Abdominal pain, peritonitis and resuscitation

Pathophysiology of Abdominal Pain & Peritoneal Innervation

Evaluating the acute abdomen is one of the most critical clinical competencies assessed in the Australian Medical Council (AMC) Examination. The acute abdomen encompasses a broad spectrum of surgical, medical, and gynaecological emergencies characterised by acute abdominal pain of rapid onset (typically lasting less than 24 to 48 hours) that frequently mandates urgent surgical or procedural intervention.

Accurate clinical assessment requires a firm understanding of the neuroanatomical origins of abdominal pain and the embryological derivation of the gastrointestinal tract.

Visceral Pain

Visceral peritoneum and the muscular walls of hollow abdominal viscera are innervated by bilateral, unmyelinated sensory C fibres that travel alongside autonomic sympathetic nerves back to corresponding spinal cord dorsal horn segments:

• Mechanisms of Stimulation: Visceral receptors are insensitive to cutting, burning, or crushing. They respond exclusively to smooth muscle stretch, distension of a hollow viscus, capsular distension of solid organs (e.g., liver, spleen), contraction against obstruction, and acute ischaemia.
• Pain Characteristics: Visceral pain is typically dull, aching, cramping, or colicky. Because sensory inputs from bilateral organs enter multiple spinal cord levels and have sparse cortical representation, visceral pain is poorly localized and always perceived in the embryological midline.
• Embryological Localization:
  • Foregut (Stomach, duodenum to ampulla of Vater, liver, biliary tree, pancreas): Innervated by sympathetic fibres from T5 to T9; pain is perceived in the epigastrium.
  • Midgut (Duodenum distal to ampulla, jejunum, ileum, appendix, caecum, ascending colon, proximal two-thirds of transverse colon): Innervated by T10 to T11; pain is perceived in the periumbilical region.
  • Hindgut (Distal one-third of transverse colon, descending colon, sigmoid colon, rectum): Innervated by T12 to L2; pain is perceived in the hypogastrium / suprapubic area.

Somatic (Parietal) Pain

The parietal peritoneum, anterior abdominal wall musculature, and root of the mesentery receive somatic sensory innervation via myelinated A-delta fibres travelling within spinal nerves T7 through L1:

• Mechanisms of Stimulation: Somatic receptors respond directly to chemical, mechanical, thermal, and infectious irritation. Irritants include gastric hydrochloric acid, pancreatic enzymes, bile, enteric contents, blood, and bacterial toxins.
• Pain Characteristics: Somatic pain is intense, sharp, constant, and precisely localized to the anatomical site of inflammation. Movement, deep inspiration, and coughing exacerbate the pain, compelling the patient to remain motionless with hips flexed.

Referred Pain Patterns

Referred pain occurs when visceral afferent fibres converge upon the same second-order neurons within the dorsal horn of the spinal cord that receive somatic afferents from distant cutaneous dermatomes:

• Diaphragmatic Irritation (Kehr Sign): Irritation of the central diaphragmatic peritoneum by blood (splenic rupture), subphrenic abscess, or perforated ulcer is mediated by the phrenic nerve ($C3, C4, C5$) and refers pain to the ipsilateral supraclavicular area / shoulder tip.
• Biliary Colic: Afferents from the gallbladder and biliary tree travel via the greater splanchnic nerves ($T5-T9$) and refer pain to the inferior angle of the right scapula (Boas sign).
• Ureteric Colic: Distension of the renal pelvis and ureter ($T10-L2$) produces loin-to-groin colic radiating into the labia majora or ipsilateral hemiscrotum.

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Signs of Localized vs. Generalized Peritonitis

Peritonitis represents inflammation of the peritoneal serosa. Clinical examination must rigorously differentiate voluntary abdominal tensing from involuntary signs of true peritoneal irritation:

Localized Peritonitis

Inflammation remains confined to a single anatomical region (e.g., localized to the right iliac fossa in uncomplicated appendicitis, or the right upper quadrant in acute cholecystitis):

• Involuntary Guarding: Reflexive spasm of the abdominal wall musculature overlying the inflamed organ upon palpation. Unlike voluntary guarding—which is a conscious contraction triggered by cold hands, anxiety, or ticklishness that softens with gentle reassurance and deep breathing—involuntary guarding cannot be relaxed voluntarily.
• Percussion Tenderness: Gentle percussion over the affected quadrant generates a localized fluid wave or peritoneal vibration that elicits exquisite focal pain. Percussion tenderness is an exceptionally sensitive marker of localized peritonitis and is far less traumatic to the patient than rebound tenderness.
• Rebound Tenderness (Blumberg Sign): Sudden release of deep manual pressure causes the parietal peritoneum to snap back against inflamed viscera, inducing severe pain. Because rebound tenderness causes severe distress, gentle percussion tenderness and the "cough test" have largely supplanted it in modern Australian surgical practice.
• Dunphy Sign: Exacerbation of localized abdominal pain elicited by coughing, indicating focal parietal peritoneal friction.
• Carnett Test: Differentiates abdominal wall pain (e.g., rectus sheath haematoma, cutaneous nerve entrapment) from intra-abdominal visceral pain. The clinician applies pressure to the tender abdominal area while the patient performs a partial sit-up or tenses the abdominal wall by lifting their head or legs. If pain increases or remains unchanged, the pathology originates within the abdominal wall; if pain decreases, the pathology is intra-abdominal (as the tensed rectus muscles shield the inflamed viscera from palpation).

Generalized Peritonitis

Generalized peritonitis arises when an intra-abdominal hollow organ ruptures (e.g., perforated duodenal ulcer, stercoral perforation of the sigmoid colon) or when a localized infection escapes physiological containment, contaminating all four quadrants:

• Board-Like Rigidity: Involuntary, unrelenting, rock-hard contraction of the entire anterior abdominal wall musculature that persists throughout all phases of respiration. It represents widespread reflex somatomotor spasm and is the hallmark of generalized peritonitis.
• Absent Bowel Sounds: Chemical and bacterial irritation of the autonomic mesenteric plexus induces a diffuse adynamic paralytic ileus, producing an eerily silent abdomen on auscultation (listening for at least 2 full minutes).
• Systemic Sepsis: Tachycardia, tachypnoea, arterial hypotension, high fevers or hypothermia, oliguria, and profound diaphoresis.

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Emergency Resuscitation & Multimodal Analgesia

The initial management of an unstable acute abdomen prioritises physiological stabilization over immediate definitive imaging:

Initial Stabilization Protocol

1. Airway and High-Flow Oxygen: Assess airway patency and administer titrated supplemental oxygen if $SpO_2 < 94\%$ (or $88-92\%$ in hypercapnic respiratory failure).
2. Large-Bore Intravenous Access: Insert two wide-bore ($16\text{G}$ or $14\text{G}$) peripheral intravenous cannulae into antecubital veins. Draw urgent bloods: full blood count, electrolytes, urea, creatinine, liver biochemistry, serum lipase, venous/arterial blood gas with lactate, coagulation profile, and group and hold / cross-match.
3. Intravenous Fluid Resuscitation: Administer an immediate bolus of balanced isotonic crystalloid (e.g., Plasmalyte or Hartmann solution, $10-20\text{ mL/kg}$ or $500-1000\text{ mL}$ over 30 minutes) to correct intravascular volume contraction resulting from third-space sequestration, vomiting, and diaphoresis.
4. Strict Nil-By-Mouth (NBM): Withhold all oral liquids and solids in anticipation of emergency general anaesthesia and surgical exploration.
5. Indwelling Urinary Catheter: Insert a urinary catheter with an hourly urometer to track end-organ perfusion, titrating fluid resuscitation to maintain urine output $\ge 0.5\text{ mL/kg/h}$.
6. Nasogastric Tube (NGT): Insert a wide-bore ($14-16\text{ Fr}$) Salem sump nasogastric tube on free drainage if bowel obstruction, intractable vomiting, or gastrointestinal perforation is suspected, preventing pulmonary aspiration and decreasing intraluminal gastric tension.
7. Urgent General Surgical Consultation: Involve the surgical team immediately upon identifying signs of peritonitis or haemodynamic collapse.

Multimodal Analgesia: Debunking the Opioid Myth

For decades, an erroneous dogma persisted in clinical medicine that administering opioid analgesia to patients with an acute abdomen would "mask physical signs," obscure peritoneal irritation, and lead to delayed or inappropriate surgical intervention.

• Current Evidence: High-quality randomized controlled trials and Cochrane systematic reviews have conclusively demonstrated that titrated intravenous opioids provide essential pain relief without diminishing diagnostic accuracy, altering peritoneal signs (guarding and rigidity persist despite analgesia), or increasing morbidity or mortality.
• Australian Standard of Care: Therapeutic Guidelines (eTG) mandate early, effective, titrated parenteral analgesia for acute abdominal pain:
  • First-Line: Intravenous morphine ($2.5-5\text{ mg}$ IV every 5 to 10 minutes, titrated to effect) or intravenous fentanyl ($25-50\ \mu\text{g}$ IV, preferred in renal impairment or haemodynamic instability due to lack of active metabolites and minimal histamine release).
  • Adjuncts: Intravenous paracetamol ($1\text{ g}$ IV 6-hourly) should be co-administered. Non-steroidal anti-inflammatory drugs (NSAIDs) such as ketorolac or ibuprofen should be avoided in undifferentiated acute abdomen until perforation, gastrointestinal bleeding, and acute renal impairment are excluded.
  • Antiemetics: Co-administer intravenous ondansetron ($4-8\text{ mg}$) or metoclopramide ($10\text{ mg}$, avoiding metoclopramide if complete mechanical bowel obstruction is suspected due to prokinetic action).

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Primary references (checked 7 October 2026): WSES perforated-ulcer guidance.