The Gastrointestinal System

The gastrointestinal (GI) system extends from the oral cavity to the anus and includes the accessory organs — liver, gallbladder, and pancreas. A systematic approach to GI history-taking and clinical examination is essential for accurate diagnosis and timely referral in Australian primary and secondary care settings. GI diseases account for a substantial burden of morbidity and mortality across all Australian populations.

In Australia, colorectal cancer is the second most common cancer by incidence and the second leading cause of cancer-related mortality, with approximately 15,500 new diagnoses annually (Australian Institute of Health and Welfare, 2023). Gastro-oesophageal reflux disease (GORD) affects an estimated 10–15% of Australian adults. Inflammatory bowel disease (IBD) prevalence exceeds 100,000 Australians, with Crohn's disease and ulcerative colitis both rising in incidence. Chronic liver disease, predominantly alcohol-related liver disease and non-alcoholic fatty liver disease (NAFLD), is the eleventh leading cause of death in Australia.

Aboriginal and Torres Strait Islander Australians are disproportionately affected by GI disease. Rates of hepatocellular carcinoma are approximately 2–4 times higher than in the non-Indigenous population, driven by higher prevalence of hepatitis B infection, hepatitis C, and harmful alcohol use. Gastric cancer and gallstone-related disease are also more prevalent. Culturally safe, trauma-informed history-taking and examination are critical.

This article provides a structured approach to the GI clinical encounter — from focused history through to systematic examination and recognition of peripheral stigmata — aligned with Australian medical curricula, the RACGP Clinical Competency Standards, and evidence-based practice.

The GI history should be comprehensive and structured. Begin with the presenting complaint and use the SOCRATES framework for pain. Always screen for alarm (red-flag) symptoms. The following domains must be explored in every GI consultation.

Abdominal Pain

Abdominal pain is the most common GI presenting complaint. Characterise using SOCRATES:

Dysphagia

Dysphagia (difficulty swallowing) is a red-flag symptom that mandates urgent investigation. Always differentiate:

• Oropharyngeal (transfer) dysphagia — difficulty initiating swallow; nasal regurgitation; aspiration; suggests neurological cause (stroke, motor neurone disease, Parkinson's disease, myasthenia gravis).
• Oesophageal (transport) dysphagia — food "sticking" retrosternally after initiating swallow. Progression from solids → liquids suggests mechanical obstruction (stricture, malignancy, Schatzki ring). Intermittent dysphagia to solids and liquids suggests motility disorder (achalasia, diffuse oesophageal spasm).

Associated questions: Is dysphagia for solids, liquids, or both? Any odynophagia (painful swallowing)? Any heartburn, regurgitation, or voice change? Prior caustic ingestion? History of radiotherapy?

Nausea and Vomiting

Assess the timing, content, and character of vomiting:

• Projectile vomiting without nausea — consider raised intracranial pressure.
• Faeculent (faeces-smelling) vomiting — suggests distal bowel obstruction or gastrocolic fistula.
• Bilious (green) vomiting — small bowel obstruction below the ampulla of Vater; also gastric outlet obstruction (when no bile present).
• Blood (haematemesis) — frank red blood (active bleeding) or "coffee-ground" (digested blood, slower bleed). Emergent assessment required.
• Timing relative to meals — within 15 minutes (gastric cause); 1–3 hours (delayed gastric emptying); faeculent (distal obstruction).

Altered Bowel Habit

Document comprehensively using the Bristol Stool Chart (Types 1–7):

Rectal Bleeding

Characterise the bleeding carefully:

• Bright red blood on paper or dripping into pan — anorectal source (haemorrhoids, anal fissure, rectal polyp).
• Mixed with stool or altered colour — colonic source (colorectal cancer, IBD, diverticular disease).
• Melaena (black, tarry, offensive stools) — upper GI source (peptic ulcer, oesophageal varices, gastric malignancy).
• Occult blood (FOBT positive, no visible bleeding) — colorectal cancer screening detection; requires colonoscopy.

Weight Loss

Unintentional weight loss is a cardinal red-flag symptom:

• >5% body weight over 6 months — investigate for malignancy, malabsorption (coeliac disease, pancreatic exocrine insufficiency), IBD, or chronic infection.
• Ask about appetite (anorexia), dietary changes, dysphagia limiting intake, vomiting, diarrhoea, and steatorrhoea.
• Cachexia (severe muscle wasting) in the context of GI symptoms strongly suggests advanced malignancy or severe chronic disease.

Jaundice

Jaundice (yellow discolouration of skin and sclerae) becomes clinically apparent when serum bilirubin exceeds ~50 µmol/L. History should include:

• Duration and progression.
• Pale stools (acholic) and dark urine (tea-coloured) → obstructive (cholestatic) jaundice: gallstones, cholangiocarcinoma, pancreatic head malignancy, benign biliary stricture.
• Normal-coloured stools with dark urine → hepatocellular jaundice: hepatitis (viral, alcoholic, autoimmune, drug-induced), cirrhosis.
• Associated RUQ pain, fever, rigors → cholangitis (Charcot's triad: RUQ pain, jaundice, fever; Reynold's pentad adds hypotension and confusion).
• Pruritus suggests cholestasis (intra- or extrahepatic).

Alcohol History

Alcohol history must be quantified and documented in every GI assessment:

• Express intake in Australian standard drinks per day and per week (1 standard drink = 10 g ethanol = 285 mL full-strength beer, 100 mL wine, 30 mL spirits).
• NHMRC guideline (2020): To reduce health risk from alcohol-related disease, healthy men and women should drink no more than 10 standard drinks per week and no more than 4 standard drinks on any one day.
• Screening tools: CAGE questionnaire (Cut down, Annoyed, Guilty, Eye-opener — ≥2 positive is significant) and AUDIT-C (Alcohol Use Disorders Identification Test — Consumption).
• Duration of heavy use is critical: cumulative lifetime alcohol exposure determines liver disease risk.
• Assess for features of alcohol dependence: morning drinking, withdrawal symptoms (tremor, sweating, seizures, hallucinations), tolerance, loss of control.

Abdominal pain can be classified by mechanism: visceral (stretching of hollow viscus or capsule of solid organ — dull, poorly localised, midline), parietal/somatic (peritoneal inflammation — sharp, well-localised, worsened by movement), and referred (perceived at a site distant from the pathology — due to shared embryological dermatomes). The following patterns are essential for clinical examination in Australia:

Peptic Ulcer Disease (PUD)

Biliary Pain (Biliary Colic & Cholecystitis)

• Site: RUQ or epigastric, radiates to right shoulder tip or right subscapular region (via phrenic nerve C3–5).
• Character: Intense, constant (not truly "colicky" despite the name), builds over 30–60 minutes then plateaus; lasts 1–6 hours.
• Precipitants: Fatty meals, post-prandial (especially evening meal); may wake from sleep.
• Associated: Nausea, vomiting, restlessness (cannot find comfortable position).
• Murphy's sign: Arrest of inspiration during RUQ palpation over the gallbladder (positive in acute cholecystitis).
• Charcot's triad (cholangitis): RUQ pain + jaundice + fever ± rigors. Reynold's pentad adds hypotension and confusion (suppurative cholangitis).

Bowel Obstruction

Peritonitis

Peritoneal inflammation produces a characteristic clinical picture:

• Generalised, severe pain — worsened by any movement; patient lies still, knees drawn up.
• Rigid (guarding) abdomen — "board-like" rigidity (involuntary).
• Rebound tenderness — pain on sudden release of palpation (release tenderness).
• Percussion tenderness — pain on gentle percussion of the abdomen.
• Absent or markedly reduced bowel sounds ("silent abdomen").
• Systemic signs: Tachycardia, pyrexia, hypotension, oliguria.

Appendicitis

The classical progression of appendicitis (Alvarado score — clinical scoring system):

Rovsing's sign: Pain in the RIF when pressure is applied to the LIF. Psoas sign: Pain on right hip extension (retrocaecal appendix irritating psoas). Obturator sign: Pain on internal rotation of flexed right hip (pelvic appendix irritating obturator internus).

The abdominal examination follows the IAPP sequence: Inspection → Auscultation → Percussion → Palpation. Auscultation is performed before percussion and palpation because the act of palpation can alter bowel sounds. Always begin with general inspection of the patient.

General Signs

• General appearance: Comfortable at rest vs. writhing in pain (renal/biliary colic) vs. lying still (peritonitis). Nutritional status — cachexia, signs of weight loss.
• Face: Jaundice (examine sclerae in natural light), pallor (anaemia), angular stomatitis (iron/B12 deficiency), parotid enlargement (alcohol use), malar flush.
• Mouth: Glossitis (smooth, red tongue — B12/iron deficiency), oral ulceration (IBD — Crohn's aphthous ulcers, Behçet's), dental erosions (chronic vomiting, GORD).
• Vital signs: Temperature, heart rate, blood pressure, respiratory rate, oxygen saturation. Tachycardia + hypotension suggests significant fluid depletion, sepsis, or haemorrhage.

Inspection

• Expose the patient from xiphisternum to symphysis pubis (draping for dignity).
• Contour: Flat, distended, scaphoid (very thin), asymmetrical.
• Distension: Generalised (ascites, obesity, bowel obstruction, pregnancy) vs. localised (organomegaly, mass, bladder distension).
• Scars: Previous surgery (midline laparotomy, right subcostal for cholecystectomy, appendicectomy scar in RIF, Pfannenstiel for Caesarean/gynaecological).
• Stomas: Type (colostomy — mucosal; ileostomy — spout), content (faeculent, bile-stained), surrounding skin (excoriation suggests high-output stoma).
• Visible masses, peristalsis, hernial orifices.
• Caput medusae: Dilated periumbilical veins radiating outward — portal hypertension (patency confirmed by direction of flow: away from umbilicus).
• Abdominal wall veins: Assess direction of flow — flow away from umbilicus (portal hypertension); flow upward from umbilicus (IVC obstruction); flow downward from umbilicus (SVC obstruction).

Auscultation

• Use the diaphragm of the stethoscope. Listen in all four quadrants for at least 30 seconds in each.
• Normal: Intermittent clicks and gurgles (5–35 sounds per minute).
• Increased (hyperactive): Loud, high-pitched "tinkling" rushes — early mechanical bowel obstruction; also gastroenteritis, brisk diarrhoea.
• Absent (silent): No bowel sounds after 3 minutes of listening — ileus (post-operative, metabolic, drugs), peritonitis, late bowel obstruction (strangulation).
• Succussion splash: Rock the patient side to side while listening over the stomach — a splash >3 hours after eating suggests gastric outlet obstruction or gastroparesis.
• Aortic bruit: Systolic bruit over the aorta — aortic stenosis or aneurysm. Renal artery bruits — lateral to midline, suggests renal artery stenosis.
• Friction rubs: Liver (perihepatitis — Fitz-Hugh-Curtis syndrome) or spleen (splenic infarct, perisplenitis).

Percussion

• Begin in the right iliac fossa and systematically percuss all nine regions.
• Liver span: Percuss from the right iliac fossa upward. Normal dullness: 6–12 cm in the mid-clavicular line (varies with body habitus). Loss of liver dullness over the RUQ may indicate free air under the diaphragm (perforation).
• Splenic percussion (Traube's space): Bounded by the left costal margin, anterior axillary line, and the horizontal line at the level of the lower border of the left tenth rib. Normally tympanitic. Dullness suggests splenomegaly (sensitivity increases when combined with percussion during inspiration).
• Shifting dullness (for ascites): Percuss from the centre outward with the patient supine. Mark the boundary between tympany and dullness. Turn the patient on their side and re-percuss — if the dullness shifts, ascites is likely. A fluid thrill (transmitted impulse) suggests large-volume ascites (>1.5 L).
• Bladder distension: Suprapubic dullness.

Palpation

Begin away from the site of pain, and ask the patient to breathe through the mouth to relax the abdominal wall muscles. Always use the flat of the hand initially (superficial palpation), then deeper pressure.

• Superficial palpation: Assess for tenderness, guarding (voluntary — patient tenses on approach; involuntary — constant rigidity indicating peritonitis), and superficial masses.
• Deep palpation: Systematically palpate all nine regions. Assess for deep masses and organomegaly.

Liver Palpation

• Start in the right iliac fossa with the flat of the hand, fingers pointing toward the right costal margin.
• Ask the patient to take a deep breath — feel the liver edge descend toward your fingers on inspiration.
• Walk your fingers cephalad after each breath until you feel the liver edge (or reach the costal margin).
• Describe: size (cm below costal margin or in cm span), surface (smooth vs. irregular/nodular), consistency (soft, firm, hard), tenderness, and edge (sharp vs. rounded).

Spleen Palpation

• Begin in the right iliac fossa, moving diagonally toward the left costal margin.
• Ask the patient to breathe deeply through the mouth. The spleen tip may be felt descending on inspiration.
• If not palpable, roll the patient onto their right side (left side up) and re-palpate — this brings the spleen forward and closer to the palpating hand.
• A normal spleen is not palpable. A palpable spleen is at least 1.5–2 times normal size.

Kidney Palpation (Bimanual Ballottement)

• Place one hand posteriorly in the renal angle (loin) and the other anteriorly on the abdomen over the expected position of the kidney.
• Press the posterior hand firmly forward and attempt to "bounce" the kidney between both hands (ballottement).
• A palpable kidney is abnormally enlarged (polycystic kidney disease, hydronephrosis, renal cell carcinoma) or displaced (horseshoe kidney).
• Percussion for renal tenderness: Gently strike the fist placed over the costovertebral angle — tenderness suggests pyelonephritis or perinephric abscess (renal angle tenderness).

Masses

When a mass is palpated, characterise using the mnemonic LLSSCC:

• Location — which region/quadrant?
• Loss of localisation (anterior vs. posterior — is it ballotable?)
• Size — measure in centimetres or use anatomical landmarks (e.g., "3 cm below costal margin")
• Surface — smooth, irregular, nodular
• Consistency — soft (lipoma, cyst), firm (fibroid), hard (malignancy, faeces)
• Characteristics — pulsatile (AAA, aortic aneurysm — assess for expansile vs. transmitted pulsation), mobile, tethered, tender

Digital Rectal Examination (DRE)

DRE is an essential component of the GI examination when rectal bleeding, faecal incontinence, prostate disease, or pelvic pathology is suspected:

• Explain the procedure and gain verbal consent. Position: left lateral (Sims' position) with knees drawn up.
• Inspect the perianal region first: fissures (sentinel pile), haemorrhoids (prolapsed, thrombosed), fistulae, abscesses, warts, malignancy.
• Lubricate the gloved index finger and gently insert, noting sphincter tone (reduced in cauda equina, pudendal neuropathy).
• Palpate circumferentially: mucosal masses, faecal loading, prostate (smooth, enlarged = benign prostatic hyperplasia; hard, irregular, fixed = carcinoma).
• Withdraw and inspect the glove for stool colour (melaena, clay-coloured) and blood.

Systemic stigmata of GI and hepatobiliary disease are frequently visible on general and targeted examination. A systematic approach — beginning with the hands, arms, face, and trunk — is essential for clinical examination and provides valuable diagnostic clues.

Hands and Arms

Face

• Jaundice: Yellow discolouration of sclerae (best examined in natural light by asking the patient to look upward), skin, and sublingual tissue. Bilirubin >50 µmol/L to become clinically apparent.
• Pallor: Anaemia — conjunctival pallor (pull down lower eyelid), palmar creases (should be pink, not white). Iron deficiency is common in coeliac disease, IBD, and GI malignancy.
• Angular stomatitis / cheilosis: Cracking at the corners of the mouth — iron deficiency, B12 deficiency, riboflavin deficiency, ill-fitting dentures.
• Glossitis: Smooth, red, painful tongue — iron deficiency (atrophic papillae), B12 deficiency (beefy red tongue).
• Parotid gland enlargement: Bilateral — chronic alcohol use; also Sjögren's syndrome, HIV, bulimia.
• Kayser-Fleischer rings: Golden-brown copper deposits at the periphery of the cornea (Descemet's membrane) — Wilson's disease (a cause of liver disease in young patients).

Spider Naevi

Spider naevi (spider angiomas) are vascular lesions consisting of a central arteriole with radiating small vessels. Key features:

• Appearance: Central red punctum with radiating "legs" (capillaries); blanch on pressure and refill from the centre outward.
• Distribution: Upper body — face, neck, upper chest, upper arms, and hands (above the level of the nipple — in the SVC drainage territory). Look in the dermatomes of C3, C4, C5.
• Clinical significance: ≥5 spider naevi are highly specific for chronic liver disease / cirrhosis (hyperoestrogenism due to impaired hepatic oestrogen metabolism). Isolated spider naevi may occur in pregnancy and are normal in children.
• Pathophysiology: Increased circulating oestrogen (normally metabolised by the liver) causes vasodilatation mediated by nitric oxide.

Palmar Erythema

Bilateral, symmetrical redness of the palms, most prominent on the thenar and hypothenar eminences, with sparing of the central palm (though in severe cases the entire palm may be involved). A common finding in chronic liver disease (occurring in up to 23% of patients with cirrhosis). Also seen in pregnancy, rheumatoid arthritis, and as a normal variant in approximately 10% of the population. Caused by hyperdynamic circulation and peripheral vasodilatation.

Gynaecomastia

Enlargement of male breast tissue due to oestrogen-androgen imbalance. Characteristically tender, subareolar, and palpable as a firm disc of tissue beneath the nipple. Distinguished from lipomastia (pseudogynaecomastia — diffuse fatty enlargement without a discrete disc) by careful palpation.

• GI causes: Cirrhosis (alcoholic and non-alcoholic — impaired oestrogen metabolism), alcoholic liver disease (direct testicular atrophy), spironolactone therapy.
• Other causes: Puberty (physiological), testicular tumours, Klinefelter syndrome, drug-induced (cimetidine, oestrogens, anabolic steroids, marijuana, phenytoin), hyperthyroidism.

Ascites

Ascites is pathological accumulation of fluid in the peritoneal cavity. Clinical examination techniques:

Causes of ascites (use serum-ascites albumin gradient [SAAG] to differentiate):

Other Peripheral Signs

• Testicular atrophy: Bilateral small, soft testes — chronic alcohol use (direct toxic effect + oestrogen excess), liver cirrhosis, Klinefelter syndrome.
• Axillary hair loss: Reduced axillary hair in women — may occur with hypoandrogenism secondary to cirrhosis.
• Loss of body hair: Generalised hair thinning — malnutrition, coeliac disease, chronic illness.
• Peripheral oedema: Bilateral pitting ankle oedema — hypoalbuminaemia (cirrhosis, nephrotic syndrome, malnutrition), right heart failure, DVT. Unilateral — DVT, venous insufficiency.
• Scratch marks (excoriations): Pruritus — cholestatic liver disease (primary biliary cholangitis, primary sclerosing cholangitis, drug-induced cholestasis, obstructive jaundice).
• Tattoo or injection marks: May indicate intravenous drug use — hepatitis B/C risk.

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