Discussion

Dual ingestions are exceedingly uncommon and present a unique set of challenges. For this case of dual ingestion, there was the risk of hepatic injury from the acetaminophen overdose, intoxication from ethanol, and direct injury to the colon from rectal administration of ethanol. Our patient was treated for both acetaminophen overdose and ethanol-induced colitis. The initial management was N-acetyl cysteine for the treatment of acetaminophen overdose to prevent hepatotoxicity [7]. Acetaminophen levels continued to decline after admission. Because the rectal ethanol ingestion was 11 hours before evaluation in the ED, he did demonstrate intoxication from ethanol. Colitis was managed conservatively. The patient’s laboratory abnormalities included white blood count (WBC) 16.4 (103 µg/mL), acetaminophen levels 108 µg/mL and aspartate aminotransferase (AST) 81 U/L. The elevated AST could either be explained by hepatic injury from the acetaminophen or ethanol. Mild AST elevation was most likely related to acute acetaminophen exposure, ethanol toxicity, or both. Although the patient had a reactive hepatitis C antibody, hepatitis C virus (HCV) RNA testing was unavailable; therefore, chronic active hepatitis could not be confirmed and should not be assumed to explain the transaminase elevation. Supportive management focused on intravenous fluid replacement for diarrhea-associated volume losses while serially monitoring hepatic and renal function.

Although ischemic, infectious, and inflammatory colitis were considered, the immediate onset of profuse bloody diarrhea following rectal ethanol administration strongly favored chemical colitis. CT imaging and colonoscopy demonstrated inflammatory mucosal injury without findings suggestive of transmural ischemia. The absence of a prior history of inflammatory bowel disease and the close temporal relationship with ethanol exposure made inflammatory bowel disease unlikely. Acetaminophen overdose rarely causes direct colonic injury and is therefore an unlikely explanation for the patient's lower gastrointestinal findings. A serum ethanol concentration was not obtained, limiting the assessment of systemic ethanol absorption. Nevertheless, the immediate onset of bloody diarrhea following rectal ethanol administration and characteristic endoscopic findings strongly supported chemical colitis.

Ethanol colitis is the inflammation of the colon after the introduction of ethanol into the colon. Colitis presents as diffuse abdominal pain, often accompanied by profuse watery diarrhea and blood, much like how our patient presented. The colonic mucosa is a site of rapid turnover, and ethanol has been shown to hinder the immunoregulatory process of the colonic mucosa along with the regenerative capacity [8]. Traditionally, we see colitis in the setting of inflammatory bowel disease, an immunological process, or in cases of ischemia or radiation. Ethanol administration has been a very rare cause of colitis. Primarily, ethanol-associated colitis cases have been seen in surgical preparation, where alcohol enemas are mixed with cleaning enemas [1]. Endoscopic findings of these patients have been consistent with those of our patient, displaying mucosal inflammation and erosions [8]. Metabolism of ethanol begins at the gastric mucosa, and the route of absorption plays a role in the first-pass metabolism of ethanol. Rectal absorption of ethanol is a mechanism that bypasses the first-pass metabolic effect by the stomach and liver; this allows for a higher concentration of blood ethanol, meaning a higher systemic concentration of ethanol [9].

Similar case reports of ethanol enemas do not have concomitant ingestions. A review of 12 reported alcohol enemas is listed in Table 2. The literature available shows that rectal alcohol administration largely involved distilled spirits, as compared to wine. Ten cases show ethanol enemas based on spirits or concentrated ethanol, and two involving wine-based enemas [1-12]. Mortality was not a common outcome, with only two reported deaths, both secondary to wine enemas [4,9]. Predominantly, the ethanol enemas resulted in inflammatory colitis, proctocolitis, or mucosal inflammation as described by six cases [3,6,10-13]. Ischemic injury was less frequent and only reported in two cases as ulcerations and a mimic of ischemic colitis [1,2].

Author (Year) | Age/ Sex | Type of Alcohol | Findings | Outcome | Other Overdose
Herrerias et al., 1983 [13] | NR | 95% Ethanol | Proctocolitis | Recovered | No
Bhalotra, 1988 [12] | NR | Ethanol solution | Mucosal inflammation | Recovered | No
Triantafillidis et al., 1994 [6] | NR | 95% ethanol | Inflammation | Recovered | No
Rodriguez-Tellez et al., 2001 [5] | NR | 96% ethanol | Proctocolitis | Recovered | No
Michopoulos et al., 2000 [11] | NR | Alcohol | Clinicopathologic colitis | Recovered | No
Randolph et al., 2005 [2] | NR | Vodka | Mimicked ischemic colitis | Recovered | No
Mian et al., 2005 [1] | 39 M | Vodka | Ulceration + ischemia | Recovered | No
Wilson et al., 2005 [4] | 55 M | Wine | Not reported | Death | No
Pizzute, 2006 [10] | 23 F | Vodka | Inflammation | Recovered | No
Andrade et al., 2003 [8] | Mice | 50% ethanol | Colitis | Recovered | No
Rosendahl et al., 2018 [3] | NR | Distilled liquor | Diffuse inflammation | Recovered | No
Peterson et al., 2014 [9] | 52 M | Sherry wine | Fatal ethanol intoxication | Death | No