Diverticular Disease

Diverticular disease refers to the formation of abnormal mucosal outpouchings (diverticula) through the colonic wall, predominantly at sites of vascular penetration, encompassing a spectrum from asymptomatic diverticulosis to symptomatic diverticular disease and acute diverticulitis with potential complications such as perforation, abscess, or fistula formation.

1. Definition and Terminology

Let's start by getting the language right — this is a topic where imprecise terminology costs marks.

Core Definitions

Diverticulum (Latin: diverticulum = "a wayside shelter" or "turning aside") — a sac-like protrusion (outpouching) of a hollow viscus ^[1]^[2]^[3]
Diverticulosis (coli) — the presence of multiple diverticula, which may be symptomatic or asymptomatic ^[2]^[3]
Diverticular disease — clinically significant and symptomatic diverticulosis ^[2]^[3]. This umbrella term encompasses:
- Diverticulitis — inflammation of a diverticulum (caused by microperforation) ^[1]^[3]
  - Acute vs. Chronic
  - Uncomplicated vs. Complicated (abscess, fistula, bowel obstruction, perforation)
- Diverticular bleeding — painless massive PR bleeding due to rupture of vasa recta draped over the diverticular dome ^[2]^[3]
  - Typically occurs in the ABSENCE of diverticulitis (the bleeding and inflammation are separate pathological processes)
  - Self-limited in ~80% of patients
- Segmental Colitis Associated with Diverticula (SCAD) / Diverticular colitis — inflammation of the interdiverticular mucosa without involvement of diverticular orifices (resembles IBD histologically but is a distinct entity) ^[3]
- Symptomatic Uncomplicated Diverticular Disease (SUDD) — persistent abdominal pain attributed to diverticula without macroscopically overt colitis or diverticulitis; CT shows wall thickening without inflammatory changes ^[3]

Key Distinction for Exams

Students often confuse diverticulosis (anatomical finding, often incidental) with diverticular disease (symptomatic). Most people with diverticulosis (~80%) are asymptomatic and will never develop complications. Only ~20% become symptomatic ^[1]^[4].

True vs. False Diverticulum

Feature	True Diverticulum	False (Pseudo) Diverticulum
Layers involved	All layers of the intestinal wall (mucosa, submucosa, muscularis propria, serosa/adventitia)	Only mucosa and submucosa herniate through muscularis propria
Example	Right-sided colonic diverticula, Meckel's diverticulum	Left-sided colonic diverticula (the vast majority of "diverticular disease"), Zenker's diverticulum
Mechanism	Usually congenital	Usually acquired (pulsion type — pushed out by intraluminal pressure)

Right-sided diverticula are true diverticula (congenital); left-sided diverticula are false diverticula (acquired) ^[1]

Other Important Diverticula (for completeness)

Meckel's diverticulum — true diverticulum arising from incomplete obliteration of the vitelline (omphalomesenteric) duct on the antimesenteric surface of the mid-to-distal ileum. Remember the "Rule of 2s": 2% prevalence, 2 feet from ileocaecal valve, 2 inches long, 2 types of ectopic tissue (gastric and pancreatic), presents by age 2 ^[3]
Zenker's diverticulum — false diverticulum arising from Killian's triangle (area of weakness between the transverse fibres of the cricopharyngeus and the oblique fibres of the lower inferior constrictor muscle of the pharynx) ^[3]

2. Epidemiology

Diverticular disease is common in the Western population ^[1]^[4]:

Prevalence increases dramatically with age:
- Rare before age 30
- ~30% by age 60
- 60% in age > 70 ^[1]
- ~65% by age 80-85 ^[1]
Mean age of diagnosis of acute diverticulitis = 63 years ^[3]
Symptomatic in about 20% of those with diverticulosis ^[1]
Of those who develop diverticulitis, ~15-25% will develop complications

Regional Variation — This Is High Yield

Feature	Western	Asian (including Hong Kong)
Predominant site	Left-sided (sigmoid colon)	Still predominantly left-sided, BUT the proportion of right-sided diverticulosis (caecum/ascending colon) is significantly higher ^[1]^[3]^[4]
Type	False (acquired)	Right-sided = True (congenital); Left-sided = False (acquired)
Clinical pitfall	Classic LLQ pain	Caecal diverticulitis mimicking appendicitis — Role of CT scan to differentiate ^[1]

Hong Kong Context — Must Know

In Hong Kong and Asia, right-sided diverticular disease is much more prevalent than in the West. A young patient presenting with RLQ pain, fever, and leucocytosis may have caecal diverticulitis rather than appendicitis. CT abdomen is the key investigation to distinguish them ^[1]^[4].

3. Risk Factors

Understanding risk factors requires understanding the pathophysiology — it's all about wall weakness + increased intraluminal pressure.

Risk Factor	Mechanism
Age (rare before 30)	Progressive degeneration of colonic wall connective tissue; reduced elastin and collagen cross-linking → weaker wall
Low-fibre diet	Low residue → smaller, harder stools → colon must generate higher intraluminal pressures to propel contents → pulsion diverticula ^[1]^[3]
Obesity	Increases intra-abdominal pressure; adipose tissue produces pro-inflammatory cytokines → increases risk of both diverticulitis and diverticular bleeding ^[3]
Fat and red meat intake	Alters gut microbiome, promotes intestinal inflammation ^[3]
Decreased physical activity / sedentary lifestyle	Reduces colonic motility → increased transit time → harder stools → higher pressures ^[3]
Constipation	Increased intraluminal pressure directly ^[4]
Smoking	Impairs mucosal blood flow and tissue healing; alters gut motility
NSAIDs	Disrupt mucosal barrier (inhibit prostaglandin synthesis → reduced mucosal blood flow, mucus and bicarbonate secretion) → promotes microperforation and bleeding ^[1]^[3]^[4]
Steroids	Immunosuppression impairs inflammatory response and healing; masks symptoms → delayed presentation
Opiates	Slow colonic transit → increased intraluminal pressure; constipation
Connective tissue diseases (Marfan syndrome, Ehlers-Danlos)	Inherent structural weakness of connective tissue in the colonic wall ^[4]

Drugs to Remember

NSAIDs, steroids, and opiates — these three drug classes all worsen diverticular disease. NSAIDs increase bleeding and perforation risk; steroids mask inflammation and delay healing; opiates increase pressure through constipation. Tell patients with known diverticulosis to avoid NSAIDs and stimulant laxatives ^[4].

4. Anatomy and Function

To understand diverticular disease, you need to understand colonic wall anatomy and the concept of points of weakness.

Colonic Wall Structure

The colon has a unique muscular arrangement compared to the small bowel:

Inner circular muscle layer — complete ring of smooth muscle
Outer longitudinal muscle layer — NOT a complete layer; instead condensed into three longitudinal bands called taeniae coli (taenia mesocolica, taenia omentalis, taenia libera)
Between the taeniae, the outer longitudinal muscle is either very thin or essentially absent → the intertaenial areas are inherently weak

Points of Weakness — Where Diverticula Form

Diverticula develop at well-defined points of weakness where the vasa recta (nutrient arteries) penetrate the circular muscle layer ^[1]^[2]^[3]^[4]:

The vasa recta are small arteries that arise from the marginal artery, travel along the mesenteric side, and penetrate through the circular muscle to reach the submucosa and mucosa
Where each vas rectum pierces the muscle, it creates a gap in the muscularis → a point of structural weakness
Under increased intraluminal pressure, the mucosa and submucosa herniate through these gaps → forming false (pulsion) diverticula

Outpouchings of the bowel wall occur at the weakest point where vasa recta penetrate circular muscle ^[1]^[2]

Why the Sigmoid Colon?

The sigmoid colon is the commonest site ^[1] because:

Laplace's Law: Wall tension = (Pressure × Radius) / (2 × Wall thickness). The sigmoid has the narrowest calibre (smallest radius) of any colonic segment → for a given wall tension, it must generate the highest intraluminal pressure to propel contents ^[1]^[4]
The sigmoid acts as a "high-pressure zone" especially during segmental non-propulsive contractions
Stool is most solid in the sigmoid (water reabsorption is largely complete) → harder to propel → more pressure needed

Why Is the Rectum Never Affected?

The rectum is never affected because the outer longitudinal smooth muscle of the rectum encompasses the full circumference (no taeniae; complete longitudinal muscle coat) → no weak intertaenial zones → no points for herniation ^[4].

Right-Sided (Asian) Diverticula

Right-sided diverticula are congenital and true diverticula (involve all layers) ^[1]
They occur predominantly in the caecum and ascending colon
Mechanism is congenital wall weakness rather than acquired pulsion
Right-sided colon has a thinner wall → a greater length of vasa recta is exposed to injury → right colon is usually the source of diverticular bleeding ^[3]
Right-sided diverticula have wider necks and domes → expose more vasa recta to luminal injury ^[3]

5. Etiology and Pathophysiology

5A. Pathogenesis of Diverticulosis (Formation of Diverticula)

The fundamental equation is: wall weakness + increased intraluminal pressure = diverticulum

Acquired (left-sided): Low fibre diet → increased intraluminal pressure ^[1]:

Low dietary fibre → smaller, harder stool boluses
Colonic segmentation contractions generate higher pressures to propel stool
Sigmoid has narrowest calibre → highest pressure (Laplace's law) ^[1]^[4]
Mucosa and submucosa herniate through weak points where vasa recta penetrate the circular muscle
Result: false diverticulum (only mucosa and submucosa)

Congenital (right-sided): Developmental weakness in the caecal/ascending colonic wall → true diverticulum (all layers) ^[1]

5B. Pathogenesis of Diverticulitis

Diverticulitis is caused by microperforation ^[1]:

Two proposed mechanisms:

Obstruction of the diverticular neck by a faecolith → stasis within the diverticulum → bacterial overgrowth → mucosal erosion → inflammation and focal necrosis → microperforation → pericolic inflammation ^[3]^[4]
Direct mechanical erosion by inspissated faecal matter → increased diverticular pressure → microperforation ^[3]

The microperforation is initially small and walled off by pericolic fat and mesentery → localised pericolic inflammation (uncomplicated diverticulitis). If the perforation is larger or the host response is inadequate → abscess, free perforation, or peritonitis (complicated diverticulitis).

5C. Pathogenesis of Diverticular Bleeding

This is a beautifully logical sequence ^[3]:

When a diverticulum herniates, it drags the penetrating vas rectum (the very vessel whose entry point created the weakness) over the dome of the diverticulum
The blood vessel is now separated from the bowel lumen only by mucosa (no muscularis protection)
The exposed vasa recta undergoes injury along its luminal aspect → eccentric intimal thickening and thinning of the media (asymmetric arterial remodelling)
These changes create segmental weakness of the artery → rupture → arterial bleeding into the lumen

This explains why diverticular bleeding is typically brisk, painless, and arterial — it's not venous oozing; it's a ruptured remodelled artery.

Why right-sided bleeding is more common:

Right-sided colon has a thinner wall ^[3]
Right-sided diverticula have wider necks and domes → more vasa recta length is exposed to luminal injury ^[3]
Therefore, right colon is usually the source of colonic diverticular bleeding even in Western populations where left-sided diverticula are more common ^[3]

Bleeding vs. Inflammation — They Don't Coexist

Diverticular bleeding typically occurs in the absence of diverticulitis. Why? Because the inflammatory process in diverticulitis causes fibrosis and obliteration of the vasa recta → the very vessels that would bleed are destroyed by the inflammation. So bleeding and inflammation are essentially mutually exclusive presentations ^[3].

5D. Pathogenesis of SUDD (Symptomatic Uncomplicated Diverticular Disease)

Altered colonic motility may be the underlying basis of symptoms — abnormal segmental contractions cause pain without overt inflammation ^[3]
Visceral hypersensitivity — after an episode of diverticulitis, there is heightened pain perception related to:
- Increased neuropeptides in the colonic wall
- Alterations in enteric innervation (a form of "post-inflammatory IBS")
- Low-grade chronic mucosal inflammation (increased mast cells, lymphocytes) ^[3]

6. Classification

6A. By Location

Site	Type	Population	Anatomical Basis
Left-sided (sigmoid > descending)	False (acquired)	Western predominant	Highest intraluminal pressure; acquired wall weakness
Right-sided (caecum, ascending)	True (congenital)	Asian (including HK) — higher proportion	Congenital wall weakness

6B. By Clinical Presentation

6C. Hinchey Classification — Prognostic Classification for Complicated Diverticulitis [4]

This is the clinical staging system for complicated diverticulitis, specifically geared towards choosing the proper surgical procedure ^[3]^[4].

Note: Hinchey classification is NOT applicable in right-sided disease ^[4]

Stage	Description	Mortality (%)	Treatment
I	Localised pericolic or mesenteric abscess	0%	Conservative: IV antibiotics ± percutaneous drainage; bowel rest and monitoring. Can be treated as outpatient if stable
II	Distant abscess (walled-off pelvic / retroperitoneal abscess)	5%	IV antibiotics + bowel rest + image-guided percutaneous drainage; possible surgical intervention
III	Generalised purulent (suppurative) peritonitis (abscess has ruptured, but bowel wall itself is intact)	25%	IV antibiotics + bowel rest + Surgery (Hartmann's operation / one-stage resection)
IV	Generalised faecal peritonitis (bowel wall perforation)	50%	IV antibiotics + bowel rest + Surgery (Hartmann's operation)

Hinchey Classification — Exam Must-Know

You must be able to differentiate Stage III (purulent peritonitis from a ruptured abscess — the bowel itself is intact) from Stage IV (faecal peritonitis from a free bowel wall perforation — faeces are in the peritoneum). Stage IV has 50% mortality — this is a surgical catastrophe. The distinction dictates surgical approach and prognosis ^[3]^[4].

7. Clinical Features

7A. Symptoms

Acute Diverticulitis (Uncomplicated)

The classic presentation triad: lower abdominal pain + fever + leucocytosis ^[4]

Symptom	Pathophysiological Basis
Lower abdominal pain	Microperforation → pericolic inflammation → visceral and somatic peritoneal irritation. Usually LLQ (sigmoid involvement in Western patients). May involve RLQ and suprapubic area due to: (a) redundant inflamed sigmoid colon lying in the pelvis/RLQ, or (b) right-sided caecal diverticulitis (common in Asians) ^[1]^[3]^[4]
Pain is constant and lasts several days prior to presentation	Unlike the colicky pain of obstruction; the constant nature reflects ongoing peritoneal inflammation rather than intermittent muscular spasm
Fever (usually low-grade)	Inflammatory response to microperforation and bacterial translocation → release of pyrogenic cytokines (IL-1, IL-6, TNF-α) acting on the hypothalamic thermoregulatory centre
Nausea and vomiting	Can result from: (a) reflex ileus — peritoneal inflammation triggers inhibitory sympathetic reflexes that reduce gut motility (paralytic ileus); (b) mechanical bowel obstruction if significant pericolic oedema or abscess compresses the lumen ^[3]
Change in bowel habit	Pericolic inflammation/oedema → luminal narrowing → constipation (more common) or diarrhoea (from mucosal irritation and altered motility)
Dysuria / urinary frequency	Inflamed sigmoid colon lies adjacent to the bladder → irritation of the bladder wall by contiguous inflammation

Diverticular Bleeding

Symptom	Pathophysiological Basis
Painless massive PR (per rectal) bleeding	Rupture of vasa recta draped over the diverticular dome → arterial haemorrhage into bowel lumen. Painless because the bleeding mechanism does NOT involve inflammation (no microperforation, no peritoneal irritation) ^[3]^[4]
Typically bright red or maroon blood	Arterial origin; if right-sided bleeding → may be darker/maroon; if left-sided → bright red. Volume of bleeding usually means blood transits quickly regardless
Self-limiting in ~80%	Arterial spasm and clot formation at the site of rupture

SUDD (Symptomatic Uncomplicated Diverticular Disease)

Symptom	Pathophysiological Basis
Colicky abdominal pain relieved by defaecation	Altered segmental colonic motility → high-pressure contractions in the diverticular segment → visceral pain. Defaecation decompresses the colon → relief ^[4]
Change in bowel habit (CIBH)	Disordered motility → alternating constipation and diarrhoea (overlaps clinically with IBS)
Bloating	Dysmotility → gas trapping in colonic segments

SUDD vs IBS — Clinical Overlap

SUDD can mimic IBS almost exactly (colicky pain, bloating, CIBH). The key difference is that SUDD occurs in the context of known diverticulosis on imaging. Some experts consider SUDD to be a form of "post-diverticulitis IBS." For exams, the distinguishing point is that SUDD patients typically have demonstrable diverticula on imaging and often a prior history of diverticulitis with persistent symptoms.

7B. Signs

Uncomplicated Acute Diverticulitis

Sign	Pathophysiological Basis
Low-grade fever (37.5–38.5°C)	Localised infection/inflammation → moderate systemic inflammatory response
LLQ tenderness (or RLQ in right-sided disease)	Parietal peritoneal irritation by the adjacent inflamed diverticulum → localised somatic pain
Localised guarding	Reflex contraction of overlying abdominal wall muscles in response to peritoneal irritation (protective mechanism)
Palpable tender mass (occasionally)	Phlegmon (inflamed mass of oedematous colon + mesentery + omentum) walling off the microperforation
Reduced bowel sounds	Localised paralytic ileus due to peritoneal inflammation → sympathetic inhibition of peristalsis
Tachycardia	Systemic inflammatory response; also may indicate hypovolaemia if bleeding co-exists

Signs of Complications (Complicated Diverticulitis)

Complication	Signs	Pathophysiological Basis
Abscess (pericolic, pelvic, psoas, hepatic)	Persistent fever and abdominal pain despite antibiotics ± tender mass on PR (digital rectal exam); swinging pyrexia; localised peritonism	Microperforation → walled-off collection of pus. Pericolic abscess may track to pelvis (pelvic abscess), along psoas muscle (psoas abscess), or rarely to liver via portal venous drainage ^[4]
Perforation → Peritonitis	Acute abdomen: diffuse rigidity ("board-like"), rebound tenderness, absent bowel sounds, generalised peritonitis; signs of sepsis (fever, tachycardia, hypotension)	Free perforation → faecal/purulent contamination of the peritoneal cavity → diffuse peritoneal inflammation. Hinchey III = purulent; Hinchey IV = faecal ^[4]
Fistula	Most common: colovesical fistula → recurrent dysuria, pneumaturia (air in urine), faecaluria (faeces in urine). Less common: colovaginal (vaginal passage of gas/faeces), coloenteric, colocutaneous	Inflamed diverticulum adheres to adjacent organ → erosion through both walls → abnormal communication. Colovesical is MC because the sigmoid lies directly on the bladder dome. More common in males (uterus acts as barrier in females) ^[4]
Intestinal obstruction	Obstipation, abdominal distension, vomiting, colicky pain; tinkling bowel sounds (mechanical) or absent bowel sounds (ileus)	LBO due to fibrosis and stricture (chronic repeated attacks → progressive fibrosis and luminal narrowing); SBO due to adhesion to inflamed bowel ^[4]
Haemorrhage	Haematochezia (fresh red blood PR), signs of hypovolaemia (tachycardia, hypotension, pallor)	Rupture of vasa recta (see above) — although this typically occurs separately from diverticulitis

Colovesical Fistula — Classic Exam Vignette

A middle-aged man with known diverticular disease presents with recurrent UTIs, pneumaturia (air bubbles in urine), and faecaluria. This is colovesical fistula until proven otherwise. It's the most common fistula type in diverticular disease. The investigation of choice is CT colonography with water-soluble rectal contrast or CT abdomen/pelvis with contrast ^[4].

7C. Clinical Features by Presentation — Summary Table

Presentation	Key Features	Distinguishing Point
Asymptomatic diverticulosis	None; incidental finding	Found on colonoscopy/imaging for other reasons
SUDD	Colicky LLQ pain, bloating, CIBH	No fever, no leucocytosis, wall thickening on CT but no inflammation
Acute uncomplicated diverticulitis	LLQ pain (constant), low-grade fever, leucocytosis	Localised peritonism; CT: pericolic fat stranding, wall thickening
Complicated diverticulitis	Above + signs of abscess/perforation/fistula/obstruction	CT with Hinchey staging
Diverticular bleeding	Painless massive PR bleed	NO fever, NO abdominal pain, NO leucocytosis
SCAD	Bloody diarrhoea, LLQ pain	Colonoscopy: interdiverticular mucosal inflammation

8. Anatomical Relationships Relevant to Clinical Features

Understanding why specific symptoms occur requires knowing what's next to the sigmoid colon:

Adjacent Structure	Clinical Consequence
Bladder	Dysuria, frequency (contiguous inflammation); colovesical fistula
Left ureter	Ureteric obstruction → hydronephrosis (rare)
Small bowel loops	Adhesion → SBO; coloenteric fistula
Uterus/vagina (females)	Colovaginal fistula (more common post-hysterectomy as the uterine barrier is removed)
Anterior abdominal wall	Colocutaneous fistula (rare)
Psoas muscle	Psoas abscess (from tracking of pericolic abscess)

9. Key Pathophysiology Diagram

High Yield Summary

Definition: Diverticula = outpouchings of bowel wall; diverticulosis = presence of diverticula; diverticular disease = symptomatic diverticulosis (diverticulitis, bleeding, SUDD).

True vs False: Right-sided = true (congenital, all layers); Left-sided = false (acquired, mucosa + submucosa only).

Epidemiology: 60% prevalence by age 70; 80% asymptomatic; left-sided predominant in West; right-sided more common in Asia → caecal diverticulitis mimics appendicitis → CT is key.

Risk factors: Age, low-fibre diet, obesity, sedentary lifestyle, NSAIDs, steroids, opiates, connective tissue disease.

Pathogenesis: Wall weakness (vasa recta penetration points) + increased intraluminal pressure (Laplace's law, sigmoid narrowest calibre) → diverticula. Diverticulitis = faecolith obstruction → microperforation. Bleeding = vasa recta rupture (separate from inflammation).

Hinchey Classification (NOT for right-sided): I = pericolic abscess (0% mortality); II = pelvic abscess (5%); III = purulent peritonitis (25%); IV = faecal peritonitis (50%).

Clinical triad of diverticulitis: Lower abdominal pain + fever + leucocytosis. LLQ in West, RLQ in Asia.

Diverticular bleeding: Painless, massive, self-limiting (80%), right colon is the usual source.

Complications: Abscess, perforation/peritonitis, fistula (MC = colovesical → pneumaturia, faecaluria), obstruction (LBO from stricture, SBO from adhesion).

Rectum never affected: Full circumferential longitudinal muscle coat.

Active Recall - Diverticular Disease (Part 1: Definition to Clinical Features)

1. Why does the sigmoid colon have the highest intraluminal pressure and is therefore the most common site for diverticula in Western populations?

Your answer

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Laplace's law: sigmoid has the narrowest calibre (smallest radius) of any colonic segment, so for a given wall tension it must generate the highest intraluminal pressure. Additionally, stool is most solid in the sigmoid as water reabsorption is complete.

2. Explain why diverticular bleeding is typically painless and occurs in the absence of diverticulitis.

Your answer

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Bleeding is caused by rupture of vasa recta draped over the diverticular dome (arterial, not inflammatory). No microperforation or peritoneal irritation occurs, so no pain. In diverticulitis, inflammation causes fibrosis and obliteration of vasa recta, so bleeding and inflammation are mutually exclusive.

3. A 45-year-old man in Hong Kong presents with RLQ pain, fever, and leucocytosis. What is an important differential to consider besides appendicitis, and how would you distinguish them?

Your answer

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Right-sided (caecal) diverticulitis, which is more common in Asian populations. CT abdomen and pelvis with contrast is the key investigation to differentiate: appendicitis shows a dilated, inflamed appendix, while caecal diverticulitis shows colonic wall thickening and pericolic fat stranding around a diverticulum.

4. Describe the Hinchey classification stages I-IV, including mortality and general management for each stage.

Your answer

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Stage I: Pericolic abscess, 0% mortality, IV antibiotics +/- drainage. Stage II: Distant (pelvic/retroperitoneal) abscess, 5% mortality, IV antibiotics + image-guided drainage. Stage III: Generalised purulent peritonitis (ruptured abscess, bowel intact), 25% mortality, surgery (Hartmann's or one-stage resection). Stage IV: Faecal peritonitis (bowel perforation), 50% mortality, surgery (Hartmann's).

5. Why is the rectum never affected by diverticular disease?

Your answer

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The outer longitudinal smooth muscle of the rectum encompasses the full circumference (unlike the colon where it is condensed into three taeniae). This complete muscle coat eliminates the weak intertaenial zones and vasa recta penetration points where diverticula would form.

6. What are the classic symptoms of a colovesical fistula complicating diverticular disease, and why is it the most common fistula type?

Your answer

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Symptoms: recurrent dysuria, pneumaturia (air in urine), faecaluria (faeces in urine). It is the most common type because the sigmoid colon lies directly on the dome of the bladder. More common in males because the uterus acts as a physical barrier between sigmoid and bladder in females.

References

^[1] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf ^[2] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf ^[3] Senior notes: felixlai.md (Diverticular disease section) ^[4] Senior notes: maxim.md (Diverticular disease section)

Differential Diagnosis of Diverticular Disease

The differential diagnosis of diverticular disease depends entirely on which presentation you're dealing with. An elderly man with painless massive PR bleeding has a completely different DDx list from a middle-aged woman with LLQ pain and fever. So let's break this down by clinical scenario — the way you'd actually think on a ward round.

Approach to the Differential Diagnosis

The key principle: diverticular disease is a mimic. It can look like cancer, appendicitis, IBD, or ischaemic colitis depending on the presentation. Your job is to systematically exclude dangerous diagnoses (especially colorectal cancer) before settling on diverticular disease as the answer.

A. Differential Diagnosis of Acute Diverticulitis

This is the scenario of lower abdominal pain + fever + leucocytosis — the classic triad ^[3]^[4]. The DDx here is essentially "what else causes localised lower abdominal pain with inflammation?"

1. Colorectal Cancer (CRC) — The Most Important DDx [3]

Why it's confusable: CRC and diverticulitis share remarkably similar features:
- Both cause bowel wall thickening on CT
- Both can present with change in bowel habit, abdominal pain, and even obstruction
- Both are diseases of the same age group (> 50 years)
How to distinguish on CT:
- Diverticulitis: pericolonic and mesenteric fat stranding/inflammation, involvement of > 10 cm of colon, absence of enlarged pericolonic lymph nodes, visible diverticula in surrounding segments ^[3]
- CRC: shorter segment of wall thickening (typically < 10 cm), "shouldering" sign (abrupt transition), pericolonic lymphadenopathy, luminal irregularity/mass
Critical point: CRC can only be excluded with colonoscopy after resolution of acute inflammation — standard practice is colonoscopy at 6–8 weeks post-recovery ^[3]^[5]

"Rule out malignancy" — colonoscopy at 6–8 weeks after acute diverticulitis is mandatory ^[5]

CRC vs Diverticulitis — The Exam Trap

Never diagnose "diverticulitis" and leave it at that. Up to 1–2% of patients diagnosed with acute diverticulitis on CT are subsequently found to have CRC on follow-up colonoscopy. The two conditions can even coexist. Always follow up with colonoscopy.

2. Acute Appendicitis [2][3][4]

Why it's confusable: Both cause RLQ pain + fever + leucocytosis. This is especially problematic in Asian populations where right-sided (caecal) diverticulitis is common ^[1]^[4]
How to distinguish:
- Appendicitis: pain classically starts periumbilical (visceral afferent T10) then migrates to RLQ (somatic, parietal peritoneum) over 12–24 hours; anorexia is prominent; younger age group (MC 5–12 years) ^[4]
- Right-sided diverticulitis: pain is localised to RLQ from the outset (no migration); older age group; CT shows colonic wall thickening with diverticula, NOT a distended appendix
- CT scan is the key investigation to differentiate — it shows either a dilated inflamed appendix (appendicitis) or colonic wall thickening with pericolic fat stranding around a diverticulum (diverticulitis) ^[1]^[3]

Caecal diverticulitis mimicking appendicitis — Role of CT scan ^[1]

3. Inflammatory Bowel Disease (IBD) [3]

Why it's confusable: IBD (especially Crohn's disease) can cause lower abdominal pain, fever, and even fistulae/strictures — complications shared with diverticular disease
How to distinguish:
- IBD: diarrhoea rather than abdominal pain is the predominant symptom ^[3]; younger age of onset; extraintestinal manifestations (arthritis, uveitis, skin lesions); chronic relapsing course; Crohn's may show skip lesions, non-caseating granulomas; UC shows continuous mucosal inflammation from rectum proximally
- Diverticulitis: abdominal pain is the predominant symptom; fever and localised peritonism; CT shows pericolic fat stranding with diverticula
- Colonoscopy (after acute phase resolves) is definitive for distinguishing

4. Infectious Colitis [3]

Why it's confusable: Infectious colitis (Salmonella, Shigella, Campylobacter, Yersinia, E. coli O157:H7, C. difficile) causes abdominal pain, fever, leucocytosis
How to distinguish:
- Infectious colitis: diarrhoea (often bloody) rather than abdominal pain is the predominant symptom ^[3]; acute onset; exposure history (travel, contaminated food, recent antibiotics for C. difficile); stool culture/PCR positive
- Diverticulitis: pain predominates; diarrhoea is not the main feature; CT shows diverticula with pericolic changes

5. Ischaemic Colitis [3]

Why it's confusable: Both occur in elderly patients with vascular risk factors; both cause lower abdominal pain
How to distinguish:
- Ischaemic colitis: rapid onset of abdominal pain with haematochezia or bloody diarrhoea ^[3]; risk factors include advanced age, hypertension, DM, dehydration, AF, recent vascular surgery, laxative use, haemodialysis; "watershed" areas affected (splenic flexure, rectosigmoid junction)
- Diverticulitis: gradual onset of constant pain over days; fever and leucocytosis more prominent; bloody stools uncommon in uncomplicated diverticulitis
- CT: ischaemia shows segmental wall thickening with "thumbprinting" in a vascular distribution, ± pneumatosis; diverticulitis shows diverticula + fat stranding

6. Gynaecological Disorders [3]

These are especially important in women of reproductive age presenting with lower abdominal/pelvic pain:

Condition	Distinguishing Features
Tubo-ovarian abscess (TOA)	History of PID; bilateral adnexal tenderness; cervical motion tenderness; purulent vaginal discharge; USS/CT shows complex adnexal mass
Ovarian torsion	Sudden onset severe unilateral pain; nausea/vomiting; Doppler USS shows absent/reduced ovarian blood flow
Ectopic pregnancy	Positive pregnancy test (β-hCG); amenorrhoea; vaginal bleeding; USS shows no intrauterine pregnancy ± adnexal mass/free fluid ^[3]
Ruptured ovarian cyst	Sudden onset pain, often during exercise/intercourse; USS shows free pelvic fluid ± collapsed cyst
PID	Recent onset pain worsening with coitus or menses; cervical motion tenderness; purulent endocervical discharge ^[2]

Golden Rule in Women of Reproductive Age

Always do a pregnancy test (urine/serum β-hCG) in any woman of reproductive age presenting with lower abdominal pain. Ruptured ectopic pregnancy is a life-threatening emergency that must be excluded before anything else.

7. Urological Disorders [3]

Condition	Distinguishing Features
Cystitis / UTI	Dysuria, frequency, urgency; positive urine dipstick (nitrites, leucocyte esterase); urine culture positive. Note: diverticulitis can cause sterile pyuria from adjacent inflammation — don't be fooled ^[3]
Nephrolithiasis / ureteric colic	Severe colicky flank-to-groin pain; haematuria (micro or macro); restlessness (patient cannot lie still, unlike peritonitis where patient lies very still); CT KUB shows calculus

8. Meckel's Diverticulitis [2]

Similar presentation as acute appendicitis ^[2]
Congenital remnant of omphalomesenteric duct located on small bowel, 2 feet from ileocaecal valve ^[3]
Small bowel may migrate into RLQ and mimic appendicitis
Diagnosis by CT scan ^[2]
Incidental finding during appendicectomy ^[2]
Treatment: antibiotics; diverticulectomy / small bowel resection ^[2]

B. Differential Diagnosis of Diverticular Bleeding

This is the scenario of painless massive PR bleeding. The DDx here is "what else causes significant lower GI haemorrhage?"

From the lecture slides, the DDx of diverticular bleeding includes ^[5]:

Angiodysplasia
Severe colitis
Rectal ulcer
Small bowel bleeding
UGIB

Let's expand on each:

DDx	Key Features	How to Distinguish from Diverticular Bleeding
Angiodysplasia (most common cause of LGIB in age > 65)	Abnormal dilated submucosal AVM; painless haematochezia; venous bleeding (tends to be less massive than diverticular bleeding); mostly right-sided (caecum, ascending colon) ^[6]	Colonoscopy: cherry red spots; angiography: "mother-in-law phenomenon" (early filling, delayed emptying); often occult/chronic causing iron deficiency anaemia rather than massive acute bleed ^[6]
Haemorrhoids (most common in age < 50)	Fresh outlet-type blood (on toilet paper, dripping into bowl, separate from stool); painless unless thrombosed; perianal mass on examination	Blood is bright red, small volume, and clearly outlet-type — not mixed with stool. Digital rectal exam and proctoscopy diagnostic
Severe colitis (infectious/IBD/ischaemic)	Bloody diarrhoea with associated symptoms (fever, tenesmus, cramping pain); mucus in stool	Pain and diarrhoea are prominent — diverticular bleeding is painless. Stool cultures, colonoscopy distinguish
Rectal ulcer (solitary rectal ulcer syndrome)	Outlet-type bleeding, mucus discharge, tenesmus, sensation of incomplete evacuation	History of straining; rigid sigmoidoscopy shows ulcer on anterior rectal wall 5–10 cm from anal verge
Small bowel bleeding	Obscure GI bleeding; may present as haematochezia if brisk; Meckel's diverticulum (especially in young), small bowel tumour, Crohn's	If colonoscopy and OGD negative → capsule endoscopy or CT enterography. Meckel's scan (Tc-99m pertechnetate) for ectopic gastric mucosa
UGIB (must not forget!)	Massive upper GI bleed can present as haematochezia (blood acts as cathartic and transits quickly); look for haemodynamic instability out of proportion to apparent blood loss	Always consider UGIB if haemodynamically unstable with PR bleed. NG tube aspirate may show blood/coffee-grounds. OGD is indicated
Colorectal cancer	Less commonly presents with massive acute bleed; more often chronic occult blood loss → iron deficiency anaemia; change in bowel habit, weight loss	Colonoscopy (after stabilisation) for definitive diagnosis

Don't Forget UGIB!

About 10-15% of patients presenting with apparent lower GI bleeding (haematochezia) actually have an upper GI source. A massive peptic ulcer bleed, for instance, can transit so rapidly that blood arrives at the rectum still bright red. If the patient is haemodynamically unstable with PR bleeding, always consider OGD before assuming a lower GI source.

C. Differential Diagnosis of SUDD

SUDD presents with colicky lower abdominal pain, change in bowel habit, bloating — essentially overlapping with functional bowel disorders:

DDx	Key Distinguishing Features
Irritable Bowel Syndrome (IBS)	Rome IV criteria: recurrent abdominal pain ≥ 1 day/week for 3 months, related to defaecation, with change in stool frequency/form; no structural abnormality; diagnosis of exclusion. SUDD is distinguished by the presence of diverticula on imaging and often a prior history of diverticulitis ^[3]
Colorectal cancer	Constitutional symptoms (weight loss, anorexia); change in stool calibre; iron deficiency anaemia; family history; colonoscopy is definitive
IBD (mild)	Chronic diarrhoea predominant; extraintestinal features; elevated faecal calprotectin; colonoscopy with biopsy diagnostic
Lactose intolerance	Symptoms temporally related to dairy ingestion; bloating and diarrhoea; hydrogen breath test diagnostic
Coeliac disease	Chronic diarrhoea, steatorrhoea, iron/folate deficiency; positive anti-tTG/EMA antibodies; duodenal biopsy shows villous atrophy

D. Differential Diagnosis of Complicated Diverticulitis (Perforation / Peritonitis)

When diverticular disease presents as an acute abdomen with generalised peritonitis, the DDx is the surgical emergency list ^[4]:

DDx	Key Distinguishing Features
Perforated peptic ulcer (PPU)	Sudden-onset epigastric pain → generalises; history of NSAID use/peptic ulcer disease; erect CXR shows pneumoperitoneum; Valentino's sign — gastric contents tracking down the right paracolic gutter causing RLQ pain mimicking appendicitis ^[4]
Perforated appendicitis	RLQ pain preceding generalised peritonitis; younger age group; CT shows perforated appendix
Ischaemic / infarcted bowel	Acute severe abdominal pain out of proportion to examination findings (early); AF or vascular risk factors; raised lactate; CT angiography shows mesenteric vessel occlusion
Sigmoid volvulus	Elderly, institutionalised patient; massive abdominal distension; "coffee bean" sign on AXR; CT shows "whirl sign" ^[6]
Strangulated hernia	Irreducible tender groin/incisional swelling; signs of obstruction and/or peritonitis
Perforated colorectal cancer	May be indistinguishable from perforated diverticulitis on initial CT; histology of resected specimen gives definitive answer

E. Differential Diagnosis by Location — The RLQ Problem (Hong Kong Relevance)

This is particularly high-yield for Hong Kong exams given the higher prevalence of right-sided diverticular disease ^[1]^[2]^[4]:

The RLQ DDx (from lecture slides) ^[2]^[4]:

Category	Conditions
Caecum/Right colon	Caecal diverticulitis, acute appendicitis, caecal/appendiceal tumour (lymphoma, carcinoid)
Terminal ileum	Crohn's disease, Meckel's diverticulitis, intestinal TB, Yersinia ileitis
Urological	Ureteric colic, testicular torsion, UTI
Gynaecological	Ovulation pain ("Mittelschmerz"), ovarian cyst complications (rupture/torsion), PID, ruptured ectopic pregnancy
Other	Mesenteric adenitis (in children), strangulated inguinal/femoral hernia, PPU with Valentino's sign

CT abdomen with IV contrast is the diagnostic test of choice when differentiating these RLQ causes — it is the single most important investigation ^[1]^[2]^[5]

Summary Table: DDx at a Glance

Presentation of Diverticular Disease	Top DDx to Exclude	Key Investigation
Acute diverticulitis (LLQ/RLQ pain, fever, leucocytosis)	CRC, appendicitis, IBD, ischaemic colitis, gynaecological causes	CT abdomen/pelvis with contrast → colonoscopy at 6–8 weeks
Diverticular bleeding (painless massive PR bleed)	Angiodysplasia, CRC, haemorrhoids, colitis, UGIB	Colonoscopy → angiography if inconclusive
SUDD (colicky pain, CIBH)	IBS, CRC, IBD, lactose intolerance	Colonoscopy to exclude organic pathology
Complicated diverticulitis (acute abdomen)	PPU, perforated appendix, ischaemic bowel, volvulus	CT abdomen/pelvis; erect CXR (pneumoperitoneum)

High Yield Summary

The single most important DDx across all presentations is colorectal cancer (CRC) — always exclude it. Colonoscopy at 6–8 weeks post-acute diverticulitis is mandatory.

Right-sided diverticulitis mimics acute appendicitis — CT abdomen is the key differentiator, especially in Asian populations including Hong Kong.

Diverticular bleeding DDx: angiodysplasia, severe colitis, rectal ulcer, small bowel bleeding, UGIB. Don't forget massive UGIB can present as haematochezia.

In women of reproductive age: always exclude ectopic pregnancy (β-hCG) and gynaecological causes (TOA, ovarian torsion, PID) before diagnosing diverticular disease.

Meckel's diverticulitis presents similarly to appendicitis; may be an incidental finding during appendicectomy; diagnosed by CT.

Ischaemic colitis has rapid onset + haematochezia (vs. gradual onset + constant pain in diverticulitis).

IBD and infectious colitis: diarrhoea predominates (vs. pain predominates in diverticulitis).

Active Recall - Differential Diagnosis of Diverticular Disease

1. Why must colonoscopy be performed 6-8 weeks after resolution of acute diverticulitis, and what is the most important diagnosis to exclude?

Your answer

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To exclude colorectal cancer (CRC). CRC and diverticulitis share similar features (bowel wall thickening on CT, same age group, change in bowel habit). Up to 1-2% of patients diagnosed with acute diverticulitis are found to have CRC on follow-up colonoscopy. Colonoscopy is avoided in the acute setting due to risk of perforation.

2. List 5 differential diagnoses for diverticular bleeding as mentioned in the lecture slides.

Your answer

Show mark scheme

Angiodysplasia, severe colitis, rectal ulcer, small bowel bleeding, UGIB. Key point: always consider UGIB in a haemodynamically unstable patient with haematochezia.

3. A 40-year-old woman in Hong Kong presents with RLQ pain, fever, and leucocytosis. Name 4 differential diagnoses and the key investigation to distinguish them.

Your answer

Show mark scheme

DDx: (1) Acute appendicitis, (2) Right-sided (caecal) diverticulitis, (3) Meckel's diverticulitis, (4) Gynaecological cause (ectopic pregnancy, ovarian torsion, PID, TOA). Key investigation: CT abdomen and pelvis with IV contrast. Also beta-hCG to exclude ectopic pregnancy in women of reproductive age.

4. How do you distinguish diverticulitis from IBD and infectious colitis clinically?

Your answer

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In IBD and infectious colitis, diarrhoea is the predominant symptom (rather than abdominal pain). Diverticulitis presents with pain as the dominant feature, localised peritonism, and fever. IBD has extraintestinal manifestations and chronic relapsing course. Infectious colitis has acute onset with exposure history and positive stool cultures.

5. What CT features help distinguish acute diverticulitis from colorectal cancer?

Your answer

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Diverticulitis: pericolic and mesenteric fat stranding, involvement of more than 10 cm of colon, absence of enlarged pericolonic lymph nodes, visible surrounding diverticula. CRC: shorter segment of wall thickening (typically less than 10 cm), shouldering sign, pericolonic lymphadenopathy, irregular luminal mass.

References

Diagnostic Criteria, Algorithm, and Investigations for Diverticular Disease

Key Principle: There Is No Single "Diagnostic Criterion" for Diverticular Disease

Unlike conditions such as rheumatic fever (Jones criteria) or SLE (ACR criteria), diverticular disease does not have formal validated diagnostic criteria with sensitivity/specificity scores. Instead, the diagnosis is clinico-radiological — you combine the clinical picture with imaging findings. Let me walk you through exactly how this works for each presentation.

1. Diagnostic Criteria by Presentation

A. Acute Diverticulitis — Clinical + Radiological Diagnosis

The clinical diagnosis rests on the triad of lower abdominal pain + fever + leucocytosis ^[1]^[4], but the definitive diagnosis requires imaging:

Component	What You're Looking For	Why
Clinical triad	Lower abdominal pain (LLQ or RLQ), fever, leucocytosis	Microperforation → localised pericolic inflammation → peritoneal irritation (pain), systemic inflammatory response (fever, leucocytosis)
CT abdomen + pelvis with IV contrast	Bowel wall thickening > 4 mm + pericolic fat stranding + visible diverticula	CT scan helps to confirm diagnosis and assess the severity ^[2] — it is both diagnostic AND prognostic (Hinchey staging)
Absence of other diagnoses	Must exclude CRC, appendicitis, IBD, gynaecological/urological causes	Diverticulitis is partly a diagnosis of exclusion in the acute setting; definitive exclusion of CRC requires colonoscopy later

Diagnosis of uncomplicated diverticulitis: CT abdomen and pelvis with IV contrast ^[5]

Avoid colonoscopy in the acute setting ^[5]

Colonoscopy at 6–8 weeks to rule out malignancy ^[5]

Why avoid colonoscopy acutely? Because the inflammation is peridiverticular (outside the bowel wall). Air insufflation during colonoscopy risks converting a sealed microperforation into a free perforation — a catastrophe. The colonoscopy won't even show much diagnostically since the disease process is extraluminal ^[3].

B. Diverticulosis (Incidental / Asymptomatic)

Incidental finding on CT, colonoscopy, or barium enema ^[5]
No specific diagnostic criteria needed — you simply see the diverticula on imaging
Investigations for diverticulosis: barium enema / colonoscopy / CT colonography (CTC) ^[5]

C. Diverticular Bleeding

Clinical: painless massive PR bleeding in a patient with known or suspected diverticulosis
Investigation of choice: colonoscopy ^[5] — both diagnostic (identify bleeding source) and therapeutic (haemostasis)
No formal diagnostic criteria; diagnosis is made by visualising a bleeding diverticulum or stigmata of recent haemorrhage at a diverticulum on colonoscopy

D. SUDD (Symptomatic Uncomplicated Diverticular Disease)

Clinical: colicky abdominal pain, altered bowel habit in a patient with known diverticulosis
CT shows wall thickening in the absence of inflammatory changes (no fat stranding, no abscess) ^[3]
Essentially a diagnosis of exclusion after ruling out diverticulitis, CRC, and IBD

2. Diagnostic Algorithm

Here is the systematic approach to a patient presenting with suspected diverticular disease, organised by clinical scenario:

The Two Phases of Diagnosis

Think of diagnosing diverticular disease in two phases:

Acute phase: CT abdomen/pelvis with IV contrast → confirm diverticulitis, stage severity (Hinchey), guide immediate management. NO colonoscopy.
Recovery phase (6–8 weeks later): Colonoscopy → definitively exclude CRC, assess for IBD/polyps, evaluate for strictures.

This two-phase approach is one of the most commonly tested concepts.

3. Investigation Modalities — Detailed Breakdown

A. Bedside Investigations

Investigation	Key Findings	Clinical Significance
Urinalysis ^[2]^[3]	Sterile pyuria	Adjacent sigmoid inflammation irritates the bladder wall → WBCs in urine without bacterial infection. Don't mistake this for UTI! ^[3]
Urine culture ^[3]^[4]	Presence of colonic flora (e.g., E. coli, Bacteroides)	Pathognomonic for colovesical fistula — bacteria from the colon have gained direct access to the urinary tract through the fistulous communication ^[3]
Pregnancy test ^[2]	Positive β-hCG	Excludes ectopic pregnancy in women of reproductive age — a critical differential for lower abdominal pain

B. Blood Investigations

Blood tests: CBC D/C, LRFT, amylase, clotting profile, ABG, type and screen ^[2]^[4]

Investigation	Key Findings	Why It's Done
CBC with differentials	Leucocytosis (raised WCC with neutrophilia)	Confirms systemic inflammatory response to infection/inflammation. Part of the diagnostic triad. Drop in Hb suggests bleeding ^[3]^[4]
CRP	Elevated	Non-specific inflammatory marker; useful for monitoring response to treatment. CRP > 200 mg/L has been associated with complicated diverticulitis
Electrolyte profile (LRFT)	Derangements in Na⁺, K⁺, urea, creatinine	Dehydration from reduced oral intake, vomiting, third-space losses; renal impairment from sepsis/hypovolaemia ^[3]
Serum amylase and lipase	Usually normal or mildly elevated	Primarily to exclude acute pancreatitis as a differential for upper/diffuse abdominal pain. Mild elevation can occur with any intra-abdominal inflammation ^[3]
LFT	Usually normal	Exclude hepatobiliary pathology; may be deranged if hepatic abscess develops from portal pyaemia
ABG and lactate ^[2]	Raised lactate, metabolic acidosis	Suggests tissue hypoperfusion — raises concern for ischaemic bowel, septic shock, or peritonitis with cardiovascular compromise
Clotting profile ^[2]	PT/INR, APTT	Essential pre-operatively and if patient is on anticoagulants (which increase bleeding risk in diverticular bleeding)
Type and screen / cross-match ^[2]	Blood group and antibody screen	Preparation for potential transfusion (especially in diverticular bleeding or if surgery anticipated)

C. Plain Radiographs — CXR and AXR

Imaging: Erect CXR, erect and supine AXR ^[2]^[3]

Finding	Significance	Pathophysiological Basis
Free gas under diaphragm (pneumoperitoneum) on erect CXR	Perforation — surgical emergency	Free bowel perforation → intraluminal air escapes into peritoneal cavity → rises to collect under the diaphragm ^[3]
Air-fluid levels with bowel dilatation on AXR	Obstruction or paralytic ileus	Mechanical obstruction (stricture from chronic diverticulitis) → proximal accumulation of gas and fluid. Alternatively, peritoneal inflammation → reflex inhibition of peristalsis (paralytic ileus) ^[3]
Dilated bowel on AXR ^[4]	Obstruction	LBO from diverticular stricture (chronic fibrosis) or SBO from adhesion to inflamed segment
Soft tissue densities	Abscess	Collection of pus and inflammatory tissue creates an area of increased soft tissue density ^[3]

Plain Films — Screening, Not Diagnostic

Erect CXR and AXR are quick, cheap screening tools done in the emergency department. They can identify life-threatening complications (perforation, obstruction) but they cannot confirm the diagnosis of diverticulitis. For that, you need CT.

D. Ultrasound (USG Abdomen)

Ultrasound can be useful as a first-line bedside investigation, especially when CT is not immediately available or to avoid radiation (e.g., young patients, pregnancy).

Finding	Significance
Diverticula in surrounding segments	Confirms underlying diverticulosis ^[3]
Bowel wall thickening > 4 mm at point of maximal tenderness (segmental mural thickening)	Localised inflammation — hallmark of diverticulitis ^[3]
Hypoechoic peridiverticular inflammatory reaction	Pericolic inflammation/phlegmon ^[3]
Mural and peridiverticular abscess ± gas bubbles	Complicated diverticulitis with abscess formation ^[3]
Anechoic mass containing echogenic debris	Abscess ^[3]
Hypoechoic area with extraluminal air bubbles extending into bladder/vagina/abdominal wall	Fistula ^[3]
Ascites, diffuse peritoneal thickening, scattered loculated fluid collections	Perforation with peritonitis ^[3]

Limitations: Operator-dependent; bowel gas obscures views; limited sensitivity for deep pelvic structures; cannot reliably stage severity (Hinchey).

E. CT Abdomen + Pelvis with IV Contrast — THE Gold Standard

This is the single most important investigation for acute diverticulitis. It does four things simultaneously ^[2]^[4]^[5]:

Diagnostic: confirms the diagnosis
Assesses complications: abscess, fistula, perforation, obstruction
Aids treatment: guides percutaneous drainage of abscess
Prognostic: enables Hinchey classification staging ^[4]

CT scan helps to confirm diagnosis and assess the severity ^[2]

CT Findings in Acute Diverticulitis [3]

CT Finding	What It Represents	Why It Occurs
Colonic diverticula	Underlying diverticulosis	Outpouchings of mucosa/submucosa through the colonic wall
Localised bowel wall thickening > 4 mm	Mural oedema and inflammation	Microperforation → inflammatory infiltrate and oedema within the bowel wall
Increased soft tissue density in pericolonic fat (fat stranding)	Pericolic inflammation	Inflammatory exudate and oedema spread from the microperforation into the surrounding mesenteric fat — this is the hallmark CT sign of diverticulitis ^[3]

CT Findings of Complications [3][4]

Complication	CT Findings	Explanation
Abscess	Fluid collection with surrounding inflammatory changes; centre may contain air, air-fluid levels, or low-attenuation necrotic debris	Walled-off collection of pus from contained microperforation. Air within the abscess comes from the bowel communication
Abscess size	5 cm is the cut-off ^[4]	< 5 cm: likely to resolve with IV antibiotics alone. ≥ 5 cm: likely requires image-guided (CT-guided) percutaneous drainage
Fistula	Extracolonic air collections within organs other than bowel (e.g., air in bladder = colovesical fistula)	Inflammatory erosion through to adjacent organ creates abnormal communication; air/gas tracks from bowel into the other organ
Obstruction	Dilated loops of bowel with air-fluid levels in proximity to an area with pericolic fat stranding	Inflammatory oedema or chronic fibrotic stricture narrows the lumen → proximal bowel dilates
Perforation	Free intraperitoneal air in patient with peritonitis	Unsealed microperforation or macro-perforation → free air escapes into peritoneal cavity

Hinchey Classification on CT [4]

Stage	CT Appearance	Management Implication
I	Small pericolic or mesenteric abscess ( < 5 cm)	IV antibiotics ± drainage
II	Larger distant abscess (pelvic, retroperitoneal)	IV antibiotics + CT-guided percutaneous drainage
III	Free fluid/gas without connection to bowel lumen; no faecal material in peritoneum	Surgery required (Hartmann's or primary resection-anastomosis)
IV	Free faecal matter and gas in peritoneal cavity; communication with bowel lumen visible	Emergency surgery (Hartmann's)

Hinchey classification: note NOT applicable in right-sided disease ^[4]

Why Hinchey Doesn't Apply to Right-Sided Disease

The Hinchey classification was developed and validated for left-sided (sigmoid) diverticulitis with its specific anatomical relationships. Right-sided diverticula are congenital and true (involving all layers), have different natural history, and right-sided complicated diverticulitis is managed differently (typically right hemicolectomy rather than Hartmann's procedure). The staging system simply doesn't translate.

CT Features Distinguishing Diverticulitis from CRC [3]

This is high-yield — you need to know this for exams:

Feature	Diverticulitis	CRC
Length of involvement	> 10 cm (long segment)	< 10 cm (short segment)
Pericolonic fat stranding	Prominent (the hallmark feature)	Mild or absent
Pericolonic lymph nodes	Absent or small/reactive	Enlarged (suggesting malignant infiltration)
Surrounding diverticula	Present in adjacent colon	May or may not be present
Transition zone	Gradual thickening	Abrupt "shouldering" (sharp transition from normal to thickened bowel)
Luminal appearance	Smooth narrowing	Irregular, eccentric mass/luminal destruction

Features suggestive of acute diverticulitis include presence of pericolonic and mesenteric inflammation, involvement of > 10 cm of colon, and absence of enlarged pericolonic lymph nodes ^[3]

The 1-2% Rule

Even with these distinguishing features, 1–2% of patients diagnosed as "uncomplicated diverticulitis" on CT will harbour an underlying CRC. With complicated diverticulitis, the rate of concurrent malignancy jumps to ~10-17% ^[5]. This is precisely why follow-up colonoscopy is non-negotiable.

From the lecture data showing studies of patients with uncomplicated vs complicated diverticulitis ^[5]:

Disease Type	Malignancy Rate
Uncomplicated diverticulitis	~0–1.1% (very low but not zero)
Complicated diverticulitis	~13–17% (significantly higher!)
Colorectal polyps (on follow-up colonoscopy)	~7–32%

This data reinforces that colonoscopy at 6–8 weeks is essential, especially after complicated disease ^[5].

F. MRI Abdomen + Pelvis

Feature	Details
When to use	When you want to avoid radiation exposure (young patients, pregnant women, recurrent imaging needed) ^[3]
Findings	Same as CT: colonic diverticula, colonic wall thickening, pericolonic exudates and oedema ^[3]
Limitations	Longer scan time; less available in emergencies; more expensive; motion artefact
Advantage	Excellent soft tissue contrast; no ionising radiation; useful for characterising pelvic abscesses and fistulae

G. Colonoscopy

Colonoscopy plays different roles depending on the clinical scenario:

In Acute Diverticulitis:

Avoid colonoscopy in the acute setting ^[5]

NO role in establishing the diagnosis of acute diverticulitis because the inflammation is peridiverticular (extraluminal) — colonoscopy only visualises the mucosal surface ^[3]
Risk of perforation during air insufflation in an already weakened, inflamed bowel wall ^[4]
Contraindication: acute diverticulitis ^[4]

Post-Recovery (6–8 Weeks):

Colonoscopy at 6–8 weeks to rule out malignancy ^[5]

Definitive diagnosis (localisation) and rule out other DDx (e.g., CRC, IBD) ^[4]
Assess complications: stenosis (fibrotic stricture from chronic disease) ^[4]
Evaluate for synchronous polyps
Standard of care after ANY episode of acute diverticulitis

In Diverticular Bleeding:

Investigation: Colonoscopy ^[5]

Endoscopic haemostasis ^[4]^[5]:
- Epinephrine injection (1:10,000) — not used alone (causes temporary vasoconstriction but doesn't achieve definitive haemostasis) ^[4]
- Endoscopic clip / band ligation — usually for diverticular bleeding ^[4]
- Argon plasma coagulation (APC) — thermal energy, usually more for angiodysplasia ^[4]
Limitations in acute massive bleeding: poor visualisation due to blood clots and lack of adequate bowel preparation ^[3]^[4]
May be difficult to identify and localise the exact bleeding diverticulum

In Diverticulosis (Asymptomatic/SUDD):

Investigations for diverticulosis: barium enema / colonoscopy / CT colonography ^[5]

Colonoscopy can directly visualise diverticula and simultaneously screen for polyps/CRC
Often the investigation that incidentally discovers diverticulosis

H. CT Colonography (Virtual Colonoscopy) with Water-Soluble Rectal Contrast

Especially useful for colovesical fistula ^[4] — water-soluble contrast instilled per rectum can be seen tracking into the bladder through the fistula
Alternative to colonoscopy when:
- Colonoscope cannot reach the caecum (stricture, tortuous colon)
- Patient cannot tolerate colonoscopy
Provides extraluminal information (unlike conventional colonoscopy)
Cannot take biopsies — if a suspicious lesion is found, colonoscopy is still needed

I. Barium Enema

NOT recommended and relatively contraindicated in the acute setting ^[3]
Risk of barium peritonitis if there is a perforation — barium is intensely irritant to the peritoneum and cannot be reabsorbed (unlike water-soluble contrast)
Contrast enema and small bowel studies are extremely useful in defining the course of fistula in complicated diverticulitis ^[3]
Largely superseded by CT colonography in modern practice
Classic finding in diverticulosis: saw-tooth pattern of the colonic mucosa with outpouchings

J. Mesenteric Angiography

Indicated when colonoscopy cannot accurately localise the diverticular bleeding source ^[3]
3-vessel mesenteric angiogram: coeliac artery, SMA, IMA ^[3]
Detects active bleeding at a rate of > 1 mL/min ^[3]
Can show: contrast extravasation at the bleeding site
Angiogram ± embolisation ^[5] — selective catheterisation and embolisation can control bleeding
However, embolisation carries risk of bowel ischaemia/gangrene — must be done selectively by experienced interventional radiologists ^[3]

K. Technetium-99m Tagged RBC Scan

Indicated when colonoscopy cannot accurately localise the diverticular bleeding source ^[3]
More sensitive than angiography: detects slow intermittent bleeding at > 0.1 mL/min ^[3]
Mechanism: patient's own RBCs are labelled with Tc-99m → reinjected → serial gamma camera images over 24 hours → localisation of tracer accumulation at the bleeding site
Useful for intermittent bleeding that may not be active at the time of angiography
Limitation: gives only approximate anatomical localisation (not precise enough for surgery alone — usually needs confirmatory angiography or colonoscopy)

4. Investigation Algorithm for Diverticular Bleeding — Stepwise Escalation

This is a critical algorithm from the lectures ^[4]^[5]:

Localisation of bleeding: colonoscopy → angiography → on-table lavage and colonoscopy → subtotal colectomy and ileostomy ^[4]

80% of diverticular bleeding is self-limiting ^[1]^[5]. Rebleeding occurs in ~20–30% ^[7]

Treatment of diverticular bleeding: endoscopic vs surgical resection ^[7]

5. Summary of Investigation Modalities by Clinical Scenario

Clinical Scenario	First-Line Investigation	Additional Investigations	What NOT to Do
Acute diverticulitis	CT abdomen + pelvis with IV contrast ^[2]^[5]	Bloods (CBC D/C, LRFT, amylase), urinalysis, erect CXR + AXR	Avoid colonoscopy ^[5]; avoid barium enema
Post-recovery from acute diverticulitis	Colonoscopy at 6–8 weeks ^[5]	CT colonography if colonoscopy incomplete	Don't skip this — rule out malignancy
Diverticular bleeding	Colonoscopy ^[5]	Mesenteric angiography, Tc-99m RBC scan, CT angiography	Don't assume it's lower GI — exclude UGIB if unstable
Asymptomatic diverticulosis	Colonoscopy / barium enema / CT colonography ^[5]	None specifically	No treatment needed if truly asymptomatic
Suspected colovesical fistula	CT colonography with water-soluble rectal contrast ^[4]	Urine culture (colonic flora), cystoscopy	Don't use barium (risk of barium peritonitis if free perforation)
Acute abdomen / suspected perforation	Erect CXR (pneumoperitoneum) → CT	Bloods including lactate, ABG	Don't delay resuscitation; don't do colonoscopy

6. Physical Examination Findings (As Part of Diagnostic Workup)

Don't forget that the examination IS part of your diagnostic algorithm ^[2]^[3]:

Abdominal Examination [3]

Finding	Significance
Tender abdominal mass	Phlegmon (inflamed mass of oedematous colon + mesentery + omentum) or peridiverticular abscess ^[3]
Peritoneal signs: rigidity, localised guarding, rebound tenderness	Localised peritonitis from pericolic inflammation; if generalised → perforation ^[3]
Absent bowel sounds	Paralytic ileus (peritoneal inflammation) or advanced obstruction
Hyperactive bowel sounds	Mechanical obstruction (stricture)

Digital Rectal Examination (DRE) [3]

Finding	Significance
Mass or tenderness	Distal sigmoid abscess — the abscess has tracked into the pelvis and is palpable through the rectal wall ^[3]
Blood on glove	Suggests bleeding or mucosal involvement
Bogginess/fullness	Pelvic abscess or collection

Investigations for acute abdomen ^[2]: Bedside tests: urinalysis, pregnancy test. Blood tests: blood count, renal and liver function, amylase, clotting profile, ABG, type and screen. Imaging: erect CXR, erect and supine AXR, USG, CT, contrast studies. Endoscopy: colonoscopy, upper endoscopy ^[2]

High Yield Summary

The diagnosis of acute diverticulitis is clinico-radiological: clinical triad (lower abdominal pain + fever + leucocytosis) confirmed by CT abdomen + pelvis with IV contrast (gold standard).

CT is diagnostic, assesses complications, aids treatment (guides drainage), and is prognostic (Hinchey staging).

Key CT findings: bowel wall thickening > 4 mm, pericolic fat stranding, visible diverticula. Complications: abscess (5 cm cut-off for drainage), fistula (extracolonic air in adjacent organs), obstruction (dilated loops), perforation (free air).

CT distinguishes diverticulitis from CRC: diverticulitis involves > 10 cm, has prominent fat stranding, no enlarged lymph nodes. CRC has short-segment involvement, shouldering, and lymphadenopathy.

Colonoscopy is CONTRAINDICATED acutely (risk of perforation). Colonoscopy at 6–8 weeks post-recovery is mandatory to exclude CRC — malignancy rate in complicated diverticulitis is ~10-17%.

Diverticular bleeding investigation: colonoscopy (first-line) → mesenteric angiography → on-table lavage and colonoscopy → subtotal colectomy if source not found.

Sterile pyuria on urinalysis = adjacent inflammation. Colonic flora on urine culture = colovesical fistula.

Hinchey classification is NOT applicable to right-sided disease.

Active Recall - Diagnosis and Investigations of Diverticular Disease

1. What is the gold standard investigation for acute diverticulitis, and name 4 roles it serves?

Your answer

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CT abdomen and pelvis with IV contrast. Four roles: (1) Diagnostic: confirms diverticulitis. (2) Assesses complications: abscess, fistula, perforation, obstruction. (3) Aids treatment: guides percutaneous drainage of abscess. (4) Prognostic: Hinchey classification staging.

2. Why is colonoscopy contraindicated in acute diverticulitis, and when should it be performed instead?

Your answer

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Contraindicated acutely because: (1) Inflammation is peridiverticular (extraluminal) so colonoscopy is not diagnostically useful. (2) Air insufflation risks converting a sealed microperforation into a free perforation. Colonoscopy should be performed at 6-8 weeks post-resolution to exclude CRC, IBD, and polyps.

3. Name 3 CT features that help distinguish acute diverticulitis from colorectal cancer.

Your answer

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Diverticulitis: (1) Involvement of more than 10 cm of colon (long segment). (2) Prominent pericolic fat stranding. (3) Absence of enlarged pericolonic lymph nodes. Also: visible surrounding diverticula, gradual thickening. CRC: short segment, shouldering sign, lymphadenopathy.

4. Describe the stepwise escalation algorithm for localising the source of diverticular bleeding.

Your answer

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Colonoscopy (first-line, both diagnostic and therapeutic) → mesenteric angiography or CT angiography (if colonoscopy inconclusive, detects bleeding more than 1 mL/min) → on-table lavage with intra-operative colonoscopy → subtotal colectomy with ileostomy if bleeding source still cannot be identified.

5. What does sterile pyuria on urinalysis suggest in a patient with suspected diverticulitis, and what does colonic flora on urine culture indicate?

Your answer

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Sterile pyuria: adjacent sigmoid inflammation irritating the bladder wall, causing WBCs in urine without bacterial infection. Colonic flora on urine culture (e.g. E. coli, Bacteroides): pathognomonic for colovesical fistula - bacteria have gained direct access from colon to urinary tract through the fistulous tract.

6. What is the CT abscess size cut-off that determines whether percutaneous drainage is likely needed, and why?

Your answer

Show mark scheme

5 cm is the cut-off. Abscesses less than 5 cm are likely to resolve with IV antibiotics alone. Abscesses 5 cm or larger are unlikely to resolve with antibiotics alone and typically require image-guided percutaneous drainage.

References

^[1] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf (p3, p4, p8) ^[2] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p12, p18, p19) ^[3] Senior notes: felixlai.md (Diverticular disease section — Diagnosis) ^[4] Senior notes: maxim.md (Diverticular disease section — Investigations) ^[5] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf (p5, p6, p7, p10, p11) ^[7] Lecture slides: GC 186. Lower and diffuse abdominal painfresh blood in stool.pdf (p9)

Management of Diverticular Disease

Management of diverticular disease is entirely dictated by which clinical entity you're dealing with — asymptomatic diverticulosis, uncomplicated diverticulitis, complicated diverticulitis (staged by Hinchey), diverticular bleeding, or chronic complications like fistula and stricture. Let me walk you through each systematically.

1. Overall Management Algorithm

2. Management of Asymptomatic Diverticulosis

Management: Conservative ^[5]

The vast majority (~80%) of people with diverticulosis remain asymptomatic and need no medical or surgical treatment — just risk factor modification to prevent progression.

Intervention	Rationale
High-fibre diet ^[4]	Increases stool bulk → reduces intraluminal pressure (the fundamental pathogenic mechanism) → fewer new diverticula form and existing diverticula are less likely to become symptomatic. Aim for 25–30 g fibre/day
Bulk laxatives (e.g., methylcellulose, psyllium/ispaghula husk) ^[4]	Hydrophilic agents that absorb water and swell → increase stool bulk → reduce colonic segmentation pressures. Unlike stimulant laxatives, these do NOT cause uncontrolled contractions
Weight reduction ^[4]	Obesity increases intra-abdominal pressure and promotes chronic inflammation
Avoid NSAIDs ^[4]	NSAIDs disrupt mucosal barrier (inhibit prostaglandin-mediated mucosal protection) → increase risk of microperforation and diverticular bleeding
Avoid stimulant laxatives ^[4]	Stimulant laxatives (e.g., senna, bisacodyl) cause forceful uncoordinated colonic contractions → increase intraluminal pressure → worsen diverticular disease. This is counterintuitive — patients think "laxatives help" but the wrong type makes things worse
Regular physical activity	Improves colonic motility and transit time, reducing intraluminal pressure

Stimulant vs Bulk Laxatives — Know the Difference

Students commonly recommend "laxatives" generically. In diverticular disease, bulk-forming laxatives (methylcellulose, psyllium) are beneficial but stimulant laxatives (senna, bisacodyl) are harmful because they cause high-pressure uncoordinated contractions. Always specify the type.

3. Management of SUDD

Antispasmodics if colicky pain ^[4]:

Mebeverine or hyoscine butylbromide — direct smooth muscle relaxants that reduce colonic spasm without affecting normal peristalsis
Plus all the conservative measures above (high-fibre diet, bulk laxatives, weight loss)
Some patients benefit from low-dose tricyclic antidepressants for visceral hypersensitivity (similar to IBS management)

4. Management of Uncomplicated Acute Diverticulitis

Treatment: IV antibiotics ^[5]

Colonoscopy at 6–8 weeks to rule out malignancy ^[5]

The goal is to control the infection from the microperforation with antibiotics and rest the bowel to allow healing.

Antibiotic Rationale

The colonic flora involved in diverticulitis include Gram-negative aerobes (e.g., E. coli, Klebsiella) and anaerobes (e.g., Bacteroides fragilis). Antibiotic regimens must therefore cover both Gram-negatives AND anaerobes ^[4].

A. Outpatient Treatment (Mild, Stable Patients)

Who qualifies: immunocompetent, tolerating oral intake, no significant comorbidities, reliable follow-up, no CT evidence of complications (Hinchey 0 — simple diverticulitis without abscess).

Regimen	Duration	Spectrum
Amoxicillin-clavulanate (Augmentin)	7–10 days	Broad-spectrum: GN aerobes + anaerobes (clavulanate = β-lactamase inhibitor extending amoxicillin's spectrum)
Metronidazole + Co-trimoxazole (TMP-SMX)	7–10 days	Metronidazole covers anaerobes; co-trimoxazole covers GN aerobes
Ciprofloxacin (+ metronidazole if needed)	7–10 days	Fluoroquinolone with excellent GN cover; add metronidazole for anaerobic coverage
Moxifloxacin	7–10 days	4th-generation fluoroquinolone with inherent anaerobic coverage (no need to add metronidazole)

^[3]

Evolving Practice — Antibiotics for Uncomplicated Diverticulitis

Recent evidence (AVOD trial 2012, DIABOLO trial 2017) suggests that antibiotics may NOT be necessary for truly uncomplicated diverticulitis in immunocompetent patients without systemic signs. Some guidelines now recommend observation without antibiotics for mild uncomplicated cases. However, for exam purposes, the standard teaching remains antibiotics for 7–10 days unless the examiner specifically asks about latest evidence.

B. Inpatient Treatment (More Severe / Cannot Tolerate PO)

Who qualifies: unable to tolerate oral intake, significant comorbidities, immunocompromised, failed outpatient treatment, or CT shows early complications.

Component	Details	Rationale
Bowel rest (NPO)	Nil by mouth	Reduces colonic motility and intraluminal pressure → allows the microperforation to seal; reduces ongoing bacterial contamination of the pericolic space
IV fluid resuscitation	Isotonic crystalloids (NS, Hartmann's)	Replace losses from reduced oral intake, vomiting, third-space fluid sequestration
IV antibiotics	Piperacillin-tazobactam (Tazocin) OR Metronidazole + Cephalosporin/Fluoroquinolone ^[3]	Piperacillin-tazobactam: ultra-broad spectrum covering GN aerobes, anaerobes, and many Gram-positives. Alternative: metronidazole (anaerobes) + ceftriaxone or ciprofloxacin (GN aerobes)
Analgesia	Paracetamol first-line; avoid opioids if possible	Opioids slow colonic transit → increase intraluminal pressure; but may be needed for severe pain
Monitoring	Clinical: pain, fever, abdominal exam, vitals; Bloods: WCC, CRP trending	Look for improvement within 48–72 hours; failure to improve suggests complication (abscess, perforation)

After resolution: Colonoscopy at 6–8 weeks to rule out malignancy ^[5]

5. Management of Complicated Diverticulitis

Resuscitation with IVF + antibiotics. Percutaneous drainage for abscess. Consider emergency surgery ^[5]

Indications for Emergency Surgery [3][5]

Consider emergency surgery when ^[5]:

Unresponsive to antibiotics
Septic shock (high fever, tachycardia, hypotension, oliguria)
Generalised peritonitis (Hinchey III and IV)

Additional indications ^[3]:

Frank (free) perforation
Colonic obstruction not amenable to conservative management
Abscess failing non-operative intervention (CT-guided drainage)

Management by Hinchey Stage

Hinchey Stage	Management	Rationale
I — Pericolic abscess	IV antibiotics ± CT-guided percutaneous drainage ^[4]^[5]	Small pericolic abscess ( < 5 cm) may resolve with antibiotics alone. Larger abscess ( ≥ 5 cm) requires drainage to achieve source control. CT-guided drainage avoids surgery in many patients
II — Distant abscess (pelvic/retroperitoneal)	IV antibiotics + CT-guided percutaneous drainage ^[4]^[5]	Distant abscess is too large and too far from the primary site to resolve with antibiotics alone; percutaneous drainage achieves source control and may serve as a "bridge" to interval elective surgery
III — Generalised purulent peritonitis	Emergency surgery ^[4]^[5]	Ruptured abscess has contaminated the peritoneal cavity → conservative management will not achieve source control → requires operative washout and resection
IV — Generalised faecal peritonitis	Emergency surgery (Hartmann's procedure) ^[4]^[5]	Free bowel perforation with faecal contamination → highest mortality (50%) → definitive surgical source control is mandatory

When Conservative Management Fails [3][4]

If a patient on IV antibiotics ± drainage does not improve within 48–72 hours (persistent fever, worsening pain, rising WCC/CRP), you must:

Repeat CT to reassess — look for enlarging abscess, new perforation, or missed diagnosis
Escalate to surgery if the source is not controllable non-operatively

6. Surgical Treatment Options

Surgical options ^[5]: Resection, Primary anastomosis, Stoma (Hartmann's), Laparoscopic lavage ^[5]

A. Colonic Resection with Primary Anastomosis (1-Stage Procedure)

Feature	Details
Indication	Hinchey I or II diverticulitis (localised contamination) where the patient can tolerate preoperative bowel preparation and tissues are not too oedematous/inflamed ^[3]
What's done	Resection of the diseased colonic segment including the abscess, with immediate anastomosis (joining the two bowel ends)
Resection margins	Proximal: where colon becomes soft, uninflamed, and non-oedematous. It is NOT necessary to resect all diverticulum-bearing colon since diverticula in the transverse or descending colon rarely cause further symptoms ^[3]. Distal: upper 1/3 of the rectum (because the rectum is NEVER involved in diverticulitis — taeniae coli have fused by that point) ^[3]
Advantage	Single operation; no stoma; better quality of life
Risk	Anastomotic leak — higher risk if performed in contaminated/inflamed field

Resection Margins — A Classic Exam Point

You do NOT need to resect every single diverticulum. The proximal margin is where the colon becomes soft and uninflamed. The distal margin must reach the upper rectum — inadequate distal margin is the most common cause of recurrent diverticulitis after resection ^[4]. This is because the diseased, high-pressure sigmoid colon must be completely removed; leaving even a short stump of sigmoid leads to recurrence.

B. Hartmann's Procedure (2-Stage Procedure)

The MOST commonly performed and preferred approach for emergency surgery ^[3]

Feature	Details
Indication	Hinchey III or IV diverticulitis (diffuse contamination) ^[3]^[4]. Also used when anastomosis is too risky (haemodynamic instability, severe contamination, immunosuppression)
Stage I	Resection of the diseased colonic segment → creation of an end colostomy (proximal limb brought out as a stoma to divert the faecal stream) + creation of a rectal stump (Hartmann's pouch) by oversewing the distal rectum ^[3]
Stage II (reversal, typically 3–6 months later)	Intestinal continuity is re-established by a descending colorectostomy (takedown of colostomy and anastomosis to the rectal stump) ^[3]
Why 2-stage?	Primary anastomosis is contraindicated in Hinchey III-IV because excessive contamination and inflamed/oedematous tissues dramatically increase the risk of anastomotic leak ^[3]^[4] — an anastomotic leak in a septic patient with peritonitis would be catastrophic
Disadvantage	Stoma-related morbidity; reversal of Hartmann's is a technically challenging operation (adhesions, difficult pelvic dissection to find the rectal stump); up to 30-40% of Hartmann's procedures are never reversed

Why is anastomotic leak so dangerous? An anastomotic leak means the joined bowel ends have separated → faecal matter leaks into the peritoneal cavity → peritonitis, sepsis, multi-organ failure. Risk factors for leak include ischaemia, tension, infection, malnutrition, steroids, and performing anastomosis in a contaminated field ^[4]. This is exactly why you DON'T do a primary anastomosis in Hinchey III-IV.

C. Colonic Resection with Primary Anastomosis + Defunctioning Loop Ileostomy (2-Stage Procedure)

Feature	Details
Indication	Hinchey III or IV in stable patients where the bowel is not excessively oedematous ^[3]; OR Hinchey I-II with relative contraindication to primary anastomosis alone
What's done	Resection + primary anastomosis (as in 1-stage) BUT with a proximal defunctioning loop ileostomy to divert the faecal stream away from the anastomosis → protects the anastomosis while it heals
Stage II	Reversal of the loop ileostomy (a technically simpler procedure than reversal of Hartmann's) ^[3]
Advantage over Hartmann's	Maintains bowel continuity from the outset; reversal of loop ileostomy is easier than takedown of a Hartmann's pouch ^[3]
Disadvantage	Only appropriate in stable patients; still requires a second operation

D. Laparoscopic Lavage

Laparoscopic lavage — feasible ^[5]

Feature	Details
Indication	Hinchey III (purulent peritonitis) — the bowel wall itself is intact (no free faecal perforation) ^[3]^[5]
What's done	Laparoscopic washout of the peritoneal cavity with warm saline + placement of drains. The diseased bowel segment is NOT resected
Rationale	In Hinchey III, the peritonitis is from a ruptured abscess (pus), not a free bowel perforation. The bowel wall is intact. So theoretically, washing out the pus and giving antibiotics may be sufficient without the morbidity of resection + stoma
Advantage	Avoids bowel resection and stoma; faster recovery; lower morbidity
Controversy	This approach remains controversial and requires additional prospective trials before formal recommendations ^[3]. The SCANDIV and LOLA trials showed higher re-intervention rates with lavage compared to resection. Current consensus: may be considered in selected cases (Hinchey III, stable patient) but NOT standard of care
Contraindication	Hinchey IV (faecal peritonitis) — you CANNOT just wash out faecal contamination without resecting the perforated bowel

7. Elective (Interval) Colectomy

Interval colectomy — this is a planned sigmoid colectomy with primary anastomosis performed after resolution of the acute episode (typically 6–12 weeks later) ^[5].

Indications for Elective Interval Colectomy [3][5]

Indication	Rationale
Previous complicated diverticulitis	History of abscess, perforation, fistula, or obstruction indicates high-risk anatomy prone to recurrence and further complications ^[3]^[5]
Immunocompromised patients	Impaired immune response means complications are harder to manage conservatively; lower threshold for surgery. These patients may not mount the usual inflammatory "walling-off" response → higher risk of free perforation
Inability to exclude malignancy	If colonoscopy post-recovery cannot definitively exclude CRC (e.g., stricture preventing passage of scope, persistent mass), resection serves both therapeutic and diagnostic purposes ^[3]
Patients with complicated disease, aged > 50, female, the privately insured, and those at teaching hospitals ^[5]	Epidemiological data showing these groups are more likely to undergo and benefit from interval colectomy
Chronic fistula	Colovesical or colovaginal fistula will not close spontaneously — requires surgical resection
Chronic stricture causing obstruction	Fibrotic stricture will not resolve with antibiotics — needs resection

What Is NO LONGER an Indication [3][5]

Recurrent episodes of uncomplicated diverticulitis — this is NO LONGER an automatic indication for surgery ^[3]

"Outcomes of > 2 episodes of attacks are not worse" ^[5]

"85% do not recur after initial medical treatment" ^[5]

Old teaching: after 2 episodes of uncomplicated diverticulitis, patients should undergo elective colectomy (the "2-strike rule") because it was believed the risk of complications increased with each recurrence
Current evidence: this has been disproven. The risk of complications does NOT significantly increase with recurrent uncomplicated episodes. Most patients (85%) will not have a recurrence after successful medical treatment of their first episode ^[3]^[5]
Current practice: decision for surgery is based on the severity of episodes and patient factors (complications, immunosuppression, inability to exclude malignancy), NOT simply the number of episodes

Recurrence rate: 10–30% in the first decade after initial attack ^[5]

Elective interval colectomy: not related to recurrence episodes ^[5]

The 2-Strike Rule Is Dead

This is a very commonly tested concept. The old "2 attacks = surgery" rule is outdated. Modern guidelines (AGA 2015, ASCRS 2020) recommend surgery based on disease severity and patient factors, not simply the number of episodes. Know this for your exam — it's a favourite trap question.

Surgical Technique for Elective Colectomy

Sigmoid colectomy with primary anastomosis (1-stage procedure)
Can be performed laparoscopically (preferred — less morbidity, faster recovery, fewer adhesions)
Same resection margin principles: proximal = soft uninflamed colon; distal = upper rectum
No stoma needed (bowel is not inflamed/contaminated at the time of elective surgery)

8. Management of Specific Complications

A. Abscess

Size / Response	Management
Small ( < 5 cm)	IV antibiotics alone — likely to resolve ^[4]
Large ( ≥ 5 cm)	CT-guided percutaneous drainage + IV antibiotics ^[4]^[5]
Failed drainage / persistent sepsis	Emergency surgery (resection ± stoma) ^[3]^[5]

Why CT-guided drainage works: inserting a drain directly into the abscess cavity under CT guidance achieves source control — the pus is evacuated, the bacterial load is dramatically reduced, and antibiotics can then sterilise the residual infection. This often converts what would have been an emergency operation into a controlled situation amenable to interval elective surgery.

B. Fistula [3][4]

Colovesical fistula (most common): Resection of affected colon + omental pedicle interposition between bowel and bladder (to prevent recurrent fistulation) + synchronous repair of bladder (primary closure) ^[4]
Colovaginal fistula: resection of affected colon + primary closure or repair of vaginal defect
Coloenteric / colocutaneous fistula: resection of affected colon ± repair of secondary organ
Management principle: control sepsis first (antibiotics, drainage), then definitive surgery — resection of the fistula-bearing colon with repair of the secondarily involved organ ^[3]

Fistula is usually managed at the index operation with resection of the affected segment of colon ^[3]

C. Obstruction

Type	Mechanism	Management
Partial obstruction (acute)	Pericolonic inflammation/oedema or compression by abscess → luminal narrowing	Conservative: bowel rest, IV fluids, NG decompression, IV antibiotics → usually resolves with resolution of inflammation
Complete obstruction (chronic)	Recurrent diverticulitis → progressive fibrosis → stricture	May require endoscopic stenting as a bridge to surgery, or direct surgical resection. Hartmann's in emergency; primary anastomosis with on-table lavage if stable
SBO from adhesion	Small bowel adheres to inflamed sigmoid colon	Standard SBO management: drip and suck → surgical adhesiolysis if not resolving

D. Perforation with Peritonitis [3][4][5]

Emergency surgery — the management depends on Hinchey stage:

Hinchey III: Hartmann's procedure OR primary anastomosis with defunctioning stoma OR laparoscopic lavage (in selected cases)
Hinchey IV: Hartmann's procedure with on-table peritoneal lavage ^[4]

9. Management of Diverticular Bleeding

Common cause of severe GI bleeding. Intermittent bleeding. 80% self-limiting ^[1]^[5]

Step 1: Resuscitation [3]

Action	Details
IV access	Two large-bore (16G or 14G) peripheral cannulae
IV fluids	Rapid bolus of isotonic crystalloid (NS or Hartmann's)
Blood transfusion	Transfuse if Hb < 7 g/dL (low-risk) or < 9 g/dL (high-risk, e.g., elderly, IHD) ^[3]
Cross-match	Group and save; cross-match 4–6 units packed RBCs
Correct coagulopathy	FFP for coagulopathy; platelets if thrombocytopaenic; withhold anticoagulants/antiplatelets (weigh against thrombotic risk) ^[3]
Monitoring	Vital signs, urine output, cardiac monitoring

Step 2: Localisation and Haemostasis — Stepwise Escalation

Investigation: Colonoscopy. Management: Conservative → Endoscopic haemostasis → Angiogram ± embolisation ^[5]

Step	Modality	Details
1st line	Conservative ^[5]	50% of diverticular bleeding stops spontaneously ^[4]. Observe with ongoing resuscitation
2nd line	Colonoscopy with endoscopic haemostasis ^[5]	Identify the bleeding diverticulum and achieve haemostasis: adrenaline injection (1:10,000) (vasoconstriction — NOT used alone) + metallic clips or band ligation (mechanical compression of the bleeding vessel) ^[3]^[4]
3rd line	Mesenteric angiography ± embolisation ^[5]	When colonoscopy fails to localise or control bleeding. Selective catheterisation of the bleeding artery → superselective embolisation (coils, gelfoam). Detects bleeding > 1 mL/min ^[3]
4th line	On-table lavage with intraoperative colonoscopy	Bowel lavage through a caecostomy/appendicostomy during laparotomy → colonoscopy to identify bleeding source intraoperatively ^[4]
Last resort	Subtotal colectomy + ileostomy ^[4]	When the bleeding source cannot be identified despite all the above. Removing the entire colon eliminates the source regardless of location. Significant morbidity — reserved as a life-saving measure

Localisation of bleeding: colonoscopy → angiography → on-table lavage and colonoscopy → subtotal colectomy and ileostomy ^[4]

Indications for Emergency Laparotomy in Diverticular Bleeding [3]

Indication	Rationale
Haemodynamically unstable despite adequate resuscitation	Ongoing arterial haemorrhage exceeding the body's compensatory capacity
Excessive blood transfusion > 6 units	Massive transfusion carries its own complications (hypothermia, coagulopathy, hyperkalaemia, citrate toxicity) — continued bleeding requiring this much blood warrants definitive surgical control
Frequent rebleeding or persistent bleeding	Endoscopic/angiographic measures have failed to achieve durable haemostasis

10. Management of Right-Sided Diverticulitis (Hong Kong Relevance)

Right-sided (caecal) diverticulitis deserves special mention because it is more common in Asian populations and is managed differently:

Feature	Approach
Uncomplicated right-sided diverticulitis	Conservative management with IV antibiotics (same principles as left-sided)
Complicated / recurrent right-sided diverticulitis	Right hemicolectomy (NOT Hartmann's — Hinchey classification does not apply to right-sided disease)
Diagnostic challenge	CT abdomen to distinguish from acute appendicitis (see DDx section)

11. Summary Table: Management by Clinical Scenario

Scenario	Management
Asymptomatic diverticulosis	Conservative: high-fibre diet, bulk laxatives, weight reduction. Avoid NSAIDs and stimulant laxatives
SUDD	Conservative + antispasmodics for colicky pain
Uncomplicated diverticulitis (outpatient)	PO antibiotics 7–10 days (Augmentin, or metronidazole + co-trimoxazole/ciprofloxacin, or moxifloxacin)
Uncomplicated diverticulitis (inpatient)	IV antibiotics (pip-taz OR metronidazole + cephalosporin/fluoroquinolone) + bowel rest
Hinchey I	IV antibiotics ± CT-guided drainage
Hinchey II	IV antibiotics + CT-guided percutaneous drainage
Hinchey III	Emergency surgery: Hartmann's / primary anastomosis + defunctioning stoma / laparoscopic lavage
Hinchey IV	Emergency surgery: Hartmann's procedure
Diverticular bleeding	Resuscitate → conservative (50% self-limiting) → colonoscopy (endoscopic haemostasis) → angiography ± embolisation → surgery
Fistula	Elective resection of affected colon + repair of secondary organ
Stricture/obstruction	Elective resection if chronic; emergency surgery if acute complete obstruction
Interval colectomy	For complicated diverticulitis history, immunocompromised, inability to exclude malignancy. NOT for recurrent uncomplicated episodes

High Yield Summary

Asymptomatic diverticulosis: conservative only — high-fibre diet, bulk laxatives (NOT stimulant laxatives), avoid NSAIDs, weight loss.

Uncomplicated diverticulitis: antibiotics covering GN aerobes + anaerobes (outpatient: Augmentin or metronidazole + ciprofloxacin; inpatient: piperacillin-tazobactam or metronidazole + cephalosporin). Colonoscopy at 6–8 weeks to exclude CRC.

Complicated diverticulitis by Hinchey stage: I–II = IV antibiotics + CT-guided drainage; III–IV = emergency surgery. Hartmann's procedure is the most commonly performed emergency operation (2-stage: resection + end colostomy → later reversal).

Primary anastomosis is contraindicated in Hinchey III–IV due to risk of anastomotic leak in the contaminated/inflamed field.

Laparoscopic lavage is feasible for Hinchey III but remains controversial.

Inadequate distal resection margin is the MC cause of recurrent diverticulitis post-surgery — always resect down to the upper rectum.

The "2-strike rule" is dead: recurrent uncomplicated diverticulitis alone is NOT an indication for surgery. 85% do not recur after initial medical treatment.

Diverticular bleeding: 80% self-limiting. Stepwise escalation: conservative → colonoscopy (clips/adrenaline) → angiography ± embolisation → on-table lavage → subtotal colectomy if source unidentifiable.

Indications for emergency surgery: free perforation, failed antibiotics, septic shock, generalised peritonitis (Hinchey III–IV), obstruction, abscess failing drainage. Indications for laparotomy in bleeding: haemodynamic instability despite resuscitation, > 6 units transfused, persistent/recurrent bleeding.

Active Recall - Management of Diverticular Disease

1. Why is primary anastomosis contraindicated in Hinchey III and IV diverticulitis, and what procedure is preferred instead?

Your answer

Show mark scheme

Primary anastomosis is contraindicated because excessive peritoneal contamination and inflammation of surrounding tissues dramatically increase the risk of anastomotic leak. Hartmann's procedure is preferred: resection of diseased segment, creation of end colostomy, and closure of rectal stump. Reversal performed later when inflammation has settled.

2. A patient with known diverticulosis presents with 3 episodes of uncomplicated diverticulitis over 5 years, each successfully treated with antibiotics. Should you recommend elective colectomy? Explain your reasoning.

Your answer

Show mark scheme

No. Recurrent uncomplicated diverticulitis is NO LONGER an indication for elective surgery (the 2-strike rule is outdated). Evidence shows that outcomes after more than 2 episodes are not worse, and 85% do not recur after initial medical treatment. Surgery should be based on disease severity and patient factors (complicated disease, immunosuppression, inability to exclude malignancy), not number of episodes.

3. Describe the stepwise escalation algorithm for managing diverticular bleeding that fails to stop spontaneously.

Your answer

Show mark scheme

Step 1: Colonoscopy with endoscopic haemostasis (adrenaline injection + metallic clips). Step 2: If colonoscopy fails, mesenteric angiography with selective embolisation. Step 3: On-table lavage with intraoperative colonoscopy to localise the source. Step 4: If source still unidentifiable, subtotal colectomy with ileostomy.

4. What is the most common cause of recurrent diverticulitis after surgical resection, and how is it prevented?

Your answer

Show mark scheme

Inadequate distal resection margin is the MC cause. The distal margin must extend to the upper third of the rectum, as the rectum is never affected by diverticular disease (taeniae coli have fused). Leaving a sigmoid stump preserves the high-pressure zone prone to recurrence.

5. Name 4 valid indications for elective interval colectomy in diverticular disease.

Your answer

Show mark scheme

1. Previous complicated diverticulitis (abscess, perforation, fistula). 2. Immunocompromised patients (lower threshold due to impaired ability to wall off perforation). 3. Inability to exclude malignancy on colonoscopy. 4. Chronic fistula (e.g. colovesical fistula) or chronic stricture causing obstruction.

6. Why should stimulant laxatives be avoided but bulk-forming laxatives are recommended in diverticular disease?

Your answer

Show mark scheme

Stimulant laxatives (e.g. senna, bisacodyl) cause forceful uncoordinated colonic contractions that increase intraluminal pressure, worsening diverticular disease. Bulk-forming laxatives (e.g. methylcellulose, psyllium) absorb water and increase stool bulk, reducing the need for high-pressure segmental contractions and thus lowering intraluminal pressure.

References

^[1] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf (p8) ^[2] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p19) ^[3] Senior notes: felixlai.md (Diverticular disease section — Treatment) ^[4] Senior notes: maxim.md (Diverticular disease section — Management) ^[5] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf (p6, p7, p10, p13, p14, p16)

Complications of Diverticular Disease

Understanding complications requires thinking about what happens when a microperforation in the colon wall goes wrong in different ways. Every complication traces back to the same fundamental event — a faecolith obstructs a diverticulum → bacterial overgrowth → mucosal erosion → microperforation — but the downstream consequences differ based on whether the perforation is walled off, tracks to an adjacent organ, causes luminal compromise, or ruptures freely into the peritoneum.

1. Abscess

Incidence and Pathophysiology

Occurs in ~17% of patients with acute diverticulitis ^[3]
When a diverticulum microperforates, the body's initial response is to wall off the contamination. The pericolic mesentery, omentum, and fat wrap around the perforation site → creating a phlegmon (inflamed mass) ^[3]
If the bacterial load overwhelms local defences, the phlegmon liquefies at its centre → a walled-off collection of pus forms = abscess
The abscess may remain localised (pericolic, Hinchey I) or track to distant sites:
- Pelvic abscess (Hinchey II) — pus gravitates into the pelvis (the most dependent peritoneal space)
- Psoas abscess — pus tracks along the psoas muscle retroperitoneally (the sigmoid colon lies directly anterior to the left psoas)
- Pyogenic liver abscess — spread of infection through the portal circulation (mesenteric veins drain to the portal vein → liver) ^[3]. This is a rare but serious complication

Clinical Features

Should be suspected in patients with no improvement in abdominal pain or a persistent fever despite 3 days of antibiotic treatment ^[3]
Swinging pyrexia (temperature spikes with intermittent defervescence — classic pattern of undrained abscess)
Persistent fever and abdominal pain despite antibiotics ± tender mass on PR (pelvic abscess palpable on digital rectal examination) ^[4]
Rising WCC and CRP despite treatment
May present as a palpable tender abdominal mass (phlegmon or large abscess)

Why 3 Days?

This is a practical clinical rule. Appropriately treated uncomplicated diverticulitis should show clinical improvement within 48–72 hours of IV antibiotics (trending down of fever, reducing pain, falling WCC). If there is no improvement by day 3, the antibiotic is either not penetrating the source (suggesting a walled-off collection that needs drainage) or there is a more serious complication.

Investigation

CT abdomen + pelvis with IV contrast — demonstrates abscess as a fluid collection with surrounding inflammatory changes containing air, air-fluid levels, or low-attenuation necrotic debris ^[3]^[4]
Abscess size 5 cm is the cut-off: < 5 cm likely resolves with antibiotics alone; ≥ 5 cm requires CT-guided percutaneous drainage ^[4]

Management

Abscess Size / Response	Management
Small ( < 5 cm)	IV antibiotics alone — high likelihood of resolution
Large ( ≥ 5 cm)	CT-guided percutaneous drainage + IV antibiotics ^[4]^[5]
Failed drainage / persistent sepsis	Emergency surgery — resection (Hartmann's or primary anastomosis + defunctioning stoma) ^[3]^[5]

2. Fistula

Pathophysiology

Inflammation from diverticulitis causes the inflamed sigmoid colon to adhere to an adjacent organ (bladder, vagina, small bowel, skin, uterus)
The inflammatory process erodes through both the colonic wall and the wall of the adjacent organ → creating an abnormal communication (fistula = Latin fistula = "pipe" or "tube")
Fistulae typically develop from a contained microperforation or small abscess that decompresses into the neighbouring structure rather than freely into the peritoneum

Types of Fistula (Ranked by Frequency)

Type	Frequency	Why?	Clinical Features
Colovesical fistula	Most common ^[3]^[4]	The sigmoid colon lies directly on the dome of the bladder — anatomical proximity. More common in males because in females the uterus interposes between sigmoid and bladder	Recurrent dysuria, pneumaturia (air bubbles in urine — pathognomonic), faecaluria (faecal particles in urine), recurrent polymicrobial UTIs ^[4]. Urine culture grows colonic flora (e.g., E. coli, Bacteroides) — essentially diagnostic ^[3]
Colovaginal fistula	Second most common ^[3]	Especially in post-hysterectomy patients — removal of the uterus eliminates the anatomical barrier between sigmoid and vagina ^[3]	Vaginal passage of faeces and flatus, foul-smelling vaginal discharge, recurrent vaginal infections
Coloenteric fistula	Uncommon ^[3]	Inflamed sigmoid adheres to adjacent small bowel loop	May be entirely asymptomatic or result in corrosive diarrhoea ^[3] — small bowel contents are diverted, and colonic bacteria contaminate the small bowel (bacterial overgrowth → malabsorption → diarrhoea)
Colocutaneous fistula	Uncommon ^[3]	Abscess tracks through the abdominal wall to the skin surface	Usually easy to identify — visible external opening with faecal discharge ^[3]

Investigation

CT colonography with water-soluble rectal contrast — contrast injected rectally is seen tracking into the bladder/vagina/skin ^[4]
Cystoscopy — for colovesical fistula: may show bullous oedema, erythema, or the fistula opening on the bladder dome
Urine culture — growth of mixed colonic flora (multiple Gram-negatives + anaerobes) is essentially pathognomonic for colovesical fistula ^[3]
Contrast enema — can delineate the fistula tract ^[3]

Management [3][4]

The management principle is: control sepsis first → then definitive surgical repair

Control sepsis: IV antibiotics + drainage of any associated abscess
Definitive surgery (usually elective):
- Resection of the affected segment of colon involved with diverticulitis, usually with a primary anastomosis ^[3]
- Simple repair of the secondarily involved organ — e.g., primary closure of bladder or vagina (may require flap depending on complexity) ^[3]
- Colovesical fistula: resection of affected colon + omental pedicle interposition between bowel and bladder (to prevent recurrent fistulation) + synchronous repair of bladder ^[4]

Fistula is usually managed at the index operation with resection of the affected segment of colon ^[3]

Omental Pedicle Interposition — Why?

After resecting the fistula-bearing colon and repairing the bladder, you place a pedicled flap of omentum between the bowel anastomosis and the bladder repair. The omentum is highly vascularised and has excellent healing properties — it physically separates the two suture lines and reduces the risk of the fistula recurring. The omentum is sometimes called the "policeman of the abdomen" because it migrates to sites of inflammation and promotes healing.

3. Obstruction

Pathophysiology

There are three distinct mechanisms by which diverticular disease causes intestinal obstruction ^[3]:

Mechanism	Type	Pathophysiology
Acute pericolonic inflammation/oedema	Partial LBO (acute)	Active diverticulitis causes significant pericolic inflammation → the bowel wall becomes oedematous and thickened → relative luminal narrowing. Alternatively, a large pericolic abscess may externally compress the lumen ^[3]
Chronic fibrosis and stricture	Complete LBO (chronic)	Recurrent attacks of acute diverticulitis result in progressive fibrosis and scarring leading to formation of intestinal strictures ^[3]. Each episode deposits more collagen → progressive narrowing → eventually complete obstruction
Adhesions to inflamed bowel	SBO	Inflamed sigmoid colon causes adjacent small bowel loops to adhere to it → kinking or compression of the small bowel → SBO ^[4]
Paralytic ileus	Functional obstruction	Localised peritoneal irritation from pericolic inflammation → reflex sympathetic inhibition of peristalsis → functional obstruction without mechanical cause ^[3]

Intestinal obstruction: LBO due to fibrosis and stricture, SBO due to adhesion to inflamed bowel ^[4]

Clinical Features

Cardinal features of intestinal obstruction (the "4 C's" — colicky pain, constipation, vomiting, and distension):
- Colicky abdominal pain — intermittent cramping as the bowel contracts against the obstruction
- Abdominal distension — proximal bowel dilates with gas and fluid
- Vomiting — initially bilious, late becomes faeculent in LBO
- Absolute constipation (obstipation) — no passage of flatus or stool
Bowel sounds: hyperactive/tinkling (mechanical obstruction) → later absent (ileus or late obstruction with bowel fatigue)

Investigation

AXR: dilated bowel loops with air-fluid levels; in LBO look for dilated colon with no gas in the rectum ^[4]
CT abdomen: identifies the transition point, distinguishes mechanical obstruction from pseudo-obstruction, evaluates for ischaemia

Management

Acute partial obstruction (from inflammation): usually resolves with conservative management (bowel rest, IV fluids, NG decompression, IV antibiotics to treat underlying diverticulitis)
Complete obstruction from stricture: may require endoscopic stenting as a bridge to surgery or direct surgical resection
Emergency: Hartmann's procedure if acute complete LBO with ischaemia/perforation signs
Elective: sigmoid colectomy with primary anastomosis after resolution of acute episode — remove the strictured segment

4. Perforation and Peritonitis

Pathophysiology

Two mechanisms of free perforation ^[3]:

Rupture of a diverticular abscess into the peritoneal cavity → the walled-off collection bursts → purulent peritonitis (Hinchey III)
Rupture of an inflamed diverticulum with faecal contamination of the peritoneum → faecal peritonitis (Hinchey IV) — this is the most catastrophic outcome

Leads to generalised purulent or faecal peritonitis ^[3]

Clinical Features

Severity ranges from diverticulitis to localised diverticular abscess to purulent peritonitis to faecal peritonitis ^[5]

Feature	Pathophysiological Basis
Sudden severe abdominal pain	Peritoneal soiling → intense irritation of the parietal peritoneum → somatic pain (sharp, well-localised initially, then generalised)
Fever, tenderness and guarding ^[2]	Systemic inflammatory response to intraperitoneal contamination; reflex abdominal wall muscle contraction (guarding) to protect the inflamed peritoneum
Board-like rigidity	Severe generalised peritonitis → diffuse reflex contraction of all abdominal wall muscles → the abdomen becomes "hard as a board"
Rebound tenderness	Sudden release of pressure stretches the inflamed parietal peritoneum → sharp pain
Absent bowel sounds	Generalised peritoneal inflammation → complete cessation of peristalsis (generalised paralytic ileus)
Septic shock: high fever, tachycardia, hypotension, oliguria ^[5]	Massive systemic inflammatory response → vasodilation (↓SVR), capillary leak, third-spacing → distributive shock → impaired organ perfusion (oliguria = acute kidney injury, altered mental state = cerebral hypoperfusion)
Pneumoperitoneum on CXR	Free intraperitoneal air from bowel perforation

Mortality — Hinchey Classification

Hinchey Stage	Type of Peritonitis	Mortality
III	Generalised purulent peritonitis (ruptured abscess, bowel wall intact)	25% ^[4]
IV	Generalised faecal peritonitis (bowel wall perforation)	50% ^[4]

Management

Resuscitation with IVF + antibiotics. Percutaneous drainage for abscess. Consider emergency surgery ^[5]

Unresponsive to antibiotics, septic shock, generalised peritonitis (III and IV) → emergency surgery ^[5]

Resuscitation: IV access, crystalloid fluid boluses, broad-spectrum IV antibiotics (piperacillin-tazobactam or metronidazole + cephalosporin), oxygen, urinary catheter, arterial line/central venous access if shocked
Emergency surgery: Hartmann's procedure (resection + end colostomy + rectal stump closure) is the standard for Hinchey III–IV ^[4]^[5]. Primary anastomosis is contraindicated in the setting of diffuse contamination and inflammation due to high risk of anastomotic leak ^[4]
On-table peritoneal lavage: copious warm saline irrigation of the peritoneal cavity to reduce bacterial load

5. Diverticular Bleeding

Pathophysiology (Recap)

When a diverticulum herniates, the vasa recta is draped over the dome → blood vessel is separated from the bowel lumen only by mucosa → eccentric intimal thickening and medial thinning → segmental arterial weakness → rupture into bowel lumen ^[3]
Right colon is usually the source because right-sided diverticula have wider necks/domes and the colonic wall is thinner → more vasa recta length exposed to injury ^[3]
Bleeding occurs in the ABSENCE of diverticulitis — the two processes are separate (inflammation causes fibrosis of vasa recta, which paradoxically protects against bleeding) ^[3]

Clinical Features

Common cause of severe GI bleeding ^[1]
Intermittent bleeding ^[1]
Painless massive PR bleeding — haematochezia (bright red to maroon blood per rectum)
80% self-limiting ^[1] — arterial spasm and clot formation at the rupture site
Rebleeding rate ~20–30% ^[7]
Can cause haemodynamic instability if blood loss is massive (tachycardia, hypotension, pallor, altered consciousness)

Management

Conservative → Endoscopic haemostasis → Angiogram ± embolisation ^[1]^[5]

Resuscitation: IV access, crystalloids, blood transfusion, correct coagulopathy
50% of bleeding stops spontaneously ^[4] → conservative observation with ongoing monitoring
Colonoscopy: endoscopic haemostasis with adrenaline injection + metallic clips ^[3]^[4]^[5]
Mesenteric angiography ± embolisation: when colonoscopy fails ^[3]
On-table lavage + intraoperative colonoscopy: when angiography fails
Subtotal colectomy + ileostomy: last resort when the bleeding source cannot be identified ^[4]

Indications for Emergency Surgery in Diverticular Bleeding [3]

Indication	Rationale
Haemodynamically unstable despite adequate resuscitation	Ongoing arterial haemorrhage exceeding compensatory capacity
Excessive blood transfusion > 6 units	Massive transfusion carries its own risks (hypothermia, coagulopathy, hyperkalaemia)
Frequent rebleeding or persistent bleeding	Endoscopic/angiographic measures have failed

6. Complications of Surgical Treatment

When patients undergo surgery for diverticular disease (whether emergency Hartmann's or elective sigmoid colectomy), they face procedure-specific complications:

A. Anastomotic Complications (If Primary Anastomosis Performed)

Complication	Timing	Features	Management
Anastomotic bleeding	Early ( < 30 days)	PR bleeding, dropping Hb	Blood transfusion, correct coagulopathy; rarely requires re-operation
Anastomotic leak	Early ( < 30 days, typically day 5–7)	Suspect if any deviation from normal post-op course: pain, fever, tachycardia, prolonged ileus, feculent/purulent drainage ^[4]	Fluid resuscitation, broad-spectrum IV antibiotics, NPO. Minor leak: CT-guided percutaneous drainage. Major leak: re-laparotomy → takedown of anastomosis + proximal diversion stoma ^[4]
Anastomotic stricture	Late ( > 30 days)	Progressive narrowing → constipation, obstructive symptoms	Majority do not require intervention. If symptomatic: endoscopic balloon dilatation ^[3]

Inadequate distal margin is the MC cause of recurrent diverticulitis after resection ^[4] — if you leave any sigmoid colon behind (rather than anastomosing to the upper rectum), the residual high-pressure sigmoid will develop recurrent diverticulitis

B. Stoma Complications (If Hartmann's or Defunctioning Stoma)

Timing	Complication	Mechanism
Early ( < 30 days)	Stomal bleeding	Mucocutaneous junction trauma or mesenteric vessel injury
	Stomal necrosis	Ischaemia of the exteriorised bowel from inadequate blood supply or excessive tension on the mesentery
	Stomal retraction	Tension on the mesentery pulls the stoma below skin level → poor appliance fitting → faecal leak and skin excoriation
	Mucocutaneous separation	Separation of the bowel from the surrounding skin sutures → peristomal wound
	Skin irritation/dermatitis	Effluent contact dermatitis — worse with ileostomy (high-output, alkaline enzymatic effluent) than colostomy
Late ( > 30 days)	Parastomal hernia	Weakness of the abdominal wall around the stoma site → peritoneal sac + bowel herniates through the defect. Risk factors: end stoma, emergency surgery, obesity
	Stomal prolapse	Intussusception of bowel through the stoma → visible protrusion. MC in loop transverse colostomy. Risk of ischaemia/necrosis
	Stomal stenosis	Scarring and fibrosis at the mucocutaneous junction → narrowing of the stoma opening → obstructive symptoms

C. Hartmann's Procedure-Specific Complications [4]

Complication	Explanation
Rectal stump leak	The oversewn rectal stump may dehisce → pelvic abscess/sepsis. This is why some surgeons bring the distal end out as a mucous fistula rather than closing it intra-abdominally (particularly if the tissues are severely inflamed)
Rectal stump abscess	Infected haematoma or seroma at the closed rectal stump
Ureteric injury	The left ureter runs very close to the sigmoid colon mesentery → at risk during dissection, especially in emergency surgery with distorted anatomy
Non-reversal	Up to 30–40% of Hartmann's procedures are never reversed — due to patient comorbidities, adhesions, or patient preference. The patient lives with a permanent end colostomy

7. Segmental Colitis Associated with Diverticula (SCAD)

While not strictly a "complication" of diverticulitis, SCAD is an important entity that can complicate the clinical picture:

Pathophysiology: Chronic mucosal inflammation in the interdiverticular mucosa (between diverticula) — the diverticular orifices themselves are spared
Why it occurs: Likely related to mucosal prolapse, altered microbiome, and chronic low-grade inflammation in diverticular segments; possibly a form of localised IBD
Clinical features: Chronic bloody diarrhoea, LLQ pain — can mimic IBD
Diagnosis: Colonoscopy with biopsy shows mucosal inflammation between diverticula with sparing of diverticular orifices
Management: 5-ASA (mesalazine) ± topical steroids; rarely requires surgery. Usually self-limiting

8. Long-Term Complications and Prognosis

Outcome	Data
Recurrence after initial medical treatment	85% do NOT recur ^[5]
Recurrence rate	10–30% in the first decade after initial attack ^[5]
Outcomes of > 2 episodes	Not worse than single episode ^[5] — this is why the "2-strike rule" for surgery is obsolete
Risk of complicated disease on recurrence	Patients who present with uncomplicated diverticulitis on their first episode tend to present with uncomplicated disease on recurrence (the disease pattern is established early)
Mortality by Hinchey stage	I = 0%, II = 5%, III = 25%, IV = 50% ^[4]

Summary Table: Complications at a Glance

Complication	Incidence / Frequency	Key Clinical Clue	Key Investigation	Management
Abscess	~17% of acute diverticulitis	Persistent fever/pain despite 3 days antibiotics; tender mass on PR	CT: fluid collection with inflammatory surround	IV Abx ± CT-guided drainage; surgery if fails
Fistula (MC: colovesical)	Most common in males	Pneumaturia, faecaluria, recurrent UTI	CT colonography; urine culture (colonic flora)	Elective resection + repair of secondary organ + omental interposition
Obstruction	Variable	Colicky pain, distension, vomiting, constipation	CT: transition point, dilated proximal bowel	Conservative if acute/partial; surgery if complete or chronic stricture
Perforation / Peritonitis	Hinchey III–IV	Acute abdomen, rigidity, absent bowel sounds, septic shock	CXR: pneumoperitoneum; CT: free air/fluid	Emergency surgery (Hartmann's)
Diverticular Bleeding	~15–55% of LGIB	Painless massive PR bleed, 80% self-limiting	Colonoscopy, angiography, Tc-RBC scan	Conservative → endoscopic → angiographic → surgical
Recurrence	10–30% in first decade	Recurrent LLQ/RLQ pain with fever	CT	Same as initial episode; surgery only for complicated disease

High Yield Summary

Abscess (17% of diverticulitis): suspect if no improvement after 3 days antibiotics. May cause pyogenic liver abscess via portal circulation. CT-guided drainage if ≥ 5 cm.

Fistula: MC = colovesical (pneumaturia, faecaluria, recurrent UTI) — more common in males. Colovaginal is second (especially post-hysterectomy). Management: resection of affected colon + repair of secondary organ + omental pedicle interposition.

Obstruction: LBO from chronic fibrotic stricture (recurrent diverticulitis → progressive fibrosis); SBO from adhesion to inflamed bowel; paralytic ileus from peritoneal irritation.

Perforation/Peritonitis: Hinchey III (purulent, abscess rupture, bowel intact) = 25% mortality; Hinchey IV (faecal, bowel wall perforation) = 50% mortality. Emergency Hartmann's procedure.

Diverticular bleeding: commonest cause of severe LGIB. Painless, arterial (vasa recta rupture), 80% self-limiting. Right colon is the usual source. Stepwise: conservative → colonoscopy → angiography → surgery.

Recurrence: 85% do not recur after initial medical treatment. 10–30% recurrence in the first decade. Outcomes after > 2 episodes are NOT worse — the "2-strike rule" is dead.

Inadequate distal resection margin is the MC cause of recurrent diverticulitis after surgery — always resect to the upper rectum.

Surgical complications: anastomotic leak (day 5–7, suspect if any post-op deviation), stoma complications (early: necrosis, retraction; late: parastomal hernia, prolapse), Hartmann's-specific (rectal stump leak, ureteric injury, 30–40% non-reversal rate).

Active Recall - Complications of Diverticular Disease

1. A patient with acute diverticulitis has persistent fever and abdominal pain despite 3 days of IV antibiotics. What complication should you suspect, and what is your next step?

Your answer

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Suspect diverticular abscess (occurs in 17% of acute diverticulitis). Next step: CT abdomen and pelvis with IV contrast to confirm abscess and assess size. If abscess is 5 cm or larger, proceed to CT-guided percutaneous drainage. If less than 5 cm, may resolve with antibiotics alone. If drainage fails, proceed to emergency surgery.

2. Explain why colovesical fistula is the most common type of fistula in diverticular disease, and why it is more common in males than females.

Your answer

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The sigmoid colon lies directly on the dome of the bladder, so inflammatory erosion most commonly tracks into the bladder. It is more common in males because in females, the uterus interposes between the sigmoid colon and bladder, acting as an anatomical barrier. Colovaginal fistula becomes the more common fistula in post-hysterectomy females because the uterine barrier has been removed.

3. Describe the two mechanisms by which diverticular disease causes free perforation and peritonitis, and state the corresponding Hinchey stages.

Your answer

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1. Rupture of a diverticular abscess into the peritoneal cavity, releasing purulent material (Hinchey III, 25% mortality). 2. Rupture of an inflamed diverticulum with direct faecal contamination of the peritoneum (Hinchey IV, 50% mortality). Hinchey III: bowel wall is intact but abscess has burst. Hinchey IV: bowel wall has perforated.

4. Why does diverticular bleeding typically occur in the absence of diverticulitis, and why is the right colon usually the source?

Your answer

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Bleeding is caused by rupture of vasa recta draped over the diverticular dome (arterial remodelling). In diverticulitis, inflammation causes fibrosis and obliteration of vasa recta, paradoxically protecting against bleeding. Right colon is the usual source because right-sided colon has thinner walls and right-sided diverticula have wider necks and domes, exposing a greater length of vasa recta to luminal injury.

5. List the three mechanisms by which diverticular disease causes intestinal obstruction, and classify each as LBO or SBO.

Your answer

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1. Acute pericolonic inflammation or oedema causing relative luminal narrowing or external compression by abscess (partial LBO, acute). 2. Recurrent diverticulitis causing progressive fibrosis and stricture formation (complete LBO, chronic). 3. Small bowel adhesion to inflamed sigmoid colon causing kinking or compression (SBO). Also: paralytic ileus from peritoneal irritation (functional, not mechanical).

6. What is the most common cause of recurrent diverticulitis after surgical resection, and how is it prevented?

Your answer

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Inadequate distal resection margin. If any sigmoid colon is left behind, the residual high-pressure sigmoid will develop recurrent diverticulitis. Prevention: the distal resection margin must extend to the upper third of the rectum, as the rectum is never affected by diverticular disease (taeniae coli have fused, providing complete longitudinal muscle coverage).

References

^[1] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf (p8, p13) ^[2] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p19) ^[3] Senior notes: felixlai.md (Diverticular disease section — Complications, Treatment) ^[4] Senior notes: maxim.md (Diverticular disease section — Investigations, Management, Hartmann's operation) ^[5] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf (p13, p16) ^[7] Lecture slides: GC 186. Lower and diffuse abdominal painfresh blood in stool.pdf (p9)