Cocaine, derived from the leaves of the Erythroxylum coca plant, is a crystalline tropane alkaloid that exerts its central action by inhibiting the reuptake of dopamine, norepinephrine, and serotonin, leading to the activation of the central and sympathetic nervous systems. [1]. This stimulation can lead to intestinal and abdominal ischemia, although the exact mechanism of cocaine-induced ischemia is not fully defined. It is suggested that three causal factors may be involved in the development of intestinal ischemia: arteriolar vasospasm, platelet activation, and accelerated atherosclerosis.

The majority of literature on cocaine-related bowel ischemia consists of case reports and small case series, indicating that the mortality associated with cocaine-induced ischemia may be high. However, many studies lack control groups, and the sample sizes are often too small to draw definitive conclusions [5].

In our case, after excluding all other potential causes, it was determined that cocaine use was the primary factor contributing to the sigmoidal perforation.

The pathophysiology of cocaine-induced ischemia is relatively well understood. Cocaine inhibits the reuptake of norepinephrine at presynaptic terminals, leading to an accumulation of catecholamines at postsynaptic membranes. This influx of catecholamines results in tachycardia, vasoconstriction, and hypertension. Vasoconstriction can cause ischemia, which, in turn, affects multiple organ systems and may lead to mesenteric vasoconstriction and localized blood pressure elevation. This focal tissue ischemia is likely to result in perforation [6].

Cocaine has been found to have additional mechanisms that can contribute to intestinal ischemia. It exerts a direct vascular constrictive effect by increasing calcium flow across the endothelial cell membrane. Some have suggested that cocaine has a direct toxic impact on the intestinal mucosa. Cocaine use also induces thrombus formation and platelet aggregation and reduces tissue fibrinolysis. Furthermore, it decreases fibrinolytic activity by stimulating plasminogen activator inhibitor activity. Some or all of these effects may explain the increased vulnerability of the colon to ischemia in individuals who abuse this drug [7].

The global incidence of gastrointestinal complications due to cocaine use is not well-documented. However, in one series from the USA, a single hospital treated 50 patients with juxtapyloric perforation over four years. This series reported only gastroduodenal perforation, and it is unclear how many other patients were admitted with different gastrointestinal complications resulting from drug abuse [8]. In Morocco, the number of reported cases is limited, although it is expected to increase with the growing number of cocaine users, which is explained in the United States by its geographical proximity to the countries producing this illicit drug [8].

Colonic perforations associated with cocaine smoking have been documented and are believed to result from deep colonic ulcerations caused by the multisystemic toxicity of freebase crack [9,10]. For example, Kram et al. reported four patients with perforated colonic ulcers due to crack use [11], and Kodali and Gordon reported upper gastrointestinal bleeding secondary to crack use [12]. Cocaine's blockade of norepinephrine reuptake leads to mesenteric vasoconstriction and focal tissue ischemia, which more frequently results in perforation [10,13].

In our case, the patient presented with abdominal pain and anorexia but without gastrointestinal hemorrhage. A CT scan revealed peritonitis due to sigmoidal perforation and inflammatory thickening of the left colon. In a study by Elramah et al., the most common symptoms included mucosal edema, pallor, and pneumatosis of the colonic wall, with thickening of the colonic wall being the most common CT finding. The prevalence of ischemia in different colon segments was as follows [5]:

• •Ischemia on the left side of the colon was observed in 7 out of 78 patients.
• •Ischemia on the right side of the colon was observed in 24 out of the 78 patients.

Cocaine-induced ischemic colitis may be an uncommon occurrence in a surgeon's clinical practice. The key point is to consider it as a potential diagnosis in patients presenting to the emergency department with acute abdominal pain, with or without rectal bleeding. Ischemic colitis is typically diagnosed through colonoscopy and often resolves without the need for surgery. However, in a few cases, it may progress to peritonitis, necessitating surgical intervention [14]. In our case, endoscopic examination was scheduled after the acute phase of peritonitis.

Elramah et al. couldn't determine whether a primary anastomosis or a colostomy should be performed as the initial surgical procedure [5]. In Chile, a right hemicolectomy was performed for toxic colonic ischemia with a cecum perforation [15]. In our case, We opted for suturing the perforation, creating a colostomy near the sigmoid colon upstream of the perforation, and performing lavage with drainage due to the patient's peritonitis.