Acid ingestion: Difference between revisions

(Moved intro into Background as bullets; removed excessive bold from bullet lead-ins; added Dysphagia DDX template)
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**Salicylate, acetaminophen, ethanol levels (if intentional ingestion)
**Salicylate, acetaminophen, ethanol levels (if intentional ingestion)
**β-hCG in women of reproductive age
**β-hCG in women of reproductive age
**Extended electrolytes including calcium and magnesium (especially for [[ydrofluoric acid]])
**Extended electrolytes including calcium and magnesium (especially for [[hdrofluoric acid]])
* Imaging:
* Imaging:
**Chest and abdominal radiograph — assess for pneumomediastinum, pneumoperitoneum, pleural effusion
**Chest and abdominal radiograph — assess for pneumomediastinum, pneumoperitoneum, pleural effusion

Revision as of 15:42, 19 March 2026

Background

  • Acid ingestion is a subcategory of caustic ingestion in which a strong acid (pH <2) causes injury to the upper gastrointestinal tract, predominantly the stomach, through coagulation necrosis.[1] Acid ingestion carries a higher mortality rate than alkali ingestion.[2]
  • Acids act as proton donors, causing cell death through protein denaturation and coagulation necrosis[1]
    • Coagulation necrosis forms a protective eschar that classically was thought to limit tissue penetration depth
    • However, recent data suggest esophageal perforation rates from acids may be higher than previously believed[3]
  • Acids tend to transit the esophagus rapidly due to low viscosity, causing preferential gastric injury
    • Pylorospasm from acid exposure prolongs gastric contact time (up to 90 minutes), leading to pooling and high-grade gastric burns[4]
    • Gastric antrum and pylorus are most commonly affected
  • Acids have a noxious taste that may trigger gagging and choking, predisposing to aspiration with subsequent airway injury[5]
  • Certain acids have unique systemic toxicity beyond local caustic effects (see Special considerations)
  • 80% of caustic ingestions worldwide occur in children (usually accidental, small-volume, often benign)[6]
  • In adults, ingestion is more often intentional (self-harm), involves larger volumes, and is more frequently life-threatening[7]

Common acids

  • Hydrochloric acid (HCl) — toilet bowl cleaners, metal cleaners, tile cleaners
  • Sulfuric acid (H₂SO₄) — car batteries, drain openers
  • Phosphoric acid — rust removers, metal cleaners
  • Hydrofluoric acid (HF) — rust removers, glass etching, industrial use
  • Oxalic acid — cleaning agents
  • Acetic acid (concentrated) — industrial solvent

Clinical features

  • Signs and symptoms are inadequate to predict the presence or severity of esophageal or gastric injury[8]
  • Absence of oropharyngeal burns does NOT exclude significant esophageal or gastric injury

Oropharyngeal

  • Burns, erythema, or ulceration of lips, tongue, oral mucosa
  • Drooling, inability to handle secretions
  • Odynophagia, dysphagia

Airway

  • Stridor, hoarseness, dysphonia (acid ingestion causes upper airway injury more often than alkali due to aspiration from gagging)[5]
  • Respiratory distress, tachypnea
  • Uvular edema

Gastrointestinal

  • Epigastric or chest pain
  • Nausea, vomiting (may be hematemesis)
  • Abdominal rigidity, guarding (suggests perforation)

Systemic

Differential diagnosis

Caustic ingestion

Other


Dysphagia

Evaluation

Workup

  • Identify the specific agent, concentration, estimated volume, time of ingestion, and intent
    • Obtain product label, MSDS/SDS when possible
    • Contact Poison control for guidance
  • Labs:
    • CBC, BMP, hepatic function panel, coagulation studies (PT/INR, fibrinogen), type and screen
    • Serum lactate, VBG/ABG (pH, lactate)
    • Lipase
    • Salicylate, acetaminophen, ethanol levels (if intentional ingestion)
    • β-hCG in women of reproductive age
    • Extended electrolytes including calcium and magnesium (especially for hdrofluoric acid)
  • Imaging:
    • Chest and abdominal radiograph — assess for pneumomediastinum, pneumoperitoneum, pleural effusion
    • CT chest/abdomen with IV contrast — useful adjunct for identifying transmural necrosis, perforation, and peritoneal free fluid; higher specificity than EGD for surgical decision-making but should not replace EGD[9]
  • Esophagogastroduodenoscopy (EGD):
    • Gold standard for grading injury severity
    • Perform within 12-24 hours of ingestion[7]
      • Too early (<12 hr) may underestimate injury extent
      • Avoid between days 5-15 post-ingestion due to maximal tissue friability and perforation risk[10]
    • Exception: do not delay surgery for EGD if perforation is already evident

Diagnosis

  • EGD findings graded by the Zargar classification:[11]
    • Grade 0 — Normal mucosa
    • Grade I — Edema and hyperemia
    • Grade IIa — Superficial ulceration, hemorrhage, erosions, blisters, exudates
    • Grade IIb — Deep, discrete, or circumferential ulceration
    • Grade IIIa — Focal necrosis (small, scattered areas of necrosis)
    • Grade IIIb — Extensive necrosis
    • Grade IV — Perforation (added in some modified classifications)
  • Grades 0, I, and IIa generally recover without long-term sequelae
  • Grades IIb and above carry significant risk of stricture formation and may require surgical intervention[12]
  • Lab markers predictive of transmural necrosis: severe metabolic acidosis (low pH, elevated lactate), leukocytosis, thrombocytopenia, elevated CRP, deranged LFTs, acute kidney injury[7]

Management

Airway

  • Assess airway immediately and continuously — may deteriorate rapidly over hours as edema progresses
  • Intubate early if stridor, voice changes, drooling, respiratory distress, or uvular edema
    • Video laryngoscopy preferred to minimize manipulation
    • Blind nasotracheal intubation is contraindicated (risk of perforation/false passage)
    • Have cricothyrotomy equipment at bedside
    • Consider nebulized racemic epinephrine while preparing for intubation if stridor present[13]

Resuscitation

  • Large-bore IV access (at least 2 sites); cardiac monitoring
  • Aggressive IV fluid resuscitation for hemorrhage, third-spacing, or shock
  • Vasopressors if hypotension refractory to fluids
  • Transfuse blood products as needed

Things to avoid

  • Do NOT induce emesis — re-exposes mucosa to caustic agent, risk of perforation and aspiration
  • Do NOT perform gastric lavage — risk of esophageal perforation
  • Do NOT attempt to neutralize with a base — exothermic reaction compounds chemical injury with thermal injury, may also induce vomiting[1]
  • Do NOT give activated charcoal — ineffective for caustics, obscures endoscopic view, aspiration risk
  • Dilution with water or milk is generally NOT recommended for liquid acid ingestions — may provoke vomiting[6]
    • Exception: dilution may have limited benefit within the first few minutes after a solid/granular caustic ingestion to remove adherent particles
  • Do NOT routinely give corticosteroids — evidence does not support efficacy in preventing stricture; may increase perforation risk[14]
  • Do NOT routinely insert NGT — risk of perforation in severely injured esophagus
    • Exception: nasogastric suction may be considered early after large-volume liquid acid ingestion (especially HF, HgCl₂, ZnCl₂) if no signs of perforation, to limit ongoing gastric and distal exposure[15]

Supportive care

  • NPO until injury severity established
  • Proton pump inhibitor or H2-receptor antagonist
  • Parenteral nutrition if prolonged NPO anticipated
  • Broad-spectrum antibiotics only if perforation suspected or confirmed
  • Pain management

Surgical consultation

  • Emergent surgical consultation for:[7]
    • Clinical signs of perforation (peritonitis, pneumoperitoneum, mediastinal air)
    • Hemodynamic instability with evidence of hemorrhage
    • Persistent metabolic acidosis or coagulopathy suggesting transmural necrosis
    • Grade IIIb injury on EGD or CT findings of transmural necrosis
  • Exploratory laparotomy is the standard approach for emergency surgery
  • Total gastrectomy may be required for extensive gastric necrosis (partial gastrectomy is not recommended due to risk of progressive necrosis in remnant)[16]

Special considerations by agent

  • Hydrofluoric acid (HF) — uniquely dangerous due to systemic fluoride toxicity[17]
    • Causes life-threatening hypocalcemia, hypomagnesemia, and hyperkalemia → cardiac dysrhythmias, QTc prolongation, cardiac arrest
    • Administer empiric IV calcium for any significant HF exposure, QTc prolongation, or dysrhythmia
    • Continuous cardiac monitoring mandatory
    • Consider early NGT suction to limit absorption
  • Sulfuric acid (H₂SO₄) — highly exothermic upon contact with water; produces high anion gap metabolic acidosis from absorbed sulfate
  • Hydrochloric acid (HCl) — concentrated ingestion >60 mL causes severe gastric and duodenal necrosis with risk of perforation; produces hyperchloremic metabolic acidosis[18]

Disposition

  • Asymptomatic, accidental, small-volume, low-concentration ingestion (child or adult):
    • Observe 4-6 hours; if tolerating PO, no symptoms, may discharge with GI follow-up and return precautions[15]
  • Symptomatic patients:
    • Admit; NPO; arrange EGD within 12-24 hours
    • GI consultation
  • Zargar Grade ≥ IIb:
    • Admit to ICU or monitored setting
    • Surgical consultation
  • Evidence of perforation, hemodynamic instability, or transmural necrosis:
    • Emergent surgical consultation and ICU admission
  • All intentional ingestions:
    • Psychiatric evaluation mandatory prior to discharge[7]
  • Long-term follow-up considerations:
    • Stricture formation occurs in up to 70-100% of Grade IIb-IIIa injuries, typically within the first 2 months; endoscopic dilation initiated at 3 weeks post-ingestion[4]
    • Upper GI bleeding risk at 2-4 weeks post-ingestion
    • Tracheoesophageal fistula may develop months after ingestion
    • 1000-fold increased risk of esophageal carcinoma (squamous cell or adenocarcinoma) after high-grade caustic burns; surveillance endoscopy recommended beginning 15-20 years post-injury[2]
    • Gastric outlet obstruction from antropyloric stenosis is a common late complication specific to acid ingestion[19]

See Also

External Links

References

  1. ↑ 1.0 1.1 1.2 Hoffman RS, Burns MM, Gosselin S. Ingestion of caustic substances. N Engl J Med. 2020;382(18):1739-1748. doi:10.1056/NEJMra1810769
  2. ↑ 2.0 2.1 Caustic ingestion
  3. ↑ Chen RJ, O'Malley RN, Salzman M. Updates on the Evaluation and Management of Caustic Exposures. Emerg Med Clin North Am. 2022;40(2):343-364. doi:10.1016/j.emc.2022.01.013
  4. ↑ 4.0 4.1 Park KS. Evaluation and management of caustic injuries from ingestion of acid or alkaline substances. Clin Endosc. 2014;47(4):301-307. doi:10.5946/ce.2014.47.4.301
  5. ↑ 5.0 5.1 Lupa M, Magne J, Guarisco JL, Amedee R. Update on the Diagnosis and Treatment of Caustic Ingestion. Ochsner J. 2009;9(2):54-59.
  6. ↑ 6.0 6.1 Caustic Ingestion. Merck Manual Professional Edition. 2025.
  7. ↑ 7.0 7.1 7.2 7.3 7.4 Chirica M, Kelly MD, Siboni S, et al. Esophageal emergencies: WSES guidelines. World J Emerg Surg. 2019;14:26. doi:10.1186/s13017-019-0245-2
  8. ↑ Previtera C, Giusti F, Guglielmi M. Predictive value of visible lesions (cheeks, lips, oropharynx) in suspected caustic ingestion: may endoscopy reasonably be omitted in completely negative pediatric patients? Pediatr Emerg Care. 1990;6(3):176-178.
  9. ↑ Chirica M, Resche-Rigon M, Pariente B, et al. Computed tomography evaluation of high-grade esophageal necrosis after corrosive ingestion to avoid unnecessary esophagectomy. Surg Endosc. 2015;29(6):1452-1461. doi:10.1007/s00464-014-3823-0
  10. ↑ De Barros SG, et al. Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017;8(2):90-98. doi:10.4292/wjgpt.v8.i2.90
  11. ↑ Zargar SA, Kochhar R, Mehta S, Mehta SK. The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc. 1991;37(2):165-169.
  12. ↑ Cheng HT, Cheng CL, Lin CH, et al. Caustic ingestion in adults: the role of endoscopic classification in predicting outcome. BMC Gastroenterol. 2008;8:31. doi:10.1186/1471-230X-8-31
  13. ↑ Emergency Care BC. Caustic Injuries — Diagnosis and Management. 2024.
  14. ↑ Katibe R, Abdelgadir I, McGrogan P, Akobeng AK. Corticosteroids for preventing caustic esophageal strictures: systematic review and meta-analysis. J Pediatr Gastroenterol Nutr. 2018;66(6):898-902. doi:10.1097/MPG.0000000000001852
  15. ↑ 15.0 15.1 Lung D. Caustic Ingestions Treatment & Management. Medscape. 2024.
  16. ↑ Corrosive Ingestion. Indian J Crit Care Med. 2019.
  17. ↑ Vohra R, et al. Hydrofluoric Acid: Burns and Systemic Toxicity, Protective Measures, Immediate and Hospital Medical Treatment. Curr Pharm Des. 2018;24(28):3327-3333. doi:10.2174/1381612824666181026150700
  18. ↑ Corrosive ingestions. Life in the Fast Lane (LITFL). 2020.
  19. ↑ Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK. Ingestion of corrosive acids: spectrum of injury to upper gastrointestinal tract and natural history. Gastroenterology. 1989;97(3):702-707.
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