Acute Appendicitis
Acute inflammation of the vermiform appendix, typically caused by luminal obstruction, presenting with periumbilical pain migrating to the right iliac fossa and requiring urgent surgical intervention.
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].
Key Concept
Think of acute appendicitis as a "closed-loop obstruction" at miniature scale — the appendix has a single opening into the caecum, so any blockage creates a sealed chamber where pressure builds, blood supply is compromised, and bacteria proliferate. This is exactly the same principle as a closed-loop bowel obstruction, just in a tiny organ.
Disease Severity Grading
A useful grading system that mirrors the pathological progression [4]:
| Grade | Description |
|---|---|
| 1 | Inflamed (simple / early) |
| 2 | Gangrenous (ischaemic necrosis of wall) |
| 3 | Perforated with localized free fluid |
| 4 | Perforated with regional abscess |
| 5 | Perforated with diffuse peritonitis |
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.
- 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.
Anatomy and Function
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].
The base is constant, but the tip is highly variable. This is critical because the position of the tip determines the clinical presentation:
| Position | Frequency | Clinical Significance |
|---|---|---|
| Retrocaecal (but intraperitoneal) | 74% | Most common. May cause flank/back pain. Psoas sign positive. May lack classic anterior abdominal signs because the appendix is "hidden" behind the caecum. |
| Pelvic | 21% | May irritate the bladder (dysuria, frequency) or rectum (diarrhoea, tenesmus). Rectal/pelvic exam important. |
| Paracaecal | 2% | Typical RIF presentation |
| Subcaecal | 1.5% | Typical RIF presentation |
| Preileal | 1% | May cause small bowel-type symptoms |
| Postileal | 0.5% | May be behind the ileum, atypical presentation |
Why does position matter so much?
The classic "textbook" presentation of acute appendicitis (periumbilical pain migrating to RIF) relies on the appendix being in a position where it can irritate the anterior parietal peritoneum. A retrocaecal appendix may never touch the anterior parietal peritoneum, so the patient may present with flank pain, back pain, or even no localizing signs — leading to delayed diagnosis and higher perforation rates. Similarly, a pelvic appendix may irritate the bladder or rectum, mimicking UTI or gastroenteritis.
- 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].
- 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).
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 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.
Aetiology
The central mechanism is obstruction of the appendiceal lumen, though non-obstructive causes exist. The causes differ by age group:
| Cause | Details | Age Group |
|---|---|---|
| Lymphoid hyperplasia | Reactive enlargement of submucosal lymphoid follicles (from viral or bacterial infection, e.g., adenovirus, EBV, measles) occludes the narrow lumen | Main cause in young patients / children [4] |
| Faecolith (fecalith) | A hard, stony mass composed of faecal material, calcium phosphates, bacteria, and epithelial debris [4]. Acts as a "stone" blocking the appendiceal orifice | Main cause in older patients [4]. Associated with low-fibre diets. |
| Tumours | Carcinoma of the caecum can obstruct the appendiceal orifice; intrinsic tumours include carcinoid tumour, adenocarcinoma, and mucocele | Elderly patients [3][4] |
| Intestinal parasites | e.g., Enterobius vermicularis (pinworm), Ascaris lumbricoides | More common in endemic areas |
| Foreign bodies | Ingested objects, fruit seeds, etc. | Rare |
| Calculi | True appendicoliths (calcified fecaliths) | Any age |
Exam Pearl
In an elderly patient presenting with features of acute appendicitis, always think about caecal carcinoma as a possible underlying cause. Post-appendicectomy, the specimen should be sent for histology, and if there is any suspicion, a follow-up colonoscopy should be arranged.
- Mucosal ulceration from viral infection (adenovirus, CMV)
- Direct bacterial invasion
- Ischaemic causes (vasculitis, e.g., in Henoch-Schönlein purpura)
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).
Perforation is the most feared progression. Risk factors include [4]:
| Risk Factor | Explanation |
|---|---|
| Male gender | Possibly due to delayed presentation |
| Extremes of age | Young children cannot articulate symptoms; elderly have atypical presentations. Both groups have higher perforation rates (up to 50–70% in < 5 years and > 65 years) |
| Diabetes mellitus | Autonomic neuropathy blunts pain perception; immunocompromised state |
| Immunosuppression | Blunted inflammatory response → delayed diagnosis |
| Previous abdominal surgery | Altered anatomy makes diagnosis difficult |
| Faecolith obstruction | More complete obstruction → faster progression to gangrene |
| Pelvic appendix | Doesn't irritate anterior parietal peritoneum → delayed diagnosis [4] |
Pathophysiology
Understanding the pathophysiology of acute appendicitis as a stepwise sequence is critical — it explains every clinical feature, complication, and management decision.
-
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.
-
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].
-
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.
-
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).
-
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.
-
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.
-
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).
-
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.
-
Outcome depends on the body's ability to contain the spillage:
Why does perforation happen faster in children?
Children have a poorly developed omentum (the "policeman of the abdomen" that walls off infection). This means that when perforation occurs in a child, generalised peritonitis is more likely than a contained abscess. Combined with their inability to articulate symptoms clearly, this explains why perforation rates in children under 5 can exceed 50%.
Classification
| Stage | Pathology | Clinical Correlate |
|---|---|---|
| Early / Catarrhal | Mucosal and submucosal inflammation only | Vague periumbilical pain, anorexia |
| Suppurative / Phlegmonous | Transmural inflammation with pus in lumen | Pain shifts to RIF, localised peritonism |
| Gangrenous | Necrosis of appendiceal wall | Severe pain, then may get paradoxical relief (nerve death) → then sudden deterioration |
| Perforated | Hole in the wall | Sudden worsening of pain, generalised peritonism, sepsis |
| Abscess | Walled-off perforation | Palpable RIF mass, swinging fever, persistent symptoms |
- 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.
Clinical Features
The classic presentation occurs in only 50–60% of patients. Always maintain a high index of suspicion.
Symptoms
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).
Classic Teaching Point
"Visceral → Somatic" pain migration is highly suggestive of acute appendicitis. The sequence is: vague periumbilical discomfort → sharp RIF pain over 12–24 hours. This pattern has a positive predictive value of ~80% for appendicitis.
Contrast this with gastroenteritis, where nausea/vomiting precedes the pain [3] — in appendicitis, pain comes first, then nausea/vomiting.
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.
- 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.
- 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.
- 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.
- 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:
- 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.
- 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).
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.
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.
- 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
- Important to assess for cervical motion tenderness (suggests PID), adnexal masses (ovarian cyst/torsion, ectopic pregnancy), and vaginal discharge.
| Sign | Suggests |
|---|---|
| High fever ( > 38.5°C) | Perforation / abscess |
| Tachycardia | Sepsis / dehydration |
| Palpable RIF mass | Appendiceal phlegmon or abscess |
| Generalised rigidity | Diffuse peritonitis |
| Absent bowel sounds | Paralytic ileus from peritonitis |
| Paradoxical pain relief followed by sudden deterioration | Gangrenous appendicitis (nerve endings in the wall die → brief pain relief → then wall perforates → sudden peritonitis) |
The 'Relief then Crash' Pattern
A patient whose pain suddenly "gets better" before dramatically worsening likely has gangrenous appendicitis progressing to perforation. The initial relief occurs because the necrotic appendiceal wall has lost its nerve supply (dead nerves don't fire pain signals). Then when perforation occurs, bacterial and faecal contamination of the peritoneal cavity causes sudden severe peritonitis. Never be falsely reassured by apparent improvement — reassess!
Special Populations
- 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).
- 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.
- 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.
- Blunted inflammatory response → minimal fever, minimal leucocytosis, minimal peritoneal signs.
- Very high risk of delayed diagnosis and perforation.
High Yield Summary
Definition: Acute inflammation of the vermiform appendix; most common acute surgical emergency. 2/3 obstructive, 1/3 non-obstructive.
Epidemiology: Peak 20s–30s adults; 4–15 years paediatric. M:F = 1.4:1. Lifetime risk ~7–8%.
Anatomy: True diverticulum of caecum. Base at convergence of taeniae coli (McBurney's point). Appendiceal artery is an END-ARTERY (thrombosis → gangrene). Retrocaecal 74%, Pelvic 21%.
Aetiology: Lymphoid hyperplasia (young), faecolith (older), tumour (elderly). Bacteria: E. coli, Bacteroides, Pseudomonas, Peptostreptococcus.
Pathophysiology: Obstruction → ↑ intraluminal pressure → venous congestion → ischaemia → bacterial invasion → transmural inflammation → gangrene → perforation → abscess or peritonitis.
Risk factors for perforation: Male, extremes of age, DM, immunosuppression, previous surgery, faecolith, pelvic appendix.
Classic symptom sequence: Anorexia → periumbilical pain (T8–10 visceral) → N/V → pain migrates to RIF (somatic, parietal peritoneum) → low-grade fever.
Key signs: McBurney's point tenderness (pointing sign), Rovsing's (RIF pain on LLQ pressure), Psoas (retrocaecal), Obturator (pelvic), rebound tenderness, guarding.
Atypical presentations: Retrocaecal (flank/back pain), Pelvic (dysuria/diarrhoea/tenesmus), Children (diffuse pain, high perforation), Elderly (vague, high perforation), Pregnancy (displaced superiorly).
Active Recall - Acute Appendicitis (Definition to Clinical Features)
[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.
Core Principle
When working through the DDx, always ask three questions: (1) What organs live in the RLQ? (2) What is the patient's age and sex? (3) Are there any atypical features that point away from appendicitis? — e.g., prominent diarrhoea (think ileitis/GE), vaginal discharge (think PID), haematuria (think ureteric colic), missed period (think ectopic pregnancy).
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)
A. Gastrointestinal Causes
- 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].
Hong Kong Exam Pearl
In any Hong Kong clinical exam or MCQ, if a middle-aged or elderly Asian patient presents with "appendicitis-like" RLQ pain, always consider right-sided diverticulitis as a differential. The CT scan is key to differentiating the two.
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.
Mesenteric Adenitis vs Appendicitis
The classic trap: a child with URTI symptoms for 2–3 days who then develops RLQ pain. Students often jump to appendicitis, but the viral prodrome + high fever + minimal peritoneal signs should flag mesenteric adenitis. In appendicitis, the pain comes first, and the fever is typically low-grade. In mesenteric adenitis, the sore throat/viral illness comes first, and the fever is often higher.
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
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2:1 male-to-female ratio
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2 inches in length
-
Found within 2 feet of the ileocaecal valve
-
2 types of ectopic tissue: gastric (60%) and pancreatic (6%)
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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.
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Diagnosis by CT scan [2]. CT may show a blind-ending tubular structure arising from the ileum with surrounding fat stranding.
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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].
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].
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
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).
- 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.
Never Miss This
Every woman of reproductive age with acute abdominal pain MUST have a pregnancy test. Missing an ectopic pregnancy is potentially fatal. This is a medicolegal standard of care.
- 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.
- 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.
- 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.
- 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.
C. Urological Causes
- 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.
- 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.
- 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.
D. Other Causes
- 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.
- 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.
- 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).
| Feature | Appendicitis | Mesenteric Adenitis | Ectopic Pregnancy | Ureteric Colic | PID | Right-Sided Diverticulitis |
|---|---|---|---|---|---|---|
| Age/Sex | Any; M > F | Children | Women of reproductive age | Any | Women of reproductive age | Older adults; common in Asians |
| Pain onset | Gradual; migrates periumbilical → RIF | Diffuse, poorly localised | Sudden, severe | Sudden, colicky | Gradual; bilateral | Gradual; RLQ |
| Prodrome | None | Recent sore throat, URTI | Missed period | None | Vaginal discharge | None |
| Fever | Low-grade | High fever | Usually none (unless infected) | None | Variable | Low-grade |
| Peritoneal signs | Localised RIF | Minimal / absent | Diffuse (haemoperitoneum) | None | Bilateral lower abdomen | Localised RIF |
| Key investigation | Clinical ± CT | USG (lymph nodes) | Pregnancy test + USG | CT KUB; urinalysis (RBC) | HVS; cervical swab | CT abdomen with contrast |
| Diarrhoea prominent? | No (unless pelvic) | Variable | No | No | No | No |
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]
High Yield Summary
Systematic DDx of RLQ pain (as per lecture slides):
GI: Acute appendicitis, caecal diverticulitis (common in Asians — CT to differentiate), mesenteric adenitis (children, URTI prodrome, minimal peritoneal signs), Meckel's diverticulitis (Rule of 2s, CT diagnosis, incidental finding at OT), ileitis (Crohn's, TB, Yersinia, Campylobacter, Salmonella — diarrhoea is predominant symptom), caecal ischaemia, cancer of caecum, PPU with Valentino's sign.
Gynaecological (all women of reproductive age — always pregnancy test!): Ruptured ectopic pregnancy (sudden pain + bleeding + collapse), ovarian cyst torsion/rupture (USG/CT, laparoscopy), PID/TOA (cervical motion tenderness, discharge), Mittelschmerz, endometriosis/endometritis.
Urological: Ureteric colic (loin-to-groin, colicky, RBC on urinalysis, patient restless), UTI, testicular torsion (always examine scrotum in males).
Other: Strangulated hernia (always examine groins), HSP (paediatric, purpuric rash), psoas abscess, DKA.
Key Differentiators:
- Pain before N/V = appendicitis; N/V before pain = gastroenteritis
- URTI prodrome + high fever + minimal peritoneal signs = mesenteric adenitis
- Asian patient + RLQ pain + older age = think caecal diverticulitis (CT to differentiate)
- Positive pregnancy test + RLQ pain = ectopic pregnancy until proven otherwise
- Loin-to-groin colicky pain + restless patient + haematuria = ureteric colic
Active Recall - Differential Diagnosis of Acute Appendicitis
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
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.
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:
| Component | Feature | Score | Explanation |
|---|---|---|---|
| M | Migratory RIF pain | 1 | The hallmark visceral → somatic pain shift (T8–10 periumbilical → RIF as parietal peritoneum becomes involved) |
| A | Anorexia | 1 | Visceral inflammation causes reflex appetite suppression via vagal afferents |
| N | Nausea and vomiting | 1 | Brainstem activation via visceral afferents; occurs after pain onset |
| T | Tenderness in RIF | 2 | Somatic pain from parietal peritoneal irritation — the most heavily weighted clinical sign |
| R | Rebound tenderness | 1 | Indicates established peritoneal inflammation |
| E | Elevated temperature ( > 37.5°C) | 1 | Systemic inflammatory response to appendiceal infection |
| L | Leucocytosis ( > 10 × 10⁹/L) | 2 | Neutrophilic response to bacterial infection — second most heavily weighted parameter |
| S | Shift to left | 1 | Increase in immature neutrophils (bands) — indicates acute bacterial infection driving emergency granulopoiesis |
| Total | 10 |
Why is Tenderness weighted 2 and Leucocytosis weighted 2?
These two features carry the highest discriminatory power. RIF tenderness (a somatic sign) means the inflammation has already reached the parietal peritoneum — it is the most reliable clinical sign. Leucocytosis is the most objective laboratory marker of acute inflammation. Together they contribute 4 out of 10 points.
| Score | Interpretation | Action |
|---|---|---|
| ≥ 7 | Strongly predictive of acute appendicitis | Consider surgery or further imaging [3][4] |
| 5–6 | Equivocal score | Requires abdominal USG or contrast-enhanced CT [3][4] |
| ≤ 4 | Appendicitis can be ruled out with greater certainty | Evaluate for other possible diagnoses [4] |
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.
- 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.
The following algorithm integrates the clinical assessment, scoring, and imaging strategy for suspected acute appendicitis:
Key Decision Points in the Algorithm
- Always pregnancy test first in women of reproductive age — ectopic pregnancy kills and must be excluded before anything else.
- Alvarado ≥ 7: Many centres will proceed directly to surgery (especially in classic presentations in young males). Some will get a confirmatory CT to reduce negative appendicectomy rates.
- Alvarado 5–6: This is the "grey zone" — imaging is essential here. CT is the modality of choice in adults.
- Alvarado ≤ 4: Think of other diagnoses, but do NOT discharge without a plan for follow-up or serial observation if the clinical suspicion persists.
- Serial examination is key in paediatrics [6] — children's presentations evolve, and a child who looks non-specific at presentation may develop clear signs hours later.
Investigations
Investigations serve three purposes: (1) support the clinical diagnosis, (2) exclude differential diagnoses, and (3) identify complications (perforation, abscess).
Bedside tests: urinalysis, pregnancy test [8]
| Test | Purpose | Key Findings | Interpretation |
|---|---|---|---|
| Urinalysis | Exclude UTI / ureteric colic; detect sterile pyuria from pelvic appendix | RBCs → ureteric colic; WBCs + nitrites + bacteria → UTI | A pelvic appendix irritating the bladder/ureter can cause sterile pyuria (WBCs but no bacteria on culture) — don't be fooled into diagnosing UTI |
| Pregnancy test (urine β-hCG) | Indicated in all women of childbearing age [4] | Positive → ectopic pregnancy until proven otherwise | Mandatory before any imaging with radiation or surgical decision-making |
| Temperature | Assess fever | > 37.5°C scores 1 point on Alvarado | High fever ( > 38.5°C) suggests perforation/abscess or alternative diagnosis |
Blood tests: blood count, renal and liver function, amylase, clotting profile, arterial blood gas, type and screen [8]
| Test | Rationale | Key Findings in Appendicitis | Caveats |
|---|---|---|---|
| CBC with differentials | Assess for leucocytosis and left shift | Leucocytosis with left shift — increased total WBC, bands, and neutrophils [4]. ↑↑↑ leucocytosis may indicate gangrenous/perforated appendix [3] | A normal WBC cannot rule out appendicitis [3]. WBC is normal in ~20% of confirmed cases. In children, the elderly, and immunosuppressed, leucocytosis may be absent. Pregnancy has physiological leucocytosis (up to 15 × 10⁹/L) |
| CRP | Inflammatory marker; more specific than WBC for duration of inflammation | ↑ CRP [4]. CRP rises ~12 hours after symptom onset. A normal CRP within the first 12 hours does not exclude appendicitis. Very high CRP ( > 100 mg/L) suggests complicated appendicitis (perforation/abscess) | CRP is a better marker of duration and severity rather than presence of appendicitis |
| Clotting profile | Pre-operative baseline | Usually normal | Required before any surgical intervention to check for bleeding diathesis [4] |
| Electrolyte profile | Assess dehydration from vomiting/poor intake | May show dehydration (↑ urea, ↑ creatinine), hypokalaemia (from vomiting) | Important for pre-operative fluid resuscitation planning |
| RFT | Baseline renal function; pre-operative; exclude renal pathology | Usually normal | Needed before contrast CT to assess eGFR (contrast is contraindicated in significant renal insufficiency) [4] |
| LFT | Baseline; marker of perforation | Mild elevations in serum bilirubin have been noted to be a marker for appendiceal perforation [4] | The mechanism is thought to be portal bacteraemia/endotoxaemia from the inflamed appendix causing hepatocyte dysfunction via portal venous drainage |
| Serum amylase | Exclude acute pancreatitis (a DDx of acute abdomen) | Normal in appendicitis; markedly elevated ( > 3× upper limit) in pancreatitis | A mildly elevated amylase can occur with any intra-abdominal inflammation — don't overcall pancreatitis |
| ABG with lactate | Assess for metabolic acidosis / raised lactate in sepsis or ischaemic bowel | Raised lactate suggests sepsis, peritonitis, or mesenteric ischaemia | Important in the unwell patient with generalised peritonitis |
| Group and screen (type and screen) | Pre-operative preparation | — | Required for any patient heading to theatre [6] |
The Bilirubin-Perforation Link
This is a commonly tested pearl: mild elevation of serum bilirubin is a marker for appendiceal perforation [4]. Why? When the appendix perforates, bacteria and endotoxins enter the portal circulation via the appendiceal vein → ileocolic vein → portal vein → liver. Endotoxins impair hepatic bilirubin excretion at the canalicular membrane, causing a mild unconjugated or mixed hyperbilirubinaemia. If you see an appendicitis patient with a mildly raised bilirubin, worry about perforation.
C. Radiological Investigations
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.
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]:
| Finding | Significance |
|---|---|
| Non-compressible appendix with double-wall thickness diameter > 6 mm | The cardinal USG sign. A normal appendix is compressible and < 6 mm. An inflamed appendix is swollen, oedematous, and rigid — it cannot be compressed by the ultrasound probe ("non-compressible blind-ending tubular structure") |
| Focal pain over appendix with compression (sonographic McBurney's sign) | The point of maximal tenderness corresponds to the visualised appendix — provides real-time correlation between anatomy and symptoms |
| Increased echogenicity of inflamed periappendiceal fat | Inflamed fat appears bright on ultrasound (compared to normal hypoechoic fat). This represents the periappendiceal inflammation/fat stranding |
| Fluid in RLQ | Free fluid around the appendix suggests transmural inflammation or early perforation |
| Presence of appendicolith (with posterior acoustic shadowing) | A calcified faecolith within the lumen. The acoustic shadowing is caused by the dense calcified structure blocking ultrasound transmission — same principle as gallstones on USG |
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]).
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]:
| Finding | Significance |
|---|---|
| Enlarged appendiceal AP diameter > 6 mm with an occluded lumen | The inflamed, obstructed appendix distends with fluid/pus. Normal appendix diameter is < 6 mm |
| Appendiceal wall thickening > 2 mm | Oedema and inflammatory infiltrate in the wall |
| Appendiceal wall enhancement | The inflamed wall takes up IV contrast avidly (hyperaemia from the inflammatory response). This is why IV contrast is used. |
| Periappendiceal fat stranding | The most sensitive CT sign. Inflammation spreads beyond the appendiceal wall into the surrounding mesenteric fat, which appears as hazy increased attenuation ("dirty fat") on CT |
| Presence of appendicolith | A calcified density within the appendiceal lumen. Present in ~25% of cases. Its presence increases the risk of perforation and treatment failure with antibiotics alone |
CT Findings Suggesting Complications:
| Finding | Complication |
|---|---|
| Focal defect in enhancing wall + extraluminal air | Perforation |
| Walled-off fluid collection with rim enhancement | Appendiceal abscess |
| Inflammatory mass without drainable fluid | Phlegmon |
| Free fluid in pelvis / paracolic gutters | Peritonitis |
| Extraluminal appendicolith | Perforation (the faecolith has escaped through the defect) |
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.
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.
Important
AVOID endoscopy for acute abdomen: a sealed-off perforation may open by gas insufflation during endoscopy [3]. This refers to upper/lower GI endoscopy (OGD/colonoscopy), NOT diagnostic laparoscopy. Laparoscopy is performed with careful insufflation in a controlled surgical setting and is safe. But blowing air into the GI lumen via endoscopy in a patient with a walled-off perforation can disrupt the seal and cause generalised peritonitis.
| Patient Group | First-Line Imaging | Second-Line Imaging | Rationale |
|---|---|---|---|
| Adult male | CT abdomen + pelvis with IV contrast | — | Highest accuracy, no radiation concerns in adults |
| Adult female of reproductive age | Urine PT first, then CT (if PT negative) | USG if gynaecological DDx likely; diagnostic laparoscopy if still equivocal | Must exclude ectopic; CT for appendicitis, but USG may diagnose gynaecological cause |
| Children | USG | CT (beware of high radiation) [1] | Minimise radiation in paediatrics; serial observation before CT |
| Pregnant women | USG | MRI (no radiation) | CT is contraindicated (radiation to foetus); MRI is safe |
| Elderly | CT abdomen + pelvis with IV contrast | Colonoscopy after resolution (exclude caecal CA) | Must exclude malignancy as underlying cause |
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]:
| 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) |
Special Considerations
- 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.
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.
High Yield Summary
Diagnostic Principle: Acute appendicitis is a CLINICAL diagnosis. Scoring systems (Alvarado/MANTRELS) and imaging SUPPORT the clinical assessment.
Alvarado (MANTRELS) Score: M-igratory RIF pain (1), A-norexia (1), N-ausea/vomiting (1), T-enderness RIF (2), R-ebound (1), E-levated temperature (1), L-eucocytosis (2), S-hift to left (1) = Total 10.
- ≥ 7: Strongly predictive → surgery/imaging
- 5–6: Equivocal → USG or CT
- ≤ 4: Unlikely → investigate other DDx
Key Bloods: CBC (leucocytosis, left shift — ↑↑↑ suggests complicated appendicitis, but normal does NOT rule it out), CRP (rises after 12 hours; very high suggests complications), LFT (↑ bilirubin = marker of perforation), pregnancy test (MANDATORY in all women of childbearing age), amylase (exclude pancreatitis).
Imaging:
- AXR: NOT recommended for appendicitis diagnosis (only 5% of faecoliths radio-opaque).
- USG: First-line in children and pregnant women. Non-compressible appendix > 6 mm.
- CT with IV contrast: HIGHEST diagnostic accuracy in adults. Appendix > 6 mm, wall thickening > 2 mm, fat stranding, appendicolith.
- MRI: Second-line in pregnant women (no radiation).
Patient-specific strategies: Adults → CT. Children → USG first, then CT if equivocal (beware radiation). Pregnant → USG first, then MRI. Girls with RLQ pain → always pregnancy test + USG + Gynae consult.
Active Recall - Diagnosis of Acute Appendicitis
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
The management of acute appendicitis rests on three pillars: resuscitation, antibiotics, and surgery. The decision tree depends critically on three factors:
- When did symptoms start? ( < 72 hours vs > 72 hours)
- Is the appendicitis complicated or uncomplicated? (simple inflammation vs gangrenous/perforated/abscess/peritonitis)
- 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].
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]
| Measure | Details | Rationale |
|---|---|---|
| NPO (nil per os) | Nothing by mouth | Patient is likely heading to theatre; eating/drinking increases aspiration risk under general anaesthesia. Also reduces stimulation of an already inflamed GI tract |
| IV fluid resuscitation | Adults: bolus crystalloid (e.g., Hartmann's or 0.9% NaCl) as needed, then maintenance. Paediatric resuscitation: NS 20 mL/kg as fast rate [6]. Maintenance: 4-2-1 rule (4 mL/kg/hr for 1st 10 kg, 2 mL/kg/hr for 2nd 10 kg, 1 mL/kg/hr for each additional kg) [4] | Patients are often dehydrated from vomiting, poor oral intake, and third-space losses from peritoneal inflammation. Adequate hydration optimises tissue perfusion and renal function pre-operatively |
| Correction of electrolyte abnormalities | Check and correct K⁺, Na⁺, etc. | Vomiting causes hypokalaemia and metabolic alkalosis. Hypokalaemia must be corrected before anaesthesia (risk of cardiac arrhythmias) |
| Pain control with analgesics | Paracetamol ± NSAIDs ± opioids (e.g., morphine, fentanyl) | Historically, there was reluctance to give analgesia before diagnosis (fear of "masking signs"). This is now considered outdated and unethical — adequate analgesia does NOT impair diagnostic accuracy and improves patient cooperation during examination |
| Close monitoring of vital signs and urine output [4] | HR, BP, temperature, urine output (target > 0.5 mL/kg/hr in adults, > 1 mL/kg/hr in children) | Detects early signs of deterioration (sepsis, perforation, haemodynamic compromise) |
| NG decompression | Nasogastric tube if vomiting is persistent or if bowel obstruction / ileus is present | Decompresses the stomach, reduces aspiration risk, and relieves distension. NG decompression is listed in the general management of paediatric surgical abdomen [6] |
IV Fluid in Paediatrics — The 4-2-1 Rule
| Weight Bracket | Hourly Rate | Daily Equivalent |
|---|---|---|
| 1st 10 kg | 4 mL/kg/hr | 100 mL/kg/day |
| 2nd 10 kg | 2 mL/kg/hr | 50 mL/kg/day |
| Each extra kg | 1 mL/kg/hr | 20 mL/kg/day |
Example: A 25 kg child → (10 × 4) + (10 × 2) + (5 × 1) = 40 + 20 + 5 = 65 mL/hr maintenance [4].
Step 2: Antibiotic Therapy
Prophylactic IV antibiotics [3] are a cornerstone of management, serving different roles at different stages:
- 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).
- Non-operative management: Antibiotics as primary treatment for uncomplicated appendicitis (the "antibiotics-first" approach).
- Post-operative continuation: Required for complicated appendicitis (perforation, abscess, peritonitis) to treat ongoing intra-abdominal sepsis.
Anaerobic coverage is essential [3]. The standard regimens target the polymicrobial flora (Gram-negatives + anaerobes):
| Regimen | Components | Rationale |
|---|---|---|
| Metronidazole AND 3rd generation cephalosporin [4] | e.g., IV metronidazole 500 mg TDS + IV ceftriaxone 2 g OD | Metronidazole ("metro" = covers anaerobes, especially Bacteroides fragilis; also has anti-protozoal activity). Ceftriaxone (3rd-gen cephalosporin — covers Gram-negatives including E. coli, Pseudomonas partially) |
| IV ceftriaxone + metronidazole [3] | As above | Same regimen, written from Maxim notes — the most commonly cited combination |
| Alternative: Amoxicillin-clavulanate (co-amoxiclav) | IV augmentin 1.2 g TDS | Broad-spectrum cover of both aerobes and anaerobes in a single agent. Sometimes used in less severe cases |
| Alternative: Piperacillin-tazobactam | IV pip-taz 4.5 g TDS | Broader spectrum — reserved for complicated/septic cases |
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.
| Scenario | Duration | Rationale |
|---|---|---|
| Non-complicated appendicitis | Continue until 24 hours post-op only [3] | The source of infection is removed at surgery; prolonged antibiotics provide no additional benefit and increase antibiotic resistance risk |
| Complicated appendicitis (abscess, phlegmon, peritonitis) | Continue 3–7 days post-op [3] | Ongoing intra-abdominal contamination requires continued treatment. Duration guided by clinical response (defervescence, normalising WCC/CRP, improving pain) |
| Conservative (antibiotics-first) approach | 7–10 days (IV then oral step-down) | As per CODA trial protocol [3] |
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 is preferred: ↓ infection risk, ↓ post-op pain, ↓ hospital stay [3]
Advantages of laparoscopic over open [4]:
| Advantage | Explanation |
|---|---|
| Lower wound infection rate | Smaller incisions; the appendix is removed through a port (often within a retrieval bag) without direct contact with the abdominal wall |
| Lower post-operative pain | Smaller incisions = less tissue trauma = less somatic pain |
| Shorter hospital stay | Faster recovery from smaller wounds, earlier mobilisation, earlier return to oral intake |
| Better cosmesis | Three small port-site scars (typically 5–12 mm) vs a larger RIF incision |
| Diagnostic advantage | The laparoscope allows inspection of the entire peritoneal cavity — useful when the diagnosis is uncertain (can visualise appendix, terminal ileum, Meckel's, ovaries, tubes, etc.) |
Disadvantages of laparoscopic [4]:
| Disadvantage | Explanation |
|---|---|
| Conversion to open may be required | If the appendix is retrocaecal with dense adhesions, or if there is uncontrollable bleeding or unclear anatomy |
| Longer operative time | Setup of laparoscopic equipment and port placement adds time |
| Higher rate of intra-abdominal abscess | Controversial — some studies suggest slightly higher post-op abscess rates with laparoscopic approach (possibly due to CO₂ insufflation disseminating bacteria, or less thorough washout). Not consistently demonstrated in recent meta-analyses |
| Higher rate of intra-operative complications | Port-related injuries (bowel, vascular), CO₂ insufflation complications |
| Higher cost | Equipment costs (disposable trocars, endoscopic staplers) |
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: 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
| Incision | Description | Advantages / Indications |
|---|---|---|
| Lanz incision | Transverse incision 2 cm below umbilicus, centred on the mid-clavicular line [3][4]. More popular [3] | Follows Langer's lines (skin tension lines) → more cosmetically pleasing with reduced scarring [3]. Preferred for most open appendicectomies |
| Gridiron incision | Incision perpendicular to the line joining ASIS to umbilicus, centred at McBurney's point [3][4] | Classic teaching incision. Muscle-splitting approach (splits external oblique, internal oblique, and transversus abdominis along their fibre direction rather than cutting across them) — less muscle damage |
| Rutherford-Morrison incision | Extends the Gridiron obliquely upwards and laterally [3] | For paracaecal appendix [3] or when wider access is needed (retrocaecal appendix, abscess, or difficult dissection) |
Lanz vs Gridiron — Exam Favourite
Both incisions are centred over the RIF, but the Lanz runs transversely (along Langer's lines → better cosmesis), while the Gridiron runs perpendicular to the ASIS-umbilicus line (a muscle-splitting incision centred at McBurney's point). In practice, the Lanz is more commonly used for its cosmetic advantage. The Rutherford-Morrison is an extended Gridiron for difficult cases.
- 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
- Access (laparoscopic ports or open incision)
- Identify the appendix by tracing the taeniae coli to their convergence at the caecal base
- Divide the mesoappendix — ligate/clip/cauterise the appendicular artery (end-artery — must be securely controlled to prevent haemorrhage)
- 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
- Specimen retrieval — place in retrieval bag (laparoscopic) to avoid contaminating the wound. Always send for histology (may find carcinoid, adenocarcinoma, mucinous neoplasm)
- Peritoneal lavage if purulent/contaminated — wash out RIF and pelvis
- Inspect the rest of the abdomen — terminal ileum, Meckel's, caecum, ovaries/tubes (in women)
- Close — port sites (laparoscopic) or layered closure (open)
| Feature | Details |
|---|---|
| Indication | Present > 72 hours AND stable [3]. The appendiceal process has already been "walled-off" [4] — an appendiceal phlegmon or abscess has formed |
| Why not operate immediately? | Immediate surgery in patients with long duration of symptoms and phlegmon formation is associated with increased morbidity due to dense adhesions and inflammation. Appendicectomy in these circumstances often requires extensive dissection and leads to injury of adjacent structures and complications necessitating ileocolectomy or caecostomy [4] |
| Initial treatment | IV antibiotics (~90% success rate) ± image-guided percutaneous drainage of abscess [3] |
| Interval appendicectomy | Laparoscopic appendicectomy 6–8 weeks later [3][4] |
| Rationale for interval appendicectomy | Prevent recurrence of appendicitis + exclude neoplasms (carcinoid, adenocarcinoma, mucinous cystadenoma, cystadenocarcinoma) especially in older adults who have higher incidence [4] |
| If age > 40 | Colonoscopy to exclude caecal carcinoma [3] |
| Treatment failure | Evidenced by bowel obstruction, sepsis, persistent pain, fever, or leucocytosis → requires immediate appendicectomy [4] |
Why 6–8 weeks?
The 6–8 week interval allows complete resolution of the inflammatory process, so that tissue planes return to normal and safe dissection is possible. Operating too early (e.g., at 2–3 weeks) risks encountering residual inflammation and dense adhesions. Operating too late (e.g., > 3 months) risks recurrence in the interim.
C. Conservative (Antibiotics-First) Management
Conservative management can be considered if uncomplicated (no perforation/abscess) and not fit for surgery [3].
| Feature | Details |
|---|---|
| Indication | Uncomplicated appendicitis (Grade 1) in patients not fit for / unwilling to undergo surgery; no appendicolith on imaging |
| Regimen | Bowel rest, IV ceftriaxone + metronidazole [3] → step down to oral antibiotics (e.g., oral co-amoxiclav) for total 7–10 days |
| Success rate | Initial resolution in ~90% of cases |
| Recurrence rate | 30% in 3 months, 40% in 1 year, 50% in 3 years [3] — this is the major drawback |
| Surgery | Antibiotics (Non-operative) | |
|---|---|---|
| Pros | Appendectomy can generally be performed with low morbidity and mortality [4]. Definitive — removes the appendix permanently. Allows histological examination (exclude tumour) | Lower pain score, lower risk of surgical complication, faster rate of recovery [4] |
| Cons | Higher pain score, higher risk of surgical complication, slower rate of recovery [4] | Risk of progression of symptoms, risk of developing complicated appendicitis, risk of recurrent appendicitis, greater risk in elderly and immunocompromised. Risk of unexpected lesion (carcinoid/carcinoma) increases with age [4] |
- 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.
When to AVOID antibiotics-first
Do NOT use the antibiotics-first approach in:
- Complicated appendicitis (gangrenous, perforated, abscess, peritonitis)
- Appendicolith present on imaging (higher failure rate — CODA trial)
- Immunocompromised patients (higher risk of progression)
- Elderly patients (risk of missed neoplasm — the removed appendix allows histological examination)
- Unreliable patients (unable to return for follow-up if symptoms worsen)
Post-operative management [4]:
| Aspect | Uncomplicated | Complicated |
|---|---|---|
| Diet | Start on clear liquid diet and advance to regular diet as tolerated [4] | Advance cautiously; may need longer NPO period if ileus present |
| Antibiotics | Antibiotics are NOT required postoperatively for non-perforated appendicitis [4]. Stop at 24 hours post-op [3] | Continue 3–7 days post-op [3] |
| Mobilisation | Early mobilisation encouraged (reduces DVT risk, promotes bowel function) | As tolerated |
| Wound care | Standard port-site or incision care | May need delayed primary closure or vacuum-assisted closure if gross contamination |
Post-operative Complications
Risks — need to know for consent! [3]
These are systematically categorised by timing:
| Complication | Explanation |
|---|---|
| Conversion to open | Inability to complete laparoscopically due to adhesions, bleeding, or unclear anatomy |
| Normal appendix found | Still removed to avoid diagnostic confusion [3] — if the appendix is left in situ, future RLQ pain episodes will always re-raise appendicitis as a possibility |
| Malignancy found requiring right hemicolectomy ± stoma | Incidental carcinoid ( > 2 cm), adenocarcinoma, or mucinous neoplasm may require oncological resection |
| Injury to surrounding organs | Caecum, small bowel, ureter, iliac vessels |
| Bleeding | From appendicular artery (end-artery), mesoappendix, or port-site vessels |
| Complication | Explanation |
|---|---|
| Wound infection (5–10%) [3] | The most common post-operative complication. Higher with complicated appendicitis. Polymicrobial (same organisms as appendicitis). Present with wound erythema, discharge, pain. Treated with wound opening, drainage, and antibiotics |
| Intra-abdominal / pelvic abscess | Spiking fever [3] — classically swinging (high spikes then near-normal troughs). Occurs when residual infected material collects in the pelvis or RIF. Diagnosed with CT. Treated with image-guided percutaneous drainage ± antibiotics |
| Post-operative ileus | Temporary failure of bowel peristalsis after abdominal surgery. Presents with distension, absence of flatus/bowel sounds, nausea. Usually self-limiting (2–5 days). Managed with NPO, IV fluids, NG tube if needed |
| Complication | Explanation |
|---|---|
| Incisional hernia | Herniation of bowel/omentum through the fascial defect at the incision site. More common with open surgery. Presents as a reducible lump at the scar |
| Adhesions | Fibrous bands that form between intra-abdominal structures as part of wound healing. Can cause adhesive small bowel obstruction months to years later. The most common cause of SBO in developed countries |
| Recurrent / stump appendicitis [3] | If the appendiceal stump is too long ( > 0.5 cm), residual appendiceal tissue can re-inflame. Rare but important — always ligate the appendix flush at its base |
| Enterocutaneous fistula | Result from an intra-peritoneal abscess that fistulises to the skin [4]. Presents with faeculent discharge from the wound. Managed with NPO, TPN, octreotide to reduce intestinal secretions, and surgical repair if persistent |
| Pylephlebitis (septic portal vein thrombosis) | Associated with high fever, chills, rigors, and jaundice. Thrombosis and infection within the portal venous system. Caused by septicaemia in the portal venous system and leads to development of intra-hepatic abscesses [4]. This occurs because the appendiceal vein drains into the portal system (appendiceal vein → ileocolic vein → SMV → portal vein). Treated with prolonged IV antibiotics ± anticoagulation |
Pylephlebitis — A Rare but Devastating Complication
If a post-appendicectomy patient develops high spiking fevers, rigors, jaundice, and RUQ pain, think of pylephlebitis — septic thrombophlebitis of the portal vein. CT with IV contrast will show portal vein thrombosis and hepatic abscesses. This requires prolonged IV antibiotics (4–6 weeks) and therapeutic anticoagulation. Mortality is significant (~10–30%) if not recognised early.
Management in Special Populations
- 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
- 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.
- 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.
| Clinical Scenario | Approach |
|---|---|
| Uncomplicated, < 72 hours, fit for surgery | Immediate laparoscopic appendicectomy |
| Complicated, < 72 hours, stable | Immediate laparoscopic appendicectomy (may need open if gross sepsis) |
| Complicated, < 72 hours, unstable / gross sepsis | Open appendicectomy with peritoneal lavage |
| Walled-off / phlegmon / abscess, > 72 hours, stable | Oschner-Sherren regimen: IV antibiotics ± percutaneous drainage → interval appendicectomy at 6–8 weeks. Colonoscopy if > 40 years old |
| Walled-off but treatment failure | Immediate appendicectomy |
| Uncomplicated, patient unfit for / declines surgery | Antibiotics-first approach (NOM): bowel rest + IV then PO antibiotics for 7–10 days. Counsel about 30–50% recurrence risk |
High Yield Summary
Resuscitation: NPO, IV fluids (4-2-1 rule in paediatrics), analgesics, electrolyte correction, close monitoring.
Antibiotics: IV metronidazole + 3rd-gen cephalosporin (e.g., ceftriaxone). Given within 60-min window before incision. Non-complicated: stop at 24h post-op. Complicated: continue 3–7 days.
Surgery — Laparoscopic appendicectomy is FIRST LINE: ↓ wound infection, ↓ pain, ↓ hospital stay. Open if gross sepsis, conversion, or no laparoscopic capability. Patient positioning: supine ± Trendelenburg + right side up.
Open Incisions: Lanz (more popular, follows Langer's lines, better cosmesis), Gridiron (at McBurney's point, muscle-splitting), Rutherford-Morrison (extended Gridiron for difficult cases).
Timing: < 72 hours → immediate surgery. > 72 hours + stable + walled-off → Oschner-Sherren regimen (IV antibiotics ± drainage → interval appendicectomy at 6–8 weeks). Colonoscopy if > 40yo to exclude CA.
Conservative (antibiotics-first): For uncomplicated, no appendicolith, not fit for surgery. ~90% initial success but 30% recur at 3 months, 40% at 1 year, 50% at 3 years. CODA trial: 10-day antibiotics non-inferior but 30% need surgery within 90 days. Avoid if appendicolith present.
Consent — Risks: Immediate: conversion to open, normal appendix removed, malignancy needing R hemicolectomy ± stoma, organ injury, bleeding. Early: wound infection (5–10%), intra-abdominal abscess (spiking fever), ileus. Late: incisional hernia, adhesions, stump appendicitis, enterocutaneous fistula, pylephlebitis.
Post-op: Non-perforated: clear liquids → advance diet, stop antibiotics at 24h. Perforated: antibiotics 3–7 days, advance diet cautiously.
Always send specimen for histology — exclude carcinoid, adenocarcinoma, mucinous neoplasm.
Active Recall - Management of Acute Appendicitis
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.
A. Complications of the Disease (Pre-operative / Untreated)
These follow the natural history of appendicitis if left untreated, or if diagnosis is delayed.
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.
Why Do the Extremes of Age Perforate More?
Children: Cannot articulate symptoms → delayed diagnosis. Underdeveloped omentum → poor ability to wall off infection. Thinner appendiceal wall → perforates more readily. Elderly: Atypical presentation, blunted inflammatory response (less fever, less leucocytosis, less pain) → delayed diagnosis. Often attributed to other causes (constipation, diverticulitis, urinary problems).
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].
- 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].
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.
Peritonitis Classification Refresher
- Primary peritonitis: Infection of ascitic fluid WITHOUT a surgically treatable intra-abdominal source (e.g., SBP in cirrhosis, CAPD-associated, TB peritonitis) [9]
- Secondary peritonitis: Infection WITH a surgically treatable source — this includes appendicitis, PPU, perforated diverticulitis, ischaemic bowel [9]
- Tertiary peritonitis: Persistent peritonitis after adequate initial therapy (e.g., anastomotic leak, opportunistic infections in ICU patients) [9]
Perforated appendicitis causes secondary bacterial peritonitis — preceded by chemical irritation from intestinal contents, then bacterial colonisation.
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].
B. Post-operative Complications (Following Appendicectomy)
These are systematically categorised by timing. Risks — need to know for consent! [3]
| Complication | Pathophysiology / Explanation | Management |
|---|---|---|
| Conversion to open [3] | Inability to complete laparoscopically — due to dense adhesions (complicated appendicitis), uncontrollable bleeding, unclear anatomy, or inability to safely identify structures | Continue via open approach. This should always be discussed during pre-operative consent |
| Normal appendix found [3] | A normal appendix is found at operation (negative appendicectomy rate is ~10–15%). Still removed to avoid diagnostic confusion [3] — if left in situ, any future RLQ pain episode would re-raise appendicitis | Appendix is removed. Thorough inspection of remainder of abdomen: terminal ileum (Crohn's, Meckel's, TB), mesenteric lymph nodes (adenitis), caecum (diverticulitis, carcinoma), gynaecological organs (women) |
| Malignancy found requiring right hemicolectomy ± stoma [3] | Incidental finding of carcinoid tumour ( > 2 cm), adenocarcinoma, or mucinous neoplasm. Appendix specimen sent to pathology for assessment of neoplasms (1% chance) [3] | Carcinoid ≤ 2 cm: appendicectomy alone is curative. Carcinoid > 2 cm or involving caecum/lymph nodes: right hemicolectomy [3]. Adenocarcinoma: right hemicolectomy ± adjuvant chemotherapy [3]. Mucinous tumours: risk assessment for pseudomyxoma peritonei [3] |
| Injury to surrounding organs [3] | Caecum, small bowel, ureter, iliac vessels — from dissection, diathermy, or port insertion | Immediate recognition and repair. Bowel injury may require primary repair or resection. Ureteric injury requires urological consultation |
| Bleeding [3] | From appendicular artery (end-artery), mesoappendix, port-site vessels | Ensure mesoappendix is adequately ligated/clipped. Intra-operative haemostasis; if uncontrollable, convert to open |
| Complication | Pathophysiology / Explanation | Clinical Features | Management |
|---|---|---|---|
| Wound infection (5–10%) [3] | The most common post-operative complication. Polymicrobial organisms (same as appendicitis: E. coli, Bacteroides). Risk increases with complicated appendicitis, contamination during surgery, obesity, diabetes | Wound erythema, warmth, discharge (purulent), pain, dehiscence. Typically day 3–7 post-op | Wound opening and drainage, swab for culture, wound packing, antibiotics if cellulitis/systemic signs |
| Intra-abdominal / pelvic abscess [3][4] | Residual infected material collects in dependent areas (pelvis, RIF, subphrenic space) after surgery. More common with complicated appendicitis. Higher rate of intra-abdominal abscess reported with laparoscopic approach in some studies [4] | Spiking fever [3] (swinging high spikes → near-normal troughs — the classic pattern of an undrained abscess). Persistent abdominal pain, ↑ WCC/CRP, tachycardia. May cause secondary ileus | CT abdomen to localise. Image-guided percutaneous drainage is first-line. IV antibiotics. Surgery if not amenable to percutaneous drainage |
| Post-operative ileus [3][4] | Temporary failure of bowel peristalsis after abdominal surgery. The peritoneal inflammation and surgical manipulation cause the enteric nervous system to enter a transient "shutdown" state. Exacerbated by opioid analgesia, electrolyte imbalance (especially hypokalaemia), and intra-abdominal sepsis | Abdominal distension, nausea/vomiting, absent flatus and bowel sounds. Typically resolves within 2–5 days | Conservative: NPO, IV fluids, NG tube for decompression if needed, correct electrolytes (especially K⁺), minimise opioids, early mobilisation. Resolves spontaneously in most cases |
Spiking Fever Post-Appendicectomy = Think Abscess
The classic post-operative fever pattern to recognise: Day 5–7 post-appendicectomy, the patient develops swinging fevers (temperature spikes to 39–40°C then drops to near-normal, recurring daily). This "picket-fence" fever pattern is highly suggestive of an undrained intra-abdominal or pelvic abscess. The mechanism: the abscess periodically releases bacteria/pyrogens into the bloodstream (transient bacteraemia), causing a fever spike, which then resolves as the immune system temporarily contains it — only for it to happen again. The definitive treatment is drainage, not just more antibiotics.
| Complication | Pathophysiology / Explanation | Clinical Features | Management |
|---|---|---|---|
| Incisional hernia [3] | Herniation of bowel/omentum through a defect in the fascial closure at the incision/port site. More common with open surgery (larger fascial defect), obesity, wound infection, malnutrition, steroid use | Reducible lump at the scar site, worse with coughing/straining | Surgical repair (mesh repair) if symptomatic or at risk of incarceration |
| Adhesions [3] | Fibrous bands form between intra-abdominal structures as part of peritoneal wound healing. Exaggerated in complicated appendicitis with peritoneal contamination. Adhesions are the most common cause of small bowel obstruction in developed countries | May be asymptomatic for years. Can present as adhesive small bowel obstruction (colicky abdominal pain, vomiting, distension, absolute constipation) at any point in the future | Conservative initially (NG decompression, IV fluids, nil by mouth) → surgery (adhesiolysis) if no resolution or signs of strangulation |
| Recurrent / stump appendicitis [3] | If the appendiceal stump is left too long ( > 0.5 cm), residual appendiceal tissue can re-inflame. The retained stump essentially behaves like a miniature appendix and can undergo the same obstructive pathophysiology as the original appendix | Recurrence of RLQ pain, fever, leucocytosis — identical presentation to the original appendicitis. History of prior appendicectomy. CT shows inflamed stump | Completion appendicectomy (removal of the stump) |
| Enterocutaneous fistula [4] | Results from an intra-peritoneal abscess that fistulises to the skin [4]. An undrained or inadequately drained abscess erodes into an adjacent bowel loop (forming an enteric communication) and then tracks through the abdominal wall to the skin surface | Faeculent discharge from the wound or drain site. May be associated with sepsis, malnutrition, electrolyte derangement (loss of intestinal contents through the fistula) | Conservative first: NPO, TPN (total parenteral nutrition), octreotide (reduces intestinal secretions by inhibiting GI hormones), wound care, antibiotics for sepsis. Many close spontaneously. Surgery if persistent ( > 6 weeks) or high-output |
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:
| Neoplasm | Frequency | Management |
|---|---|---|
| Carcinoid tumour | Most common appendiceal neoplasm (~0.3–0.7% of appendicectomy specimens) | ≤ 2 cm: appendicectomy alone is curative. > 2 cm or involving caecum/lymph nodes: right hemicolectomy ± stoma [3] |
| Adenocarcinoma | Rare. Highly malignant | Right hemicolectomy ± adjuvant chemotherapy [3] |
| Mucinous neoplasms | Mucinous cystadenoma / cystadenocarcinoma | Mucinous tumours have risk of perforation and seeding → pseudomyxoma peritonei (PMP). Low risk: colonoscopy + surveillance. High risk: cytoreductive surgery + heated intraperitoneal chemotherapy (HIPEC) [3] |
Pseudomyxoma Peritonei — A Rare but High-Yield Concept
PMP ("pseudo" = false; "myxoma" = mucous tumour; "peritonei" = of the peritoneum) is a condition where the peritoneal cavity fills with mucinous (jelly-like) material, usually from a ruptured mucinous appendiceal tumour. The mucinous cells implant on peritoneal surfaces and continue secreting mucin, causing progressive abdominal distension ("jelly belly"). Treatment is aggressive: cytoreductive surgery (removing all visible tumour from every peritoneal surface) + HIPEC (heated chemotherapy solution bathed directly in the peritoneal cavity during surgery to kill residual microscopic tumour cells). This is why mucinous appendiceal tumours, even when "benign-appearing," must be taken seriously.
- 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.
High Yield Summary
Disease Complications (natural history if untreated):
- Perforation: Suspect when fever > 39.4°C, WBC > 15 × 10⁹/L, RLQ fluid collection on imaging. Risk factors: male, extremes of age, DM, immunosuppression, faecolith, pelvic appendix.
- Appendiceal abscess/phlegmon: Walled-off perforation. Presents with persistent fever, RLQ mass, elevated inflammatory markers. Manage with IV antibiotics ± percutaneous drainage → interval appendicectomy at 6–8 weeks. Do NOT operate immediately through a phlegmon (risk of ileocolectomy/caecostomy).
- Generalised peritonitis: Perforation NOT walled off. Board-like rigidity, absent bowel sounds, septic shock. Surgical emergency — open appendicectomy + peritoneal lavage.
- Pylephlebitis: Septic portal vein thrombosis → hepatic abscesses. High fever, rigors, jaundice. CT shows portal vein thrombus + liver abscesses. Prolonged IV antibiotics + anticoagulation.
Post-operative Complications (consent risks):
- Immediate: Conversion to open, normal appendix still removed, incidental malignancy needing R hemicolectomy ± stoma, organ injury, bleeding.
- Early: Wound infection (5–10%, most common), intra-abdominal/pelvic abscess (spiking fever — drain it), post-op ileus.
- Late: Incisional hernia, adhesions (most common cause of SBO), stump appendicitis, enterocutaneous fistula, pylephlebitis.
Incidental Neoplasms (1% of specimens): Carcinoid (≤ 2 cm = appendicectomy sufficient; > 2 cm = R hemicolectomy), adenocarcinoma (R hemicolectomy + chemo), mucinous tumours (risk of pseudomyxoma peritonei → cytoreductive surgery + HIPEC if high risk).
Always send the appendix specimen for histology.
Active Recall - Complications of Acute Appendicitis
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)
High Yield Summary
Definition: Acute inflammation of the vermiform appendix; most common acute surgical emergency. 2/3 obstructive, 1/3 non-obstructive.
Epidemiology: Peak 20s–30s adults; 4–15 years paediatric. M:F = 1.4:1. Lifetime risk ~7–8%.
Anatomy: True diverticulum of caecum. Base at convergence of taeniae coli (McBurney's point). Appendiceal artery is an END-ARTERY (thrombosis → gangrene). Retrocaecal 74%, Pelvic 21%.
Aetiology: Lymphoid hyperplasia (young), faecolith (older), tumour (elderly). Bacteria: E. coli, Bacteroides, Pseudomonas, Peptostreptococcus.
Pathophysiology: Obstruction → ↑ intraluminal pressure → venous congestion → ischaemia → bacterial invasion → transmural inflammation → gangrene → perforation → abscess or peritonitis.
Risk factors for perforation: Male, extremes of age, DM, immunosuppression, previous surgery, faecolith, pelvic appendix.
Classic symptom sequence: Anorexia → periumbilical pain (T8–10 visceral) → N/V → pain migrates to RIF (somatic, parietal peritoneum) → low-grade fever.
Key signs: McBurney's point tenderness (pointing sign), Rovsing's (RIF pain on LLQ pressure), Psoas (retrocaecal), Obturator (pelvic), rebound tenderness, guarding.
Atypical presentations: Retrocaecal (flank/back pain), Pelvic (dysuria/diarrhoea/tenesmus), Children (diffuse pain, high perforation), Elderly (vague, high perforation), Pregnancy (displaced superiorly).
High Yield Summary
Systematic DDx of RLQ pain (as per lecture slides):
GI: Acute appendicitis, caecal diverticulitis (common in Asians — CT to differentiate), mesenteric adenitis (children, URTI prodrome, minimal peritoneal signs), Meckel's diverticulitis (Rule of 2s, CT diagnosis, incidental finding at OT), ileitis (Crohn's, TB, Yersinia, Campylobacter, Salmonella — diarrhoea is predominant symptom), caecal ischaemia, cancer of caecum, PPU with Valentino's sign.
Gynaecological (all women of reproductive age — always pregnancy test!): Ruptured ectopic pregnancy (sudden pain + bleeding + collapse), ovarian cyst torsion/rupture (USG/CT, laparoscopy), PID/TOA (cervical motion tenderness, discharge), Mittelschmerz, endometriosis/endometritis.
Urological: Ureteric colic (loin-to-groin, colicky, RBC on urinalysis, patient restless), UTI, testicular torsion (always examine scrotum in males).
Other: Strangulated hernia (always examine groins), HSP (paediatric, purpuric rash), psoas abscess, DKA.
Key Differentiators:
- Pain before N/V = appendicitis; N/V before pain = gastroenteritis
- URTI prodrome + high fever + minimal peritoneal signs = mesenteric adenitis
- Asian patient + RLQ pain + older age = think caecal diverticulitis (CT to differentiate)
- Positive pregnancy test + RLQ pain = ectopic pregnancy until proven otherwise
- Loin-to-groin colicky pain + restless patient + haematuria = ureteric colic
High Yield Summary
Diagnostic Principle: Acute appendicitis is a CLINICAL diagnosis. Scoring systems (Alvarado/MANTRELS) and imaging SUPPORT the clinical assessment.
Alvarado (MANTRELS) Score: M-igratory RIF pain (1), A-norexia (1), N-ausea/vomiting (1), T-enderness RIF (2), R-ebound (1), E-levated temperature (1), L-eucocytosis (2), S-hift to left (1) = Total 10.
- ≥ 7: Strongly predictive → surgery/imaging
- 5–6: Equivocal → USG or CT
- ≤ 4: Unlikely → investigate other DDx
Key Bloods: CBC (leucocytosis, left shift — ↑↑↑ suggests complicated appendicitis, but normal does NOT rule it out), CRP (rises after 12 hours; very high suggests complications), LFT (↑ bilirubin = marker of perforation), pregnancy test (MANDATORY in all women of childbearing age), amylase (exclude pancreatitis).
Imaging:
- AXR: NOT recommended for appendicitis diagnosis (only 5% of faecoliths radio-opaque).
- USG: First-line in children and pregnant women. Non-compressible appendix > 6 mm.
- CT with IV contrast: HIGHEST diagnostic accuracy in adults. Appendix > 6 mm, wall thickening > 2 mm, fat stranding, appendicolith.
- MRI: Second-line in pregnant women (no radiation).
Patient-specific strategies: Adults → CT. Children → USG first, then CT if equivocal (beware radiation). Pregnant → USG first, then MRI. Girls with RLQ pain → always pregnancy test + USG + Gynae consult.
High Yield Summary
Resuscitation: NPO, IV fluids (4-2-1 rule in paediatrics), analgesics, electrolyte correction, close monitoring.
Antibiotics: IV metronidazole + 3rd-gen cephalosporin (e.g., ceftriaxone). Given within 60-min window before incision. Non-complicated: stop at 24h post-op. Complicated: continue 3–7 days.
Surgery — Laparoscopic appendicectomy is FIRST LINE: ↓ wound infection, ↓ pain, ↓ hospital stay. Open if gross sepsis, conversion, or no laparoscopic capability. Patient positioning: supine ± Trendelenburg + right side up.
Open Incisions: Lanz (more popular, follows Langer's lines, better cosmesis), Gridiron (at McBurney's point, muscle-splitting), Rutherford-Morrison (extended Gridiron for difficult cases).
Timing: < 72 hours → immediate surgery. > 72 hours + stable + walled-off → Oschner-Sherren regimen (IV antibiotics ± drainage → interval appendicectomy at 6–8 weeks). Colonoscopy if > 40yo to exclude CA.
Conservative (antibiotics-first): For uncomplicated, no appendicolith, not fit for surgery. ~90% initial success but 30% recur at 3 months, 40% at 1 year, 50% at 3 years. CODA trial: 10-day antibiotics non-inferior but 30% need surgery within 90 days. Avoid if appendicolith present.
Consent — Risks: Immediate: conversion to open, normal appendix removed, malignancy needing R hemicolectomy ± stoma, organ injury, bleeding. Early: wound infection (5–10%), intra-abdominal abscess (spiking fever), ileus. Late: incisional hernia, adhesions, stump appendicitis, enterocutaneous fistula, pylephlebitis.
Post-op: Non-perforated: clear liquids → advance diet, stop antibiotics at 24h. Perforated: antibiotics 3–7 days, advance diet cautiously.
Always send specimen for histology — exclude carcinoid, adenocarcinoma, mucinous neoplasm.
High Yield Summary
Disease Complications (natural history if untreated):
- Perforation: Suspect when fever > 39.4°C, WBC > 15 × 10⁹/L, RLQ fluid collection on imaging. Risk factors: male, extremes of age, DM, immunosuppression, faecolith, pelvic appendix.
- Appendiceal abscess/phlegmon: Walled-off perforation. Presents with persistent fever, RLQ mass, elevated inflammatory markers. Manage with IV antibiotics ± percutaneous drainage → interval appendicectomy at 6–8 weeks. Do NOT operate immediately through a phlegmon (risk of ileocolectomy/caecostomy).
- Generalised peritonitis: Perforation NOT walled off. Board-like rigidity, absent bowel sounds, septic shock. Surgical emergency — open appendicectomy + peritoneal lavage.
- Pylephlebitis: Septic portal vein thrombosis → hepatic abscesses. High fever, rigors, jaundice. CT shows portal vein thrombus + liver abscesses. Prolonged IV antibiotics + anticoagulation.
Post-operative Complications (consent risks):
- Immediate: Conversion to open, normal appendix still removed, incidental malignancy needing R hemicolectomy ± stoma, organ injury, bleeding.
- Early: Wound infection (5–10%, most common), intra-abdominal/pelvic abscess (spiking fever — drain it), post-op ileus.
- Late: Incisional hernia, adhesions (most common cause of SBO), stump appendicitis, enterocutaneous fistula, pylephlebitis.
Incidental Neoplasms (1% of specimens): Carcinoid (≤ 2 cm = appendicectomy sufficient; > 2 cm = R hemicolectomy), adenocarcinoma (R hemicolectomy + chemo), mucinous tumours (risk of pseudomyxoma peritonei → cytoreductive surgery + HIPEC if high risk).
Always send the appendix specimen for histology.
Sketchy memory palace for Acute Appendicitis
| No. | Visual Cue | Meaning |
|---|---|---|
| 1 | Specific age hikers and 1.4:1 ratio | Peak incidence in 4-15 and 20s-30s; slight male predominance |
| 2 | Three vines converging at tunnel base | Appendix base at taeniae coli convergence (McBurney's point) |
| 3 | Red hose with 'Stop' clamp | End-artery supply; thrombosis causes rapid gangrene |
| 4 | Entrance stone or purple seeds | Obstruction via faecolith (older) or lymphoid hyperplasia (young) |
| 5 | Swelling walls with E. coli beetles | Increased pressure, ischemia, and bacterial invasion |
| 6 | Pain moving from navel to right hip | Migrating pain from periumbilical (T8-10) to Right Iliac Fossa |
| 7 | Refusing food and low-heat fire | Classical symptoms of anorexia and low-grade fever |
| 8 | Left bridge pressure causing right pain | Rovsing's Sign: RIF pain on palpation of the left lower quadrant |
| 9 | Pain extending hip over a log | Psoas Sign: Clinical indicator of a retrocaecal appendix |
| 10 | Asian architectural tea house | Differential: Caecal diverticulitis (common in Asian populations) |
| 11 | Pregnancy test stick and crystal ball | Rule out ectopic pregnancy; USG is first-line in pregnancy |
| 12 | Restless hiker with bag of rocks | Differential: Ureteric colic presents with restless pacing |
| 13 | Alvarado scoreboard showing score of 7 | Alvarado score >= 7 warrants surgery or imaging |
| 14 | Goggles showing thick walls and fat | CT with IV contrast is gold standard imaging in adults |
| 15 | Hourglass and laparoscopic arm | Laparoscopic appendicectomy; antibiotics given 60m pre-incision |
| 16 | Burst tunnel wall leaking mud | Complication: Perforation, abscess, or peritonitis |
| 17 | Icy river blocking portal flow | Complication: Pylephlebitis (septic portal vein thrombosis) |
| 18 | Histology jar with hidden crab | Post-op histology to exclude carcinoid or other neoplasms |
Bariatric Surgery
Bariatric surgery encompasses surgical procedures that modify the gastrointestinal tract to induce sustained weight loss in patients with severe obesity, primarily through restrictive, malabsorptive, or combined mechanisms.
Anal Fissure
An anal fissure is a longitudinal tear in the mucosa of the anal canal, typically at the posterior midline, causing severe pain during defecation and minor rectal bleeding.