Acid ingestion: Difference between revisions

(Created page with "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.<ref name="Hoffman2020">Hoffman RS, Burns MM, Gosselin S. Ingestion of caustic substances. ''N Engl J Med''. 2020;382(18):1739-1748. doi:10.1056/NEJMra1810769</ref> Acid ingestion carries a higher mortality rate than alkali ingestion.<ref name="WikEM">Caustic...")
 
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Acid ingestion is a subcategory of [[Caustic ingestion|caustic ingestion]] in which a strong acid (pH <2) causes injury to the upper gastrointestinal tract, predominantly the stomach, through coagulation necrosis.<ref name="Hoffman2020">Hoffman RS, Burns MM, Gosselin S. Ingestion of caustic substances. ''N Engl J Med''. 2020;382(18):1739-1748. doi:10.1056/NEJMra1810769</ref> Acid ingestion carries a higher mortality rate than alkali ingestion.<ref name="WikEM">[[Caustic ingestion]]</ref>
==Background==
==Background==
*Acid ingestion is a subcategory of [[Caustic ingestion|caustic ingestion]] in which a strong acid (pH <2) causes injury to the upper gastrointestinal tract, predominantly the stomach, through coagulation necrosis.<ref name="Hoffman2020">Hoffman RS, Burns MM, Gosselin S. Ingestion of caustic substances. ''N Engl J Med''. 2020;382(18):1739-1748. doi:10.1056/NEJMra1810769</ref> Acid ingestion carries a higher mortality rate than alkali ingestion.<ref name="WikEM">[[Caustic ingestion]]</ref>
*Acids act as proton donors, causing cell death through protein denaturation and '''coagulation necrosis'''<ref name="Hoffman2020"/>
*Acids act as proton donors, causing cell death through protein denaturation and '''coagulation necrosis'''<ref name="Hoffman2020"/>
**Coagulation necrosis forms a protective eschar that classically was thought to limit tissue penetration depth
**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<ref name="Chen2022">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</ref>
**However, recent data suggest esophageal perforation rates from acids may be higher than previously believed<ref name="Chen2022">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</ref>
*Acids tend to transit the esophagus rapidly due to low viscosity, causing '''preferential gastric injury'''
*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<ref name="Park2014">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</ref>
**Pylorospasm from acid exposure prolongs gastric contact time (up to 90 minutes), leading to pooling and high-grade gastric burns<ref name="Park2014">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</ref>
**Gastric antrum and pylorus are most commonly affected
**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<ref name="Lupa2009">Lupa M, Magne J, Guarisco JL, Amedee R. Update on the Diagnosis and Treatment of Caustic Ingestion. ''Ochsner J''. 2009;9(2):54-59.</ref>
*Acids have a noxious taste that may trigger gagging and choking, predisposing to aspiration with subsequent airway injury<ref name="Lupa2009">Lupa M, Magne J, Guarisco JL, Amedee R. Update on the Diagnosis and Treatment of Caustic Ingestion. ''Ochsner J''. 2009;9(2):54-59.</ref>
*Certain acids have unique '''systemic toxicity''' beyond local caustic effects (see [[#Special considerations by agent|Special considerations]])
*Certain acids have unique systemic toxicity beyond local caustic effects (see [[#Special considerations by agent|Special considerations]])
*80% of caustic ingestions worldwide occur in children (usually accidental, small-volume, often benign)<ref name="Merck">Caustic Ingestion. ''Merck Manual Professional Edition''. 2025.</ref>
*80% of caustic ingestions worldwide occur in children (usually accidental, small-volume, often benign)<ref name="Merck">Caustic Ingestion. ''Merck Manual Professional Edition''. 2025.</ref>
*In adults, ingestion is more often intentional (self-harm), involves larger volumes, and is more frequently life-threatening<ref name="Chirica2017">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</ref>
*In adults, ingestion is more often intentional (self-harm), involves larger volumes, and is more frequently life-threatening<ref name="Chirica2017">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</ref>
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==Clinical features==
==Clinical features==
*'''Signs and symptoms are inadequate to predict the presence or severity of esophageal or gastric injury'''<ref name="Previtera1990">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.</ref>
* Signs and symptoms are inadequate to predict the presence or severity of esophageal or gastric injury<ref name="Previtera1990">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.</ref>
*'''Absence of oropharyngeal burns does NOT exclude significant esophageal or gastric injury'''
* Absence of oropharyngeal burns does NOT exclude significant esophageal or gastric injury


===Oropharyngeal===
===Oropharyngeal===
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*[[Retropharyngeal abscess]]
*[[Retropharyngeal abscess]]
*[[Foreign body ingestion]]
*[[Foreign body ingestion]]
{{Dysphagia DDX}}


==Evaluation==
==Evaluation==
===Workup===
===Workup===
*'''Identify the specific agent, concentration, estimated volume, time of ingestion, and intent'''
* Identify the specific agent, concentration, estimated volume, time of ingestion, and intent
**Obtain product label, MSDS/SDS when possible
**Obtain product label, MSDS/SDS when possible
**Contact [[Poison control]] for guidance
**Contact [[Poison control]] for guidance
*'''Labs:'''
* Labs:
**CBC, BMP, hepatic function panel, coagulation studies (PT/INR, fibrinogen), type and screen
**CBC, BMP, hepatic function panel, coagulation studies (PT/INR, fibrinogen), type and screen
**Serum lactate, VBG/ABG (pH, lactate)
**Serum lactate, VBG/ABG (pH, lactate)
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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 [[hydrofluoric acid]])
*'''Imaging:'''
* Imaging:
**Chest and abdominal radiograph — assess for pneumomediastinum, pneumoperitoneum, pleural effusion
**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<ref name="Chirica2015">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</ref>
** 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<ref name="Chirica2015">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</ref>
*'''Esophagogastroduodenoscopy (EGD):'''
* Esophagogastroduodenoscopy (EGD):
**Gold standard for grading injury severity
**Gold standard for grading injury severity
**Perform within '''12-24 hours''' of ingestion<ref name="Chirica2017"/>
**Perform within 12-24 hours of ingestion<ref name="Chirica2017"/>
***Too early (<12 hr) may underestimate injury extent
***Too early (<12 hr) may underestimate injury extent
***Avoid between days 5-15 post-ingestion due to maximal tissue friability and perforation risk<ref name="DeBarros2017">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</ref>
***Avoid between days 5-15 post-ingestion due to maximal tissue friability and perforation risk<ref name="DeBarros2017">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</ref>
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===Diagnosis===
===Diagnosis===
*EGD findings graded by the '''Zargar classification:'''<ref name="Zargar1991">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.</ref>
*EGD findings graded by the Zargar classification:<ref name="Zargar1991">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.</ref>
**'''Grade 0''' — Normal mucosa
** Grade 0 — Normal mucosa
**'''Grade I''' — Edema and hyperemia
** Grade I — Edema and hyperemia
**'''Grade IIa''' — Superficial ulceration, hemorrhage, erosions, blisters, exudates
** Grade IIa — Superficial ulceration, hemorrhage, erosions, blisters, exudates
**'''Grade IIb''' — Deep, discrete, or circumferential ulceration
** Grade IIb — Deep, discrete, or circumferential ulceration
**'''Grade IIIa''' — Focal necrosis (small, scattered areas of necrosis)
** Grade IIIa — Focal necrosis (small, scattered areas of necrosis)
**'''Grade IIIb''' — Extensive necrosis
** Grade IIIb — Extensive necrosis
**'''Grade IV''' — Perforation (added in some modified classifications)
** Grade IV — Perforation (added in some modified classifications)
*Grades 0, I, and IIa generally recover without long-term sequelae
*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<ref name="Cheng2008">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</ref>
*Grades IIb and above carry significant risk of stricture formation and may require surgical intervention<ref name="Cheng2008">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</ref>
*'''Lab markers predictive of transmural necrosis:''' severe metabolic acidosis (low pH, elevated lactate), leukocytosis, thrombocytopenia, elevated CRP, deranged LFTs, acute kidney injury<ref name="Chirica2017"/>
* Lab markers predictive of transmural necrosis: severe metabolic acidosis (low pH, elevated lactate), leukocytosis, thrombocytopenia, elevated CRP, deranged LFTs, acute kidney injury<ref name="Chirica2017"/>


==Management==
==Management==
===Airway===
===Airway===
*Assess airway '''immediately and continuously''' — may deteriorate rapidly over hours as edema progresses
*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
* Intubate early if stridor, voice changes, drooling, respiratory distress, or uvular edema
**Video laryngoscopy preferred to minimize manipulation
**Video laryngoscopy preferred to minimize manipulation
**Blind nasotracheal intubation is '''contraindicated''' (risk of perforation/false passage)
**Blind nasotracheal intubation is '''contraindicated''' (risk of perforation/false passage)
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*'''Do NOT attempt to neutralize''' with a base — exothermic reaction compounds chemical injury with thermal injury, may also induce vomiting<ref name="Hoffman2020"/>
*'''Do NOT attempt to neutralize''' with a base — exothermic reaction compounds chemical injury with thermal injury, may also induce vomiting<ref name="Hoffman2020"/>
*'''Do NOT give activated charcoal''' — ineffective for caustics, obscures endoscopic view, aspiration risk
*'''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<ref name="Merck"/>
* Dilution with water or milk is generally NOT recommended for liquid acid ingestions — may provoke vomiting<ref name="Merck"/>
**Exception: dilution may have limited benefit within the first few minutes after a solid/granular caustic ingestion to remove adherent particles
**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<ref name="Katibe2018">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</ref>
*'''Do NOT routinely give corticosteroids''' — evidence does not support efficacy in preventing stricture; may increase perforation risk<ref name="Katibe2018">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</ref>
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*Proton pump inhibitor or H2-receptor antagonist
*Proton pump inhibitor or H2-receptor antagonist
*Parenteral nutrition if prolonged NPO anticipated
*Parenteral nutrition if prolonged NPO anticipated
*Broad-spectrum antibiotics '''only''' if perforation suspected or confirmed
*Broad-spectrum antibiotics only if perforation suspected or confirmed
*Pain management
*Pain management


===Surgical consultation===
===Surgical consultation===
*'''Emergent surgical consultation''' for:<ref name="Chirica2017"/>
* Emergent surgical consultation for:<ref name="Chirica2017"/>
**Clinical signs of perforation (peritonitis, pneumoperitoneum, mediastinal air)
**Clinical signs of perforation (peritonitis, pneumoperitoneum, mediastinal air)
**Hemodynamic instability with evidence of hemorrhage
**Hemodynamic instability with evidence of hemorrhage
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===Special considerations by agent===
===Special considerations by agent===
*'''[[Hydrofluoric acid exposure|Hydrofluoric acid (HF)]]''' — uniquely dangerous due to systemic fluoride toxicity<ref name="Vohra2018">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</ref>
* [[Hydrofluoric acid exposure|Hydrofluoric acid (HF)]] — uniquely dangerous due to systemic fluoride toxicity<ref name="Vohra2018">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</ref>
**Causes '''life-threatening hypocalcemia, hypomagnesemia, and hyperkalemia''' → cardiac dysrhythmias, QTc prolongation, cardiac arrest
**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
**Administer empiric IV calcium for any significant HF exposure, QTc prolongation, or dysrhythmia
**Continuous cardiac monitoring mandatory
**Continuous cardiac monitoring mandatory
**Consider early NGT suction to limit absorption
**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
* 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<ref name="LITFL">Corrosive ingestions. ''Life in the Fast Lane (LITFL)''. 2020.</ref>
* Hydrochloric acid (HCl) — concentrated ingestion >60 mL causes severe gastric and duodenal necrosis with risk of perforation; produces hyperchloremic metabolic acidosis<ref name="LITFL">Corrosive ingestions. ''Life in the Fast Lane (LITFL)''. 2020.</ref>


==Disposition==
==Disposition==
*'''Asymptomatic, accidental, small-volume, low-concentration ingestion (child or adult):'''
* 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<ref name="Medscape"/>
**Observe 4-6 hours; if tolerating PO, no symptoms, may discharge with GI follow-up and return precautions<ref name="Medscape"/>
*'''Symptomatic patients:'''
* Symptomatic patients:
**Admit; NPO; arrange EGD within 12-24 hours
**Admit; NPO; arrange EGD within 12-24 hours
**GI consultation
**GI consultation
*'''Zargar Grade ≥ IIb:'''
* Zargar Grade ≥ IIb:
**Admit to ICU or monitored setting
**Admit to ICU or monitored setting
**Surgical consultation
**Surgical consultation
*'''Evidence of perforation, hemodynamic instability, or transmural necrosis:'''
* Evidence of perforation, hemodynamic instability, or transmural necrosis:
**Emergent surgical consultation and ICU admission
**Emergent surgical consultation and ICU admission
*'''All intentional ingestions:'''
* All intentional ingestions:
**Psychiatric evaluation mandatory prior to discharge<ref name="Chirica2017"/>
**Psychiatric evaluation mandatory prior to discharge<ref name="Chirica2017"/>
*'''Long-term follow-up considerations:'''
* 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<ref name="Park2014"/>
**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<ref name="Park2014"/>
**Upper GI bleeding risk at 2-4 weeks post-ingestion
**Upper GI bleeding risk at 2-4 weeks post-ingestion
**Tracheoesophageal fistula may develop months after 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<ref name="WikEM"/>
** 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<ref name="WikEM"/>
**Gastric outlet obstruction from antropyloric stenosis is a common late complication specific to acid ingestion<ref name="Zargar1989">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.</ref>
**Gastric outlet obstruction from antropyloric stenosis is a common late complication specific to acid ingestion<ref name="Zargar1989">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.</ref>


Latest revision as of 09:29, 22 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 hydrofluoric 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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