Diverticular disease K57.32

Authors: Prof. Dr. med. Peter Altmeyer, Prof. Dr. med. Guido Gerken

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Last updated on: 29.10.2020

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Synonym(s)

Diverticulitis

Definition
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A "diverticular disease" of the colon occurs when diverticulosis leads to clinically significant symptoms and/or complications. Diverticulosis of the colon and diverticular disease are among the most common diseases of the gastrointestinal tract. The special clinical significance of diverticulosis results from its possible complications, such as the life-threatening occurrence of covered or open perforations and diverticular bleeding. Diverticular disease can lead to painful relapses, stenoses or fistulas in the medium to long term.

Classification
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The German S 2k guideline Diverticular Disease/Diverticulitis proposes a new classification (Classification of Diverticular Disease - CDD). Diverticular hemorrhages are a special form of CDD, which are the most common cause of lower gastrointestinal bleeding:

Classification of Diverticular Diseases (varies according to Böhm SK 2020):

  • Type 0 Asymptomatic diverticulosis, random findings (80%)
  • Type 1 Acute uncomplicated diverticular disease (non-perforated diverticulitis)
    • Type 1a: Diverticulitis without environmental reaction (conservative therapy)
    • Type 1b: Diverticulitis (peridiverdiculitis) with phlegmonous environmental reaction (conservative, avoidance of antibiotics in the absence of risk factors)
  • Type 2 Acute complicated diverticular disease (like type 1b with additional findings)
    • Type 2a: Microabscess; covered perforated diverticulitis; CT microabscess < 1cm (conservative, antibiotics, surgical only if there is no improvement)
    • Type 2b: Macroabscess: freely perforated diverticulitis; CT macroabscess >1cm (initially conservative, antibiotics, in case of abscess > 3-4cm possibly drainage in the course of elective laparoscopic sigmoid contingency transection)
    • Type 2c: Free perforation, free air, generalized peritonitis (emergency surgery; sigmoid resection, continuity resection)
      • Type 2c1: Purulent peritonitis (emergency surgery)
      • Type 2c2: Faecal peritonitis (emergency surgery)
  • Type 3 Chronic recurrent diverticular disease/recurrent or persistent symptomatic diverticular disease (op-indication depending on the symptoms)
    • Type 3a: Symptomatic uncomplicated chronic recurrent diverticular disease (SUDD) (conservative: rifaximin, mesalzine)
    • Type 3b: recurrent diverticulitis without complications (recurrent signs of inflammation with CT findings in type 1a/b (conservative, rifaximin, mesallizine, probiotics, possibly surgical = laparascopic sigmoid-continuity transection)
    • Type 3c: Recurrent diverticulitis with complications (stenosis, fistulas, conglomerate tumor. elective laparascopic sigmo-continuity transection)
  • Type 4: Diverticular hemorrhage (caused by a rupture of the rectal vasa, clinically evident by hematochezia, in severe cases with circulatory reactions; drop in RR and rise in pulse; therapy: colonoscopy with hemostasis; resection if necessary)

Occurrence/Epidemiology
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Diverticulosis: There is a clear age dependency in terms of prevalence. There is also a clear age dependency in the incidence, with some increase in younger patients.

Prevalences:

  • 40-49 years old: about 25 %.
  • 50-59 years: approx. 35
  • 60-69 years of age: approx. 50
  • 70-79 years: approx. 65
  • > 80 years: approx. 70

The incidence of diverticulitis shows a 50% increase over the last 20 years. 20% of patients with sympothless diverticulosis develop symptomatic diverticulitis during their lifetime. Of the patients with a first relapse of diverticulitis, about 20% have a further relapse or several further relapses within a year.

Etiopathogenesis
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Due to changing luminal filling levels, the colonic wall has a high degree of elasticity. The mucosa is present in excess as a "substrate" for diverticular formation. Internal pressures of up to 90 mmHg can occur in the colon. Such high pressures are essential factors for the protrusion of the mucosa along the transmuscular connective tissue perivascular septa. Other potential factors for the development of diverticulitis are:

  • Local ischemia of the prolapsed tissue
  • Increased exposure to germs with bacterial translocation
  • Mechanical ulceration due to retained faecolith (stercoral trauma)
  • Microperforations of a diverticular tip covered only by serosa
  • Changes in connective tissue, enteric musculature, enteric nervous system and intestinal motility

Role of age and genetics: According to a twin study, the influence of genetic factors in the development of diverticular disease is 40% compared to 60% for environmental factors. Some rare genetic syndromes are strongly predisposed to the development of colonic diverticula, such as Marfan's syndrome, Ehlers-Danlos syndrome, Williams-Beuren syndrome, Coffin-Lowry syndrome, polycystic kidney disease. In genetically predisposed people, colonic diverticula develop at a young age (Suster SM et al. 1984, Beighton PH et al. 1969).

Environmental factors influencing the risk of developing diverticulosis/ diverticular disease:

  • Dietary fibre/life style: Lack of dietary fibre in the diet of the population of Western industrialised nations as opposed to the diet of African or Asian peoples seems to be a relevant lifestyle-associated risk factor for the development of diverticulosis and diverticular disease. An increased risk for the development of diverticular disease still exists for:
  • red meat
  • Smoking
  • Overweight

Drugs:

  • Non-steroidal anti-inflammatory drugs (Tsuruoka N et al (2011), acetylsalicylic acid (ASA), paracetamol, corticosteroids and opioids increase the risk of developing diverticular disease. The risk of diverticular bleeding is 1.74-fold higher with regular consumption of NSAIDS alone, 1.70-fold higher for aspirin and 2.02-fold higher for the combination of NSAIDS and aspirin (Strate L et al. 2011). Furthermore:
  • Corticosteroids: The risk of diverticular perforation due to simultaneous intake of corticosteroids is 2.74 times higher.
  • Immunosuppressive therapy modalities: Various studies indicate a more severe course of diverticular disease in patients under immunosuppression (Hwang SS et al. 2010).
  • Calcium antagonists: The intake of calcium antagonists is recognised as an independent risk factor for diverticular hemorrhage (Jansen A et al. 2009).

Comorbidities as a risk factor for the occurrence of diverticular disease including diverticular hemorrhage:

  • Arterial hypertension
  • Hyperlipidemia
  • Hyperuricemia
  • Coronary heart disease
  • Allergic dispositions (from Rahden BH et al. 2012).

No influence on the risk of developing a diverticular disease including diverticular hemorrhage:

  • Coffee has no influence on the risk. In the HPFS cohort, no association was found between coffee consumption and the occurrence of diverticular disease.
  • Coxibe (COX-2 inhibitors) can be used without risk.
  • Calcium antagonists and statins rather have a protective effect.
  • Data for alcohol are inconsistent.

Positive factors that can reduce the risk of developing diverticular disease:

  • Dietary fiber
  • Nuts
  • Grains
  • Corn, popcorn
  • Physical activity

Clinical features
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Remark: The symptoms of the symptomatic uncomplicated diverticular disease overlap with irritable bowel syndrome (Jung HK et al. 2010)

Sigmoid diverticulitis: Spontaneous pain possibly tenesmus frequently in the left lower quadrant, defence tension, pain of relinquishment, inflammatory roll palpable, possibly fever "left appendicitis". Stool irregularities (opstipation/diarrhoea) Flatulence. Leukocytosis, CRP increased.

Coecum diverticulitis: pain in the right middle/lower abdomen. Diverticulitis affects C. ascendens or coecum). It is then often misdiagnosed as appendicitis. Rectal examination (sensitivity to pain, rarely blood); (Differential diagnosis: gynaecological causes - pelvic inflammation, ectopic pregnancy, pedunculated adnexal tumor). Caution: Hard abdomen, diffuse defensive tension and hemodynamic instability signal free perforation and generalized peritonitis.

Bleeding (in 5% of diverticular diseases)

Diagnostics
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Note: The suspected diagnosis of sigmoid diverticulitis is based on the patient's medical history, clinical findings, basic laboratory tests and urine status.

Medical history: Usually relatively unspecific symptoms; in case of an extensive differential diagnosis the medical history is usually not decisive for the primary diagnosis.

Physical examination:

  • Vital parameters (especially temperature, pulse, blood pressure)
  • Abdominal examination (pain often in the left lower quadrant, defensive tension, pain of release, inflammatory roll palpable).
  • Localization of symptoms: Diverticulitis may (more rarely) occur on the right side (C. ascendens or coecum) and is then often misdiagnosed as appendicitis. Rectal examination (sensitivity to pain, rarely blood); if necessary gynaecological examination (differential diagnosis of the gynaecological cause of the complaints. Hard abdomen, diffuse defensive tension and haemodynamic instability signal free perforation and generalised peritonitis)

Instrumental diagnostics:

  • Colonoscopy in acute diverticulitis: Colonoscopy has no significance for the diagnosis of acute diverticulitis (the inflammatory process takes place beyond the endoscopically assessable mucosa). Caution: danger of perforation!
  • Colonoscopy in case of uncharacteristic clinical picture or course: in this constellation a colonoscopy can be performed with probably slightly increased risk of perforation in acute diverticulitis, if covered perforation and abscessation is excluded in sectional imaging.
  • Colonoscopy with different indications: 4-6 weeks after a conservatively treated diverticulitis has healed or before an elective sigmoid resection, the indication for colonoscopy can be generously given: diseases with similar symptoms can be excluded e.g. enteritis regionallis (Crohn's disease), irritable bowel syndrome, adenomas or carcinomas.
  • For diverticular hemorrhage (type 4-CDD), early colonoscopy (< 24h) is the method of choice. 75-92 % of diverticular bleeding stops spontaneously! With delayed endoscopy, identification of the source of bleeding is often no longer possible!

Imaging
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Evidence of a diverticulitic change in sectional imaging (sonography, CT). CT is still the most accurate and safest method for the detection of diverticulitis or possible complications (stage classification).

MRI: There is only limited experience with MRI, both in studies and in practice. From the point of view of radiation hygiene, MRI can be an alternative to CT, especially for younger patients.

Laboratory
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Basic laboratory: Na, K, creatinine, GPT, LDH, lipase, lactate, blood count, CRP, BSG, PTT, INR, urine status, leukocytosis, CRP, if necessary BSG: detection of inflammatory activity, secondly differentiation from SUDD (type 3a CCD) or acute uncomplicated diverticulitis type 1a.

Acute uncomplicated diverticulitis (type 1 CCD) rarely involves leukocytosis, CRP and FHR are regularly elevated. In contrast, all three parameters are elevated in acute complicated diverticulitis and to a greater extent than in type 1 CCD.

CRP < 50 mg/l: perforation unlikely; CRP > 200 mg/l: strong indicator of perforation. Calprotectin in faeces is unsuitable for acute diagnosis, the valence in the differential diagnosis of SUDD (type 3a CDD) and irritable bowel syndrome is not sufficiently clarified.

Histology
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Histopathologically, prominent mucosal protrusions with disturbed crypt architecture and cryptitis, ulcerations with lymphocytic and neutrophilic infiltrates, fibrosis of the lamina propria mucosae as well as hyperplasia and fragmentation of the lamina muscularis mucosae are evident. In the long term, recurrent inflammatory episodes can lead to local fibrosis, wall thickening and stenosis, possibly with the formation of a so-called diverticulitic tumor (Goldstein NS et al. (1997). In some cases, overlaps with histopathological findings can be observed, which are typically present in chronic inflammatory bowel diseases (e.g. granulomas, transmural inflammatory infiltrates, lymphoid aggregates, panethcell metaplasia).

Diagnosis
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Classification of the test results:

First episode of diverticular disease (without acute abdomen): in addition to the clinical symptoms, signs of inflammation (e.g. CRP) may indicate the type of diverticulitis. Sonography and if necessary CT-abdomen allow an exact classification. Colonoscopy at intervals.

Chronically recurrent diverticulitis: in this constellation (with a known history), sonography and, if necessary, CT-abdomen and colonoscopy make it possible to confirm the diagnosis. Clarification of stenoses or fistulas.

Acute abdomen: Patients are treated surgically after appropriate imaging (sonography, X-ray abdomen overview - free air in the case of perforations, mirror in the case of obstructions, CT abdomen). Patients without an acute abdomen must be carefully classified and treated according to the valid classification criteria.

Differential diagnosis
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Common inflammatory bowel diseases

Rare inflammatory disease patterns

  • appendicitis epiploica
  • Meckel's diverticulitis

Obstructive clinical pictures

  • Constipation
  • Incarcerated hernia
  • Invagination
  • Volvulus

Urogenital causes

  • Pyelonephritis
  • Kidney stone
  • Ureteral stone
  • Cystitis
  • Prostatitis
  • seminal vesiculitis

For moderate pain

  • Adnexitis
  • Torsion of the ovary
  • Hemorrhagic or ruptured ovarian cyst
  • Varicosis pelvis (pelvic congestion syndrome)
  • Uterine myomas
  • Endometriosis
  • Ovarian tumor
  • Ectopes or tubal pregnancy
  • Miscarriage

Vascular causes

  • Aortitis/Vasculitis
  • Vascular dissection/aneurysm

Other causes

  • Abdominal wall abscess
  • Abdominal wall hematoma
  • Psoas abscess
  • retroperitoneal bleeding

Therapy
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The therapeutic procedure depends essentially on the exact classification of the disease types. The classification according to CDD provides the framework for the indicated therapeutic measures.

The majority of patients with uncomplicated diverticulitis can be treated on an outpatient basis without antibiotics (type 1a, b): low-fibre diet, small intestine absorbable low-molecular formula diet. Patients with complicated diverticulitis (type 2a, b) are treated on an inpatient basis with antibiotics. Abscesses > 3-4 cm require the insertion of a drainage. Patients with a free perforation (type 2c) require emergency surgical therapy.

Prerequisites for outpatient therapy (S 2k guideline): absence of fever, leukocytosis, immune system tension, stool retention, CRP only slightly elevated, ensuring adequate compliance, oral food and fluid intake, close medical supervision, presence of uncomplicated diverticulitis (CDD type 1a, b). Diet/Nutrition: Nutritional recommendations in acute phases of the disease can hardly be based on data. In many cases, a diet with clear fluids for 2-3 days with a transition to a low-fibre diet if the pain improves is recommended for the types 1a, b and 2a. At least for the uncomplicated diverticulitis, an ad libitum diet does not seem to have any disadvantages.

In-patients: Patients with a severe form of the disease should be on a diet until stabilisation. After the diverticulitis has healed, a diet rich in fibre and poor in red meat is recommended.

Pain therapy: First choice preparations are paracetamol and spasmolytics like Buscopan or Dicyclomine. For refractory pain, opioids are used despite the association with perforations.

Pharmacotherapy: Antibiotics: Patients with uncomplicated diverticulitis (type 1 CDD) can be treated without antibiotics in over 90% of cases in the absence of fever > 38.5 °C, signs of bacteremia or septicaemia, severe comorbidities, especially immunosuppression. Antibiotic therapy neither accelerates convalescence nor helps to avoid complications. The choice of preparations requires an individual decision, which takes into account the patient's general condition and risk profile as well as the local resistance situation. Rifaximin and mesalazine are preferred.

Typical antibiotic regimens for the treatment of acute diverticulitis of varying severity. The doses apply to patients with normal kidney and liver function.

  • Outpatient mono-therapy scheme over 4-7 days:
    • Co-Amoxicillin (clavulanic acid / amoxicillin) 625mg (500/125 mg) 3 × 1/day p. o.
    • Alternatively: Co-amoxicillin 1000 (875/125 mg) 2 × 1/d p. o. Moxifloxacin 400 mg 1 × 1/d p. o.
    • Outpatient combination therapy scheme over 4-7 days:
    • Ciprofloxacin 500 mg 2 × 1/day p. o. plus metronidazole 500 mg 3 × 1/day p. o.
    • Alternatively: Levofloxacin 750 mg 1 × 1/day p. o. plus metronidazole 500 mg 3 × 1/day p. o.
    • Alternatively: Trimethoprim/Sulfamethoxazole 160/800 mg 2 × 1/ day plus Metronidazole 500 mg 3 × 1/day p. o.
  • Stationary monotherapy regimen: mild to moderate complicated diverticulitis for 4-7 days:

Ertapenem 1 g 1 × / day i. v.

Alternative: Moxifloxacin 400 mg 1 × 1/ day i. v.

  • Stationary combination therapy scheme: mild to moderate complicated diverticulitis, peritonitis for 4-7 days

Cefuroxime 1,5 g 3 × /d i.v. plus metronidazole 500 mg 2-3 ×/the i.v.

Alternatively: Ceftriaxone 2 g 1 × /d i.v. plus metronidazole 500 mg 2-3 ×/the i.v.

Alternative: Ciprofloxacin 400 mg 2 × 1/d i.v. plus metronidazole 500 mg 2-3 ×/the i.v.

  • Stationary monotherapy: severe complicated diverticulitis, peritonitis for 4-7 days:

imipenem-cilastatin 500 mg 4 × 1/d IV or imipenem-cilastatin 1 g 3 × 1/d IV

Alternatively: Meropenem 1 g 3 × 1/d i. v.

Alternatively: piperacillin-tazobactam 4,5 g 3 × 1/d i.v.

  • Stationary combination therapy: severe complicated diverticulitis, peritonitis for 4-7 days:

Cefepim 2 g 3 × 1/d i.v. plus metronidazole 500 mg 2-3 × /d i.v.

Alternative: Ceftazidim 2 g 3 × 1/d IV plus metronidazole 500 mg 2-3 × /d IV

Alternatively, ciprofloxacin 400 mg 2 × 1/d IV plus metronidazole 500 mg 2-3 × /d IV

Alternative: Levofloxacin 500 mg 2 × 1/d IV plus metronidazole 500 mg 2-3 × /d IV

Interventional therapy: endovascular, superselective embolization treatment in acute arterial diverticular hemorrhages (type 4 CDD); sonographically or CT-guided drainage of abscesses > 3-4 cm

Progression/forecast
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Prognosis decisively depends on the AZ and the stage of the disease.

Risk of a new episode after a first episode after 10 years: approx. 20 %, after a second episode after 10 years: approx. 55 %, after a third episode after 3 years: approx. 40 %. Risk of abscess or perforation shortly after an episode of uncomplicated diverticulitis: 2%. 40% of patients with an episode of uncomplicated diverticulitis report mild to moderate abdominal pain 1 year after the episode.

Themortality rate of acute complicated diverticulitis (type II) is between 5%-15%.

The lethality is significantly higher in patients under immunosuppressive therapy.

Emergency surgical intervention therapy is required in 2-62% of patients. The earlier and more severe the first diverticulitis attack, the more likely it is that surgery will be required.

Literature
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  1. Beighton PH et al (1969) Gastrointestinal complications of the Ehlers-Danlos syndrome. Good 1969; 10: 1004-1008
  2. Böhm S et al (2017) Diverticulitis. Domain of conservative or drug therapy? Internist 2017; 58: 745-752
  3. Böhm SK et al (2017) Life style and other risk factors for diverticulitis. Minerva Gastroenterol Dietol 63: 110-118
  4. Böhm SK (2012) . Diagnosis and classification of diverticular disease. Visceral medicine 28: 171-181
  5. Böhm SK (2020) Diverticular disease. In: Riemann JF (Hrsg) Reference Gastroenterology Thieme Verlag p. 535
  6. Cuomo R et al (2014) Italian consensus conference for colonic diverticulosis and diverticular disease. UEG Journal 2: 413-442
  7. Goldstein NS et al (1997) Histology of the mucosa in sigmoid colon specimens with diverticular disease: observations for the interpretation of sigmoid colonoscopic biopsy specimens. At J Clin Pathol 107: 438-444
  8. Hwang SS et al (2010) Diverticulitis in transplant patients and patients on chronic corticosteroid therapy: a systematic review. Diseases of the colon and rectum 53: 1699-1707
  9. Jansen A et al (2009) Risk factors for colonic diverticular bleeding: a Westernized community based hospital study. World journal of gastroenterology: WJG 15: 457-461
  10. Jung HK et al (2010) Diarrhea-predominant irritable bowel syndrome is associated with diverticular disease: a population-based study. The American journal of gastroenterology 105: 652-661208.
  11. Leifeld L, Germer CT, Böhm S et al. S 2k guideline diverticular disease/ diverticulitis. Z Gastroenterol 201; 52: 663-710
  12. Lembcke B. Ultrasonography in acute diverticulitis - credit where credit is due. Z Gastroenterol 2016; 54: 47-57
  13. Pustelnik D, Elsholtz FHJ, Bojarski C et al. The CDD system in com- putertomographic diagnostics of diverticular disease. Progress Röntgenstr 2017; 189: 740-747
  14. Schreyer AG, Layer G. S 2k Guideline Diverticular Disease and Diverticulitis: Diagnostics, Classification and Therapy for Radiology. Progress Röntgenstr 2015; 187: 676-684
  15. Stollman N et al (2004) Diverticular disease of the colon. Lancet 363: 631-639 14th Simpson J et al (2002) Pathogenesis of colonic diverticula. The British journal of surgery 89: 546-554
  16. Strate LL et al (2011) Use of aspirin or nonsteroidal anti-inflammatory drugs increases risk for diverticulitis and diverticular bleeding. Gastroenterology 140: 1427-1433
  17. Suster SM et al (1984) Diverticulosis coli in association with Marfan's syndrome. Arch Internal Med 144: 203.
  18. Swanson SM, Strate LL. Acute colonic diverticulitis. Ann Intern Med 2018; 168: ITC 65-ITC 80
  19. Tsuruoka N et al (2011) NSAIDs are a significant risk factor for colonic diverticular hemorrhage in elder patients: evaluation by a case-control study. Journal of gastroenterology and hepatology 26: 1047-1052
  20. by Rahden BH et al (2012) Allergic predisposition, histamine and histamine receptor expression (H1R, H2R) are associated with complicated courses of sigmoid diverticulitis. Journal of gastrointestinal surgery: official journal of the Society for Surgery of the Alimentary Tract 16: 173-182

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Last updated on: 29.10.2020