Self-administered alcohol enema causing chemical proctocolitis

Introduction

Orally ingested alcohol does not cause damage to the upper gastrointestinal tract. However, in an animal experiment, mucosa of the rat colon was damaged with 10% alcohol.¹ Here, we report the case of a patient who experienced extensive chemical proctocolitis by transanally administering a large quantity of 35% alcohol, with a review on the clinical course of previous reports.

Case report

A 21-year-old male with no medical history was found lying on the bathroom floor in his home by his family who called an ambulance and had him transported to our hospital. On arrival, he experienced disturbance of consciousness with Glasgow Coma Score 6 (eye, verbal, motor responses: E2V1M3), pulse 101/min, blood pressure 118/66 mmHg, respiratory rate 18 respirations/min, and 35.5°C body temperature. He was not wearing clothing on his lower body, and a small quantity of melena was found from his anus. Blood tests revealed increased levels of white blood cells (23,900/μL) and hemoglobin (Hb) (17.5 g/dL). Blood gas analysis results were as follows: pH 7.299, bicarbonate (HCO₃⁻) 19.9 mmol/L, base excess (BE) −6.0 mmol/L, and lactate 5.4 mmol, indicating metabolic acidosis and hyperlactacidemia. Results of drug toxicity screening (Triage^® DOA) were negative. Brain CT revealed no intracranial hemorrhagic lesions. Non-contrast enhanced CT of the abdomen and pelvis disclosed thickening of the wall from ascending colon to the rectum (Figure 1).

Figure 1 Wall thickening of the sigmoid colon and rectum.

Development after admission: While we were preparing for further tests in the ICU to determine the cause of disturbance of consciousness (eg, acute poisoning by a substance that could not be detected with Triage^® DOA or post-ictal disturbance), his level of consciousness gradually improved, and the patient declared that he used a manual siphon pump to inject 1.8 L of white distilled liquor (35% alcohol) into his anus. Thus, the cause of disturbance of consciousness was believed to be acute alcohol poisoning by anally administered alcohol. Because we were unable to measure blood alcohol levels at our hospital, we could not definitively diagnose the cause of disturbance of consciousness. A lower digestive tract endoscopy was performed to examine the edematous changes extending from the colon to the rectum on abdominal CT suspected to be caused by alcohol-induced chemical proctocolitis (Figure 2). Diffuse bleeding, mucosal edema, ulcer, and submucosal bleeding were found from the ascending colon to the rectum. There were no lesions in the mucosal surface of the ileum. Prednisolone (60 mg) was rectally administered. Although the increase in lactic acid levels was immediately improved by fluid therapy and was thought to be due to dehydration, not due to intestinal necrosis. The patient was administered conservative treatment as per the standard treatment for ischemic colitis (fluid therapy with fasting). By the second day of illness, melena disappeared. Lower digestive tract endoscopy on the seventh day of illness showed improved inflammation; hence, he was initiated on an oral diet. There was no recurrence of melena, and the patient was discharged on the ninth day. He was followed up by a nearby physician who noted no delayed onset complications such as intestinal stenosis at two months of follow up. During hospitalization, the patient was asked why he transanally administered alcohol. He responded that he was suffering from insomnia due to severe anxiety as he prepared for his university entrance examinations and learned on the internet about anally administering alcohol with a siphon pump as a method to quickly induce sleep.

Figure 2 Endoscopic view of transverse colon mucosa showing diffuse redness, erosion, ulcer, and hemorrhage.

Discussion

To the best of our knowledge, there are only 13 reports, including this case, of chemical proctocolitis induced by transanally administered alcohol (Table 1).^2–13 There are little is known about alcohol lesions in the colonic mucosa, compared from gastric mucosa. In a rat animal model, mucosa of the rat colon was damaged with 10% alcohol,¹ and the histological appearance of acute lesions (10 mins after 30% ethanol enema) showed complete destruction of the surface epithelium. Necrosis extended throughout the depth of the mucosal layer but did not penetrate the muscularis mucosa. The mucosal injury in the colon also may be mediated by prostaglandin pathways, because intrarectal administration of prostaglandins decreases the damage.¹⁴ Previous reports listed the intention of suicide, sexual pleasure, and medical accidents as reasons for anally administering alcohol. Metabolism of ethanol begins as soon as it reaches gastric mucosa. Rectal absorption of ethanol bypasses the first pass metabolism, allowing for a higher systemic concentration of blood ethanol, greater potential for central nerve system depression. To feel alcohol effects quickly, alcohol enemas have been performed since ancient times, and pottery has been found representing that Mayan priests are injecting alcohol from the anus.¹⁵ In recent years, it has been noted as a dangerous alcohol intake method called “butt chugging” among university students in the USA.¹⁶ Clinical symptoms included melena, tenesmus, and burning sensation in the anus. Little abdominal pain has been reported, as observed in this patient who did not complain of abdominal pain. Colonoscopy findings showed diffuse redness, edema, bleeding, erosion, and ulcer of the intestinal mucosa, which were similar to the endoscopic findings of ischemic colitis.^2–8 In this study case, moderate edematous changes were found in the ascending colon to the rectum, particularly in the transverse colon, as well as multiple lesions of submucosal bleeding and erosion. Histopathological findings showed sloughed epithelial cells, interstitial edema, capillary dilation, bleeding of the lamina propria and submucosa, and a nonspecific inflammatory response, which were also similar to those of ischemic colitis.^5,8,11,12 In this case, since no pathological examination has been conducted, no histological evaluation could be obtained. Regarding the relationship between the concentration of alcohol in the injected fluid and the resulting damage, previous studies reported relatively good course with conservative therapy, even for a patient who injected 96% alcohol and required hospitalization for 7 days.⁶ Intestinal perforation and necrosis were not reported in any of the previous cases. This patient, who administered 35% alcohol, was discharged after 9 days of hospital stay with conservative therapy alone. In terms of the relationship between the volume of alcohol injected and extent of damage, 200 mL reached only the descending colon, whereas 1,000 mL caused damage in the transverse colon as well. This individual administered 1,800 mL, which was the highest quantity among the existing reports, and the damage was observed in the ascending colon. The extent of damage in alcohol-induced chemical proctocolitis depends on the quantity administered; however, clinical symptoms and course are similar to ischemic colitis and can be treated with conservative therapy.

Table 1 Clinical features of alcohol-induced proctitis

Conclusions

We experienced a rare case of chemical proctocolitis induced by transanally administering alcohol. Clinical symptoms and course were similar to ischemic colitis.