Rlq Pain

• Incidence ~233/100,000/year globally ^[3]
• Peak incidence in the 2nd to 3rd decades of life (teens to 30s), rare in infancy and the very elderly ^[1][3]
• Male-to-female ratio = 1.4:1 overall (lifetime risk ~8.6% males vs 6.7% females) ^[1][3]
• Perforation risk is highest at extremes of age (children < 5, elderly > 65) — because young children cannot articulate symptoms and the elderly have blunted inflammatory responses, leading to delayed presentation ^[1]

• Mean age of diagnosis of acute diverticulitis = 63 years ^[1]
• In Western populations diverticulosis is predominantly left-sided (sigmoid)
• In Asian populations (including Hong Kong), the proportion of right-sided diverticulosis (involving the caecum) is significantly higher — this is often confused with acute appendicitis ^[1][2]

• Obesity — increases intra-abdominal pressure
• Low-fibre diet — decreases stool bulk → increased intraluminal pressure
• NSAIDs, steroids, opiates — impair mucosal defence or increase constipation ^[1][2]
• Decreased physical activity
• Smoking
• High fat and red meat intake ^[1]

• Ectopic pregnancy: prior PID, previous ectopic, tubal surgery, IUD use, assisted reproduction
• Testicular torsion: cryptorchidism, bell-clapper deformity (occurs in 5–10% of individuals, usually bilateral — testes lack normal attachment to tunica vaginalis → increased mobility) ^[1]
• Ureteric colic: dehydration, high oxalate/protein/sodium diet, low fluid intake, family history, anatomical abnormalities (medullary sponge kidney, horseshoe kidney) ^[1]

This is critical for understanding clinical signs:

• The appendix is a true diverticulum of the caecum — it contains all layers including mucosa, submucosa, longitudinal and circular muscularis, and serosa ^[1][3]
• Position of the appendix tip: ^[1][3]

• Why does position matter? Because the tip of the appendix determines which somatic structures it irritates when inflamed:

  • Retrocaecal → may irritate the psoas muscle (positive psoas sign) and may not produce classic anterior abdominal tenderness → delayed diagnosis
  • Pelvic → may irritate the bladder (dysuria, frequency) or rectum (diarrhoea, tenesmus) → mimics UTI or gastroenteritis → delayed diagnosis → higher perforation rate ^[1]

• Blood supply: appendicular artery, a terminal branch of the ileocolic artery (from SMA) ^[1][3]

  • This is an end-artery — if thrombosed (from inflammation/oedema compressing it), the entire appendix becomes ischaemic → gangrenous appendicitis ^[2][3]

• Lymphoid tissue: the appendix contains prominent lymphoid tissue (compared to the rest of the caecum) ^[3]

  • This lymphoid tissue is most active in childhood and adolescence → prone to lymphoid hyperplasia which can obstruct the lumen → this is why appendicitis peaks in the young
  • Lymphoid tissue undergoes atrophy with age — which is why appendicitis is rare in the elderly ^[1]

• Mesoappendix: contains the appendicular artery, 4–6 lymphatic channels (drain to ileocaecal lymph nodes), and fat (fat content increases in adults; in children the mesoappendix may be transparent) ^[3]

This is the foundation for understanding the classical migratory pain of appendicitis:

Why does appendicitis pain migrate? Initially, distension and inflammation of the appendix stimulate visceral afferents (travelling with T10 sympathetics from the midgut) → periumbilical pain. Over 12–24 hours, transmural inflammation reaches the serosa and irritates the overlying parietal peritoneum → somatic nerve fibres localise the pain to the RLQ. This is the classic visceral-to-somatic pain migration of appendicitis.

Relevant because ureteric stones lodge at these sites and can cause RLQ pain:

1. Pelvi-ureteric junction (PUJ) — where the renal pelvis joins the ureter
2. Pelvic inlet — where the ureter crosses the pelvic brim near the bifurcation of the common iliac artery
3. Vesico-ureteric junction (VUJ) — where the ureter pierces the bladder wall ^[1]

A stone at the VUJ on the right side will cause RLQ pain with urinary symptoms (frequency, urgency, dysuria).

From the lecture slides, the following causes of RLQ pain are explicitly listed: ^[4]

The lecture slides explicitly note that the following can cause pain at left AND right side:

• Ureteric colic
• Ruptured ectopic pregnancy
• Torsion of ovarian cyst
• Inguinal/femoral hernia
• Testicular pathology

This is the paradigmatic RLQ pathology. Understanding the pathophysiology from first principles:

Step-by-step: ^[1][2][3]

1. Luminal obstruction (present in ~2/3 of cases; 1/3 are non-occlusive) ^[2]
   • Causes of obstruction:
     • Faecolith ("faeco" = faeces, "lith" = stone): a hard stony mass of faeces — the most common cause in adults ^[2]
     • Lymphoid hyperplasia (the usual cause in the young) — lymphoid tissue in the appendiceal wall swells in response to infections (gastroenteritis, URTI, measles) or inflammation (e.g., Crohn's disease) ^[3]
     • Rare: tumour (carcinoma of caecum), intestinal parasites, foreign bodies ^[2]
2. Mucosal secretion continues → fluid accumulates in the obstructed lumen → raised intraluminal pressure
3. Venous outflow obstruction → when intraluminal pressure exceeds venous pressure, venous congestion occurs → mucosal oedema and ischaemia
4. Bacterial invasion → the ischaemic mucosa loses its barrier function → enteric bacteria (E. coli, Pseudomonas aeruginosa, Peptostreptococcus, Bacteroides) ^[1] invade the wall → suppurative inflammation
5. Arterial compromise → the appendicular artery is an end-artery → inflammation and oedema compress it → gangrenous appendicitis ^[2][3]
6. Perforation → necrotic wall perforates → if the omentum and adjacent bowel loops wall it off → appendiceal abscess; if not → generalised peritonitis ^[2]

Disease Severity Grading: ^[1]

"Diverticulum" → Latin "divertere" = to turn aside; an outpouching from the bowel wall

• False diverticula (as in diverticulosis coli): only mucosa and submucosa herniate through the muscularis propria (the full muscular wall is NOT involved) ^[2]
• Pathophysiology: ^[1][2]
  • Bowel wall weakening with ageing + increased intraluminal pressure (constipation, obesity)
  • The sigmoid has the narrowest lumen → highest pressure (Laplace's law: Pressure = Wall tension / Radius; smaller radius → higher pressure for a given wall tension) ^[2]
  • Outpouchings occur at the weakest points — where the vasa recta penetrate the circular muscle ^[2]
  • In Asia, right-sided diverticula are common → caecal diverticulitis mimics appendicitis
  • Obstruction of a diverticulum by a faecolith → stasis and bacterial overgrowth → inflammation ^[2]
  • The rectum is never affected because the outer longitudinal muscle layer encompasses the full circumference of the rectum (no weak points) ^[2]

• A stone lodges at one of the three anatomical narrowings of the ureter → obstructs urine flow → proximal hydronephrosis → distension of the renal pelvis and ureter → stimulation of visceral afferents → severe colicky pain radiating loin to groin ^[1]
• A right-sided VUJ stone will cause RLQ pain + urinary symptoms
• Pain is colicky because the ureter undergoes peristaltic contractions against the obstruction

• Ectopic implantation (usually in the fallopian tube) → growing trophoblast erodes the tubal wall → tubal rupture → haemoperitoneum
• Blood irritates the parietal peritoneum → localised RLQ pain (if right-sided) ± referred shoulder-tip pain (diaphragmatic irritation → phrenic nerve → C3-C5)
• Haemodynamic instability if significant blood loss

• Viral or bacterial infection (often Yersinia enterocolitica, adenovirus) → reactive enlargement of mesenteric lymph nodes, especially in the ileocaecal region
• Inflamed nodes cause visceral pain mimicking appendicitis
• Self-limiting; important differential in children

• The right colon receives blood from the ileocolic artery and right colic artery (both branches of SMA)
• Watershed areas (Griffiths' point at the splenic flexure, Sudeck's point at the rectosigmoid junction) are classically vulnerable ^[3]
• However, the caecum itself can be ischaemic in non-occlusive mesenteric ischaemia (low-flow states in critically ill patients)
• Pathophysiology: hypoperfusion → mucosal ischaemia → reperfusion injury → transmural necrosis (in prolonged ischaemia) ^[3]

• Meckel's diverticulum: a true diverticulum (contains all layers) — remnant of the vitelline (omphalomesenteric) duct
• "Rule of 2s": 2% of population, 2 feet from ileocaecal valve, 2 inches long, 2 types of ectopic tissue (gastric and pancreatic), presents before age 2 (in children)
• Ectopic gastric mucosa secretes acid → ulceration of adjacent ileal mucosa → bleeding or perforation
• Can also become inflamed (Meckel's diverticulitis) → clinically indistinguishable from appendicitis

• Torsion of the spermatic cord → venous outflow obstruction → congestion → arterial compromise → testicular ischaemia → infarction if not relieved within 6 hours
• Bell-clapper deformity → testes lack normal posterior fixation to tunica vaginalis → lie transversely → free to rotate ^[1]
• Pain often radiates to the ipsilateral lower abdomen/RLQ (because the testis is innervated by T10 sympathetics, the same as the periumbilical region)

In all females of reproductive age presenting with RLQ pain, you MUST take a full gynaecological history (menstrual cycle, vaginal discharge, possibility of pregnancy) and perform a urine pregnancy test ^[3]

Differential diagnosis of acute abdominal pain in children (the spectrum is different from adults):

Key principle: should ALWAYS take a full gynaecological history and consider pelvic causes

The main additional differentials beyond GI causes are:

• PID — pain is lower than appendicitis and usually bilateral
• Ovarian cyst complications (rupture, torsion)
• Ectopic pregnancy — pain is characteristically non-migrating
• Mittelschmerz — mid-cycle pain, self-limiting

• Right-sided colon cancer — insidious, iron-deficiency anaemia, change in bowel habit
• Caecal volvulus — presents with large bowel obstruction
• Ischaemic colitis — sudden cramping pain + rectal bleeding within 24 hours
• Strangulated femoral hernia — classic trap; always check hernial orifices
• Perforated appendicitis — elderly patients have blunted inflammatory responses → present late → high perforation rate

The operative decision should be based on a clinical and laboratory-based scoring system (Alvarado score) ^[1][10]

The original Alvarado score uses the mnemonic MANTRELS:

Note: The Modified Alvarado Score (MANTREL) drops the "Shift" component (total out of 9 instead of 10) because a manual differential count is not always readily available ^[3][10].

Interpretation: ^[1][2][3]

WBC > 10 × 10⁹/L or CRP > 10 mg/L will give a PPV of 61.5% and NPV of 88.1% ^[3]

This means: if both WBC and CRP are normal, you can be reasonably confident (88% negative predictive value) that appendicitis is unlikely — but you cannot exclude it entirely. Serial clinical observation remains essential.

A more modern alternative to Alvarado, used in some centres:

Interpretation: 0–4 = low risk; 5–8 = intermediate (image); 9–12 = high risk (surgery). The AIR score incorporates CRP (which Alvarado does not) and is considered to have better discriminative ability.

If pancreatitis is suspected as a cause of RLQ pain (or as a differential), the diagnosis requires ≥ 2 out of 3 criteria ^[3]:

1. Epigastric pain: acute onset of persistent, severe epigastric pain often radiating to the back
2. Elevated serum lipase/amylase to ≥ 3× ULN
3. Characteristic imaging findings on contrast CT, MRI, or transabdominal USG

If the pain is felt to be more RUQ/upper abdominal, the TG13 diagnostic criteria apply ^[3]:

• Suspected diagnosis = 1× local sign + 1× systemic sign
• Definite diagnosis = 1× local sign + 1× systemic sign + 1× imaging finding

There are no formal "diagnostic criteria" — the diagnosis is clinical and requires urgent surgical exploration regardless of investigation results ^[8]. However, the following clinical features strongly suggest torsion:

• Sudden onset severe scrotal pain
• High-riding testis with horizontal lie
• Absent cremasteric reflex
• Doppler USG (if diagnosis uncertain): decreased testicular blood flow, whirlpool sign, increased resistive index ^[8]

In children, the lecture slides specifically mention: investigations include leucocytosis, plain XR (rarely), USG, CT (beware of high radiation) ^[11]

USG is the first-line imaging in pregnant women and children ^[1][2][3]

Imaging of choice by site of pain: ^[6]

Site of Pain	Imaging of Choice
RUQ	USG
LUQ	CT
RLQ	CT with IV contrast
LLQ	CT with IV contrast
Suprapubic	USG (TAS or TVS)

CT abdomen + pelvis with IV contrast is the imaging of choice for RLQ pain and has the highest diagnostic accuracy and lowest non-diagnostic rate for appendicitis ^[1][2][3][6].

From the lecture slides: endoscopy (colonoscopy, upper endoscopy) is listed as an investigation modality for lower abdominal pain ^[4]

Diagnostic laparoscopy serves as both the final diagnostic step AND a therapeutic intervention ^[6]:

• Indicated when clinical assessment and imaging are inconclusive
• Allows direct visualisation of the appendix, terminal ileum, mesentery, ovaries, and fallopian tubes
• If appendicitis is confirmed → proceed to laparoscopic appendicectomy in the same sitting
• If the appendix is normal → look for alternative pathology (Meckel's diverticulum, mesenteric adenitis with enlarged lymph nodes, ovarian pathology, Crohn's ileitis)
• Intra-operative finding in Yersiniosis: inflammation around appendix/terminal ileum with enlarged lymph nodes but normal appendix → excise mesenteric lymph node for culture ^[3]

Resuscitation, NPO, IV fluids, analgesics ^[2]

• Adequate hydration with IV fluid resuscitation ^[1]
  • Paediatric resuscitation bolus = 10–20 mL/kg full-rate ^[1]
  • Maintenance fluid therapy using the 4-2-1 rule (Holliday-Segar):

• Correction of electrolyte abnormalities ^[1]
• Close monitoring of vital signs and urine output ^[1]
• Pain control with analgesics ^[1] — paracetamol ± opioids (morphine, fentanyl). Do NOT withhold analgesia while awaiting surgical review.

Prophylactic IV antibiotics ^[2]

This is a critical component. The rationale differs depending on the clinical scenario:

Antibiotic choices: ^[1][2][3]

• Metronidazole AND 3rd-generation cephalosporin (e.g., ceftriaxone + metronidazole) ^[1][2]
• Alternative: cefoxitin or cefotetan or cefazolin 2g + metronidazole 500mg IV ^[3]

Why metronidazole? "Metro" = metre (measure), "nidazole" = nitroimidazole class. Metronidazole is a nitroimidazole that is selectively activated by anaerobic organisms (they reduce the nitro group → cytotoxic intermediates that damage DNA). Appendicitis involves mixed aerobic-anaerobic flora (E. coli, Bacteroides fragilis, Peptostreptococcus) — metronidazole provides the anaerobic coverage ^[2], while the cephalosporin covers Gram-negative aerobes.

Conservative management can be considered if uncomplicated (no perforation/abscess) and patient is not fit for surgery ^[2]

Indications: ^[3]

• Uncomplicated diverticulitis as evidenced by CT
• Microperforation (localised pericolic air or small fluid on CT) — NOT considered complicated disease
• Small diverticular abscesses ( < 4–5 cm) or not amenable to percutaneous drainage

Regimen: ^[3]

• Diet: NPO (bowel rest) → clear fluid diet → high-fibre low-residual diet
• IV fluids + analgesics
• Antibiotics: IV augmentin or cefuroxime + metronidazole × 10–14 days → IV tazocin if severe
• Clinical resolution typically in 3–5 days → switch to oral antibiotics

Follow-up: ^[2][3]

• Elective colonoscopy at 6 weeks — because colorectal cancer can present similarly to diverticulitis on CT (2.8% positive rate) ^[3]
• Interval colectomy is usually NOT required — recurrence rate is low
• Number of recurrent attacks (traditionally ≥ 2) is no longer an indication for interval colectomy — prior uncomplicated attacks do NOT predict increased incidence/severity of future attacks ^[3]

Indication: large abscesses > 4–5 cm in a favourable location ^[3]

• Approach: trans-abdominal (majority); trans-gluteal for deep pelvic abscesses
• Leave drainage catheter until output is minimal (can take up to 30 days)

Required in 15% of acute diverticulitis ^[3]

Indications: ^[3]

• Diffuse peritonitis (Hinchey stage 3–4)
• Failure of medical treatment in 3–5 days
• Chronic diverticulitis
• Obstruction (to obtain histology to rule out colorectal cancer)
• Fistula

Surgical options: ^[3]

Management of diverticular bleeding: ^[1]

• Fluid resuscitation and blood transfusion
• Colonoscopy to identify and treat the bleeding site (adrenaline injection, metallic clips)
• Indications for laparotomy and subtotal/total colectomy:
  • Haemodynamically unstable despite adequate resuscitation
  • Excessive blood transfusion > 6 units
  • Frequent rebleeding or persistent bleeding

First-line pain control: NSAIDs (e.g., diclofenac, ketorolac) — more effective than opioids for renal colic and reduce ureteric smooth muscle spasm ^[12]

Chance of spontaneous passage (for ureteric stones): ^[12]

• ≤ 4 mm: 95% pass spontaneously
• 4–10 mm: progressively decreasing chance, especially for proximal stones
• ≥ 10 mm: unlikely to pass spontaneously → definitive stone removal indicated

Medical expulsion therapy (MET): ^[12]

• Best for distal ureteric stones > 5 mm (the distal ureter has a large number of α₁-adrenergic receptors → α-blockers relax ureteric smooth muscle → facilitate stone passage)
• Regimen: tamsulosin 0.4 mg once daily × 4 weeks (off-label use)
• α-blockers make stones 1.45× more likely to pass; most useful for 5–10 mm stones

Indications: ^[12]

• Uncontrolled sepsis (urosepsis)
• Progressively worsening renal function
• (Intractable pain)

Methods:

• JJ ureteric stent (under fluoroscopy) — more comfortable but not possible in BPH, non-compliant bladder, stone impaction
• Percutaneous nephrostomy (PCN) — quicker (preferred in septic shock) but contraindicated in bleeding tendency, distorted anatomy, obesity ^[12]

Indications (the "7 Ss"): Symptomatic, Sepsis, Solitary kidney with obstruction, Size > 10 mm, Social reasons (e.g., airline pilot), Stone growth on follow-up, Significant obstruction ^[12]

ESWL (Extracorporeal Shock Wave Lithotripsy): ^[1][12]

• Minimally invasive; does not require anaesthesia
• Uses high-energy shock waves for stone fragmentation
• Contraindications: pregnancy, active UTI/urosepsis, uncontrolled bleeding diathesis, obstruction distal to stone ^[1]
• Limitations: poor efficacy in obese patients (long skin-to-stone distance), hard stones (cystine, calcium oxalate monohydrate, brushite), lower pole stones, complex renal anatomy ^[1]

These are the complications that arise from the surgery itself — important for consent discussions and post-operative monitoring ^[1][2][3].

• Occurs in 17% of patients with acute diverticulitis ^[1]
• Should be suspected in patients with no improvement in abdominal pain or a persistent fever despite 3 days of antibiotic treatment ^[1]
• May develop a pyogenic liver abscess due to spread of infection through the portal circulation ^[1] — same mechanism as pylephlebitis in appendicitis (bacteria drain via mesenteric veins → portal vein → liver)
• Clinical presentation:
  • Persistent fever despite antibiotics ^[1]
  • NO improvement in abdominal pain despite antibiotics ^[1]
  • Palpable tender mass on examination or on digital rectal examination (DRE) if distal sigmoid abscess ^[1]
• Management: Percutaneous CT-guided drainage (if > 4–5 cm) + IV antibiotics; small abscesses ( < 4–5 cm) may respond to antibiotics alone

• Inflammation may result in formation of fistula between colon and adjacent organs ^[1]
• A fistula forms when the inflammatory process erodes through the wall of two adjacent hollow structures, creating an abnormal communication

Types of fistula (by frequency): ^[1]

Management of fistula: ^[1]

• Control sepsis with antibiotics and drainage
• Resection of the affected segment of colon involved with diverticulitis, usually with primary anastomosis
• Simple repair of the secondarily involved organ (e.g., primary closure of bladder or vagina)

• Partial colonic obstruction occurs from luminal narrowing due to pericolonic inflammation or compression from a diverticular abscess ^[1]
• Complete colonic obstruction occurs because recurrent attacks of acute diverticulitis result in progressive fibrosis and scarring leading to formation of intestinal strictures ^[1]
• Localised irritation can lead to development of paralytic ileus ^[1]
• Clinical presentation:
  • Abdominal pain + abdominal distension + vomiting + constipation ^[1]
  • Bowel sounds: hyperactive with mechanical obstruction; absent or sluggish with paralytic ileus ^[1]
• Key point: always exclude colorectal cancer as the cause of a colonic stricture — diverticular stricture and malignant stricture can look identical on CT. Colonoscopy with biopsy after resolution of acute inflammation is mandatory.

• Rupture of a diverticular abscess into the peritoneal cavity ^[1]
• Rupture of an inflamed diverticulum with fecal contamination of the peritoneum ^[1]
• Leads to generalised purulent or fecal peritonitis ^[1]
• Clinical presentation:
  • Haemodynamic instability (hypotension, shock) ^[1]
  • Peritoneal signs: guarding, rigidity, rebound tenderness ^[1]
  • Absent bowel sounds ^[1]
• This corresponds to Hinchey stage III (purulent peritonitis) or stage IV (fecal peritonitis) — both require emergency surgery
• Prognosis: mortality up to 20% if perforated with diffuse peritonitis ^[3]

• Most common cause of massive PR bleeding (30–50% of lower GI bleeds) ^[3]
• Mechanism: the vasa recta (arterial branches that penetrate the colonic wall at the site of diverticula) are draped over the dome of the diverticulum → chronic pulsation and injury weakens the vessel wall → rupture into the diverticular lumen → painless massive haematochezia ^[3]
• Diverticulitis and diverticular bleeding rarely co-exist ^[3] — this is because the pathophysiology is different: bleeding is from arterial erosion, while diverticulitis is from obstruction and infection
• 80% are self-limiting; 50% have a history of previous PR bleed ^[3]
• Appearance: dark/maroon-coloured in right-sided vs bright red in left-sided ^[3]

Only 30% remain asymptomatic long-term after the first episode of acute diverticulitis ^[3]

• Recurrence: ~1/3 patients (especially females and younger patients) — but NOT associated with increased risk of complications ^[3]
• Chronic abdominal pain due to persistent low-grade diverticulitis or IBS-related ^[3]
• Diverticular colitis: IBD-like segmental colitis following acute diverticulitis, cause unknown ^[3]
• Diverticular stricture leading to acute/chronic obstruction due to progressive fibrosis/scarring ^[3]