Transcript Differential Diagnosis of Hepatomegaly

Differential Diagnosis
of Hepatomegaly
Hepatomegaly is an important physical sign of
large
number of diseases.
Following characteristics of the liver should be
noticed on physical examination:
1. Liver size ( Upper and lower borders of the
liver, which are determined by percussion by
Kurlov’s method. Normal sizes by Kurlov’s
are; on mid clavicular line-9-10 cm, on
median line-8 cm, and on left costal arch-7
cm).
2. Surface (smooth, nodular).
3. Consistency (dense, soft, firm, hard).
4. Margins (sharp, rounded).
5. Tenderness.
6. Pulsations.
7.Bruit/fraction rub
At palpation of liver it is necessary to define
properties of margins of liver (soft, dense,
sharp,
rounded), tenderness, morbidity and
surface
(smooth, nodular or tubercle).
1. The soft margins of liver with moderately
dense consistency, rounded and smooth
surface of liver is observed at acute and
chronic hepatitis, heart failure, hepatosis,
and liver echinococcosis.
2. The sharp margins, dense consistency,
rough and microtubercular surface of the
liver determines liver cirrhosis,
amyloidosis of liver.
3. Very dense consistency (stone like),
rough, macrotubercular surface indicates
liver cancer.
Diagnostic work for finding out the causes
of hepatomegaly begins with:
- Questioning of the patient, careful collection of
anamnesis.
- Patient’s contacts with patients of acute viral
hepatitis.
- Presence of predisposing factors e.g. blood
transfusions, operative interventions, injections,
alcohol abuse.
- Possible communication of hepatomegaly with
professional intoxications or with reception of
some drugs.
- It is necessary to establish illnesses of relatives.
- Physical examination of the patient is directed
towards the finding of yellowness of sclera,
pigmentation of skin and to find extrahepatic
signs such as vascular stellas, hepatic palms,
gynecomastia, xanthalasm and ascites.
The basic biochemical investigations:
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Levels of serum bilirubin.
Activity of serum transaminases (ALT, AST)
Alkaline phosphatase.
Common protein and albuminous fraction,
albumin sedimentary tests.
Prothrombin index.
Serum cholesterol.
Level of bilirubin and urobilinogen in urine,
stercobilin in feces.
Markers of viral hepatitis A,B,C,D,E.
Immunological researches ( defining of
immunoglobulins IgM, IgG, IgA, auto
antibodies to subcellular structures,
antinuclear antibodies, auto antibodies to
smooth muscles and mitochondria).
Level of concentration of alpha-fetoprotein.
Elementary instrumental methods of
investigation:
(With their help to successfully confirm
lesion of liver and to differentiate focal
and diffuse pathology)
- Ultrasonography of liver.
- Scanning of liver with C189 and Tc199.
Research under indications:
- Laparoscopy.
- Selective angiography.
- Puncture biopsy of liver under control of
ultrasonography.
- CT-scan.
- Bromsulphaleony test.
- Latex-Agglutination test.
- Definition of alpha-fetoprotein by reaction of
Abelov-Tataryne.
Classification of hepatomegaly
The diseases accompanying pre-eminently
increase of liver sizes could be divided into
3 major groups.
I-st group of liver diseases:
1. Acute liver diseases:
- Acute viral hepatitis (A,B,C,D,E).
- Acute drug induced hepatitis.
- Acute toxic hepatitis.
- Acute alcoholic hepatitis.
- Acute hepatosis.
2. Chronic liver diseases:
- Chronic hepatitis (Viral, autoimmune,
drug-induced, cryptogenic)
- Liver cirrhosis (viral, druginduced,
toxic, alcoholic, autoimmune, billiary,
cryptogenic).
- Hereditary hepatosis.
3. Focal lesions of liver:
- Primary cancer of liver.
- Liver echinococcosis.
4. Diseases of vessels of liver:
- Budd-Chiari syndrome and disease.
- Thrombosis of hepatic veins.
5. Lesions of liver at other diseases
(systemic diseases, endocrine disorders,
diseases of organs of hematogenesis,
parasitic
diseases of liver).
II-nd group of liver diseases (Diseases
Of accumulation):
-
Fatty hepatosis.
Wilson- Konovalov disease.
Hemochromatosis.
Amyloidosis of liver.
Alpha-antitrypsin insufficiency.
IIIrd group of liver diseases (Diseases
of cardiovascular system):
- Right heart failure.
- Constrictive pericarditis.
- Congestion of liver.
To distinguish the diseases, accompanying
pre-eminently increase of liver sizes, it is
important to remember their diagnostic
criteria:
Acute Viral Hepatitis
Viral hepatitis A, B, C, D, E.
1. Unfavorable epidemiological anamnesis
(Contact with patient of hepatitis A, E)
2. To find out data of blood transfusion and
its preparations.
3. Parenteral manipulations, repeated
injections (At hepatitis B, C, D.)
4. Period of disease (At hepatitis A, E last
from 1.5-3 weeks, at hepatitis B, C, d till
7-8 weeks).
5. The preicteric period:
- Fever, subfebril, on later stages
temperature is reduced.
- Dyspeptic syndrome: decreased
appetite, nausea, vomiting, bitterness of
mouth, abdominal distension.
- Catarrhal syndrome: same as Grippe
(Flu).
- Intoxication syndrome: weakness, pain
in joints and bones.
- Astenovegetaitve syndrome: general
weakness, muscular weakness,
decreased work ability.
- Objective examination in preicteric
period reveals hepatomegaly and dark
urine.
6.
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Icteric period:
Syndrome of hepatocellular insufficiency
Dark urine.
Acholic stool.
Jaundice of skin.
Itching.
Hepatomegaly.
Hemorrhage.
Nasal bleeding.
Sharply increased activity of
transaminases (ALT, AST, LDH3)
Hyperbilirubinemia(increased conjugated
and nonconjugated serum bilirubin)
Dysproteinemia (Increased alpha-2 and
beta globulins and hypoalbuminemia).
7. Detection of serological markers of viral
hepatitis:
- Hepatitis A virus- AntiHAVIgM
- Hepatitis B virus- HBs Ag, HBeAg, Anti
HBc IgM, and DNA-polymerase.
- Hepatitis C virus- Anti HCVIgM, HCVRNA.
- Hepatitis D virus- Anti HDVIgM, HDVRNA + markers of HBV.
- Hepatitis E viruse- Anti HEVIgM.
Drug induced and Toxic Hepatitis
1. Drugs with hepatotoxic effects are:
Tetracyclines, Aminosine, Anti TB drugs,
Dopegite, Sulphanilamide, Flothane.
2. Hepatotoxic poisons are chlorinated hydrogen, 4chloride carbons, salts of heavy metals e.g.
Mercury, phosphorus, etc.
3. Drug induced and toxic hepatitis develop rapidly
after the period of sensibilization.
4. It has acute onset with expressed signs of
intoxication.
5. Usually it is accompanied with expressed allergic
manifestations (Urticaria, itching, vasculitis).
6. Expressed cholestatic syndrome is observed with
symptoms of jaundice, itching, dark urine, and
acholic stool.
7. Hepatomegaly is also seen.
8. CBC reveals eosinophillia.
9. Increased levels of alkaline phophatase,
conjugated bilirubin and cholesterol.
Acute Hepatosis
(Acute toxic dystrophy of liver)
It is disease of liver described by
dystrophic changes of its parenchyma
without expressed mesenchymalcellular
reaction. It is caused by various
reasons
(Heavy poisoning with phosphorus,
Arsenic, Heavy intake of alcohol and/or
hepatotoxic medications.
Acute Alcoholic Hepatosis
1. In anamnesis heavy alcohol abuse.
2. Dyspeptic syndrome: Nausea, vomiting,
diarrhea, anorexia and weight loss.
3. Astenovegetative syndrome.
4. Pain syndrome (Pain in right hypochondrium
and epigastric area).
5. Jaundice of hemolytic character.
6. Fever.
7. Blood serum reveals hypercholesterinemia,
hypertriglyceridemia, anemia (hemolytic
character).
8. Hyperbilirubinemia (Nonconjugated and
conjugated).
9. Modorately increased transaminase activity
(ALT, AST).
10. Liver biopsy reveals fatty liver (Excessive
adipose deposition in hepatocytes).
Echinococcosis of Liver
1. Disease is caused by larval stage of Echinococcosus
Granulosus.
2. Epidemiological anamnesis reveals contact with dogs,
use of water and green vegetables contaminated with
dog feces.
3. Disease has slow course.
4. Allergic reactions are seen at early stages (Urticaria,
eosinopillia, skin itching).
5. Pain (Feeling of pressure or dull pain) in right
hypochondrium or epigastric area.
6. Hepatomegaly (Soft consistency, painless smooth
surface).
7. On later stages may appear jaundice and ascites.
8. Positive reaction of Kassoni.
9. Positive reaction of Latex-agglutination with antigens
from liquid of echinococcal cyst.
10. Chest X-ray (Upward lifting of right dome of
diaphragm)
11. USG and scintigraphy of liver.
12. CT-scan(Focal volumetric formation with regular
borders).
Budd-Chiari Disease & Syndrome
1. It is obliterating endophlebitis of hepatic vein. If it is
primary, it is named as disease but if it occurs
secondarily it is termed and syndrome.
2. In either case infringement of outflow of blood from
liver promotes development of portal hypertension.
3. Clinically obliteration of hepatic veins leads to
development of triad of symptoms.
- Hepatomegaly.
- Ascites.
- Splenomegaly.
4. Hepatomegaly is similar to cirrhosis but there is no
cytolytic syndrome or cholestasis.
5. There are no structural infringements of hepatocytes
which are characteristic for cirrhosis.
6. Diagnosis is confirmed with help of angiography or
spleeno-portography or cavagraphy.
7. Etiology of secondary Budd-Chiari Syndrome are:
peritonitis, focal lesions of liver, pericarditis
(especially adhesive pericarditis), thrombophlebitis of
lower extremities, polycythemia and other conditions.
Primary Cancer of Liver
Is characterized by:
1. Hepatomegaly (Lower borders of liver reaches
below level of umbilicus, consistency is stone
like, macro tubercular, liver is deformed due
to non-uniform increase in size and palpation
is sharply painful)
2. Constant pain syndrome at right
hypochondrium, syndrome of minor signs.
3. Intoxication syndrome (Fever, general
weakness, loss of appetite and weight).
4. Jaundice and ascites.
5. LFTs are normal.
6. Leukocytosis and considerable elevation of
ESR.
7. Positive reaction of Iatrein-Abelov on alphafetoprotein.
8. Scientigraphy of liver and CT-scan reveals
focal defects.
VIRAL CIRRHOSIS OF LIVER
(leading syndrome of hepatic
insufficiency)
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developes after chronic viral hepatitis B, C, D
very early in phase replication appears signs hepatic
insufficiency (pain, heaviness in right hypochondria) after
error in diet physical exercise, asthenic dyspeptic hemarogic
(nasal bloodflow, syndrome of hepatic encephalopathy,
jaundice, fever), portal hypertension ascites appears in late
stage
Objectively jaundice may be hepatic smell from mouth, signs
of hepar encephalopathy and hepar coma, teleangiectasy,
hepar is increased in size, densively tuberosity, edge is not
right, splenomegaly
palmary erythema, red colored tongue
blood: anemia, thrombocytopenia, signs hypersplenism –
dysproteinemia (hypoalbuminemia, hyper alpha-2 and gamma
- globulinemia) increased of activity of transaminase ALT,
hyperbilirubinemia, conginetive, hypoholesterinemia,
hypoprothrombinemia, positive serological markers of viral
hepatitis
VIRAL CIRRHOSIS OF LIVER
(leading syndrome of hepatic
insufficiency)
- urine: urobilinuria
- faeces may be aholic
- Ultrasound: structure of liver heterogeneous,
increased different echodensity, forms of liver are
deformed, increased size of liver and spleen
- radioisotope scanning: a big defect of cumullation
of drugs
- poor cumullations in liver
- biopsy of liver – signs macronodular cirrhosis
liver
ALCOHOLIC CIRRHOSIS OF LIVER
(Leading syndrome of portal
hypertension)
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develops in sequence of linering use of alcohol
(daily usage of alcohol in quantity of 60-70 ml
within 10-15 years)
early appearance of portal hypertension, late
stage – hepatic insufficiency
objective signs: malnutrition, pale skin surface,
palmary erythema, vascular stars, ascites, foot
edema, strawberry tongue, varicose diletates.
Liver of small size, spleen is increased
blood: hupo- and normochrom anemia, signs of
hypersplenism, dysproteinemia,
hypoalbuminemia, hyper-gamma globulinemia,
positive sedimentary tests,
hypoprothrombinemia
urine: urobilinuria, many estrogens
ALCOHOLIC CIRRHOSIS OF LIVER
(Leading syndrome of portal
hypertension)
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X-ray – varicose veins esophagus, stomach
ultrasound structure of liver is heterogeneous,
increased different echodensity, forms of liver
are deformed, small size of liver and big size of
spleen, extension of portal vein diameter more
1,3sm, spleen vein more 0,8sm
radioisotope scanning, small increase and
unequal forms of liver, unequal cumulating of
drugs, size of spleen is increased
liver biopsy – signs of micronodular cirrhosis,
giallin bodies of Mallori
AUTOIMMUNE HEPATITIS – CIRRHOSIS LIVER
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female part is more
early signs of inflammation syndrome (or
autoimmune or mesenchimal – inflammatory
syndrome) systemic and off-liver inflammations
(mialgia, artralgia, vasculitis, miocardit, pericardit,
glomerulonefrit, lymphoadenopathia), may be other
autoimmune distinctions (tireoidit, Shegren
syndrome, nonspecific ulcer colitis)
objective signs: jaundice, vasculitis,
lymphoadenopathia, allergic skin efflorescence,
hepatosplenomegaly
progressive flow
blood – erythrocyte sedimentation rate is increased,
hemolytic anemia, distinct hyper-gamma
globulinemia, an absence of B, C, D viral hepatitis
markers – autoantibodies to different liver elements
(antinuclear, smooth-muscle antibodies, antibodies
to liver membrane), high rate of Ig A, M, G may be
appearance of LE-cells, low rate of T-lymphocytes,
harsh increase of aminotransferases more than 10
times, and bilirubine rate conjuncted and non
conjuncted
BILIARY CIRRHOSIS
Biliary cirrhosis results from prolonged
biliary obstruction anywhere between the
small interlobular bile ducts and papilla
of Vater
TYPES:
- Primary
- Secondary
PRIMARY BILIARY CIRRHOSIS
Primary biliary cirrhosis is a chronic
disorder in which small interlobular bile
ducts of the liver become progressively
damaged and eventually leading to
cirrhosis. Women are affected in 90% of
cases in the age range 40-50 years.
Etiology is unknown, immunological
mechanisms may play a part because
antimitochondrial antibodies are found in
almost all patiens.
CLINICAL FEATURES
Symptoms:
1. Pruritus (itching): often preceding jaundice a
few years (this is the earliest symptom) and is
produced by accumulation of bile acids.
2. Jaundice is occasionally present in early stages.
3. Diarrhea – resulting from malabsorbtion of fat
sometimes occur (because fat absorbtion requires
bile salts which are not available in the gut due to
cholestasis)
4. Bone pain or fracture: due to osteomalacia from
malabsorbtion of vitamin D which is fat soluble and
requires bile salts for absorbtion.
CLINICAL FEATURES
Signs:
1. Jaundice
2. Zanthelasma – yellowish deposition of
cholesterol around the eyes and in xreases of hand
(because cholasterol is not excreted in bile due to
cholestasis)
3. Hepatomegaly is almost present while the
splenomegaly occurs late when portal
hypertension develops.
PRIMARY BILIARY CIRRHOSIS
Investigations
1. LFT: very alkaline phosphatase
2. Antimitochondrial antibodies (AMA) present in
>95% of cases
3. Serum cholesterol is high
4. Ultrasound: diffuse alteration in liver
architecture
5. Liver biopsy shows:
- infiltration of portal tract lymphocytes and
plasma cells
- loss of small bile ducts
- portal tract fibrosis
- granulomas in about 40% cases
PRIMARY BILIARY CIRRHOSIS
1.
2.
3.
4.
Diagnosis
Pruritus
Serum alkaline phosphatase very high
Antimitochondrial antibodies present
No extrahepatic bile duct obstruction on
ultrasound
5. Liver biopsy