Abdominal Pain
Abdominal pain is a symptom of discomfort felt between the chest and pelvis, arising from visceral, parietal, or referred mechanisms, that signals a wide range of gastrointestinal, genitourinary, vascular, or systemic conditions.
What Is "Abdominal Pain"?
Abdominal pain is not a diagnosis — it is a symptom that reflects activation of nociceptive (pain-sensing) pathways originating from abdominal viscera, the parietal peritoneum, or structures that refer pain to the abdomen. Understanding abdominal pain requires understanding the three fundamental pain mechanisms at play:
| Pain Type | Mechanism | Character | Localisation | Example |
|---|---|---|---|---|
| Visceral pain | Stretch, distension, ischaemia or spasm of hollow viscus walls activating unmyelinated C-fibre afferents travelling with autonomic (sympathetic) nerves → poorly mapped in the somatosensory cortex | Dull, crampy, colicky, poorly localised, midline | Referred to the dermatome of embryological origin (foregut → epigastrium; midgut → periumbilical; hindgut → suprapubic/hypogastrium) | Early appendicitis (periumbilical), biliary colic (epigastric) |
| Parietal (somatic) pain | Direct irritation of the parietal peritoneum activating myelinated Aδ-fibre afferents in somatic intercostal nerves → well-represented in cortex | Sharp, constant, well-localised, worsened by movement/coughing | Localises to the exact quadrant of the inflamed peritoneum | Late appendicitis (RLQ), perforated peptic ulcer (epigastric → generalised) |
| Referred pain | Visceral afferents converge on the same spinal cord dorsal horn neurons as somatic afferents from a distant dermatome → brain "misinterprets" the source | Felt at a site distant from the pathology | Predictable dermatomal pattern | Diaphragmatic irritation → shoulder tip (C3-C5 via phrenic nerve); biliary → right scapula (T6-T9) |
Why does early appendicitis cause periumbilical pain? Because the appendix is a midgut structure; visceral afferents from the midgut enter the spinal cord at T10 — the same dermatome as the umbilicus. Only when the inflamed appendix irritates the parietal peritoneum of the RLQ does pain shift there (somatic pain).
- Abdominal pain accounts for ~5-10% of all Emergency Department presentations worldwide and is the single most common chief complaint in EDs [1][2].
- In Hong Kong, acute abdominal pain is among the top 5 presenting complaints in public hospital A&E departments.
- Approximately 30-40% of patients presenting with acute abdominal pain will have a non-specific or self-limiting cause after full workup.
- Age distribution matters enormously:
- Young adults (20-40): appendicitis, ovarian pathology, ectopic pregnancy, peptic ulcer disease
- Middle-aged (40-60): biliary disease, pancreatitis, diverticulitis, malignancy
- Elderly ( > 60): mesenteric ischaemia, AAA, malignancy, bowel obstruction, diverticulitis
- Sex matters: In women of reproductive age, always rule out ectopic pregnancy — it is a life-threatening cause of abdominal pain. Ovarian torsion, ruptured ovarian cyst, and PID are additional considerations [1].
- Key Hong Kong epidemiological points: Right-sided diverticular disease is significantly more common in the Asian population compared to the Western sigmoid predominance, and is frequently confused with acute appendicitis [3].
Anatomy and Function Relevant to Abdominal Pain
The abdominal cavity is lined by peritoneum — a serous membrane with two layers:
- Parietal peritoneum: lines the abdominal wall. Innervated by somatic nerves (intercostal and subcostal nerves T7-L1). This is why parietal peritoneal irritation produces sharp, well-localised pain.
- Visceral peritoneum: covers the abdominal organs. Innervated by autonomic (visceral) afferents only — hence dull, poorly localised pain.
This is the single most important concept for understanding abdominal pain localisation:
| Embryological Division | Structures | Arterial Supply | Spinal Segments | Pain Referral Zone |
|---|---|---|---|---|
| Foregut | Oesophagus (lower), Stomach, Duodenum (D1-D2), Liver, Gallbladder, Pancreas (head), Spleen | Coeliac trunk | T5-T9 | Epigastrium |
| Midgut | Duodenum (D3-D4), Jejunum, Ileum, Caecum, Appendix, Ascending colon, Proximal 2/3 of transverse colon | Superior mesenteric artery (SMA) | T8-T12 (primarily T10) | Periumbilical |
| Hindgut | Distal 1/3 of transverse colon, Descending colon, Sigmoid, Rectum (upper) | Inferior mesenteric artery (IMA) | T11-L1 | Suprapubic / Hypogastrium |
Why does cholecystitis cause epigastric pain first? The gallbladder is a foregut derivative. Visceral afferents travel via the coeliac plexus to T5-T9, so early gallbladder distension is felt as epigastric/RUQ discomfort. Only when the inflamed gallbladder irritates the parietal peritoneum does the pain become sharply localised to the RUQ with Murphy's sign.
- Coeliac trunk → foregut organs
- SMA → midgut; major branches include the ileocolic artery (which gives off the appendiceal artery — an end-artery, meaning thrombosis leads to appendiceal necrosis) [3]
- IMA → hindgut
- Watershed areas (vulnerable to ischaemia):
These watershed areas explain why ischaemic colitis classically affects the splenic flexure and rectosigmoid junction — they are the "last meadows" between two irrigation systems.
Knowing the anatomy of peritoneal recesses explains how fluid/pus tracks:
- Right paracolic gutter communicates directly with the right subphrenic and subhepatic (Morrison's pouch) spaces — a perforated duodenal ulcer leaks gastric content down the right paracolic gutter, causing RIF pain (mimicking appendicitis) and right shoulder tip pain (diaphragmatic irritation → phrenic nerve C3-C5).
- Left paracolic gutter is partially obstructed by the phrenicocolic ligament, so fluid tracks less freely to the left subphrenic space.
- Pouch of Douglas (rectouterine/rectovesical pouch) is the most dependent part of the peritoneal cavity in the upright position — fluid/pus accumulates here.
| Structure | Nerve Supply | Clinical Relevance |
|---|---|---|
| Parietal peritoneum (anterior) | Intercostal nerves (T7-T12), subcostal (L1) | Sharp, localised pain; guarding, rigidity, rebound tenderness |
| Parietal peritoneum (diaphragmatic, central) | Phrenic nerve (C3-C5) | Referred shoulder tip pain (e.g., ruptured spleen, subphrenic abscess) |
| Visceral peritoneum & abdominal viscera | Autonomic afferents (sympathetic chain) | Dull, midline, poorly localised pain |
Etiology (Focus on Hong Kong)
The causes of abdominal pain are vast. A structured approach by anatomical location and acuity is most practical for clinical reasoning.
This is the classic approach taught at the bedside [1][2]:
Right Upper Quadrant (RUQ)
- Biliary colic — gallstone impacted in cystic duct causing smooth muscle spasm (actually a "false colic" because it is constant, not truly waxing/waning) [2]
- Acute cholecystitis — cystic duct obstruction → gallbladder distension → secondary inflammation/infection [2][5]
- Acute cholangitis — CBD obstruction → biliary stasis → ascending infection (Charcot's triad: RUQ pain, fever, jaundice; Reynold's pentad adds hypotension + confusion) [2]
- Hepatitis — liver capsule (Glisson's capsule) distension from hepatocellular swelling
- Liver abscess — pyogenic (Klebsiella pneumoniae particularly common in Hong Kong and Asia, especially in diabetics) [5] or amoebic (Entamoeba histolytica — consider in travellers)
- Ruptured HCC — important in Hong Kong given high prevalence of hepatitis B; presents with sudden RUQ pain + haemodynamic instability
Epigastric
- Peptic ulcer disease (PUD) — H. pylori (92% DU, 70% GU), NSAIDs, stress ulcers; imbalance between aggressive factors (acid, pepsin) and protective factors (mucus, bicarbonate, prostaglandins, mucosal blood flow) [2][6]
- Acute gastritis/duodenitis
- Acute pancreatitis — premature intracellular activation of trypsin → pancreatic autodigestion → NF-κB mediated systemic inflammation [7]
- Perforated peptic ulcer (PPU) — chemical peritonitis followed by bacterial peritonitis [2]
- GERD/Oesophagitis — reflux of gastric acid onto squamous oesophageal epithelium [8]
- Abdominal aortic aneurysm (AAA) — can present with epigastric/back pain ± pulsatile mass [9]
Left Upper Quadrant (LUQ)
- Splenic pathology (infarction, rupture, abscess)
- Gastric ulcer (lesser curvature)
- Pancreatitis (tail of pancreas)
- Left lower lobe pneumonia (referred)
Right Lower Quadrant (RLQ)
- Acute appendicitis — luminal obstruction (faecolith, lymphoid hyperplasia, tumour, parasites) → venous congestion → ischaemia → gangrene/perforation [3][10]
- Right-sided diverticulitis — significantly more common in Asian populations including Hong Kong; frequently confused with appendicitis [3][11]
- Mesenteric lymphadenitis — especially in children/young adults; viral
- Crohn's disease — terminal ileum is the commonest site
- Ectopic pregnancy (women of reproductive age — always check β-hCG)
- Ovarian torsion / Ruptured ovarian cyst
- Ureteric colic (right distal ureter)
Right Iliac Fossa (RIF) / Left Iliac Fossa (LIF) overlap: caecal pathology (right) vs sigmoid pathology (left)
Left Lower Quadrant (LLQ)
- Sigmoid diverticulitis — "left-sided appendicitis" in Western populations (but remember right-sided predominance in Asia) [3][11]
- Colorectal carcinoma — sigmoid is a common site
- Left ureteric colic
- Ovarian pathology (left)
- IBD (ulcerative colitis — continuous from rectum, often involves sigmoid)
Suprapubic / Hypogastric
- Urinary retention (AROU)
- Cystitis / UTI
- Pelvic inflammatory disease (PID)
- Degenerating fibroid
- Endometriosis / Adenomyosis
Diffuse / Non-specific Abdominal Pain [1]
- Gastroenteritis
- Constipation
- Intestinal obstruction (mechanical or functional)
- Generalised peritonitis (from any perforated viscus)
- Intra-abdominal haemorrhage
- Medical causes: DKA, hypercalcaemia, herpes zoster, anaphylaxis, porphyria [1]
Life-Threatening Causes of Acute Abdomen — Must Know
The following must NEVER be missed [1]:
- Perforated viscus (e.g., PPU)
- Ruptured AAA
- Acute mesenteric ischaemia
- Acute intestinal obstruction (especially closed-loop with strangulation)
- Severe acute pancreatitis
- Ruptured HCC (especially relevant in Hong Kong due to hepatitis B)
- Medical conditions: DKA, acute MI, Addisonian crisis
- Obstetric conditions: ruptured ectopic pregnancy, placental abruption
| Mechanism | Examples | Pathophysiology of Pain |
|---|---|---|
| Inflammation | Appendicitis, cholecystitis, pancreatitis, diverticulitis, PID, IBD | Inflammatory mediators (prostaglandins, bradykinin, histamine) sensitise nociceptors → lower pain threshold. Peritoneal inflammation adds parietal component. |
| Obstruction / Distension | Biliary colic, ureteric colic, intestinal obstruction, urinary retention | Smooth muscle spasm or luminal distension stretches wall → activates mechanoreceptors and nociceptive C-fibres in visceral wall |
| Ischaemia | Mesenteric ischaemia, strangulated hernia, ischaemic colitis, ovarian torsion, testicular torsion | Tissue hypoxia → anaerobic metabolism → lactate + H⁺ accumulation → direct nociceptor activation. Often pain "out of proportion" to examination (classic for mesenteric ischaemia) |
| Perforation | PPU, perforated diverticulum, perforated appendix | Leakage of irritant contents (acid, bile, faeces) onto peritoneum → intense chemical peritonitis → parietal pain |
| Haemorrhage | Ruptured AAA, ruptured ectopic pregnancy, ruptured HCC, splenic rupture | Peritoneal irritation by blood + haemodynamic instability |
| Functional | IBS, functional dyspepsia | Visceral hypersensitivity, altered motility, dysregulated brain-gut axis, serotonergic imbalance [12] |
Pathophysiology of Pain Generation (Deep Dive)
- Noxious stimuli (distension, ischaemia, inflammation, chemical irritation) activate nociceptors on visceral afferent nerve endings in the gut wall.
- These are predominantly unmyelinated C-fibres that travel alongside sympathetic nerves through the coeliac, superior mesenteric, and inferior mesenteric plexuses → enter the spinal cord via dorsal root ganglia at specific spinal levels (T5-L1).
- In the dorsal horn, visceral afferents converge with somatic afferents from the corresponding dermatome → this is the basis of referred pain and the reason visceral pain is poorly localised.
- Signal ascends via spinothalamic tract to thalamus and then somatosensory cortex.
In chronic conditions (IBS, functional dyspepsia), there is peripheral sensitisation (lowered threshold of visceral nociceptors) and central sensitisation (amplification of pain signals in the dorsal horn) → patients feel pain at lower thresholds of distension/stimulation. This explains why IBS patients report pain with normal bowel gas volumes.
Understanding the pathophysiology of peritonitis is crucial:
- Peritoneum becomes hyperaemic, oedematous and covered with fibrinous exudate → fluid shifts into the peritoneal cavity (third-spacing) → hypovolaemia [13].
- This leads to septicaemia, endotoxaemia, shock, hypovolaemia and multi-organ failure [13].
Classification of Peritonitis
| Type | Definition | Key Points |
|---|---|---|
| Primary | Ascitic fluid infection without a surgically treatable intra-abdominal source | Common in liver cirrhosis (SBP); also CAPD peritonitis, TB peritonitis [13] |
| Secondary | Infection with a surgically treatable intra-abdominal source | Chemical irritation first (gastric juice, bile, pancreatic juice, urine, blood) then bacterial [13]. Causes: Perforation (PPU, perforated bowel/diverticulum), Ischaemia (bowel ischaemia), Infection (appendiceal/perinephric abscess), Inflammation (cholecystitis, cholangitis, appendicitis, pancreatitis, diverticulitis), Others (incarcerated hernia, anastomotic leakage) [13] |
| Tertiary | Opportunistic infection with normally non-pathogenic flora | Associated with prolonged antibiotic use in persistent intra-abdominal infection; organisms include Staphylococcus, Enterococcus, Candida [13] |
Relevant Classification Systems
- Acute abdominal pain ( < 1 week, often < 48 hours): surgical emergency until proven otherwise
- Chronic abdominal pain ( > 3 months): more likely functional, malignant, or chronic inflammatory
- Acute-on-chronic: e.g., IBD flare, recurrent biliary colic
- Surgical abdomen: requires operative intervention (e.g., perforated viscus, strangulated obstruction, ruptured AAA)
- Medical abdomen: managed non-operatively (e.g., DKA, acute pancreatitis [initially], acute MI, porphyria)
Acute Appendicitis Severity (Disease Severity Score) [3]:
| Grade | Description |
|---|---|
| 1 | Inflamed |
| 2 | Gangrenous |
| 3 | Perforated with localised free fluid |
| 4 | Perforated with regional abscess |
| 5 | Perforated with diffuse peritonitis |
Hinchey Classification (Complicated Diverticulitis) [11]:
| Stage | Description | Treatment |
|---|---|---|
| I | Pericolic or mesenteric abscess | Conservative: antibiotics, bowel rest, monitoring (outpatient if stable) |
| II | Walled-off pelvic abscess | IV antibiotics + bowel rest + image-guided drainage ± surgery |
| III | Generalised purulent peritonitis | IV antibiotics + bowel rest + surgery |
| IV | Generalised faecal peritonitis | IV antibiotics + bowel rest + surgery |
Los Angeles Classification (GERD/Oesophagitis) [8] — Grades A-D based on extent of mucosal breaks.
Clinical Features
The history is the most powerful diagnostic tool in abdominal pain. Use the SOCRATES framework but expand it with system-specific questions [1][2]:
S — Site: Which quadrant? Localised or diffuse?
- Localised → somatic/parietal pain (think peritoneal irritation)
- Diffuse/midline → visceral pain (think hollow organ distension/ischaemia)
- Any shifting: e.g., appendicitis shifts from periumbilical to RLQ; pancreatitis epigastric to back [2]
O — Onset: Sudden (seconds) → perforation, rupture, torsion, vascular event. Gradual (hours) → inflammation, obstruction.
C — Character:
- Colicky (waxing and waning) → obstruction of a hollow tube (bowel, ureter, bile duct) — because smooth muscle contracts in peristaltic waves against the obstruction
- Constant → inflammation (appendicitis, cholecystitis), ischaemia, or peritonitis
- Burning → mucosal inflammation (PUD, GERD)
R — Radiation [2]:
| Radiation Pattern | Suggests |
|---|---|
| Back | Pancreatitis, AAA, aortic dissection, posterior peptic ulcer |
| Shoulder tip | Haemoperitoneum (ruptured ectopic, splenic rupture) — diaphragmatic irritation → phrenic nerve C3-C5 |
| Right scapula / Scapular spine | Gallbladder disease (T6-T9 dermatomal referred pain) |
| Loin to groin | Renal/ureteric colic |
| Testicles to flank | Testicular torsion |
| Flanks | Pyelonephritis, retroperitoneal haematoma, AAA |
A — Associations: System-specific screening [1][2]:
- GI: nausea/vomiting, bowel habit changes, melaena/haematemesis, PR bleeding
- Hepatobiliary/Pancreatic: jaundice, tea-coloured urine, pale stools
- Genitourinary: dysuria, haematuria, frothy urine
- Gynaecological: vaginal discharge, PV bleeding, LMP, possibility of pregnancy
- Constitutional: fever, weight loss, night sweats, anorexia
T — Time course [2]:
- Constant: ulcers, peritonitis
- Colicky with pain-free intervals: intestinal, renal, biliary colic
- Steady increase then constant: biliary colic ("false colic"), pancreatitis
- Progressive: appendicitis, diverticulitis
- Catastrophic onset: ruptured AAA, perforated viscus
E — Exacerbating / Relieving factors [1][2]:
- Peritonitis: ↑ by movement → patient lies still (PPU classic: patient motionless on bed)
- Colic: often ↓ by movement (patient writhes around)
- Food: GU pain exacerbated by eating; DU pain relieved by eating (food buffers acid in duodenum but stimulates acid secretion in stomach) [2]
- Fatty meals: exacerbate biliary colic and pancreatitis (CCK release → gallbladder contraction)
- Position: GERD, pancreatitis, and pancreatic cancer relieved by leaning forward (reduces pressure on retroperitoneal pancreas); PPU worsened by movement [1]
- Defecation: IBS pain characteristically associated with and relieved by defecation [12]
- Vomiting: gastric ulcer pain ↓ by vomiting (decompresses the stomach); intestinal obstruction pain ↓ by vomiting (decompresses proximal dilated bowel) [2]
S — Severity: Use numerical rating scale; "worst pain of life" → think perforation, torsion, ruptured AAA, renal colic
Always ask about:
- NSAIDs (peptic ulcer, NSAID gastropathy, diverticular complications, colitis)
- Aspirin (mucosal ulceration)
- Steroids (mask peritoneal signs, increase perforation risk)
- Bisphosphonates (oesophageal ulceration)
- Opiates (constipation, paralytic ileus)
- Anticholinergics (constipation, paralytic ileus)
- Anticoagulants (retroperitoneal haematoma, intramural haematoma)
Red flags that mandate urgent investigation:
- Age > 55 with new-onset dyspepsia (risk of gastric/oesophageal malignancy)
- Family history of upper GI cancer
- Significant unintentional weight loss
- Dysphagia / early satiety (obstruction or malignancy)
- GI bleeding: coffee-ground vomiting, fresh haematemesis, melaena, PR bleeding
- Unexplained iron-deficiency anaemia
- Persistent vomiting
- Palpable mass or lymphadenopathy
- Jaundice
Symptoms with Pathophysiological Basis
- Classical course: periumbilical pain (visceral, midgut → T10) → low-grade fever, vomiting, anorexia (note: in appendicitis, pain precedes vomiting; in gastroenteritis, vomiting precedes pain — a useful differentiator) → pain migrates to RLQ after 12-24h (parietal peritoneum of RLQ becomes involved → somatic pain)
- Why anorexia? Vagal afferents from the inflamed appendix stimulate the vomiting centre and suppress appetite via the nucleus tractus solitarius.
- Peak incidence: 20s-30s, M:F = 1.4:1 [3]
- Pelvic appendix may cause suprapubic pain and diarrhoea (irritation of rectum/bladder) — can be confusing [3]
- Retrocaecal appendix may cause flank/back pain and have minimal anterior abdominal signs (because it is shielded from the anterior parietal peritoneum by the caecum) [3]
Biliary Colic [2]:
- Risk factors: Fat, Female, Fertile, Forty (cholesterol gallstones)
- Intense, dull discomfort in RUQ or epigastrium — actually a misnomer ("colic") because the pain is constant (smooth muscle in sustained spasm), though it has excruciating exacerbations [2]
- Usually lasts ≥ 30 minutes, plateaus within 1 hour, resolves ≤ 6 hours if uncomplicated [2]
- Associated with nausea, vomiting, diaphoresis (vagal response) ± jaundice (if CBD stone)
- Why "colic" is actually constant: the gallbladder contracts against an impacted stone; unlike intestinal peristalsis (which has rhythmic contractions with rest periods), gallbladder contraction is sustained tetanic spasm.
- Sudden, prolonged RUQ or epigastric pain > 4-6 hours (distinguishes from biliary colic which resolves < 6h)
- May radiate to back or tip of right scapula (T6-T9 dermatomal referral)
- Exacerbated by moving and breathing (parietal peritoneal irritation)
- Associated with fever (secondary bacterial infection of obstructed, distended gallbladder)
- Murphy's sign: arrest of inspiration on palpation of RUQ — the inflamed gallbladder descends with the diaphragm during inspiration and contacts the examiner's fingers → pain → patient stops breathing in.
Acute Cholangitis [2]:
- Charcot's triad: RUQ pain + fever (intermittent with rigors) + obstructive jaundice
- Reynold's pentad: adds hypotension + mental obtundation (indicating septic shock with biliary sepsis)
- Pathophysiology: CBD obstruction (stone, stricture, tumour) → biliary stasis → ascending bacterial infection → bacteraemia → sepsis
- Gastric ulcer: pain immediately after meal → patients are often afraid of eating → weight loss. Pain ↓ by vomiting (decompresses stomach). Why? Food stimulates acid secretion which bathes the ulcer.
- Duodenal ulcer: pain 2h after meal (when gastric contents including acid enter the duodenum), ↓ by eating (food buffers acid in the duodenum → patients often have good appetite). Classic "hunger pain" or nocturnal pain (no food to buffer overnight acid).
- Drug history: ask about ANY drug ingested — especially aspirin, NSAIDs, alendronate [2]
Perforated Peptic Ulcer (PPU) [2]:
- Sudden severe and constant epigastric pain that quickly reaches maximum intensity and remains severe for hours
- Gradually extends to the whole abdomen (as gastric acid and duodenal contents spread throughout the peritoneal cavity)
- ↑ by movement → patient lies completely still on bed (parietal peritoneal irritation)
- Important: pain and guarding may decrease after 4-6h as the acid gets diluted — but the peritonitis is still progressing! This is a classic trap [2].
- History of previous dyspepsia, steroids, NSAIDs
Acute Pancreatitis [7]:
- Epigastric pain (can be RUQ or rarely LUQ) — radiates to the back (pancreas is retroperitoneal; pain transmitted through the retroperitoneum)
- Rapid onset (gallstone-related) or less abrupt (alcohol-related)
- Severe, persistent for hours to days
- Relieved by sitting up or leaning forward (reduces tension on the retroperitoneal pancreas by allowing it to fall away from the posterior abdominal wall)
- Associated with nausea and vomiting (visceral autonomic response + paralytic ileus)
- Dyspnoea may occur due to diaphragmatic inflammation, pleural effusions (especially left-sided), or ARDS [7]
Intestinal Obstruction [14]:
- Colicky abdominal pain (peristalsis against obstruction causes rhythmic cramping — spasm → partial relaxation → spasm)
- Abdominal distension (proximal bowel dilates with gas and fluid)
- Vomiting (early in proximal/SBO; late in distal/LBO). Faeculent vomiting in late LBO (bacterial overgrowth in stagnant intestinal contents).
- Absolute constipation (obstipation — no passage of faeces OR flatus) — indicates complete obstruction
- High-pitched tinkling bowel sounds (proximal hyperperistalsis trying to overcome obstruction)
- Common causes: adhesions (post-surgical — #1 cause of SBO), hernias (#2 cause), malignancy (#1 cause of LBO), volvulus
Mesenteric Ischaemia [4]:
- Pain out of proportion to physical findings — the hallmark! (early visceral ischaemia activates nociceptors intensely but there is minimal peritoneal inflammation initially)
- Sudden onset (embolic) or more gradual (thrombotic on pre-existing atherosclerosis)
- Associated with AF (source of emboli), peripheral vascular disease, cardiac disease [4]
- Late features: bloody diarrhoea, peritonitis, metabolic acidosis, elevated lactate — indicate bowel infarction (irreversible)
- Sudden onset cramping abdominal pain — milder and more lateral than mesenteric ischaemia
- Mild-to-moderate rectal bleeding within 24h of pain onset
- Typically in elderly women ( > 60)
- Usually non-occlusive (transient low-flow states) affecting watershed areas [4][15]
- Clinical triad: lower abdominal pain + fever + leucocytosis [11]
- Pathophysiology: obstruction of diverticulum by faecolith → stasis and bacterial overgrowth → inflammation [11]
- In Western populations: LLQ pain (sigmoid diverticulitis)
- In Asian populations (including Hong Kong): RLQ pain (right-sided diverticulosis) — frequently confused with acute appendicitis [3][11]
- Mean age of diagnosis: 63 years [11]
Inflammatory Bowel Disease — Ulcerative Colitis [16]:
- Abdominal pain — typically LLQ/left-sided (sigmoid and rectal involvement)
- Bloody diarrhoea — shallow mucosal ulceration → bleeding
- Urgency, tenesmus — rectal inflammation
- Occurs between 30-70s, no gender predominance [16]
- Protective factors: prior appendicectomy, smoking [16]
Volvulus [17]:
- Sigmoid volvulus: older males (mean age 70), constipation history, "bent inner-tube" sign on AXR
- Caecal volvulus: younger females (mean age 33-53), congenital failure of right colon fixation
- Acute onset abdominal pain + distension + obstipation
IBS [12]:
- Recurrent abdominal pain with variable intensity
- Cramping/colicky pain ± bloating, flatulence, belching
- Characteristically associated with defecation (relieved or worsened)
- ↑ by emotional stress, meals, and throughout the day
- No red flag features (no weight loss, no bleeding, no nocturnal symptoms)
- Epidemiology: ~15% in US, up to 25% in East Asia, 3.7% in HK (Rome II criteria); more common in younger ( < 50y) and females [12]
The pain should be linked with the menstrual history, coitus and the possibility of an early pregnancy [1].
- IUCD → increases risk of salpingitis, ectopic pregnancy [1]
- Infertility history → think endometriosis, salpingitis [1]
- Tubal surgery → ectopic pregnancy [1]
- For recurrent and chronic pain, instruct the patient to keep a diary over two menstrual cycles [1]
| Condition | Pain Character | Pathophysiology |
|---|---|---|
| Ectopic pregnancy | Sudden unilateral lower abdominal pain ± vaginal bleeding ± shoulder tip pain (if ruptured with haemoperitoneum) | Implantation in fallopian tube → tubal distension → rupture → haemoperitoneum |
| Ruptured ovarian cyst | Sudden onset unilateral lower abdominal pain | Cyst rupture → peritoneal irritation by cyst contents/blood |
| Ovarian torsion | Severe, sudden, unilateral lower abdominal pain ± nausea/vomiting | Torsion of ovarian pedicle → venous then arterial occlusion → ischaemia |
| PID | Bilateral lower abdominal pain, fever, vaginal discharge | Ascending infection from cervix → endometritis → salpingitis → tubo-ovarian abscess |
| Endometriosis | Cyclical pain (dysmenorrhoea), dyspareunia, dyschezia | Ectopic endometrial tissue responds to hormonal cycling → bleeding, inflammation, adhesions |
| Degenerating fibroid | Acute lower abdominal pain ± fever | Fibroid outgrows its blood supply → central necrosis ("red degeneration" in pregnancy) |
Signs with Pathophysiological Basis
- Lying perfectly still → peritonitis (any movement irritates inflamed parietal peritoneum)
- Writhing, unable to get comfortable → colic (ureteric, biliary, intestinal — visceral pain without peritoneal irritation)
- Tachycardia, hypotension → hypovolaemia (haemorrhage, third-spacing in obstruction/pancreatitis/peritonitis), sepsis
- Shallow respiration → peritonitis (patient avoids diaphragmatic excursion to minimise peritoneal movement) [2]
- Jaundice → biliary/hepatic pathology
- Pallor → anaemia from chronic/acute GI bleeding
- Distension → obstruction (gas + fluid proximal to obstruction), ascites, ileus
- Visible peristalsis → intestinal obstruction (hypertrophied bowel contracting against obstruction)
- Surgical scars → adhesive obstruction, hernia
- Hernia orifices → always examine! Incarcerated hernia is a common missed cause of obstruction [14]
- Guarding: voluntary contraction of abdominal wall muscles in response to palpation — indicates underlying peritoneal inflammation. Why? The patient (and reflexly the nervous system) contracts the muscles to splint and protect the inflamed area.
- Rigidity (involuntary guarding / "board-like rigidity"): reflex, involuntary spasm of abdominal wall muscles. Indicates severe peritonitis (e.g., generalised peritonitis from PPU) [2]. The afferent limb is via peritoneal somatic nerves → reflex arc at spinal cord level → efferent limb via motor nerves to rectus abdominis.
- Rebound tenderness: pain on sudden release of pressure (as the parietal peritoneum snaps back to its original position → stretches inflamed peritoneum). Indicates peritonitis.
- Murphy's sign: arrest of inspiration during RUQ palpation → inflamed gallbladder descends on inspiration and contacts examiner's hand → pain → patient catches breath. Positive in acute cholecystitis [2].
- McBurney's point tenderness: maximal tenderness at 1/3 distance from ASIS to umbilicus → overlies the base of the appendix [3][10].
- Rovsing's sign: RLQ pain upon palpation of LLQ → displacement of peritoneal gas/fluid transmits pressure to the inflamed RLQ peritoneum [10].
- Psoas sign: increased RLQ pain upon extending the hip against resistance → inflamed retrocaecal appendix overlying the psoas muscle is stretched [10].
- Obturator sign: pain on internal rotation of flexed right hip → inflamed pelvic appendix irritates the obturator internus muscle.
- Pulsatile abdominal mass → AAA [9].
- Loss of liver dullness → pneumoperitoneum (free gas from perforated viscus replaces the normally dull liver → tympanic note) [2].
- Shifting dullness → ascites
- Tympany → distended gas-filled bowel (obstruction, ileus)
- High-pitched tinkling bowel sounds → mechanical obstruction (bowel trying to overcome obstruction)
- Absent bowel sounds → paralytic ileus or late/severe peritonitis (bowel has "given up")
- Borborygmi → increased gut motility (gastroenteritis, early obstruction)
- Always perform in acute abdomen
- Empty rectum → obstruction proximal to rectum
- Melaena → upper GI bleeding
- Blood on glove → lower GI pathology (malignancy, IBD, ischaemic colitis)
- Tenderness in Pouch of Douglas → pelvic abscess, collection
- Boggy mass → pelvic abscess
- Speculum (preferably bivalve type) and bimanual palpation [1]
- Cervical excitation (chandelier sign) → ectopic pregnancy, PID
- Adnexal mass → ovarian cyst, ectopic pregnancy, tubo-ovarian abscess
- Uterine tenderness → endometritis, PID
Key Examination Approach
In the assessment of abdominal pain in women, use the traditional abdominal and pelvic examination to identify the site of tenderness, rebound tenderness, and any abdominal or pelvic masses. The pelvis should be examined by speculum and bimanual palpation. Proper assessment can be difficult if the patient cannot relax, if there is abdominal scarring or obesity, or if extreme tenderness is present — so a gentle, caring vaginal examination with appropriate explanation and reassurance is critical, especially in the younger and apprehensive patient [1].
As mentioned in the lecture slides [1]:
- FBE / ESR / CRP
- Urine MC&S
- Chlamydia PCR (in women with lower abdominal pain / PID suspected)
- β-hCG (all women of reproductive age)
- Additional based on clinical suspicion: LFTs, amylase/lipase, lactate, blood gas, imaging (AXR, erect CXR, USG, CT)
Always consider non-abdominal causes of abdominal pain [1]:
- Depression (somatic presentation of depression can present as chronic abdominal pain)
- Drugs (NSAIDs, opiates, etc.)
- Spinal dysfunction (referred pain from thoracolumbar spine to abdomen — T7-L1 dermatomal distribution)
- UTI (lower abdominal/suprapubic pain)
- "Is the patient trying to tell me something?" — can be very relevant. Consider various problems and sexual dysfunction [1].
Nerve Entrapment and Referred Pain to Pelvis
The lecture slides specifically mention nerve entrapment as a cause of pelvic pain, and referred pain to the pelvis from: appendicitis, cholecystitis, diverticulitis, UTI [1]. Don't forget these — a patient with "pelvic pain" may actually have appendicitis!
| Condition | Site | Character | Radiation | Timing | Exacerbating/Relieving | Key Associated Features |
|---|---|---|---|---|---|---|
| Appendicitis | Periumbilical → RLQ | Dull → sharp | None typical | Progressive over 12-24h | ↑ movement | Anorexia, low-grade fever, vomiting (after pain) |
| Biliary colic | RUQ/epigastric | Constant, intense (false colic) | Right scapula | ≥30min, <6h | ↑ fatty meals | N/V, diaphoresis |
| Cholecystitis | RUQ | Constant, severe | Back, right scapula | >4-6h | ↑ movement, breathing | Fever, Murphy's sign |
| Cholangitis | RUQ | Constant | — | Persistent | — | Charcot's triad/Reynold's pentad |
| PPU | Epigastric → generalised | Sudden, severe, constant | — | Maximal immediately | ↑ movement | Board-like rigidity, ↓liver dullness |
| Gastric ulcer | Epigastric | Burning | — | With meals | ↑ eating, ↓ vomiting | Weight loss, afraid of eating |
| Duodenal ulcer | Epigastric | Burning, "hunger pain" | Back (posterior ulcer) | 2h post-meal, nocturnal | ↓ eating | Good appetite |
| Pancreatitis | Epigastric | Severe, constant | Back | Hours to days | ↓ leaning forward | N/V, dyspnoea |
| SBO | Periumbilical | Colicky | — | Intermittent | ↓ vomiting | Distension, vomiting, constipation |
| LBO | Lower abdomen | Colicky | — | Intermittent | — | Distension ++, late vomiting |
| Mesenteric ischaemia | Diffuse/periumbilical | Severe, constant | — | Sudden or subacute | — | Pain >> signs, AF history, lactic acidosis |
| Diverticulitis | LLQ (West) / RLQ (Asia) | Constant | — | Progressive | — | Fever, leucocytosis |
| Renal colic | Loin → groin | Colicky, severe | Loin to groin | Paroxysmal | ↓ movement is NOT helpful (writhing) | Haematuria, N/V |
| AAA rupture | Abdominal/back | Severe, sudden | Back | Catastrophic | — | Hypotension, pulsatile mass |
High Yield Summary
-
Three pain types: Visceral (dull, midline, autonomic afferents), Parietal/Somatic (sharp, localised, somatic nerves), Referred (distant site, convergence in dorsal horn).
-
Embryological pain referral: Foregut → epigastrium; Midgut → periumbilical; Hindgut → suprapubic.
-
Life-threatening causes NEVER to miss: PPU, ruptured AAA, mesenteric ischaemia, strangulated obstruction, severe pancreatitis, ruptured HCC/ectopic, DKA, acute MI, Addisonian crisis.
-
Appendicitis: Midgut visceral pain (periumbilical T10) → shifts to RLQ (parietal peritoneal irritation). Appendiceal artery is an END-ARTERY → thrombosis = necrosis. Peak 20s-30s, M > F.
-
Biliary colic: "False colic" — actually constant. ≥30min, <6h. Risk factors: Fat, Female, Fertile, Forty.
-
PPU: Sudden maximal epigastric pain → generalised. Board-like rigidity. ↓Liver dullness (pneumoperitoneum). Pain may transiently ↓ after 4-6h as acid dilutes — BUT peritonitis is still progressing!
-
Pancreatitis: Epigastric → back. Relieved by leaning forward. Autodigestion by premature trypsin activation.
-
Mesenteric ischaemia: Pain out of proportion to findings. Think AF, atherosclerosis. Lactate↑.
-
Asian diverticular disease: Right-sided predominance; confused with appendicitis.
-
Peritonitis classification: Primary (SBP in cirrhosis), Secondary (surgically treatable), Tertiary (opportunistic after prolonged antibiotics).
-
Watershed areas: Griffiths' point (splenic flexure), Sudeck's point (rectosigmoid junction).
-
Women of reproductive age: ALWAYS check β-hCG. Link pain with menstrual history, coitus, pregnancy possibility. Examine speculum + bimanual.
-
Masquerades: Depression, Drugs, Spinal dysfunction (referred), UTI. "Is the patient trying to tell me something?"
Active Recall - Abdominal Pain (Definition to Clinical Features)
[1] Lecture slides: murtagh merge.pdf (Abdominal pain in women section) [2] Senior notes: Ryan Ho Fundamentals.pdf (p268-276, Causes of Upper Abdominal Pain, Abdominal Pain History) [3] Senior notes: felixlai.md (Acute appendicitis section) [4] Senior notes: felixlai.md (Mesenteric ischaemia / ischaemic colitis section) [5] Senior notes: felixlai.md (Cholecystitis, Liver abscess sections) [6] Senior notes: Ryan Ho GI.pdf (p76, Peptic Ulcer Disease) [7] Senior notes: felixlai.md (Acute pancreatitis section) [8] Senior notes: felixlai.md (GERD section) [9] Senior notes: Ryan Ho Cardiology.pdf (p222, Abdominal Aortic Aneurysms) [10] Senior notes: maxim.md (Acute appendicitis section) [11] Senior notes: felixlai.md (Diverticular disease section); maxim.md (Diverticular disease section) [12] Senior notes: Ryan Ho GI.pdf (p118, Irritable Bowel Syndrome) [13] Senior notes: felixlai.md (Peritonitis section) [14] Senior notes: felixlai.md (Bowel obstruction section) [15] Senior notes: Ryan Ho GI.pdf (p146, Ischaemic Colitis) [16] Senior notes: felixlai.md (Ulcerative colitis section) [17] Senior notes: felixlai.md (Volvulus section)
Differential Diagnosis of Abdominal Pain
The differential diagnosis of abdominal pain is enormous. Rather than trying to memorise every single cause, the key is to have a structured framework that you apply every single time. There are several complementary frameworks you can use simultaneously:
- By anatomical quadrant (where is the pain?) — narrows the organ
- By acuity (acute vs chronic vs recurrent) — narrows the tempo of disease
- By mechanism (inflammation, obstruction, ischaemia, perforation, haemorrhage, functional) — narrows the pathology
- By patient demographics (age, sex, ethnicity, comorbidities) — narrows the probability
- By Murtagh's diagnostic strategy (probability diagnosis → serious disorders not to be missed → pitfalls → masquerades → "is the patient trying to tell me something?") — a systematic safety net [1]
The beauty of Murtagh's framework is that it forces you to think about common things first, then actively look for the dangerous mimics and the "often missed" diagnoses. This is exactly how a good clinician thinks.
Murtagh's Diagnostic Strategy — Acute Abdominal Pain in Adults [1]
This is the lecture-slides framework. Every single entry below comes from or is cross-referenced with the Murtagh slides. Understand the logic behind each category.
These are the conditions you will see most often in clinical practice:
| Condition | Why It's Common | Key Distinguishing Feature |
|---|---|---|
| Acute gastroenteritis | Most common cause of acute abdominal pain worldwide; viral/bacterial | Diffuse crampy pain + diarrhoea + vomiting (N/V typically before pain — contrast with appendicitis where pain precedes vomiting) |
| Acute appendicitis | Lifetime risk ~7-8%; peak 20s-30s | Migratory pain periumbilical → RLQ; anorexia; low-grade fever |
| Mittelschmerz / Dysmenorrhoea | Extremely common in women of reproductive age | Mid-cycle (Mittelschmerz = "middle pain" in German, i.e., pain at ovulation) or cyclical with menses |
| Irritable bowel syndrome | Prevalence up to 25% in East Asia | Recurrent crampy pain related to defecation; no red flags; diagnosis of exclusion [12][18] |
| Biliary colic / Renal colic | Gallstones affect ~10-15% of adults; renal stones ~5% | Biliary: constant RUQ/epigastric < 6h; Renal: loin-to-groin colicky pain with haematuria |
| Peptic ulcer | Lifetime risk ~10% | Epigastric burning; meal-related; NSAID/H. pylori history [6][18] |
These are the ones that kill or maim if you miss them. You must actively consider and exclude these in every patient with acute abdominal pain.
Vascular — Why vascular causes are deadly: large-vessel events cause rapid exsanguination or irreversible organ ischaemia:
| Condition | Mechanism of Pain | Key Clinical Clue |
|---|---|---|
| Myocardial infarction (esp. inferior) [1] | Inferior MI can refer pain to the epigastrium via shared T5-T9 autonomic afferents from the diaphragmatic surface of the heart | ECG changes; cardiac risk factors; epigastric pain + nausea/diaphoresis in an elderly patient with no peritoneal signs — always do an ECG! |
| Splenic infarction [1] | Embolic occlusion of splenic artery → splenic ischaemia → capsular distension | LUQ pain ± left shoulder tip pain; AF, endocarditis, myeloproliferative disorders |
| Ruptured AAA [1] | Aortic wall rupture → retroperitoneal/intraperitoneal haemorrhage | Classical triad: severe abdominal/back pain + hypotension + pulsatile abdominal mass [9] |
| Dissecting aneurysm of aorta [1] | Intimal tear → blood dissects through medial layer → stretches adventitia (nociceptive) | "Tearing" interscapular/back pain; BP differential between arms; wide mediastinum on CXR |
| Mesenteric artery occlusion [1] | SMA embolism/thrombosis → midgut ischaemia/infarction | Pain out of proportion to examination; AF or vascular disease history; metabolic acidosis + ↑lactate [4] |
Cancer [1]:
- Bowel cancer with large or small bowel obstruction — Colorectal carcinoma is the commonest cause of LBO in adults. Think of this in any elderly patient with new-onset colicky pain + distension + change in bowel habit.
Infection [1]:
| Condition | Why Serious | Distinguishing Features |
|---|---|---|
| Acute cholecystitis | Can progress to empyema, gangrenous cholecystitis, perforation | RUQ pain > 4-6h + fever + Murphy's sign [2][5] |
| Acute salpingitis | Can cause tubo-ovarian abscess, sepsis, infertility | Bilateral lower abdominal pain + fever + vaginal discharge; cervical motion tenderness |
| Peritonitis / SBP | Septicaemia → multi-organ failure | Generalised guarding/rigidity; SBP in cirrhotic patients [13] |
| Ascending cholangitis | Biliary sepsis → septic shock | Charcot's triad / Reynold's pentad [2] |
| Intra-abdominal abscess | Persistent sepsis | Persistent fever despite antibiotics; CT shows collection [3][11] |
Other serious conditions [1]:
| Condition | Mechanism | Key Feature |
|---|---|---|
| Pancreatitis | Autodigestion → systemic inflammatory cascade → organ failure | Epigastric → back; ↓ leaning forward; ↑amylase/lipase ≥ 3× ULN [7] |
| Ectopic pregnancy | Tubal implantation → rupture → haemoperitoneum | +β-hCG, amenorrhoea, unilateral pain ± shoulder tip pain if ruptured |
| Small bowel obstruction / Strangulated hernia [1] | Luminal obstruction → bowel ischaemia if strangulated | Colicky pain + vomiting + distension + absolute constipation; always check hernial orifices! [14] |
| Sigmoid volvulus [1] | Sigmoid colon twists on mesentery → closed-loop obstruction | Elderly constipated male; massive abdominal distension; "coffee-bean sign" on AXR [17] |
| Perforated viscus (esp. PPU) [1] | Free leakage of GI contents → chemical then bacterial peritonitis | Sudden maximal epigastric pain → generalised; board-like rigidity; loss of liver dullness [2] |
Always Check Hernial Orifices
Incarcerated hernias are a leading cause of complications related to bowel obstruction [14]. A strangulated inguinal or femoral hernia is easily missed if the groins are not examined — a cardinal sin in the assessment of acute abdominal pain. Femoral hernias are particularly treacherous because they are small, more common in women, and have a high rate of strangulation.
These are the diagnoses that are frequently overlooked, leading to diagnostic delay:
| Condition | Why It's Missed | How to Catch It |
|---|---|---|
| Acute appendicitis (atypical) [1] | Retrocaecal (minimal anterior signs), pelvic (suprapubic/urinary/rectal symptoms), or malrotated appendix | Maintain a high index of suspicion in any RLQ/RIF pain; serial examination is key; CT if in doubt [3][10][18] |
| Myofascial tear / Muscle wall pain [1] | Abdominal wall pathology masquerading as intra-abdominal | Carnett sign: tenderness that increases when the patient tenses the abdominal wall muscles (sit-up position) → points to abdominal wall origin [18] |
| Pulmonary causes: pneumonia, PE [1] | Lower lobe pneumonia (especially right) refers pain to upper abdomen via diaphragmatic irritation (phrenic nerve C3-C5) | CXR; pleuritic pain; cough; hypoxia; high respiratory rate |
| Faecal impaction (elderly) [1] | Elderly, immobile or demented patients may present with vague abdominal pain; easily diagnosed on PR exam | Always do a PR exam in elderly patients with abdominal pain |
| Acute diverticulitis [1] | Right-sided diverticulitis in Asian patients mimics appendicitis [3][11]; sigmoid diverticulitis may be mild | CT abdomen with contrast is the diagnostic test of choice [3] |
| Herpes zoster [1] | Pre-eruptive phase causes dermatomal pain before the rash appears → can mimic visceral pain | Look for rash in a dermatomal distribution; unilateral; burning/lancinating quality |
| Acute hepatitis [1] | RUQ pain from liver capsule distension; may be subtle | LFTs (markedly ↑ALT/AST); jaundice; travel/drug/sexual history |
| Inflammatory bowel disease [1] | Insidious onset; may present acutely in young patients | Bloody diarrhoea (UC); chronic diarrhoea + weight loss + perianal disease (Crohn's) [16] |
Rarities (low probability but examinable) [1]:
- Porphyria ("purple urine" — actually port-wine) — intermittent severe colicky abdominal pain with neuropsychiatric features; check urine porphyrins
- Lead poisoning — colicky pain + constipation + basophilic stippling on blood film + blue line on gums (Burton's line)
- Haemochromatosis — RUQ pain from hepatomegaly; bronze skin; diabetes; arthropathy; ↑ferritin, ↑transferrin saturation
- Haemoglobinuria / Sickle cell anaemia [1] — vaso-occlusive crises cause severe diffuse abdominal pain; sickle cell patients have a high rate of cholesterol gallstones too
- Addison disease [1] — acute adrenal crisis presents as an acute abdomen with diffuse abdominal pain, nausea, vomiting, fever, hypotension and shock [19]; hypoNa, hyperK, hypoglycaemia
These are non-abdominal conditions that present with abdominal pain. The concept is that the abdomen is a "great mimicker" — and equally, other conditions can mimic abdominal pathology.
| Masquerade | Mechanism | Clinical Clue |
|---|---|---|
| Depression [1] | Somatic presentation of psychiatric illness; visceral hypersensitivity from altered brain-gut signalling | Chronic/recurrent pain with no organic cause found; associated with sleep disturbance, anhedonia, psychomotor changes |
| Diabetes (ketoacidosis) [1] | DKA causes an acute abdomen — diffuse abdominal pain, nausea, vomiting due to ileus (metabolic acidosis → impaired GI motility) [19] | Kussmaul respiration, fruity breath, polyuria/polydipsia history, hyperglycaemia ≥ 11 mmol/L with ketonuria + metabolic acidosis |
| Drugs [1] | NSAIDs → PUD/gastropathy; iron tablets → GI irritation; narcotics → constipation/ileus; cytotoxics → mucositis, neutropenic enterocolitis | Always take a thorough drug history |
| Anaemia (sickle cell) [1] | Vaso-occlusive crisis → microinfarction of mesenteric vasculature, splenic infarction, or hepatic sequestration | Known sickle cell disease; acute pain crisis; ↓Hb; sickle cells on film |
| Spinal dysfunction (referred) [1] | Thoracolumbar spinal pathology (T7-L1) can refer pain to the abdomen via somatic nerve roots | Dermatomal distribution; associated with back pain; tenderness follows dermatome, not organ |
| UTI (including urosepsis) [1] | Lower urinary tract infection → suprapubic pain; pyelonephritis → flank/loin pain; urosepsis → diffuse abdominal pain with systemic toxicity | Dysuria, frequency, urgency; pyuria on urine MC; fever with rigors in urosepsis |
"Is the patient trying to tell me something?" [1] — May be very significant. Consider Munchausen syndrome, sexual dysfunction and abnormal stress [1]. This is the final safety net in Murtagh's framework: some patients present with abdominal pain as a vehicle to discuss other concerns.
DKA as an Acute Abdomen
DKA can perfectly mimic a surgical acute abdomen [1][19]. The mechanism is multifactorial: severe metabolic acidosis causes paralytic ileus (impaired smooth muscle contractility), gastric distension, and direct peritoneal irritation from ketone bodies. The clinical presentation includes diffuse abdominal pain, guarding, nausea, and vomiting — making it virtually indistinguishable from peritonitis on examination alone. Always check blood glucose and ketones in any patient with acute abdominal pain, especially if young, thin, or with known T1DM. Performing an unnecessary laparotomy on a DKA patient is a classic exam and real-life disaster.
Murtagh's Diagnostic Strategy — Chronic / Recurrent Abdominal Pain in Adults [1]
The chronic DDx overlaps with the acute list but shifts the probabilities significantly toward functional, inflammatory and neoplastic causes.
- Irritable bowel syndrome — #1 cause of chronic abdominal pain; Rome IV criteria (recurrent pain ≥ 1 day/week for 3 months, associated with ≥ 2 of: related to defecation, change in stool frequency, change in stool form) [12]
- Mittelschmerz / Dysmenorrhoea — cyclical, mid-cycle or menstrual
- Constipation — common especially in elderly, immobile, drug-related (opioids, CCB, anticholinergics)
- Peptic ulcer / Gastritis — chronic, meal-related epigastric pain [6]
- Mesenteric artery ischaemia (chronic) — "intestinal angina": postprandial pain (increased metabolic demand of gut exceeds compromised blood supply) → food fear → weight loss. Classic triad: postprandial pain, food avoidance, weight loss [4].
- AAA — vague, indolent abdominal/back pain; stretching of aneurysm sac indicates impending rupture [9]
- Cancer: bowel, stomach, pancreatic, ovarian [1] — Weight loss, constitutional symptoms, change in bowel habit, new dyspepsia in elderly
- Hepatitis (chronic) — insidious; RUQ discomfort, fatigue, jaundice
- Recurrent PID — recurrent lower abdominal pain with vaginal discharge
- Adhesions — prior abdominal surgery; intermittent colicky pain from partial SBO
- Appendicitis (grumbling / recurrent) — atypical, chronic RLQ pain
- Biliary disease: gallstones, sludge — recurrent biliary colic episodes
- Food allergies / Lactase deficiency — diarrhoea, bloating, pain related to specific dietary intake (dairy in lactose intolerance)
- Hernia — intermittent pain at hernial orifice; worse with straining/standing
- Constipation / Faecal impaction [1]
- Chronic pancreatitis [1] — chronic epigastric pain radiating to back; history of alcohol; pancreatic calcifications on imaging; exocrine insufficiency (steatorrhoea)
- Coeliac disease [1] — diarrhoea, steatorrhoea, iron/B12/folate deficiency anaemia, weight loss; positive anti-tTG antibodies; duodenal biopsy shows villous atrophy
- Inflammatory bowel disease [1] — Crohn's (any part of GIT, transmural, skip lesions, granulomas) vs UC (continuous from rectum, mucosal, pseudopolyps) [16]
- Crohn disease [1] — specifically mentioned; terminal ileum commonest site; RLQ pain, chronic diarrhoea ± PR bleeding, perianal disease, weight loss
- Endometriosis [1] — cyclical pain, dyspareunia, dyschezia; ectopic endometrial tissue
- Diverticular disease [1] — recurrent LLQ/RLQ pain; change in bowel habit
- Subacute obstruction (cancer, adhesions) [1] — intermittent colicky pain, vomiting, distension
Rarities [1]:
- Tropical infections (hydatids, melioidosis, strongyloides) — travel history!
- Uraemia — chronic renal failure → GI symptoms
- Lead poisoning, Porphyria, Sickle cell, Hypercalcaemia, Addison disease [1]
Probability diagnosis: Primary dysmenorrhoea, Mittelschmerz, Pelvic/abdominal adhesions, Endometriosis [1]
Serious disorders not to be missed [1]:
- Vascular: internal iliac claudication (rare but important)
- Neoplasms: ovary, uterus, other pelvic structures [1]
- Infection: PID, pelvic abscess, appendicitis [1]
- Other: ectopic pregnancy [1] — the single most dangerous diagnosis to miss in a woman of reproductive age
Pitfalls (often missed) [1]:
- Endometriosis / Adenomyosis
- Torsion of ovary or pedunculated fibroid
- Constipation / Faecal impaction
- Pelvic congestion syndrome — chronic pelvic pain from dilated pelvic veins; worse with standing/end of day
- Misplaced IUCD
- Nerve entrapment [1] — ilioinguinal or iliohypogastric nerve entrapment (e.g., post-surgical) causing chronic localised pain
Referred pain to pelvis [1]: appendicitis, cholecystitis, diverticulitis, UTI — always consider these even when the pain appears pelvic.
| Category | Diagnoses |
|---|---|
| Probability diagnosis | Infant 'colic' (2-16 weeks), Gastroenteritis (all ages), Mesenteric adenitis |
| Serious - not to miss | Acute appendicitis (mainly 5-15y) — more likely complicated in children due to delayed presentation [18]; Pneumonia (esp. right lower lobe); Pyelonephritis; Peritonitis; Intussusception (peaks 6-9 months); Bowel obstruction; Coeliac disease; Strangulated inguinal hernia; colon cancer (rare) |
| Pitfalls | Child abuse; Constipation; Torsion of testes; Lactose intolerance; Peptic ulcer; Infections (mumps, tonsillitis, pneumonia, EBV, UTI, hepatitis) |
Key pearl for children: Intussusception (telescoping of proximal bowel into distal bowel, classically ileocolic) presents with episodic severe colicky pain (child draws up legs and screams) + "redcurrant jelly" stools (mixed blood and mucus) + sausage-shaped mass in RUQ. Peak age 6-9 months. Pathophysiology: lead point (often Peyer's patch / lymphoid hyperplasia) gets caught in peristaltic wave → intussusception → venous congestion → ischaemia → bloody mucus extrusion.
| Category | Diagnoses |
|---|---|
| Probability | Non-organic RAP, Constipation, Recurrent viral illness / mesenteric adenitis |
| Serious | Recurrent UTI / ureteric reflux, Parasitic infection (pinworm, strongyloides), TB, Hydronephrosis, colon cancer (rare) |
| Pitfalls | IBD, Childhood migraine equivalent (periodic syndrome), Food allergy / lactose intolerance, Gastritis / GERD; Rarities: Meckel's diverticulum, temporal lobe epilepsy, sickle cell disease, HSP, IBS |
DDx Organised by Location — Expanded Detail
This section integrates the quadrant-based approach from multiple senior notes [2][18] with the Murtagh framework above. The purpose is to have a single, comprehensive, location-based DDx you can recall at the bedside.
| Organ System | Differential | Key Distinguishing Feature |
|---|---|---|
| Biliary (commonest) | Biliary colic | Constant RUQ < 6h, post-fatty meal, ± jaundice (CBD stone) |
| Acute cholecystitis | > 4-6h, fever, Murphy's sign [5] | |
| Acute cholangitis | Charcot's / Reynold's pentad [2] | |
| Sphincter of Oddi dysfunction | Pain < 6h, intermittent; normal labs and imaging [5] | |
| Liver | Acute hepatitis | Capsular distension; markedly ↑ALT/AST; jaundice |
| Liver abscess | Fever (90%), guarding/rebound; Klebsiella in HK/diabetics, amoebic if travel history [5] | |
| HCC or metastasis | Underlying cirrhosis/HBV carrier; sudden RUQ pain if ruptured | |
| Budd-Chiari syndrome | RUQ pain + massive ascites + LL oedema + jaundice; thrombotic RFs [2] | |
| Portal vein thrombosis | Background cirrhosis; acute RUQ pain + fever [2] | |
| Fitz-Hugh-Curtis syndrome | Pleuritic RUQ pain ± radiation to right shoulder; perihepatic adhesions from PID ("violin-string" adhesions) [2] | |
| Pancreatic | Acute pancreatitis | Epigastric → back; ↓ leaning forward; gallstones/alcohol [7] |
| GI | PUD | Epigastric burning; may radiate to RUQ [2] |
| Colorectal diseases | Hepatic flexure pathology | |
| Others | Pyelonephritis, renal stone, RCC | Flank/loin pain, CVA tenderness, haematuria |
| Basal pneumonia, pleural effusion, basal MI | Referred from thorax; CXR, ECG [2] | |
| Herpes zoster, abdominal wall pain | Dermatomal; Carnett sign [2] |
| Differential | Key Feature |
|---|---|
| PUD (GU / DU) | Meal-related; NSAID/H. pylori [6] |
| PPU | Sudden maximal severity; board-like rigidity; ↓liver dullness [2] |
| Acute pancreatitis | → back; ↓ leaning forward [7] |
| GERD / Oesophagitis | Retrosternal burning; ↑ lying flat [8] |
| Acute gastritis / Duodenitis | Drug history; milder |
| AAA (symptomatic/ruptured) | Pulsatile mass; hypotension [9] |
| Gastric / Pancreatic cancer | Weight loss; new dyspepsia in > 55 |
| Functional dyspepsia | 75% of dyspepsia; diagnosis of exclusion (Rome IV criteria); postprandial fullness, early satiety, epigastric pain/burning; no structural disease [18][20] |
| Differential | Key Distinguishing Feature |
|---|---|
| Acute appendicitis | Migratory pain; McBurney's point; anorexia → vomiting → pain sequence [3][10] |
| Right-sided diverticulitis | More common in Asian populations; CT shows pericolonic inflammation > 10 cm involvement, no enlarged LN [3][11] |
| Meckel's diverticulitis | Congenital remnant 2 feet from ileocaecal valve on antimesenteric border; can mimic appendicitis; usually incidental finding at surgery [3] |
| Acute ileitis | Acute bacterial (Yersinia, Campylobacter, Salmonella); diarrhoea is a prominent symptom [3] |
| Crohn's disease | Chronic; fever, prolonged diarrhoea, weight loss, perianal disease [3] |
| Tubo-ovarian abscess | Reproductive age women; complication of PID [3] |
| Ruptured ovarian cyst | Sudden onset; during exercise/intercourse [3] |
| Ovarian / Fallopian tube torsion | Severe sudden pain; torsion of ovarian pedicle → ischaemia [3] |
| PID | Pain worsens during coitus or near menses; purulent endocervical discharge; cervical motion tenderness [3] |
| Ectopic pregnancy | Positive β-hCG; no IUP on USS [3] |
| Endometritis | Post-delivery or post-procedure [3] |
| Endometriosis | Cyclical; dyspareunia; ectopic endometrial tissue [3] |
| Ureteric colic | Loin-to-groin; haematuria |
| Strangulated inguinal/femoral hernia | Irreducible groin lump + signs of obstruction [1] |
| Differential | Key Distinguishing Feature |
|---|---|
| Sigmoid diverticulitis | "Left-sided appendicitis" in Western populations; triad of LLQ pain + fever + leucocytosis [11] |
| CRC (sigmoid) | Elderly; change in bowel habit; PR bleeding; iron-deficiency anaemia |
| UC / IBD | Bloody diarrhoea; continuous from rectum [16] |
| Ischaemic colitis | Elderly; sudden crampy pain + rectal bleeding < 24h; watershed areas [4][15] |
| Gynaecological | As per RLQ (left-sided equivalents) |
| Ureteric colic (left) | Loin-to-groin |
DDx by Specific Clinical Scenario — Cross-Referencing Key Conditions
When a patient presents with epigastric pain radiating to the back:
- Peptic ulcer disease — burning, meal-related, no ↑amylase/lipase
- Choledocholithiasis / Cholangitis / Cholecystitis — overlaps significantly (gallstones are the commonest cause of pancreatitis!); jaundice, RUQ predominant
- Hepatitis — ↑↑ALT/AST, not amylase/lipase
- Mesenteric ischaemia — pain out of proportion; AF/vascular risk; ↑lactate [4]
- Intestinal obstruction — colicky; distension; vomiting
- Myocardial infarction [7] — always do an ECG in upper abdominal pain; inferior MI can mimic pancreatitis perfectly
- Colorectal cancer — similar presentation + bowel wall thickening on CT. CRC can only be excluded with colonoscopy after resolution of acute inflammation [3]. CT features favouring diverticulitis: pericolonic/mesenteric inflammation, involvement > 10 cm of colon, absence of enlarged pericolonic LN [3].
- Acute appendicitis — periumbilical → RLQ migration; younger patients
- Inflammatory bowel disease — diarrhoea predominant rather than pain [3]
- Infectious colitis — diarrhoea predominant [3]
- Ischaemic colitis — rapid onset pain + hematochezia; elderly with vascular risk factors [3]
- Gynaecological disorders — tubo-ovarian abscess, ovarian torsion, ectopic pregnancy [3]
- Urological disorders — cystitis, nephrolithiasis [3]
- Aortic dissection — tearing interscapular pain; BP differential
- Ulcerated aortic plaque — chronic atheroembolism
- Acute pancreatitis — ↑amylase/lipase
- Acute peritonitis — peritoneal signs
- Acute MI [9] — ECG
- Gallbladder polyps — adenoma (commonest benign neoplastic), cholesterol polyps (commonest benign non-neoplastic — "strawberry gallbladder"), adenomyomatosis [5]
- Acute cholecystitis — pain > 6h, fever, Murphy's sign [5]
- Sphincter of Oddi dysfunction — pain < 6h, intermittent, normal labs [5]
- Functional gallbladder disorder — pain < 6h, intermittent, normal labs and imaging [5]
| Condition | Age | Key Features |
|---|---|---|
| Acute appendicitis | MC 5-12y | Similar to adults but more likely complicated due to delayed presentation |
| Mesenteric adenitis | Children/young adults | Viral illness prodrome; high fever ( > 38.5°C — contrast with appendicitis which has low-grade fever); mimics appendicitis |
| Meckel's diverticulitis | Any age | Painless PR bleeding (ectopic gastric mucosa causing ulceration) OR mimic appendicitis |
| Intussusception | Peak 6-9 months | Episodic colicky pain; "redcurrant jelly" stools; sausage-shaped mass; USS "target sign" |
| Testicular torsion | Adolescent males | Sudden severe scrotal pain; absent cremasteric reflex; high-riding testis; surgical emergency — testicular viability < 6h |
| HSP | 3-10 years | Purpuric rash (lower limbs/buttocks) + abdominal pain (GI vasculitis) + arthritis + nephritis |
| DKA | Any age | As per adults; always check glucose [19] |
"Upper abdominal pain is caused by lesions of the upper GIT. Lower abdominal pain is caused by lesions of the lower GIT or pelvic organs." [1]
"Early severe vomiting indicates a high obstruction of the GIT." [1] — Because proximal obstruction has less bowel to accommodate the backed-up secretions, so vomiting occurs earlier and more prominently.
High Yield Summary
-
Murtagh's framework: Probability → Serious not to miss → Pitfalls → Masquerades → "Is the patient trying to tell me something?" Apply this systematically to every patient.
-
Life-threatening DDx of acute abdomen: PPU, ruptured AAA, acute mesenteric ischaemia, acute IO, severe pancreatitis, ruptured HCC, DKA, acute MI, Addisonian crisis, ruptured ectopic, placental abruption.
-
Masquerades: Depression, DKA, Drugs (NSAIDs, opioids, cytotoxics), Sickle cell anaemia, Spinal dysfunction (referred pain), UTI/urosepsis.
-
DKA mimics surgical acute abdomen — always check blood glucose and ketones.
-
Inferior MI mimics upper abdominal pain — always do an ECG in epigastric pain.
-
Right-sided diverticulitis in Asia mimics appendicitis — CT abdomen is the differentiator.
-
CRC can only be excluded with colonoscopy after resolution of acute diverticulitis inflammation.
-
Women of reproductive age: always β-hCG; ectopic pregnancy is the single most dangerous miss.
-
Children: appendicitis more likely complicated (delayed); intussusception peaks 6-9 months; mesenteric adenitis has higher fever than appendicitis.
-
Carnett sign differentiates abdominal wall pain from intra-abdominal: tenderness increases with muscle tensing → wall origin.
-
Early severe vomiting = high GI obstruction; late vomiting = distal obstruction.
-
Always examine hernial orifices — incarcerated hernia is a leading cause of bowel obstruction complications.
Active Recall - Differential Diagnosis of Abdominal Pain
References
[1] Lecture slides: murtagh merge.pdf (Abdominal pain acute in adults p4-6; Abdominal pain in women p1-2; Abdominal pain acute in children p8; Abdominal pain chronic/recurrent in adults p11-12; Abdominal pain recurrent in children p14) [2] Senior notes: Ryan Ho Fundamentals.pdf (p268-276, p307-308, Causes of Upper Abdominal Pain, RUQ Pain) [3] Senior notes: felixlai.md (Acute appendicitis section, Diverticulitis DDx section) [4] Senior notes: felixlai.md (Mesenteric ischaemia section) [5] Senior notes: felixlai.md (Cholecystitis section, Biliary colic DDx section) [6] Senior notes: Ryan Ho GI.pdf (p76, Peptic Ulcer Disease) [7] Senior notes: felixlai.md (Acute pancreatitis section) [8] Senior notes: felixlai.md (GERD section) [9] Senior notes: Ryan Ho Cardiology.pdf (p222, Abdominal Aortic Aneurysms); felixlai.md (AAA DDx section) [10] Senior notes: maxim.md (Acute appendicitis section) [11] Senior notes: felixlai.md (Diverticular disease section); maxim.md (Diverticular disease section) [12] Senior notes: Ryan Ho GI.pdf (p118-119, Irritable Bowel Syndrome) [13] Senior notes: felixlai.md (Peritonitis section) [14] Senior notes: felixlai.md (Bowel obstruction section) [15] Senior notes: Ryan Ho GI.pdf (p146, Ischaemic Colitis) [16] Senior notes: felixlai.md (Ulcerative colitis section) [17] Senior notes: felixlai.md (Volvulus section) [18] Senior notes: maxim.md (Paediatric surgical abdomen section; Acute appendicitis section) [19] Senior notes: Ryan Ho Endocrine.pdf (p71, Adrenal insufficiency; p91, DKA) [20] Senior notes: felixlai.md (Dyspepsia section); Ryan Ho Fundamentals.pdf (p263, Approach to Dyspepsia)
Diagnostic Approach to Abdominal Pain
The diagnostic approach to abdominal pain is fundamentally about pattern recognition guided by structured clinical reasoning, followed by targeted investigations to confirm or refute your clinical hypothesis. There is no single diagnostic criterion for "abdominal pain" itself — instead, we use condition-specific criteria alongside a systematic investigative algorithm.
The first question is always: Is this patient haemodynamically stable? If not, resuscitate first. The second question: Is this a surgical abdomen requiring immediate intervention?
Imaging Choice by Pain Location
This is a high-yield, practical rule from the senior notes [21]:
| 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) |
Why USG for RUQ? Because the commonest causes are biliary (gallstones, cholecystitis) and hepatic — USG is highly sensitive (95%) for gallstones and can demonstrate gallbladder wall thickening, pericholecystic fluid, and sonographic Murphy's sign [2][22].
Why CT for LUQ, RLQ, LLQ? Because CT provides the best anatomical detail for bowel pathology (diverticulitis, appendicitis, malignancy, ischaemia) and retroperitoneal structures. CT with IV contrast is preferred to demonstrate bowel wall enhancement and vascular pathology [3][21].
Why USG for suprapubic? Pelvic pathology (ovarian cysts, ectopic pregnancy, fibroids, bladder) is well-visualised by transabdominal (TAS) or transvaginal (TVS) ultrasonography without radiation [21].
A useful checklist from the lecture slides [1]:
- General appearance
- Oral cavity (dehydration, jaundice)
- Vital parameters including temperature, pulse
- Abdominal examination: inspection, auscultation, palpation and percussion (in that order) [1]
- Rectal examination
- Inguinal region (hernial orifices)
- Vaginal examination (if appropriate) [1]
- Urine analysis [1]
Why auscultation before palpation? Because palpation can stimulate peristalsis and alter bowel sounds, invalidating your assessment. Auscultate first to get a true baseline.
| Sign | How to Elicit | Positive Finding | Pathophysiological Basis |
|---|---|---|---|
| Guarding | Palpate the abdomen | Voluntary muscle contraction over tender area | Patient consciously or subconsciously protects inflamed peritoneum |
| Rigidity | Palpate the abdomen | Involuntary board-like muscle spasm | Reflex arc: peritoneal somatic afferents → spinal cord → motor efferents to rectus abdominis. Indicates severe peritonitis [2] |
| Rebound tenderness | Press slowly then release suddenly | Pain on release worse than on pressing | Rapid peritoneal rebound stretches inflamed peritoneum |
| Murphy's sign | Palpate GB fossa; ask patient to inspire deeply | Patient catches breath (inspiratory arrest) | Inflamed GB descends with diaphragm and contacts examiner's fingers → pain. Sensitivity 97%, Specificity 48% [22] |
| Sonographic Murphy's sign | USG probe pressed on visualised gallbladder | Maximal tenderness when probe directly over GB | Same principle as clinical Murphy's but confirms anatomical correlation — the tenderness is definitely from the gallbladder, not adjacent structures [2][22] |
| McBurney's point | Palpate 1/3 distance from ASIS to umbilicus | Maximal tenderness at this point | Overlies the base of the appendix where taeniae coli converge on caecum [3][10] |
| Rovsing's sign | Deep palpation of LLQ | Pain felt in RLQ | Displacement of peritoneal gas/fluid to the right → stretches inflamed RLQ peritoneum [3][10] |
| Psoas sign | Passive right hip extension (patient lies on left side) | RLQ pain | Inflamed retrocaecal appendix overlies psoas muscle → stretching the muscle stretches inflamed tissue [3][10] |
| Obturator sign | Passive internal rotation of flexed right hip | RLQ pain | Inflamed pelvic appendix irritates obturator internus [3] |
| Carnett sign | Ask patient to tense abdominal wall (lift head) | Tenderness increases with muscle tensing | Abdominal wall pathology (not intra-abdominal) — contracted muscles would normally shield viscera, so if pain increases it must be in the wall [20] |
| Boas' sign | Check for hyperaesthesia below right scapula | Increased sensitivity in T6-T9 dermatome | Referred pain from gallbladder inflammation via sympathetic afferents to T6-T9 spinal segments [22] |
| Loss of liver dullness | Percuss over liver area | Tympanic instead of dull | Pneumoperitoneum — free gas from perforated viscus rises to the highest point under the diaphragm [2] |
| Succussion splash | Shake the patient's abdomen while auscultating | Splashing sound | Retained fluid + gas in the stomach — indicates gastric outlet obstruction (or recent large meal) [6] |
Key Investigations — Systematic Approach
| Test | What It Tells You | When to Order |
|---|---|---|
| Urinalysis (dipstick + microscopy) [1] | Haematuria (renal/ureteric stones), pyuria/nitrites (UTI), glycosuria + ketonuria (DKA), proteinuria | Every patient with abdominal pain |
| Urine pregnancy test [1][2] | β-hCG positivity → must rule out ectopic pregnancy | All women of childbearing age — non-negotiable! [3][21] |
| ECG | Inferior MI mimicking epigastric pain; arrhythmias (AF → mesenteric embolism) | Every patient with upper abdominal pain [1][21]; also if elderly, cardiac risk factors, or unexplained tachycardia |
| Capillary blood glucose | DKA (hyperglycaemia ≥ 11 mmol/L with ketoacidosis mimics acute abdomen) [19] | If any suspicion of DKA; young patients, known diabetes |
Non-Negotiable Bedside Tests
Three tests that must NEVER be omitted in acute abdominal pain:
- Urine pregnancy test in all women of childbearing age (ectopic pregnancy kills)
- ECG in all patients with upper abdominal pain (inferior MI mimics abdominal pathology)
- Capillary glucose if any suspicion of DKA (DKA mimics surgical abdomen)
Missing any of these is a patient safety failure.
| Test | Key Findings & Interpretation | Clinical Relevance |
|---|---|---|
| FBE / CBC with differential [1] | ↑WBC with left shift (↑bands/neutrophils) → infection/inflammation. Markedly ↑↑WBC ( > 16 × 10⁹/L) → may suggest gangrenous/perforated appendicitis [3][23]. Normal WBC does NOT rule out appendicitis [23]. RBC indices → microcytic anaemia from chronic bleeding (takes 48h for haemodilution post-acute bleed) [2] | Every patient |
| ESR / CRP [1] | Non-specific inflammatory markers. CRP > 3 mg/dL is one of the TG13 systemic criteria for cholecystitis [22][24]. WBC > 10 × 10⁹/L or CRP > 10 mg/L gives PPV 61.5% and NPV 88.1% for appendicitis [23] | Every patient |
| LFT [1] | Hepatocellular pattern (↑↑ALT/AST) → hepatitis. Cholestatic pattern (↑ALP, ↑GGT, ↑bilirubin) → biliary obstruction, cholangitis. Mild non-specific derangement → cholecystitis. ↑Bilirubin/GGT should raise suspicion of CBD obstruction [22] | RUQ pain, jaundice, suspected biliary/hepatic pathology |
| RFT [2] | Hydration status (↑urea:creatinine ratio → pre-renal). HypoK/hypoCl → prolonged vomiting. HypoK/hypoCa → can cause ileus. Cr → suitability for contrast CT [2] | Every patient |
| Serum amylase [1] | Peaks 6-12h of onset, normalises in 3-5 days [21]. ≥ 3× ULN → diagnostic of acute pancreatitis (with compatible clinical features) [7][21]. Amylase > 1000 is virtually diagnostic of acute pancreatitis [2]. Prolonged elevation → complications (e.g., pseudocyst) [21]. False positives: PPU, ruptured AAA, DKA, macroamylasaemia [21]. If equivocal or delayed presentation: urine amylase (rises within 24-48h, persists 1 week) [21] | Epigastric pain, suspected pancreatitis |
| Serum lipase [1] | Rises within 4-8h, normalises in 8-14 days (longer half-life) [21]. More specific than amylase and preferred for delayed presentation > 24h [21]. ≥ 3× ULN → diagnostic of pancreatitis [7] | Preferred if patient presents > 24h after onset |
| Clotting profile + Type & Screen | Pre-operative preparation; DIC in severe sepsis/pancreatitis | Surgical abdomen, GI bleeding, suspected AAA |
| Cardiac enzymes (Troponin) | Exclude acute MI (inferior MI mimics epigastric pain) [1][2] | Upper abdominal pain, elderly, cardiac risk factors |
| Blood glucose | DKA: hyperglycaemia ≥ 11 mmol/L [19] | Young patients, known diabetics, metabolic acidosis |
| ABG + Lactate [2][21] | Metabolic acidosis + ↑lactate → intestinal ischaemia (classic and critical finding) [4]. Metabolic alkalosis → prolonged vomiting. Respiratory alkalosis → early sepsis (compensatory hyperventilation) | Suspected ischaemic bowel, sepsis, shock |
| CaPO₄ [21] | Hypercalcaemia (cause of pancreatitis and abdominal pain); hypocalcaemia in severe pancreatitis (saponification of calcium by fat necrosis) | Suspected pancreatitis |
| H. pylori tests [1] | Urea breath test (non-invasive, best for confirming eradication); stool antigen test; serology (indicates exposure, not active infection); CLO test on biopsy (rapid urease test) | Suspected PUD/dyspepsia [6] |
| Faecal blood (FOBT) [1] | Occult GI bleeding not visible to the naked eye | Suspected GI malignancy, chronic anaemia |
| Fecal calprotectin | Elevated in inflammatory bowel disease; normal in IBS — useful to differentiate [12] | Chronic abdominal pain with diarrhoea, suspected IBD vs IBS |
Why does amylase have false positives? Amylase is not exclusively produced by the pancreas — salivary glands also produce it (salivary amylase), and damaged bowel wall (as in PPU or ischaemia) can release it. This is why lipase is more specific — it is produced almost exclusively by pancreatic acinar cells. In clinical practice, most centres now prefer lipase.
C. Imaging — Systematic Approach [1][2][21]
The single most important first radiograph in acute abdominal pain — not the AXR! Why?
- Free gas under diaphragm (pneumoperitoneum) → perforation of a hollow viscus (PPU being the commonest) [2]. The patient must be sitting upright for ≥ 10 minutes before the film to allow free gas to rise. Even a small amount of free gas ( < 1 mL) can be detected on erect CXR.
- Also screens for basal pneumonia (referred abdominal pain) and pleural effusion (pancreatitis — especially left-sided).
- Sensitivity for pneumoperitoneum: ~80% — i.e., 20% of perforations may NOT show free gas. If clinical suspicion is high, proceed to CT.
Why Erect CXR Before AXR?
Many students instinctively order an AXR first. But the erect CXR is more important because:
- It detects pneumoperitoneum (perforation — a surgical emergency requiring immediate action)
- It excludes thoracic causes of abdominal pain (pneumonia, PE, pleural effusion)
- It is more sensitive for free gas than a supine AXR
If there is free gas under the diaphragm and the patient has peritoneal signs, you go straight to theatre — you don't need a CT.
| Finding | Interpretation | Clinical Condition |
|---|---|---|
| Proximal dilatation + distal collapse | Mechanical obstruction | Intestinal obstruction — '3-6-9 rule': SB > 3 cm, LB > 6 cm, caecum > 9 cm [23] |
| Air-fluid levels on erect AXR | Bowel loops with trapped air above fluid | > 5 air-fluid levels is diagnostic of intestinal obstruction [2][23] |
| Coffee-bean sign | Massively dilated, bent loop of sigmoid | Sigmoid volvulus — loop extends from LLQ to RUQ [2][17][23] |
| Sentinel loop sign | Solitary dilated loop of bowel near an inflammatory focus | Localised ileus indicating adjacent inflammation (e.g., pancreatitis — dilated jejunal loop near pancreas) [2][21] |
| Colonic cut-off sign | Dilated colon from ascending to mid-transverse with abrupt paucity distal to splenic flexure | Acute pancreatitis — inflammatory spasm of colon at splenic flexure [21] |
| Obliteration of psoas outline | Loss of the normally visible psoas shadow | Retroperitoneal fluid/pathology (e.g., retroperitoneal extension of pancreatitis) [21] |
| Radio-opaque stones | Calcified structures in RUQ, renal areas, or along ureters | 90% of urinary stones are radio-opaque; only 15% of gallstones are radio-opaque (only pigmented stones — majority cholesterol stones are radiolucent) [2] |
| Pancreatic calcification | Calcified deposits in the pancreatic region | Chronic pancreatitis [2] |
| Rigler's triad | Pneumobilia + SBO + ectopic gallstone | Gallstone ileus — gallstone erodes through gallbladder into duodenum and impacts at ileocaecal valve |
| Thumb-printing | Thickened bowel wall with scalloped pattern | Ischaemic colitis or IBD (thickened, oedematous mucosal folds indent the gas column) [23] |
| Faecal loading | Multiple faecal densities throughout colon/rectum | Faecal impaction / Constipation |
Gasless abdomen on AXR: In some cases of IO, bowel loops may be completely filled with fluid with minimal gas. Look for the "string of pearls" sign — collection of small intraluminal gas bubbles along the superior bowel wall separated by valvulae conniventes [23].
USG is the first-line imaging for RUQ and suprapubic/pelvic pain.
| Application | Key Findings | Sensitivity/Specificity |
|---|---|---|
| Gallstones | Hyperechoic focus with posterior acoustic shadowing | 95% sensitivity [2] |
| Acute cholecystitis | Thickened GB wall ( > 3 mm), pericholecystic fluid, stone at neck of GB, sonographic Murphy's sign (tenderness maximal when probe presses on visualised gallbladder) [2][22] | Sens 88%, Spec 80% [22] |
| CBD dilatation | CBD diameter > 6 mm ( > 8 mm post-cholecystectomy) → suggests distal obstruction | Problem: distal CBD often obscured by bowel gas [2] |
| Acute appendicitis | Non-compressible appendix with double-wall thickness > 6 mm, focal pain with compression, increased echogenicity of periappendiceal fat, RLQ fluid, ± appendicolith [3] | Lower sensitivity than CT; operator-dependent; reserved for pregnant women and children to avoid radiation [3][23] |
| Acute pancreatitis | Swollen, diffusely enlarged, hypoechoic pancreas; peripancreatic anechoic fluid collection; gallstones/biliary obstruction as underlying cause [22]. May be obscured by bowel gas from paralytic ileus [22] | — |
| Pelvic pathology | Ovarian cysts, ectopic pregnancy (empty uterus + adnexal mass + free fluid), fibroids, AROU | TAS for screening; TVS for better pelvic detail |
| AAA | Aortic diameter measurement; peri-aortic haematoma | Screening and monitoring; CT for acute assessment |
CT is the workhorse investigation for most causes of acute abdominal pain, particularly when the diagnosis is unclear or the clinical situation is complex. Contrast-enhanced CT (CECT) provides the most information.
| Application | Key CT Findings | Notes |
|---|---|---|
| Acute appendicitis | Distended appendix AP > 6 mm with occluded lumen, wall thickening > 2 mm, periappendiceal fat stranding, wall hyperenhancement, ± appendicolith [3][23] | Highest diagnostic accuracy and lowest non-diagnostic rate among all imaging. Standard for most non-pregnant adults [3][23] |
| Acute diverticulitis | Pericolonic fat stranding, bowel wall thickening, ± abscess, ± free air. Features favouring diverticulitis over CRC: involvement > 10 cm of colon, pericolonic/mesenteric inflammation, absence of enlarged pericolonic LN [3][11] | CT is the diagnostic test of choice for diverticulitis [3] |
| Acute pancreatitis | Focal or diffuse pancreatic enlargement with homogeneous enhancement, peripancreatic fat stranding, ± necrosis (hypoenhancement on contrast — not visible on early CT, best seen ≥ 3 days after onset) [22]. May also show gallstones, biliary dilatation [22] | NOT needed in majority of cases, especially if mild — diagnosis is usually clinical + biochemical [22]. Indicated if diagnostic uncertainty, severe pancreatitis, or suspicion of complications |
| Acute cholecystitis | GB wall thickening, distension, pericholecystic fat stranding, ± stone. Fat stranding seen on CT but NOT on USG [22] | Sens 94%, Spec 59% [22]. Usually used to rule out complications/alternative diagnoses |
| Intestinal obstruction | Transition point (dilated proximal → collapsed distal), cause of obstruction (hernia, mass, adhesion band), features of strangulation (mesenteric oedema, poor bowel wall enhancement, pneumatosis) [23] | CT superior to AXR for identifying cause and complications of IO |
| Mesenteric ischaemia (CTA) | Embolic: oval thrombus in proximal SMA surrounded by contrast. Thrombotic: thrombus superimposed on calcified atherosclerotic lesion at SMA ostium. Bowel changes: focal/segmental wall thickening, pneumatosis intestinalis, portal venous gas, bowel dilatation with mesenteric stranding [4][23] | CTA is the most important investigation for diagnosis in stable patients [4]. No oral contrast should be given (delays and obscures) [4]. Unstable → diagnosis often made at laparotomy. |
| Perforated viscus | Free intraperitoneal gas (even tiny amounts), extraluminal fluid, thickened bowel/ulcer crater at site of perforation | CT more sensitive than erect CXR for free gas. If erect CXR shows obvious free gas + peritoneal signs → go straight to theatre without CT |
| AAA | Aortic diameter, extent, relationship to renal arteries (infra- vs supra-renal), mural thrombus, retroperitoneal haematoma if ruptured [9] | CTA for pre-operative planning |
| Bowel ischaemia (colonic) | Bowel wall thickening, submucosal oedema/haemorrhage, thumbprinting, pneumatosis (only in advanced ischaemia), mesenteric stranding | CTA with coronal/sagittal reconstruction |
Radiation concerns: CT involves significant radiation. In pregnant women and children, prefer USG or MRI to avoid radiation when possible [3].
Contrast concerns: IV contrast is contraindicated in renal insufficiency (risk of contrast-induced nephropathy — check Cr/eGFR beforehand) and contrast allergy [3]. In such patients, consider non-contrast CT, USG, or MRI.
| Modality | Application | Key Points |
|---|---|---|
| MRI abdomen/pelvis | Appendicitis in pregnancy; pancreatitis (pancreatic oedema: ↓T1W, ↑T2W [22]); equivocal CT findings | No radiation; limited by availability, cost, and scan time |
| MRCP | 2nd line after USG for biliary pathology [2]; better than CT for bile duct stones and ductal anatomy | Non-invasive; useful when ERCP not yet indicated |
| ERCP | Diagnostic AND therapeutic for gallstone disease and cholangitis [2]; stone extraction, sphincterotomy, stent placement | Invasive; risk of post-ERCP pancreatitis. AVOID endoscopy for acute abdomen if sealed-off perforation may open by gas insufflation [21] |
| Cholescintigraphy (HIDA scan) | Alternative to USG for acute cholecystitis. IV ⁹⁹ᵐTc-labelled HIDA taken up by hepatocytes → excreted into bile → no entry into GB = obstructed cystic duct [22] | Sens 90-97%, Spec 71-90% [22]. Rarely available in many centres |
| Mesenteric arteriogram | Direct visualisation of mesenteric vasculature; can combine with catheter-directed thrombolysis | If CTA equivocal or for endovascular intervention [4] |
| MR venography | More sensitive for mesenteric venous occlusion than CT [4] | Consider if venous thrombosis suspected and CTA inconclusive |
| Diagnostic laparoscopy | When all non-invasive investigations are inconclusive but clinical suspicion remains high | Allows direct visualisation + therapeutic intervention (e.g., appendicectomy); avoids unnecessary laparotomy [21] |
AVOID Endoscopy in Acute Abdomen
AVOID endoscopy for acute abdomen [21]: a sealed-off perforation may be opened by gas insufflation during endoscopy, converting a contained situation into free perforation and generalised peritonitis. The only exception is ERCP in the context of acute cholangitis or gallstone pancreatitis, where the benefit of biliary decompression outweighs the risk.
Consider upper GI endoscopy [1] for:
- Investigation of dyspepsia with alarm features (age > 55, weight loss, dysphagia, GI bleeding, anaemia)
- Suspected PUD — diagnostic + biopsy (H. pylori, exclude malignancy in gastric ulcers)
- Upper GI bleeding — diagnostic + therapeutic (adrenaline injection, clipping, thermal coagulation)
- Not indicated in the acute abdomen setting unless for specific upper GI bleeding management
Condition-Specific Diagnostic Criteria
Diagnosis of acute cholecystitis can be made by a combination of local and systemic signs of inflammation correlated with imaging findings [5].
| Category | Criteria |
|---|---|
| A: Local signs of inflammation | Murphy's sign (Sens 50-65%, Spec 79-96% [22]); RUQ mass, pain or tenderness |
| B: Systemic signs of inflammation | Fever; ↑WBC count; ↑CRP ( > 3 mg/dL) [22][24] |
| C: Imaging findings | Imaging findings characteristic of acute cholecystitis — USG as 1st line (thickened GB wall > 3 mm, pericholecystic fluid, stone at neck, sonographic Murphy's sign). Alternatives: CECT, Doppler USG, HIDA [22][24] |
- Suspected diagnosis = One item in A + One item in B
- Definite diagnosis = One item in A + One item in B + One item in C
Why three categories? Because local signs alone (e.g., RUQ tenderness) could be biliary colic, PUD, or hepatitis. Adding systemic inflammation increases specificity. Adding imaging confirms the pathology is in the gallbladder specifically.
Diagnosis requires ≥ 2 out of 3 of [7][21][22]:
| Criterion | Detail |
|---|---|
| Clinical | Acute onset of persistent, severe, epigastric pain often radiating to the back |
| Biochemical | Serum amylase or lipase ≥ 3× upper limit of normal |
| Radiological | Characteristic imaging findings on USG, contrast-enhanced CT, or MRI |
Why is imaging not always needed? If a patient has classic epigastric-to-back pain AND amylase/lipase ≥ 3× ULN, that satisfies 2/3 criteria — the diagnosis is made without imaging. Imaging is reserved for diagnostic uncertainty (is it really pancreatitis or could it be PPU?) or to assess severity and complications [22].
Important caveats on pancreatic enzymes [21]:
- Amylase cut-off is 3× ULN — it is NOT indicative of severity [21]. A patient with amylase of 10,000 does not necessarily have more severe pancreatitis than one with amylase of 1,000.
- Serum amylase: rises within 6-12h, normalises in 3-5 days. False positives: PPU, ruptured AAA, DKA, macroamylasaemia [21].
- Serum lipase: rises within 4-8h, normalises in 8-14 days — preferred for delayed presentation > 24h because of its longer half-life and greater specificity [21].
- If equivocal or delayed: urine amylase (rises within 24-48h, persists 1 week) [21].
Diagnosis of acute appendicitis is essentially clinical [3]. However, clinical diagnosis alone has a negative appendectomy rate (NAR) of 15-30% [23]. The Alvarado/MANTREL score is used for risk stratification:
| Component | Score |
|---|---|
| M — Migratory RLQ pain | 1 |
| A — Anorexia | 1 |
| N — Nausea or vomiting | 1 |
| T — Tenderness in RLQ | 2 |
| R — Rebound tenderness in RLQ | 1 |
| E — Elevated temperature ( > 37.5°C) | 1 |
| L — Leukocytosis (WBC > 10 × 10⁹/L) | 1 |
| Total | 8 |
- 0-3 (previously ≤ 4): Appendicitis unlikely → evaluate for other diagnoses
- 4-6 (previously 5-6): Equivocal → imaging recommended (USG or contrast CT)
- ≥ 7: Strongly predictive of acute appendicitis → consider surgery (may proceed to imaging if available to confirm and plan)
Why is this scoring system useful? It structures the subjective clinical assessment into an objective score. The key high-value items are Tenderness in RLQ (2 points — the most discriminating sign) and Leukocytosis (objective lab data). The mnemonic MANTREL (or MANTRELS with the original 10-point scale) makes it easy to remember.
| Criterion | Threshold | Explanation |
|---|---|---|
| Dilated bowel | '3-6-9 rule': SB > 3 cm, LB > 6 cm, caecum > 9 cm [23] | Bowel dilated proximal to obstruction due to accumulated gas and fluid |
| Air-fluid levels | > 5 air-fluid levels on erect AXR = diagnostic of IO [2] | Gas-fluid interfaces in obstructed, dilated bowel loops |
| Transition point | Dilated proximal + collapsed distal bowel | Identifies the level of obstruction |
| SB vs LB | SB: central location, valvulae conniventes (cross full diameter — "stack-of-coins"), featureless (ileum). LB: peripheral, haustral folds (irregularly spaced, not crossing full diameter) [23] | Critical to distinguish SBO from LBO — different management |
Recurrent abdominal pain on average ≥ 1 day/week, associated with ≥ 2 of [12]:
- Related to defecation
- Associated with change in frequency of stools
- Associated with change in form (appearance) of stools
For the past 3 months, with symptom onset ≥ 6 months before diagnosis [12].
IBS is a diagnosis of exclusion. Alarm features that alert to alternative diagnosis: weight loss, constitutional symptoms, PR bleeding, old age of onset, family history of CRC or IBD, positive FOBT, anaemia, leukocytosis, ↑ESR, abnormal biochemistry [12].
One or more of:
- Postprandial fullness
- Early satiety
- Epigastric pain or burning
With NO evidence of structural disease on investigation to explain symptoms. Symptoms present for last 3 months with onset ≥ 6 months before diagnosis [20].
GERD is overdiagnosed in dyspepsia [20] — do NOT conclude GERD unless there are typical symptoms of heartburn or regurgitation.
Diagnostic Approach by Clinical Scenario — Decision Trees
This is the classic "test-and-treat" approach for H. pylori in young patients without alarm features — it avoids unnecessary endoscopy while still catching H. pylori-related PUD [20].
"Upper abdominal pain is caused by lesions of the upper GIT." [1]
"Lower abdominal pain is caused by lesions of the lower GIT or pelvic organs." [1]
"Early severe vomiting indicates a high obstruction of the GIT." [1]
These simple maxims help generate your initial differential before investigations even return.
Special Situations
- USG = first-line imaging (no radiation) [3]
- MRI = second-line (no radiation, excellent for appendicitis in pregnancy) [3]
- CT is contraindicated in the first trimester but may be used in life-threatening situations with informed consent
- β-hCG quantitation guides management of suspected ectopic pregnancy
- Lower threshold for CT — atypical presentations are common; examination may be unreliable (decreased pain perception, immunosuppression masking inflammation)
- Always check for mesenteric ischaemia (pain out of proportion, lactate, CTA) [4]
- Always do PR exam — faecal impaction is a very common and easily treatable cause [1]
- Consider ruptured AAA in any elderly patient with back/abdominal pain and haemodynamic instability [9]
- Rule out UTI with urinalysis — blood, protein and leucocytes may all be present with acute appendicitis; nitrites are more specific for UTIs [1]
- FBE/ESR/CRP
- Scanning according to findings [1]
- Consider gentle abdominal palpation with a soft toy [1] — reduces anxiety and improves examination quality in young children
- USG preferred over CT (no radiation) for appendicitis in children [3][23]
High Yield Summary
-
Erect CXR is the most important first radiograph — detects pneumoperitoneum (perforation), basal pneumonia, pleural effusion. If free gas + peritoneal signs → straight to theatre.
-
Three non-negotiable bedside tests: Urine pregnancy test (all women of childbearing age), ECG (all upper abdominal pain), Capillary glucose (DKA suspicion).
-
Imaging by pain site: RUQ → USG; LUQ → CT; RLQ/LLQ → CT with IV contrast; Suprapubic → USG (TAS/TVS).
-
Acute cholecystitis (TG13): Suspected = 1× local sign + 1× systemic sign. Definite = + 1× imaging finding. USG is 1st line (Sens 88%, Spec 80%).
-
Acute pancreatitis (Revised Atlanta): ≥ 2/3 of clinical pain, amylase/lipase ≥ 3× ULN, imaging. Amylase cut-off NOT indicative of severity. Lipase preferred if > 24h.
-
Appendicitis (MANTREL): ≤ 3 = unlikely; 4-6 = image; ≥ 7 = surgery. CT is gold standard in adults. USG for pregnant/children.
-
IO on AXR: 3-6-9 rule (SB > 3, LB > 6, caecum > 9 cm). > 5 air-fluid levels on erect AXR = diagnostic.
-
Amylase false positives: PPU, ruptured AAA, DKA, macroamylasaemia. Lipase is more specific.
-
90% urinary stones are radio-opaque; only 15% gallstones are radio-opaque (only pigmented stones).
-
CTA is the most important investigation for mesenteric ischaemia in stable patients. No oral contrast. Metabolic acidosis + ↑lactate = ischaemic bowel until proven otherwise.
-
AVOID endoscopy in acute abdomen — sealed-off perforation may open with gas insufflation.
-
IBS: Rome IV — pain ≥ 1 day/week for 3 months, a/w ≥ 2 of: related to defecation, change in stool frequency, change in stool form. Diagnosis of exclusion.
Active Recall - Diagnostic Criteria and Investigations for Abdominal Pain
References
[1] Lecture slides: murtagh merge.pdf (Abdominal pain acute in adults p6; Abdominal pain acute in children p9) [2] Senior notes: Ryan Ho Fundamentals.pdf (p262-263, p278-279, p307-308, Investigations, Physical Examination, RUQ Pain, Approach to Dyspepsia) [3] Senior notes: felixlai.md (Acute appendicitis — Diagnosis section, Radiological tests) [4] Senior notes: felixlai.md (Mesenteric ischaemia section); Ryan Ho GI.pdf (p145, Evaluation of mesenteric ischaemia) [5] Senior notes: felixlai.md (Cholecystitis — Diagnosis, Tokyo criteria 2013) [6] Senior notes: felixlai.md (PUD — Diagnosis section) [7] Senior notes: felixlai.md (Acute pancreatitis — Diagnostic criteria) [9] Senior notes: Ryan Ho Cardiology.pdf (p222, AAA) [10] Senior notes: maxim.md (Acute appendicitis section) [11] Senior notes: felixlai.md (Diverticular disease section) [12] Senior notes: Ryan Ho GI.pdf (p118-119, IBS — Rome IV criteria) [17] Senior notes: felixlai.md (Volvulus section) [19] Senior notes: Ryan Ho Endocrine.pdf (p91, DKA) [20] Senior notes: felixlai.md (Dyspepsia section); Ryan Ho Fundamentals.pdf (p263, Approach to Dyspepsia); Ryan Ho GI.pdf (p53, Approach to Dyspepsia) [21] Senior notes: maxim.md (Investigations section p87, Acute pancreatitis investigation p299) [22] Senior notes: Ryan Ho GI.pdf (p247-248, Acute cholecystitis — Diagnostic imaging, TG13; p340-341, Acute pancreatitis — Diagnostic evaluation) [23] Senior notes: Ryan Ho GI.pdf (p136, IO — Diagnostic evaluation; p150, Appendicitis — Approach to workup, Alvarado score, Imaging) [24] Senior notes: Ryan Ho GI.pdf (p248, TG13 diagnostic criteria)
Management of Abdominal Pain
The management of abdominal pain follows a universal framework before branching into condition-specific treatment. Think of it as a pyramid: stabilise the patient first, then diagnose, then treat the specific condition.
This is the "Schema for all surgical Mx" framework [2]:
Diet — Activity — Vitals — Investigations — Drugs (mnemonic: DAVID)
| Component | Detail | Rationale |
|---|---|---|
| Diet: NPO [2][25] | All patients with acute abdominal pain should be kept nil by mouth initially | Prevents aspiration during potential anaesthesia induction; reduces bowel stimulation; prepares for possible surgery |
| IV Fluids [2][25] | Secure IV access (large bore if resuscitation required). Routine: 2D1S Q8h (2 bags dextrose 5% : 1 bag NS 0.9%, one 500 mL bag every 8 hours ≈ 1.5 L/day) [2]. If clinically dehydrated: 500 mL bolus crystalloid then reassess by UO [2]. Replace losses: vomiting (hypochloraemic hypokalaemic metabolic alkalosis), third-spacing (peritonitis, IO, pancreatitis) | Restores intravascular volume depleted by vomiting, third-space losses, and reduced oral intake. Crystalloids (NS, Ringer's lactate, Hartmann's) are first-line [25] |
| NG tube | Placed on free drainage with 4-hourly aspiration or continuous suction [25][26] | Decompresses proximal bowel (IO); reduces aspiration risk during anaesthesia; achieves "gastric rest" in pancreatitis. Functions: decompression + prevention of aspiration [25] |
| Activity | Bed rest; haemodynamic monitoring | Minimise metabolic demand; allow serial examination |
| Vitals | BP/Pulse, Temperature, Fluid balance (Foley catheter → keep UO > 0.5 mL/kg/h [2]), ± CVP if severe [2] | Early detection of deterioration; guides fluid resuscitation |
| Investigations | Serial abdominal examination to assess changes [2]; bloods and imaging as per diagnostic algorithm | Ongoing reassessment is critical — a "benign" abdomen can evolve into peritonitis |
| Drugs | IV broad-spectrum antibiotics if infective aetiology [2]; Analgesics as indicated [2] | Treat infection; control pain (see below) |
Analgesia in Acute Abdominal Pain
There is an old surgical myth that giving analgesia "masks" peritoneal signs and impairs diagnosis. This has been comprehensively debunked. Opioid analgesia is usually NOT associated with decreased diagnostic accuracy [2]. Withholding pain relief is inhumane and counterproductive — a patient in severe pain cannot cooperate with examination. Give analgesia early and reassess.
Analgesic choices:
- Paracetamol IV — safe first-line; no GI effects
- NSAIDs (e.g., ketorolac, diclofenac) — excellent for renal colic (1st line for ureteric stones [27]) and biliary colic; avoid in pancreatitis (can worsen and cause renal failure) [22] and PUD
- Opioids (fentanyl, tramadol, morphine, pethidine) — for severe pain; in pancreatitis, prefer fentanyl/hydromorphone/tramadol/pethidine; avoid morphine because morphine increases sphincter of Oddi pressure [22]
Condition-Specific Management
Below is detailed management for the major causes of abdominal pain, organised by the conditions most likely to appear in exams.
General principles: Resuscitation, NPO, IV fluids, analgesics [10]
- Prophylactic IV antibiotics with anaerobic coverage [10]
- Regimen: IV ceftriaxone + metronidazole [10] (alternatives: cefoxitin/cefotetan/cefazolin 2g + metronidazole 500mg IV [23])
- Non-complicated: continue until 24h post-op [10]
- Complicated (e.g., abscess, phlegmon): continue 3-7 days post-op [10]
Definitive treatment: Laparoscopic appendicectomy (first line!) [10]
| Scenario | Approach | Details |
|---|---|---|
| Present within 72h and fit for surgery [10] | Immediate surgery | Laparoscopic preferred (↓infection risk, ↓post-op pain, ↓hospital stay) [10][23]. Open if gross sepsis [10]. A short delay of < 12-24h for preparation is NOT associated with ↑risk of perforation [23]. |
| Present > 72h and stable [10] | Interval surgery (Ochsner-Sherren regimen) | By > 72h, inflammation has often become walled-off (appendiceal mass/phlegmon). IV antibiotics (~90% success rate [10]) ± image-guided drainage of abscess. Laparoscopic appendicectomy 6-8 weeks later. Colonoscopy if > 40 years old to exclude CA [10][23]. |
| Complicated and unstable | Urgent surgery | Consider open approach if gross sepsis [10] |
Non-operative (conservative) management [10]:
- Can be considered if uncomplicated (no perforation/abscess) and not fit for surgery
- Bowel rest + IV ceftriaxone + metronidazole
- Compared to surgery: shorter disability but risk of complications and recurrence (recurrence rate: 30% at 3 months, 40% at 1 year, 50% at 3 years) [10]
- The CODA trial (2020) showed 10-day antibiotics non-inferior to appendicectomy, but 30% chance of appendicectomy within 90 days [10]
- Positioning: supine ± Trendelenburg and right side up (allows small bowel to fall away from operative field) [10]
- Open incisions:
- Lanz (more popular): transverse incision ~2 cm below umbilicus, centred on mid-clavicular line — follows Langer's lines, more cosmetically pleasing [10]
- Gridiron: perpendicular to line joining ASIS to umbilicus at McBurney's point [10]
- Rutherford-Morrison: extends Gridiron obliquely upwards and laterally (for paracaecal/retrocaecal appendix) [10]
- Unexpected findings [23]: Normal appendix → still remove (↓diagnostic confusion), exclude terminal ileitis, Meckel's, tubo-ovarian pathology. Appendicular tumour: carcinoid < 2 cm → simple appendicectomy; > 2 cm → R hemicolectomy. Adenocarcinoma → R hemicolectomy [23].
Risks (for consent) [10]:
- Immediate: conversion to open, normal appendix (still removed), malignancy requiring R hemicolectomy ± stoma, injury to surrounding organs, bleeding
- Early: wound infection (5-10%), intra-abdominal/pelvic abscess (spiking fever), post-op ileus
- Late: incisional hernia, adhesions, recurrent/stump appendicitis
Medical treatment [5]:
- NPO + continuous monitoring of vitals + blood tests including crossmatch [5]
- IV fluids
- Analgesics: Pain control with NSAIDs (effective for biliary pain; inhibit prostaglandins that mediate gallbladder inflammation) [5]
- IV Antibiotics [5]: Secondary bacterial infection occurs in 15-30% of cholecystitis cases. Empirical antibiotics should cover Gram-negative aerobes and anaerobes:
- Ampicillin-sulbactam / Piperacillin-tazobactam / Ticarcillin-clavulanate (OR)
- Metronidazole + 3rd-generation cephalosporin (e.g., Ceftriaxone) (OR)
- Metronidazole + Fluoroquinolone (e.g., Ciprofloxacin/Levofloxacin) [5]
Surgical treatment — Laparoscopic cholecystectomy [5]:
Guided by TG13 severity grading [5][24]:
| Severity | Criteria | Management |
|---|---|---|
| Mild (Grade I) | Does not meet criteria for moderate or severe | Early laparoscopic cholecystectomy (within 72h of admission — early is better than delayed) |
| Moderate (Grade II) | WBC > 18,000, palpable RUQ mass, duration > 72h, marked local inflammation (gangrenous, emphysematous, pericholecystic abscess, hepatic abscess, biliary peritonitis) | Either early LC OR antibiotics followed by delayed LC [5] |
| Severe (Grade III) | Organ dysfunction (cardiovascular, neurological, respiratory, renal, hepatic, haematological) | Antibiotics + gallbladder drainage by percutaneous cholecystostomy (patient too unfit for surgery) followed by delayed LC once medically optimised [5] |
Why early cholecystectomy? Performing LC within 72h of admission (during the same admission) reduces total hospital stay and is safe. Waiting for the inflammation to "cool down" was the traditional approach but has been shown to be inferior — the inflammation actually gets worse over time, making delayed surgery technically more difficult.
Acalculous cholecystitis [5]: Occurs in critically ill patients (TPN, burns, sepsis, major surgery). Requires urgent intervention — percutaneous USG/CT-guided cholecystostomy is treatment of choice (diagnostic and therapeutic — decompresses infected gallbladder). Definitive treatment: interval cholecystectomy [5].
Approach: Generally supportive: fluid replacement, nutritional support, antibiotics, analgesics + management of complications + management of underlying cause [22]
Supportive management [22]:
| Component | Detail | Rationale |
|---|---|---|
| Organ support | ICU/HDU if severe; arterial line, vasopressor, RRT, mechanical ventilation as needed [22] | Severe pancreatitis causes SIRS → organ failure |
| Aggressive IV fluid resuscitation | 5-10 mL/kg/h isotonic crystalloids initially [22]; adjust by clinical assessment, haematocrit, urea. Hct > 44% = intravascular fluid depletion (independent RF for pancreatic necrosis) [22] | Massive third-space losses from peritoneal/retroperitoneal inflammation; maintains pancreatic perfusion and prevents necrosis |
| Nutritional management | NPO + NGT aspiration if persistent vomiting/ileus [22]. Early enteral feeding ( < 48-72h) is preferred over parenteral — associated with ↓mortality, ↓organ failure, ↓infection, ↓surgery [22]. Oral feeding can be initiated ≤ 24h if mild and no ileus/N/V [22]. Parenteral feeding only if cannot tolerate enteral [22] | Gastric rest reduces pancreatic stimulation; but early enteral feeding maintains gut mucosal barrier integrity, reducing bacterial translocation |
| Analgesics | Opioids preferred: fentanyl, hydromorphone, tramadol, pethidine. NOT morphine (↑sphincter of Oddi pressure → worsens biliary pancreatitis) [22]. NSAIDs NOT preferred (worsen pancreatitis and cause renal failure) [22] | Uncontrolled pain → haemodynamic instability; morphine causes Oddi spasm |
| Antibiotics | Routine in HK due to ↑proportion of biliary pancreatitis [22]. Prophylactic Abx NOT routinely recommended in guidelines but commonly given. Amoxicillin for interstitial oedematous pancreatitis (cover cholangitis); Imipenem for necrosis [22]. Therapeutic Abx for infected necrosis: imipenem, quinolone, ceftazidime/cefepime + metronidazole [22] | Prophylactic Abx controversial globally but pragmatic in HK given biliary predominance |
| Monitoring | HDU care if severe; serial vitals, electrolytes, glucose, ABG [22]. Contrast CT at day 3 for severe pancreatitis to assess complications [22] | Early CT will not show necrosis (takes ≥ 3 days to demarcate) |
| Others | Stress ulcer prophylaxis (PPI) [22] | Critically ill patients at risk of stress ulcers |
Management of complications [22]:
| Complication | Timing | Management |
|---|---|---|
| Acute peripancreatic fluid collection | Early | None needed — majority resolve spontaneously [22] |
| Acute necrotic collection | Early | Sterile necrosis: conservative Mx for ≥ 4 weeks [22]. Infected necrosis: empirical Abx → percutaneous/endoscopic drainage → surgical debridement (necrosectomy) if drainage fails (step-up approach) [22]. Delay all interventions to > 4 weeks when collection is walled off — early debridement has poor outcomes [22] |
| Walled-off necrosis | Late ( > 4 weeks) | Drainage/debridement if symptomatic, infected, ongoing organ failure [22] |
| Pseudoaneurysm | Variable | Angiographic embolisation (endoscopic drainage of collection absolutely contraindicated!) [22] |
| Abdominal compartment syndrome | Variable | Intra-abdominal pressure > 20 mmHg + new organ failure → surgical decompression [22] |
| Splanchnic venous thrombosis | Variable | Treat underlying pancreatitis; anticoagulate if extends into portal/SMV [22] |
Management of underlying cause [22]:
- Gallstone pancreatitis: ERCP for stone clearance (low threshold in HK; early ERCP ≤ 72h especially if cholangitis or CBD obstruction) [22]. Interval cholecystectomy during same admission if mild, or 6 weeks later if severe.
- Alcohol: cessation counselling, multivitamins
- Hypertriglyceridaemia: if TG > 11.3 mmol/L → insulin infusion, plasmapheresis
- Hypercalcaemia: treat underlying cause (e.g., primary hyperparathyroidism)
General approach [25]:
Conservative (non-operative) management [25]:
- IV and electrolyte rehydration + NGT decompression may be curative — 70% of SBO (especially adhesive) recover with bowel rest and decompression [26]
- Exclusion of complicated obstruction is required before conservative management [25]
- Duration of observation: 48-72 hours [25]. If no improvement → surgical exploration
- Monitor for resolution: ↓abdominal distension, ↓NGT output, passage of flatus/stool, resolution on AXR [25]
Supportive management ("Drip and Suck") [25]:
| Component | Detail |
|---|---|
| NPO | Limit further bowel distension [25] |
| IV fluids | Replace external (vomiting) and internal (third-space sequestration) losses; crystalloids (NS, Ringer's, Hartmann's); K⁺ replacement cautiously (risk of AKI from dehydration) [25] |
| NGT decompression | Non-vented (Ryle) or vented (Salem Sump); free drainage with 4-hourly aspiration [25] |
| Pain relief | Opioids reasonable though mechanical pain often poorly responsive to analgesics [25] |
| Antibiotic prophylaxis | Broad-spectrum Abx due to bacterial overgrowth; mandatory for all surgical patients [25] |
Gastrografin (water-soluble contrast) meal and follow-through [25][26]:
- Both diagnostic AND therapeutic [25][26]
- Diagnostic: detects level of obstruction; whether partial or complete. X-ray taken every 30 min until 4 hours. GGF reaching colon ≤ 24h is highly predictive of resolution with conservative Mx [26].
- Therapeutic: Hyperosmolar → draws fluid into bowel lumen → decreases intestinal wall oedema → stimulates peristalsis ("laxative-like" effect) [25][26]. Demonstrated to shorten hospital stay and believed to reduce operation rate from 30% to 10% [26].
- Indication: adhesive IO unresponsive to conservative treatment at 48h [26]
Indications for urgent surgery [25][26]:
- Strangulated (complicated) obstruction
- Closed-loop obstruction
- Peritonitis
- Incarcerated or strangulated hernia
- Complete obstruction with failure to resolve
Surgical management [26]:
| Procedure | Indication |
|---|---|
| Operative decompression | Milk SB content retrograde to stomach → orogastric aspiration [26] |
| Bowel resection | Non-viable bowel (gangrenous, necrotic, perforated) [26] |
| Adhesiolysis (enterolysis) | Adhesive IO [26] |
| Stricturoplasty | Strictures (e.g., Crohn's) [26] |
| Hernia repair | Incarcerated hernia [26] |
| Surgical reduction of intussusception | Intussusception failing non-operative reduction |
Large bowel obstruction [26]:
Majority of LBO are managed surgically (unlike SBO which often resolves conservatively) [26]:
| Scenario | Management |
|---|---|
| Sigmoid volvulus | Non-operative decompression by sigmoidoscopy or Ryle's tube (initial detorsion). Note: requires interval sigmoidectomy because 50% recur [26] |
| Malignant obstruction | Endoscopic stenting (self-expanding metallic stent) as bridge to surgery (definitive OT 1-2 weeks after stenting) or as palliative treatment in unresectable disease [26]. Advantages: avoids emergency surgery (↑↑morbidity/mortality > 10%), allows bowel prep for elective surgery, better staging. C/I: perforated/strangulated, coagulopathy, distal rectal lesion ≤ 5 cm from anal verge [26] |
| Complicated LBO (peritonitis, perforation) | Emergency surgery: Hartmann's procedure (usually procedure of choice — sigmoid resection + end colostomy + rectal stump closure) [26] or primary anastomosis ± diverting ileostomy in selected patients [26] |
Conservative treatment (majority of uncomplicated cases) [26]:
- NPO → clear fluid diet → high-fibre low-residual diet
- IV fluids + analgesics
- Antibiotics: IV augmentin or cefuroxime + metronidazole × 10-14 days → IV tazocin if severe [26]. Clinical resolution expected in 3-5 days → switch to PO antibiotics [26].
- Note: per WSES 2016, antibiotics may not be indicated in immunocompetent patients with uncomplicated diverticulitis and no systemic signs of infection — but this practice is still controversial and not standard in HK [26].
Follow-up [26]:
- Elective colonoscopy at 6 weeks: CRC can present similarly to diverticulitis on CT (2.8% positive rate for malignancy) [26]
- Interval colectomy: usually NOT required (recurrence rate is low). Possible indications: high-risk (immunocompromised), complicated (stenosis, fistulae, recurrent bleeding), persistent symptoms [26]. Number of recurrent attacks (traditionally ≥ 2) is no longer an indication for interval colectomy [26].
Percutaneous CT-guided drainage [26]:
- Indication: large abscesses > 4-5 cm with favourable location
Surgical management (required in ~15%) [26]:
- Indications: diffuse peritonitis (Hinchey 3-4), failure of medical treatment in 3-5 days, chronic diverticulitis, obstruction (r/o CA), fistula [26]
- Hartmann's procedure: usually procedure of choice for emergency (sigmoid resection + end colostomy). Subsequent reversal is technically difficult and done in only ~50-60% [26].
- Primary anastomosis ± diverting ileostomy: advocated in some cases with similar mortality/morbidity but ↓length of stay and ↑stoma reversal rate [26]
Initial management [4]:
- Supportive: NPO, NGT decompression, IV fluids, O₂ supplement
- Stop ALL vasopressors [4] — vasopressors worsen splanchnic vasoconstriction
- Systemic anticoagulation by unfractionated heparin [4] — prevents clot propagation
- Empirical broad-spectrum antibiotics [4]
- PPI [4]
Subsequent management [4]:
| Clinical Scenario | Intervention |
|---|---|
| Stable, no features of advanced ischaemia | Endovascular intervention: pharmacomechanical thrombolysis if within 8h of pain onset (but majority diagnosed late); angioplasty with stenting as alternative [4] |
| Features of advanced ischaemia (peritonitis, sepsis, pneumatosis intestinalis) | Immediate surgery: exploratory laparotomy → revascularisation (open SMA embolectomy or SMA bypass) → resection of non-viable segments → delayed closure with second-look laparotomy 24-48h post-op to reassess viability [4] |
Why second-look laparotomy? Bowel viability is difficult to assess intraoperatively. Marginally perfused bowel may look viable initially but declare itself non-viable over the next 24-48h. A planned re-look avoids leaving behind necrotic bowel that will cause sepsis and death.
Ischaemic colitis [26]:
- Majority resolve with supportive care (non-occlusive, transient)
- Conservative for low/moderate risk: NPO, NGT, IV fluids, broad-spectrum Abx ± TPN, rectal tube decompression ± antithrombotics if occlusive [26]
- Abdominal exploration for high-risk individuals or those with infarction/necrosis: emergency laparotomy → resection of ischaemic segments ± primary anastomosis → second-look procedure [26]
- Prognosis: mortality < 5% non-gangrenous; 50-75% if gangrene develops [26]
Initial management: Resuscitation, NPO, IV fluids, NGT decompression, IV PPI (omeprazole 80 mg bolus then 8 mg/h infusion), broad-spectrum IV antibiotics (cover Gram-negatives and anaerobes).
Definitive surgery:
- Omental patch repair (Graham patch) — the standard: the perforation is closed with a plug of omentum sutured over the defect
- Laparoscopic repair is increasingly preferred where expertise is available
- Gastric ulcer: requires biopsy (may be malignant) → simple plication + biopsy, or ulcerectomy/partial gastrectomy [2]
- Post-operative: test and treat H. pylori; discontinue NSAIDs; PPI
Approach [5]:
- Supportive: resuscitation if necessary, monitor vitals
- Percutaneous drainage: diagnostic + therapeutic — indicated for ALL liver abscesses (some studies show small abscesses < 3 cm can be treated by antibiotics alone) [5]
- Needle aspiration if small (≤ 5 cm); catheter placement if large ( > 5 cm)
- USG-guided (small/superficial) or CT-guided
- Antibiotics:
- Pyogenic: broad-spectrum (cover Gram-negatives, anaerobes) — empirical then targeted by culture
- Amoebic: metronidazole (highly effective; drainage only if fails or imminent rupture)
- Surgical drainage: seldom done now; indicated if failed percutaneous drainage, multiloculated abscess, concomitant surgical pathology
- Emergency resuscitation: IV access × 2 large bore, crossmatch, permissive hypotension (SBP ~80-90 mmHg) to avoid dislodging clot
- Immediate surgery: Open repair (traditional) or EVAR (endovascular aneurysm repair) where anatomy is suitable and resources available [9]
- For uncomplicated AAA: indications for elective repair include all AAA > 5 cm (5.5 cm in Caucasians), symptomatic aneurysm of any size, rapidly expanding > 1 cm/year or > 0.5 cm/6 months, saccular aneurysm [9]
Supportive [27]:
- Pain control: NSAIDs are first-line (e.g., diclofenac, ketorolac) — highly effective because they reduce prostaglandin-mediated ureteric smooth muscle spasm and renal pelvic pressure. Opioids (hydromorphone, tramadol) as second-line.
- α-blockers (e.g., tamsulosin) can reduce recurrent colic and facilitate spontaneous stone passage (medical expulsive therapy — MET)
- Antibiotics if complicated by infection
Urgent decompression [27]:
- Indications: uncontrolled sepsis, progressively worsening renal function, intractable pain
- JJ stent (under fluoroscopy) or percutaneous nephrostomy (PCN)
- PCN: quicker (preferred in septic shock); C/I: bleeding tendency, distorted anatomy, obesity
- JJ stent: more comfortable; not possible in BPH, incompliant bladder, impacted stone
Definitive management (by stone size and location) [27]:
- Conservative (most stones < 5 mm pass spontaneously)
- ESWL (extracorporeal shockwave lithotripsy) — for renal/proximal ureteral stones < 20 mm
- RIRS (retrograde intrarenal surgery) — flexible ureteroscopy with laser lithotripsy
- PCNL (percutaneous nephrolithotomy) — for large renal stones > 20 mm
- Ureteroscopy — for ureteral stones
- Dietary changes: avoid dairy (secondary lactose malabsorption) [2]
- ORS: replace established deficits + ongoing losses + daily requirement. IV fluids if shock, unconscious, ileus, or failed oral rehydration [2]
- Antibiotics: NOT indicated unless inflammatory, severe watery diarrhoea, or high-risk patients [2]. Empirical: azithromycin (inflammatory) or fluoroquinolones. Specific: metronidazole (C. difficile), amoxicillin/co-trimoxazole (Listeria) [2].
- Anti-diarrhoeal (loperamide): use with caution in inflammatory diarrhoea (may prolong illness) [2]
Multifaceted approach [12]:
- Reassurance and education may already be sufficient [12]
- Dietary changes: low FODMAP diet [12]; high dietary fibre for constipation-predominant
Pharmacotherapy directed towards predominant symptom [12]:
| Predominant Symptom | Treatment Options |
|---|---|
| Diarrhoea (IBS-D) | Opioid agonist (loperamide); bile salt sequestrants (cholestyramine); probiotics; rifaximin [12] |
| Constipation (IBS-C) | Dietary fibre (psyllium); laxative (PEG); chloride channel activator (lubiprostone); guanylate cyclase C agonist (linaclotide) [12] |
| Abdominal pain | Peppermint oil; antispasmodics (otilonium, mebeverine); TCA (amitriptyline, desipramine); SSRI (citalopram, paroxetine, sertraline) [12] |
- Psychological treatment if refractory to medications [12]
Why do TCAs work in IBS? Tricyclic antidepressants modulate the brain-gut axis through central and peripheral mechanisms: they ↓visceral hypersensitivity (by modulating descending pain inhibitory pathways), have anticholinergic effects (↓motility — useful in IBS-D), and improve mood/anxiety. They work at low doses (10-25 mg) — much lower than antidepressant doses.
- Non-operative reduction preferred (high success rate) [28]
- Preparation: stabilisation + IV fluid resuscitation + prophylactic antibiotics (risk of perforation) [28]
- Method: Pneumatic technique (air/CO₂) is preferred over hydrostatic (NS) — reduces intussusception more easily and advantageous if perforation occurs [28]. Ultrasound guidance preferred over fluoroscopic [28].
- Successful reduction indicators: appearance of water/bubbles in terminal ileum, free flow of contrast/air into terminal ileum, relief of symptoms, disappearance of mass [28]
- Post-reduction: observation with hospitalisation for 12-24h (fever common from bacterial translocation; risk of recurrence from residual inflammation) [28]
- Surgical treatment indications: critically ill, suspected perforation, refractory to non-operative reduction [28]. Manual reduction at surgery; resection with primary anastomosis if irreducible or lead point identified [28].
| Drug Class | Indications in Abdominal Pain | Contraindications / Cautions |
|---|---|---|
| NSAIDs | Biliary colic (1st line for cholecystitis pain [5]), renal colic (1st line [27]) | Avoid in PUD (exacerbates); avoid in pancreatitis (worsens + renal failure) [22]; caution in renal impairment, bleeding risk |
| Morphine | Severe pain (general) | Avoid in biliary/pancreatic pain (↑sphincter of Oddi pressure) [22] |
| Fentanyl / Tramadol / Pethidine | Severe pain in pancreatitis and biliary disease [22] | Respiratory depression (fentanyl); seizure risk (tramadol, pethidine in high doses) |
| Metronidazole | Anaerobic coverage in appendicitis, diverticulitis, peritonitis, C. difficile, amoebic abscess | Disulfiram-like reaction with alcohol; peripheral neuropathy with prolonged use |
| 3rd-gen Cephalosporins (Ceftriaxone) | Gram-negative coverage in appendicitis, cholecystitis, peritonitis | Allergy; biliary sludge with prolonged use (ceftriaxone) |
| Piperacillin-tazobactam (Tazocin) | Broad-spectrum for severe intra-abdominal infections [26] | Allergy; interstitial nephritis |
| Imipenem | Infected pancreatic necrosis [22] | Seizures at high doses; allergy |
| PPI (Omeprazole, Pantoprazole) | PUD, PPU, stress ulcer prophylaxis, GERD | Long-term: ↓Mg, ↓Ca absorption, C. difficile risk, fundic gland polyps |
| Gastrografin | Diagnostic + therapeutic in adhesive SBO [25][26] | Aspiration risk if not given via NGT in obtunded patients; not for suspected complete LBO |
High Yield Summary
-
Universal initial Mx: NPO + IV fluids (2D1S Q8h; bolus if dehydrated) + NGT if IO/vomiting + analgesia + IV Abx if infective + serial examination. Keep UO > 0.5 mL/kg/h.
-
Appendicitis: Lap appendicectomy is 1st line. Within 72h → immediate surgery. > 72h stable → Ochsner-Sherren (IV Abx → interval surgery 6-8 weeks). Prophylactic IV ceftriaxone + metronidazole.
-
Cholecystitis: TG13 severity guides Mx. Mild → early LC. Moderate → early or delayed LC. Severe → percutaneous cholecystostomy → delayed LC. IV Abx cover Gram-negatives + anaerobes.
-
Pancreatitis: Aggressive fluids (5-10 mL/kg/h). Analgesia (fentanyl/tramadol — NOT morphine). Early enteral feeding < 48-72h. ERCP if biliary cause. Infected necrosis → step-up (Abx → drainage → necrosectomy). Delay interventions > 4 weeks.
-
IO: 70% SBO resolves with "drip and suck". Gastrografin study at 48h is diagnostic AND therapeutic. Urgent surgery if strangulation, closed-loop, peritonitis, incarcerated hernia. LBO: mostly surgical.
-
Mesenteric ischaemia: STOP vasopressors. Heparin. IV Abx. Stable → endovascular. Unstable/advanced → laparotomy + revascularisation + resection + second-look 24-48h.
-
PPU: IV PPI + IV Abx + omental patch repair. Always biopsy gastric ulcers.
-
Diverticulitis: Conservative majority. IV augmentin or cefuroxime + metro. Colonoscopy at 6 weeks to exclude CRC. Surgery for Hinchey 3-4.
-
Drug pearls: NSAIDs 1st line for renal/biliary colic but AVOID in pancreatitis and PUD. Morphine AVOID in biliary/pancreatic pain. Gastrografin is diagnostic + therapeutic in adhesive SBO.
-
IBS: Low FODMAP diet. Pharmacotherapy by predominant symptom. TCAs for pain. Psychological treatment if refractory.
Active Recall - Management of Abdominal Pain
References
[2] Senior notes: Ryan Ho Fundamentals.pdf (p257, p280, p289, Initial Management, Schema for Surgical Mx, Mx of GE) [3] Senior notes: felixlai.md (Acute appendicitis section) [4] Senior notes: felixlai.md (Mesenteric ischaemia section); Ryan Ho GI.pdf (p145, Initial and Subsequent Mx of mesenteric ischaemia) [5] Senior notes: felixlai.md (Cholecystitis — Treatment section) [9] Senior notes: felixlai.md (AAA — Treatment section); Ryan Ho Cardiology.pdf (p222, AAA) [10] Senior notes: maxim.md (Acute appendicitis — Management section) [11] Senior notes: felixlai.md (Diverticular disease section) [12] Senior notes: Ryan Ho GI.pdf (p118-119, IBS — Management) [22] Senior notes: Ryan Ho GI.pdf (p344-346, Acute pancreatitis — Management, Complications) [23] Senior notes: Ryan Ho GI.pdf (p150-152, Appendicitis — Approach to management, Appendicectomy) [24] Senior notes: Ryan Ho GI.pdf (p248, TG13 severity assessment) [25] Senior notes: felixlai.md (Intestinal obstruction — Treatment section) [26] Senior notes: Ryan Ho GI.pdf (p137-139, IO Management; p147, Ischaemic colitis Mx; p158-159, Diverticulitis Mx) [27] Senior notes: Ryan Ho Urogenital.pdf (p140, Renal colic — Acute management) [28] Senior notes: felixlai.md (Intussusception — Treatment section)
Complications of Abdominal Pain Conditions
Complications arise when the primary pathology progresses unchecked or as a consequence of treatment itself. Understanding complications from first principles means asking: "What happens if this disease process continues?" — the answer is almost always a progression along the spectrum of inflammation → necrosis → perforation → sepsis → organ failure → death.
This section covers complications in two broad categories:
- Complications of the primary abdominal conditions (disease-related)
- Complications of surgical treatment (iatrogenic)
I. Complications of Primary Abdominal Conditions
The natural history of untreated appendicitis follows a predictable cascade:
Luminal obstruction → mucosal inflammation → transmural inflammation → venous congestion (appendiceal artery is an end-artery → no collateral rescue) → ischaemia → gangrene → perforation
| Complication | Mechanism | Clinical Features | Management |
|---|---|---|---|
| Perforation | Necrosis of the appendiceal wall (worsened by the end-artery blood supply — once the appendiceal artery thromboses, the entire wall becomes ischaemic). Occurs in 13-20% of patients [23]. Risk factors: male gender, ↑age, ≥ 3 comorbidities [23] | Walled-off perforation: localised RLQ pain, inflammatory mass (phlegmon/abscess). Free perforation: diffuse pain, generalised peritonitis [23]. Suspect when fever > 39.4°C, WBC > 15 × 10⁹/L, imaging shows RLQ fluid collection [29] | Walled-off + stable → Ochsner-Sherren. Free perforation/unstable → emergency appendicectomy [23] |
| Appendiceal abscess | Localised collection of pus from a walled-off perforation (omentum wraps around the inflamed appendix → containment → but ongoing bacterial proliferation) | Persistent/spiking fever, RLQ mass palpable, failure to improve with antibiotics | IV Abx + percutaneous image-guided drainage ± interval appendicectomy 6-8 weeks [23] |
| Generalised peritonitis | Free perforation → faecal and bacterial contamination of the entire peritoneal cavity | Diffuse abdominal pain, board-like rigidity, absent bowel sounds, sepsis | Emergency laparotomy + appendicectomy + peritoneal lavage [13][23] |
| Pylephlebitis (septic portal vein thrombosis) | Septicaemia in the portal venous system from the inflamed appendix → thrombosis and infection propagating via the portal vein → intra-hepatic abscesses [29] | High fever, chills, rigors, jaundice [29] | IV antibiotics + anticoagulation ± drainage of hepatic abscesses |
Post-operative complications of appendicectomy [10][23][29]:
| Timing | Complication | Detail |
|---|---|---|
| Early ( < 1 week) | Wound infection (5-10%) | Pain and erythema of wound on post-op day 4-5. Usually mixed Gram-negative bacilli and anaerobic bacteria (Bacteroides, Streptococcus). Mx: wound drainage + antibiotics [23] |
| Intra-abdominal / pelvic abscess (~8%) | Spiking fever, malaise, anorexia post-op day 5-7. May be interloop, paracolic, pelvic, or subphrenic. Mx: drainage ± laparotomy [23] | |
| Post-operative ileus | Expected for 24-72h. > 4-5 days indicates continuing intra-abdominal sepsis (especially if fever) [23] | |
| Haemorrhage | Intra-abdominal, abdominal wall haematoma, scrotal haematoma [23] | |
| Late ( > 1 week) | Adhesions | Most common long-term complication of any abdominal surgery. Causes: intestinal obstruction, chronic pelvic pain. Adhesive SBO is the #1 cause of SBO overall [23][25] |
| Enterocutaneous fistula | Results from intraperitoneal abscess that fistulises to the skin [29] | |
| Stump appendicitis | Retained appendiceal stump with recurrent inflammation — rare but dangerous [23] | |
| Incisional hernia | Abdominal wall defect at the incision site [10] |
Why is perforation more common in children and the elderly? In children, the omentum is underdeveloped and cannot effectively wall off the inflamed appendix → free perforation is more likely. In the elderly, reduced immune response leads to delayed diagnosis and late presentation → the appendix has more time to necrose before treatment.
| Complication | Mechanism | Clinical Features |
|---|---|---|
| Empyema of gallbladder | Pus accumulates in the obstructed gallbladder (secondary bacterial infection in the setting of persistent cystic duct obstruction) | High fever, severe RUQ pain, rigors, high WBC — essentially an intra-abdominal abscess |
| Gangrenous cholecystitis | Prolonged ischaemia of the gallbladder wall (distension → vascular compromise) → necrosis | Clinical deterioration despite antibiotics; carries high risk of perforation |
| Gallbladder perforation | Gangrenous wall ruptures → bile and pus leak into the peritoneal cavity | Localised (if contained by adhesions) or generalised peritonitis. Type I (free perforation → peritonitis), Type II (localised abscess), Type III (cholecystoenteric fistula) |
| Emphysematous cholecystitis | Gas-forming organisms (Clostridium, E. coli) infect the gallbladder wall | Crepitus over RUQ; gas in gallbladder wall on CT. More common in diabetics. Surgical emergency. |
| Mirizzi syndrome | Impacted stone in the cystic duct or Hartmann's pouch extrinsically compresses the common hepatic duct | Obstructive jaundice mimicking choledocholithiasis but with an intact CBD |
| Gallstone ileus | Large gallstone erodes through the gallbladder into the adjacent duodenum (cholecystoduodenal fistula) → enters the bowel lumen → impacts at the narrowest point (ileocaecal valve) → mechanical SBO | Rigler's triad on AXR: pneumobilia + SBO + ectopic gallstone [23]. Elderly women classically affected. |
| Cholangitis | Stone migrates into or co-existing stone in CBD → stasis + ascending infection | Charcot's triad / Reynold's pentad [2] |
Pancreatitis complications are divided into local and systemic categories. The Revised Atlanta Classification 2013 provides the framework for local complications.
| Complication | Definition & Timing | Clinical Features | Management |
|---|---|---|---|
| Acute peripancreatic fluid collection (APFC) | Non-encapsulated fluid collection within first 4 weeks; no necrosis | Often asymptomatic; detected incidentally on CT | Resolves spontaneously in 7-10 days; no drainage needed [30] |
| Acute necrotic collection | Non-encapsulated collection containing both fluid and necrotic tissue, < 4 weeks | Persistent fever, clinical deterioration | Sterile → conservative. Infected necrosis → empirical Abx → step-up approach (percutaneous drainage → surgical necrosectomy if fails) [22]. Usually occurs > 10 days post-onset; > 75% monomicrobial with gut-derived organisms [22] |
| Pseudocyst | Encapsulated fluid collection with well-defined wall; > 4 weeks; no necrotic component | Persistent abdominal pain, palpable epigastric mass, visceral obstruction | Drain if symptomatic, infected, or causing complications [22] |
| Walled-off necrosis (WON) | Encapsulated necrotic collection with well-defined wall; > 4 weeks | Persistent fever, failure to improve, organ failure | Delay interventions > 4 weeks (necrotic tissue poorly demarcated early → incomplete debridement → poor outcome). Evaluate by CT/MRI ± EUS-guided FNA. Drain/debride if symptomatic/infected/ongoing organ failure [22] |
Why delay drainage/debridement to > 4 weeks? In the early phase, necrotic tissue is poorly demarcated with intense inflammation. Attempting debridement results in incomplete removal, bleeding, and worsening inflammation. By 4 weeks, the necrosis has "matured" — the wall has formed and the necrotic tissue is better demarcated, making debridement safer and more effective.
Peripancreatic vascular complications [30]:
| Complication | Mechanism | Clinical Features | Management |
|---|---|---|---|
| Splanchnic venous thrombosis | Splenic, portal, or SMV thrombosis from close proximity to the inflammatory process | Hepatic decompensation; compromise of bowel perfusion | Treat underlying pancreatitis (may resolve spontaneously). Anticoagulation if extends into portal/SMV [22][30] |
| Pseudoaneurysm | Pancreatic enzyme erosion into adjacent arteries (GDA, left gastric, splenic arteries most common) | Unexplained GI bleeding, ↓Hb, sudden expansion of pancreatic fluid collection [30] | Angiographic embolisation [30]. Endoscopic drainage of collection absolutely contraindicated (catastrophic haemorrhage!) [22] |
Systemic complications [30]:
- Respiratory: ARDS (inflammatory mediators → alveolar capillary leak → non-cardiogenic pulmonary oedema)
- Cardiovascular: coronary artery disease, high-output heart failure
- GI: paralytic ileus, abdominal compartment syndrome (tissue oedema + ascites + ileus → intra-abdominal pressure > 20 mmHg + new organ failure → surgical decompression) [22]
- Renal: acute kidney injury (hypovolaemia, SIRS, nephrotoxic drugs)
- Haematology: retroperitoneal bleeding (haemorrhagic pancreatitis → Cullen's sign, Grey Turner's sign, Fox's sign)
- Endocrine: insulin deficiency → hyperglycaemia (destruction of islet cells)
- SIRS → organ failure: the leading cause of early mortality in pancreatitis. Cytokine cascade (TNF-α, IL-1, IL-6) → multiorgan dysfunction [7][30]
| Complication | Mechanism | Clinical Features | Prognosis |
|---|---|---|---|
| Strangulation | Blood supply compromised from: ↑intraluminal pressure, direct pressure on bowel wall, or interrupted mesenteric blood flow → ischaemia → necrosis → perforation [29] | Continuous/worsening pain (cf. intermittent colicky pain of simple obstruction), fever, tachycardia, peritoneal signs [29]. Biochemical: leukocytosis, metabolic acidosis. Radiological: pneumoperitoneum, pneumatosis intestinalis, portal venous gas [29] | Mortality: 2% (non-strangulated) vs 10-30% (strangulated) [26] |
| Closed-loop obstruction | Obstruction at two points along the bowel → isolated segment cannot decompress in either direction → rapid rise in intraluminal pressure → ischaemia | Rapid clinical deterioration; volvulus is a classic example | Surgical emergency — cannot resolve with conservative management |
| Perforation | Necrotic bowel wall ruptures → faecal peritonitis | Pneumoperitoneum on CXR/AXR; generalised peritonitis | Emergency laparotomy |
| Aspiration pneumonia | Proximal bowel distension → vomiting → aspiration (especially in obtunded patients or those without NGT decompression) | Respiratory distress post-emesis; CXR infiltrates | Antibiotics; intubation if severe; prevention by NGT |
| Dehydration and electrolyte disturbance | Third-space fluid sequestration into dilated bowel loops + vomiting losses → intravascular depletion + electrolyte derangement | Tachycardia, ↓BP, ↓UO, ↑urea:Cr ratio; hypokalaemia (vomiting), metabolic alkalosis (loss of H⁺ and Cl⁻ in vomitus) | Aggressive IV fluid and electrolyte replacement |
| Bacterial translocation and sepsis | Bacterial overgrowth in stagnant bowel contents → disrupted mucosal barrier (ischaemia) → bacteria translocate across bowel wall into peritoneal cavity/bloodstream | Fever, SIRS, septic shock | IV broad-spectrum antibiotics; source control (surgery) |
| Complication | Frequency/Mechanism | Clinical Features | Management |
|---|---|---|---|
| Abscess | Occurs in 17% of acute diverticulitis. Microperforation contained by pericolic tissues/mesentery [29] | Persistent fever and no improvement in abdominal pain despite 3 days of antibiotics [29]. May lead to pyogenic liver abscess via portal circulation [29] | Small ( < 4-5 cm) → IV Abx. Large ( > 4-5 cm) → percutaneous CT-guided drainage [26] |
| Fistula | Inflammation erodes into adjacent organs. Most commonly colovesical (bladder), followed by colovaginal (especially post-hysterectomy) [29] | Colovesical: pneumaturia, fecaluria, recurrent dysuria/UTI [11][29]. Colovaginal: vaginal passage of faeces and flatus [29] | Control sepsis → resect affected colon segment + primary repair of secondarily involved organ [29] |
| Obstruction | Partial: pericolonic inflammation/abscess compressing lumen. Complete: progressive fibrosis and scarring from recurrent attacks → stricture formation [29] | Abdominal pain + distension + vomiting + constipation. Hyperactive bowel sounds (mechanical) or absent (paralytic ileus from peritoneal inflammation) [29] | Conservative initially; surgical resection for complete obstruction or stricture |
| Perforation | Rupture of diverticular abscess into peritoneal cavity (purulent peritonitis) OR rupture of inflamed diverticulum with faecal contamination (faecal peritonitis) [29] | Haemodynamic instability (hypotension, shock); peritoneal signs (guarding, rigidity, rebound); absent bowel sounds [29] | Emergency surgery: Hartmann's procedure (Hinchey 3-4) [26] |
| Diverticular bleeding | Rupture of vasa recta at the neck of the diverticulum (the artery is draped over the dome of the diverticulum where it is most vulnerable) | Painless massive PR bleeding [11] — this is the most common cause of massive lower GI bleeding [26]. Dark/maroon (right-sided) vs bright red (left-sided) [26] | Majority (80%) self-limiting. Colonoscopy is initial diagnostic + therapeutic procedure. Failed → angiography/RBC scan → segmental colectomy [26] |
| Chronic sequelae [26] | Chronic pain (persistent low-grade diverticulitis or IBS-related); diverticular colitis (IBD-like segmental colitis); diverticular stricture → chronic/acute obstruction | Variable | Depends on specific sequela |
Why is diverticular bleeding painless? Diverticular bleeding occurs from rupture of the vasa recta WITHOUT significant inflammation. This distinguishes it from diverticulitis (which has inflammation but rarely bleeds). The two conditions rarely coexist [26].
| Complication | Mechanism | Clinical Features |
|---|---|---|
| Bleeding | Ulcer erodes into a blood vessel (gastroduodenal artery in posterior DU is a classic site) | Haematemesis (frank blood or coffee-ground), melaena, haematochezia (if massive) [6] |
| Perforation | Ulcer erodes through all layers of the gut wall → peritonitis | Sudden severe epigastric pain → generalised; board-like rigidity; ↓liver dullness [2] |
| Penetration | Ulcer erodes through serosa but is contained by adhesion to an adjacent organ (pancreas posteriorly for DU; liver for GU) | Change in pain character: more intense, longer duration, shift to localised back pain, NOT relieved by food or antacids [6] |
| Gastric outlet obstruction (GOO) | Chronic ulceration at the pylorus or duodenal bulb → fibrosis + scarring + oedema → narrowing of the lumen | Epigastric pain after eating, early satiety, bloating, nausea/vomiting, weight loss. Succussion splash on examination [6]. Dehydration + hypokalaemic hypochloraemic metabolic alkalosis (loss of H⁺ and Cl⁻ in vomitus) |
| Fistulisation | Gastrocolic or duodenocolic fistula (ulcer erodes into adjacent colon) | Feculent vomiting, postprandial diarrhoea, dyspepsia, weight loss [6] |
| Complication | Mechanism | Management |
|---|---|---|
| Stricture | Repeated inflammation → muscle hypertrophy and fibrosis → luminal narrowing. Should be considered malignant until proven otherwise by endoscopy + biopsy [30] | Endoscopy + biopsy to exclude malignancy |
| Fulminant colitis | Severe pan-colonic inflammation → > 10 stools/day, continuous bleeding, abdominal pain, distension, acute severe toxic symptoms (fever, anorexia, tachycardia) [30] | Medical: IV steroids, cyclosporine/infliximab. Surgical: total abdominal colectomy with end ileostomy if refractory [30] |
| Toxic megacolon | Inflammation extends beyond mucosa to involve muscle layers → loss of colonic tone → non-obstructive dilatation ≥ 6 cm or caecum > 9 cm + systemic toxicity [30] | Bowel rest + TPN + IV steroids + electrolyte correction. Failure → emergency surgery |
| Perforation | Most commonly as consequence of toxic megacolon → necrotic, dilated bowel wall ruptures | Generalised peritonitis; high mortality [30] |
| Colorectal cancer | Chronic mucosal inflammation → dysplasia → carcinoma sequence. Risk increases with disease duration and extent | Regular endoscopic surveillance in long-standing disease [30] |
Crohn's Disease [30]:
| Complication | Mechanism | Clinical Features |
|---|---|---|
| Fistula formation | Transmural inflammation → sinus tracts penetrate serosa → connect to adjacent organs [30] | Enteroenteric (palpable mass), enterovesical (UTI, pneumaturia), enterovaginal (passage of gas/faeces per vaginum), enterocutaneous (skin drainage), retroperitoneal (psoas abscess, hydronephrosis) [30] |
| Abscess formation | Sinus tract leads to walled-off collection | Acute localised peritonitis, fever, tenderness [30] |
| Stricture / Intestinal obstruction | Chronic transmural inflammation → fibrosis → luminal narrowing | Colicky pain, distension, vomiting. Strictureplasty or resection |
| Perianal disease | Terminal ileum → rectal involvement → perianal inflammation | Skin tags, anal fissures, perirectal abscess, anorectal fistulas [30] |
| Malnutrition | Reduced intake (food fear), malabsorption (inflamed/resected ileum), protein-losing enteropathy | Weight loss, vitamin deficiencies (B12, fat-soluble vitamins), anaemia |
Complications of ruptured AAA and its repair [9]:
| Complication | Mechanism |
|---|---|
| Massive blood loss and transfusion-related effects | Haemorrhagic shock; DIC, hypothermia from massive transfusion [9] |
| Cardiorespiratory complications | Haemodynamic stress of rupture and aortic clamping → myocardial ischaemia, arrhythmias |
| Renal failure | Shock (pre-renal) or suprarenal aortic clamping (direct renal ischaemia) [9] |
| Bowel ischaemia | Much higher risk than in non-ruptured AAA [9] — IMA ligation during repair + hypotension → colonic ischaemia |
| Paralytic ileus | Retroperitoneal haematoma irritates the autonomic plexus → bowel dysmotility [9] |
| Abdominal compartment syndrome | Reperfusion injury → massive tissue oedema + ascites → intra-abdominal pressure > 20 mmHg + new organ failure → decompressive laparotomy [9] |
| Graft infection | Late complication; aortoenteric fistula (graft erodes into duodenum → GI bleeding) is a feared complication |
Complications of elective AAA repair (EVAR-specific) [9]:
- Endoleak: persistent blood flow into the aneurysm sac outside the graft. Types I-V classified by source of leak [9]. Type I (attachment site) and Type III (graft defect) require intervention. Type II (retrograde flow from branch vessels) — most common, usually benign.
- Graft migration, limb thrombosis, graft infection
Any abdominal surgery can result in complications classified by timing [10]:
| Timing | Category | Examples |
|---|---|---|
| Immediate ( < 1h) | Local | Primary haemorrhage (bleeding from an unsecured vessel), damage to neighbouring structures |
| Systemic | Shock (blood loss), atelectasis (anaesthesia → reduced surfactant, shallow breathing) | |
| Laparoscopy-specific | Organ puncture, vascular injury, nerve injury, port-site hernia; pneumoperitoneum-related: subcutaneous emphysema, pneumothorax, arrhythmia [10] | |
| Early (24-48h) | Local | Reactionary haemorrhage (within 24h: vasoconstriction during surgical stress masks a bleeding vessel → when stress response wanes, vessel dilates → bleeding) [10] |
| Systemic | Acute confusion (dehydration, sepsis), pneumonia, AROU, UTI [10] | |
| Late ( > 48h) | Local | Wound infection (post-op day 4-5); secondary haemorrhage (7-10 days post-op: pseudoaneurysm from infection → mesenteric angiogram for diagnosis) [10]; adhesive intestinal obstruction; incisional hernia [10] |
| Systemic | Fever, acute confusion, cardiac (arrhythmia, MI), DVT/PE [10] |
Anastomotic complications (specific to bowel surgery) [29]:
| Complication | Timing | Clinical Features | Management |
|---|---|---|---|
| Anastomotic bleeding | Early ( < 30 days) | PR bleeding, haemodynamic instability | Blood transfusion + correct coagulopathy [29] |
| Anastomotic leakage | Early (day 5-7) | Pain, fever, tachycardia, feculent or purulent drainage. Radiological: fluid/gas-containing collections [29] | Fluid resuscitation + broad-spectrum IV Abx + bowel rest + image-guided percutaneous drainage ± fecal diversion or re-operation [29] |
| Anastomotic stricture | Late ( > 30 days) | Features of partial/subacute obstruction | Finger dilatation (low) or endoscopic balloon dilatation (high) [29] |
| Anastomotic fistula | Late ( > 30 days) | Enterocutaneous (most close spontaneously), rectovaginal, rectourinary [29] | Enterocutaneous → conservative. Rectovaginal/rectourinary → proximal fecal diversion [29] |
Stoma complications [29]:
| Timing | Complication | Detail |
|---|---|---|
| Early | Stomal bleeding, stomal necrosis (ischaemia), stomal retraction, mucocutaneous separation | Necrosis: dusky/black stoma — may need revision. Retraction: stoma sinks below skin level → poor appliance fit → leakage |
| Skin irritation and dermatitis | Most common in end and loop ileostomy due to high-output and highly alkaline enzymatic effluent [29] — the proteolytic enzymes digest the skin | |
| Late | Parastomal hernia, stomal prolapse, stomal stenosis | Parastomal hernia: most common long-term stoma complication (fascial defect around the stoma allows bowel herniation) |
III. Complications of Specific Medical Causes of Abdominal Pain
- Cerebral oedema (especially in children during treatment — rapid correction of glucose/osmolality causes osmotic fluid shifts into brain cells)
- Hypokalaemia during treatment (insulin drives K⁺ intracellularly; always replace K⁺ before or with insulin infusion)
- ARDS (severe cases)
- Aspiration pneumonia (obtunded patient with vomiting)
- Mucormycosis (rhinocerebral fungal infection in poorly controlled diabetics)
- Recurrent DKA if precipitant not addressed
- Haemoperitoneum → haemorrhagic shock
- Infertility (tubal damage — especially if salpingectomy required)
- Recurrent ectopic (15% risk in subsequent pregnancies)
- Tubal adhesions (from inflammation)
High Yield Summary
-
Appendicitis complications: Perforation (13-20%) → walled-off abscess or generalised peritonitis. Post-op: wound infection (5-10%), intra-abdominal abscess (~8%), adhesions (long-term SBO risk), pylephlebitis (rare but serious).
-
Cholecystitis complications: Empyema → gangrenous cholecystitis → perforation → peritonitis. Emphysematous cholecystitis (diabetics, gas-formers). Mirizzi syndrome. Gallstone ileus (Rigler's triad: pneumobilia + SBO + ectopic stone).
-
Pancreatitis complications: Local: APFC (resolves spontaneously), acute necrotic collection, pseudocyst, WON (delay intervention > 4 weeks). Vascular: splanchnic thrombosis, pseudoaneurysm (angiographic embolisation — NEVER drain collection endoscopically!). Systemic: ARDS, AKI, abdominal compartment syndrome, SIRS → organ failure.
-
IO complications: Strangulation (mortality 10-30% vs 2% non-strangulated). Signs: continuous pain, fever, tachycardia, peritoneal signs, metabolic acidosis, pneumatosis, portal venous gas. Closed-loop obstruction is a surgical emergency.
-
Diverticulitis complications: Abscess (17%), fistula (colovesical MC → pneumaturia, fecaluria), obstruction (fibrosis/stricture), perforation (Hinchey 3-4), diverticular bleeding (painless massive PR bleed — MC cause of massive LGIB).
-
PUD complications: Bleeding, perforation, penetration, GOO (succussion splash, hypokalaemic hypochloraemic metabolic alkalosis), fistulisation.
-
UC complications: Stricture (malignant until proven otherwise), fulminant colitis, toxic megacolon (≥ 6 cm + systemic toxicity), perforation, CRC (surveillance needed).
-
Anastomotic leakage: Day 5-7 post-op. Pain + fever + tachycardia + feculent drainage. Mx: IV Abx + drainage ± re-operation.
-
Reactionary haemorrhage: Within 24h (stress vasoconstriction wanes → bleeding). Secondary haemorrhage: 7-10 days (pseudoaneurysm from infection → "warning bleed" then torrential bleed).
-
Stoma dermatitis: Worst with ileostomy (alkaline proteolytic effluent digests skin).
Active Recall - Complications of Abdominal Pain Conditions
References
[2] Senior notes: Ryan Ho Fundamentals.pdf (p268-276, Causes of Upper Abdominal Pain) [5] Senior notes: felixlai.md (Cholecystitis section) [6] Senior notes: felixlai.md (PUD — Complications section) [7] Senior notes: felixlai.md (Acute pancreatitis — Pathophysiology section) [9] Senior notes: Ryan Ho Cardiology.pdf (p222, p228, AAA, Complications of ruptured AAA) [10] Senior notes: maxim.md (Post-op complications section, Appendicitis management section) [11] Senior notes: felixlai.md (Diverticular disease section); maxim.md (Diverticular disease section) [13] Senior notes: felixlai.md (Peritonitis section) [16] Senior notes: felixlai.md (Ulcerative colitis section) [19] Senior notes: Ryan Ho Endocrine.pdf (p91, DKA) [22] Senior notes: Ryan Ho GI.pdf (p344-346, Pancreatitis — Management of complications) [23] Senior notes: Ryan Ho GI.pdf (p150-153, Appendicitis — Perforated appendix, Post-op complications) [25] Senior notes: felixlai.md (Intestinal obstruction — Treatment and Complications sections) [26] Senior notes: Ryan Ho GI.pdf (p138-139, IO Management; p147, Ischaemic colitis; p158-160, Diverticulitis) [29] Senior notes: felixlai.md (Appendicitis — Post-op complications section; Colorectal surgery — Anastomotic and stoma complications) [30] Senior notes: felixlai.md (Pancreatitis — Complications section; Crohn's disease — Complications section; UC — Complications section); Ryan Ho GI.pdf (p350, Chronic pancreatitis complications)
High Yield Summary
-
Three pain types: Visceral (dull, midline, autonomic afferents), Parietal/Somatic (sharp, localised, somatic nerves), Referred (distant site, convergence in dorsal horn).
-
Embryological pain referral: Foregut → epigastrium; Midgut → periumbilical; Hindgut → suprapubic.
-
Life-threatening causes NEVER to miss: PPU, ruptured AAA, mesenteric ischaemia, strangulated obstruction, severe pancreatitis, ruptured HCC/ectopic, DKA, acute MI, Addisonian crisis.
-
Appendicitis: Midgut visceral pain (periumbilical T10) → shifts to RLQ (parietal peritoneal irritation). Appendiceal artery is an END-ARTERY → thrombosis = necrosis. Peak 20s-30s, M > F.
-
Biliary colic: "False colic" — actually constant. ≥30min, <6h. Risk factors: Fat, Female, Fertile, Forty.
-
PPU: Sudden maximal epigastric pain → generalised. Board-like rigidity. ↓Liver dullness (pneumoperitoneum). Pain may transiently ↓ after 4-6h as acid dilutes — BUT peritonitis is still progressing!
-
Pancreatitis: Epigastric → back. Relieved by leaning forward. Autodigestion by premature trypsin activation.
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Mesenteric ischaemia: Pain out of proportion to findings. Think AF, atherosclerosis. Lactate↑.
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Asian diverticular disease: Right-sided predominance; confused with appendicitis.
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Peritonitis classification: Primary (SBP in cirrhosis), Secondary (surgically treatable), Tertiary (opportunistic after prolonged antibiotics).
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Watershed areas: Griffiths' point (splenic flexure), Sudeck's point (rectosigmoid junction).
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Women of reproductive age: ALWAYS check β-hCG. Link pain with menstrual history, coitus, pregnancy possibility. Examine speculum + bimanual.
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Masquerades: Depression, Drugs, Spinal dysfunction (referred), UTI. "Is the patient trying to tell me something?"
High Yield Summary
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Murtagh's framework: Probability → Serious not to miss → Pitfalls → Masquerades → "Is the patient trying to tell me something?" Apply this systematically to every patient.
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Life-threatening DDx of acute abdomen: PPU, ruptured AAA, acute mesenteric ischaemia, acute IO, severe pancreatitis, ruptured HCC, DKA, acute MI, Addisonian crisis, ruptured ectopic, placental abruption.
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Masquerades: Depression, DKA, Drugs (NSAIDs, opioids, cytotoxics), Sickle cell anaemia, Spinal dysfunction (referred pain), UTI/urosepsis.
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DKA mimics surgical acute abdomen — always check blood glucose and ketones.
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Inferior MI mimics upper abdominal pain — always do an ECG in epigastric pain.
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Right-sided diverticulitis in Asia mimics appendicitis — CT abdomen is the differentiator.
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CRC can only be excluded with colonoscopy after resolution of acute diverticulitis inflammation.
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Women of reproductive age: always β-hCG; ectopic pregnancy is the single most dangerous miss.
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Children: appendicitis more likely complicated (delayed); intussusception peaks 6-9 months; mesenteric adenitis has higher fever than appendicitis.
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Carnett sign differentiates abdominal wall pain from intra-abdominal: tenderness increases with muscle tensing → wall origin.
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Early severe vomiting = high GI obstruction; late vomiting = distal obstruction.
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Always examine hernial orifices — incarcerated hernia is a leading cause of bowel obstruction complications.
High Yield Summary
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Erect CXR is the most important first radiograph — detects pneumoperitoneum (perforation), basal pneumonia, pleural effusion. If free gas + peritoneal signs → straight to theatre.
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Three non-negotiable bedside tests: Urine pregnancy test (all women of childbearing age), ECG (all upper abdominal pain), Capillary glucose (DKA suspicion).
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Imaging by pain site: RUQ → USG; LUQ → CT; RLQ/LLQ → CT with IV contrast; Suprapubic → USG (TAS/TVS).
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Acute cholecystitis (TG13): Suspected = 1× local sign + 1× systemic sign. Definite = + 1× imaging finding. USG is 1st line (Sens 88%, Spec 80%).
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Acute pancreatitis (Revised Atlanta): ≥ 2/3 of clinical pain, amylase/lipase ≥ 3× ULN, imaging. Amylase cut-off NOT indicative of severity. Lipase preferred if > 24h.
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Appendicitis (MANTREL): ≤ 3 = unlikely; 4-6 = image; ≥ 7 = surgery. CT is gold standard in adults. USG for pregnant/children.
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IO on AXR: 3-6-9 rule (SB > 3, LB > 6, caecum > 9 cm). > 5 air-fluid levels on erect AXR = diagnostic.
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Amylase false positives: PPU, ruptured AAA, DKA, macroamylasaemia. Lipase is more specific.
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90% urinary stones are radio-opaque; only 15% gallstones are radio-opaque (only pigmented stones).
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CTA is the most important investigation for mesenteric ischaemia in stable patients. No oral contrast. Metabolic acidosis + ↑lactate = ischaemic bowel until proven otherwise.
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AVOID endoscopy in acute abdomen — sealed-off perforation may open with gas insufflation.
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IBS: Rome IV — pain ≥ 1 day/week for 3 months, a/w ≥ 2 of: related to defecation, change in stool frequency, change in stool form. Diagnosis of exclusion.
High Yield Summary
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Universal initial Mx: NPO + IV fluids (2D1S Q8h; bolus if dehydrated) + NGT if IO/vomiting + analgesia + IV Abx if infective + serial examination. Keep UO > 0.5 mL/kg/h.
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Appendicitis: Lap appendicectomy is 1st line. Within 72h → immediate surgery. > 72h stable → Ochsner-Sherren (IV Abx → interval surgery 6-8 weeks). Prophylactic IV ceftriaxone + metronidazole.
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Cholecystitis: TG13 severity guides Mx. Mild → early LC. Moderate → early or delayed LC. Severe → percutaneous cholecystostomy → delayed LC. IV Abx cover Gram-negatives + anaerobes.
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Pancreatitis: Aggressive fluids (5-10 mL/kg/h). Analgesia (fentanyl/tramadol — NOT morphine). Early enteral feeding < 48-72h. ERCP if biliary cause. Infected necrosis → step-up (Abx → drainage → necrosectomy). Delay interventions > 4 weeks.
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IO: 70% SBO resolves with "drip and suck". Gastrografin study at 48h is diagnostic AND therapeutic. Urgent surgery if strangulation, closed-loop, peritonitis, incarcerated hernia. LBO: mostly surgical.
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Mesenteric ischaemia: STOP vasopressors. Heparin. IV Abx. Stable → endovascular. Unstable/advanced → laparotomy + revascularisation + resection + second-look 24-48h.
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PPU: IV PPI + IV Abx + omental patch repair. Always biopsy gastric ulcers.
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Diverticulitis: Conservative majority. IV augmentin or cefuroxime + metro. Colonoscopy at 6 weeks to exclude CRC. Surgery for Hinchey 3-4.
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Drug pearls: NSAIDs 1st line for renal/biliary colic but AVOID in pancreatitis and PUD. Morphine AVOID in biliary/pancreatic pain. Gastrografin is diagnostic + therapeutic in adhesive SBO.
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IBS: Low FODMAP diet. Pharmacotherapy by predominant symptom. TCAs for pain. Psychological treatment if refractory.
High Yield Summary
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Appendicitis complications: Perforation (13-20%) → walled-off abscess or generalised peritonitis. Post-op: wound infection (5-10%), intra-abdominal abscess (~8%), adhesions (long-term SBO risk), pylephlebitis (rare but serious).
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Cholecystitis complications: Empyema → gangrenous cholecystitis → perforation → peritonitis. Emphysematous cholecystitis (diabetics, gas-formers). Mirizzi syndrome. Gallstone ileus (Rigler's triad: pneumobilia + SBO + ectopic stone).
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Pancreatitis complications: Local: APFC (resolves spontaneously), acute necrotic collection, pseudocyst, WON (delay intervention > 4 weeks). Vascular: splanchnic thrombosis, pseudoaneurysm (angiographic embolisation — NEVER drain collection endoscopically!). Systemic: ARDS, AKI, abdominal compartment syndrome, SIRS → organ failure.
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IO complications: Strangulation (mortality 10-30% vs 2% non-strangulated). Signs: continuous pain, fever, tachycardia, peritoneal signs, metabolic acidosis, pneumatosis, portal venous gas. Closed-loop obstruction is a surgical emergency.
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Diverticulitis complications: Abscess (17%), fistula (colovesical MC → pneumaturia, fecaluria), obstruction (fibrosis/stricture), perforation (Hinchey 3-4), diverticular bleeding (painless massive PR bleed — MC cause of massive LGIB).
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PUD complications: Bleeding, perforation, penetration, GOO (succussion splash, hypokalaemic hypochloraemic metabolic alkalosis), fistulisation.
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UC complications: Stricture (malignant until proven otherwise), fulminant colitis, toxic megacolon (≥ 6 cm + systemic toxicity), perforation, CRC (surveillance needed).
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Anastomotic leakage: Day 5-7 post-op. Pain + fever + tachycardia + feculent drainage. Mx: IV Abx + drainage ± re-operation.
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Reactionary haemorrhage: Within 24h (stress vasoconstriction wanes → bleeding). Secondary haemorrhage: 7-10 days (pseudoaneurysm from infection → "warning bleed" then torrential bleed).
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Stoma dermatitis: Worst with ileostomy (alkaline proteolytic effluent digests skin).