7.1 Acute Abdomen: Peritonitis, Appendicitis & Acute Cholecystitis

Neuroanatomy & Clinical Triage of the Acute Abdomen

The term acute abdomen denotes acute intra-abdominal disease of sudden onset that frequently necessitates urgent surgical evaluation and intervention. Effective clinical triage begins with understanding the neuroanatomical origins of abdominal pain, which dictate its quality, localization, and progression.

Visceral Pain vs. Somatic Parietal Pain

• Visceral Pain: Arises from mechanical stretching, distension, ischemia, or smooth muscle spasm affecting hollow abdominal organs. It is transmitted via unmyelinated autonomic C-fibers travelling with sympathetic nerves to the central nervous system. Because sensory innervation to the viscera is multi-segmental with few nerve endings, visceral pain is dull, deep, crampy, poorly localized, and referred to the midline according to the embryological origin of the affected organ:
  • Foregut Structures (Stomach, Duodenum Proximal to the Major Papilla, Liver, Gallbladder, Pancreas): Innervated by T5 to T9 spinal segments via the greater splanchnic nerve; pain is referred to the epigastrium.
  • Midgut Structures (Duodenum Distal to the Major Papilla, Jejunum, Ileum, Appendix, Cecum, Ascending Colon, Proximal Two-Thirds of Transverse Colon): Innervated by T10 to T11 spinal segments via the lesser splanchnic nerve; pain is referred to the periumbilical region.
  • Hindgut Structures (Distal Third of Transverse Colon, Descending Colon, Sigmoid Colon, Rectum): Innervated by T12 to L1 spinal segments via lumbar splanchnic nerves; pain is referred to the hypogastrium (suprapubic region).
• Somatic (Parietal) Pain: Arises when the overlying parietal peritoneum becomes irritated by inflammation, bacterial contamination, or chemical agents (gastric acid, bile, blood). It is transmitted via myelinated A-delta nerve fibers within somatic spinal nerves (T6 to L1). Somatic pain is intense, sharp, constant, and precisely localized to the anatomical site of the inflamed peritoneal surface.

Clinical Hallmarks of Peritonitis

Peritonitis represents inflammation of the peritoneal serosa and is classified as localized (confined to a single anatomical quadrant or recess) or generalized (diffuse involvement of the peritoneal cavity):

1. Involuntary Guarding: Reflexive spasm and contraction of the abdominal wall musculature elicited by gentle palpation, reflecting localized somatic parietal peritoneal irritation. Unlike voluntary guarding (which relaxes with slow, deep exhalation or reassurance), involuntary guarding is persistent and uncontrollable.
2. Board-Like Muscular Rigidity: Severe, involuntary, tonic contraction of the entire abdominal wall musculature. It is the hallmark of generalized peritonitis, characteristically seen in catastrophic chemical peritonitis following a perforated peptic ulcer or acute feculent peritonitis from colonic perforation.
3. Percussion Tenderness: Eliciting sharp pain by gentle tapping over the abdominal wall. Percussion produces minimal displacement of the peritoneum and is far more humane and diagnostic for detecting peritoneal inflammation than aggressive manual rebound testing.
4. Rebound Tenderness (Blumberg's Sign): Sharp, stabbing pain experienced when deep, sustained manual pressure on the abdominal wall is abruptly released. While historically popular, it causes unnecessary patient discomfort and should be superseded by gentle percussion tenderness or coughing tenderness.
5. Coughing Tenderness (Dunphy's Sign): An acute increase in localized pain triggered when the patient is instructed to cough, shifting the inflamed parietal peritoneum against the visceral organs.

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Acute Appendicitis: Pathophysiology & Clinical Progression

Acute appendicitis is the most common non-traumatic surgical emergency worldwide, with a lifetime risk of approximately 7% to 8%.

Pathophysiological Cascade

1. Luminal Obstruction: The primary inciting event in over 80% of cases. In adults, obstruction is most commonly caused by an appendicolith (fecalith), inspissated barium, foreign bodies, or rarely an underlying carcinoid (neuroendocrine) tumor or cecal adenocarcinoma. In children, adolescents, and young adults, obstruction is predominantly driven by lymphoid follicular hyperplasia in the submucosa, often provoked by acute viral infections (adenovirus, measles) or gastroenteritis.
2. Increased Intraluminal Pressure & Venous Congestion: The appendiceal mucosal epithelium continues to secrete mucus, distending the closed-loop lumen. As intraluminal pressure exceeds capillary and venous filling pressure (around 20 to 30 mmHg), mucosal venous outflow becomes obstructed, producing mucosal edema, cellular ischemia, and loss of the protective mucosal barrier.
3. Bacterial Invasion & Transmural Necrosis: Commensal colonic bacteria (principally Escherichia coli, Bacteroides fragilis, Peptostreptococcus, and Pseudomonas) proliferate rapidly and invade the ischemic appendiceal wall. Bacterial invasion accelerates transmural inflammation, progressing to gangrenous appendicitis.
4. Perforation & Peritonitis: Continued arterial thrombosis leads to full-thickness ischemic gangrene (typically along the antimesenteric border where blood supply is poorest). The appendix perforates, discharging purulent and fecal contents into the peritoneal cavity, resulting in either a contained phlegmon/abscess or diffuse generalized peritonitis.

The Classic Symptom Progression

• Early Visceral Stage (0 to 12 Hours): Obstruction and acute luminal distension stimulate unmyelinated visceral afferent fibers travelling with the sympathetic nervous system to the T10 spinal level. The patient experiences dull, aching, crampy, poorly localized pain centered in the periumbilical region, accompanied by autonomic symptoms: profound anorexia (the 'hamburger sign', where the patient refuses favorite food), nausea, and one or two episodes of vomiting.
• Late Somatic Stage (12 to 24 Hours): As transmural inflammation extends through the serosa to irritate the adjacent somatic parietal peritoneum of the right iliac fossa, the pain migrates to the right lower quadrant (McBurney's point). The pain transforms into a sharp, constant, intense, localized ache exacerbated by walking, coughing, or sudden movement.
• McBurney's Point: Anatomically located precisely one-third of the distance along a line drawn from the right anterior superior iliac spine (ASIS) to the umbilicus.

Physical Examination Signs

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The Alvarado Clinical Scoring System (MANTRELS)

The Alvarado score stratifies patients presenting with suspected acute appendicitis to guide admission, imaging, or urgent operative intervention:

• Symptoms:
  • Migration of pain to the right lower quadrant: 1 point
  • Anorexia: 1 point
  • Nausea or vomiting: 1 point
• Signs:
  • Tenderness in the right lower quadrant: 2 points (cardinal sign)
  • Rebound tenderness in the right lower quadrant: 1 point
  • Elevated temperature (>= 37.3°C / 99.1°F): 1 point
• Laboratory Findings:
  • Leukocytosis (WBC >= 10.0 x 10^9/L): 2 points (cardinal sign)
  • Shift of leukocytes to the left (neutrophils >= 75%): 1 point
• Total Possible Score: 10 points

Clinical Interpretation & Action Thresholds

• Score 1 to 4 (Low Probability): Consider discharge only if clinically well, symptoms are improving and follow-up is reliable; give clear return precautions. Persistent or worsening symptoms require reassessment.
• Score 5 to 6 (Intermediate Probability): Use observation, serial examinations and appropriate imaging: ultrasound first in children/pregnancy, with MRI if pregnancy ultrasound is inconclusive; CT is highly accurate in non-pregnant adults.
• Score 7 to 8 (High Probability): Obtain urgent surgical assessment. The score alone neither confirms appendicitis nor mandates appendectomy.
• Score 9 to 10 (Very High Probability): Prompt surgical assessment is required. Selected young adults with a convincing presentation may proceed to diagnostic/therapeutic laparoscopy without CT; other patients benefit from imaging to confirm the diagnosis or identify alternatives.

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Diagnostic Imaging & Operative Management of Appendicitis

Diagnostic Imaging Modalities

• Graded Compression Ultrasonography: The initial imaging modality of choice in children, adolescents, and pregnant women to eliminate ionizing radiation exposure. Ultrasonographic diagnostic criteria for acute appendicitis include:
  • Non-compressible, blind-ending, aperistaltic tubular structure in the right iliac fossa.
  • Outer transverse diameter > 6 mm.
  • Distinct 'target' or 'halo' sign in cross-section with mucosal thickening.
  • Presence of an echogenic appendicolith with posterior acoustic shadowing.
  • Periappendiceal hyperechoic fat stranding or fluid collection.
• Contrast-Enhanced Abdominal/Pelvic CT: The diagnostic gold standard in adult men, non-pregnant women, and elderly patients, boasting sensitivity and specificity > 95%. CT diagnostic criteria include:
  • Enlarged appendiceal caliber > 6 mm with circumferential wall thickening (> 2 mm).
  • Distinct wall hyperenhancement ('halo' or 'target' sign).
  • Periappendiceal mesenteric fat stranding, thickened cecal apex ('arrowhead sign').
  • Detection of complications: extraluminal gas bubbles, loculated abscess, phlegmon, or appendiceal wall discontinuity indicating perforation.

Operative Timing & Antibiotic Protocols

• Appendectomy: Laparoscopic appendectomy is the international standard of care, offering lower rates of wound infection, reduced postoperative pain, shorter hospital stays, and faster return to baseline activity compared to open appendectomy. In uncomplicated acute appendicitis, surgery should ideally be performed within 12 to 24 hours of admission.
• Perioperative Antibiotics: All patients undergoing appendectomy must receive prophylactic broad-spectrum intravenous antibiotics targeting enteric Gram-negative bacilli (E. coli, Klebsiella) and anaerobes (Bacteroides fragilis), such as IV Ceftriaxone (1 to 2 g) plus IV Metronidazole (500 mg), or IV Piperacillin-Tazobactam. In uncomplicated catarrhal or phlegmonous appendicitis, a single preoperative dose (or continuation for < 24 hours postoperatively) is sufficient. For complicated appendicitis, give a short postoperative antibiotic course after adequate source control (typically 2–3 days under WSES2025). Persistent sepsis requires reassessment for residual infection; incomplete source control may require longer individualized treatment.
• Appendiceal Phlegmon & Abscess Management: Patients presenting late (> 5 to 7 days after symptom onset) with a palpable, well-circumscribed inflammatory mass in the right iliac fossa frequently have an appendiceal phlegmon or walled-off abscess. Immediate surgical intervention carries high morbidity, including high rates of ileocecal resection and fecal fistula formation due to dense, friable inflammatory adhesions. Standard management comprises the conservative Ochsner-Sherren regimen:
  • Strict bowel rest, IV fluid resuscitation, and broad-spectrum IV antibiotics.
  • Serial marking of mass borders and continuous clinical monitoring (pulse, temperature, WBC).
  • Percutaneous Image-Guided Drainage (CT or Ultrasound): Indicated for well-defined, loculated appendiceal abscesses >= 3 to 4 cm in diameter.
  • Interval Appendectomy: Elective laparoscopic appendectomy performed 6 to 8 weeks following complete resolution of acute inflammation, particularly recommended in patients over 40 years of age to rule out underlying cecal or appendiceal malignancy (e.g. neuroendocrine tumor, mucinous adenocarcinoma) via colonoscopy or interval imaging.

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Acute Cholecystitis: Pathophysiology & Tokyo Guidelines

Acute cholecystitis represents acute inflammation of the gallbladder, classified as calculous (> 90% to 95% of cases) or acalculous (5% to 10%, seen in critically ill, septic, burn, or major trauma patients with prolonged total parenteral nutrition and bile stasis).

Pathophysiological Mechanism of Calculous Cholecystitis

1. Cystic Duct Impaction: A gallstone becomes impacted in the neck of the gallbladder (Hartmann's pouch) or cystic duct during gallbladder contraction provoked by a fatty meal.
2. Luminal Distension & Chemical Inflammation: Persistent cystic duct occlusion prevents gallbladder emptying. Luminal secretions accumulate, raising intraluminal pressure up to 200 to 300 mm H2O. Mucosal phospholipase A2 hydrolyzes luminal lecithin into toxic lysolecithin, which incites direct chemical inflammation and mucosal ulceration.
3. Ischemia & Secondary Infection: High intraluminal tension compresses intramural arterioles and venules, compromising mucosal perfusion. While initially sterile, secondary bacterial colonization supervenes in over 50% to 70% of cases, commonly involving E. coli, Klebsiella pneumoniae, Enterococcus faecalis, and anaerobic species.

Clinical Presentation & Murphy's Sign

• Symptoms: Constant, unremitting, severe pain in the right upper quadrant (RUQ) or epigastrium, lasting > 6 hours (distinguishing it from the transient < 4-6 hour colic of uncomplicated biliary colic). Pain typically radiates to the right infrascapular region or right shoulder, mediated by phrenic nerve afferents (C3-C5) and sympathetic splanchnic afferents (T7-T9). Accompanied by low-grade pyrexia, anorexia, nausea, and vomiting.
• Murphy's Sign: The examiner palpates deeply beneath the right costal margin at the midclavicular line while instructing the patient to take a slow, deep inspiration. As the descending diaphragm pushes the inflamed gallbladder fundus against the examining fingers, the patient experiences an abrupt, sharp increase in pain resulting in sudden arrest of inspiration. A positive Murphy's sign is pathognomonic for acute cholecystitis.

Tokyo Guidelines 2018 (TG18) Diagnostic Criteria

Definite diagnosis of acute cholecystitis requires fulfillment of three criteria:

• A. Local Signs of Inflammation: (1) Murphy's sign, (2) RUQ mass, pain, or tenderness.
• B. Systemic Signs of Inflammation: (1) Fever, (2) Elevated C-reactive protein (CRP), or (3) Elevated WBC count.
• C. Imaging Findings: Characteristic ultrasonographic or CT findings of acute cholecystitis.
• Diagnostic Threshold: 1 item from A + 1 item from B confirms suspected diagnosis; 1 from A + 1 from B + C establishes definite diagnosis.

Ultrasonographic Hallmarks of Acute Cholecystitis

Transabdominal ultrasound is the primary imaging modality (sensitivity 88%, specificity 80%):

1. Gallbladder wall thickening > 4 mm (in the absence of chronic liver disease, ascites, or congestive heart failure).
2. Sonographic Murphy's Sign: Maximal focal tenderness elicited by direct pressure of the ultrasound transducer over the visualized gallbladder.
3. Pericholecystic Fluid: Hypoechoic rim of fluid tracking around the gallbladder wall or fundus.
4. Cholelithiasis with Acoustic Shadowing: Impacted calculus visualized at the gallbladder neck or cystic duct.
5. Gallbladder hydrops/distension (longitudinal axis > 8 cm, transverse diameter > 4 cm).

Management & Timing of Cholecystectomy

• Early Laparoscopic Cholecystectomy: The definitive gold standard treatment. International randomized controlled trials establish that early cholecystectomy performed within 72 hours of admission (and within 7 days of symptom onset) is superior to delayed interval cholecystectomy, significantly reducing overall hospital length of stay, treatment costs, and emergency readmission rates without increasing conversion rates to open surgery or bile duct injury risks.
• Percutaneous Transhepatic Cholecystostomy (PTC): Reserved for critically ill, septic, or medically fragile patients (severe Tokyo Grade III acute cholecystitis with hemodynamic instability, multi-organ failure, or severe cardiac comorbidities) who are unfit for general anesthesia. PTC provides temporizing external biliary drainage, converting acute sepsis into a manageable subacute state.

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Acute Cholangitis: Charcot's Triad, Reynolds' Pentad & ERCP

Acute ascending cholangitis is a potentially fatal infection of the biliary tree caused by the lethal combination of biliary outflow tract obstruction and rapid bacterial proliferation within the ductal system.

Etiological Spectrum

• Choledocholithiasis (80%): Secondary common bile duct (CBD) stones migrating from the gallbladder, or primary intraductal calculi.
• Benign Biliary Strictures: Post-cholecystectomy surgical clip placement or ischemic ductal strictures, chronic pancreatitis, Primary Sclerosing Cholangitis (PSC).
• Malignant Biliary Obstruction: Pancreatic ductal adenocarcinoma (head of pancreas), cholangiocarcinoma (Klatskin tumor), ampullary carcinoma, duodenal adenocarcinoma, or extrinsic compression by metastatic lymphadenopathy.
• Biliary Stents & Instrumentation: Occluded plastic biliary endoprostheses, post-ERCP manipulation.

Clinical Manifestations

• Charcot's Triad: (1) Severe right upper quadrant pain, (2) Jaundice (scleral icterus, dark urine, acholic pale stools), and (3) Spiking fevers with shaking rigors. Present in approximately 50% to 70% of patients.
• Reynolds' Pentad: Charcot's triad PLUS (4) Hypotension / Septic shock and (5) Altered mental status / Acute delirium. Reynolds' pentad indicates acute toxic suppurative cholangitis with intrabiliary pressure exceeding 25 cm H2O, which overcomes the hepatic sinusoidal barrier and discharges massive quantities of bacteria and endotoxins directly into the systemic hepatic venous circulation. Mortality approaches 100% without emergency intervention.

Emergency Resuscitation & Decompression Protocols

1. Immediate Resuscitation: Place two large-bore IV lines, administer balanced isotonic crystalloids to restore perfusion, insert an indwelling urinary catheter, and obtain urgent baseline laboratory studies (WBC, bilirubin, alkaline phosphatase, aminotransferases, serum lactate, coagulation profile, and two sets of peripheral blood cultures).
2. Empiric Broad-Spectrum IV Antibiotics: Administer immediately within 1 hour: IV Piperacillin-Tazobactam (4.5 g every 8 hours), or IV Ceftriaxone (2 g once daily) plus IV Metronidazole (500 mg every 8 hours), or Meropenem for septic shock.
3. Definitive Biliary Decompression:
   • Emergency Endoscopic Retrograde Cholangiopancreatography (ERCP): The diagnostic and therapeutic intervention of choice. After cannulation, establish biliary drainage with a stent or nasobiliary drain. Combine sphincterotomy and stone extraction when the patient can tolerate definitive treatment; in severe instability or significant bleeding risk, decompress first and defer duct clearance.
   • Timing: In patients presenting with septic shock, organ dysfunction, or Reynolds' pentad, emergency ERCP decompression must be achieved within 12 hours. In stable or moderately ill patients responding to initial antibiotics, decompression is performed urgently within 24 to 48 hours.
   • Percutaneous Transhepatic Biliary Drainage (PTBD): Second-line rescue decompression when ERCP fails, is technically impossible (e.g. surgically altered Roux-en-Y gastric bypass anatomy, severe duodenal diverticulum), or when high proximal hilar obstruction prevents transpapillary drainage.

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Differential Matrix of the Acute Abdomen