The initial abscess started pericolonically following perforated diverticulitis in the left anterior peritoneal space abutting the rectus abdominis. Fistulas usually develop secondary to a foreign body, radiation, inflammation, epithelialization, neoplasm, or distal obstruction [5]. Colonic inflammation from appendicitis and diverticular disease has also been associated with fistula formation [6]. Our patient had several of these risk factors, including inflammation from diverticulitis, the introduction of a foreign body by IR, and colonic abscess formation. We hypothesize that the intraperitoneal sigmoid colon diverticular abscess was the root cause, and the secondary abscess that was in the anterior extraperitoneal space adjacent to the rectus abdominis was the abscess that drained into the left scrotum.
Abscess formation is a well-known complication of perforated diverticulitis. It often occurs intraperitoneally and can typically be treated with antibiotics alone if the abscess is less than three centimeters. Percutaneous abscess drainage (PAD) is required for larger abscesses [7]. One study that systematically reviewed the outcomes after treatment of acute diverticulitis with abscess formation showed that of patients treated nonoperatively (antibiotics or PAD), 25% experienced a recurrent episode during long-term follow-up, and of the patients undergoing PAD, 2.5% experienced procedure-related complications [8].
The most common organisms that cause cutaneous abscesses are gram-positive bacteria, such as Staphylococcus aureus, which are found on flora of human skin and mucous membranes [9]. However, anaerobic bacteria are frequently isolated, with the true prevalence of these infections undetermined due to slow growth, difficulty in culturing, and polymicrobial nature of the infection [10]. Abscesses associated with diverticulitis are due to diverticular microperforations and extravasation of enteric commensals, with Escherichia coli and Bacteroides species being the most frequently isolated [11].
The evolution of cultures from the scrotal abscess site supports the hypothesis that enteric spread caused the secondary abscess. Cultures of the scrotal abscess from the initial bedside incision and drainage showed a predominant growth of coagulase-negative staphylococcus, gram-positive cocci, and mixed anaerobic bacteria. The presence of coagulase-negative staphylococcus indicates that there was likely floral contamination that contributed to this initial abscess formation [12]. Subsequent cultures showed growth of Enterobacter cloacae, which has been the most common cause of nosocomial infection within the last decade [13]. This shift in culture suggests that the initial scrotal abscess was unrelated to the pericolonic abscess; however, the secondary scrotal abscess was associated with the intraperitoneal abscess as the isolated species were related to organisms that typically reside within the gastrointestinal tract. We can postulate that the formation of a fistulous tract between the peritoneum and abdominal wall allowed for direct extension, which was confirmed with CT imaging and intraoperatively.
The fistulous tract that developed anteriorly dissected through the transversalis fascia, rectus sheath, and invested in Scarpa’s fascia before spreading inferiorly into the scrotum. Scarpa’s fascia is contiguous with the Dartos fascia below the pubic symphysis which can provide a direct route from the anterior abdominal wall into the scrotum for potential spread [14]. A retroperitoneal tract has also been hypothesized to be a cause of abscess tracking to the scrotum. A retroperitoneal abscess formation tracking to the scrotum has been described in the literature. An ascending and descending colonic perforation with subsequent spread along the retroperitoneal fascial planes resulting in scrotal abscess with fecal contents in the scrotum has been reported [15]. The postulated mechanism is that the inflammation from the retroperitoneum caused the abscess to dissect through the transversalis fascia through the deep inguinal ring. Another pathway to the scrotum is with a patent processus vaginalis.
Documented scrotal abscess formation from an intraperitoneal source most commonly occurs in the pediatric population, often associated with a patent processus vaginalis. The patent processus vaginalis serves as a communication between the peritoneal cavity and the scrotum, with several case reports describing a phenomenon of peritoneal extension of an abscess associated with perforated appendicitis. The presenting symptom of appendicitis in these cases is scrotal swelling in young boys [4]. A patent processus vaginalis has been estimated to be present in 80–95% of newborn males, with 15–37% of those persisting into adulthood [2,3,4]. However, a patent processus vaginalis will typically close within the first 24 months of life and is unlikely to cause a scrotal abscess via intraperitoneal extension in an adult. Instead, scrotal extension of an intraperitoneal abscess in an adult can be caused by direct extension [16]. It is rare for fluid collection to drain into the scrotum without a patent processus vaginalis, especially in adults. We conclude that there are extraperitoneal planes that can lead to scrotal abscess collection from an abdominal source.