Acetic acid intoxication by rectal administration

Author(s): Satoshi Fujita , Mikito Kawamata , Takahisa Mayumi , Akiyoshi Namiki , Keiichi Omote and Sinzou Sumita

 

Source: Journal of Toxicology: Clinical Toxicology. 32.3 (May 1994): p333.

INTRODUCTION

While intoxication by acid ingestion is well recognized [1-3], acute acid intoxication by rectal administration is little known [4]. Acid burns of the colon and rectum are an unusual occurrence but may lead to more extensive damage than induced in the esophagus and stomach by ingestion [4].

Case Report

A 5-year-old, 16 kg boy experienced abdominal discomfort after swimming. At the doctor's office he received 50 mL of 9% acetic acid rather than the prescribed glycerin enema, but the error was not discovered. At 5 h after treatment he experienced severe abdominal pain and macrohematuria and was immediately hospitalized.

On admission oral temperature was 38.6 [degrees] C; systolic blood pressure 60 mm Hg; heart rate 180 bpm and respiratory rate 40/min. He was drowsy, the extremities showed signs of dehydration and cyanosis, the abdomen was distended and guarded with absent bowel sounds. Laboratory data included the following: WBC 25,500/[mm.sup.3]; hematocrit 44.9%; platelets 245,000/[mm.sup.3]; prothrombin time 16.8 sec (control below 12.0 sec); partial thromboplastin time 48 sec (control 32 sec); serum Na 140 mEq/L; K 5.4 mEq/L; AST 546 U; ALT 164 U; LDH 3379 U (up to 500 U); myoglobin in serum 610 ng/mL; myoglobin in urine 2660 ng/mL; [beta.sub.2] microglobulin in serum 2.1 mg/mL; and [beta.sub.2] microglobulin in urine 8000 mg/mL. The serum specimen was hemolyzed. Arterial blood gases (room air): pH 7.208; [PaO.sub.2] 63 mm Hg; [PaCO.sub.2] 24 mm Hg; and Base Excess -11.6 mEq/L. Abdominal ultrasonography showed ascites and a distended colon with fluid.

A laparotomy approximately 9 h after the enema showed colonic necrosis extending from the left transverse colon to the sigmoid colon but there was no perforation. A hemicolectomy and colorectostomy were accomplished despite wound bleeding. On proctoscopy the mucous membranes of the rectum were edematous and eroded. Post-operatively the administration of the acetic acid enema was discovered.

Shock and respiratory distress responded to fluids, fresh frozen plasma, dopamine and mechanical ventilation. The hemolysis improved after administration of haptoglobulin 2000 U but oliguria developed.

The postoperative laboratory data indicated DIC, acute renal failure and acute liver dysfunction. He was treated with 2 U of fresh blood and 3 U of fresh-frozen plasma, and 8 U of fresh packed platelet for 2 days with a gradual resolution. Acute renal failure was treated with hemodiafiltration through d 15 by which time serum creatinine was normal. The high level of serum transaminases returned to their normal ranges by day 15. Sepsis with blood cultures positive for Staph. aureus was treated with antibiotics through d 15.

The pathologic diagnosis of resected colon and rectum was extensive necrosis of the colon down to smooth muscle with engorged vessels, fibrin and neutrophilic infiltration.

DISCUSSION

A 9% acetic acid solution would not seem to pose a serious danger upon ingestion, as vinegar contains 4 - 6% acetic acid, but 5% acetic acid injected into the colon with immediate irrigation induced colitis in rats [5]. After acid ingestion the rapid transit through the esophagus, lined with squamous epithelium, the greater thickness of the three muscle layers of the gastric wall and dilution by gastric juice or food may contribute to the low incidence of gastric necrosis [6]. In contrast, an acid solution by enema has a longer contact time with little neutralization or dilution. Rectal administration of 40 mL of a 3 % acetic acid is fatal to rabbits within 1 h, but only after 6 d by gastric route [7].

We are aware of only one report describing an acid (95% sulfuric acid) burn of the colon and rectum [4]. In that case the rectum and transverse colon were gangrenous, but no perforation was noted [4]. Subtotal proctocolectomy was done soon after the burn, and the patient recovered uneventfully [4]. In contrast, our patient who had a hemicolectomy about 9 h after administration, developed hemolysis, acute renal failure, DIC and acute liver dysfunction. Acute renal failure is a well-known complication after acid ingestion [7], and DIC and acute liver dysfunction have also resulted from acid ingestion [8.9], but not all in the same patient [8-12].

The mechanism of caustic-induced DIC remains unclear, but extensive acid-induced tissue necrosis can lead to procoagulant formation and DIC [9]. Direct activation of the coagulation system by acetic acid is another possibility. DIC is also a complication of many disease states with many different causes, including acidosis, shock and sepsis [10].

Two patients who ingested glacial acetic acid developed acute necroinflammatory changes of the liver [11]. It is proposed that liver dysfunction is caused by thrombosis and circulatory disturbances in the portal vein and intralobular capillaries after acetic acid ingestion [12].

In toxicology, the route of administration is critical to the prediction of risk. This case is a reminder that rectal administration of relatively dilute caustic, 9% acetic acid, can cause bowel necrosis of high morbidity and mortality.

REFERENCES

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