Acute Appendicitis

Definition

Acute appendicitis is an acute inflammation of the vermiform appendix, most commonly resulting from obstruction of the appendiceal lumen. The term derives from Latin: appendix = "something attached" + -itis = "inflammation." It is the most common acute surgical emergency of the abdomen and the most common acute paediatric surgical condition ^[1][2].

Approximately two-thirds of cases are due to luminal occlusion, while one-third are non-occlusive (the exact mechanism in non-occlusive cases remains debated but likely involves mucosal ulceration from viral infection or lymphoid hyperplasia) ^[3].

Disease Severity Grading

A useful grading system that mirrors the pathological progression ^[4]:

This grading matters operatively — Grade 1–2 can often be managed laparoscopically with ease, while Grade 4–5 may require open conversion, drainage, and intensive post-operative antibiotics.

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Epidemiology

• Peak incidence in the 2nd and 3rd decades of life (20s–30s) in adults ^[4].
• Peak age in paediatrics: between 4 and 15 years ^[1].
• Increasingly common through childhood and early adult life, then declines in the elderly ^[4].
• Male : Female ratio ≈ 1.4 : 1 ^[4].
• Lifetime risk: approximately 7–8%.
• Rare in infants < 2 years (the appendiceal lumen is wide and funnel-shaped, making obstruction less likely, and lymphoid tissue is underdeveloped).
• In the elderly, acute appendicitis is less common but carries higher morbidity and mortality due to delayed presentation, atypical symptoms, and higher perforation rates.

Epidemiology in Hong Kong Context

• Hong Kong has a relatively high incidence of right-sided diverticulitis compared to Western populations, which is an important differential (more on this in DDx later) ^[4].
• The availability of CT scanning and emergency ultrasonography in Hong Kong's public hospital system (HA hospitals) has improved diagnostic accuracy, but clinical diagnosis remains paramount in straightforward presentations.

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Anatomy and Function

Gross Anatomy

The vermiform appendix is a true diverticulum of the caecum, meaning it contains all layers of the colonic wall: mucosa, submucosa, muscularis (both longitudinal and circular layers), and serosa ^[4].

• Base: Located at the posteromedial wall of the caecum, approximately 2 cm below the ileocaecal valve, at the point where the three taeniae coli converge on the caecum ^[3][4].
  • This convergence point is constant regardless of the position of the tip — this is why during surgery, the appendix can always be traced by gentle traction on the taeniae coli ^[3].
• Surface landmark: The base corresponds to McBurney's point — defined as the point one-third of the distance from the anterior superior iliac spine (ASIS) to the umbilicus ^[3].
• Length: Typically 6–9 cm (range 2–20 cm).
• In colonoscopy: The appendiceal orifice is visualized on the posteromedial wall of the caecum, approximately 2 cm below the ileocaecal valve ^[3].

Position of the Appendix Tip

The base is constant, but the tip is highly variable. This is critical because the position of the tip determines the clinical presentation:

• The appendix's position is affected by embryological rotation. The caecum undergoes continuous growth during foetal life, rotating the appendix into its retrocaecal (but intraperitoneal) position during childhood. A pelvic appendix may result from absence of this rotation ^[4].
• Position can also be dramatically altered by malrotation or non-rotation of the caecum (e.g., the caecum may end up in the RUQ or even LUQ) ^[3].

Neurovascular Supply

• Arterial supply: The appendiceal artery, which is a terminal branch of the ileocolic artery (itself a branch of the superior mesenteric artery, SMA) ^[3][4].
  • Crucially, this is an end-artery — there is no collateral blood supply. This means that thrombosis of the appendiceal artery causes necrosis of the entire appendix (gangrenous appendicitis) ^[3]. This explains why the progression from inflammation to gangrene can be rapid and irreversible.
• Venous drainage: Appendiceal vein → ileocolic vein → superior mesenteric vein → portal vein.
  • This portal venous drainage explains why appendicitis can (rarely) cause pylephlebitis (septic thrombophlebitis of the portal vein) and hepatic abscess.
• Lymphatic drainage: To the ileocolic lymph nodes.
• Nerve supply: Sympathetic and parasympathetic fibres via the superior mesenteric plexus. Visceral afferent pain fibres enter the spinal cord at T8–T10 — this is why early appendiceal pain is referred to the periumbilical region (T10 dermatome).

Function

The appendix was historically considered "vestigial," but it is now understood to have roles in:

• Immune function: The wall contains abundant lymphoid tissue (sometimes called the "abdominal tonsil"), particularly in children and young adults. This lymphoid tissue is part of gut-associated lymphoid tissue (GALT) and participates in IgA secretion.
  • Lymphoid tissue undergoes atrophy with age ^[4], which partly explains why appendicitis becomes less common in the elderly.
• Gut microbiome reservoir: The appendix may serve as a "safe house" for commensal bacteria, allowing recolonization of the colon after diarrhoeal illness.

The Mesoappendix

The appendix is suspended by a mesoappendix (a triangular fold of peritoneum), which contains the appendicular artery and vein ^[3]. During appendicectomy, the mesoappendix must be ligated to control the appendicular artery before the appendix is divided at its base.

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Aetiology

The central mechanism is obstruction of the appendiceal lumen, though non-obstructive causes exist. The causes differ by age group:

Causes of Luminal Obstruction

Non-Obstructive Appendicitis (~1/3 of cases)

• Mucosal ulceration from viral infection (adenovirus, CMV)
• Direct bacterial invasion
• Ischaemic causes (vasculitis, e.g., in Henoch-Schönlein purpura)

Bacteriology

Once the appendix becomes inflamed and ischaemic, polymicrobial bacterial overgrowth occurs. The common organisms reflect normal colonic flora ^[4]:

• Escherichia coli (most common aerobe)
• Bacteroides spp. (most common anaerobe — especially B. fragilis)
• Pseudomonas aeruginosa
• Peptostreptococcus spp.

This mixed aerobic-anaerobic flora is why antibiotic regimens for appendicitis must cover both Gram-negatives and anaerobes (e.g., cefuroxime + metronidazole, or amoxicillin-clavulanate).

Risk Factors for Perforation

Perforation is the most feared progression. Risk factors include ^[4]:

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Pathophysiology

Understanding the pathophysiology of acute appendicitis as a stepwise sequence is critical — it explains every clinical feature, complication, and management decision.

Step-by-Step Pathogenesis

Detailed Explanation of Each Step

1. Luminal obstruction: The appendix has a narrow lumen (especially in adults). Obstruction creates a "closed-loop" obstruction ^[1] — the appendix has only one opening into the caecum, so once blocked, secretions have nowhere to go.

2. Continued mucus secretion: The appendiceal mucosa continues to secrete mucus (approximately 1 mL/day). Continuous mucus secretion and inflammatory exudation leads to increased intraluminal and intramural pressure ^[4].

3. Rising intraluminal pressure: Pressure within the lumen exceeds venous pressure first (veins are thin-walled and low-pressure), then lymphatic pressure, and eventually arterial pressure.

4. Venous congestion → lymphatic stasis: Thrombosis and occlusion of small vessels in the appendiceal wall, and stasis of lymphatic flow ^[4]. The appendix becomes oedematous, engorged, and hyperaemic. This is the "early appendicitis" stage (Grade 1).

5. Mucosal ischaemia and bacterial invasion: As the mucosa becomes ischaemic, the mucosal barrier breaks down. Bacterial overgrowth occurs within the diseased appendix, and intraluminal bacteria subsequently invade the appendiceal wall ^[4]. This is when the process becomes truly infective.

6. Transmural inflammation: The entire wall is now inflamed. When inflammation reaches the serosa (outermost layer), it irritates the adjacent parietal peritoneum — this is when the pain shifts from periumbilical to RIF.

7. Arterial compromise: Because the appendiceal artery is an end-artery, once arterial inflow is compromised (by oedema compressing the artery, or thrombosis), the entire appendix undergoes gangrenous necrosis (Grade 2).

8. Perforation (Grade 3–5): Once significant inflammation and necrosis occurs, the appendix is at risk of perforation ^[4]. The weakened, necrotic wall gives way, releasing pus, faecal material, and bacteria into the peritoneal cavity.

9. Outcome depends on the body's ability to contain the spillage:

   • If the omentum and adjacent bowel loops can migrate to wall off the perforation → appendiceal abscess (Grade 4) → may later cause adhesive small bowel obstruction ^[3].
   • If the infection is not walled off → generalised peritonitis (Grade 5) ^[3] — a life-threatening surgical emergency.

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Classification

By Pathological Stage (Clinical-Pathological Correlation)

By Complexity

• Uncomplicated: Inflamed but not gangrenous/perforated (Grade 1)
• Complicated: Gangrenous (Grade 2), perforated (Grade 3), abscess (Grade 4), or diffuse peritonitis (Grade 5)

This distinction is important for management — uncomplicated appendicitis may be managed conservatively with antibiotics in select cases (the "antibiotics-first" approach), while complicated appendicitis almost always requires surgery ± drainage.

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Clinical Features

The classic presentation occurs in only 50–60% of patients. Always maintain a high index of suspicion.

Symptoms

1. Abdominal Pain — The Cardinal Symptom

The migratory pattern of pain is the single most important diagnostic feature:

Phase 1: Visceral Pain (Early)

• Periumbilical pain: crampy, intermittent, poorly localized ^[3]
• Why periumbilical? The appendix is a midgut structure. Visceral afferent nerve fibres from the appendix travel with sympathetic nerves and enter the spinal cord at T8–T10 levels ^[4]. T10 is the dermatome of the umbilicus. Since visceral pain is transmitted by unmyelinated C-fibres that converge on shared spinal cord segments, the brain cannot localise it precisely — hence the vague, poorly localised periumbilical ache.
• Character: Dull, crampy, colicky (due to peristaltic contractions of the appendiceal smooth muscle trying to expel the obstruction).
• Aggravated by moving and coughing ^[3] (even at this stage, movement jostles the inflamed viscus).

Phase 2: Somatic Pain (Later — typically after 12–24 hours)

• Pain migrating to the right lower quadrant (RLQ) after 12–24 hours: constant, sharp, well-localised pain ^[3][4]
• Why does it migrate? Once transmural inflammation extends to the serosa, it irritates the overlying parietal peritoneum. Unlike the viscera, the parietal peritoneum is innervated by somatic nerves (myelinated A-delta fibres) that provide precise localisation ^[4]. The pain now shifts to wherever the inflamed appendix is located — classically the RIF.
• Character: Sharp, constant, worse with movement (the patient lies still and resists any jostling).

Atypical Pain Locations (based on appendix position):

• Retrocaecal appendix: Pain may be in the right flank or back; may mimic renal colic. Anterior abdominal signs may be minimal.
• Pelvic appendix: Suprapubic pain; may mimic UTI or gynecological pathology. May cause rectal pain or urinary symptoms.
• Long appendix crossing midline: Left-sided pain (rare but described).
• Malrotated caecum: Pain may be anywhere in the abdomen.

2. Anorexia (Loss of Appetite)

• Anorexia is a classical feature ^[4] — present in > 90% of cases.
• Why? Visceral inflammation causes a reflex suppression of appetite via vagal afferents to the brainstem vomiting/appetite centres. The peritoneal irritation also causes ileus and gastric stasis, reducing the desire to eat.
• Clinically useful: If a patient is hungry and eating normally, think twice about appendicitis.

3. Nausea and Vomiting

• Nausea and vomiting are classical features ^[4].
• Why? Visceral afferent stimulation from the inflamed appendix activates the area postrema and nucleus tractus solitarius in the brainstem. Peritoneal irritation also reflexly causes gastric stasis and reverse peristalsis.
• Key timing: In appendicitis, pain precedes nausea/vomiting. In gastroenteritis, nausea/vomiting typically precedes pain ^[3]. This is a commonly tested distinction.
• Vomiting is usually mild (1–2 episodes) and not profuse.

4. Low-Grade Fever

• Low-grade fever ^[3] — typically 37.5–38.5°C.
• Why? The inflammatory response generates pyrogens (IL-1, IL-6, TNF-α, PGE₂) that act on the hypothalamic thermoregulatory centre.
• High fever ( > 38.5°C) should raise suspicion for perforation, abscess, or an alternative diagnosis.

5. Other Non-Specific Symptoms

• Indigestion, flatulence ^[4] — due to reflex ileus.
• Diarrhoea ^[4] — especially with a pelvic appendix irritating the rectum (causes increased rectal peristalsis). Can mimic gastroenteritis.
• Tenesmus ^[4] — again due to a pelvic appendix irritating the rectum (a feeling of incomplete evacuation and the urge to defaecate).
• Malaise ^[4] — general systemic inflammation.
• Dysuria / urinary frequency — a pelvic appendix lying close to the bladder can irritate it, mimicking a UTI.
• Constipation — due to reflex ileus; some patients develop absolute constipation with peritonitis.

The classic sequence: Anorexia → periumbilical pain → nausea ± vomiting → pain migration to RIF → low-grade fever. This sequence (sometimes called Murphy's sequence or the chronology of symptoms) is present in ~50% of cases but is highly specific when present.

Signs

The physical examination in suspected appendicitis follows a systematic approach. Signs are best understood in terms of what they are testing:

1. General Inspection

• The patient often lies still with hips slightly flexed (because extension of the right hip stretches the psoas and irritates the inflamed appendix).
• Facial expression of pain when asked to move or cough.
• May be flushed with low-grade fever.
• Foetor oris (bad breath) — due to dehydration and reduced oral intake.

2. Abdominal Inspection

• The abdomen may be still on the affected side (reduced respiratory excursion due to guarding).
• No specific visible abnormality in early appendicitis.
• A distended abdomen may indicate complications (ileus, peritonitis, or abscess with obstruction).

3. Palpation — Tenderness and Peritonism

Pointing sign: Maximum tenderness at McBurney's point ^[3]

• McBurney's point is the surface landmark of the appendiceal base.
• The patient can often point with one finger to the site of maximum pain — this is the "pointing sign."
• Why here? The inflamed appendix (or its base) lies deep to this point, and pressure here compresses inflamed tissue against the psoas/iliacus, causing sharp somatic pain.

Localised guarding

• Involuntary contraction of the abdominal wall muscles overlying the inflamed area.
• Why? A protective reflex mediated by spinal cord reflex arcs — when somatic pain fibres from the parietal peritoneum are stimulated, motor neurones to the overlying rectus/oblique muscles cause contraction to "splint" the area and prevent further irritation.

Rebound tenderness

• Pain that is worse on sudden release of deep palpation than on compression.
• Why? Sudden release causes the peritoneum to spring back into contact with the inflamed appendix, generating a burst of somatic nerve firing. This is a sign of parietal peritoneal irritation.

Rigidity (Board-like abdomen)

• Indicates diffuse peritonitis (Grade 5) — suggests perforation with generalised contamination.
• The entire abdominal wall is involuntarily rigid.

4. Special Signs

Rovsing's sign: RLQ pain upon deep palpation (or rebound) of the LLQ ^[3]

• Why? Pressing on the left side of the abdomen pushes bowel gas and intestinal contents towards the caecum and RIF, distending the caecum and jostling the inflamed appendix. Pain is felt in the RIF, not the LLQ. This confirms that the source of irritation is in the RIF.

Psoas sign (Cope's psoas test): Increased RIF pain upon passive extension of the right hip (or asking the patient to flex the right hip against resistance) ^[3]

• Why? The psoas major muscle lies in the retroperitoneum along the right iliac fossa. A retrocaecal appendix lies directly on or near the psoas. Extending the hip stretches the psoas, which moves against the inflamed appendix, causing pain.
• This sign is most useful for retrocaecal appendicitis.

Obturator sign: RIF pain on passive internal rotation of the flexed right hip

• Why? The obturator internus muscle forms part of the lateral pelvic wall. A pelvic appendix lying near this muscle will be irritated when the muscle moves during internal rotation.
• This sign is most useful for pelvic appendicitis.

Dunphy's sign: Increased pain with coughing

• Why? Coughing raises intra-abdominal pressure, causing the parietal peritoneum to move against the inflamed appendix.

Cough test / Percussion tenderness

• Gently percussing the RIF causes pain — a gentler way of eliciting peritoneal irritation than deep palpation.

5. Rectal Examination (DRE)

• Classically taught as part of the assessment.
• May reveal right-sided pelvic tenderness if the appendix is in a pelvic position.
• A palpable mass may indicate an appendiceal abscess.
• In practice, DRE adds limited information if imaging is available, but it should be performed if:
  • The diagnosis is unclear
  • A pelvic appendix is suspected
  • Pelvic pathology (e.g., pelvic abscess, TOA, ectopic pregnancy) is in the differential

6. Vaginal Examination (in women of reproductive age)

• Important to assess for cervical motion tenderness (suggests PID), adnexal masses (ovarian cyst/torsion, ectopic pregnancy), and vaginal discharge.

7. Signs Suggesting Complications

Special Populations

Children (Paediatric Appendicitis)

• Most common acute paediatric surgical condition ^[1].
• Peak age between 4 and 15 years ^[1].
• Higher perforation rate (up to 30–50%), especially in younger children, because:
  • Cannot articulate symptoms clearly → delayed diagnosis
  • Underdeveloped omentum → poor ability to wall off infection
  • Thinner appendiceal wall → perforates more readily
• May present with diffuse abdominal pain, irritability, refusal to eat/walk, and diarrhoea more commonly than adults.
• Neonates and infants: Extremely rare. If it occurs, almost always presents as perforation with peritonitis (diagnosis is rarely made pre-operatively).

Elderly

• Atypical presentations are the rule, not the exception.
• Lower temperature response, less prominent leucocytosis, vague symptoms.
• High perforation rate (50–70%) due to delayed presentation and delayed diagnosis.
• Must rule out caecal carcinoma as the underlying cause.

Pregnancy

• Most common non-obstetric surgical emergency in pregnancy.
• The growing uterus displaces the caecum and appendix superiorly and laterally — pain may be in the right flank or even RUQ rather than RIF, especially in the 2nd and 3rd trimesters.
• Leucocytosis is normal in pregnancy (up to 15,000/µL) → less reliable as a diagnostic marker.
• Ultrasound is the first-line imaging (no ionising radiation); MRI is second-line.
• Perforation risk is higher because of delayed diagnosis, and maternal/foetal morbidity is significant with perforation → maintain a low threshold for surgery.

Immunocompromised Patients (HIV, transplant recipients, on chemotherapy)

• Blunted inflammatory response → minimal fever, minimal leucocytosis, minimal peritoneal signs.
• Very high risk of delayed diagnosis and perforation.

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Summary of Clinical Approach (Pre-Diagnosis)

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Active Recall - Acute Appendicitis (Definition to Clinical Features)

1. Why is the appendiceal artery clinically significant in the pathogenesis of gangrenous appendicitis?

Your answer

Grade

Show mark scheme

It is a terminal branch (end-artery) of the ileocolic artery with no collateral supply. Thrombosis leads to complete necrosis of the appendiceal wall (gangrenous appendicitis).

2. Explain the pathophysiological basis for pain migration from the periumbilical region to the right iliac fossa in acute appendicitis.

Your answer

Grade

Show mark scheme

Early: visceral afferents from appendix enter spinal cord at T8-T10 (periumbilical dermatome) causing vague, poorly localised pain. Later: transmural inflammation involves serosa, irritating parietal peritoneum innervated by somatic nerves, causing sharp, well-localised RIF pain.

3. A pelvic appendix may mimic which conditions and why?

Your answer

Grade

Show mark scheme

UTI (bladder irritation causing dysuria/frequency), gastroenteritis (rectal irritation causing diarrhoea/tenesmus), and gynaecological pathology (suprapubic pain). Because the pelvic appendix lies close to the bladder, rectum, and adnexa.

4. What is the most common cause of appendiceal obstruction in young patients versus older patients?

Your answer

Grade

Show mark scheme

Young: lymphoid hyperplasia (reactive to viral/bacterial infection). Older: faecolith (hard mass of faecal material, calcium phosphates, bacteria, epithelial debris). Elderly: also consider tumours (caecal carcinoma, carcinoid).

5. Why do children have higher perforation rates in acute appendicitis compared to adults?

Your answer

Grade

Show mark scheme

Three reasons: (1) Cannot articulate symptoms clearly leading to delayed diagnosis, (2) Underdeveloped omentum cannot wall off infection, (3) Thinner appendiceal wall perforates more readily.

6. Describe the mechanism behind Rovsing's sign.

Your answer

Grade

Show mark scheme

Deep palpation of the LLQ pushes bowel gas and contents towards the caecum/RIF, distending the caecum and jostling the inflamed appendix against the parietal peritoneum, causing referred pain in the RIF (not the LLQ).

References

^[1] Lecture slides: GC 203. The child needs an operation Common emergencies and surgery in childhood.pdf (p39) ^[2] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf ^[3] Senior notes: maxim.md (Section 4.6 - Acute appendicitis) ^[4] Senior notes: felixlai.md (Acute appendicitis section)

Differential Diagnosis of Acute Appendicitis

The differential diagnosis of RLQ pain is one of the broadest in surgery. The key challenge is that the RLQ is a "crowded neighbourhood" — the terminal ileum, caecum, appendix, right ureter, right ovary/tube, psoas muscle, and various vascular structures all live here. A systematic organ-based approach is essential.

Overview: Causes of RLQ Pain

From the lecture slides, the following is the comprehensive list of causes of RLQ pain ^[2]:

Acute appendicitis, Caecal diverticulitis, Ureteric colic, Ruptured ectopic pregnancy, Mesenteric adenitis, Torsion of ovarian cyst, Ileitis, Meckel's diverticulitis, Caecal ischaemia, Cancer of caecum, Inguinal/femoral hernia*, Testicular pathology*, Perforated peptic ulcer, Acute cholecystitis*** ^[2]

(asterisked conditions can cause pain on either side)

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A. Gastrointestinal Causes

1. Caecal / Right-Sided Diverticulitis

• Right colon diverticulosis is common in Asians ^[5]. This is a critical Hong Kong-specific point — while diverticular disease in Western populations predominantly affects the left/sigmoid colon, in Asia (including Hong Kong, Japan, Korea), right-sided (caecal) diverticulitis is more common ^[4][5].
• Caecal diverticulitis mimics appendicitis ^[5] — both present with RLQ pain, fever, leucocytosis, and localised peritonism. The two can be virtually indistinguishable clinically.
• Why does it mimic appendicitis? The caecum and appendix are anatomically adjacent. Inflammation of a caecal diverticulum irritates the same parietal peritoneum in the RIF.
• How to differentiate: CT abdomen with contrast is the diagnostic test of choice in patients with suspected acute diverticulitis ^[4]. CT shows pericolic fat stranding centred on the caecal wall (rather than an inflamed appendix), diverticula, and colonic wall thickening.
• The role of CT scan in distinguishing caecal diverticulitis from appendicitis is emphasised in the lecture ^[5].
• Features more suggestive of diverticulitis over appendicitis on CT include: pericolonic/mesenteric inflammation, involvement of > 10 cm of colon, and absence of enlarged pericolonic lymph nodes ^[4].

2. Mesenteric Adenitis

This is a classic mimic of appendicitis, especially in children.

• Often misdiagnosed as acute appendicitis ^[2].
• Causative organisms: β-haemolytic Streptococcus, E. coli, Streptococcus viridans, Yersinia, Coxsackievirus, rubeola virus, and adenovirus ^[2].
• Usually in children ^[2].
• Recent sore throat and high fever ^[2] — this is the key distinguishing feature. The child typically has a viral prodrome (URTI symptoms) preceding the abdominal pain by a few days.
• Not much peritoneal sign ^[2] — this is a crucial clinical differentiator. In mesenteric adenitis, the enlarged mesenteric lymph nodes cause visceral-type pain but do not cause significant parietal peritoneal irritation. So you get tenderness but minimal guarding or rebound tenderness, and no true localised peritonism.
• Why does it cause RLQ pain? The mesenteric lymph nodes draining the terminal ileum and caecum are concentrated in the RIF (ileocolic lymph nodes). When they enlarge from infection, they cause pain referred to the RLQ.
• Diagnosis: Presence of enlarged lymph nodes found during operation ^[2] (historically a finding at laparotomy/laparoscopy when the appendix is normal). Now, USG can detect mesenteric lymphadenopathy pre-operatively ^[6].
• Management: Conservative — it is a self-limiting condition. Antibiotics are not needed unless a specific bacterial pathogen is identified.

3. Meckel's Diverticulitis

Meckel's diverticulitis presents similar to acute appendicitis ^[2] and may be an incidental finding during appendicectomy ^[2].

• What is a Meckel's diverticulum? It is a true congenital diverticulum (contains all bowel wall layers) located on the anti-mesenteric aspect of the small intestine, arising from incomplete obliteration of the vitelline duct (omphalomesenteric duct — the embryological connection between the midgut and the yolk sac) ^[7].

The Rule of 2s (classic mnemonic) ^[7]:

• 2% of the population

• 2% become symptomatic, often by age 2

• 2:1 male-to-female ratio

• 2 inches in length

• Found within 2 feet of the ileocaecal valve

• 2 types of ectopic tissue: gastric (60%) and pancreatic (6%)

• Why does it mimic appendicitis? The Meckel's diverticulum is located on the ileum approximately 2 feet (60 cm) proximal to the ileocaecal valve. When it becomes inflamed (Meckel's diverticulitis), the small bowel may migrate into the RLQ and mimic symptoms of acute appendicitis ^[4]. The inflammation of a visceral peritoneal structure in the RLQ region produces virtually identical pain patterns.

• Diagnosis by CT scan ^[2]. CT may show a blind-ending tubular structure arising from the ileum with surrounding fat stranding.

• Treatment: Antibiotics + Diverticulectomy or small bowel resection ^[2].

• Complications include: massive painless haematochezia (from acid secretion by ectopic gastric mucosa eroding adjacent ileal mucosa), intestinal obstruction (intussusception with Meckel's as lead point, volvulus), and Littre's hernia (hernia containing Meckel's diverticulum) ^[7].

4. Ileitis

Ileitis is inflammation of the terminal ileum, which lies in the RIF and can closely mimic appendicitis. It is sometimes misdiagnosed as acute appendicitis and can be an incidental finding of inflamed terminal ileum during operation ^[2].

Causes of ileitis ^[2]:

• Crohn's disease — chronic granulomatous transmural inflammation. Look for: prolonged diarrhoea with abdominal pain ± gross bleeding, weight loss, fatigue, perianal disease, extraintestinal manifestations (arthritis, uveitis, erythema nodosum) ^[4]. Crohn's classically affects the terminal ileum.
• TB — intestinal TB is not uncommon in Hong Kong. Presents similarly to Crohn's but with risk factors (immigration from endemic areas, HIV, immunosuppression). Ileocaecal region is the most common site.
• Radiation enteritis — history of pelvic/abdominal radiotherapy.
• Bacterial infection: Campylobacter, Yersinia, Salmonella ^[2][4] — acute self-limited bacterial ileitis. Should be considered when acute diarrhoea is a prominent symptom ^[4]. Yersinia enterocolitica has a particular predilection for the terminal ileum and mesenteric lymph nodes and is a classic appendicitis mimic (sometimes called "pseudoappendicitis").

How to differentiate from appendicitis: Diarrhoea is the predominant symptom in ileitis/colitis, whereas in appendicitis, pain is the dominant symptom and diarrhoea is mild/absent or occurs only with a pelvic appendix ^[4].

5. Cancer of the Caecum

• Cancer of caecum ^[2] can present as RLQ pain, especially if it causes obstruction of the appendiceal orifice (leading to secondary appendicitis) or if the tumour itself perforates or becomes locally advanced.
• In elderly patients with RLQ pain, always consider caecal carcinoma.
• CRC can only be excluded with colonoscopy after resolution of acute inflammation ^[4].
• Features suggestive of malignancy: weight loss, iron-deficiency anaemia, change in bowel habit, palpable RIF mass, family history of colorectal cancer.

6. Perforated Peptic Ulcer (PPU) — Valentino's Sign

• Perforated peptic ulcer ^[2] can mimic appendicitis via Valentino's sign ^[3]: gastric/duodenal contents leak from a perforated ulcer and track down the right paracolic gutter to the RIF, causing RLQ pain and peritonism.
• PPU: epigastric pain → RLQ (Valentino's sign) ^[3].
• How to differentiate: History of preceding epigastric pain, NSAID use, known PUD, erect CXR showing free gas under the diaphragm (pneumoperitoneum). The pain starts in the epigastrium and later involves the RLQ — the reverse direction of appendicitis pain migration.

7. Intussusception (Paediatric)

• In the paediatric differential diagnosis, intussusception must be considered ^[6].
• Classical triad: colicky abdominal pain (episodic, with pain-free intervals), "redcurrant jelly" stools (blood and mucus), and a palpable sausage-shaped mass.
• Most common in infants 6–36 months — typically younger than the peak age for appendicitis.
• Differentiation: Intussusception has episodic pain with pain-free intervals (the child may appear completely well between episodes), whereas appendicitis pain is more continuous and progressive.

8. Acute Cholecystitis

• Acute cholecystitis ^[2] usually causes RUQ pain but can occasionally cause referred pain or pain that extends to the RLQ.
• Rarely a true mimic — Murphy's sign, fever, and RUQ tenderness usually point to the correct diagnosis. USG shows gallstones, thickened gallbladder wall, and pericholecystic fluid.

9. Acute Pancreatitis

• Acute pancreatitis ^[3] — epigastric pain radiating to the back, associated with vomiting. Raised serum amylase/lipase. Usually not confused with appendicitis, but mentioned for completeness as a cause of acute abdominal pain.

10. Caecal Ischaemia

• Caecal ischaemia ^[2] — seen in elderly patients with vascular risk factors (AF, atherosclerosis, recent cardiac surgery, hypotension). The caecum is a watershed area between SMA and IMA territories.
• Presents with sudden-onset RLQ pain, bloody diarrhoea. CT angiography or colonoscopy may show mucosal ischaemia.

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B. Gynaecological Causes

In all women of reproductive age presenting with RLQ pain, gynaecological pathology must be actively excluded. The key first step is always: check a pregnancy test (urine β-hCG).

1. Ruptured Ectopic Pregnancy

• Presents with sudden severe pain, bleeding, and circulatory collapse ^[2].
• Investigations: pregnancy tests, blood count, type and screen ^[2].
• Diagnosis: USG ^[2].
• Treatment: large-bore IV cannula and resuscitation → urgent laparoscopy and salpingotomy/salpingectomy ^[2].
• Why it mimics appendicitis: A right-sided tubal ectopic can cause RLQ pain and peritonism due to tubal rupture and haemoperitoneum.
• Key differentiator: Positive pregnancy test strongly suggests presence of an ectopic pregnancy if an intrauterine pregnancy cannot be visualized ^[4]. Amenorrhoea/missed period, vaginal bleeding, haemodynamic instability.

2. Torsion or Ruptured Ovarian Cyst

• Ovarian cyst complications: ruptured, torsion, infarct ^[2].
• Lower abdominal pain ± tenderness and guarding ^[2].
• Diagnosis confirmed by USG or CT ^[2].
• Treatment is laparoscopic ovarian cystectomy/oophorectomy ^[2].
• Ruptured cyst: Pain often begins during strenuous physical activity such as exercise or intercourse ^[4]. Sudden onset of sharp unilateral lower abdominal pain, no fever (unless secondary infection).
• Ovarian torsion: Refers to twisting of the ovary on its ligamentous supports, often resulting in impedance of its blood supply ^[4]. Presents with sudden severe unilateral pain, nausea/vomiting (due to peritoneal irritation), and a palpable adnexal mass. It is a surgical emergency — delay leads to ovarian infarction and loss.
• How to differentiate from appendicitis: Onset is typically more sudden, pain is often suprapubic or in the iliac fossa (lower than McBurney's point), and there may be a known history of ovarian cysts. USG is diagnostic.

3. Pelvic Inflammatory Disease (PID) / Tubo-Ovarian Abscess (TOA)

• PID: recent onset of pain that worsens during coitus or during/shortly after menses are particularly suggestive ^[4].
• Purulent endocervical discharge, cervical motion tenderness, and adnexal tenderness on physical examination are particularly suggestive ^[4].
• TOA: inflammatory mass involving ovary, fallopian tube, and adjacent pelvic organs including bladder and bowels. Most commonly found in reproductive-age women resulting from upper genital tract infection, usually a complication of PID ^[4].
• Why it mimics appendicitis: PID can cause RLQ pain and peritonism. However, PID is usually bilateral (both adnexae tender), whereas appendicitis is strictly right-sided. PID patients often have a history of vaginal discharge, recent sexual activity, or IUD insertion.
• Key differentiators: Cervical motion tenderness ("chandelier sign"), bilateral adnexal tenderness, vaginal/cervical discharge, high vaginal swab positive for Chlamydia trachomatis or Neisseria gonorrhoeae.

Fitz-Hugh-Curtis syndrome: PID can also cause RUQ pain due to perihepatic inflammation (violin-string adhesions between the liver capsule and anterior abdominal wall), further broadening its mimicry.

4. Mittelschmerz ("Middle Pain")

• Mittelschmerz pain (ovulation) ^[3] — mid-cycle ovulatory pain caused by follicular rupture and release of follicular fluid/blood, which irritates the peritoneum.
• Typically mild, self-limiting, occurring around day 14 of the menstrual cycle.
• Usually does not cause significant peritonism or fever — differentiating it from appendicitis.

5. Endometriosis / Acute Endometritis

• Endometriosis: presence of endometrial glands and stroma at extrauterine sites ^[4]. Can cause chronic or cyclical RLQ pain (especially if endometriotic implants are on the right ovary, appendix, or peritoneum).
• Acute endometritis: occurs after obstetrical delivery or invasive uterine procedure ^[4]. Usually causes diffuse lower abdominal/pelvic pain with uterine tenderness and fever.

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C. Urological Causes

1. Ureteric Colic

• Presence of stones in the right or left ureter ^[2].
• True colic, severe, gripping in nature ^[2] — this is a key differentiator. Ureteric colic comes in waves (the ureter contracts rhythmically trying to push the stone along), whereas appendicitis pain is constant once somatic pain develops.
• Starts at the loin and radiates to the groin region ^[2] — the classic loin-to-groin radiation follows the dermatomes of the ureter (T11–L2).
• Presence of RBC in urinalysis ^[2] — microscopic haematuria is present in ~85% of cases. However, note that a pelvic appendix lying near the ureter can also cause mild haematuria.
• Diagnosis confirmed by X-ray or plain CT abdomen ^[2] (non-contrast CT KUB is the gold standard for ureteric calculi).
• Treatment is mostly conservative and pain relief as majority of stones pass spontaneously ^[2].
• How to differentiate from appendicitis: The patient with renal colic is restless and cannot find a comfortable position (rolling around in agony), whereas the appendicitis patient lies still (movement aggravates peritoneal irritation). Colic is episodic; appendicitis pain is continuous. Urinalysis with haematuria points towards colic.

2. UTI / Pyelonephritis

• Dysuria, frequency, urgency, and suprapubic pain suggest cystitis.
• Fever + flank pain + pyuria suggest pyelonephritis.
• A pelvic appendix can cause dysuria by irritating the bladder, potentially mimicking UTI — but in appendicitis, the urinalysis will show only a few WBCs (sterile pyuria) and no bacteria on culture, whereas true UTI will have significant bacteriuria and positive culture.

3. Testicular Torsion

• Testicular torsion ^[3] — must be considered in young males with RLQ pain, as the pain can be referred from the testis to the RIF via the genitofemoral nerve (L1–L2).
• Always examine the scrotum in any male presenting with lower abdominal pain. The testis will be high-riding, horizontally oriented ("bell-clapper deformity"), and exquisitely tender. Absent cremasteric reflex.
• This is a surgical emergency — testicular salvage drops dramatically after 6 hours.

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D. Other Causes

1. Strangulated Inguinal / Femoral Hernia

• Inguinal/femoral hernia ^[2] can cause RLQ (or LLQ) pain, especially if incarcerated or strangulated.
• Always examine the groin — a tender, irreducible lump at the inguinal or femoral region with associated RLQ pain and signs of obstruction (vomiting, distension) should prompt urgent surgical assessment.
• Femoral hernias are more common in women and have a high strangulation rate due to the rigid femoral ring.

2. Henoch-Schönlein Purpura (HSP) — Paediatric

• HSP is listed as a differential for appendicitis in children ^[1][6].
• HSP is an IgA-mediated small vessel vasculitis presenting with the classic tetrad: palpable purpura (typically on the buttocks and lower limbs), abdominal pain, arthritis, and renal involvement (glomerulonephritis) ^[6].
• Why does it mimic appendicitis? Intestinal vasculitis causes colicky abdominal pain, and HSP can also cause intussusception (especially ileo-ileal). The abdominal pain may precede the rash, causing diagnostic confusion.
• Key differentiator: The characteristic purpuric rash on the buttocks and extensor surfaces of the legs. If in doubt, USG abdomen to rule out intussusception.

3. Psoas Abscess

• Infection of the psoas muscle (from TB spondylitis, Crohn's disease, or haematogenous seeding) can cause RIF pain, hip flexion, and fever — mimicking a retrocaecal appendicitis.
• CT scan is diagnostic (shows fluid collection within the psoas).

4. Medical Causes Mimicking Acute Abdomen

From the general acute abdomen DDx ^[3]:

• DKA: Can cause diffuse abdominal pain; always check blood glucose and ketones.
• Gastroenteritis: N/V followed by pain in GE ^[3] (contrast with appendicitis where pain precedes N/V).

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Systematic Approach: Differentiating Key Mimics

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Paediatric-Specific Differential Diagnosis

The paediatric differential diagnosis ^[1][6] deserves special attention because presentations are vaguer:

• Mesenteric adenitis: viral illness prodrome, USG detects lymphadenopathy ^[6]
• Meckel's diverticulitis: CT abdomen ^[6]
• Gynaecological causes (in adolescent girls) ^[6]
• HSP: look for purpuric rash, arthritis, abdominal pain ± intussusception
• Intussusception: episodic colicky pain, vomiting, "redcurrant jelly" stools, sausage-shaped mass
• Gastroenteritis: vomiting and diarrhoea precede pain; no localising signs
• UTI / stone disease
• DKA (if diabetic child)

For girls: always ask LMP, order pregnancy test and USG abdomen. Do NOT perform PV examination on your own — consult Gynaecology! ^[6]

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Active Recall - Differential Diagnosis of Acute Appendicitis

1. Why is right-sided (caecal) diverticulitis particularly important in the Hong Kong context, and how is it differentiated from acute appendicitis?

Your answer

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Right-sided diverticulosis is more common in Asian populations (unlike left-sided predominance in Western populations). It closely mimics appendicitis with RLQ pain, fever, and peritonism. CT abdomen with contrast is the diagnostic test of choice — shows pericolonic fat stranding centred on the caecal wall rather than an inflamed appendix.

2. List three clinical features that distinguish mesenteric adenitis from acute appendicitis in a child.

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(1) Recent URTI/sore throat prodrome preceding abdominal pain, (2) Higher fever than typically seen in appendicitis, (3) Minimal or absent peritoneal signs despite abdominal tenderness. Causative organisms include beta-haemolytic Strep, Yersinia, adenovirus.

3. A 25-year-old woman presents with sudden-onset RLQ pain. She missed her last period. What is the most important immediate investigation and why?

Your answer

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Urine pregnancy test (beta-hCG). A positive pregnancy test in the context of RLQ pain and amenorrhoea strongly suggests ruptured ectopic pregnancy until proven otherwise. Follow up with pelvic USG. This is a life-threatening emergency requiring urgent laparoscopy if confirmed.

4. What is Valentino's sign and what condition does it indicate?

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Valentino's sign is RLQ pain caused by a perforated peptic ulcer (PPU) — gastric/duodenal contents leak and track down the right paracolic gutter to the RIF, mimicking appendicitis. Key differentiator: the pain starts in the epigastrium (opposite direction to appendicitis pain migration), and erect CXR may show pneumoperitoneum.

5. How do you clinically differentiate ureteric colic from acute appendicitis at the bedside?

Your answer

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Ureteric colic: patient is restless/cannot lie still, pain is colicky (comes in waves), radiates loin-to-groin, urinalysis shows RBCs, no peritoneal signs. Appendicitis: patient lies still (movement worsens pain), pain is constant (once somatic), localised peritoneal signs present, urinalysis usually normal.

6. State the 'Rule of 2s' for Meckel's diverticulum.

Your answer

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2% of population, 2% become symptomatic (often by age 2), 2:1 male-to-female ratio, 2 inches long, found within 2 feet of ileocaecal valve, 2 types of ectopic tissue (gastric and pancreatic). It is a true diverticulum from incomplete obliteration of the vitelline (omphalomesenteric) duct.

References

^[1] Lecture slides: GC 203. The child needs an operation Common emergencies and surgery in childhood.pdf (p39–41) ^[2] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p5, p14, p16, p17, p20, p22, p25, p27) ^[3] Senior notes: maxim.md (Section 4.6 – Acute appendicitis; Section 2.4 – Acute abdomen) ^[4] Senior notes: felixlai.md (Acute appendicitis – Differential diagnosis; Diverticulitis DDx) ^[5] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf (p4) ^[6] Senior notes: maxim.md (Section 3.3 – Paediatric surgical abdomen) ^[7] Senior notes: maxim.md (Meckel diverticulum section)

Diagnostic Criteria, Algorithm, and Investigations

Fundamental Diagnostic Principle

Diagnosis of acute appendicitis is essentially clinical ^[2][4]. Diagnosis is often clinical ^[8].

This is the single most important statement to internalise. Unlike many conditions where you depend heavily on a single definitive test, acute appendicitis is diagnosed by putting together the clinical picture — history, examination, basic bloods, and scoring systems — and then using imaging to confirm or exclude in equivocal cases. No blood test or imaging modality alone can definitively rule in or rule out appendicitis.

Why is clinical diagnosis so central? Because the pathological process is dynamic and evolves over hours. A patient seen at 6 hours may have a completely different examination from the same patient at 18 hours. This is why serial examination is important ^[6] — particularly in children where the presentation is vague. The diagnosis often becomes clearer with time as pain localises.

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The Alvarado (MANTRELS) Score

The Alvarado score is the most widely used clinical scoring system for risk-stratifying suspected appendicitis ^[3][4]. It is a clinical and laboratory-based scoring system that helps guide the operative decision ^[4].

MANTRELS is the mnemonic — each letter represents a component:

Interpreting the Alvarado Score

Practical nuance: The Alvarado score was originally designed for adult males. It has lower specificity in women of reproductive age (because gynaecological pathology can produce similar symptoms and signs) and in children (who may not mount a robust leucocytosis and whose symptoms are vague). In these groups, a lower threshold for imaging is appropriate.

Other Scoring Systems (Brief Mention)

• Appendicitis Inflammatory Response (AIR) Score: Incorporates CRP levels in addition to clinical features. More discriminatory than Alvarado in some studies, particularly for identifying complicated appendicitis.
• Paediatric Appendicitis Score (PAS): Modified for children — includes right lower quadrant cough/hop/percussion tenderness instead of rebound tenderness (which is harder to elicit reliably in children).
• Adult Appendicitis Score (AAS): Newer score incorporating CRP and clinical features with better sensitivity/specificity profiles.

For exams, the Alvarado (MANTRELS) score is the one you must know inside out. The others are good to be aware of.

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Diagnostic Algorithm

The following algorithm integrates the clinical assessment, scoring, and imaging strategy for suspected acute appendicitis:

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Investigations

Investigations serve three purposes: (1) support the clinical diagnosis, (2) exclude differential diagnoses, and (3) identify complications (perforation, abscess).

A. Bedside Tests

Bedside tests: urinalysis, pregnancy test ^[8]

B. Blood Tests

Blood tests: blood count, renal and liver function, amylase, clotting profile, arterial blood gas, type and screen ^[8]

C. Radiological Investigations

The imaging of choice for RLQ pain is CT with IV contrast ^[3][8].

1. Plain Abdominal X-ray (AXR)

AXR: faecoliths (only 5% radio-opaque) ^[3]

• Not recommended in the diagnostic workup of suspected appendicitis, nor do findings on plain radiograph change the level of suspicion for appendicitis ^[4].
• Plain XR (rarely) used in paediatric assessment ^[1].
• Why is it still sometimes done? Primarily to exclude other causes of acute abdomen (e.g., bowel obstruction with dilated loops and air-fluid levels, pneumoperitoneum from perforated viscus — though erect CXR is better for this).
• Possible findings (non-specific and unreliable):
  • Radio-opaque faecolith in RIF (only 5% of appendicoliths are calcified enough to be visible)
  • Localised ileus ("sentinel loop") — a dilated loop of small bowel in the RIF due to localised inflammation
  • Loss of the right psoas shadow (from retroperitoneal inflammation)
  • Scoliosis concave to the right (from psoas spasm)
• Bottom line: AXR is a low-yield investigation for appendicitis specifically. Its value lies in excluding other diagnoses.

2. Ultrasound (USG) Abdomen and Pelvis

USG: low sensitivity, for pregnant women/children ^[3]. Ultrasound and CT scan may be helpful ^[8].

Advantages (+) ^[4]:

• No ionising radiation — safe for children and pregnant women
• No intravenous contrast required
• Can assess gynaecological pathology simultaneously (ovarian cyst, ectopic pregnancy, PID)
• Real-time, bedside, repeatable

Disadvantages (−) ^[4]:

• Lower diagnostic accuracy compared to CT
• Higher non-diagnostic rate (cannot visualise the appendix in 15–50% of cases)
• Operator dependent — accuracy varies with sonographer experience
• Patient-specific limitations: body habitus (obesity significantly reduces sensitivity), discomfort (pressure on tender abdomen), appendix location relative to overlying bowel (retrocaecal appendix hidden by gas-filled bowel)

USG Findings of Appendicitis ^[4]:

Graded compression technique: The sonographer applies gentle, graduated pressure with the transducer in the RIF. Normal bowel loops are displaced and compressed. The inflamed appendix, being rigid and non-compressible, remains visible as a target-like structure on transverse view.

Strategy in children: USG is the first-line imaging in paediatrics ^[1][3]. If USG is positive → proceed to surgery. If USG is negative or equivocal but clinical suspicion remains → serial observation or CT (bearing in mind radiation concerns — beware of high radiation ^[1]).

3. CT Abdomen and Pelvis with IV Contrast

This is the imaging modality with the highest diagnostic accuracy ^[3][4] and the lowest non-diagnostic rate ^[4].

• Sensitivity: 94–98%
• Specificity: 95–98%
• Negative predictive value: > 97% (a truly negative CT essentially excludes appendicitis)

Advantages (+) ^[4]:

• Highest diagnostic accuracy
• Lowest non-diagnostic rate
• Excellent for identifying complications (abscess, phlegmon, perforation)
• Can identify alternative diagnoses (right-sided diverticulitis, mesenteric adenitis, ovarian pathology, ureteric calculi)

Disadvantages (−) ^[4]:

• Radiation is contraindicated in infants and pregnancy — CT involves significant ionising radiation (effective dose ~10 mSv for an abdominal CT). In children, radiation risk is amplified due to longer remaining lifespan for cancer development. Beware of high radiation in paediatrics ^[1].
• Contrast is contraindicated in renal insufficiency or hypersensitivity — iodinated contrast can cause contrast-induced nephropathy (especially if eGFR < 30) or anaphylactoid reactions.

CT Findings of Appendicitis ^[3][4]:

CT Findings Suggesting Complications:

4. MRI Abdomen and Pelvis

MRI abdomen and pelvis with contrast ^[4]

• Advantages: No ionising radiation ^[4] — the primary reason it is used.
• Disadvantages: Higher non-diagnostic rate ^[4], longer scan time (20–30 min vs 5 min for CT), requires patient cooperation (difficult in young children without sedation), less widely available on an emergency basis, more expensive.
• When to use: Second-line imaging in pregnant women when USG is equivocal. Also increasingly used in paediatric centres where availability allows.
• Findings: Similar to CT — enlarged appendix, wall thickening, periappendiceal fluid/inflammation. T2-weighted sequences show the inflamed appendix as high signal.

5. Diagnostic Laparoscopy

Diagnostic laparoscopy ^[3] is both diagnostic AND therapeutic.

• Used when the diagnosis remains uncertain despite clinical assessment and imaging.
• Particularly useful in women of reproductive age (can simultaneously assess the appendix, ovaries, tubes, and uterus).
• If appendicitis is confirmed → proceed to laparoscopic appendicectomy in the same sitting.
• If the appendix is normal → inspect the terminal ileum (Crohn's, Meckel's, mesenteric adenitis), gynaecological organs, and remainder of the abdomen.

Summary: Imaging Strategy by Patient Group

Investigations for Acute Abdomen — Quick Reference

From the lecture slides, the general investigation approach for acute abdominal pain ^[8]:

Bedside tests: urinalysis, pregnancy test Blood tests: blood count, renal and liver function, amylase, clotting profile, arterial blood gas, type and screen Imaging: erect CXR, erect and supine AXR, USG, CT, contrast studies Endoscopy: colonoscopy, upper endoscopy

And the site-specific imaging guidance from senior notes ^[3]:

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Special Considerations

Paediatric Diagnosis

• Investigations: leucocytosis, plain XR (rarely), USG, CT (beware of high radiation) ^[1].
• Clinical diagnosis — serial examination is important ^[6].
• For boys: usually no need for imaging unless suspected delayed abscess or unclear diagnosis ^[6].
• For girls: ask LMP, order pregnancy test and USG abdomen. Do NOT perform PV on your own — consult Gynaecology!! ^[6].
• The approach in children is more conservative with imaging because: (1) radiation risk is significant, (2) clinical observation with serial exams is often sufficient, (3) USG can be used as first-line to avoid radiation.

When the Appendix Appears Normal at Surgery

If a normal appendix is found at operation ^[3]:

• The appendix is still removed — to avoid diagnostic confusion in the future (if the appendix is left in situ, a future episode of RLQ pain would re-raise appendicitis as a possibility).
• The surgeon must systematically inspect: terminal ileum (Crohn's, Meckel's diverticulum, TB ileitis), mesenteric lymph nodes (mesenteric adenitis), right colon (diverticulitis, carcinoma), gynaecological organs (women), and omentum/small bowel mesentery.
• The specimen is sent for histology — incidental carcinoid tumours and other pathology are occasionally found.

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Active Recall - Diagnosis of Acute Appendicitis

1. List the 8 components of the Alvarado (MANTRELS) score and their point values.

Your answer

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M - Migratory RIF pain (1), A - Anorexia (1), N - Nausea/vomiting (1), T - Tenderness in RIF (2), R - Rebound tenderness (1), E - Elevated temperature above 37.5C (1), L - Leucocytosis above 10x10^9/L (2), S - Shift to left (1). Total = 10. Score 7-10 = strongly predictive, 5-6 = equivocal (needs imaging), 0-4 = unlikely.

2. What are the 5 key CT findings of acute appendicitis?

Your answer

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(1) Enlarged appendiceal diameter > 6 mm with occluded lumen, (2) Appendiceal wall thickening > 2 mm, (3) Periappendiceal fat stranding (most sensitive sign), (4) Appendiceal wall enhancement (hyperaemia), (5) Presence of appendicolith.

3. Why is USG preferred over CT as first-line imaging in children with suspected appendicitis?

Your answer

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USG involves no ionising radiation, which is critical in children due to their higher radiation sensitivity and longer remaining lifespan for cancer development. CT involves significant radiation dose (~10 mSv). USG is also non-invasive, requires no contrast, and can be repeated. CT is reserved for equivocal USG results.

4. A patient with suspected appendicitis has a mildly elevated serum bilirubin but otherwise normal LFTs. What does this suggest and what is the mechanism?

Your answer

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Mild elevation of serum bilirubin is a marker for appendiceal perforation. Mechanism: perforation causes bacteria/endotoxins to enter portal circulation via appendiceal vein to ileocolic vein to portal vein to liver. Endotoxins impair hepatic bilirubin excretion at the canalicular membrane, causing mild hyperbilirubinaemia.

5. What is the first investigation you must order in a 22-year-old woman presenting with RLQ pain, and why?

Your answer

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Urine pregnancy test (beta-hCG). Mandatory in ALL women of childbearing age to exclude ectopic pregnancy, which is a life-threatening emergency. A positive result with RLQ pain and no intrauterine pregnancy on USG strongly suggests ectopic pregnancy. Must be done before any imaging or surgical planning.

6. Why should you AVOID colonoscopy or OGD in a patient with suspected acute abdomen?

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Gas insufflation during endoscopy can disrupt a sealed-off (walled-off) perforation, converting a contained situation into generalised peritonitis. This applies to upper and lower GI endoscopy, NOT to diagnostic laparoscopy which is performed under controlled surgical conditions.

References

^[1] Lecture slides: GC 203. The child needs an operation Common emergencies and surgery in childhood.pdf (p39, p41) ^[2] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p5, p9, p14, p15) ^[3] Senior notes: maxim.md (Section 4.6 – Acute appendicitis; Section 2.4 – Acute abdomen) ^[4] Senior notes: felixlai.md (Acute appendicitis – Diagnosis, Biochemical tests, Radiological tests) ^[6] Senior notes: maxim.md (Section 3.3 – Paediatric surgical abdomen) ^[8] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p12, p15)

Management of Acute Appendicitis

General Principles

The management of acute appendicitis rests on three pillars: resuscitation, antibiotics, and surgery. The decision tree depends critically on three factors:

1. When did symptoms start? ( < 72 hours vs > 72 hours)
2. Is the appendicitis complicated or uncomplicated? (simple inflammation vs gangrenous/perforated/abscess/peritonitis)
3. Is the patient stable or unstable?

Treatment: Antibiotics + Appendicectomy (Laparoscopic vs open) ^[2]

Appendectomy is the preferred treatment for complicated or uncomplicated acute appendicitis ^[4]. It can generally be performed with low morbidity and mortality ^[4].

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Management Algorithm

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Step 1: Initial Resuscitation and Supportive Care

Before any definitive treatment, every patient needs resuscitation. This is not unique to appendicitis — it applies to any acute surgical abdomen ^[3][4]:

Resuscitation, NPO, IV fluids, analgesics ^[3]

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Step 2: Antibiotic Therapy

Prophylactic IV antibiotics ^[3] are a cornerstone of management, serving different roles at different stages:

Indications for Antibiotics [4]

1. Pre-operative prophylaxis: Perioperative antibiotics are required and given within a 60-minute "window" before the initial incision ^[4] — this ensures therapeutic antibiotic levels in tissue at the time of surgical incision, reducing surgical site infection (SSI).
2. Non-operative management: Antibiotics as primary treatment for uncomplicated appendicitis (the "antibiotics-first" approach).
3. Post-operative continuation: Required for complicated appendicitis (perforation, abscess, peritonitis) to treat ongoing intra-abdominal sepsis.

Antibiotic Choice

Anaerobic coverage is essential ^[3]. The standard regimens target the polymicrobial flora (Gram-negatives + anaerobes):

Why must we cover anaerobes? Because Bacteroides fragilis is the most common anaerobic organism in the appendix, and it is the principal cause of intra-abdominal abscess formation after appendicitis. Metronidazole provides excellent anaerobic cover and penetrates abscess cavities well.

Duration of Antibiotics

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Step 3: Definitive Surgical Management

A. Immediate Surgery (Presentation < 72 hours)

Patients who present within 72 hours will undergo immediate appendicectomy ^[4].

Why 72 hours as the cut-off? Within the first 72 hours, the inflammatory process is still evolving — tissue planes are identifiable, adhesions are not yet dense, and the appendix can be safely dissected. After 72 hours, dense adhesions and phlegmon formation make surgery technically hazardous ^[4].

Laparoscopic Appendicectomy — First Line [3]

Laparoscopic is preferred: ↓ infection risk, ↓ post-op pain, ↓ hospital stay ^[3]

Advantages of laparoscopic over open ^[4]:

Disadvantages of laparoscopic ^[4]:

Patient positioning: Supine ± Trendelenburg and right side up ^[3] — tilting the patient head-down and right side up causes the small bowel to fall away from the operative field in the RIF by gravity, improving visualisation.

Open Appendicectomy

Open: indicated if gross sepsis ^[3]

Indications for open approach:

• Gross sepsis / diffuse peritonitis (Grade 5) — open approach allows better peritoneal lavage
• Haemodynamic instability
• Failed laparoscopic approach (conversion)
• Lack of laparoscopic equipment/expertise
• Appendiceal mass requiring right hemicolectomy

Methods of Incision (Open Surgery) [3][4]

Pre-operative Preparation [4]

• Orogastric tube to decompress the stomach — reduces gastric distension and aspiration risk during induction of anaesthesia
• Foley catheter or voiding prior to operation — an empty bladder reduces the risk of iatrogenic bladder injury and provides intra-operative urine output monitoring
• Perioperative antibiotics — within 60-minute window before incision

Surgical Steps (Simplified)

1. Access (laparoscopic ports or open incision)
2. Identify the appendix by tracing the taeniae coli to their convergence at the caecal base
3. Divide the mesoappendix — ligate/clip/cauterise the appendicular artery (end-artery — must be securely controlled to prevent haemorrhage)
4. Divide the appendix at its base — ligate the stump with absorbable suture or secure with endoscopic stapler/loop. Some surgeons invaginate the stump into the caecal wall (purse-string or Z-stitch) — this is controversial and increasingly omitted
5. Specimen retrieval — place in retrieval bag (laparoscopic) to avoid contaminating the wound. Always send for histology (may find carcinoid, adenocarcinoma, mucinous neoplasm)
6. Peritoneal lavage if purulent/contaminated — wash out RIF and pelvis
7. Inspect the rest of the abdomen — terminal ileum, Meckel's, caecum, ovaries/tubes (in women)
8. Close — port sites (laparoscopic) or layered closure (open)

B. Interval Surgery — The Oschner-Sherren Regimen (Presentation > 72 hours, Stable, Walled-Off)

C. Conservative (Antibiotics-First) Management

Conservative management can be considered if uncomplicated (no perforation/abscess) and not fit for surgery ^[3].

Surgery vs Antibiotics — Comparison

Key Evidence for Conservative Management [3]

• CODA trial (2020): 10-day antibiotics non-inferior to appendicectomy for uncomplicated appendicitis. However, 30% chance of requiring appendicectomy within 90 days, and increased risk of failure if appendicoliths present.
• APPAC I/II/III trials: Finnish trials demonstrating that antibiotic therapy is a safe and feasible alternative for uncomplicated appendicitis, though with significant recurrence rates.
• APPIC trial: Further supporting evidence for antibiotics-first approach.

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Post-operative Management

Post-operative management ^[4]:

Post-operative Complications

Risks — need to know for consent! ^[3]

These are systematically categorised by timing:

Immediate Complications (Intra-operative)

Early Complications (Days to Weeks)

Late Complications (Weeks to Months)

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Management in Special Populations

Paediatric Appendicitis

• Laparoscopic appendicectomy ± open ^[6]
• Non-operative management (NOM) can be considered in selected patients (no complications, no appendicoliths) ^[6]
• Resuscitation: NS 20 mL/kg fast rate ^[6]
• NG decompression, correct electrolytes, type and screen for OT ^[6]
• Children often present later with complicated appendicitis → higher rates of open conversion and prolonged antibiotic courses

Pregnancy

• Surgery should NOT be delayed — the risk of perforation and foetal loss from complicated appendicitis far exceeds the risk of surgery.
• Laparoscopic approach is safe in all trimesters (slight modification of port placement in late pregnancy).
• Left lateral tilt to prevent aortocaval compression by the gravid uterus.
• Avoid excessive CO₂ insufflation pressure.

Elderly

• Maintain a low threshold for surgery — atypical presentations lead to delayed diagnosis and higher perforation rates.
• Always send the specimen for histology and consider follow-up colonoscopy to exclude underlying caecal malignancy.

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Summary of Management Decision Tree

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Active Recall - Management of Acute Appendicitis

1. What is the standard antibiotic regimen for acute appendicitis, and what organisms does each component cover?

Your answer

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IV metronidazole + 3rd generation cephalosporin (e.g., ceftriaxone). Metronidazole covers anaerobes (especially Bacteroides fragilis). Ceftriaxone covers Gram-negatives (E. coli, Pseudomonas). Given within 60-min window before incision. Non-complicated: 24h post-op. Complicated: 3-7 days post-op.

2. A patient presents with RLQ pain, CT shows an appendiceal abscess, and symptoms have been present for 5 days. The patient is haemodynamically stable. What is the management plan?

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Oschner-Sherren regimen: (1) IV antibiotics (metronidazole + ceftriaxone), (2) Image-guided percutaneous drainage of the abscess, (3) Interval laparoscopic appendicectomy at 6-8 weeks, (4) Colonoscopy if age > 40 to exclude caecal carcinoma. Rationale: > 72 hours, walled-off process — immediate surgery risks dense adhesions, organ injury, and need for ileocolectomy.

3. List 3 advantages and 3 disadvantages of laparoscopic vs open appendicectomy.

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Advantages of laparoscopic: (1) Lower wound infection rate, (2) Lower post-op pain, (3) Shorter hospital stay. Also: better cosmesis, diagnostic advantage. Disadvantages of laparoscopic: (1) May need conversion to open, (2) Longer operative time, (3) Higher cost. Also: possibly higher intra-abdominal abscess rate, higher intra-operative complication rate.

4. Name the three open incisions used for appendicectomy and state the key feature of each.

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Lanz: transverse incision 2cm below umbilicus, follows Langer's lines (most popular, best cosmesis). Gridiron: perpendicular to ASIS-umbilicus line at McBurney's point (muscle-splitting, classic teaching incision). Rutherford-Morrison: extended Gridiron obliquely upwards and laterally (for paracaecal/retrocaecal appendix or difficult access).

5. What is pylephlebitis and why does it occur after appendicitis?

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Pylephlebitis = septic thrombophlebitis of the portal vein. Occurs because the appendiceal vein drains via ileocolic vein to SMV to portal vein. Bacterial septicaemia from the inflamed/perforated appendix spreads through this venous system, causing portal vein thrombosis and intrahepatic abscesses. Presents with high fever, rigors, jaundice, and RUQ pain. Treated with prolonged IV antibiotics and anticoagulation.

6. What are the recurrence rates for the antibiotics-first (conservative) approach to uncomplicated appendicitis, and which factor increases the risk of treatment failure?

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Recurrence rate: 30% at 3 months, 40% at 1 year, 50% at 3 years. Presence of appendicolith on imaging significantly increases the risk of treatment failure (CODA trial). Other risk factors for failure: complicated appendicitis, immunosuppression, elderly age.

References

^[1] Lecture slides: GC 203. The child needs an operation Common emergencies and surgery in childhood.pdf (p41) ^[2] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p15) ^[3] Senior notes: maxim.md (Section 4.6 – Acute appendicitis, Management) ^[4] Senior notes: felixlai.md (Acute appendicitis – Treatment, Supportive treatment, Medical treatment, Laparoscopic appendicectomy, Post-operative management) ^[6] Senior notes: maxim.md (Section 3.3 – Paediatric surgical abdomen)

Complications of Acute Appendicitis

Complications of acute appendicitis can be divided into two broad categories: complications of the disease itself (if untreated or inadequately treated) and post-operative complications (following appendicectomy). Understanding both is critical for exam purposes and for informed consent discussions with patients.

The key concept linking all disease complications is the pathological progression we covered earlier: obstruction → inflammation → gangrene → perforation → abscess or peritonitis. Every complication is essentially a consequence of where the patient falls on this spectrum and whether the body can contain the infection.

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A. Complications of the Disease (Pre-operative / Untreated)

These follow the natural history of appendicitis if left untreated, or if diagnosis is delayed.

1. Perforation

Perforation of the appendix ^[4] is the most feared complication and the natural endpoint of untreated appendicitis.

• Pathophysiology: Patients develop inflammation and necrosis of the appendix. Increased risk of perforation once significant inflammation and necrosis occurs, which leads to localised abscess formation or diffuse peritonitis ^[4]. As the appendiceal wall undergoes gangrenous necrosis (recall: the appendiceal artery is an end-artery — once thrombosed, the entire wall dies), the weakened wall gives way, releasing intraluminal contents (pus, bacteria, faecal material) into the peritoneal cavity.
• Clinical suspicion: Considered in patients when fever > 39.4°C, WBC > 15 × 10⁹/L, and imaging studies reveal fluid collection in RLQ ^[4].
• Risk factors for perforation: Male gender, extremes of age, DM, immunosuppression, previous abdominal surgery, faecolith obstruction, pelvic appendix ^[4].
• Time course: Perforation rarely occurs within the first 12 hours of symptom onset. Risk increases significantly after 36–48 hours of untreated symptoms. In children < 5 years and adults > 65 years, perforation rates can reach 50–70% because of delayed diagnosis.
• The "relief then crash" phenomenon: As the appendiceal wall becomes gangrenous, nerve endings within the wall die → pain may temporarily improve. Then perforation occurs → sudden severe generalised abdominal pain, tachycardia, fever, and peritoneal signs. This pattern is a classic clinical trap.

2. Appendiceal Abscess

Walled off: forms appendiceal abscess → may cause obstruction ^[3].

• Pathophysiology: When the appendix perforates, the greater omentum (the "policeman of the abdomen") and adjacent loops of bowel migrate towards the inflamed area and wall off the contamination, forming a contained collection of pus — an appendiceal abscess. This is the body's defence mechanism to prevent generalised peritonitis.
• Clinical features: Signs of complications: high fever, RLQ mass, imaging shows abscess/phlegmon (inflammatory mass) ^[3]. Classically presents with:
  • Persistent or swinging (spiking) fever despite initial treatment
  • Palpable, tender RLQ mass
  • Persistent RLQ pain
  • Elevated and rising inflammatory markers (WCC, CRP)
• Imaging: CT abdomen with contrast is the gold standard — shows a rim-enhancing fluid collection with surrounding fat stranding.
• Complications of the abscess itself:
  • May cause adhesive small bowel obstruction (loops of bowel become adherent to the inflammatory mass)
  • May fistulise to adjacent structures (see enterocutaneous fistula below)
  • May rupture, causing secondary generalised peritonitis
• Management: IV antibiotics ± image-guided percutaneous drainage → interval appendicectomy at 6–8 weeks ^[3].

3. Appendiceal Phlegmon

• A phlegmon is an inflammatory mass composed of the inflamed appendix, adherent omentum, and loops of bowel — without a drainable fluid collection (distinguishing it from an abscess).
• It represents an earlier/milder stage of the same walling-off process.
• On CT, it appears as an ill-defined soft tissue mass with fat stranding in the RIF, but without a discrete fluid pocket.
• Management is the same as abscess: IV antibiotics → interval appendicectomy ^[3][4]. Importantly, immediate surgery in patients with phlegmon formation is associated with increased morbidity due to dense adhesions and inflammation — operating through a phlegmon often requires extensive dissection and leads to injury of adjacent structures and complications necessitating ileocolectomy or caecostomy ^[4].

4. Generalised (Diffuse) Peritonitis

Not walled off: generalised peritonitis ^[3].

• Pathophysiology: When the omentum and adjacent structures fail to wall off the perforation, faecal and purulent material spreads freely throughout the peritoneal cavity. This is secondary bacterial peritonitis — a surgical emergency ^[9]. Acute secondary bacterial peritonitis can be caused by severe inflammation of abdominal organs (e.g., diverticulitis, cholecystitis, appendicitis), perforations of the GI tract, anastomotic leakage, or ischaemia of abdominal organs ^[9].
• Why does it fail to wall off? In children (underdeveloped omentum), in immunosuppressed patients (blunted inflammatory response cannot organise a wall), or when the contamination is overwhelming (massive perforation with faecal spillage).
• Clinical features:
  • Severe, generalised abdominal pain — the patient lies absolutely still
  • Board-like rigidity — involuntary contraction of the entire abdominal wall musculature (a reflex arc: inflamed peritoneum → somatic afferent nerves → spinal cord → motor efferents → abdominal wall muscles)
  • Absent bowel sounds — the bowel enters a state of paralytic ileus in response to the generalised peritoneal inflammation (the enteric nervous system "shuts down" when the peritoneum is inflamed)
  • Sepsis / septic shock — tachycardia, hypotension, fever (or hypothermia in severe sepsis), altered mental status
  • Rebound tenderness and guarding (generalised, not localised)
• Grading: This corresponds to Grade 5 in the disease severity score (perforated with diffuse peritonitis) ^[4].
• Management: This is a surgical emergency — requires open appendicectomy (or laparoscopic if expertise available), thorough peritoneal lavage, and prolonged post-operative IV antibiotics (3–7 days minimum). Haemodynamic resuscitation takes priority.

5. Pylephlebitis (Septic Portal Vein Thrombosis)

Pylephlebitis (septic portal vein thrombosis) ^[4] — a rare but devastating pre- or post-operative complication.

• Etymology: "pyle" (Greek) = gate (referring to the porta hepatis / portal vein); "phlebitis" = vein inflammation.
• Pathophysiology: Thrombosis and infection within the portal venous system. Caused by septicaemia in the portal venous system ^[4]. The appendiceal vein drains via the ileocolic vein → superior mesenteric vein → portal vein. When the appendix is severely infected or perforated, bacteria enter this venous system, causing septic thrombophlebitis that propagates along the portal vein to the liver, leading to development of intra-hepatic abscesses ^[4].
• Clinical features: Associated with high fever, chills and rigors, and jaundice ^[4]. The patient is severely septic. Jaundice occurs because: (1) hepatic abscesses disrupt bile canaliculi, and (2) portal vein thrombosis causes hepatic congestion and impaired bilirubin metabolism.
• Diagnosis: CT abdomen with IV contrast — shows filling defect in the portal vein (thrombus) and ring-enhancing hepatic abscesses. Blood cultures are typically positive.
• Management: Prolonged IV antibiotics (4–6 weeks), therapeutic anticoagulation (to prevent thrombus propagation), ± percutaneous drainage of hepatic abscesses. Mortality is significant (~10–30%).

Connection to liver abscess: Pylephlebitis from appendicitis is a recognised cause of pyogenic liver abscess — spread from portal vein (20% of liver abscess causes): intra-abdominal infections e.g., acute appendicitis, diverticulitis, Crohn's ^[10].

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B. Post-operative Complications (Following Appendicectomy)

These are systematically categorised by timing. Risks — need to know for consent! ^[3]

Immediate Complications (Intra-operative / < 1 hour)

Early Complications (24 hours to weeks)

Late Complications (Weeks to months/years)

Incidental Appendiceal Neoplasms — A Special "Complication" to Know

Appendix specimen sent to pathology for assessment of neoplasms (1% chance) ^[3].

The resected appendix must always be sent for histological examination. In approximately 1% of cases, an unsuspected neoplasm is found:

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Summary: Complications at a Glance

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Mortality

• Non-perforated appendicitis: Mortality < 0.1% — extremely low with modern surgical care.
• Perforated appendicitis: Mortality 0.5–5%, rising significantly in the elderly and immunocompromised.
• Generalised peritonitis with septic shock: Mortality can exceed 10–30% depending on patient comorbidities and time to intervention.
• The key determinant of outcome is time to diagnosis and treatment — every hour of delay increases the risk of progression along the complication spectrum.

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Active Recall - Complications of Acute Appendicitis

1. What clinical parameters suggest appendiceal perforation, and what are the risk factors?

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Suspect perforation when: fever > 39.4C, WBC > 15 x 10^9/L, imaging shows fluid collection in RLQ. Risk factors: male gender, extremes of age, DM, immunosuppression, previous abdominal surgery, faecolith obstruction, pelvic appendix position.

2. Why is immediate surgery contraindicated in a patient presenting more than 72 hours after symptom onset with an appendiceal phlegmon?

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After 72 hours with phlegmon formation, there are dense adhesions and inflammation. Immediate surgery requires extensive dissection, risks injury to adjacent structures (caecum, ureter, iliac vessels, small bowel), and may necessitate ileocolectomy or caecostomy. Instead, manage with IV antibiotics (+/- percutaneous drainage if abscess present) then interval appendicectomy at 6-8 weeks when inflammation has resolved.

3. A patient develops swinging fevers on day 6 after appendicectomy for perforated appendicitis. What is the most likely diagnosis, how would you investigate, and how would you manage?

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Most likely diagnosis: intra-abdominal or pelvic abscess. Investigation: CT abdomen with IV contrast (shows rim-enhancing fluid collection). Management: image-guided percutaneous drainage (first-line) + IV antibiotics. Surgery if not amenable to percutaneous drainage.

4. Explain the pathophysiology of pylephlebitis as a complication of acute appendicitis, including the anatomical venous drainage pathway.

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Appendiceal vein drains to ileocolic vein to superior mesenteric vein to portal vein. Bacteria from the infected/perforated appendix enter this venous system, causing septic thrombophlebitis that propagates along the portal vein. Thrombus and infection reach the liver via portal vein, leading to intrahepatic abscesses. Presents with high fever, rigors, jaundice. Treat with prolonged IV antibiotics (4-6 weeks) and anticoagulation.

5. An appendicectomy specimen reveals a 2.5 cm carcinoid tumour. What is the appropriate next step and why?

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Right hemicolectomy is required. Carcinoid tumours > 2 cm or involving the caecum/lymph nodes have significant metastatic potential (especially to regional lymph nodes and liver). Appendicectomy alone is only curative for carcinoids 2 cm or smaller confined to the appendix without lymph node involvement.

6. List the post-operative complications of appendicectomy categorised by timing (immediate, early, late) with at least two examples for each.

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Immediate: conversion to open, normal appendix removed, incidental malignancy needing R hemicolectomy, organ injury, bleeding. Early: wound infection (5-10%), intra-abdominal/pelvic abscess (spiking fever), post-op ileus. Late: incisional hernia, adhesions (leading to SBO), stump appendicitis, enterocutaneous fistula, pylephlebitis.

References

^[3] Senior notes: maxim.md (Section 4.6 – Acute appendicitis, Management, Risks, Appendix specimen pathology) ^[4] Senior notes: felixlai.md (Acute appendicitis – Treatment, Post-operative complications, Prognosis/Complications) ^[9] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p39) ^[10] Senior notes: maxim.md (Liver abscess – Etiology)