GI System Clinical Examination

1. History Taking

Chief Complaint & Character of Symptoms

• Site: Localizes to a quadrant (e.g., RUQ → biliary/hepatic, RLQ → appendix/ileocecal, LLQ → sigmoid/colon, epigastric → gastric/duodenal/pancreatic)
• Onset: Sudden ("bolt of lightning") suggests perforation or vascular catastrophe; insidious suggests inflammation or neoplasm
• Character: Crampy/colicky (hollow viscus — bowel obstruction, biliary colic), burning (PUD, GERD), tearing (aortic dissection), dull/aching (solid organ)
• Radiation: To the right shoulder (biliary/diaphragmatic); to the back (pancreatitis, AAA); to the groin (ureteral colic)
• Severity & Timing: Constant vs. episodic; relationship to meals (biliary pain after fatty foods; duodenal ulcer relieved by eating; gastric ulcer or mesenteric ischemia worsened by eating)
• Exacerbating/relieving factors: Peritonitis → patient lies still; visceral pain (renal colic, early appendicitis) → patient writhes

Associated Symptoms

• Nausea & vomiting: Clear vomitus → gastric outlet obstruction; feculent vomitus → distal small bowel or colonic obstruction
• Dysphagia/odynophagia: Points to esophageal pathology
• Anorexia, weight loss: Suggest malignancy, chronic inflammation, malabsorption
• Bowel habit changes: Diarrhea, constipation, tenesmus, hematochezia, melena, steatorrhea
• Jaundice, dark urine, pale stools: Biliary obstruction or hepatocellular disease
• Fever, chills, night sweats: Infectious or inflammatory process
• Flatulence, bloating: Malabsorption, IBS, bacterial overgrowth

Past Medical & Drug History

Family & Social History

2. General Inspection

• General appearance: Pallor (anemia from GI blood loss), cachexia (malignancy, malabsorption), jaundice
• Posture and movement: A patient lying absolutely still, guarding the abdomen → peritonitis; a patient writhing → visceral/colic pain. Gentle shaking of the bed elicits sharp pain in peritonitis but not visceral pain
• Vital signs: Hemodynamic instability (hypotension, tachycardia) → urgent surgical cause (perforated viscus, ruptured AAA, hemorrhage). Tachypnea may indicate metabolic acidosis (DKA, mesenteric ischemia)
• Breathing pattern: Shallow, rapid breathing → intraabdominal sepsis or peritonitis

3. Peripheral Signs (Hands to Toes)

4. Abdominal Examination

4.1 Inspection

• Abdominal distension: The 6 Fs — Fat, Fluid (ascites), Flatus, Faeces, Foetus, Fibroid/mass; or the catastrophic 7th — Fatal (obstruction/volvulus)
• Surgical scars: Location suggests prior procedures; may hint at adhesion-related obstruction
• Dilated veins (caput medusae): Periumbilical venous engorgement radiating outward implies recanalization of the umbilical vein in portal hypertension

• Skin findings: Herpes zoster (dermatomal vesicles suggesting zoster affecting T6–T12); striae (Cushing's syndrome, rapid weight gain); jaundiced skin
• Cullen's sign: Periumbilical ecchymosis → retroperitoneal hemorrhage (e.g., acute hemorrhagic pancreatitis, ruptured AAA)
• Grey-Turner's sign: Flank ecchymosis → same causes as Cullen's
• Visible peristalsis: Suggests gastric outlet obstruction or small bowel obstruction (ladder pattern)
• Pulsatile mass in epigastrium: Suggests AAA
• Umbilical hernias: Often present in long-standing ascites

4.2 Auscultation

• Normal bowel sounds: Intermittent, low-pitched gurgles every 5–15 seconds
• Absent bowel sounds: Listen for at least 2 minutes in more than one quadrant before declaring silent. Complete absence → peritonitis or adynamic (paralytic) ileus
• High-pitched, rushing, hyperactive sounds synchronous with crampy pain → mechanical small bowel obstruction (the "borborygmi" or "tinkling" of obstruction)
• Bruit over the aorta/renal arteries: Vascular stenosis, AVM
• Succussion splash: Splashing sound on shaking the patient → gastric outlet obstruction (retained fluid in stomach)
• Stethoscope palpation trick: Press the stethoscope gently onto an area of suspected tenderness while appearing to auscultate — notable discrepancy with manual palpation suggests functional/non-organic pain

4.3 Percussion

• Tympany (resonance): Air-filled bowel — normal over most of abdomen
• Dullness: Solid organ or fluid

• Tympanic throughout → gaseous distension (obstruction, ileus, aerophagia)
• Dullness in flanks (flank dullness) → ascites (highest sensitivity at 94%)

1. Patient supine — percuss from midline toward the right flank until dullness is detected (the air-fluid interface)
2. Mark the spot; ask the patient to roll toward you (lateral decubitus)
3. Re-percuss at the same spot — if now tympanic, shifting dullness is confirmed (fluid has moved with gravity)
4. Repeat on the other side for confirmation

• Shifting dullness is the most sensitive clinical sign for ascites; its absence reliably rules it out

• Place the ulnar border of an assistant's hand firmly on the abdomen's midline (to dampen transmission through the abdominal wall)
• Tap one lateral flank sharply — the transmitted wave is felt by the examiner's other hand on the opposite flank
• Positive fluid wave has highest specificity for ascites among bedside signs
• Positive predictors (in order of sensitivity): flank dullness 94%, shifting dullness, fluid wave

• Liver is dull on percussion
• Percuss the right upper quadrant from above (noting upper border of liver dullness, normally ~5th intercostal space) and from below (ascending from RLQ until dullness is reached)
• Liver span in the mid-clavicular line: normally 6–12 cm
• Diminished span → cirrhosis (shrunken liver) or free gas (perforated viscus produces loss of liver dullness)
• Increased span → hepatomegaly (congestion, infiltration, malignancy, NAFLD)

• Dullness to percussion between the 9th and 11th ribs in the left midaxillary line suggests splenomegaly
• Normally, the left midaxillary line is tympanic (gastric air bubble)
• Traube's space (6th rib above, midaxillary line laterally, left costal margin below): dullness here suggests splenomegaly or pleural effusion

4.4 Palpation

• Detects superficial tenderness, guarding, skin hypersensitivity
• Guarding: Involuntary reflex increase in abdominal wall muscle tone, present throughout the respiratory cycle (vs. voluntary guarding, which relaxes during inspiration or with distraction)
• Rigidity: Severe form of involuntary guarding — "board-like" abdomen; indicates advanced peritonitis
• Pain with gentle percussion or light palpation → peritonitis
• The traditional rebound tenderness test (deep pressure then sudden release) should be abandoned — it causes unnecessary pain and is no more accurate than percussion for detecting peritonitis

• Detects organomegaly, masses, deep tenderness
• A pulsatile, tender epigastric mass → AAA
• Evaluate all hernial orifices (inguinal, femoral, umbilical) and surgical scars for incarcerated hernias

4.5 Organ-Specific Palpation

Liver

• Begin in the right lower quadrant and move upward toward the costal margin, so the edge is felt as you ascend on inspiration
• Normal liver edge: smooth, slightly tender, up to 2 cm below the right costal margin in thin individuals
• Hepatomegaly: Tender, enlarged, smooth → acute viral hepatitis, alcoholic hepatitis, hepatic congestion (right heart failure); Hard, irregular → cirrhosis; Multiple nodules → metastatic disease
• Scratch test: Bell of stethoscope over RUQ; scratch the skin moving from mid-abdomen toward the liver — amplified sound localizes the liver edge (useful when obesity or ascites obscures palpation)
• Ballot test / dipping method: In the presence of ascites, apply a quick downward pressure with fingertips below the costal margin to "ballot" the liver edge up through the fluid

Gallbladder

• Not normally palpable
• Murphy's sign: Place fingers under the right costal margin at the midclavicular line; ask the patient to take a deep breath — a positive sign is the patient abruptly stopping inspiration due to pain as the inflamed gallbladder descends onto the examiner's fingers; indicates acute cholecystitis (sensitivity ~65%, specificity ~87%)
• Courvoisier's law: A palpable, non-tender gallbladder in a jaundiced patient → malignant biliary obstruction (pancreatic head carcinoma), not cholelithiasis

Spleen

• Begin in the right lower quadrant and move diagonally toward the left costal margin (an enlarged spleen enlarges toward the RLQ)
• Normal spleen is not palpable; a palpable spleen tip = splenomegaly
• Ballotment: If not palpable, place one hand behind the left lower thorax and push forward; palpate anteriorly to feel the spleen between both hands
• Splenomegaly in chronic liver disease → portal hypertension; also seen in acute viral hepatitis, infiltrative disorders
• The splenic notch may be felt on its medial border, distinguishing it from other masses

Kidneys

• Bimanual palpation: one hand posteriorly in the renal angle, one anteriorly on the abdomen — "ballot" the kidney
• Normal kidneys are not palpable except in thin individuals
• Ballottable, enlarged kidneys → polycystic kidney disease, hydronephrosis, renal tumors
• Renal angle tenderness (CVAT): Fist percussion at the costovertebral angle → pain in pyelonephritis or perinephric abscess

4.6 Special Maneuvers

5. Rectal Examination (Digital Rectal Examination, DRE)

• Anal sphincter tone: Decreased in neurological disease; increased in anal fissure (protective spasm)
• Rectal masses or polyps
• Stool character: Presence, consistency, color; test for occult blood (FOBT)
• Blood: Bright red (lower GI source) or melaenic stool (upper GI source)
• Prostate (in males): Size, tenderness, consistency — enlarged/nodular → carcinoma; tender → prostatitis
• Uterus/cervix (in females): Via vaginal/rectal palpation of the pelvis
• Peritoneal inflammation: "Hot Douglas" — exquisite tenderness on anterior wall of rectum (anterior pouch of Douglas) → pelvic peritonitis, pelvic abscess, perforated appendix

6. Completion of the Examination

• Hernia orifices: Inguinal, femoral, umbilical, incisional
• Genitalia: Always examined in patients with acute abdominal pain; scrotal edema in ascites
• Chest examination: Rales and elevated JVP → right heart failure causing hepatic congestion; basal dullness → pleural effusion (hepatic hydrothorax)
• Cardiovascular: Atrial fibrillation → mesenteric arterial embolism
• Lymphadenopathy: Axillary, inguinal, Virchow's node (left supraclavicular) for GI malignancy
• Skin: Jaundice, scratch marks, ecchymoses, telangiectasias

7. Summary: Key Signs and Their Significance

Conditions Causing Eosinophilia

Master Mnemonic: "NAACP DIABETES"

(Each letter = a category)

Simpler Mnemonic: "CHINA PAD"

(Commonly used in clinical exams)

Detailed Category Breakdown

1. Parasites — "WASH" (most common worldwide cause)

Wuchereria bancrofti · Ascaris · Strongyloides · Hookworm

• Tissue-invasive helminths cause higher eosinophilia than luminal parasites
• Trichinella (muscle invasion), Toxocara (visceral larva migrans) → marked eosinophilia
• Protozoa: Dientamoeba fragilis, Isospora belli (rare)

2. Allergic / Atopic Diseases

• Asthma, allergic rhinitis, urticaria, atopic dermatitis
• Mechanism: IgE-mediated → IL-5 surge → eosinophil recruitment

3. Pulmonary Eosinophilia — "TALE"

Tropical pulmonary eosinophilia · Acute eosinophilic pneumonia · Löffler syndrome · Eosinophilic chronic pneumonia + ABPA

• Löffler syndrome: Transient pulmonary infiltrates + eosinophilia during larval lung migration
• TPE: Paroxysmal cough, bronchospasm, very high eosinophilia; caused by Wuchereria bancrofti
• ABPA (Allergic bronchopulmonary aspergillosis): Asthmatic + IgE ↑ + central bronchiectasis

4. Drugs

• Drug reaction with eosinophilia and systemic symptoms = DRESS syndrome

5. Neoplasms

• Hodgkin lymphoma and peripheral T-cell lymphoma: Paraneoplastic cytokine-driven eosinophilia
• Eosinophilic leukemia (FIP1L1-PDGFRA mutation): Clonal, responds to imatinib
• Myeloproliferative neoplasms, mastocytosis
• Solid tumors (lung, cervix, bladder): Advanced-stage paraneoplastic

6. Connective Tissue / Vasculitis

• EGPA (Churg-Strauss syndrome): Asthma + sinusitis + eosinophilia + small-vessel vasculitis
• PAN, SLE, RA

7. Idiopathic Hypereosinophilic Syndrome (HES)

• Eosinophils >1500/µL for >6 months + no secondary cause + end-organ damage (cardiac, neurologic, pulmonary)
• Subtypes: Myeloid (PDGFRA/B mutations) vs. lymphocytic vs. idiopathic

8. Addison's Disease (Adrenal Insufficiency)

• Cortisol normally promotes eosinophil apoptosis; its deficiency → accumulation
• Classic teaching: morning cortisol trough causes physiologic eosinophilia → exaggerated in Addison's

9. Skin Disorders

• Eosinophilic fasciitis, eosinophilic cellulitis (Wells syndrome), eosinophilic folliculitis, episodic angioedema with eosinophilia

10. GI Disorders

• Eosinophilic esophagitis, eosinophilic gastroenteritis, eosinophilic colitis
• IBD can have mild eosinophilia

11. Miscellaneous

• Transplant rejection
• Retroviral infections: HIV, HTLV-1
• Eosinophilia-myalgia syndrome: L-tryptophan ingestion (historical)
• Atheroembolic disease
• Interstitial nephritis
• Premature birth (neonatal eosinophilia — ~75% of low-birth-weight infants)

Degree of Eosinophilia: Quick Reference

Quick Recall Summary Mnemonic: "INDIA"

(For rapid exam recall — the 5 most tested causes)