Alkali ingestion: Difference between revisions

(Created page with "==Background== *Alkali (caustic/corrosive) ingestion refers to oral exposure to substances with a pH ≥ 12, which cause '''liquefactive necrosis''' — saponification of fats, protein denaturation, and cell membrane destruction that penetrates deeply into tissue<ref name="hoffman">Hoffman RS, Burns MM, Gosselin S. Ingestion of caustic substances. ''N Engl J Med''. 2020;382(18):1739-1748. PMID 32348644.</ref> *Unlike acids (which cause coagulative necrosis with a protect...")
 
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==Background==
==Background==
*Alkali (caustic/corrosive) ingestion refers to oral exposure to substances with a pH ≥ 12, which cause '''liquefactive necrosis''' — saponification of fats, protein denaturation, and cell membrane destruction that penetrates deeply into tissue<ref name="hoffman">Hoffman RS, Burns MM, Gosselin S. Ingestion of caustic substances. ''N Engl J Med''. 2020;382(18):1739-1748. PMID 32348644.</ref>
*Alkali (caustic/corrosive) ingestion refers to oral exposure to substances with a pH ≥ 12, which cause liquefactive necrosis — saponification of fats, protein denaturation, and cell membrane destruction that penetrates deeply into tissue<ref name="hoffman">Hoffman RS, Burns MM, Gosselin S. Ingestion of caustic substances. ''N Engl J Med''. 2020;382(18):1739-1748. PMID 32348644.</ref>
*Unlike acids (which cause coagulative necrosis with a protective eschar), alkalis penetrate through tissue layers and can cause '''transmural injury and perforation'''<ref name="hoffman"/>
*Unlike acids (which cause coagulative necrosis with a protective eschar), alkalis penetrate through tissue layers and can cause transmural injury and perforation<ref name="hoffman"/>
*Alkali ingestions are more common than acid ingestions in the US and are the most frequent cause of serious caustic GI injury<ref name="statpearls">Alkali Toxicity. In: ''StatPearls''. Treasure Island (FL): StatPearls Publishing; 2023. PMID 31082166.</ref>
*Alkali ingestions are more common than acid ingestions in the US and are the most frequent cause of serious caustic GI injury<ref name="statpearls">Alkali Toxicity. In: ''StatPearls''. Treasure Island (FL): StatPearls Publishing; 2023. PMID 31082166.</ref>
*Common alkali substances:
*Common alkali substances:
**'''Drain cleaners / oven cleaners:''' Sodium hydroxide (NaOH) or potassium hydroxide (KOH) — "lye"; most common cause of severe injury
**Drain cleaners / oven cleaners: Sodium hydroxide (NaOH) or potassium hydroxide (KOH) — "lye"; most common cause of severe injury
**'''Hair relaxers/straighteners:''' Sodium hydroxide or calcium hydroxide
**Hair relaxers/straighteners: Sodium hydroxide or calcium hydroxide
**'''Laundry/dishwasher detergent pods (LDPs):''' Concentrated alkaline surfactants; increasingly common pediatric exposure
**Laundry/dishwasher detergent pods (LDPs): Concentrated alkaline surfactants; increasingly common pediatric exposure
**'''Household bleach (NaOCl):''' Low concentration (3–8%) rarely causes serious injury; industrial-strength bleach or international formulations may have higher concentration
**Household bleach (NaOCl): Low concentration (3–8%) rarely causes serious injury; industrial-strength bleach or international formulations may have higher concentration
**'''Ammonia:''' Household cleaners
**Ammonia: Household cleaners
**'''Disc/button batteries:''' Generate alkali via electrolysis at the anode; cause focal liquefactive necrosis on contact with mucosa
**Disc/button batteries: Generate alkali via electrolysis at the anode; cause focal liquefactive necrosis on contact with mucosa
*Epidemiology:
*Epidemiology:
**'''Children < 5 years:''' Accidental ingestion; usually small volumes → less severe injury
**Children < 5 years: Accidental ingestion; usually small volumes → less severe injury
**'''Adolescents / Adults:''' Intentional ingestion (suicidal); typically larger volumes → more severe injury and higher mortality<ref name="statpearls"/>
**Adolescents / Adults: Intentional ingestion (suicidal); typically larger volumes → more severe injury and higher mortality<ref name="statpearls"/>
*Severity of injury depends on: pH, titratable alkali reserve (TAR), volume ingested, concentration, physical form (liquid vs. solid vs. gel), and duration of tissue contact<ref name="chirica">Chirica M, Bonavina L, Kelly MD, Sarfati E, Cattan P. Caustic ingestion. ''Lancet''. 2017;389(10083):2041-2052. PMID 28045663.</ref>
*Severity of injury depends on: pH, titratable alkali reserve (TAR), volume ingested, concentration, physical form (liquid vs. solid vs. gel), and duration of tissue contact<ref name="chirica">Chirica M, Bonavina L, Kelly MD, Sarfati E, Cattan P. Caustic ingestion. ''Lancet''. 2017;389(10083):2041-2052. PMID 28045663.</ref>
*Liquid alkalis tend to cause more extensive injury (spread distally to esophagus and stomach); solid/granular alkalis tend to adhere to oropharynx and proximal esophagus
*Liquid alkalis tend to cause more extensive injury (spread distally to esophagus and stomach); solid/granular alkalis tend to adhere to oropharynx and proximal esophagus
*'''Long-term complications:''' Esophageal stricture (most common long-term sequela), gastric outlet obstruction, and a '''1,000-fold increased risk of esophageal carcinoma''' decades after injury<ref name="hoffman"/>
*Long-term complications: Esophageal stricture (most common long-term sequela), gastric outlet obstruction, and a 1,000-fold increased risk of esophageal carcinoma decades after injury<ref name="hoffman"/>


==Clinical Features==
==Clinical Features==
*Presentation ranges from '''asymptomatic''' to '''cardiac arrest''' depending on severity
*Presentation ranges from asymptomatic to cardiac arrest depending on severity
*'''Absence of oropharyngeal burns does NOT exclude significant esophageal or gastric injury''' — up to 10–30% of patients without visible oral burns have esophageal injury on endoscopy<ref name="hoffman"/>
*Absence of oropharyngeal burns does NOT exclude significant esophageal or gastric injury — up to 10–30% of patients without visible oral burns have esophageal injury on endoscopy<ref name="hoffman"/>


===Oropharyngeal===
===Oropharyngeal===
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===Airway===
===Airway===
*Stridor, hoarseness, dysphonia — '''signs of laryngeal/epiglottic edema; may progress rapidly to complete obstruction'''
*Stridor, hoarseness, dysphonia — signs of laryngeal/epiglottic edema; may progress rapidly to complete obstruction
*Cough, tachypnea, respiratory distress
*Cough, tachypnea, respiratory distress
*Aspiration → chemical pneumonitis
*Aspiration → chemical pneumonitis
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==Differential Diagnosis==
==Differential Diagnosis==
*[[Acid ingestion|Acid/corrosive ingestion]]
*[[Caustic ingestion]]
*[[Boron toxicity|Boric acid ingestion]]
*[[Boron toxicity|Boric acid ingestion]]
*Foreign body ingestion (especially [[Button battery ingestion|button battery]])
*Foreign body ingestion (especially [[Button battery ingestion|button battery]])
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==Evaluation==
==Evaluation==
===Workup===
===Workup===
*'''Airway assessment is the first priority''' — examine for stridor, drooling, voice changes, respiratory distress
*Airway assessment is the first priority — examine for stridor, drooling, voice changes, respiratory distress
*'''Do NOT delay airway management''' — early intubation if any concern for progressive airway edema; airway can deteriorate rapidly<ref name="rumpf">Rumpf JJ, Settmacher U, Rauchfuss F. Acute emergency care and airway management of caustic ingestion in adults. ''Scand J Trauma Resusc Emerg Med''. 2016;24:45. PMID 27068117.</ref>
*'''Do NOT delay airway management''' — early intubation if any concern for progressive airway edema; airway can deteriorate rapidly<ref name="rumpf">Rumpf JJ, Settmacher U, Rauchfuss F. Acute emergency care and airway management of caustic ingestion in adults. ''Scand J Trauma Resusc Emerg Med''. 2016;24:45. PMID 27068117.</ref>
*'''Labs:'''
*Labs:
**CBC (leukocytosis may indicate severe injury/necrosis)
**CBC (leukocytosis may indicate severe injury/necrosis)
**BMP/CMP (electrolytes, renal function, bicarbonate)
**BMP/CMP (electrolytes, renal function, bicarbonate)
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**Lipase (if concern for pancreatic injury)
**Lipase (if concern for pancreatic injury)
**Serum β-hCG in women of reproductive age
**Serum β-hCG in women of reproductive age
*'''Imaging:'''
*Imaging:
**'''CXR and upright abdominal XR:''' Evaluate for pneumomediastinum, pneumoperitoneum, pleural effusion, aspiration
**CXR and upright abdominal XR: Evaluate for pneumomediastinum, pneumoperitoneum, pleural effusion, aspiration
**'''Contrast-enhanced CT (neck/chest/abdomen):''' Increasingly used as first-line imaging in adults; can identify transmural necrosis (absence of post-contrast wall enhancement), perforation, and extent of injury<ref name="chirica"/>
**Contrast-enhanced CT (neck/chest/abdomen): Increasingly used as first-line imaging in adults; can identify transmural necrosis (absence of post-contrast wall enhancement), perforation, and extent of injury<ref name="chirica"/>
***CT should be performed 3–6 hours post-ingestion per WSES guidelines
***CT should be performed 3–6 hours post-ingestion per WSES guidelines
***High specificity for severe injury; may reduce need for emergent endoscopy in some centers
***High specificity for severe injury; may reduce need for emergent endoscopy in some centers
*'''Endoscopy (EGD):'''
*Endoscopy (EGD):
**Standard for grading injury severity using the '''Zargar classification'''<ref name="zargar">Zargar SA, Kochhar R, Mehta S, et al. The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. ''Gastrointest Endosc''. 1991;37(2):165-169. PMID 2032601.</ref>
**Standard for grading injury severity using the Zargar classification<ref name="zargar">Zargar SA, Kochhar R, Mehta S, et al. The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. ''Gastrointest Endosc''. 1991;37(2):165-169. PMID 2032601.</ref>
**Should be performed '''within 12–24 hours''' (do not delay beyond 48 hours — perforation risk increases after this point)
**Should be performed '''within 12–24 hours''' (do not delay beyond 48 hours — perforation risk increases after this point)
**Typically performed by GI or surgery; not an ED procedure
**Typically performed by GI or surgery; not an ED procedure


===Diagnosis===
===Diagnosis===
*Diagnosis is '''clinical''' — based on history of alkali exposure and consistent symptoms
*Diagnosis is clinical — based on history of alkali exposure and consistent symptoms
*'''Zargar Endoscopic Classification:'''<ref name="zargar"/>
*Zargar Endoscopic Classification:<ref name="zargar"/>
{| class="wikitable"
{| class="wikitable"
|-
|-
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==Management==
==Management==
===Airway (First Priority)===
===Airway (First Priority)===
*'''Early intubation''' if any evidence of airway compromise (stridor, voice changes, drooling, respiratory distress, significant oropharyngeal edema)<ref name="rumpf"/>
*Early intubation if any evidence of airway compromise (stridor, voice changes, drooling, respiratory distress, significant oropharyngeal edema)<ref name="rumpf"/>
*Have a '''difficult airway plan''' ready — consider early involvement of anesthesia; awake fiberoptic intubation or surgical airway may be needed if severe laryngeal edema
*Have a '''difficult airway plan''' ready — consider early involvement of anesthesia; awake fiberoptic intubation or surgical airway may be needed if severe laryngeal edema
*50% of patients with intentional alkali ingestion in one series required intubation<ref name="rumpf"/>
*50% of patients with intentional alkali ingestion in one series required intubation<ref name="rumpf"/>


===Resuscitation===
===Resuscitation===
*'''IV access (two large-bore)''' and crystalloid resuscitation
*IV access (two large-bore) and crystalloid resuscitation
*'''NPO''' — nothing by mouth until injury is graded
*NPO — nothing by mouth until injury is graded
*'''Correct coagulopathy and acidosis''' as needed
*Correct coagulopathy and acidosis as needed
*'''Blood products''' if hemorrhaging
*Blood products if hemorrhaging


===What NOT To Do===
===What NOT To Do===
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===Dilution (Controversial / Limited Role)===
===Dilution (Controversial / Limited Role)===
*'''Small volumes''' of water or milk (120–240 mL) may be offered '''within 30 minutes''' of ingestion of '''solid/granular''' alkali only — goal is to dislodge particles adhering to mucosa<ref name="statpearls"/>
*Small volumes of water or milk (120–240 mL) may be offered '''within 30 minutes''' of ingestion of '''solid/granular''' alkali only — goal is to dislodge particles adhering to mucosa<ref name="statpearls"/>
*Do NOT use for liquid alkali ingestions (risk of inducing emesis outweighs benefit)
*Do NOT use for liquid alkali ingestions (risk of inducing emesis outweighs benefit)
*Do NOT delay other management for dilution
*Do NOT delay other management for dilution


===Supportive Care===
===Supportive Care===
*'''Pain management:''' IV opioid analgesia as needed
*Pain management: IV opioid analgesia as needed
*'''PPI therapy:''' IV proton pump inhibitor (reduces acid exposure to injured tissue); routinely initiated though evidence is limited
*PPI therapy: IV proton pump inhibitor (reduces acid exposure to injured tissue); routinely initiated though evidence is limited
*'''Antibiotics:''' Not routinely indicated; give if perforation suspected or documented, or if the patient develops signs of sepsis
*Antibiotics: Not routinely indicated; give if perforation suspected or documented, or if the patient develops signs of sepsis
*'''Corticosteroids:'''
*Corticosteroids:
**Role is '''controversial'''
**Role is controversial
**Some evidence supports high-dose methylprednisolone (starting within 48 hours) for '''grade 2b''' injuries to reduce stricture formation<ref name="usta">Usta M, Erkan T, Cokugras FC, et al. High doses of methylprednisolone in the management of caustic esophageal burns. ''Pediatrics''. 2014;133(6):e1518-e1524. PMID 24864180.</ref>
**Some evidence supports high-dose methylprednisolone (starting within 48 hours) for grade 2b injuries to reduce stricture formation<ref name="usta">Usta M, Erkan T, Cokugras FC, et al. High doses of methylprednisolone in the management of caustic esophageal burns. ''Pediatrics''. 2014;133(6):e1518-e1524. PMID 24864180.</ref>
**Steroids are NOT indicated for grade 1, 2a (unnecessary) or grade 3 (may mask perforation signs and impair healing)
**Steroids are NOT indicated for grade 1, 2a (unnecessary) or grade 3 (may mask perforation signs and impair healing)
**Decision should be made in consultation with GI/surgery after endoscopic grading
**Decision should be made in consultation with GI/surgery after endoscopic grading


===Surgical Consultation===
===Surgical Consultation===
*'''Emergent surgery''' is indicated for:<ref name="chirica"/>
*Emergent surgery is indicated for:<ref name="chirica"/>
**Evidence of perforation (pneumomediastinum, pneumoperitoneum)
**Evidence of perforation (pneumomediastinum, pneumoperitoneum)
**Zargar grade 3b on endoscopy (extensive necrosis)
**Zargar grade 3b on endoscopy (extensive necrosis)
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==Disposition==
==Disposition==
*'''Discharge after 4–6 hour observation:'''
*Discharge after 4–6 hour observation:
**Asymptomatic patients with '''accidental''' ingestion of '''small volume''' of '''low-concentration''' alkali (e.g. small taste of dilute household bleach, household ammonia cleaner)
**Asymptomatic patients with accidental ingestion of small volume of low-concentration alkali (e.g. small taste of dilute household bleach, household ammonia cleaner)
**Must tolerate PO challenge without difficulty prior to discharge
**Must tolerate PO challenge without difficulty prior to discharge
**Ensure close follow-up; consider outpatient GI referral for delayed EGD
**Ensure close follow-up; consider outpatient GI referral for delayed EGD
*'''Admit:'''
*Admit:
**All symptomatic patients
**All symptomatic patients
**All '''intentional''' ingestions regardless of symptoms
**All intentional ingestions regardless of symptoms
**All pediatric patients with suspected significant ingestion
**All pediatric patients with suspected significant ingestion
**Any patient requiring endoscopy or CT for injury grading
**Any patient requiring endoscopy or CT for injury grading
**Patients with abnormal labs (acidosis, elevated lactate, leukocytosis)
**Patients with abnormal labs (acidosis, elevated lactate, leukocytosis)
*'''ICU admission:'''
*ICU admission:
**Airway compromise or intubation
**Airway compromise or intubation
**Hemodynamic instability
**Hemodynamic instability
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**Evidence of perforation
**Evidence of perforation
**Multiorgan dysfunction, DIC, or severe metabolic acidosis
**Multiorgan dysfunction, DIC, or severe metabolic acidosis
*'''Surgical consultation:''' Early for all significant ingestions; emergent for perforation or grade 3b injury
*Surgical consultation: Early for all significant ingestions; emergent for perforation or grade 3b injury
*'''Psychiatric evaluation:''' '''Mandatory''' for all intentional ingestions prior to hospital discharge<ref name="chirica"/>
*Psychiatric evaluation: Mandatory for all intentional ingestions prior to hospital discharge<ref name="chirica"/>
*'''Poison Control:''' '''1-800-222-1222'''
*Poison Control: 1-800-222-1222


==See Also==
==See Also==

Latest revision as of 09:29, 22 March 2026

Background

  • Alkali (caustic/corrosive) ingestion refers to oral exposure to substances with a pH ≥ 12, which cause liquefactive necrosis — saponification of fats, protein denaturation, and cell membrane destruction that penetrates deeply into tissue[1]
  • Unlike acids (which cause coagulative necrosis with a protective eschar), alkalis penetrate through tissue layers and can cause transmural injury and perforation[1]
  • Alkali ingestions are more common than acid ingestions in the US and are the most frequent cause of serious caustic GI injury[2]
  • Common alkali substances:
    • Drain cleaners / oven cleaners: Sodium hydroxide (NaOH) or potassium hydroxide (KOH) — "lye"; most common cause of severe injury
    • Hair relaxers/straighteners: Sodium hydroxide or calcium hydroxide
    • Laundry/dishwasher detergent pods (LDPs): Concentrated alkaline surfactants; increasingly common pediatric exposure
    • Household bleach (NaOCl): Low concentration (3–8%) rarely causes serious injury; industrial-strength bleach or international formulations may have higher concentration
    • Ammonia: Household cleaners
    • Disc/button batteries: Generate alkali via electrolysis at the anode; cause focal liquefactive necrosis on contact with mucosa
  • Epidemiology:
    • Children < 5 years: Accidental ingestion; usually small volumes → less severe injury
    • Adolescents / Adults: Intentional ingestion (suicidal); typically larger volumes → more severe injury and higher mortality[2]
  • Severity of injury depends on: pH, titratable alkali reserve (TAR), volume ingested, concentration, physical form (liquid vs. solid vs. gel), and duration of tissue contact[3]
  • Liquid alkalis tend to cause more extensive injury (spread distally to esophagus and stomach); solid/granular alkalis tend to adhere to oropharynx and proximal esophagus
  • Long-term complications: Esophageal stricture (most common long-term sequela), gastric outlet obstruction, and a 1,000-fold increased risk of esophageal carcinoma decades after injury[1]

Clinical Features

  • Presentation ranges from asymptomatic to cardiac arrest depending on severity
  • Absence of oropharyngeal burns does NOT exclude significant esophageal or gastric injury — up to 10–30% of patients without visible oral burns have esophageal injury on endoscopy[1]

Oropharyngeal

  • Oral pain, drooling, dysphagia, odynophagia
  • Erythema, edema, ulceration, or white/gray pseudomembranes of the lips, tongue, palate, and posterior pharynx
  • Refusal to swallow (children)

Airway

  • Stridor, hoarseness, dysphonia — signs of laryngeal/epiglottic edema; may progress rapidly to complete obstruction
  • Cough, tachypnea, respiratory distress
  • Aspiration → chemical pneumonitis

Esophageal / Gastric

  • Chest pain, epigastric pain, back pain
  • Hematemesis
  • Signs of perforation: severe chest/abdominal pain, rigidity, subcutaneous emphysema

Systemic (Severe Ingestions)

  • Hypotension, tachycardia (hemorrhage, third-spacing, sepsis)
  • Metabolic acidosis (lactic acidosis from tissue necrosis and hypoperfusion)
  • Fever, leukocytosis
  • Disseminated intravascular coagulation
  • Multiorgan failure

Delayed Complications

  • Esophageal/gastric stricture (weeks to months)
  • Esophageal perforation (greatest risk in first 5–14 days post-ingestion when tissue is weakest during granulation)
  • Esophageal carcinoma (years to decades)

Differential Diagnosis

Evaluation

Workup

  • Airway assessment is the first priority — examine for stridor, drooling, voice changes, respiratory distress
  • Do NOT delay airway management — early intubation if any concern for progressive airway edema; airway can deteriorate rapidly[4]
  • Labs:
    • CBC (leukocytosis may indicate severe injury/necrosis)
    • BMP/CMP (electrolytes, renal function, bicarbonate)
    • VBG/ABG with lactate (metabolic acidosis and elevated lactate are predictive of transmural necrosis)[3]
    • LFTs (hepatic injury in severe cases)
    • Coagulation studies (PT/INR) — coagulopathy may develop
    • Type and screen/crossmatch (anticipate hemorrhage)
    • Lipase (if concern for pancreatic injury)
    • Serum β-hCG in women of reproductive age
  • Imaging:
    • CXR and upright abdominal XR: Evaluate for pneumomediastinum, pneumoperitoneum, pleural effusion, aspiration
    • Contrast-enhanced CT (neck/chest/abdomen): Increasingly used as first-line imaging in adults; can identify transmural necrosis (absence of post-contrast wall enhancement), perforation, and extent of injury[3]
      • CT should be performed 3–6 hours post-ingestion per WSES guidelines
      • High specificity for severe injury; may reduce need for emergent endoscopy in some centers
  • Endoscopy (EGD):
    • Standard for grading injury severity using the Zargar classification[5]
    • Should be performed within 12–24 hours (do not delay beyond 48 hours — perforation risk increases after this point)
    • Typically performed by GI or surgery; not an ED procedure

Diagnosis

  • Diagnosis is clinical — based on history of alkali exposure and consistent symptoms
  • Zargar Endoscopic Classification:[5]
Grade Findings Prognosis
0 Normal No injury
1 Mucosal edema, hyperemia Excellent; heals without sequelae
2a Superficial ulceration, exudates, friability Good; low stricture risk
2b Deep or circumferential ulceration Moderate; significant stricture risk (~70%)
3a Focal/scattered necrosis Poor; high perforation and stricture risk
3b Extensive necrosis Surgical emergency; high mortality
  • Abnormal labs (severe acidosis, elevated lactate, leukocytosis, thrombocytopenia, elevated CRP, renal injury) are predictive of transmural necrosis and poor outcomes[3]
  • Initial normal labs do NOT exclude transmural necrosis — serial monitoring is essential

Management

Airway (First Priority)

  • Early intubation if any evidence of airway compromise (stridor, voice changes, drooling, respiratory distress, significant oropharyngeal edema)[4]
  • Have a difficult airway plan ready — consider early involvement of anesthesia; awake fiberoptic intubation or surgical airway may be needed if severe laryngeal edema
  • 50% of patients with intentional alkali ingestion in one series required intubation[4]

Resuscitation

  • IV access (two large-bore) and crystalloid resuscitation
  • NPO — nothing by mouth until injury is graded
  • Correct coagulopathy and acidosis as needed
  • Blood products if hemorrhaging

What NOT To Do

  • Do NOT induce emesis — re-exposes esophagus to caustic agent; risk of aspiration and perforation[1]
  • Do NOT attempt neutralization (i.e. do not give a weak acid) — exothermic reaction causes thermal injury on top of chemical injury[2]
  • Do NOT place a nasogastric tube blindly — risk of esophageal perforation
  • Do NOT give activated charcoal — does not adsorb alkalis; obscures endoscopy; aspiration risk[1]
  • Do NOT perform gastric lavage — contraindicated due to perforation risk[2]

Dilution (Controversial / Limited Role)

  • Small volumes of water or milk (120–240 mL) may be offered within 30 minutes of ingestion of solid/granular alkali only — goal is to dislodge particles adhering to mucosa[2]
  • Do NOT use for liquid alkali ingestions (risk of inducing emesis outweighs benefit)
  • Do NOT delay other management for dilution

Supportive Care

  • Pain management: IV opioid analgesia as needed
  • PPI therapy: IV proton pump inhibitor (reduces acid exposure to injured tissue); routinely initiated though evidence is limited
  • Antibiotics: Not routinely indicated; give if perforation suspected or documented, or if the patient develops signs of sepsis
  • Corticosteroids:
    • Role is controversial
    • Some evidence supports high-dose methylprednisolone (starting within 48 hours) for grade 2b injuries to reduce stricture formation[6]
    • Steroids are NOT indicated for grade 1, 2a (unnecessary) or grade 3 (may mask perforation signs and impair healing)
    • Decision should be made in consultation with GI/surgery after endoscopic grading

Surgical Consultation

  • Emergent surgery is indicated for:[3]
    • Evidence of perforation (pneumomediastinum, pneumoperitoneum)
    • Zargar grade 3b on endoscopy (extensive necrosis)
    • Absence of post-contrast wall enhancement on CT (transmural necrosis)
    • Clinical deterioration despite supportive care (peritonitis, hemodynamic instability, worsening acidosis)
  • Surgical options include esophagogastrectomy with delayed reconstruction

Disposition

  • Discharge after 4–6 hour observation:
    • Asymptomatic patients with accidental ingestion of small volume of low-concentration alkali (e.g. small taste of dilute household bleach, household ammonia cleaner)
    • Must tolerate PO challenge without difficulty prior to discharge
    • Ensure close follow-up; consider outpatient GI referral for delayed EGD
  • Admit:
    • All symptomatic patients
    • All intentional ingestions regardless of symptoms
    • All pediatric patients with suspected significant ingestion
    • Any patient requiring endoscopy or CT for injury grading
    • Patients with abnormal labs (acidosis, elevated lactate, leukocytosis)
  • ICU admission:
    • Airway compromise or intubation
    • Hemodynamic instability
    • Zargar grade 2b or higher on endoscopy
    • Evidence of perforation
    • Multiorgan dysfunction, DIC, or severe metabolic acidosis
  • Surgical consultation: Early for all significant ingestions; emergent for perforation or grade 3b injury
  • Psychiatric evaluation: Mandatory for all intentional ingestions prior to hospital discharge[3]
  • Poison Control: 1-800-222-1222

See Also

External Links

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Hoffman RS, Burns MM, Gosselin S. Ingestion of caustic substances. N Engl J Med. 2020;382(18):1739-1748. PMID 32348644.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 Alkali Toxicity. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2023. PMID 31082166.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Chirica M, Bonavina L, Kelly MD, Sarfati E, Cattan P. Caustic ingestion. Lancet. 2017;389(10083):2041-2052. PMID 28045663.
  4. ↑ 4.0 4.1 4.2 Rumpf JJ, Settmacher U, Rauchfuss F. Acute emergency care and airway management of caustic ingestion in adults. Scand J Trauma Resusc Emerg Med. 2016;24:45. PMID 27068117.
  5. ↑ 5.0 5.1 Zargar SA, Kochhar R, Mehta S, et al. The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc. 1991;37(2):165-169. PMID 2032601.
  6. ↑ Usta M, Erkan T, Cokugras FC, et al. High doses of methylprednisolone in the management of caustic esophageal burns. Pediatrics. 2014;133(6):e1518-e1524. PMID 24864180.
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