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SN10 SHORT NOTE 5M

Write a short note on the clinical approach to hepatomegaly and splenomegaly.

General Medicine · Final Professional

Definition and Clinical Assessment

The liver is normally palpable up to 1–2 cm below the right costal margin in thin individuals and in children, and normal liver span is 12–15 cm in the midclavicular line by percussion. A palpable liver edge is not synonymous with hepatomegaly — it may be displaced downwards by hyperinflated lungs in COPD or by a subdiaphragmatic collection, which is why percussion of the upper border is essential before declaring enlargement.

The normal spleen is NOT palpable — it must enlarge to about twice its size before becoming palpable. It is distinguished from a renal mass by: enlarging towards the right iliac fossa, having a notch on its medial border, being dull to percussion, having no palpable upper border (you cannot get above it), moving early and markedly with respiration, and not being ballotable.

Grading of splenomegaly: just palpable; moderate (up to the umbilicus); massive (crossing the midline or reaching the pelvis).

Causes of Hepatomegaly

CategoryCausesCharacter of liver
CongestiveRight heart failure, constrictive pericarditis, Budd–Chiari, tricuspid regurgitationSmooth, tender; PULSATILE in tricuspid regurgitation; hepatojugular reflux
InfectiveViral hepatitis, amoebic and pyogenic liver abscess, malaria, kala-azar, enteric fever, tuberculosis, hydatid cystSmooth and tender in acute infection
Infiltrative / storageFatty liver (NAFLD, alcohol), amyloidosis, Gaucher's and Niemann–Pick disease, glycogen storage disease, haemochromatosisSmooth, non-tender, firm
MalignantSecondary metastases (commonest malignant cause), hepatocellular carcinoma, lymphoma, leukaemiaHard, irregular, nodular; may have a bruit (HCC)
HaematologicalChronic haemolytic anaemia, myeloproliferative neoplasms, thalassaemiaFirm
BiliaryBiliary obstruction, primary biliary cholangitisSmooth, may be tender
CirrhosisEarly cirrhosis (later the liver shrinks)Firm, irregular, non-tender, with a hard edge

Causes of Splenomegaly

DegreeCauses
Massive (crossing the midline or reaching the pelvis)Chronic myeloid leukaemia, myelofibrosis, kala-azar (visceral leishmaniasis), chronic malaria and tropical splenomegaly syndrome, Gaucher's disease
ModeratePortal hypertension with congestive splenomegaly, lymphoma, chronic lymphocytic leukaemia, thalassaemia major, storage disorders
MildAcute infections — enteric fever, infective endocarditis, EBV, malaria, viral hepatitis, brucellosis; autoimmune — SLE, rheumatoid arthritis (Felty's syndrome), sarcoidosis, amyloidosis; haemolytic anaemias; acute leukaemia
CLINICAL PEARL

In India, the differential for MASSIVE splenomegaly is short and worth memorising: chronic myeloid leukaemia, myelofibrosis, kala-azar, chronic malaria (tropical splenomegaly syndrome), and Gaucher's disease. Two bedside tests will often settle it — a peripheral smear (leucocytosis with the full myeloid spectrum and basophilia in CML; tear-drop cells in myelofibrosis; parasites in malaria) and an rK39 rapid test for kala-azar in a patient from Bihar, Jharkhand, West Bengal or eastern UP.

CAUSES OF HEPATOSPLENOMEGALY (both together)

  • Portal hypertension / cirrhosis — the commonest
  • Haematological malignancy — leukaemia (acute and chronic), lymphoma, myeloproliferative neoplasms
  • Infections — kala-azar, malaria, enteric fever, brucellosis, infective endocarditis, EBV, CMV, HIV, disseminated tuberculosis
  • Haemolytic anaemias — thalassaemia major, sickle cell disease, hereditary spherocytosis
  • Storage and infiltrative disorders — Gaucher's, Niemann–Pick, amyloidosis, sarcoidosis
  • Congestive — right heart failure, constrictive pericarditis
  • Autoimmune — SLE, adult-onset Still's disease

Clinical Approach

History:

  • duration and rate of onset
  • fever and its pattern
  • travel to and residence in endemic areas (kala-azar belt, malaria)
  • weight loss and night sweats (B symptoms)
  • alcohol and drug history
  • risk factors for viral hepatitis
  • bleeding, bruising and recurrent infection (marrow disease)
  • jaundice, dark urine and pallor (haemolysis)
  • family history and consanguinity (storage disease, haemoglobinopathy)
  • cardiac symptoms.

Examination:

  • Characterise the organs — size, consistency, surface, edge, tenderness, and any bruit or rub.
  • Look for the company they keep: lymphadenopathy (lymphoma, leukaemia, infection), stigmata of chronic liver disease and ascites, pallor, jaundice, purpura, raised JVP and cardiac signs, skin changes (hyperpigmentation in kala-azar and haemochromatosis), joint signs, and fundoscopy.

Investigations

  • CBC with peripheral smear — the single highest-yield test: blasts, the myeloid spectrum with basophilia (CML), tear-drop cells (myelofibrosis), atypical lymphocytes (EBV), parasites (malaria), spherocytes, target cells, pancytopenia.
  • Liver function tests, INR, albumin; renal function; LDH and uric acid.
  • Infective screen — malaria smear and rapid test, rK39 for kala-azar, blood cultures, Widal, brucella serology, viral hepatitis serology, HIV, EBV and CMV serology, Mantoux/IGRA.
  • Ultrasound abdomen with Doppler — organ size and texture, focal lesions, portal vein diameter and flow, splenic vein, ascites, lymph nodes.
  • CECT abdomen for masses, lymphadenopathy and staging.
  • Bone marrow aspiration and biopsy — for haematological malignancy, marrow infiltration, and to demonstrate LD bodies in kala-azar.
  • Lymph node biopsy where there is lymphadenopathy; liver biopsy in selected cases.
  • Specific tests as directed: haemoglobin electrophoresis, autoimmune profile, serum ACE, enzyme assays for storage disorders, and upper GI endoscopy for varices where portal hypertension is suspected.

Management

Treat the underlying cause — this is the whole of management. Additional considerations:

  • Avoid contact sports and trauma with significant splenomegaly, because of the risk of splenic rupture — advice that is regularly forgotten.
  • Manage hypersplenism (cytopenias) — treat the cause; splenectomy or splenic artery embolisation in selected cases.
  • If splenectomy is performed: vaccinate against pneumococcus, meningococcus and *Haemophilus influenzae* type b at least 2 weeks beforehand, give lifelong penicillin prophylaxis, and provide a patient alert card — overwhelming post-splenectomy infection is rapidly fatal and entirely preventable.

All questions in Hepatology / GIT

  1. Q1Discuss the aetiology, serology, clinical features, complications and management of viral hepatitis. ★
  2. Q2Discuss the aetiology, clinical features, complications, investigations and management of cirrhosis of the liver. ★
  3. Q3Discuss the causes, clinical assessment and management of upper gastrointestinal bleeding. ★
  4. Q4Discuss the aetiology, clinical features, severity assessment, complications and management of acute pancreatitis. ★
  5. SN1Write a short note on the approach to jaundice and interpretation of liver function tests.
  6. SN2Write a short note on acute liver failure.
  7. SN3Write a short note on non-alcoholic fatty liver disease and alcoholic liver disease.
  8. SN4Write a short note on portal hypertension and ascites.
  9. SN5Write a short note on hepatic encephalopathy.
  10. SN6Write a short note on hepatorenal syndrome.
  11. SN7Write a short note on spontaneous bacterial peritonitis and secondary peritonitis.
  12. SN8Write a short note on amoebiasis — intestinal and hepatic.
  13. SN9Write a short note on Wilson's disease.
  14. SN10Write a short note on the clinical approach to hepatomegaly and splenomegaly.
  15. SN11Write a short note on peptic ulcer disease, Helicobacter pylori and Zollinger-Ellison syndrome.
  16. SN12Write a short note on gastro-oesophageal reflux disease.
  17. SN13Write a short note on chronic diarrhoea and malabsorption.
  18. SN14Write a short note on inflammatory bowel disease.
  19. SN15Write a short note on acute infective diarrhoea — cholera and bacillary dysentery.
  20. SN16Write a short note on lower gastrointestinal bleeding.

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