Diverticular Disease

Meet the patient

A 68-year-old man arrives with three days of constant left lower quadrant pain, a low-grade fever, and on examination a tender, palpable mass in the left iliac fossa. He has known diverticulosis, found incidentally at a screening colonoscopy two years ago. He is systemically well, his observations are stable, and a CT with IV contrast is booked.[2]

Two questions frame everything that follows for this man, exactly as they frame every diverticular-disease stem at 3am: is the process contained, or has it perforated? (the CT and the abdomen answer that between them), and is this really diverticulitis — or is a cancer hiding behind it? (only a colonoscopy, six to eight weeks after the acute episode settles, can settle that). Hold those two questions and the whole topic slots into place.[1][2]

Sort the three words first — diverticulum, diverticulosis, diverticulitis

Examiners fail candidates for conflating three look-alike words — sort them before you touch management, every single time. A diverticulum (plural: diverticula) is a localised outpouching of the wall of a hollow viscus. Etymology for viva gold: the word is from the Latin diverticare, "to turn aside" — the bowel wall turns aside, and a pocket forms; and Laplace's law, which explains why, is named for the French physicist Pierre-Simon Laplace.[1]

The true-versus-false distinction is the single most tested fact in the topic, so learn it as a face-off:[1]

[1]

Discriminator beneath the face-off: muscularis in the wall means true (think Meckel's); muscularis absent means false (think the sigmoid at 70).[1]

Now sort the three clinical terms — the confusion examiners exploit:[1][2]

• Diverticulosis — the mere anatomical presence of diverticula, almost always asymptomatic. Incidental diverticula at colonoscopy need only reassurance.
• Diverticulitis — inflammation of one or more diverticula, usually from microperforation.
• Diverticular disease — the umbrella clinical term for the whole spectrum, including SUDD and complicated disease.[1][2]

The clinical stakes are bimodal — most patients never know they have it, but the minority who perforate face mortality up to 30%. The disease is best read as a spectrum whose entire challenge is to find, at each end, the patient who needs urgent intervention rather than reassurance.[3]

Why the sigmoid? Laplace, the vasa recta, and the pulsion event

Diverticula form where anatomy meets pressure — and in the sigmoid, both conspire. The colonic wall has four layers: mucosa, submucosa, muscularis propria (inner circular, outer longitudinal), and serosa. The outer longitudinal muscle is not continuous but gathered into three flat bands, the taeniae coli; between them the circular muscle is exposed and traversed by the vasa recta, the straight end-arteries that supply the wall. Those penetrating vessels are the inherent weak points — and it is precisely there that diverticula herniate.[1]

[1]

Formation is a pulsion event driven by raised intraluminal pressure, and the model every candidate must reproduce combines Laplace's law with segmentation. By Laplace's law (T = P × r), wall tension tracks radius and pressure; the narrowest segment of colon sustains the greatest wall tension, which is why the sigmoid — the narrowest colonic segment — bears the brunt. Layered on this is segmentation: the colon contracts in discrete rings that compartmentalise the lumen into closed chambers, each behaving as a small-bore tube to which Laplace's law applies, generating pressures that can exceed 90 mmHg locally.[1]

[1]

Three structural changes accompany and promote the disease, and a registrar should be able to name all three. Elastosis — increased elastin in the taeniae and circular muscle — shortens and thickens the bowel (the characteristic palpable, cord-like sigmoid at laparotomy) and reduces wall compliance, so the same contractile force produces a higher pressure. Myochosis is thickening of the circular and longitudinal muscle even without overt inflammation. And the diverticular wall itself, lacking a muscular layer, is structurally fragile: a faecolith in its neck can erode through it, and a vasa recta draped over the fundus can be eroded into the massive arterial-type bleed that defines diverticular haemorrhage.[1]

This anatomy also explains why inflammation and bleeding are mechanistically separate — an examiner favourite. Diverticulitis arises from microperforation of the fundus; diverticular haemorrhage arises from erosion of the vasa recta at the neck or fundus. Most patients who bleed have never had diverticulitis, and most patients with recurrent diverticulitis never bleed. Examiners deliberately test that distinction.[1][3]

Who gets it, and why fibre is the lever

Diverticular disease is a disease of affluent, low-fibre societies and of age. It was uncommon before the twentieth century, and its rise tracks the industrial refinement of carbohydrate and the loss of dietary fibre in the West. Age is the strongest risk factor: rare before 40 (under 5%), it affects roughly 50% of people older than 60 and 65% of those older than 80, with essentially equal prevalence in men and women (women present slightly later).[1][2]

[1]

Fibre is the central environmental lever. Low intake reduces stool bulk, increases segmentation, raises intraluminal pressure, and shortens the period over which the pulsion mechanism operates. The classical fibre hypothesis is supported by the near-absence of the disease in rural African and Asian populations on high-fibre diets and its appearance within a generation of migration to a Western diet; the protective effect is strongest for fruit, vegetable, and cereal fibre (particularly cellulose).[1]

[1]

The clinical course is a predictable stepped progression examiners expect you to articulate out loud. Of 100 patients with diverticulosis, 75 to 80 remain asymptomatic for life; 15 to 25 develop SUDD or a single episode of uncomplicated diverticulitis; of those who develop diverticulitis, roughly 20% develop a complication (abscess, fistula, perforation, stricture); and only 3 to 5% ever suffer a major diverticular bleed. Recurrence after a first episode of diverticulitis runs 20 to 30%, and recurrent episodes are increasingly likely to be complicated.[1][6]

From a faecolith to peritonitis — the inflammatory cascade

The diverticula form by pulsion; the clinical disease begins when one of them blocks and bursts. A faecolith impacts in the narrow neck, the obstructed diverticulum distends, its thin wall is rendered ischaemic by the distension and by the chemical insult of retained stool, and the wall gives way. The resulting perforation is initially microscopic and is contained by pericolic fat, mesocolon, and omentum as a pericolic abscess or phlegmon — the substrate of uncomplicated to moderately complicated diverticulitis. If containment fails, the perforation extends to a distant abscess, then to purulent, then to faecal peritonitis.[1]

[1]

Bacteriology dictates the antibiotic choice, so name the organisms. The colon harbours a dense mixed flora, and the organisms cultured from a diverticular abscess or peritoneal washings reflect it. The dominant aerobes are Escherichia coli, Klebsiella, Proteus, and Enterococcus; the dominant anaerobes are Bacteroides fragilis, Clostridium, Peptostreptococcus, and Fusobacterium. Anaerobes outnumber aerobes 1000 to 1, which is why empirical therapy must cover both Gram-negative aerobes and anaerobes, and why amoxicillin alone is inadequate. In regions with high ESBL rates, empirical piperacillin-tazobactam or a carbapenem may be needed, then de-escalated on culture.[1]

The microbiome and SUDD. Contemporary research implicates a low-grade chronic inflammation and an altered gut microbiota in SUDD — the patient with recurrent left lower quadrant pain, bloating, and altered bowel habit but no acute inflammation on imaging. Biopsies show microscopic lymphocytosis and mucosal neutrophilia, with visceral hypersensitivity resembling irritable bowel syndrome. This is the rationale for the still-debated use of mesalazine, rifaximin, and probiotics in SUDD, and it explains why SUDD and IBS are so easily confused clinically.[1][6]

Hinchey, WSES, and the clinical spectrum — three maps for one disease

Three complementary maps describe one disease, and each drives a different decision. The clinical spectrum sorts severity; the Hinchey classification (1978) grades the anatomical extent of peritoneal contamination in perforated disease; and the WSES 2015 severity grade (Sartelli et al, 2016) is CT-based and has largely superseded the older Ambrosetti grading in emergency practice.[4]

The clinical spectrum

The spectrum, from silent to lethal:[1]

The Hinchey classification (1978) — for perforated diverticulitis

Hinchey is the bedrock of surgical communication in perforated diverticulitis — it grades the anatomical extent of peritoneal contamination and maps directly onto the operation. The modified Hinchey classification (Wasvary or Kaiser) subdivides stages I and II to fold in CT findings (pericolic air versus abscess, small versus large abscess), but the four-stage original remains the framework examiners expect you to reproduce.[5]

[5]

The WSES 2015 severity grade — CT-based, decision-driving

The WSES guidelines (Sartelli 2016) introduce a CT-driven severity grade that links the imaging appearance directly to a management recommendation, and it is now the dominant system in European emergency-surgical practice because it is objective and reproducible.[4]

[4]

WSES and Hinchey are related but not identical: WSES grades 0 to 2 correspond broadly to the non-perforated or contained spectrum (uncomplicated to Hinchey I to II), while WSES grades 3 and 4 map onto Hinchey III and IV. The advantage of WSES is that it is decided at the CT scanner, before theatre, and it tells the surgeon whether percutaneous drainage (grades 1b to 2) or surgery (grades 3 to 4) is required.[4]

The bedside picture — LLQ pain, and when it stops being localised

The presentation is dominated by left lower quadrant pain because the sigmoid is the most common site — the history and a deliberate abdominal exam will identify most cases before imaging.[2]

Acute uncomplicated diverticulitis

The classic presentation every candidate must reproduce:[2][3]

Complicated diverticular disease

The presentation pivots the moment a complication develops — the cardinal sign is the loss of the localised picture. Peritonitis becomes generalised, fever becomes septic, or a new symptom (pneumaturia, massive bleeding, obstruction) declares the complication.[1]

[1]

Diverticular bleeding — the distinct clinical entity

Diverticular bleeding is mechanistically separate from diverticulitis and is the single commonest cause of major lower gastrointestinal bleeding. The bleed arises when a vasa recta, draped over the fundus of a diverticulum, is eroded at the point where it penetrates the diverticular neck. The result is an arterial-type bleed: sudden, painless, and massive, producing maroon or bright red haematochezia (unlike the slow, occult bleeding of a caecal cancer). Around 75 to 80% of diverticular bleeds stop spontaneously, but 20 to 25% recur, and a minority need urgent endoscopic, radiological, or surgical haemostasis. Right-sided diverticula bleed disproportionately relative to their frequency.[1][3]

The differential — and the cancer you must not call a stricture

The differential of left lower quadrant pain with fever is broad; the discriminator is persistent localised tenderness with systemic inflammation plus a CT showing bowel-wall thickening with fat stranding.[3]

[3]

The classic trap: attributing a diverticular-looking stricture or mass to diverticulitis without excluding cancer. The two can coexist and look identical on CT, which is why every patient recovering from a first episode of diverticulitis must undergo colonoscopy 6 to 8 weeks after the acute inflammation has settled. A stricture labelled "diverticular" that turns out to be a cancer six months later is the preventable disaster of this topic.[3]

CT first, scope later — the investigation order that prevents perforation

Investigation serves three purposes — confirm diverticulitis, grade severity (Hinchey or WSES), and exclude mimics, principally colorectal cancer — and the order follows the clinical question.[2][4]

CT findings and severity grading

The CT findings of acute diverticulitis are bowel-wall thickening (over 4 to 5 mm), pericolic fat stranding, diverticula, and — with increasing severity — pericolic fluid, abscess, free gas, or free fluid; the distribution of gas and fluid determines the WSES grade. A retrospective review of the SCANDIV trial data confirmed that preoperative CT accurately predicts the Hinchey or WSES grade in most patients, although it tends to under-stage faecal peritonitis — which is why a normal-looking CT never over-rules a rigid, septic abdomen.[4][11]

Severity drives everything — from reassurance to emergency Hartmann's

Management is entirely severity-driven and follows the Hinchey or WSES grade; the principle is to reserve surgery for those who need it — drain the pus, resect the faeces, and resect electively only a carefully selected minority.[2][4]

Asymptomatic diverticulosis

The vast majority need only reassurance. Counsel that 70 to 80% will never develop symptoms; advise a high-fibre diet (25 to 30 g per day) with whole grains, fruit, vegetables, and legumes, adequate fluid (2 L per day), regular exercise, and avoidance of unnecessary NSAIDs. The historical instruction to avoid nuts, seeds, and popcorn is obsolete — large cohort data show no increased risk and possibly a protective effect. There is no role for routine follow-up colonoscopy for diverticulosis found incidentally, other than participation in population screening.[1][6]

Acute uncomplicated diverticulitis (WSES 0 to 1a)

Most patients can be managed as outpatients with oral antibiotics covering Gram-negatives and anaerobes, a brief period of clear fluids, and paracetamol-based analgesia, with a clear safety-net to return if pain or fever worsen.[2][6]

• Antibiotics: amoxicillin-clavulanate 625 mg PO TDS for 7 to 10 days (first line); alternatives are ciprofloxacin 500 mg PO BD + metronidazole 400 mg PO TDS, or co-trimoxazole 960 mg PO BD + metronidazole 400 mg PO TDS, or moxifloxacin 400 mg PO OD (monotherapy).
• Diet: clear fluids for 24 to 48 hours, advancing to a low-residue diet as symptoms settle.
• Analgesia: paracetamol (avoid NSAIDs — they increase perforation and bleeding risk; avoid opioids — they cause constipation and may precipitate pseudo-obstruction).
• Admit if the patient is systemically unwell, immunocompromised, unable to tolerate oral intake, elderly with comorbidity, or if there are high-risk features on CT (WSES 1b or above).[1]

The 3 to 4 cm threshold that turns antibiotics into drainage

An abscess changes management: admit, make the patient nil by mouth, give IV fluids and IV antibiotics, and decide on drainage.[4][5]

[4]

Consultant confession: the 3 to 4 cm threshold is softer than it reads. A 3.5 cm abscess in a septic 80-year-old gets drained today; a 4.5 cm abscess in a stable, improving patient may drain tomorrow. The number is the guide; the patient, the trend in CRP, and the fever curve make the decision. Treat the patient, not the calipers.[5]

Hinchey IV — the one that gets a Hartmann's

Generalised peritonitis with free gas is a surgical emergency. Resuscitate aggressively — IV fluids, oxygen, IV antibiotics covering Gram-negatives and anaerobes, urinary catheter, central access if shocked — then operate. The operation chosen depends on the grade, the patient's physiology, and the surgeon's expertise.[4][5]

[4]

Hartmann's procedure — the operation Hinchey IV buys you

The Hartmann's procedure (resection with end colostomy and a closed rectal stump) is the operation examiners most often ask you to describe for perforated sigmoid diverticulitis — master the steps in sequence.[5]

Indications. Hinchey IV (faecal peritonitis); Hinchey III in an unstable, comorbid, or heavily contaminated patient; failed conservative management with perforation; perforation in a frail patient unfit for the physiological insult of an anastomosis.[4]

[5]

Hartmann's reversal (3 to 6 months later). Only 30 to 50% of patients ever undergo reversal — many are too old or comorbid, some decline, and some develop recurrence or other disease in the interval.[5]

• Pre-operative work-up: barium enema or flexible sigmoidoscopy to assess the rectal stump length and exclude pathology; assess fitness (cardiopulmonary); counsel that reversal is a major operation with an anastomotic leak rate of 5 to 10%.
• Technique: open or, increasingly, laparoscopic; the colo-rectal anastomosis is stapled (double-staple) or hand-sewn; a temporary defunctioning loop ileostomy is fashioned if there is concern about anastomotic integrity.
• Pitfalls: the rectal stump can be hard to find (dense pelvic adhesions); the left ureter is at risk during mobilisation; pelvic nerve damage (sexual or urinary dysfunction) is a recognised risk.[1]

Consultant confession: I counsel every Hartmann's patient at the outset that reversal may never happen. Half to two-thirds never come back for it, and very often that is the right call — the reversal is a bigger operation than the index surgery, and a stoma that works is better than an anastomosis that leaks.[5]

Laparoscopic lavage — DILALA, LOLA, SCANDIV, and why it is not routine

Laparoscopic peritoneal lavage (without resection) for Hinchey III purulent peritonitis was proposed as a less invasive alternative to resection; three landmark trials have since pulled practice back from routine lavage. The premise was that the source has often sealed by the time of surgery, so washing out the pus and placing drains may suffice. The combined message of the trials is that lavage is feasible but carries a higher reintervention price than resection.[7][8][9][10]

[7] [8] [9]

The Cirocchi meta-analysis (Tech Coloproctol 2017) pooled these data and concluded that laparoscopic lavage is associated with a higher rate of reoperation and reintervention than resection, without a clear benefit in mortality or stoma-free survival.[10]

Primary anastomosis vs Hartmann's — the DIVA verdict

The old dogma was that emergency perforated diverticulitis mandates a stoma; the DIVA trial has overturned that for fit patients with Hinchey III disease. Primary resection with anastomosis (with or without a defunctioning loop ileostomy) achieves a higher rate of stoma-free survival at 12 months, with comparable mortality and morbidity to Hartmann's. The trade-off is the risk of anastomotic leak (5 to 10%), mitigated by a defunctioning ileostomy. The decision is individualised: Hartmann's for the unstable, comorbid, or faecally contaminated patient; primary anastomosis ± ileostomy for the fit, stable patient with purulent peritonitis.[12]

Fistulae — the chronic complication that needs elective resection

A fistula is a chronic complication arising when a peridiverticular abscess erodes into an adjacent organ, and it almost always needs elective surgical resection — because the source (the diseased sigmoid) persists and conservative management rarely closes a diverticular fistula.[1][3]

Colovesical fistula is the commonest diverticular fistula. The triad is pneumaturia, faecaluria, and recurrent polymicrobial UTI (classically with mixed enterococci and anaerobes resistant to single-agent antibiotics). CT (air and contrast in the bladder, bladder wall thickening adjacent to the sigmoid) and CT cystogram (contrast passing into the colon) confirm the diagnosis; cystoscopy shows nonspecific inflammation around the fistula but rarely the tract itself. The Cuellar–Camarasa modification of the Hinchey staging is sometimes invoked here. Management is elective one-stage sigmoid resection with primary colorectal anastomosis; the bladder defect is usually small and heals with catheter drainage for 10 to 14 days, so a formal bladder repair is rarely needed.[1]

Colovaginal fistula presents with transvaginal passage of gas or faeces and recurrent vaginitis, often in a woman who has had a hysterectomy (the vaginal vault is the weak point). Management is sigmoid resection with primary anastomosis and repair or omental interposition over the vaginal defect.[1]

Colocutaneous fistula typically follows percutaneous drainage of an abscess or a surgical anastomotic leak. Many close spontaneously once distal obstruction is excluded and nutrition is optimised; persistent fistulae require resection.[1]

Diverticular bleeding — resuscitate, localise, then treat

Diverticular bleeding is an emergency of resuscitation and localisation, not of inflammation — and the order of the algorithm matters.[3]

[1]

Two principles dominate. First, diverticular bleed is arterial and massive but usually self-limiting — do not rush unstable patients to theatre before an attempt at localisation. Second, localise before you resect: a blind segmental colectomy for unlocalised bleeding has a high rebleed rate because diverticula are pan-colonic. Right-sided diverticula bleed disproportionately, so a presumed diverticular bleed localised to the right colon may warrant a right hemicolectomy.[1]

Elective resection — individualised, never a fixed count

The question of when to offer elective sigmoid resection after diverticulitis has been one of the most revised areas in colorectal surgery — and examiners test the current, not the historical, view.[6]

[6]

After recovery from a complicated episode (especially perforation managed non-operatively or by drainage), an elective laparoscopic sigmoid resection with primary anastomosis is often advised, because recurrence and the risk of a future emergency are higher. The resection must remove the entire thickened sigmoid down to the proximal rectum; leaving diverticular bowel behind increases recurrence. The recurrence rate after a properly performed elective sigmoid resection is 5 to 10%.[5][6]

The antibiotic doses — oral and IV, byte for byte

Outpatient (uncomplicated) — 7 to 10 days oral

• Amoxicillin-clavulanate 625 mg PO TDS (covers Gram-negatives and anaerobes — first line).
• Alternative: ciprofloxacin 500 mg PO BD + metronidazole 400 mg PO TDS.
• Alternative: co-trimoxazole 960 mg PO BD + metronidazole 400 mg PO TDS.
• Alternative (monotherapy): moxifloxacin 400 mg PO OD.
• Adjunctive: clear fluids for 24 to 48 hours, then low-residue diet; paracetamol for analgesia (avoid NSAIDs, avoid opioids); safety-net advice.[1]

Inpatient (complicated, Hinchey I to IV) — IV, then step down

• Co-amoxiclav 1.2 g IV TDS + metronidazole 500 mg IV TDS.
• Alternative: cefuroxime 1.5 g IV TDS + metronidazole 500 mg IV TDS.
• Alternative (monotherapy, broad): piperacillin-tazobactam 4.5 g IV TDS to QDS.
• Alternative: ciprofloxacin 400 mg IV BD + metronidazole 500 mg IV TDS.
• Severe sepsis / faecal peritonitis / ESBL risk: meropenem 1 g IV TDS (de-escalate on culture).
• Duration: 7 to 14 days IV, step down to oral when the patient is afebrile, the WCC/CRP are falling, and pain is resolving; total course typically 10 to 14 days.[1]

The principle is empirical cover of Gram-negative aerobes and anaerobes, narrowed once cultures are available, with attention to local resistance (ESBL) and to the patient's allergies and renal function.[4]

Special populations — the young, the old, the immunosuppressed, the pregnant

• Young patients (under 50). Historically thought to follow a more aggressive course, justifying early elective surgery. Contemporary data do not support age alone as an indication; young patients are managed like any other, with surgery reserved for recurrent complicated disease or persistent symptoms.[6]
• The elderly. More likely to present atypically (confusion, minimal pain, near-normal WCC) and to bleed (diverticular haemorrhage peaks after 70). Higher operative mortality for emergency surgery; consider primary anastomosis cautiously, and favour Hartmann's or damage-control in the very frail.[3]
• The immunocompromised (transplant, chemotherapy, chronic steroids, HIV). Present later, with blunted signs; higher rates of perforation and sepsis; lower threshold to image and to operate; elective resection considered after a single complicated episode.[3]
• Pregnant women. Right-sided pain can be confusing; image with MRI or limited CT after the first trimester if essential; manage surgically with a colorectal and obstetric team, with a low threshold for early intervention to protect mother and fetus.[1]
• Patients on anticoagulants or NSAIDs. Higher bleeding risk; reversible risk factors addressed during any bleeding episode; NSAIDs avoided long-term after diverticulitis.[1]

Complications — of the disease, and of the surgery

Complications of the disease include abscess, perforation (purulent or faecal peritonitis), fistula (colovesical, colovaginal, colocutaneous, coloenteric), stricture with large-bowel obstruction, and diverticular haemorrhage; distant complications include portal pyaemia and liver abscess, and sepsis with multi-organ failure.[1]

Complications of surgery (Hartmann's, primary anastomosis, elective resection) include anastomotic leak (5 to 10% for colo-rectal anastomosis, less for elective), pelvic or abdominal collection, wound infection (higher after faecal peritonitis), incisional hernia, stoma complications (necrosis, retraction, parastomal hernia, skin excoriation), left ureteric injury during sigmoid mobilisation, pelvic nerve damage (urinary and sexual dysfunction), and the morbidity and mortality of a Hartmann's reversal that may never occur. The failure to reverse a Hartmann's (50 to 70% of patients) is itself a recognised long-term complication, and is a key argument for primary anastomosis in fit patients.[5][12]

Prognosis and follow-up — and the colonoscopy no one must forget

Prognosis is excellent at the benign end and grave at the severe end. Uncomplicated diverticulitis treated medically resolves in over 90% with no sequelae; recurrence is 20 to 30% over 5 to 10 years. Complicated diverticulitis carries higher recurrence and the risk of future emergency surgery. Faecal peritonitis (Hinchey IV) has a mortality of up to 30%, driven by sepsis and comorbidity in the elderly. Diverticular bleeding has an inpatient mortality of 2 to 5% in modern series, mostly from comorbidity rather than exsanguination.[1][3]

Follow-up after a first episode of diverticulitis is built around two principles: a colonoscopy at 6 to 8 weeks to exclude colorectal cancer, and lifestyle counselling (high-fibre diet, hydration, exercise, avoidance of unnecessary NSAIDs and smoking) to reduce recurrence. Patients who have had a complicated episode are reviewed in an outpatient clinic with a view to elective resection in selected cases. After a Hartmann's procedure, a decision about reversal is made at 3 to 6 months once the patient has recovered and has been fully investigated.[3][6]

Exam pearls — HINCHEY, the twelve pearls, and the mantra

When an examiner asks about diverticular disease, they are testing one of six discriminations: true vs false diverticulum, diverticulosis vs diverticulitis vs diverticular disease, the Hinchey stage and its operation, when NOT to scope (acute episode), the bleeding algorithm (resuscitate-localise-treat), and when to offer elective surgery (individualised, not a fixed count). Frame every answer around these axes.[2][4]

[4]

High-yield MCQ topics. One: false diverticulum = mucosa + submucosa only (vs Meckel's = true). Two: Hinchey IV = faecal peritonitis = Hartmann's. Three: right-sided diverticular in Asians. Four: no colonoscopy or barium during an acute attack (perforation risk); wait 6 to 8 weeks. Five: nuts, seeds, and popcorn are NOT contraindicated (debunked myth). Six: colovesical fistula — pneumaturia, faecaluria, recurrent polymicrobial UTI. Seven: diverticular bleed — painless, massive, arterial-type; usually self-limiting. Eight: antibiotics — amoxicillin-clavulanate or cipro plus metronidazole (cover anaerobes). Nine: laparoscopic lavage is NOT routine; DILALA positive but LOLA and SCANDIV negative; contraindicated in Hinchey IV. Ten: elective surgery is individualised — young age alone is not an indication.[1][6]

The mantra, one more time: Resuscitate, grade by Hinchey, drain the pus, resect the faeces.[4][5]

Ward-round test — two stems, thirty seconds each

Self-test: a 72-year-old with sudden painless massive maroon haematochezia and haemodynamic compromise. Known diverticulosis. What is the correct sequence of management?

Resuscitate first — IV access, fluids, crossmatch 4 to 6 units, reverse anticoagulants, transfuse to Hb 70 to 90 g/L. Then localise: haemodynamically unstable → CT angiography followed by mesenteric angiography with superselective embolisation of the bleeding vasa recta; stable → urgent colonoscopy within 24 h after bowel purge (adrenaline, clips, band ligation, APC). Around 75 to 80% stop spontaneously. Reserve surgery (segmental resection, ideally after localisation) for uncontrolled or recurrent bleeding. Do not rush to theatre before an attempt at localisation, because diverticula are pan-colonic and a blind resection rebleeds.[1][3]

Self-test: a 60-year-old with three days of LLQ pain and fever has CT showing a 5 cm pelvic abscess (Hinchey II). What is the management?

Admit, nil by mouth, IV fluids, and IV antibiotics covering Gram-negatives and anaerobes (e.g., co-amoxiclav 1.2 g IV TDS + metronidazole 500 mg IV TDS). Add CT-guided percutaneous drainage because the abscess is ≥3 to 4 cm. After resolution (4 to 6 weeks), perform colonoscopy to exclude malignancy and consider elective laparoscopic sigmoid resection with primary anastomosis, because complicated diverticulitis has a higher recurrence and future-emergency risk. This pathway converts an emergency into a planned, lower-risk operation.[4][5]

Exam application bank (NEET-PG / INICET)

One-line answer

Diverticular disease encompasses a spectrum from asymptomatic diverticulosis (70 to 80% of cases) through symptomatic uncomplicated diverticular disease (SUDD) to acute diverticulitis and its life-threatening complications. False (pseudodiverticula) = mucosa and submucosa herniate through the muscularis propria at sites of vasa recta penetration. The sigmoid colon is affected in 90% of Western populations (right-sided in 15 to 75% of Asians). Over 50% of people older than 60 are affected. Hinchey classification (stages I to IV) and the WSES 2015 severity grade guide surgical management of perforated diverticulitis. Management ranges from dietary modification to emergency Hartmann's procedure for faecal peritonitis.[1]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose or route if drug therapy is standard. [1]

Stem 2 — Unstable or complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. [1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. [1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. [1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU, ICU, or theatre, and what follow-up is mandatory. [1]

Rapid viva checklist

1. Definition and classification.
2. Pathophysiology chain.
3. Bedside signs and criteria.
4. Score with exact components (if any).
5. Emergency bundle.
6. Definitive therapy with doses.
7. Complications of disease and of treatment.
8. Special populations.
9. Guideline or trial name if classic.
10. Three exam traps.[1]

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Diverticular Disease.[1]

References

1. [1]Tursi A, et al. Colonic diverticular disease Nat Rev Dis Primers, 2020.PMID 32218442
2. [2]Wilkins T, et al. Diagnosis and management of acute diverticulitis Am Fam Physician, 2013.PMID 23668524
3. [3]Swanson SM, et al. Acute Colonic Diverticulitis Ann Intern Med, 2018.PMID 29710265
4. [4]Sartelli M, et al. WSES Guidelines for the management of acute left sided colonic diverticulitis in the emergency setting World J Emerg Surg, 2016.PMID 27478494
5. [5]McDermott FD, et al. Minimally invasive and surgical management strategies tailored to the severity of acute diverticulitis Br J Surg, 2014.PMID 24258427
6. [6]Peery AF, et al. AGA Clinical Practice Update on Medical Management of Colonic Diverticulitis: Expert Review Gastroenterology, 2021.PMID 33279517
7. [7]Schultz JK, et al. One-year results of the SCANDIV randomized clinical trial of laparoscopic lavage versus primary resection for acute perforated diverticulitis Br J Surg, 2017.PMID 28631827
8. [8]Vennix S, et al. Laparoscopic peritoneal lavage or sigmoidectomy for perforated diverticulitis with purulent peritonitis: a multicentre, parallel-group, randomised, open-label trial Lancet, 2015.PMID 26209030
9. [9]Angenete E, Thornell A, Burcharth J, et al. 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, 2016.PMID 25489672
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