What should a pathologist report in a gastric fluid sample from a patient with a history of acid intake?

Pathology Reporting for Gastric Fluid After Acid Ingestion

In a patient with a history of acid (corrosive) ingestion, the pathologist must report the presence and severity of gastric mucosal injury, specifically documenting transmural necrosis, hemorrhagic gastritis, and the anatomic distribution of damage, as these findings directly determine the need for emergency surgical intervention.

Critical Pathologic Features to Report

Severity and Depth of Mucosal Injury

• Transmural necrosis is the most critical finding requiring immediate surgical intervention and must be explicitly documented if present 1
• The pathologist should describe whether injury is superficial (mucosal only) or full-thickness (transmural), as this distinction determines surgical versus medical management 1
• Hemorrhagic gastritis patterns should be documented, noting that superficial hemorrhagic changes may progress over the first 24-48 hours after acid ingestion 1

Anatomic Distribution of Damage

• The prepyloric antrum is almost always injured after mineral acid ingestion and must be specifically assessed 2
• Fundus and cardia involvement should be documented, particularly noting that these areas are more likely to be injured if the stomach was empty at the time of ingestion 2
• Esophageal involvement should be noted if present, though clinically significant esophageal injury occurs in less than 20% of acid ingestion cases (in contrast to alkali ingestion) 2

Distinction from Other Gastric Pathology

Differentiation from Other Conditions

• The pathologist must distinguish acid-induced injury from stress ulcers (multiple superficial fundal lesions in critically ill patients), reactivation of pre-existent ulcer disease, or drug-induced gastritis 3
• Unlike stress ulcers which are typically multiple and superficial, acid ingestion produces more extensive antral injury with potential for transmural necrosis 3, 2

Mechanism-Related Features

• Acid ingestion causes direct mucosal barrier disruption with backdiffusion of hydrogen ions, leading to intramural acidosis and cell death 3, 4
• The pathologist may observe evidence of mucosal ischemia contributing to injury, as impaired mucosal buffering leads to intramural acidosis 3

Clinical Implications for Reporting

Prognostic Indicators

• Transmural necrosis at any level (stomach, duodenum, or esophagus) is an absolute indication for emergency surgery and must be prominently stated 1
• The report should facilitate surgical decision-making, as subtotal gastrectomy with Billroth I reconstruction is typically required for severe injury 2
• Documentation should note that even without immediate transmural necrosis, late gastric outlet obstruction may develop, making surgical therapy eventually mandatory 2

Supporting Laboratory Context

• While not part of the pathology report itself, the pathologist should be aware that findings correlate with severe acidosis, elevated lactate, deranged liver function tests, leukocytosis, and elevated CRP as predictors of transmural necrosis 1

Common Pitfalls to Avoid

• Do not underestimate antral injury: The prepyloric antrum bears the brunt of acid ingestion damage and requires careful assessment 2
• Do not assume esophageal involvement: Unlike alkali ingestion, acid typically causes less esophageal damage but more gastric injury 2
• Do not delay reporting transmural necrosis: This finding requires immediate surgical consultation, as mortality increases with delayed intervention 1