Colonic Diverticular Disease

Jason F. Hall, Willem A. Bemelman

Key Concepts

  • Our understanding of the pathophysiology of diverticular disease is evolving.
  • Many behavioral and environmental factors may influence the development of diverticular disease.
  • Some patients with early uncomplicated diverticulitis can be treated without antibiotics.
  • The decision to perform elective surgery after several episodes of recurrent uncomplicated diverticulitis should be individualized.
  • The decision to perform elective surgery after successful non-operative management of a diverticular abscess should be individualized.
  • Laparoscopic lavage can be employed in some patients with Hinchey III diverticulitis.
  • Minimally invasive surgery is an acceptable option for managing diverticulitis and its complications.


Diverticular disease of the colon is one of the most commonly diagnosed gastrointestinal conditions[1],[2]. Symptomatic diverticular disease represents a spectrum of disease ranging from mild abdominal symptoms to free perforation with peritonitis and sepsis. In the past few decades, there has been renewed enthusiasm for research in this area, and many practice patterns have been challenged. Presentations of diverticulitis are stratified into complicated or uncomplicated diverticulitis.

Complicated disease includes diverticulitis associated with free perforation, fistula, abscess, stricture, or obstruction. Uncomplicated diverticulitis is defined as diverticulitis which is not associated with any of the aforementioned features. Microperforation with small amounts of contained extraluminal gas, in the absence of a systemic inflammatory response, is considered uncomplicated diverticulitis[3]. Symptomatic uncomplicated diverticular disease (SUDD) is defined as diverticulosis associated with chronic abdominal pain. These patients do not have clinically overt colitis[4].

This chapter focuses on the pathophysiology, evaluation, and treatment of left-sided colonic diverticulitis. Diverticular hemorrhage is associated with diverticulosis and not diverticulitis. The management of diverticular bleeding is covered in the chapter on lower gastrointestinal bleeding.


The prevalence of diverticula-related illness has risen in the United States over the past few decades[5],[6]. A recent report utilizing information from the National Inpatient Sample (NIS) suggested that the rate of hospitalization for diverticulitis increased from 74.1/100,000 in the year 2000 to 96.0/100,000 in 2008[1]. Peery recently examined data from the National Ambulatory Medical Care Survey and the National Hospital Ambulatory Medical Care Survey. In 2010, there were more than 2.7 million discharges in the ambulatory setting associated with a diagnosis of diverticular disease. In 2012 there were >340,000 emergency department visits for diverticulitis[7]. More recent data revealed that in 2014, there were 1.92 million patients diagnosed with diverticular disease in the ambulatory setting[2]. The estimated aggregate national cost of caring for patients with diverticular disease in the emergency setting was $1.6 billion in 2013[8].

Histology and Pathology

Many of the microscopic features of diverticulitis include thickening of the lamina propria, mucin depletion, and Paneth cell hyperplasia. Crypt abscesses and ulceration are also observed in some cases[9]. Many of the histologic features are similar to those associated with inflammatory bowel disease[10]. Hinchey developed pathologic criteria to classify the severity of diverticular disease. This classification has been used and is divided into Stages I–IV[11]. Stage I includes patients with diverticulitis and a pericolic abscess. Stage II represents patients with distant abscesses such as a pelvic or retroperitoneal. Stage III and IV are patients with purulent and feculent peritonitis, respectively. A number of attempts have been made to extend the Hinchey criteria to preoperative staging based on CT scan[12].

Role of Fiber

A number of authors have postulated that diverticular disease is related to fiber deficiency. Painter and Burkitt studied colonic transit times and fiber contents in patients in Uganda and the United Kingdom. Patients with a higher fiber intake had more frequent bowel movements, faster colonic transit times, and larger stool volumes. They postulated that a progressively more processed diet removes a large source of fiber from the Western diet[13]. These observations are confounded by a number of factors, including differing life expectancies in industrialized and non-industrialized countries[14]. It is interesting to note that as non-industrialized societies have adopted a more Western diet, a number of authors have noted an increasing prevalence of diverticular disease[15].

A number of studies have examined dietary factors in large patient populations with and without diverticular disease and found an inverse association between incidence and fiber intake[16],[17]. The relative risks associated with fruit and vegetable fiber intake were 0.62 and 0.55, respectively[16]. Fiber found in fruits and vegetables conferred the most protective effect (compared with fiber from cereal) and a high intake of fat and red meat increased the incidence of diverticular disease.

Manousos et al.[17] compared individuals who ate a vegetarian diet to those who predominantly ate meat. The risk of developing diverticular disease was 50-fold greater in meat eaters. In a more recent cohort study of 47,228 male health professionals, popcorn, nut, and seed consumption were inversely correlated with diverticulosis or diverticular complications. This study refutes the adage that “nuts, corn, seeds and popcorn” cause diverticulitis and should be avoided in patients who have had an attack of diverticulitis[18].

Recent data has examined the association between eating a “Western” diet (high in red meat, refined grains, and high-fat dairy) and the risk of developing diverticulitis. In a study of men from the Health Professionals Follow-Up Study, Western diet was associated with an increased risk of diverticulitis when compared to a “prudent approach” (high in fruits, vegetables, and whole grains). Men who had the highest consumption of a Western diet had a multivariate hazard ratio of 1.55 (95% CI: 1.20–1.99) for diverticulitis compared to men in the lowest quintile. The authors suggested that this association was related primarily to the intake of less fiber and more red meat[19].

Another group demonstrated a similar pattern when they studied 907 incident cases of diverticulitis. The cohort was divided into patients with low- and high-risk lifestyles. The components of a low-risk lifestyle are an average red meat intake (<51 g per day), dietary fiber intake in the top 40% of the cohort (about 23 g per day), approximately 2 hours of exercise weekly, normal BMI, and never smoked. These authors demonstrated an inverse linear relationship between the number of low-risk lifestyle factors and the incidence of diverticulitis (p for trend <0.001). Although there were numerous contributors to the lower risk of disease, it appears that fiber has an important role to play in the pathogenesis of this disease[20].



The progression of normal colonic architecture to diverticulosis and subsequent diverticulitis is not well understood. Multiple lines of evidence suggest that this progression is multifactorial and may involve diet, the microbiome, lifestyle, and genetics[21],[22].

A hereditary basis for diverticular disease was suggested by a number of sources. Hall demonstrated that a family history of diverticular disease is associated with a higher risk of recurrence in patients with an incident case of diverticulitis[23]. Two large, twin studies compared the risk of diverticular disease in monozygotic and dizygotic twins. The risk of developing diverticular disease in a twin pair was significantly higher among monozygotic as opposed to dizygotic twins. These authors estimated that heritability accounted for 40–50% of the risk for diverticular disease[24],[25].

Although these clinical observations have been important in establishing a hereditary predisposition to the disease, localization of a specific gene is still in flux. A recent genome-wide association study identified several gene variants (COLQ, ARHGAP15, and FAM155A) that may contribute to diverticular disease[26]. Many of these genes are thought to influence important cellular functions such as regulation of immunity, cell adhesion, membrane transport, intestinal motility, and immunity[21].

Other authors have detected several single-nucleotide polymorphisms in the TNFSF15 gene in a cohort of patients with diverticular disease who required surgery[27]. Variations in this gene have also been implicated in the pathogenesis of Crohn’s disease[28]. Coble used whole exome sequencing to examine genes that are associated with early onset diverticulitis. LAMB4, a gene localized to the colonic myenteric plexus, was found to alter the function of the enteric nervous system and was proposed as a potential contributor to early onset diverticular disease[29].


The human gastrointestinal tract contains a variety of microorganisms, which harbor approximately 1012 to 1014 genes. The size of this genome is estimated to be at least 100 times larger than the size of our own genome[30]. The aggregate of these varied microorganisms is referred to as the microbiome. Several authors have postulated that an altered microbiome could influence the pathogenesis of diverticulitis[31].

The human metabolism and inflammatory response can be influenced by genetic information outside our genome. However, insights into the influence of microorganisms on gastrointestinal function and diverticular disease are in their infancy and rely on extrapolation from other disease states. Patients with obesity, colon cancer, irritable bowel syndrome, and inflammatory bowel disease have all been proposed to have altered microbiomes[31],[32],[33],[34].

There have been a few small studies that examined the role of the microbiome in the pathogenesis of diverticular disease. There is some evidence that patients with diverticular disease have lower levels of bacteria that metabolize fiber into short-chain fatty acids (SCFA)[35]. SCFA are thought to increase the production of antimicrobial and mucus peptides in the gut. In this way they help to regulate intestinal barrier function and cell proliferation[36].

Other authors have demonstrated that patients who had colonic resections for diverticulitis had higher levels of Bifidobacterium when compared to patients with colon cancer or IBD[37]. Another group compared the microbiome of patients with diverticulitis undergoing colonoscopy to asymptomatic controls. They found that the diversity of Proteobacteria was higher in patients with diverticulitis[38]. Other studies have demonstrated lower levels of Clostridial organisms in patients with a history of diverticulitis when compared to controls with asymptomatic diverticulosis[39],[40].

The fecal microbiome appears to be important to normal gut function. Its role in the pathogenesis of diverticular disease is still to be determined. It is not clear whether the aforementioned changes are causal or simply associated with the development of the disease.

Risk Factors for Disease


Diverticular disease tends to affect patients during middle age; the incidence rises from 5% at age 40% to 80% by age 80[3]. Historically, diverticulitis in patients under the age of 50 years was thought to be more virulent and associated with more complications[3]. More contemporary data suggests that young age is not associated with worse clinical outcomes.

Younger patients do have higher recurrence rates compared with older patients. However, younger patients do not seem to have more complicated recurrences[41],[42],[43]. This observation is bolstered by data from multiple national databases and systematic reviews, which demonstrate that younger patients are more likely to require repeat hospitalization for diverticulitis, but are not more likely to undergo emergency surgery[44],[45],[46].


Diverticulitis is more common in men. Previous estimates suggest between a 3:2 and 3:1 male-to-female ratio[47]. Others have reported that patients with symptomatic diverticular disease under the age of 65 tend to be male. Hall demonstrated that younger male patients may present with more severe CT findings of diverticulitis than female patients[48]. Etzioni reported that women are at higher risk of treatment failure when managed as outpatients[49]. A similar pattern was noted in a paper examining recurrence of diverticulitis in the National Health Service (United Kingdom)[44].

Physical Activity

Several studies have examined the effect of exercise on the development of diverticular disease[50],[51]. The risk of developing diverticular disease and levels of physical activity appeared to be inversely related. This difference persisted even when the authors adjusted for differences in dietary fiber intake. These findings were later replicated in 2009. Strate demonstrated that men who had >57.4 metabolic equivalent hours per week (MET-h/week) had a RR of 0.75 for diverticulitis and 0.54 for bleeding, as compared with men in the lowest quintile (< or = 8.2 MET-h/week). Vigorous activity appeared to be particularly important and was inversely related to diverticulitis (multivariable RR, 0.66; 95% CI, 0.51–0.86). Nonvigorous activity was not associated with a similar benefit[52].


Although the association between smoking and diverticular disease was once considered controversial, more recent data suggests a strong association. One large case-control study demonstrated that smokers had three times the risk of developing complications from diverticular disease compared to nonsmokers[53]. Aune performed a meta-analysis of 5 studies examining 6076 cases of diverticular disease. Current smokers had a much higher incidence of diverticular disease when compared to former smokers and ever smokers. The relative risk associated with developing a complication of diverticular disease (abscess or perforation) was 2.54 for current smokers and 1.83 for ever smokers[54].

Non-steroidal Anti-inflammatory Agents

The use of non-steroidal anti-inflammatory (NSAID) agents has been associated with the development of multiple gastrointestinal complications. A number of cohort studies have consistently demonstrated an association between NSAID use and diverticular disease[55],[56],[57],[58]. While the health professionals’ follow-up study showed an increased incidence of uncomplicated diverticular disease in patients who used NSAIDs compared with their asymptomatic counterparts, additional studies have also noted an increased risk of complicated diverticulitis with NSAID use[59]. A retrospective study by Corder demonstrated a 23% higher risk of perforating diverticulitis in patients who took NSAIDs regularly compared with patients with diverticular disease who did not take NSAIDs[60]. An additional study of hospitalized patients reported chronic NSAID use to be much higher in patients admitted with diverticular disease than the population as a whole. In addition these patients were four times more likely to develop perforated diverticulitis than patients with no history of NSAID use[61].


A number of retrospective case series have noted increased rates of obesity in patients with diverticulitis, particularly patients under the age of 40[62],[63],[64]. In addition, two prospective cohort studies (the Health Professionals Follow-up Study and a Swedish study) have shown an association between body mass index (BMI) and diverticular disease[65],[66],[67]. A prospective cohort from the Nurses’ health study demonstrated that women who gained ≥20 kg had a 73% increased risk of diverticulitis (95% CI, 27–136%) compared to women who maintained the same weight from age 18 years to the present[68].

Aune examined the role of obesity in a meta-analysis of five studies. They found that the relative risk for an incident episode of diverticulitis was 1.31 for each 5 unit increase in BMI. Similarly, they found that the relative risk for a diverticular complication was 1.20 for each 5 unit increase in BMI[69].

Clinical Manifestations and Physical Findings

Differential Diagnosis

The differential diagnosis for suspected diverticular disease includes appendicitis, bowel obstruction, ruptured aortic aneurysm, colorectal cancer, ischemic colitis, pyelonephritis, gynecologic disease, inflammatory bowel disease, and irritable bowel syndrome. Other diagnoses that should be entertained include endometriosis, tubo-ovarian abscess, pelvic inflammatory disease, ureteral calculi, volvulus, stercoral ulcer, and ovarian torsion. Modern cross-sectional imaging is often helpful in diagnosing many of these clinical entities. An important diagnosis to exclude on initial presentation is colorectal cancer.

History and Physical Examination

Patients with acute diverticulitis typically present with left-sided abdominal pain, fever, and leukocytosis. Physical findings include left lower quadrant tenderness on examination. Patients with free perforation will typically present with diffuse peritonitis and signs of systemic toxicity. When there is a significant phlegmon involving the colon, an abdominal mass may be palpable or appreciated on rectal or pelvic exam. Many patients present with some degree of abdominal distention. Right-sided tenderness can be a presentation in patients who have a redundant sigmoid colon that extends to the right side of the abdomen. Free perforation is associated with diffuse abdominal pain, sometimes referred pain in the shoulder, and shortness of breath.

Many patients often describe changes in their bowel habits such as constipation, or an alteration in stool caliber. Rectal bleeding rarely occurs as a presentation of acute diverticulitis. If present, rectal bleeding is more suggestive of ischemic colitis or inflammatory bowel disease. In complicated presentations, an inflammatory phlegmon can be associated with a small or large bowel obstruction. Patients with an associated obstruction will present with abdominal distention and sometimes nausea and vomiting.

Patients with fistulas may have minimal abdominal complaints and often present initially to a urologist or gynecologist. Colovesical fistulas may present with pneumaturia, pyuria, or fecaluria, while patients with colovaginal fistulas present with vaginal discharge, vaginal air, or stool per vagina.

A number of patients with “chronic” or atypical diverticular disease will present with pain as their predominant symptom in the absence of other physical findings. The pain is typically persistent and boring, and remains constant over long periods of time. It does not tend to be “crampy” in nature as in patients with irritable bowel syndrome, but is difficult to distinguish from this entity[70]. Recently, symptomatic uncomplicated diverticular disease (SUDD) has been used to describe this group of patients. Many patients with SUDD have continuing symptoms and quality of life limitations even after recovery from an acute episode of diverticulitis. Often, there are no imaging findings which correlate with their symptoms[71].

Diagnostic Evaluation

Most laboratory tests are not terribly helpful in the evaluation of acute diverticulitis. Many patients with acute diverticulitis present with leukocytosis. Patients with colovesical fistulas may have an abnormal urinalysis and/or a urine culture with enteric organisms. C-reactive protein (CRP), procalcitonin, and fecal calprotectin have been considered as potential adjuncts in assessing diverticulitis severity[72],[73],[74]. In multiple case series, CRP has been examined as a marker of complicated diverticulitis. Much of the available data is limited as the series are small and the suggested cutoff values vary[75],[76],[77],[78],[79].

In one study, CRP >150 mg/L significantly discriminated acute uncomplicated from complicated diverticulitis. This study also examined the use of CRP and CT imaging findings. A CRP >150 mg/L and free fluid on CT scan were associated with increased mortality[80]. Another recent study used procalcitonin levels to discriminate between patients with uncomplicated and complicated disease[72]. Although laboratory testing may play an important predictive role in the future, evidence supporting its routine use is limited at present.

Although a number of different modalities have been used to evaluate patients with suspected diverticular disease, computed tomography has emerged as the study of choice. Flat and upright plain films of the abdomen are commonly obtained in the evaluation of the patient with acute abdominal pain to exclude obstruction or free intraperitoneal air. In patients with diverticular disease, the findings of plain films tend to be nonspecific[81]. Ultrasound has not gained wide acceptance in the United States. Contrast enemas are seldom currently used in the evaluation and management of diverticulitis. Water-soluble contrast studies may be useful when an obstructing stricture is suspected.

A CT scan is usually the most useful test in the evaluation of patients with acute abdominal pain. CT findings associated with diverticulitis were first described over 30 years ago. These signs included the presence of diverticula, pericolic fat stranding, colonic wall thickening more than 4 mm, and abscess formation[73]. CT has the ability to stage the severity of disease and may provide a road map for percutaneous drainage of an associated abscess. CT has the added advantage of detecting other intraperitoneal findings including hepatic abscesses, pylephlebitis, small bowel obstruction, colonic strictures/obstruction, and colovesical fistulas.

The first system for classifying the severity of diverticulitis on CT findings to guide clinical management was proposed by Ambrosetti. CT findings consistent with mild diverticulitis included localized wall thickening (>5 mm) and inflammation of the pericolic fat. Severe CT findings were the combination of localized wall thickening and inflammation of the pericolic fat with abscess, extraluminal air, or extraluminal contrast. When the natural history of patients with diverticulitis was stratified by these CT criteria, the authors found that patients with severe CT findings underwent operative intervention more frequently than those patients with mild findings (33% vs. 15%). Patients under 50 years of age with severe findings on CT scan were more likely to have recurrence or complications[74].

In a prospectively collected dataset, patients with findings of severe diverticulitis on CT scan during an index attack treated with antibiotics were more likely to have recurrent attacks of diverticulitis, when compared to patients with mild diverticulitis (39% vs. 14%)[75]. Poletti explored CT and demographic predictors for nonoperative treatment failure in 312 patients with a first episode of left-sided diverticulitis and concluded that the presence of an abscess or extraluminal air >5 cm in diameter was a significant predictor of treatment failure[76].

CT findings which are relevant to clinical management were reclassified based on the Hinchey classification system. In grade 0, there is colonic wall thickening but not pericolonic fat stranding. Grade 1a consists of wall thickening and pericolonic fat stranding, while grade 1b includes pericolonic or mesocolic abscess. Patients with grade 2 disease have distant intra-abdominal or pelvic abscesses. Patients with grade 3 and grade 4 disease have purulent and fecal peritonitis, respectively. CT is somewhat limited in distinguishing between patients with grade 3 and grade 4 disease, as purulent and fecal peritonitis often cannot be distinguished on imaging[77].

Kaiser found that disease severity using the modified CT Hinchey classification system correlated with postoperative morbidity and mortality. This group also found that the CT stage correlated with recurrence in patients managed nonoperatively. The presence of a diverticulitis with an associated abscess was one particular factor highly associated with an increased risk of failed nonoperative management[78].

Endoscopic Evaluation

Endoscopic evaluation of the colon is typically recommended following an acute episode of diverticulitis. This approach is generally advocated to exclude the presence of a malignancy or an alternative diagnosis such as ischemic colitis or inflammatory bowel disease. In actual practice, finding a malignancy is rare. Bryan evaluated 307 patients with flexible sigmoidoscopy (20%) or colonoscopy (80%) following an acute episode of diverticulitis. They found only two patients with colorectal carcinomas[82]. These findings were mirrored by Lau. Of 319 patients who underwent endoscopic evaluation, 26% had polyps (9 polyps >1 cm) and 2.8% were found to have colorectal cancer[83].

Patients with the highest prevalence of malignancy diagnosed after an acute presentation of apparent diverticulitis are those with complicated diverticular disease. A recent systematic review demonstrated that the incidence of malignancy was 7.9% in patients following an attack of complicated diverticulitis and 1.3% following an attack of uncomplicated diverticulitis[84]. Sharma found that the risk of malignancy was 11% in patients with complicated diverticulitis versus 0.7% in those with uncomplicated diverticulitis[85]. A recently published meta-analysis examining 17 studies and 3296 patients demonstrated that the pooled prevalence of colorectal cancer in all patients with diverticulitis was 2.1% (95% CI 1.5–3.1%). In patients with uncomplicated acute diverticulitis, the prevalence of colorectal carcinoma was 0·5 (0·2–1·2) percent[59].

Endoscopic procedures (flexible sigmoidoscopy and colonoscopy) are generally not advocated during an acute episode of diverticulitis. A delay of 6 weeks following resolution of symptoms is typically recommended. This approach is encouraged in order to avoid potential conversion of a sealed microperforation into a free perforation[60]. This position has been questioned by other groups who have demonstrated that colonoscopy during an acute episode of diverticulitis can be safe. However, when colonoscopy is performed in the acute setting, a significant number of the procedures cannot be completed[61],[86].

Cystoscopy or cystography have been used to identify suspected colovesical fistulas associated with diverticulitis. However, in the CT era, the presence of air in the urinary bladder in the absence of instrumentation may be considered diagnostic[87].

Management of Diverticulitis

Acute Uncomplicated Diverticulitis

The number of patients that are admitted for diverticulitis is rising, particularly in the young[1],[88]. Ten percent of these patients develop complications requiring additional management[89]. The vast majority of patients with CT confirmed uncomplicated diverticulitis can be managed without the need for surgery. A number of areas of controversy still exist as new data continues to emerge that influences medical practice.


Two large randomized trials performed in immunocompetent and stable patients questioned the use of antibiotics for the treatment of uncomplicated diverticulitis (DIABOLO and AVOD). In DIABOLO, a proportion of patients with small abscesses were included. In both trials, there were no differences with respect to development of complicated diverticulitis in the short or long term, nor in rates of recurrent diverticulitis based on antibiotic usage[90],[91],[92]. Antibiotic-related complications were reported up to 8% in the DIABOLO trial. Although the aforementioned trials provide level I evidence for non-antibiotic treatment of uncomplicated diverticulitis, there is still not broad agreement in actual practice. The combined SAGES/EAES guideline failed to achieve consensus[93]. The 2020 ASCRS guidelines for the treatment of left-sided diverticulitis are in press and recommend that “selected patients with uncomplicated diverticulitis can be treated without antibiotics/”

Ambulatory Management

Most patients with uncomplicated diverticulitis can be treated in an outpatient setting[94]. General practitioners successfully treat many patients without hospitalization, with low rates of readmission (7%). These patients rarely require percutaneous drainage, and outpatient management is associated with considerable costs savings. Patient selection is paramount. Outpatient treatment candidates should be hemodynamically stable and generally healthy appearing and without major comorbidities or immunosuppression[94],[95].

Dietary Changes

Dietary changes have been applied as non-surgical management of acute uncomplicated diverticulitis. There is little data that suggests that a change in dietary approach can alter the course of diverticulitis. For this reason, the patients should be allowed to have a normal diet as tolerated[96],[97].

Management of Acute Complicated Diverticulitis

Complicated diverticulitis is defined as acute diverticulitis associated with fistula, free perforation, abscess, and/or large bowel obstruction.

Diverticular Abscesses (Hinchey Stages Ib and II)

Literature on the management of diverticular abscesses is difficult to interpret because of significant selection bias. Smaller abscesses (<3 cm) are predominantly treated with antibiotics only, while larger abscesses are treated with percutaneous drainage or even surgery. The failure rates of management of abscesses are therefore difficult to compare.

A recent large multicenter observational study including 447 patients demonstrated a significantly higher rate of treatment failure in the percutaneous drainage group compared to antibiotic treatment (36% vs 24%, p = 0.013). In this study, there were more complications in the subgroup of patients with a large or distant abscess (Hinchey 2)[98]. However, the majority of smaller abscesses were treated with antibiotics and the larger ones with percutaneous drainage.

In a systematic review of 7653 patients treated with antibiotics, the overall recurrence rate was 25.5%; in patients treated with percutaneous drainage, the recurrence rate was 15%[99]. Although the optimal role of percutaneous drainage is not completely clear, it may be considered in patients with a diverticular abscess larger than 3 centimeters. Other patients may initially be treated with antibiotics, as may be patients with an abscess inaccessible for percutaneous drainage. Emergent surgery is appropriate for patients who do not respond to standard non-surgical treatments[100],[101],[102],[103].

Hinchey Stage III Diverticulitis

Nonoperative Management

Hinchey III diverticulitis is suspected when the CT scan shows free air and free fluid. It is important to tailor the management of perforated diverticulitis toward the patient’s clinical condition and CT images. If the patient is clinically stable and without fever, hemodynamic changes, or toxicity, an attempt at antibiotic therapy should be considered. CT scan with the addition of rectal contrast to oral/IV contrast administration can rule out an overt connection between the bowel lumen and the peritoneal cavity (Hinchey IV). There are four case series indicating that in select patients with CT diagnosed perforated diverticulitis, nonoperative management is effective in the majority[104],[105],[106],[107].

Laparoscopic Lavage

There have been three randomized trials and numerous cohort studies looking at the efficacy of laparoscopic lavage compared to resectional surgery. In all three trials, the surgical approach was not uniform and the trials examined different primary outcomes[108],[109],[110]. In the LOLA trial, the primary outcome was a composite of morbidity and mortality. The primary outcome in the SCANDIV trial was the rate of severe postoperative complications at 90 days (Clavien-Dindo >3a). The DILALA trial compared reoperation rates within 12 months of surgery[108],[109],[110],[111].

The LOLA trial was closed early by the data monitoring board because an interim analysis demonstrated an increased rates of serious short-term adverse events in the lavage group (39% vs. 19%, p = 0.04)[112]. In addition, the laparoscopic lavage required more surgical re-interventions (20% vs. 7%, p = 0.12) and had more abscesses that required drainage (20% vs. 0%, p = 0.002). The composite endpoint of morbidity/mortality was comparable between the laparoscopic lavage and sigmoid resection groups at 12 months (67% vs. 60%, p = 0.58). Interestingly, 52% of patients in the laparoscopic lavage group did not require any acute or elective surgical intervention, and 74% of patients never required a stoma[112].

In the SCANDIV trial, there was no difference in the rate of severe complications between the groups at 90 days. These results remained consistent at 1 year after surgery[110],[113]. The laparoscopic lavage group had a higher rates of deep surgical site infection (32% vs. 13%, p = 0.006) and unplanned reoperation (27% vs. 10%, p = 0.01). There were lower rates of superficial wound infection (1% vs. 17%, p = 0.001) and stoma formation (14% vs. 42%, p < 0.001) in the laparoscopic lavage group. Four patients undergoing laparoscopic lavage were ultimately found to have colon adenocarcinoma.

In the DILALA trial, there was no difference in the rate of early re-interventions (30 days) between the laparoscopic lavage and Hartmann groups (13.2% vs. 17.1%, p = 0.67). When long-term results were assessed, the laparoscopic lavage group had a 45% reduction in the risk of undergoing of reoperation within 24 months of surgery[109],[114].

A number of meta-analyses have been performed to summarize the evidence surrounding this technique. Laparoscopic lavage was associated with initial success rate in three out of four patients; similarly, ~3/4 of patients remain stoma free at 1 year. Secondary surgery appears to be necessary in one out of four because of ongoing complaints, who then most often undergo laparoscopic resection. Laparoscopic lavage, however, was associated with a significantly increased risk of intra-abdominal abscess, peritonitis, and future emergency reoperation[108],[110],[111],[115],[116]. Figure 38.1 shows the different outcomes of the three trials at 1 year.

Fig. 38.1
Descriptive text is not available for this image
Shows the different outcomes of the three trials at 1 year. (
) DILALA trial[111],[115], LOLA trial[117], (
) SCANDIV trial[110],[116]

The trade-off with lavage is a higher initial re-intervention rate, but overall morbidity and mortality at 1 year and the need for subsequent intervention is similar to resectional surgery. Lavage has been shown to be more cost-effective[118].

Technique: Diagnostic Laparoscopy and Laparoscopic Lavage

During diagnostic laparoscopy, it is important to examine and irrigate the whole peritoneal cavity. When purulent peritonitis is noted, the abdominal cavity is extensively lavaged until the return is clear. Fibrinous exudate may be evacuated if it can be readily removed without damaging the small bowel. The whole peritoneal cavity must be inspected, in particular the pelvis, to ensure there is not an underlying feculent peritonitis. If necessary, the inflammatory mass should be elevated to ensure there is not fecal contamination hidden deep in the pelvis.

Omentum covering the inflamed sigmoid should be carefully removed, but left alone if densely adherent. Laparoscopic lavage for purulent peritonitis is usually effective if the initial diverticular perforation is sealed. Early failure of laparoscopic lavage can be caused by misdiagnosed Hinchey IV diverticulitis or perforated colorectal cancer. Both are conditions that require sigmoid colectomy. Endoscopic insufflation enables detection of a patent perforation.

Hinchey IV Diverticulitis

Hinchey stage IV perforation is characterized by the presence of feculent peritonitis. Resection of the perforated segment is imperative to control sepsis. Segmental resection has been extensively studied in both Hinchey III as well as Hinchey IV perforations. It is important note that in the acute setting, formal mesenteric resection is not necessary unless there is concern for malignancy. If malignancy is suspected, then oncologic resection with high ligation is suggested.

In hemodynamically stable and immunocompetent patients, it has been shown that anastomosis after sigmoid colectomy +/− diverting loop ileostomy is safe and associated with a much higher rate of subsequent stoma reversal (Tables 38.1, 38.2, and 38.3). If a definitive anastomosis is to be performed, then a proper diverticular resection should be undertaken to minimize recurrence (see below); if a Hartmann procedure is chosen, only the perforated segment needs be initially resected. When the colostomy is taken down after full recovery of the patient, a proper completion sigmoidectomy can be performed.

Table 38.1: Randomized trials comparing sigmoidectomy with anastomosis to Hartmann’s procedure for Hinchey III and IV perforated diverticulitis (cumulative at 1 year)


Stoma closure

Overall morbidity


PA (%)

HP (%)

PA (%)

HP (%)

























Table 38.2: Cohort studies comparing sigmoidectomy with anastomosis to Hartmann’s procedure for Hinchey III and IV perforated diverticulitis

PA Primary anastomosis, HP Hartmann’s procedure[123]


MR* (%) p<0.0001

MB (%)

MB reversal* (%) p = 0.005

SSI (%)

SSI deep* (%) p = 0.003

Hernia (%)

ReOK (%)

Stoma closure (%)





















Table 38.3: Inclusion and exclusion criteria of the trials

Age limit


Pelvic radiotherapy


Hemodynamically unstable


Not mentioned


<18 yrs


<18 yrs





>85 yrs

>20 mg




Chronic Diverticular Disease

Chronic Uncomplicated Disease

Traditionally, elective sigmoid resection was recommended after the second episode of diverticulitis[124],[125],[126]. However, complications of diverticulitis are most likely to occur with a first episode and prophylactic surgery to prevent complicated disease is not justified[23],[127],[128]. Therefore, the decision to perform surgery should be a shared one, which weighs the potential improvement in quality of life against the risks of surgery. The decision for surgery should be individualized, based on severity of symptoms and interference with overall quality of life. Patients should have CT confirmation of the diagnosis of acute diverticulitis, as symptoms from irritable bowel syndrome may mimic ongoing inflammation or recurrent attacks. A randomized study comparing optimal conservative management versus surgery for ongoing complaints or recurrent attacks showed superior quality of life with surgery, despite a relatively high complication rate (DIRECT trial)[129].

The Young

Younger patients do not appear to have more virulent disease than their older counterparts. However, the younger patients have a higher lifetime risk of developing recurrent disease owing to the greater number of remaining years at risk[130]. The relative risk of having an emergent operation in the younger cohort was slightly higher in a systematic review (7.3% vs. 4.9%)[131]. However, this may represent a more aggressive approach to this cohort or a higher rate of misdiagnosis (e.g., appendicitis), rather than the nature of disease.

The Immunocompromised

Complicated diverticulitis may be more aggressive in immunocompromised patients, with a higher incidence of free perforation[132],[133]. However, overall, the incidence of complicated diverticulitis is only slightly higher (1%) in this cohort[134]. The same individualized assessment and approach toward elective resection after an acute episode of diverticulitis appears appropriate.


Complicated diverticular disease can be associated with fistulas to adjacent organs. Diverticular fistulas typically form when a diverticular abscess decompresses through a nearby viscus. Colovesical fistulas are characterized by pneumaturia, fecaluria, and recurrent urinary tract infections. Cross-sectional imaging revealing air in the bladder or a urinary culture with a multiple gut microorganism is usually diagnostic in patients with diverticulitis. Colovesical fistulas may also be identified on cystoscopy. Most patients who are medically fit should be offered surgery to avoid recurrent urosepsis.

Colovaginal fistulas typically arise in patients who have had prior hysterectomies. Most patients will complain of passing gas or stool per vagina. Cross-sectional imaging typically is sufficient for diagnosis. Most patients with a significant colovaginal fistula will desire repair because of the associated distressing symptoms and drainage.

Colocutaneous fistula usually results from a longstanding abscess which drains though the abdominal wall. Initially, these can be managed expectantly. As with other fistulas, patients with significant symptoms usually will require or wish to have an elective operation.


Diverticulitis-related obstructions should be treated surgically. Colonic stenting is generally not successful in benign conditions. It is important to differentiate diverticular stricture from colorectal cancer, owing to the need for oncologic resection in the latter circumstance.

Technical Aspects of Surgery


Three randomized trials and three meta-analyses have evaluated the application of laparoscopy to sigmoid colectomy for diverticulitis. Two of them showed superiority of the laparoscopic approach compared to open surgery[135],[136],[137],[138]. Laparoscopy within an enhanced recovery after surgery program is usually the preferred approach in suitable cases and is associated with earlier recovery and less complications[139]. Pfannenstiel incisions are associated with low incisional hernia rates[140]. In emergency surgery, the evidence is accumulating that a laparoscopic approach may also be of benefit[141].

Transection Margins

Most literature regarding the extent of resection is based on retrospective data and is not very robust. The distal margin of the sigmoidectomy should be the proximal rectum. Colorectal as opposed to colocolic anastomoses have a lower frequency of recurrent disease[142],[143],[144],[145],[146]. The proximal margin of the sigmoidectomy should be chosen where the bowel is not diseased, as evidenced by the absence of bowel wall thickening. The presence of diverticula per se should not guide the proximal margin of resection.

Inferior Mesenteric Artery Preservation

If there is suspicion of malignancy, an oncologic resection should be done with appropriate proximal ligation of the inferior mesenteric vessels. In cases where malignancy is not suspected, an extensive mesenteric resection is not necessary. One randomized trial showed improved intestinal function when the mesentery is preserved[147]. Another study reported a lower radiological and clinical leak rate[148]. Both systematic reviews and cohort studies have reported that leak rates are either lower or the same with vessel preserving surgery[149],[150],[151],[152],[153],[154]. High pedicle ligation seems therefore warranted in cases where cancer cannot be excluded, whereas IMA preservation may otherwise be beneficial.

Splenic Flexure Mobilization

Routine splenic flexure mobilization has not been tested in a systematic way. Nonetheless, creation of a tension-free, well-vascularized anastomosis is desired. In many cases, mobilization of the flexure is necessary to achieve a tension-free anastomosis. The few studies on this topic suggest that splenic flexure mobilization should be done on an individualized basis, depending on the anatomy, disease extent, and the need for additional length to create a tension-free anastomosis[155],[156]. One study suggested that splenic flexure mobilization is associated with increased risk of superficial surgical site infections (10.6% vs. 8.4%, p < 0.0002)[157].

Ureteral Stents

Available evidence suggests that routine ureteral stenting in surgery for diverticular disease is associated with a longer operative time, longer length of stay, and higher costs[158],[159],[160]. Analysis of the protective impact of ureteral stents against ureteral injury in the literature is always confounded by selection bias, as higher-risk patients are more likely to receive stents. As such, comparable rates of injury in stent vs no stent groups may actually be evidence to support their efficacy. A selective approach appears appropriate.

Anastomotic Leak Testing

Anastomotic leak testing may be simply performed by instilling air transanally while submerging the anastomosis under saline in the pelvis (air bubble test). A positive result identifies patients at higher risk of having a clinical leak[161],[162]. This allows the surgeon to repair or revise and then retest the anastomosis[163]. A randomized trial comparing leak testing versus no leak testing in 145 colorectal anastomoses showed that leak testing significantly reduced the incidence of postoperative clinical and radiological leaks[164].

Right-Sided Diverticulitis

There are distinct differences between left- and right-sided diverticulitis. While left-sided diverticula consist of a protrusion of the mucosa through the bowel wall and are by definition false diverticula, the right-sided diverticula are most often true diverticula consisting of all layers of the bowel wall. They are more common in Asia[3]. The scarce literature on right-sided diverticulitis suggests that right-sided diverticulitis is less often associated with a complicated course. The management of complicated diverticulitis, be it left- or right-sided, is generally similar[165],[166].


Colonic diverticular disease is associated with a wide spectrum of presentations and treatment options. While many of the current treatment methods have been in use for the greater part of a century, new approaches to treatment continue to evolve. The initial goal of therapy is to control inflammation and infection, if present. Increasingly, attenuation of the inflammatory response itself will become a target of medical therapy. Individualized assessment is the key to surgical decision-making.


  1. Wheat CL, Strate LL. Trends in Hospitalization for Diverticulitis and Diverticular Bleeding in the United States From 2000 to 2010. Clin Gastroenterol Hepatol. 2016;14(1):96-103.e1.  [PMID:25862988]
  2. Peery AF, Crockett SD, Murphy CC, et al. Burden and Cost of Gastrointestinal, Liver, and Pancreatic Diseases in the United States: Update 2018. Gastroenterology. 2019;156(1):254-272.e11.  [PMID:30315778]
  3. Hall J, Hammerich K, Roberts P. New paradigms in the management of diverticular disease. Curr Probl Surg. 2010;47(9):680-735.  [PMID:20684920]
  4. Rezapour M, Ali S, Stollman N. Diverticular disease: an update on pathogenesis and management. Gut Liver. 2018;12:125–32. PubMed
  5. Heise CP. Epidemiology and pathogenesis of diverticular disease. J Gastrointest Surg. 2008;12(8):1309-11.  [PMID:18278535]
  6. Ricciardi R, Baxter NN, Read TE, et al. Is the decline in the surgical treatment for diverticulitis associated with an increase in complicated diverticulitis? Dis Colon Rectum. 2009;52(9):1558-63.  [PMID:19690482]
  7. Peery AF, Crockett SD, Barritt AS, et al. Burden of Gastrointestinal, Liver, and Pancreatic Diseases in the United States. Gastroenterology. 2015;149(7):1731-1741.e3.  [PMID:26327134]
  8. Bollom A, Austrie J, Hirsch W, et al. Emergency Department Burden of Diverticulitis in the USA, 2006-2013. Dig Dis Sci. 2017;62(10):2694-2703.  [PMID:28332105]
  9. West AB, NDSG. The pathology of diverticulitis. J Clin Gastroenterol. 2008;42(10):1137-8.  [PMID:18936652]
  10. Goldstein NS, Leon-Armin C, Mani A. Crohn's colitis-like changes in sigmoid diverticulitis specimens is usually an idiosyncratic inflammatory response to the diverticulosis rather than Crohn's colitis. Am J Surg Pathol. 2000;24(5):668-75.  [PMID:10800985]
  11. Hinchey EJ, Schaal PG, Richards GK. Treatment of perforated diverticular disease of the colon. Adv Surg. 1978;12:85-109.  [PMID:735943]
  12. Wasvary H, Turfah F, Kadro O, et al. Same hospitalization resection for acute diverticulitis. Am Surg. 1999;65(7):632-5; discussion 636.  [PMID:10399971]
  13. Painter NS, Burkitt DP. Diverticular disease of the colon: a deficiency disease of Western civilization. Br Med J. 1971;2(5759):450-4.  [PMID:4930390]
  14. Commane DM, Arasaradnam RP, Mills S, et al. Diet, ageing and genetic factors in the pathogenesis of diverticular disease. World J Gastroenterol. 2009;15(20):2479-88.  [PMID:19468998]
  15. Kiguli-Malwadde E, Kasozi H. Diverticular disease of the colon in Kampala, Uganda. Afr Health Sci. 2002;2(1):29-32.  [PMID:12789112]
  16. Aldoori WH, Giovannucci EL, Rimm EB, Wing AL, Trichopoulos DV, Willett WC. A prospective study of diet and the risk of symptomatic diverticular disease in men. Am J Clin Nutr. 1994;60:757–64. PubMed
  17. Manousos O, Day NE, Tzonou A, et al. Diet and other factors in the aetiology of diverticulosis: an epidemiological study in Greece. Gut. 1985;26(6):544-9.  [PMID:3924745]
  18. Strate LL, Liu YL, Syngal S, et al. Nut, corn, and popcorn consumption and the incidence of diverticular disease. JAMA. 2008;300(8):907-14.  [PMID:18728264]
  19. Strate LL, Keeley BR, Cao Y, et al. Western Dietary Pattern Increases, and Prudent Dietary Pattern Decreases, Risk of Incident Diverticulitis in a Prospective Cohort Study. Gastroenterology. 2017;152(5):1023-1030.e2.  [PMID:28065788]
  20. Liu PH, Cao Y, Keeley BR, et al. Adherence to a Healthy Lifestyle is Associated With a Lower Risk of Diverticulitis among Men. Am J Gastroenterol. 2017;112(12):1868-1876.  [PMID:29112202]
  21. Strate LL, Morris AM. Epidemiology, Pathophysiology, and Treatment of Diverticulitis. Gastroenterology. 2019;156(5):1282-1298.e1.  [PMID:30660732]
  22. Schafmayer C, Harrison JW, Buch S, et al. Genome-wide association analysis of diverticular disease points towards neuromuscular, connective tissue and epithelial pathomechanisms. Gut. 2019;68(5):854-865.  [PMID:30661054]
  23. Hall JF, Roberts PL, Ricciardi R, et al. Long-term follow-up after an initial episode of diverticulitis: what are the predictors of recurrence? Dis Colon Rectum. 2011;54(3):283-8.  [PMID:21304297]
  24. Granlund J, Svensson T, Olén O, et al. The genetic influence on diverticular disease--a twin study. Aliment Pharmacol Ther. 2012;35(9):1103-7.  [PMID:22432696]
  25. Strate LL, Erichsen R, Baron JA, et al. Heritability and familial aggregation of diverticular disease: a population-based study of twins and siblings. Gastroenterology. 2013;144(4):736-742.e1; quiz e14.  [PMID:23313967]
  26. Sigurdsson S, Alexandersson KF, Sulem P, et al. Sequence variants in ARHGAP15, COLQ and FAM155A associate with diverticular disease and diverticulitis. Nat Commun. 2017;8:15789.  [PMID:28585551]
  27. Connelly TM, Berg AS, Hegarty JP, et al. The TNFSF15 gene single nucleotide polymorphism rs7848647 is associated with surgical diverticulitis. Ann Surg. 2014;259(6):1132-7.  [PMID:24814505]
  28. Connelly TM, Choi CS, Berg AS, et al. Diverticulitis and Crohn's disease have distinct but overlapping tumor necrosis superfamily 15 haplotypes. J Surg Res. 2017;214:262-269.  [PMID:28624054]
  29. Coble JL, Sheldon KE, Yue F, et al. Identification of a rare LAMB4 variant associated with familial diverticulitis through exome sequencing. Hum Mol Genet. 2017;26(16):3212-3220.  [PMID:28595269]
  30. Gill SR, Pop M, Deboy RT, et al. Metagenomic analysis of the human distal gut microbiome. Science. 2006;312(5778):1355-9.  [PMID:16741115]
  31. Daniels L, Philipszoon LE, Boermeester MA. A hypothesis: important role for gut microbiota in the etiopathogenesis of diverticular disease. Dis Colon Rectum. 2014;57(4):539-43.  [PMID:24608313]
  32. Strate LL. Lifestyle factors and the course of diverticular disease. Digest Dis (Basel, Switzerland). 2012;30:35–45.
  33. Bäckhed F, Ding H, Wang T, Hooper LV, Koh GY, Nagy A, Semenkovich CF, Gordon JI. Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome. Gastroenterol. 2012;143(4):913–6.e7.
  34. Bäckhed F, Ding H, Wang T, et al. The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci U S A. 2004;101(44):15718-23.  [PMID:15505215]
  35. Barbara G, Scaioli E, Barbaro MR, et al. Gut microbiota, metabolome and immune signatures in patients with uncomplicated diverticular disease. Gut. 2017;66(7):1252-1261.  [PMID:27618836]
  36. Koh A, De Vadder F, Kovatcheva-Datchary P, et al. From Dietary Fiber to Host Physiology: Short-Chain Fatty Acids as Key Bacterial Metabolites. Cell. 2016;165(6):1332-1345.  [PMID:27259147]
  37. Gueimonde M, Ouwehand A, Huhtinen H, et al. Qualitative and quantitative analyses of the bifidobacterial microbiota in the colonic mucosa of patients with colorectal cancer, diverticulitis and inflammatory bowel disease. World J Gastroenterol. 2007;13(29):3985-9.  [PMID:17663515]
  38. Daniels L, Budding AE, de Korte N, et al. Fecal microbiome analysis as a diagnostic test for diverticulitis. Eur J Clin Microbiol Infect Dis. 2014;33(11):1927-36.  [PMID:24894339]
  39. Frank DN, St Amand AL, Feldman RA, et al. Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases. Proc Natl Acad Sci U S A. 2007;104(34):13780-5.  [PMID:17699621]
  40. Gevers D, Kugathasan S, Denson LA, et al. The treatment-naive microbiome in new-onset Crohn's disease. Cell Host Microbe. 2014;15(3):382-392.  [PMID:24629344]
  41. Li D, de Mestral C, Baxter NN, et al. Risk of readmission and emergency surgery following nonoperative management of colonic diverticulitis: a population-based analysis. Ann Surg. 2014;260(3):423-30; discussion 430-1.  [PMID:25115418]
  42. Katz LH, Guy DD, Lahat A, et al. Diverticulitis in the young is not more aggressive than in the elderly, but it tends to recur more often: systematic review and meta-analysis. J Gastroenterol Hepatol. 2013;28(8):1274-81.  [PMID:23701446]
  43. van de Wall BJ, Draaisma WA, van Iersel JJ, et al. Elective resection for ongoing diverticular disease significantly improves quality of life. Dig Surg. 2013;30(3):190-7.  [PMID:23838742]
  44. El-Sayed C, Radley S, Mytton J, et al. Risk of Recurrent Disease and Surgery Following an Admission for Acute Diverticulitis. Dis Colon Rectum. 2018;61(3):382-389.  [PMID:29420430]
  45. Mathews SN, Lamm R, Yang J, et al. Factors Associated with Repeated Health Resource Utilization in Patients with Diverticulitis. J Gastrointest Surg. 2017;21(1):112-120.  [PMID:27613732]
  46. Hupfeld L, Burcharth J, Pommergaard HC, Rosenberg J. Risk factors for recurrence after acute colonic diverticulitis: a systematic review. Int J Color Dis. 2017;32:611–22.
  47. Parks TG. Natural history of diverticular disease of the colon. A review of 521 cases. Br Med J. 1969;4(5684):639-42.  [PMID:5359917]
  48. Hall JF, Roberts PL, Ricciardi R, et al. Colonic diverticulitis: does age predict severity of disease on CT imaging? Dis Colon Rectum. 2010;53(2):121-5.  [PMID:20087085]
  49. Etzioni DA, Chiu VY, Cannom RR, et al. Outpatient treatment of acute diverticulitis: rates and predictors of failure. Dis Colon Rectum. 2010;53(6):861-5.  [PMID:20484998]
  50. Aldoori WH, Giovannucci EL, Rimm EB, Wing AL, Trichopoulos DV, Willett WC. A prospective study of diet and the risk of symptomatic diverticular disease in men. Am J Clin Nutr. 1994;60(5):757–64. PubMed
  51. Heaton KW, Thompson WG. Exercise and diverticular disease. BMJ. 1995;310(6990):1332.  [PMID:7773067]
  52. Strate LL, Liu YL, Aldoori WH, et al. Physical activity decreases diverticular complications. Am J Gastroenterol. 2009;104(5):1221-30.  [PMID:19367267]
  53. Papagrigoriadis S, Macey L, Bourantas N, et al. Smoking may be associated with complications in diverticular disease. Br J Surg. 1999;86(7):923-6.  [PMID:10417566]
  54. Aune D, Sen A, Leitzmann MF, Tonstad S, Norat T, Vatten LJ. Tobacco smoking and the risk of diverticular disease – a systematic review and meta-analysis of prospective studies. Color Dis. 2017;19:621–33.
  55. Kvasnovsky CL, Papagrigoriadis S, Bjarnason I. Increased diverticular complications with nonsteriodal anti-inflammatory drugs and other medications: a systematic review and meta-analysis. Color Dis. 2014;16:O189–96.
  56. Aldoori WH, Giovannucci EL, Rimm EB, et al. Use of acetaminophen and nonsteroidal anti-inflammatory drugs: a prospective study and the risk of symptomatic diverticular disease in men. Arch Fam Med. 1998;7(3):255-60.  [PMID:9596460]
  57. Humes DJ, Fleming KM, Spiller RC, et al. Concurrent drug use and the risk of perforated colonic diverticular disease: a population-based case-control study. Gut. 2011;60(2):219-24.  [PMID:20940283]
  58. Strate LL, Liu YL, Huang ES, et al. Use of aspirin or nonsteroidal anti-inflammatory drugs increases risk for diverticulitis and diverticular bleeding. Gastroenterology. 2011;140(5):1427-33.  [PMID:21320500]
  59. Rottier SJ, van Dijk ST, Ünlü Ç, et al. Complicated Disease Course in Initially Computed Tomography-Proven Uncomplicated Acute Diverticulitis. Surg Infect (Larchmt). 2019;20(6):453-459.  [PMID:30932745]
  60. Lahat A, Yanai H, Sakhnini E, et al. Role of colonoscopy in patients with persistent acute diverticulitis. World J Gastroenterol. 2008;14(17):2763-6.  [PMID:18461662]
  61. Lahat A, Yanai H, Menachem Y, et al. The feasibility and risk of early colonoscopy in acute diverticulitis: a prospective controlled study. Endoscopy. 2007;39(6):521-4.  [PMID:17554647]
  62. Sheth AA, Longo W, Floch MH. Diverticular disease and diverticulitis. Am J Gastroenterol. 2008;103(6):1550-6.  [PMID:18479497]
  63. Dobbins C, Defontgalland D, Duthie G, et al. The relationship of obesity to the complications of diverticular disease. Colorectal Dis. 2006;8(1):37-40.  [PMID:16519636]
  64. Zaidi E, Daly B. CT and clinical features of acute diverticulitis in an urban U.S. population: rising frequency in young, obese adults. AJR Am J Roentgenol. 2006;187(3):689-94.  [PMID:16928931]
  65. Aldoori WH, Giovannucci EL, Rimm EB, et al. A prospective study of alcohol, smoking, caffeine, and the risk of symptomatic diverticular disease in men. Ann Epidemiol. 1995;5(3):221-8.  [PMID:7606311]
  66. Strate LL, Liu YL, Aldoori WH, et al. Obesity increases the risks of diverticulitis and diverticular bleeding. Gastroenterology. 2009;136(1):115-122.e1.  [PMID:18996378]
  67. Rosemar A, Angerås U, Rosengren A. Body mass index and diverticular disease: a 28-year follow-up study in men. Dis Colon Rectum. 2008;51(4):450-5.  [PMID:18157570]
  68. Ma W, Jovani M, Liu PH, Nguyen LH, Cao Y, Tam I, Wu K, Giovannucci EL, Strate LL, Chan AT. Association between obesity and weight change and rsk of diverticulitis in women. Gastroenterology. 2018;155, 58:–66.e4.
  69. Aune D, Sen A, Leitzmann MF, et al. Body mass index and physical activity and the risk of diverticular disease: a systematic review and meta-analysis of prospective studies. Eur J Nutr. 2017;56(8):2423-2438.  [PMID:28393286]
  70. Horgan AF, McConnell EJ, Wolff BG, et al. Atypical diverticular disease: surgical results. Dis Colon Rectum. 2001;44(9):1315-8.  [PMID:11584207]
  71. Rezapour M, Ali S, Stollman N. Diverticular disease: an udate on pathogenesis and management. Gut Liver. 2018;12(2):125–32. PubMed
  72. Jeger V, Pop R, Forudastan F, Barras JP, Zuber M, Piso RJ. Is there a role for procalcitonin in differentiating uncomplicated and complicated diverticulitis in order to reduce antibiotic therapy? A prospective diagnostic cohort study. Swiss Med Weekly. 2017;147:w14555.
  73. Kiewiet JJ, Andeweg CS, Laurell H, Daniels L, Lameris W, Reitsma JB, Hendriks JC, Bleichrodt RP, van Goor H, Boermeester MA. External validation of two tools for the clinical diagnosis of acute diverticulitis without imaging. Digest Liver Dis. 2014;46:119–24.
  74. Tursi A, Elisei W, Picchio M, Brandimarte G. Increased faecal calprotectin predicts recurrence of colonic diverticulitis. Int J Color Dis. 2014;29:931–5.
  75. Hogan J, Sehgal R, Murphy D, et al. Do Inflammatory Indices Play a Role in Distinguishing between Uncomplicated and Complicated Diverticulitis? Dig Surg. 2017;34(1):7-11.  [PMID:27336407]
  76. Kechagias A, Rautio T, Kechagias G, et al. The role of C-reactive protein in the prediction of the clinical severity of acute diverticulitis. Am Surg. 2014;80(4):391-5.  [PMID:24887672]
  77. Kechagias A, Rautio T, Makela J. The early C-reactive protein trend does not hve a role in monitoring acute diverticulitis progression. Chirurgia (Bucharest, Romania : 1990). 2016;111:43–7.
  78. Makela JT, Klintrup K, Rautio T. The role of low CRP values in the prediction of the development of acute diverticulitis. Int J Color Dis. 2016;31:23–7.
  79. Nizri E, Spring S, Ben-Yehuda A, et al. C-reactive protein as a marker of complicated diverticulitis in patients on anti-inflammatory medications. Tech Coloproctol. 2014;18(2):145-9.  [PMID:23807310]
  80. Mäkelä JT, Klintrup K, Takala H, et al. The role of C-reactive protein in prediction of the severity of acute diverticulitis in an emergency unit. Scand J Gastroenterol. 2015;50(5):536-41.  [PMID:25665622]
  81. Rosen MP, Sands DZ, Longmaid HE, et al. Impact of abdominal CT on the management of patients presenting to the emergency department with acute abdominal pain. AJR Am J Roentgenol. 2000;174(5):1391-6.  [PMID:10789801]
  82. van de Wall BJ, Reuling EM, Consten EC, van Grinsven JH, Schwartz MP, Broeders IA, Draaisma WA. Endoscopic evaluation of the colon after an episode of diverticulitis: a call for a more selective approach. Int J Color Dis. 2012;27:1145–50.
  83. Lau KC, Spilsbury K, Farooque Y, et al. Is colonoscopy still mandatory after a CT diagnosis of left-sided diverticulitis: can colorectal cancer be confidently excluded? Dis Colon Rectum. 2011;54(10):1265-70.  [PMID:21904141]
  84. Meyer J, Orci LA, Combescure C, et al. Risk of Colorectal Cancer in Patients With Acute Diverticulitis: A Systematic Review and Meta-analysis of Observational Studies. Clin Gastroenterol Hepatol. 2019;17(8):1448-1456.e17.  [PMID:30056181]
  85. Sharma PV, Eglinton T, Hider P, et al. Systematic review and meta-analysis of the role of routine colonic evaluation after radiologically confirmed acute diverticulitis. Ann Surg. 2014;259(2):263-72.  [PMID:24169174]
  86. Sakhnini E, Lahat A, Melzer E, et al. Early colonoscopy in patients with acute diverticulitis: results of a prospective pilot study. Endoscopy. 2004;36(6):504-7.  [PMID:15202046]
  87. Touzios JG, Dozois EJ. Diverticulosis and acute diverticulitis. Gastroenterol Clin N Am. 2009;38:513–25.
  88. Binda GA, Mataloni F, Bruzzone M, et al. Trends in hospital admission for acute diverticulitis in Italy from 2008 to 2015. Tech Coloproctol. 2018;22(8):597-604.  [PMID:30196450]
  89. Bolkenstein HE, van Dijk ST, Consten ECJ, Heggelman BGF, Hoeks CMA, Broeders I, Boermeester MA, Draaisma WA. Conservative treatment in diverticulitis patients with pericolic extraluminal air and the role of antibiotic treatment. J Gastrointest Sur. 2019;23(11):2269–76.
  90. Chabok A, Påhlman L, Hjern F, et al. Randomized clinical trial of antibiotics in acute uncomplicated diverticulitis. Br J Surg. 2012;99(4):532-9.  [PMID:22290281]
  91. Daniels L, Ünlü Ç, de Korte N, van Dieren S, Stockmann HB, Vrouenraets BC, Consten EC, van der Hoeven JA, Eijsbouts QA, Faneyte IF, Bemelman WA, Dijkgraaf MG, Boermeester MA, Dutch Diverticular Disease (3D) Collaborative Study Group. Randomized clinical trial of observational versus antibiotic treatment for a first episode of CT-proven uncomplicated acute diverticulitis. Br J Surg.
  92. van Dijk ST, Daniels L, Ünlü Ç, et al. Long-Term Effects of Omitting Antibiotics in Uncomplicated Acute Diverticulitis. Am J Gastroenterol. 2018;113(7):1045-1052.  [PMID:29700480]
  93. Francis NK, Sylla P, Abou-Khalil M, et al. EAES and SAGES 2018 consensus conference on acute diverticulitis management: evidence-based recommendations for clinical practice. Surg Endosc. 2019;33(9):2726-2741.  [PMID:31250244]
  94. Biondo S, Golda T, Kreisler E, et al. Outpatient versus hospitalization management for uncomplicated diverticulitis: a prospective, multicenter randomized clinical trial (DIVER Trial). Ann Surg. 2014;259(1):38-44.  [PMID:23732265]
  95. van Dijk ST, Bos K, de Boer MGJ, Draaisma WA, van Enst WA, Felt RJF, Klarenbeek BR, Otte JA, Puylaert J, van Geloven AAW, Boermeester MA. A systematic review and meta-analysis of outpatient treatment for acute diverticulitis. Int J Color Dis. 2018;33:505–12.
  96. van de Wall BJ, Draaisma WA, van Iersel JJ, et al. Dietary restrictions for acute diverticulitis: evidence-based or expert opinion? Int J Colorectal Dis. 2013;28(9):1287-93.  [PMID:23604409]
  97. Stam MA, Draaisma WA, van de Wall BJ, Bolkenstein HE, Consten EC, Broeders IA. An unrestricted diet for uncomplicated diverticulitis is safe: results of a prospective diverticulitis diet study. Color Dis. 2017;19:372–7.
  98. Lambrichts DPV, Bolkenstein HE, van der Does DCHE, et al. Multicentre study of non-surgical management of diverticulitis with abscess formation. Br J Surg. 2019;106(4):458-466.  [PMID:30811050]
  99. Gregersen R, Mortensen LQ, Burcharth J, et al. Treatment of patients with acute colonic diverticulitis complicated by abscess formation: A systematic review. Int J Surg. 2016;35:201-208.  [PMID:27741423]
  100. Vennix S, Morton DG, Hahnloser D, Lange JF, Bemelman WA. Systematic review of evidence and consensus on diverticulitis: an analysis of national and international guidelines. Color Dis. 2014;16:866–78.
  101. Brandt D, Gervaz P, Durmishi Y, et al. Percutaneous CT scan-guided drainage vs. antibiotherapy alone for Hinchey II diverticulitis: a case-control study. Dis Colon Rectum. 2006;49(10):1533-8.  [PMID:16988856]
  102. Kumar RR, Kim JT, Haukoos JS, et al. Factors affecting the successful management of intra-abdominal abscesses with antibiotics and the need for percutaneous drainage. Dis Colon Rectum. 2006;49(2):183-9.  [PMID:16322960]
  103. Ambrosetti P, Chautems R, Soravia C, et al. Long-term outcome of mesocolic and pelvic diverticular abscesses of the left colon: a prospective study of 73 cases. Dis Colon Rectum. 2005;48(4):787-91.  [PMID:15747071]
  104. Costi R, Cauchy F, Le Bian A, et al. Challenging a classic myth: pneumoperitoneum associated with acute diverticulitis is not an indication for open or laparoscopic emergency surgery in hemodynamically stable patients. A 10-year experience with a nonoperative treatment. Surg Endosc. 2012;26(7):2061-71.  [PMID:22274929]
  105. Dharmarajan S, Hunt SR, Birnbaum EH, et al. The efficacy of nonoperative management of acute complicated diverticulitis. Dis Colon Rectum. 2011;54(6):663-71.  [PMID:21552049]
  106. Sallinen VJ, Mentula PJ, Leppäniemi AK. Nonoperative management of perforated diverticulitis with extraluminal air is safe and effective in selected patients. Dis Colon Rectum. 2014;57(7):875-81.  [PMID:24901689]
  107. Titos-Garcia A, Aranda-Narvaez JM, Romacho-Lopez L, Gonzalez-Sanchez AJ, Cabrera-Serna I, Santoyo-Santoyo J. Nonoperative management of perforated acute diverticulitis with extraluminal air: results and risk factors of failure. Int J Color Dis. 2017;32:1503–7.
  108. Vennix S, Musters G, Mulder I, Swank H, Consten E, Belgers E, Geloven A, Gerhards M, Govaert M, Grevenstein W, Hoofwijk A, Kruyt P, Nienhuijs S, Boermeester M, Vermeulen J, Dieren S, Lange J, Bemelman W. Laparoscopic peritoneal lavage or sigmoidectomy for perforated diverticulitis with purulent peritonitis: a multicentre, parallel-group, randomised, open-label trial. Lancet (London, England). 2015; https://​doi.​org/​10.​1016/​S0140-6736(15)61168-0.
  109. Angenete E, Thornell A, Burcharth J, Pommergaard H, Skullman S, Bisgaard T, Jess P, Läckberg Z, Matthiessen P, Heath J, Rosenberg J, Haglind E. Laparoscopic lavage is feasible and safe for the treatment of perforated diverticulitis with purulent peritonitis: the first results from the randomized controlled trial DILALA. Ann Surg. 2017; https://​doi.​org/​10.​1097/​SLA.​0000000000001061​.
  110. Schultz JK, Yaqub S, Wallon C, et al. Laparoscopic Lavage vs Primary Resection for Acute Perforated Diverticulitis: The SCANDIV Randomized Clinical Trial. JAMA. 2015;314(13):1364-75.  [PMID:26441181]
  111. Thornell A, Angenete E, Bisgaard T, et al. Laparoscopic Lavage for Perforated Diverticulitis With Purulent Peritonitis: A Randomized Trial. Ann Intern Med. 2016;164(3):137-45.  [PMID:26784672]
  112. Vennix S, Musters GD, Mulder IM, et al. Laparoscopic peritoneal lavage or sigmoidectomy for perforated diverticulitis with purulent peritonitis: a multicentre, parallel-group, randomised, open-label trial. Lancet. 2015;386(10000):1269-1277.  [PMID:26209030]
  113. Schultz J, Wallon C, Blecic L, Forsmo H, Folkesson J, Buchwald P, Korner H, Dahl F, Oresland T, Yaqub S. One-year results of the SCANDIV randomized clinical trial of laparoscopic lavage versus primary resection for acute perforated diverticulitis. Br J Surg. 2017; https://​doi.​org/​10.​1002/​bjs.​10567 .
  114. Kohl A, Rosenberg J, Bock D, et al. Two-year results of the randomized clinical trial DILALA comparing laparoscopic lavage with resection as treatment for perforated diverticulitis. Br J Surg. 2018;105(9):1128-1134.  [PMID:29663316]
  115. Angenete E, Bock D, Rosenberg J, Haglind E. Laparoscopic lavage is superior to colon resection for perforated purulent diverticulitis-a meta-analysis. Int J Color Dis. 2017;32:163–9.
  116. Schultz JK, Wallon C, Blecic L, Forsmo HM, Folkesson J, Buchwald P, Kørner H, Dahl FA, Øresland T, Yaqub S. One-year results of the SCANDIV randomized clinical trial of laparoscopic lavage versus primary resection for acute perforated diverticulitis. Br J Surg. 2017;104:1382–92. PubMed
  117. Vennix S, Musters G, Swank H, Mulder I, Consten E, Boermeester M, Dieren S, Lange J, Bemelman W. Laparoscopic peritoneal lavage or sigmoidectomy for generalized peritonitis due to perforated diverticulitis; results: of a multicenter randomised trial (the ladies trial). Surg Endosc Other Interv Tech. 2015; https://​doi.​org/​10.​1007/​s00464-015-4135-8 .
  118. Vennix S, van Dieren S, Opmeer BC, et al. Cost analysis of laparoscopic lavage compared with sigmoid resection for perforated diverticulitis in the Ladies trial. Br J Surg. 2017;104(1):62-68.  [PMID:28000941]
  119. Oberkofler CE, Rickenbacher A, Raptis DA, et al. A multicenter randomized clinical trial of primary anastomosis or Hartmann's procedure for perforated left colonic diverticulitis with purulent or fecal peritonitis. Ann Surg. 2012;256(5):819-26; discussion 826-7.  [PMID:23095627]
  120. Binda GA, Karas JR, Serventi A, Sokmen S, Amato A, Hydo L, Bergamaschi R. Primary anastomosis vs nonrestorative resection for perforated diverticulitis with peritonitis: a prematurely terminated randomized controlled trial. Color Dis. 2012;14:1403–10.
  121. Bridoux V, Regimbeau JM, Ouaissi M, et al. Hartmann's Procedure or Primary Anastomosis for Generalized Peritonitis due to Perforated Diverticulitis: A Prospective Multicenter Randomized Trial (DIVERTI). J Am Coll Surg. 2017;225(6):798-805.  [PMID:28943323]
  122. Lambrichts DPV, Vennix S, Musters GD, et al. Hartmann's procedure versus sigmoidectomy with primary anastomosis for perforated diverticulitis with purulent or faecal peritonitis (LADIES): a multicentre, parallel-group, randomised, open-label, superiority trial. Lancet Gastroenterol Hepatol. 2019;4(8):599-610.  [PMID:31178342]
  123. Gachabayov M, Oberkofler CE, Tuech JJ, Hahnloser D, Bergamaschi R. Resection with primary anastomosis vs nonrestorative resection for perforated diverticulitis with peritonitis: a systematic review and meta-analysis. Color Dis. 2018;20:753–70.
  124. Köhler L, Sauerland S, Neugebauer E. Diagnosis and treatment of diverticular disease: results of a consensus development conference. The Scientific Committee of the European Association for Endoscopic Surgery. Surg Endosc. 1999;13(4):430-6.  [PMID:10094765]
  125. Wong WD, Wexner SD, Lowry A, et al. Practice parameters for the treatment of sigmoid diverticulitis--supporting documentation. The Standards Task Force. The American Society of Colon and Rectal Surgeons. Dis Colon Rectum. 2000;43(3):290-7.  [PMID:10733108]
  126. Feingold D, Steele SR, Lee S, et al. Practice parameters for the treatment of sigmoid diverticulitis. Dis Colon Rectum. 2014;57(3):284-94.  [PMID:24509449]
  127. Ritz JP, Lehmann KS, Frericks B, et al. Outcome of patients with acute sigmoid diverticulitis: multivariate analysis of risk factors for free perforation. Surgery. 2011;149(5):606-13.  [PMID:21145569]
  128. Haglund U, Hellberg R, Johnsén C, et al. Complicated diverticular disease of the sigmoid colon. An analysis of short and long term outcome in 392 patients. Ann Chir Gynaecol. 1979;68(2):41-6.  [PMID:507737]
  129. van de Wall BJM, Stam MAW, Draaisma WA, et al. Surgery versus conservative management for recurrent and ongoing left-sided diverticulitis (DIRECT trial): an open-label, multicentre, randomised controlled trial. Lancet Gastroenterol Hepatol. 2017;2(1):13-22.  [PMID:28404008]
  130. Rafferty J, Shellito P, Hyman NH, et al. Practice parameters for sigmoid diverticulitis. Dis Colon Rectum. 2006;49(7):939-44.  [PMID:16741596]
  131. van de Wall BJ, Poerink JA, Draaisma WA, et al. Diverticulitis in young versus elderly patients: a meta-analysis. Scand J Gastroenterol. 2013;48(6):643-51.  [PMID:23330633]
  132. Biondo S, Borao JL, Kreisler E, et al. Recurrence and virulence of colonic diverticulitis in immunocompromised patients. Am J Surg. 2012;204(2):172-9.  [PMID:22444713]
  133. Pourfarziani V, Mousavi-Nayeeni SM, Ghaheri H, et al. The outcome of diverticulosis in kidney recipients with polycystic kidney disease. Transplant Proc. 2007;39(4):1054-6.  [PMID:17524890]
  134. Oor JE, Atema JJ, Boermeester MA, et al. A systematic review of complicated diverticulitis in post-transplant patients. J Gastrointest Surg. 2014;18(11):2038-46.  [PMID:25127673]
  135. Gervaz P, Inan I, Perneger T, et al. A prospective, randomized, single-blind comparison of laparoscopic versus open sigmoid colectomy for diverticulitis. Ann Surg. 2010;252(1):3-8.  [PMID:20505508]
  136. Gervaz P, Mugnier-Konrad B, Morel P, et al. Laparoscopic versus open sigmoid resection for diverticulitis: long-term results of a prospective, randomized trial. Surg Endosc. 2011;25(10):3373-8.  [PMID:21556992]
  137. Klarenbeek BR, Veenhof AA, Bergamaschi R, et al. Laparoscopic sigmoid resection for diverticulitis decreases major morbidity rates: a randomized control trial: short-term results of the Sigma Trial. Ann Surg. 2009;249(1):39-44.  [PMID:19106674]
  138. Raue W, Paolucci V, Asperger W, Albrecht R, Buchler MW, Schwenk W. Laparoscopic sigmoid resection for diverticular disease has no advantages over open approach: midterm results of a randomized controlled trial. Langenbecks Arch Surg/Deutsche Gesellschaft fur Chirurgie. 2011;396:973–80.
  139. Vlug MS, Wind J, Hollmann MW, et al. Laparoscopy in combination with fast track multimodal management is the best perioperative strategy in patients undergoing colonic surgery: a randomized clinical trial (LAFA-study). Ann Surg. 2011;254(6):868-75.  [PMID:21597360]
  140. Bartels SA, Vlug MS, Hollmann MW, et al. Small bowel obstruction, incisional hernia and survival after laparoscopic and open colonic resection (LAFA study). Br J Surg. 2014;101(9):1153-9.  [PMID:24977342]
  141. Vennix S, Lips DJ, Di Saverio S, van Wagensveld BA, Brokelman WJ, Gerhards MF, van Geloven AA, van Dieren S, Lange JF, Bemelman WA. Acute laparoscopic and open sigmoidectomy for perforated diverticulitis: a propensity score-matched cohort. Surg Endosc. 2016;30:3889–96. PubMed
  142. Benn PL, Wolff BG, Ilstrup DM. Level of anastomosis and recurrent colonic diverticulitis. Am J Surg. 1986;151(2):269-71.  [PMID:3946763]
  143. Bergamaschi R, Arnaud JP. Anastomosis level and specimen length in surgery for uncomplicated diverticulitis of the sigmoid. Surg Endosc. 1998;12(9):1149-51.  [PMID:9716770]
  144. Bressan A, Marini L, Michelotto M, Frigo AC, Da Dalt G, Merigliano S, Polese L. Risk factors including the presence of inflammation at the resection margins for colorectal anastomotic stenosis following surgery for diverticular disease. Color Dis. 2018;20:923–30.
  145. Thaler K, Baig MK, Berho M, et al. Determinants of recurrence after sigmoid resection for uncomplicated diverticulitis. Dis Colon Rectum. 2003;46(3):385-8.  [PMID:12626916]
  146. Wolff BG, Ready RL, MacCarty RL, et al. Influence of sigmoid resection on progression of diverticular disease of the colon. Dis Colon Rectum. 1984;27(10):645-7.  [PMID:6489070]
  147. Masoni L, Mari FS, Nigri G, et al. Preservation of the inferior mesenteric artery via laparoscopic sigmoid colectomy performed for diverticular disease: real benefit or technical challenge: a randomized controlled clinical trial. Surg Endosc. 2013;27(1):199-206.  [PMID:22733197]
  148. Tocchi A, Mazzoni G, Fornasari V, et al. Preservation of the inferior mesenteric artery in colorectal resection for complicated diverticular disease. Am J Surg. 2001;182(2):162-7.  [PMID:11574089]
  149. Borchert DH, Schachtebeck M, Schoepe J, et al. Observational study on preservation of the superior rectal artery in sigmoid resection for diverticular disease. Int J Surg. 2015;21:45-50.  [PMID:26192969]
  150. De Nardi P, Gazzetta P. Does inferior mesenteric artery ligation affect outcome in elective colonic resection for diverticular disease? ANZ J Surg. 2018;88(11):E778-E781.  [PMID:30062801]
  151. Lehmann RK, Brounts LR, Johnson EK, et al. Does sacrifice of the inferior mesenteric artery or superior rectal artery affect anastomotic leak following sigmoidectomy for diverticulitis? a retrospective review. Am J Surg. 2011;201(5):623-7.  [PMID:21545911]
  152. Posabella A, Rotigliano N, Tampakis A, von Flue M, Fuglistaler I. Peripheral vs pedicle division in laparoscopic resection of sigmoid diverticulitis: a 10-year experience. Int J Color Dis. 2018;33:887–94.
  153. Sohn M, Schlitt HJ, Hornung M, Zulke C, Hochrein A, Moser C, Agha A. Preservation of the superior rectal artery: influence of surgical technique on anastomotic healing and postoperative morbidity in laparoscopic sigmoidectomy for diverticular disease. Int J Color Dis. 2017;32:955–60.
  154. Cirocchi R, Popivanov G, Binda GA, et al. Sigmoid resection for diverticular disease - to ligate or to preserve the inferior mesenteric artery? Results of a systematic review and meta-analysis. Colorectal Dis. 2019;21(6):623-631.  [PMID:30609274]
  155. Schlussel AT, Wiseman JT, Kelly JF, et al. Location is everything: The role of splenic flexure mobilization during colon resection for diverticulitis. Int J Surg. 2017;40:124-129.  [PMID:28259692]
  156. Simon T, Orangio GR, Ambroze WL, et al. Factors associated with complications of open versus laparoscopic sigmoid resection for diverticulitis. JSLS. 2005;9(1):63-7.  [PMID:15791973]
  157. Carlson RM, Roberts PL, Hall JF, et al. What are 30-day postoperative outcomes following splenic flexure mobilization during anterior resection? Tech Coloproctol. 2014;18(3):257-64.  [PMID:23907675]
  158. Chiu AS, Jean RA, Gorecka J, et al. Trends of ureteral stent usage in surgery for diverticulitis. J Surg Res. 2018;222:203-211.e3.  [PMID:29100586]
  159. Speicher PJ, Goldsmith ZG, Nussbaum DP, et al. Ureteral stenting in laparoscopic colorectal surgery. J Surg Res. 2014;190(1):98-103.  [PMID:24656474]
  160. Coakley KM, Kasten KR, Sims SM, et al. Prophylactic Ureteral Catheters for Colectomy: A National Surgical Quality Improvement Program-Based Analysis. Dis Colon Rectum. 2018;61(1):84-88.  [PMID:29215477]
  161. Wu Z, van de Haar RC, Sparreboom CL, Boersema GS, Li Z, Ji J, Jeekel J, Lange JF. Is the intraoperative air leak test effective in the prevention of colorectal anastomotic leakage? A systematic review and meta-analysis. Int J Color Dis. 2016;31:1409–17.
  162. Ricciardi R, Roberts PL, Marcello PW, et al. Anastomotic leak testing after colorectal resection: what are the data? Arch Surg. 2009;144(5):407-11; discussion 411-2.  [PMID:19451481]
  163. Daams F, Wu Z, Lahaye MJ, et al. Prediction and diagnosis of colorectal anastomotic leakage: A systematic review of literature. World J Gastrointest Surg. 2014;6(2):14-26.  [PMID:24600507]
  164. Beard JD, Nicholson ML, Sayers RD, et al. Intraoperative air testing of colorectal anastomoses: a prospective, randomized trial. Br J Surg. 1990;77(10):1095-7.  [PMID:2136198]
  165. Kim SH, Byun CG, Cha JW, et al. Comparative study of the clinical features and treatment for right and left colonic diverticulitis. J Korean Soc Coloproctol. 2010;26(6):407-12.  [PMID:21221241]
  166. Chung BH, Ha GW, Lee MR, et al. Management of Colonic Diverticulitis Tailored to Location and Severity: Comparison of the Right and the Left Colon. Ann Coloproctol. 2016;32(6):228-233.  [PMID:28119866]
Last updated: January 26, 2022