hydrogen ions (H+) of acid are responsible for principal toxic effects
  • Acids can donate a proton in an aqueous solution causing a chemical reaction → coagulation necrosis:
    • Desiccation or denaturation of superficial tissue proteins
    • Thromboses of mucosal microvasculature
  • Effects:
    • Formation of an eschar or coagulum (which is protective, lessening the damage of deeper tissues)
    • In < 5 days, the eschar sloughs off and granulation tissue fills in, rendering the area susceptible to perforation
    • Obstruction can occur as the scar contracts.
  • Causes pain upon contact in the oropharynx: limits the amount of acidic substances ingested
  • Significant exposure may result in the GI absorption of acidic substances, which can affect other systems:
    • Metabolic acidosis
    • Hemolysis
    • AKI

Notable factors affecting injury

  • pH:
    • > 12: considered a strong base
    • < 2: considered a strong acid
  • Substance consistency:
    • Alkaline: viscous (longer contact time)
    • Acid: flows/passes down more quickly
  • Duration of contact: ↑ time, ↑ damage
  • Commonly affected anatomy:
    • Alkaline ingestion: esophagus is commonly damaged
    • Acidic ingestion:
      • Upper airway (pain on contact, causing gagging and choking, which damage the upper airway) 
      • Stomach 
  • Volume and concentration of the ingested solution: Large volumes and higher concentrations result in more extensive damage.
  • Physical form:
    • Solid: localized effect/injury, as these can adhere to the mucosa and not reach the stomach
    • Liquid: affect larger surfaces/areas

Mnemonic

To help recall the damage caused by alkalis and acids, the following mnemonic may be used:

Alkaline = liquefactive necrosis 

Acidic = coagulation necrosis

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Clinical Presentation

  • Oropharyngeal injury:
    • Oral pain
    • Hypersalivation
    • Whitening of the tongue 
    • Oropharyngeal burns and ulcerations
  • Laryngeal damage:
    • Hoarseness
    • Stridor
  • Esophageal damage:
    • Dysphagia
    • Odynophagia
  • Gastric damage: 
    • Epigastric pain
    • Hematemesis
    • Retrosternal or back pain (signifies perforation or mediastinitis)
    • Rebound abdominal pain and rigidity (suggests peritonitis)
  • Other features signifying extensive injury:
    • Fever
    • Respiratory distress
    • Shock (e.g., hypotension, tachycardia)
    • Altered mental status
    • Deaths commonly from perforation and mediastinitis

Diagnosis

  • Attempt to identify the specific agent ingested:
    • Concentration
    • pH
    • Quantity 
  • Laboratory tests:
    • Tests:
      • CBC
      • Comprehensive metabolic panel including ionized calcium
      • Lactate
      • Toxicology screening
      • Blood gas
      • CRP
    • Findings:
      • Leukocytosis, low platelet count, severe acidosis, elevated CRP, renal failure, and liver-function abnormalities are indicative of poor outcomes.
      • Abrupt, life-threatening hypocalcemia can occur with the ingestion of hydrogen fluoride.
  • ECG: Check for ischemia and/or arrhythmia.
  • Imaging:
    • X-ray:
      • Chest: Check for pneumomediastinum, aspiration pneumonia, and presence of a foreign body (e.g., battery).
      • Abdominal: Check for pneumoperitoneum and presence of a foreign body. 
    • CT scan: 
      • Check the depth of necrosis. 
      • Determines presence of perforation and helps assess the need for emergency surgery
  • Upper endoscopy:
    • 1st step is to stabilize the patient.
    • Contraindicated in hemodynamic instability and GI perforation
    • Preferably within 24 hours (average 12–48 hours)
    • Early endoscopy may not correctly indicate the extent of injury, while delayed endoscopy increases the risk of perforation.
    • Pathological classification of injury:
      • 1st-degree injury: superficial mucosa affected; erythema, edema, hemorrhage expected during healing
      • 2nd-degree injury: ulcers, exudates affect up to submucosal layer; scarring and strictures possible
      • 3rd-degree injury: transmural in depth, with deep ulcers and wall perforation

Management and Complications

Management

Asymptomatic patients without significant ingestion or oral burns can be safely discharged.

Management of symptomatic patients and individuals with significant ingestion includes the following:

  • Secure airway (laryngoscopy).
  • Fluid resuscitation and pain control
  • Decontamination (remove clothes, skin irrigation) 
  • No nasogastric intubation
  • Medications:
    • Use IV proton pump inhibitors.
    • Avoid emetics (vomiting worsens burn/injury) and use neutralizing agents or corticosteroids.
  • Mild injury needs only supportive management.
  • More severe injury:
    • Observe for signs of perforation.
    • May require tube feedings 
    • Possible surgery (laparotomy and esophagectomy)

Complications

  • Airway/cardiorespiratory:
    • Airway edema or obstruction may occur immediately or up to 48 hours after exposure.
    • Mediastinitis
    • Pericarditis
    • Pleuritis
  • Gastroenterological:
    • Gastroesophageal perforation occurring with a possible delay of 4 days (up to 3 weeks) post ingestion
    • Formation of esophageal stricture:
      • Most common complication
      • May be prevented by dilatation or stenting after 3–4 weeks
    • Fistula formation:
      • Tracheoesophageal fistula formation
      • Esophageal-aortic fistula formation
    • Upper GI hemorrhage and ulcers
    • Peritonitis
    • ↑ Risk of squamous cell carcinoma (SCC) with lye ingestion (surveillance upper endoscopy after 15–20 years to screen for SCCs)

Differential Diagnosis

  • Esophageal cancer: a malignant tumor of the esophagus. Nearly all esophageal cancers are either adenocarcinomas or SCCs. Early-stage cancer is often asymptomatic, with dysphagia and weight loss presenting as the disease progresses. Diagnosis of esophageal cancer is by endoscopic biopsy or image-guided biopsy of the metastatic site. Management depends on the disease stage. Alkali ingestion is a risk factor for SCC.
  • Esophageal stricture: an abnormal narrowing in the esophagus, which might occur due to benign or malignant conditions. Benign (non-cancerous) strictures may occur due to the buildup of fibrous tissue and collagen deposits from ulcers, or chronic inflammation of the esophagus.
  • Esophagitis: inflammation or irritation of the esophagus. The major variants of esophagitis are medication-induced, infectious, eosinophilic, corrosive, and acid-reflux esophagitis. Patients typically present with odynophagia, dysphagia, and retrosternal chest pain. Diagnosis is by endoscopy and biopsy. Management depends on the etiology, but includes medications and possible surgery.
  • Herbicides: substances used to control the growth of unwanted plants and in the construction industry. Paraquat is an example of an herbicide that is potentially fatal when ingested. Clinical manifestations range from local oral burns to vomiting, diarrhea, renal failure, and respiratory distress. Early detection (based on history) is important to prevent further toxicity. Management depends on the ingested quantity and time since exposure. Hemodialysis is recommended in certain cases.
  • Pesticides: chemical substances used to control pests, including weeds. Commonly used pesticides include organochlorines, carbamates, and organophosphates. Ingestion of different pesticides result in different clinical manifestations, which include nausea, vomiting, and neurotoxicity. Early detection after exposure is important to prevent further toxicity. Management involves supportive therapy and may include antidotes depending on the ingested pesticide.

References

  1. De Lusong, M., Timbol, A., & Tuazon, D. (2017). Management of esophageal caustic injury. World Journal of Gastrointestinal Pharmacology and Therapeutics, 8(2), 90–98. https://doi.org/10.4292/wjgpt.v8.i2.90
  2. Dire, D. (2020). Disk Battery Ingestion. Emedicine. Retrieved March 15, 2021, from https://emedicine.medscape.com/article/774838-overview
  3. Lung, D. (2020). Caustic Ingestions Clinical Presentation. Emedicine. Retrieved March 14, 2021, from https://emedicine.medscape.com/article/813772-clinical
  4. Triadafilopoulos, G. (2020). Caustic esophageal injury in adults. UpToDate. Retrieved March 15, 2021, from https://www.uptodate.com/contents/caustic-esophageal-injury-in-adults

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