What is the management approach for acid ingestion?

Management of Acid Ingestion

Acid ingestion requires immediate assessment of injury severity through esophagogastroduodenoscopy (EGD), with management focused on preventing systemic complications, perforation, and late stricture formation—acid ingestions carry significantly higher morbidity and mortality than alkali ingestions. 1, 2

Immediate Assessment and Stabilization

Initial Evaluation

• Identify the specific acid ingested, concentration, volume, and whether ingestion was intentional or accidental to stratify risk—strong acids like hydrochloric, sulfuric, and glacial acetic acid cause the most severe injuries. 1, 3, 2
• Contact Poison Control Centers immediately to evaluate systemic toxicity potential of the specific agent. 1
• Assess airway patency and respiratory status—severe caustic injury to the upper respiratory tract may require emergent endotracheal intubation. 3, 4
• Obtain arterial blood gas to detect severe acidosis, which indicates systemic absorption and extensive tissue injury. 5

Critical Laboratory Studies

• Renal function tests (urea, creatinine) to assess injury severity and detect acute kidney injury from hemolysis. 1, 4
• Complete blood count to identify hemolysis and anemia. 4
• Liver function tests and C-reactive protein—elevations suggest transmural necrosis. 1
• Coagulation studies to detect disseminated intravascular coagulation. 4
• β-HCG in women of childbearing age. 1

Diagnostic Imaging

Esophagogastroduodenoscopy (EGD)

• EGD is the gold standard for determining presence and severity of corrosive esophageal and gastric lesions—perform within 12-24 hours when patient is stable. 1, 3
• Assign Zargar grade to guide management decisions and predict complications. 3
• Early endoscopy is safe and provides crucial prognostic information—the grade of mucosal injury is the strongest predictor of systemic complications, GI complications, and mortality (relative risk 9). 2

Computed Tomography

• CT imaging increasingly plays a role in defining extent of injury, particularly when perforation is suspected. 3
• Useful for detecting transmural necrosis and planning surgical intervention. 1

Medical Management

Acute Phase Treatment

• Bowel rest is mandatory to prevent further injury and allow healing. 3
• Proton pump inhibitor (PPI) therapy—initiate high-dose PPI (twice-daily dosing) to reduce acid-mediated secondary injury. 6, 1, 3
• Corticosteroids may be considered depending on extent of injury, though evidence is limited. 3
• Broad-spectrum antibiotics if transmural injury or perforation is suspected. 3
• Aggressive fluid resuscitation and hemodynamic support for shock. 4

Management of Systemic Complications

• For severe hemolysis: Plasma separation is the quickest and most effective detoxification method; exchange transfusion may be necessary in severe cases. 4
• For acute kidney injury: Hemodialysis for secondary renal failure. 4
• For disseminated intravascular coagulation: Low-dose heparin, antithrombin III substitution, and blood product replacement. 4
• Careful acid-base management throughout treatment course. 4

Surgical Intervention

Indications for Surgery

• Esophageal or gastric perforation requires immediate surgical intervention—this occurs in approximately 6% of acid ingestions. 3, 2
• Massive gastric hemorrhage, though uncommon, necessitates urgent surgery. 7
• Serial laparoscopic evaluations may be needed to assess evolving gastrointestinal tract injuries. 5
• Total gastrectomy may be required for extensive gastric necrosis. 5

Long-Term Management

Stricture Prevention and Treatment

• Gastric outlet obstruction is a common late complication that may develop after an asymptomatic interval—maintain high index of suspicion. 7
• Strictures develop in approximately 15-17% of patients regardless of acid vs. alkali ingestion. 2
• Endoscopic dilation is successful in only 34% of patients with strictures; most require primary (n=7) or secondary (n=11) surgical intervention. 2
• Continue PPI therapy indefinitely at lowest effective dose for patients with documented mucosal injury. 6, 1

Prognostic Factors

Poor Prognostic Indicators

• Acid ingestion carries significantly worse outcomes than alkali ingestion: higher rates of mucosal injury (median grade 2 vs. 1), longer hospital stays (9.9 vs. 7.2 days), more ICU admissions (44% vs. 22%), more systemic complications (24% vs. 3%), higher perforation rates (6% vs. 0%), and higher mortality (14% vs. 2%). 2
• Glacial acetic acid ingestion is particularly lethal—400 ml of 25% acetic acid is normally considered a lethal dose. 2, 4
• Grade of mucosal injury at endoscopy is the strongest predictive factor for complications and mortality. 2

Critical Pitfalls to Avoid

• The absence of severe symptoms soon after acid ingestion is often misleading—patients may appear stable initially but develop severe complications later. 7
• Do not delay EGD based on lack of symptoms—early endoscopy provides essential prognostic information. 2
• Do not underestimate systemic toxicity—monitor for hemolysis, acidosis, and renal failure even with seemingly limited oral exposure. 5, 4
• Inadequate monitoring for late complications, particularly gastric outlet obstruction, leads to delayed diagnosis. 7