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NO LIST OF DIAGNOSIS PATHO/RISK FACTORS/ CAUSES CLINICAL PRESENTATION/ COMPLICATIONS INVESTIGATION MANAGEMENT
1 Portal hypertension - Hepatic venous pressure gradient (HVPG) Cx; Ascites, spontaneous bacterial peritonitis Ultrasound (Liver & Spleen) – dilated splenic and SMV,
≥6mmHg (bet hepatic & portal vein) (SBP), formation of portosystemic shunts, hepatic splenomegaly >12cm, dilated portal vein, porto-systemic
- Chronic increase in portal P d/t mechanical encephalopathy collaterals, ascites, nodular liver
obstruction as consequence of cirrhosis
- Causes; Pre-sinusoidal, Sinusoidal, Post-
sinusoidal
2 Ascites - Progressive liver cirrhosis obstruct intra- Progressive abdominal distension, painless, SAAG; Conservative; low salt diet, fluid restriction,
hepatic vasculature Portal HTN abdominal discomfort, weight gain, SOB, early - ≥1.1g/dL; liver cirrhosis, alcoholic hepatitis, CHF, Budd- monitor
splanchnic vasodilation satiety Chiari syndrome, portal vein thrombosis Pharmacological; Diuresis (spironolactone,
- Low effective intra-abdominal blood V Fever, abdominal tenderness, altered mental - <1.1g/dL; peritoneal carcinomatosis, peritoneal TB, furosemide), Antibiotics (if suspect SBP) (IV
- Renal hypoperfusion RAAS stimulated status (AMS) suspect SBP pancreatitis, pancreatic ascites, nephrotic syndrome ceftriaxone or oral quinolones)
vasoconstriction, high aldosterone salt and PE; abdominal distension, flank dullness, shifting FBC, U/E/Cr, LFT, CXR, Liver & Spleen US/CT scan Therapeutic paracentesis + IV albumin 20%
water retention dullness, fluid thrill, CLD stigmata, raised JVP, Peritoneal tap infusion
anasarca (in nephrotic syndrome) Surgical – liver transplantation and shunts
Treat underlying cause, Liver transplant for
cirrhosis
3 Liver haemangioma - Benign vascular lesions. Endothelium Usually asymptomatic, incidental finding Do not biopsy (risk of fatal haemorrhage) Asymptomatic, <4cm – observation
hamartomatous outgrowth made of widened Pain from liver capsule stretch, non-specific Ultrasound; well circumscribed, homogenous, hyperechoic Symptomatic/ complicated lesions – surgical
blood vessels abdominal fullness, vague abdominal pain, mass lesion, compressibility of lesion (pathognomonic) removal
- Most common benign liver tumour effects Triphasic CT scan; peripheral enhancement (arterial phase), Large, unresectable – low-dose radiotherapy or
- Vascular malformation enlarged by ectasia Cx; life-threatening haemorrhage, CHF, centripetal filling (portal venous phase), contrast retention + embolization
Kasabach-Merritt syndrome (consumptive appears brightest + uniformly enhanced (delayed phase) Spontaneous rupture – arterial
coagulopathy) Gadolinium-enhanced MRI; hyperintense on T2-weighted angioembolization then definitive resection
images (“light bulb sign”)
4 Focal Nodular - Benign, nodular in appearance. Central stellate Asymptomatic, incidental on imaging Triphasic CT scan; bright homogenous enhancement w Conservative Mx for asymptomatic
Hyperplasia (FNH) scar Symptomatic; RUQ pain hypoattenuating central scar (arterial phase), isoattenuating Surgery/ Liver resection for symptomatic
- Second commonest benign liver tumour (portal venous phase), hyper-attenuation of central scar
(delayed phase)
Sulphur colloid scan – have Kupffer cells, will take up sulphur
colloid
MRI – central scar hyperintense on T2 weighted images
5 Hepatic adenoma - Benign proliferation of hepatocytes Asymptomatic Triphasic CT scan; sharply defined borders, homogenous Conservative Mx for small, asymptomatic lesions
Symptomatic – spontaneous rupture and enhancement (arterial phase), isodensity (portal venous and Surgical resection for symptomatic lesion or
intraperitoneal haemorrhage of lesions >5cm, delayed phase) lesions > 4-5cm
abdominal pain, vague symptoms of fullness, Sulphur colloid scan (cold) – no Kupffer cells thus no uptake If got acute haemorrhage, proceed to hepatic
RUQ discomfort MRI – hypervascular tumour angioembolization followed by surgery
Histology – lack bile duct glands and Kupffer cells, no true
lobules, congested hepatocytes
6 Hepatic cysts - Classification; Non parasitic (simple, Asymptomatic Simple liver cyst – percutaneous aspiration with
polycystic, neoplastic), Echinococcal (hydatid) Symptomatic – RUQ tenderness, hepatomegaly, sclerotherapy or laparoscopic “unroofing” if
cysts bleeding, infection, torsion, mass effect of IVC symptomatic
compression, CBD compression, portal HTN, Polycystic liver disease – laparoscopic
fistulation “unroofing” or liver resection if symptomatic
Neoplastic cyst – resection or enucleation
Hydatid cyst – surgery or unroofing
7 Hepatocellular - Risk factors; CLD, chronic HBV/HCV infection, Local S&S; upper abdominal pain, dull, persistent, Diagnostic approach Curative; surgical resection, liver transplantation
carcinoma alcohol, NAFLD, autoimmune (PBC, SBC), early satiety, vomiting, constitutional symptoms, Triphasic CT scan as GOLD STANDARD – early enhancement Palliative;
metabolic (haemochromatosis, A1AT pyrexia, jaundice + hyper-dense lesion (arterial phase), dull/wash out + hypo- - Local – radiofrequency ablation, microwave
deficiency), others (diet, aflatoxins B1, DM, Tumour rupture; severe abdominal pain, pallor dense (portal venous phase), tumour capsule (delayed ablation, thermal ablation, cryotherapy
smoking) Features of decompensated CLD phase) - Regional – TACE, selective internal
- Chronic inflammation or on-going Features of portal HTN Hallmark – arterial hypervascularity + venous/ late phase radiotherapy
hepatocellular damage with high cellular Metastases; bone pain, dyspnoea washout - Systemic – sorafenib/ Lenvatinib
regeneration leading to increased mutation Paraneoplastic syn; hypoglycemia, hyperCa, etc Lipiodol contrast CT scan, AFP, hepatic markers, MRI, USG Others – symptomatic treatment
Hepatobiliary – Hepatobiliary – Hepatobiliary MOZZAR
Histology – Hallmark; stromal invasion
Staging studies
Biochemical assessment via Child-Pugh score
Indocyanine green (ICG) assessment
CT volumetry
ECOG performance scale
8 Secondary liver - Metastatic liver tumours more common than Metastasis to liver parenchyma; incidental Biochemical Ix Usually palliative except in selected cases
malignancy primary liver tumours d/t liver dual blood finding, fullness in RUQ, RHC pain, constitutional Triphasic liver CT scan; hypodense (arterial phase), Colorectal liver metastases – liver resection
supply symptoms increasing contrast uptake (portal venous and delayed recommended
PE; hard, irregular, nodular hepatomegaly. Late phases) Neuroendocrine liver metastases – hepatic
jaundice resection if resectable