What is the treatment for Hydrochloric acid (HCl) poisoning?

Treatment of Hydrochloric Acid (HCl) Poisoning

Do not induce vomiting, do not give activated charcoal, and do not attempt neutralization with water or milk—immediately remove contaminated clothing, irrigate exposed skin/eyes with copious water, and rapidly transport to a medical facility for endoscopic evaluation and supportive care. 1

Immediate Pre-Hospital Management

Scene Safety and Decontamination

• Ensure your own safety first by assessing for toxic fumes and chemical hazards before approaching the patient 2, 3
• Remove all contaminated clothing from around the mouth and face area to prevent continued exposure 1
• For skin exposure, immediately irrigate the affected area with copious amounts of water for at least 15-20 minutes 1
• For eye exposure, perform continuous water irrigation while transporting to the hospital 1

Critical "Do NOT" Actions

• Do not administer water or milk for dilution—this lacks evidence and may induce vomiting and aspiration 1
• Do not give activated charcoal—it is completely ineffective for caustic substances and will obscure subsequent endoscopic visualization 1, 4
• Do not induce vomiting with ipecac—this causes intractable emesis and delays definitive care 1
• Do not attempt chemical neutralization—this generates heat and worsens tissue injury 1

Initial Stabilization

• Assess and secure the airway immediately, as respiratory distress may develop rapidly from laryngeal edema or aspiration 1, 5
• Establish IV access and begin fluid resuscitation 1
• Contact Poison Control immediately for expert guidance 3, 1

Hospital-Based Management

Diagnostic Evaluation Timeline

• Within 3-6 hours: Perform contrast-enhanced CT to detect transmural injuries and guide surgical decision-making 1
• Within 12-48 hours: Perform upper endoscopy (esophagogastroduodenoscopy) to determine injury severity using Zargar grading, which directly guides prognosis and management 1, 5
• Obtain laboratory studies including CBC, comprehensive metabolic panel, liver function tests, arterial blood gas, and serum lactate to identify systemic complications 1

Understanding the Injury Pattern

HCl causes coagulative necrosis that forms an eschar, which paradoxically may limit deeper penetration compared to alkali injuries 1. However, acids preferentially cause severe gastric injury rather than esophageal injury because the liquid rapidly transits through the esophagus and pools in the stomach 1, 6. The duodenopancreatic region is particularly vulnerable, and extension of necrosis to this area carries extremely high mortality (48% in one series) 6.

Medical Management Based on Severity

For metabolic acidosis:

• Administer sodium bicarbonate (1-2 mEq/kg IV) only after establishing effective ventilation 1
• Monitor serial arterial blood gases and electrolytes 1

For patients without transmural necrosis:

• Implement bowel rest with nasogastric decompression if needed 5
• Consider proton pump inhibitors, though evidence is limited 5
• Antibiotics may be indicated based on clinical judgment and risk of perforation 5
• Steroids remain controversial with no strong evidence supporting routine use 5
• Close clinical monitoring with serial examinations and imaging 1

For patients with transmural necrosis:

• Emergency surgery is potentially lifesaving and should be considered immediately 1, 7
• Surgical options include discontinuous gastrectomy with delayed reconstruction, as successfully demonstrated in case reports 7
• Minimally invasive approaches (laparoscopic or robotic) may be feasible in select cases 7

Critical Prognostic Factors

The single most important prognostic factor is extension of necrosis to the duodenopancreatic region 6. In a series of 25 patients, all 12 deaths occurred in patients with esophagogastric massive necrosis extending to the duodenopancreatic frame, while 10 patients without duodenal involvement survived 6.

Important Clinical Caveats

• Absence of oral burns or pain does not exclude severe internal injury—clinical symptoms correlate poorly with the extent of gastrointestinal damage 1
• Cardiovascular complications are rare but potentially fatal—obtain serial ECGs even without cardiac complaints, as acute myocardial infarction has been reported 8
• Systemic complications may include hemolysis, acute renal failure, and severe metabolic acidosis 8
• The concentration and volume ingested directly correlate with mortality—as little as 8.19 mL of concentrated HCl has been documented as a lethal dose 9

Long-Term Complications

Survivors may develop esophageal or gastric strictures requiring endoscopic dilation 1. However, avoid dilation procedures within the first 3 weeks post-ingestion due to significantly higher complication rates during this healing phase 1.

Key Pitfalls to Avoid

• Do not delay imaging and endoscopy waiting for symptom development—injury severity cannot be predicted clinically 1, 5
• Do not assume the absence of esophageal injury means safety—the stomach and duodenum are at highest risk 1, 6
• Do not miss the narrow window for surgical intervention in transmural necrosis—delayed surgery dramatically worsens outcomes 6, 7
• Do not forget to monitor for delayed complications including perforation, which may occur days after initial presentation 5, 7