Category Archives: Hepatobiliary Surgery

Main Clinical Manifestations of Chronic Cholecystitis

Chronic cholecystitis denotes persistent, low-grade inflammation of the gall-bladder wall, usually in the setting of recurrent mechanical irritation by gallstones or, less commonly, chronic infection or metabolic deposition. Symptoms are episodic and less dramatic than those of acute cholecystitis, but they may culminate in fibrosis, loss of function, or acute exacerbation.

  1. Recurrent biliary colic
    Episodic, post-prandial right-upper-quadrant or epigastric pain lasting 15–60 min, often precipitated by fatty foods and radiating to the inter-scapular region or right shoulder. Pain is typically self-limiting but becomes more frequent over time.
  2. Dyspeptic syndrome
    Early satiety, eructation, bloating, and nausea reflect impaired gall-bladder emptying and coexist with colicky episodes.
  3. Fat intolerance
    Patients report loose stools or diarrhoea following meals rich in fat, attributable to inadequate bile acid delivery to the duodenum.
  4. Vague upper-abdominal discomfort
    A dull, non-colicky heaviness or fullness persists between attacks, especially when the gall-bladder is distended by viscous bile or sludge.
  5. Tender hepatomegaly
    The liver edge remains smooth and mildly tender; the gall-bladder fundus may be palpable as a soft, non-distended mass that moves with respiration.
  6. Laboratory changes
    Serum alkaline phosphatase and γ-glutamyl transferase may be intermittently elevated; total bilirubin is usually normal unless common bile-duct stones coexist. Repeated episodes can raise C-reactive protein minimally.
  7. Acute exacerbation
    Sudden intensification of pain, high fever, or guarding signals progression to acute cholecystitis, gangrene, or empyema and mandates urgent evaluation.
Symptom / SignTypical Presentation
Recurrent colicPost-prandial RUQ pain 15–60 min, fatty trigger
DyspepsiaEarly satiety, bloating, eructation
Fat intoleranceLoose stools after rich meals
Vague discomfortDull heaviness between attacks
Tender organSoft, mildly tender gall-bladder edge
LaboratoryIntermittent ↑ ALP/GGT, normal bilirubin
ExacerbationSudden severe pain, fever, guarding

Main Clinical Manifestations of Acute Cholecystitis

Acute cholecystitis is acute inflammation of the gall-bladder wall, initiated most often by cystic-duct obstruction with secondary bacterial infection. The clinical picture evolves over hours, and recognition of its characteristic features guides early imaging, antibiotic therapy, and timely surgical intervention.

  1. Right-upper-quadrain pain
    Persistent, often severe pain begins beneath the costal margin, may radiate to the right scapula or inter-scapular region, and is exacerbated by deep inspiration or movement. Pain typically lasts > 6 h and is unrelenting.
  2. Murphy sign
    Inspiratory arrest elicited by palpation of the right upper quadrant during deep inspiration is a reliable physical finding; a positive Murphy sign has high diagnostic accuracy.
  3. Fever and systemic response
    Low-grade pyrexia (37.5–38.5 °C) with chills is usual; higher temperatures or rigors suggest suppurative complications such as empyema or gangrene.
  4. Nausea and vomiting
    Gastric stasis and vagal reflexes produce repeated retching that may transiently lessen pain but contributes to dehydration and electrolyte imbalance.
  5. Tender hepatomegaly and guarding
    The gall-bladder fundus is palpable as a smooth, exquisitely tender mass; voluntary guarding progresses to board-like rigidity if peritonism develops.
  6. Laboratory inflammation
    Leukocytosis with neutrophil left shift, elevated C-reactive protein, and modest rise in serum alkaline phosphatase and transaminases are characteristic; total bilirubin may be mildly elevated unless common bile-duct stones coexist.
  7. Local complications
    Persistent high fever, unrelenting pain, or palpable emphysematous crepitus indicates gangrene, perforation, or emphysematous cholecystitis and mandates urgent intervention.
Symptom / SignTypical Presentation
RUQ painPersistent > 6 h, radiates to scapula
Murphy signInspiratory arrest on palpation
FeverLow-grade, chills; high if suppurative
Nausea/vomitingRepeated, may relieve pain transiently
Tender massSmooth, exquisitely tender gall-bladder
LaboratoryLeukocytosis, ↑ CRP, ↑ ALP/ALT
Alarm signsHigh fever, crepitus, unrelenting pain

Main Clinical Manifestations of Portal Vein Thrombosis

Portal vein thrombosis (PVT) is the partial or complete occlusion of the portal venous system by thrombus. Presentation is determined by the tempo of obstruction (acute vs. chronic), the extent of mesenteric involvement, and the presence of underlying cirrhosis or malignancy. Symptoms range from incidental imaging findings to life-threatening intestinal ischemia.

  1. Abdominal pain
    Colicky or constant upper-abdominal discomfort is the commonest early feature, reported in up to 90 % of acute cases. Pain may be non-specific, but when disproportionate to physical signs it heralds mesenteric vein extension and impending bowel infarction .
  2. Fever and systemic inflammatory response
    Low-grade pyrexia, rigors, and elevated C-reactive protein are frequent even in the absence of documented bacteraemia, reflecting thrombus-induced inflammation .
  3. Ascites
    New-onset, usually small-volume ascites develops in ~50 % of acute non-cirrhotic cases, secondary to sinusoidal hypertension and fluid extravasation; tense ascites suggests extensive thrombosis or intestinal ischemia .
  4. Gastrointestinal bleeding
    Haematemesis, melaena, or rectal bleeding occur when thrombosis aggravates pre-existing portal hypertension, producing oesophageal, gastric, or choledochal varices. Bleeding is the presenting event in up to 40 % of chronic cases and carries a higher mortality when superimposed on cirrhosis .
  5. Splenomegaly and hypersplenism
    Acute venous congestion enlarges the spleen; thrombocytopenia or leucopenia may appear within days. Persistent splenomegaly indicates chronic portal hypertension and cavernous transformation .
  6. Intestinal ischaemia
    Extension into the superior mesenteric vein produces diarrhoea, haematochezia, rebound tenderness, and ileus. Persistent lactic acidosis, rising lactate, or multi-organ dysfunction signals bowel infarction and mandates emergency intervention .
  7. Hepatic encephalopathy (rare)
    Acute shunting of nitrogenous products through collaterals can precipitate confusion, asterixis, and coma even in the absence of underlying cirrhosis.
  8. Chronic portal hypertension sequelae
    After cavernoma formation, patients may remain asymptomatic for years, but long-term risks include repeated variceal bleeding, ascites, and portal cholangiopathy with cholestasis or cholangitis .
Symptom / SignTypical Presentation
Abdominal painColicky or constant, may herald mesenteric extension
FeverLow-grade, rigors, elevated CRP
AscitesNew, small-volume; tense if ischaemia present
GI bleedingHaematemesis/melaena from varices
SplenomegalyAcute congestion or chronic hypersplenism
Intestinal ischaemiaDiarrhoea, haematochezia, rebound tenderness
Hepatic encephalopathyConfusion, asterixis (rare, acute)
Chronic sequelaeRecurrent bleeding, ascites, cholangitis

Main Clinical Manifestations of Biliary Tract Tumours

Biliary tract tumours comprise neoplasms of the gall-bladder, cystic duct, extra-hepatic bile ducts, and intra-hepatic bile ducts. Most are malignant (gall-bladder carcinoma, cholangiocarcinoma) and present late; benign lesions are rare and usually detected incidentally. Symptom patterns reflect anatomical location, growth morphology, and degree of biliary obstruction.

  1. Painless obstructive jaundice
    Progressive conjugated hyper-bilirubinaemia with scleral icterus, dark urine, and acholic stools is the hallmark of hilar or distal cholangiocarcinoma and of advanced gall-bladder carcinoma. Pruritus is often intense and may precede visible icterus.
  2. Right-upper-quadrain pain
    A constant dull ache or vague heaviness is typical of gall-bladder cancer; intermittent colicky pain suggests concomitant cholelithiasis or cholangiocarcinoma mimicking biliary colic.
  3. Systemic features
    Fatigue, early satiety, unintentional weight loss, and low-grade night sweats reflect tumour cachexia and chronic cholestasis.
  4. Recurrent cholangitis
    Intermittent fever with rigors, elevated C-reactive protein, and right-sided tenderness occur when malignant obstruction becomes super-infected, fulfilling Charcot triad.
  5. Palpable gall-bladder (Courvoisier sign)
    A distended, non-tender gall-bladder may be felt below the right costal margin in distal bile-duct obstruction where the cystic duct remains patent.
  6. Hepatomegaly and lobar atrophy–hypertrophy complex
    The obstructed lobe atrophies while the contralateral lobe enlarges, producing a firm, nodular liver edge and visible abdominal asymmetry.
  7. Laboratory cholestasis
    Serum alkaline phosphatase and γ-glutamyl transferase are elevated in > 90 % of cases; total bilirubin climbs steadily as ductal involvement extends.
  8. Advanced disease indicators
    Persistent fever, ascites, palpable left-supraclavicular node, or rapidly rising bilirubin suggests unresectable disease or distant spread.
Symptom / SignTypical Presentation
Painless jaundiceProgressive, conjugated, with pruritus
RUQ painDull ache or intermittent colic
SystemicFatigue, weight loss, night sweats
CholangitisFever + RUQ pain + rising bilirubin
Courvoisier signNon-tender, distended gall-bladder
HepatomegalyFirm, nodular, lobar asymmetry
Laboratory↑ ALP, ↑ GGT, ↑ total bilirubin
AdvancedAscites, fever, distant nodes

Main Clinical Manifestations of Congenital Biliary Malformations

Congenital biliary malformations encompass a spectrum of structural defects in the extra- and intrahepatic bile ducts. The phenotypic expression is determined by the embryologic stage at which development is arrested and by the subsequent impairment of bile flow. Three cardinal symptom complexes dominate the clinical picture: cholestatic jaundice, recurrent cholangitis, and secondary hepatic dysfunction.

  1. Cholestatic Jaundice
    Conjugated hyperbilirubinemia is the earliest and most consistent finding. In neonates it is usually recognized after the physiological jaundice window (>2 weeks of life) and is marked by progressive acholic stools and dark urine reflecting absent intra-intestinal bilirubin. In older children jaundice may fluctuate, often precipitated by intercurrent infection or intermittent cystic distension.
  2. Abdominal Pain and Palpable Mass
    Dilation of the extrahepatic duct (choledochal cyst) produces right-upper-quadrant discomfort or colicky pain. A discrete, non-tender, cystic mass is palpable in up to 60 % of affected infants. Sudden enlargement may herald complete obstruction or intracystic hemorrhage.
  3. Cholangitis and Systemic Sepsis
    Stagnant bile predisposes to bacterial ascent, presenting as fever, rigors, and elevated serum C-reactive protein. Repeated episodes accelerate periportal fibrosis and may precipitate acute-on-chronic liver failure.
  4. Growth Failure and Fat-Soluble Vitamin Deficiency
    Chronic cholestasis impairs enterohepatic circulation of bile acids, leading to steatorrhea, hypoalbuminemia, and deficiencies of vitamins A, D, E, and K. Manifestations include rachitic rosary, coagulopathy, and failure to thrive despite adequate caloric intake.
  5. Portal Hypertension and Cirrhosis
    Untreated malformations evolve toward biliary cirrhosis, with subsequent splenomegaly, thrombocytopenia, and variceal bleeding. Hepatopulmonary syndrome with digital clubbing and exertional dyspnea may supervene, mandating transplant evaluation.
  6. Pancreaticobiliary Reflux–Associated Pancreatitis
    Anomalous pancreaticobiliary junction permits activation of pancreatic enzymes within the common channel, producing episodic hyperamylasemia and acute pancreatitis.
  7. Miscellaneous Anomalies
    Gall-bladder agenesis is usually silent, yet concomitant ductal atresia can reproduce the full cholestatic phenotype. Intrahepatic gall-bladder predisposes to cholelithiasis and recurrent biliary colic.
Age GroupDominant SymptomsCommon Laboratory/Imaging Correlates
0–6 monthsObstructive jaundice, hepatomegaly, acholic stoolsConjugated bilirubin ↑, US: cystic or atretic ducts
6 months–4 yearsIntermittent jaundice, abdominal pain, feverALT/AST ↑, MRCP: choledochal cyst, hyperamylasemia
>4 yearsRecurrent pancreatitis, cirrhosis, portal hypertensionLow albumin, prolonged PT, thrombocytopenia, varices on endoscopy

Main Clinical Manifestations of Biliary Tract Diseases

Biliary tract diseases encompass a spectrum of disorders affecting the gallbladder, cystic duct, and extra- or intra-hepatic bile ducts. Symptoms arise from obstruction, inflammation, infection, or neoplastic change, and often overlap among entities such as cholelithiasis, cholecystitis, cholangitis, and cholangiocarcinoma. Recognition of characteristic patterns guides timely imaging and intervention.

  1. Biliary colic
    Paroxysmal, post-prandial pain located in the epigastrium or right upper quadrant, radiating to the inter-scapular region or right shoulder, peaking over ≥30 min and resolving spontaneously within 6 h.
  2. Nausea and vomiting
    Vagal stimulation and gastric compression produce repeated retching that may transiently relieve pain.
  3. Fluctuating or progressive jaundice
    Conjugated hyper-bilirubinaemia manifests as scleral icterus, dark urine, and clay-coloured stools; levels oscillate with stone impaction or steadily rise with malignant stricture.
  4. Fever and rigors
    High spiking temperature with chills signals bacterial infection (cholecystitis, cholangitis) or central tumour necrosis.
  5. Tender hepatomegaly and Murphy sign
    A smooth, hot liver edge that arrests inspiration on palpation indicates acute cholecystitis; diffuse tenderness accompanies acute cholangitis.
  6. Pruritus
    Cutaneous deposition of bile salts produces intense itching, often preceding visible jaundice.
  7. Systemic features
    Fatigue, early satiety, and unintentional weight loss suggest chronic cholestasis or malignancy.
  8. Acute complications
    Persistent hypotension, confusion, or unrelenting pain heralds septic shock (Reynolds pentad), acute pancreatitis, or perforation.
Symptom / SignTypical Presentation
Biliary colicPost-prandial RUQ/epigastric pain ≥30 min
Nausea/vomitingRepeated, may relieve pain
JaundiceFluctuating (stones) or progressive (tumour)
Fever/rigorsHigh spiking, chills
Tender hepatomegalyHot edge, positive Murphy sign
PruritusIntense, precedes icterus
SystemicFatigue, weight loss, early satiety
Alarm signsHypotension, confusion, unrelenting pain

Main Clinical Manifestations of Bile-Duct Stones

Choledocholithiasis denotes the presence of calculi within the extra- or intrahepatic bile ducts. Symptoms arise when a stone obstructs flow, triggers inflammation, or provokes infection. The presentation ranges from silent imaging findings to life-threatening sepsis.

  1. Biliary colic
    Epigastric or right-upper-quadrant pain begins 30–60 min post-prandially, peaks for ≥30 min, and radiates to the inter-scapular region or right shoulder. Movement does not relieve the discomfort, and analgesics are often required.
  2. Nausea and vomiting
    Gastric stasis and vagal reflexes produce repeated retching that may transiently lessen pain.
  3. Fluctuating jaundice
    Intermittent elevation of conjugated bilirubin produces scleral icterus, dark urine, and clay-coloured stools that wax and wane as stones impact or disimpact.
  4. Cholangitis
    Complete obstruction plus bacterial contamination yields Charcot triad: spiking fever with rigors, constant RUQ pain, and deepening jaundice. Suppurative forms add hypotension and mental confusion (Reynolds pentad), indicating pus under pressure.
  5. Acute pancreatitis
    Impaction at the ampulla obstructs both bile and pancreatic flow, leading to epigastric pain radiating to the back, intractable vomiting, and elevated serum amylase/lipase.
  6. Tender hepatomegaly
    The liver edge is smooth, hot and exquisitely tender; inspiratory arrest on palpation (Murphy sign) is frequent when concomitant acute cholecystitis is present.
  7. Laboratory cholestasis
    Serum alkaline phosphatase and γ-glutamyl transferase rise early; total bilirubin climbs steadily as obstruction persists.
Symptom / SignTypical Presentation
Biliary colicPost-prandial RUQ/epigastric pain ≥30 min
Nausea/vomitingRepeated, may transiently relieve pain
JaundiceFluctuating, dark urine, pale stools
CholangitisFever + RUQ pain + jaundice (Charcot triad)
Acute pancreatitisEpigastric pain to back, ↑ amylase/lipase
Tender hepatomegalyHot, painful edge, positive Murphy sign
Laboratory↑ ALP, ↑ GGT, ↑ total bilirubin

Main Clinical Manifestations of Cholangitis

Cholangitis denotes acute bacterial infection within the biliary tree, most commonly precipitated by obstruction from stones, strictures, or neoplasia. The spectrum ranges from mild ductal inflammation to life-threatening sepsis. Recognition of its cardinal features guides urgent biliary decompression and antimicrobial therapy.

Complication warnings
Persistent fever despite antibiotics, uncontrolled hypotension, or new-onset renal dysfunction suggests progressive sepsis and requires urgent endoscopic or percutaneous biliary drainage.

Charcot triad
Intermittent high spiking fever with rigors, constant right-upper-quadrant pain, and conjugated hyper-bilirubinaemia constitute the classical presentation seen in ~70 % of patients with incomplete or partial obstruction.

Reynolds pentad
Addition of hypotension (systolic BP < 90 mmHg) and altered mental status marks suppurative cholangitis with septic shock; this combination mandates emergency ductal drainage.

Jaundice and pruritus
Scleral icterus, dark urine, and clay-coloured stools reflect impaired bile flow; intractable pruritus results from cutaneous deposition of bile salts.

Tender hepatomegaly
The liver edge is hot, exquisitely painful to percussion, and may show a soft bulge over the obstructed segment; inspiratory arrest on palpation (Murphy sign) is frequent when concomitant acute cholecystitis is present.

Gastro-intestinal upset
Anorexia, nausea, and intermittent vomiting are common; large duct obstruction produces early satiety and eructation.

Systemic toxicity
Tachycardia > 100 beats min⁻¹, prolonged capillary refill, elevated lactate, and leukocytosis with left shift indicate bacteraemia and impending septic shock.

Laboratory cholestasis
Serum alkaline phosphatase and γ-glutamyl transferase rise early; total bilirubin climbs steadily as obstruction persists; blood cultures frequently yield enteric Gram-negative bacilli.

Symptom / SignTypical Presentation
Charcot triadFever + RUQ pain + jaundice
Reynolds pentadAbove + hypotension + confusion
JaundiceConjugated, dark urine, pale stools
Tender hepatomegalyHot, painful edge, positive Murphy
GI upsetNausea, vomiting, early satiety
Systemic toxicityTachycardia, leukocytosis, elevated lactate
Laboratory↑ ALP, ↑ GGT, ↑ bilirubin, positive blood cultures
Alarm signsRefractory fever, shock, renal dysfunction

Main Clinical Manifestations of Hilar Cholangiocarcinoma

Hilar cholangiocarcinoma (Klatskin tumour) arises at or near the confluence of the right and left hepatic ducts. Because the lesion obstructs the central bile ducts early, symptoms are usually biliary and appear while the tumour is still relatively small.

  1. Painless jaundice
    Conjugated hyper-bilirubinaemia develops insidiously, producing progressive yellowing of skin and sclera, dark urine and clay-coloured stools; pruritus is often intense and may precede visible icterus.
  2. Right-upper-quadrant discomfort
    A dull, non-colicky ache or sensation of fullness is common; pain is usually mild and does not parallel the degree of jaundice.
  3. Cholangitis episodes
    Intermittent fever with rigors, right-sided tenderness and elevated C-reactive protein occur when malignant obstruction becomes infected, fulfilling Charcot triad.
  4. Systemic features
    Fatigue, early satiety, unintentional weight loss and low-grade night sweats reflect chronic cholestasis and tumour cachexia.
  5. Palpable gallbladder (Courvoisier sign)
    A distended, non-tender gallbladder may be felt below the right costal margin if the cystic duct remains patent—more frequent in distal tumours but occasionally present in hilar lesions.
  6. Hepatomegaly and lobar atrophy–hypertrophy complex
    The obstructed lobe atrophies while the contralateral lobe compensates, leading to a firm, nodular liver edge and visible abdominal asymmetry.
  7. Laboratory cholestasis
    Serum alkaline phosphatase and γ-glutamyl transferase are elevated in > 90 % of cases; total bilirubin climbs steadily as ductal involvement extends.
  8. Advanced disease indicators
    Persistent fever, ascites, palpable left-supraclavicular node or rapidly rising bilirubin suggest unresectable disease or distant spread.
Symptom / SignTypical Presentation
Painless jaundiceProgressive, conjugated, with pruritus
RUQ discomfortDull ache, mild, non-colicky
CholangitisFever + RUQ pain + rising bilirubin
SystemicFatigue, weight loss, night sweats
Palpable gallbladderNon-tender, distended (Courvoisier)
HepatomegalyFirm, nodular, lobar asymmetry
Laboratory↑ ALP, ↑ GGT, ↑ total bilirubin
AdvancedAscites, fever, distant nodes

Main Clinical Manifestations of Hepatic Ascites

Ascites is the pathological accumulation of fluid within the peritoneal cavity secondary to portal hypertension, hypoalbuminaemia and sodium retention. In patients with chronic liver disease it marks the transition from compensated to decompensated cirrhosis. The severity ranges from mild, detected only by imaging, to gross, producing marked physical and metabolic disturbances.

Metabolic disturbances
Hyponatraemia, muscle cramps and hypervolaemic dilutional anaemia reflect advanced renal sodium retention and impaired free-water clearance.

Progressive abdominal distension
Painless increase in girth is usually the first complaint; patients note tight clothing, difficulty bending forward, and a sensation of heaviness in the flanks.

Shifting dullness and fluid thrill
On percussion, dullness moves toward the dependent side when the patient turns; a fluid thrill may be elicited in tense ascites.

Weight gain and ankle oedema
Rapid daily increments (≥0.5 kg) reflect active sodium-water retention; gravitational oedema often precedes detectable peritoneal fluid.

Early satiety and nausea
Elevation of the diaphragm and compression of the stomach reduce gastric capacity, leading to post-prandial fullness, eructation and occasional vomiting.

Dyspnoea and orthopnoea
Basal atelectasis and elevation of the diaphragm decrease functional residual capacity, producing exertional dyspnoea and inability to lie flat.

Umbilical hernia and striae
Increased intra-abdominal pressure stretches the linea alba, leading to eversion of the umbilicus and occasionally painful incarceration.

Spontaneous bacterial peritonitis (SBP) warning
New-onset fever, abdominal pain, rebound tenderness or altered mental status indicate infection of ascitic fluid and require immediate diagnostic paracentesis.

Symptom / SignTypical Presentation
Abdominal distensionProgressive, painless, flank bulging
Shifting dullnessPercussion dullness moves with posture
Weight gain / oedema≥0.5 kg/day, ankle swelling
Early satietyPost-prandial fullness, nausea
DyspnoeaExertional, orthopnoea from raised diaphragm
Umbilical herniaEverted umbilicus, incarceration risk
SBP warningFever, pain, rebound tenderness
MetabolicHyponatraemia, muscle cramps