This document provides information on signs of abnormal liver and spleen, as well as mechanisms and causes of hepatomegaly, splenomegaly, and hepatosplenomegaly. It describes how the liver and spleen should feel on examination and lists various conditions that can lead to enlargement. These include increased cell size/number from storage diseases, inflammation, infiltrating cells from tumors or infections, increased vascular/biliary spaces from congestion, and idiopathic causes. Specific infectious, oncologic, metabolic, and hematologic etiologies are outlined.

2. Hepatomegaly

3. · >3.5cm below the right costal margin in
a newborn
· Rubbery (hepatitis)
·Tender (acute hepatitis, right heart
failure, venous congestion)
· Firm (cirrhosis)
· Nodular (malignancy)
Signs of an Abnormal Liver

4.  Note that liver is easily palpated in most
children at 1-2 cm below the right costal
margin. A normal liver should feel soft
and is easily moveable upon inspiration.

5. Mechanisms of Hepatomegaly
INCREASE INTHE NUMBER OR
SIZE OFTHE CELLS INTRINSICTO
THE LIVER
INFILTRATION OF
CELLS
INCREASED SIZE OF
VASCULAR SPACE
INCREASED SIZE OF
BILIARY SPACE
IDIOPATHIC
(? “BENIGN”)

6. Mechanisms of Hepatomegaly
1INCREASE INTHE NUMBER OR SIZE OFTHE CELLS
INTRINSICTOTHE LIVER
Storage
Fat:malnutrition, obesity, metabolic liver disease (diseases of
fatty acid oxidation and Reye syndrome–like illnesses), lipid
infusion (total parenteral nutrition), cystic fibrosis, diabetes
mellitus, medication related, pregnancy
Specific lipid storage diseases: Gaucher, Niemann-Pick,
Wolman disease
Glycogen:glycogen storage diseases (multiple enzyme defects);
total parenteral nutrition; infant of diabetic mother, Beckwith
syndrome
Miscellaneous: α1-antitrypsin dificiency, Wilson disease,
hypervitaminosis A, neonatal iron storage disease

7. Inflammation
Hepatocyte enlargement (hepatitis)
Viral:acute and chronic
Bacterial:sepsis, abscess, cholangitis
Toxic:drugs
Autoimmune
Kupffer cell enlargement
Sarcoidosis
Systemic lupus erythematosus
Mast cell activating syndrome
2INFILTRATION OF CELLS
Primary LiverTumors
Benign
Hepatocellular
Focal nodular hyperplasia
Nodular regenerative hyperplasia

8. Hepatocellular adenoma
Mesodermal
Infantile hemangioendothelioma
Mesenchymal hamartoma
Cystic masses
Choledochal cyst
Hepatic cyst
Hematoma
Parasitic cyst
Pyogenic or amebic abscess
Malignant
Hepatocellular
Hepatoblastoma
Hepatocellular carcinoma
Mesodermal
Angiosarcoma
Undifferentiated embryonal sarcoma

9. Secondary or metastatic processes
Lymphoma
Leukemia
Histiocytosis
Neuroblastoma
Wilms tumor
3INCREASED SIZE OFVASCULAR SPACE
Intrahepatic obstruction to hepatic vein outflow
Veno-occlusive disease
Hepatic vein thrombosis (Budd-Chiari syndrome)
Hepatic vein web
Suprahepatic
Congestive heart failure
Pericardial disease
Tamponade
Constrictive pericarditis
Hematopoietic:sickle cell anemia, thalassemia

10. 4INCREASED SIZE OF BILIARY SPACE
Congenital hepatic fibrosis
Caroli disease
Extrahepatic obstruction
5IDIOPATHIC (? “BENIGN”)

11. Significant hepatomegaly
with minimal or absent
splenomegaly
 Liver abscess
 Hydatid cyst
 Glycogen storage diseases
 Cirrhosis
 Primary or metastatic malignancy
 Mucopolysaccharidosis
 Veno occlusive disease
 Budd Chiari syndrome

12. Splenomegaly

13. >2 cm below left costal margin
Abnormally rough surface
Tender
Hard
Signs of Abnormal Spleen

14. NOTE
 A soft, thin spleen may be palpable in
15% of neonates, 10% of normal
children, and 5% of adolescents.
 In most individuals, the spleen must be
2–3 times its normal size before it is
palpable

15. Pathophysiology of splenomegaly
ANATOMIC
LESIONS
HYPERPLASIA
CAUSED BY
HEMATOLOGIC
DISORDERS
INFECTIONS[†]
IMMUNOLOGIC
AND
INFLAMMATORY
PROCESSES[*]
CONGESTIVE[*] STORAGE
DISEASES
MALIGNANCIES

16. Pathophysiology of
splenomegaly
 1ANATOMIC LESIONS
Cysts, pseudocysts ,Hamartomas, Polysplenia
syndrome Hemangiomas and lymphangiomas
Hematoma or rupture (traumatic) Hamartoma
2HYPERPLASIA CAUSED BY HEMATOLOGIC
DISORDERS
Acute and Chronic Hemolysis[*]
Hemoglobinopathies (sickle cell disease in
infancy with or without sequestration crisis

17. and sickle variants, thalassemia major, unstable
hemoglobins)
Erythrocyte membrane disorders (hereditary
spherocytosis, elliptocytosis, pyropoikilocytosis)
Erythrocyte enzyme deficiencies (severe G6PD
deficiency, pyruvate kinase deficiency) Immune
hemolysis (autoimmune and isoimmune hemolysis)
Paroxysmal nocturnal hemoglobinuria
Chronic Iron Deficiency
Extramedullary hematopoiesis
Severe hemolytic anemias

18.  Myeloproliferative diseases:
 chronic myelogenous leukemia (CML), juvenile CML,
myelofibrosis with myeloid metaplasia, polycythemia vera
 Osteopetrosis
 Patients receiving granulocyte and granulocyte-macrophage
colony-stimulating factors
3 INFECTIONS[†]
 Bacterial
 Acute sepsis: Salmonella typhi, Streptococcus pneumoniae,
Haemophilus influenzae type b, Staphylococcus aureus
 Chronic infections: infective endocarditis, chronic
meningococcemia, brucellosis, tularemia, cat-scratch disease
 Local infections: splenic abscess (S. aureus, streptococci,
less often Salmonella species, polymicrobial species),
pyogenic liver abscess (anaerobic bacteria, gram-negative
enteric bacteria), cholangitis

19.  Viral[*]
 Acute viral infections, especially in children
Congenital cytomegalovirus (CMV), herpes simplex,
rubella Hepatitis, A, B, and C;CMV Epstein-Barr virus
(EBV)Viral hemophagocytic syndromes: CMV, EBV,
HHV-6 Human immunodeficiency virus (HIV)
Spirochetal
 Syphilis, especially congenital syphilis Leptospirosis
 Rickettsial
 Rocky Mountain spotted fever Q feverTyphus
 Fungal/Mycobacterial Miliary tuberculosis
 Disseminated histoplasmosis South American
blastomycosis Systemic candidiasis (in
immunosuppressed patients)

20.  Parasitic
 MalariaToxoplasmosis, especially congenital
Toxocara canis,Toxocara cati (visceral larva migrans)
Leishmaniasis (kala-azar) Schistosomiasis (hepatic-
portal involvement)Trypanosomiasis Fascioliasis
4IMMUNOLOGICAND INFLAMMATORY
PROCESSES[*]
 Systemic lupus erythematosus Rheumatoid arthritis,
Mixed connective tissue disease Systemic vasculitis
,Serum sickness, Drug hypersensitivity, especially to
phenytoin ,Graft vs host disease, Sjögren syndrome,
Cryoglobulinemia ,Amyloidosis ,Sarcoidosis, Large
granular lymphocytosis and neutropenia
,Histiocytosis syndromes, Hemophagocytic
syndromes (nonviral, familial)

21.  5MALIGNANCIES
 Primary:leukemia (acute, chronic), lymphoma,
angiosarcoma, Hodgkin disease
 Metastatic
 6STORAGE DISEASES
 Lipidosis (Gaucher disease, Niemann-Pick disease,
infantile GM1 gangliosidosis)
Mucopolysaccharidoses (Hurler, Hunter-type)
Mucolipidosis (I-cell disease, sialidosis, multiple
sulfatase deficiency, fucosidosis)
Defects in carbohydrate metabolism:
galactosemia, fructose intolerance Sea-blue
histiocyte syndrome

22.  7CONGESTIVE[*]
Heart failure
Intrahepatic cirrhosis or fibrosis
Extrahepatic portal (thrombosis), splenic,
and hepatic vein obstruction (thrombosis,
Budd-Chiari syndrome

23. Massive splenomegaly with
minimal hepatomegaly
 Portal hypertension
 Thalassemia major
 CML
 Myeloid metaplasia
 Chronic malaria
 Kala azar
 Gaucher’s disease
 Amyloidosis

24. *DO NOT MISS:
sequestration crisis in sickle disease is a
medical emergency with 10-15% mortality in
the pediatric population!

25. Hepatosplenomegaly

26. Hepatosplenomegaly: Causes
 Infective:
 Viral: Hepatotrophic (A,B,C,D,E) and other viruses (herpes,
cytomegalo, Ebstein-Barr, varicella,HIV, rubella, adeno,
entero, arbo.)
 Protozoal: malaria, kalazar, amoebic, toxoplasma
 Bacterial: sepsis; tuberculosis, brucellosis, syphilis,
 Helminths: hydatid, visceral larva migrans
 Fungal: histoplasmosis

27.  Haemopoetic:
 Haemolytic: haemolytic disease of newborn thalassaemia;
 Anaemia
 Metabolic:
 Neiman-Pick, gangliosidosis, Gaucher, fucosidosis,Wolman,
glycogen storage, sialiodosis, galactosialiodosis, a-
mannosidosis.
 Malignancies:
 Leukemia, histiocytic syndromes, myeloproliferative
syndromes, lymphomas,
 Immunological:
 Chronic granulomatous, heriditory neutrophilia, Ommen
syndrome.

28. Developmental:
Congenital hepatic fibrosis
Congestive:
Hepatic vein obstruction, constrictive pericarditis

29. Hepatosplenomegaly
with Rash

30. Hepatosplenomegaly with
Rash
Differential diagnosis
1 Infections
Bacterial
Typhoid , brucellosis , syphilis
Viral
Infectious mononucleosis , rubella
Cytomegalovirus,hepatitis B virus infection
Parasitic
toxoplasmosis

31. 2 Autoimmune
Systemic type of rheumatoid arthritis , SLE
3Drugs
Phenytoin
4Others
Langerhan’s cell histiocytosis

32. Lymphadenopathy
 Most lymph nodes are not usually palpable in
the newborn.With antigenic exposure,
lymphoid tissue increases in volume so that the
cervical, axillary, and inguinal nodes are often
palpable during childhood.
 They are not considered enlarged until their
diameter is:
 > 1 cm for cervical and axillary nodes
 > 1.5 cm for inguinal nodes.

33. Lymphadenopathy
 Lymph node enlargement is
caused by proliferation of normal
lymphoid elements or by
infiltration with malignant or
phagocytic cells
• Acutely infected nodes are usually tender. There may
also be erythema and warmth of the overlying skin
• Fluctuance - abscess formation.
•Tuberculous nodes may be matted.
•Chronic infection- many signs are not present.
•Tumor-bearing nodes -firm and nontender and may
be matted or fixed to the skin or underlying
structures.

34.  Generalized adenopathy (enlargement of >2
noncontiguous node regions) is caused by
systemic disease and is often accompanied by
abnormal physical findings in other systems.
 Regional adenopathy is most frequently the
result of infection in the involved node and/or
its drainage area
 When due to infectious agents other than bacteria,
adenopathy may be characterized by atypical anatomic
areas, a prolonged course, a draining sinus, lack of prior
pyogenic infection, and unusual clues in the history (cat
scratches, tuberculosis exposure, venereal disease).

35. Generalized Lymphadenopathy
INFANT CHILD ADOLESCENT
COMMON CAUSES
Syphilis Viral infection Viral infection
Toxoplasmosis EBV EBV
CMV CMV CMV
HIV HIV HIV
Toxoplasmosis Toxoplasmosis
Syphilis

36. RARE CAUSES
Chagas disease
(congenital)
Serum sickness Serum sickness
Congenital leukemia SLE, JRA SLE, JRA
Congenital tuberculosis Leukemia/lymphoma Leukemia/lymphoma/Ho
dgkin disease
Reticuloendotheliosis Tuberculosis Lymphoproliferative
disease
Lymphoproliferative
disease
Measles Tuberculosis
Metabolic storage disease Sarcoidosis Histoplasmosis
Histiocytic disorders Fungal infection Sarcoidosis
Plague Fungal infection
Langerhan cell
histiocytosis
Plague
Chronic granulomatous
disease
Drug reaction
Sinus histiocytosis Castleman disease
Drug reaction

37. Local Lymphadenopathy
CERVICAL
 Oropharyngeal infection
(viral or group A
streptococcal,
staphylococcal)
 Scalp infection
 Mycobacterial
lymphadenitis
(tuberculosis and
nontuberculous
mycobacteria)

 Viral infection (EBV, CMV,
HHV-6)
 Cat-scratch disease
 Toxoplasmosis
 Kawasaki disease
 Thyroid disease
 Sinus histiocytosis
 Autoimmune
lymphoproliferative
disease

38. ANTERIOR AURICULAR- Conjuctivitis ,Other
eye infection, Oculoglandular
tularemia,Facial cellulitis
POSTERIOR AURICULAR- Otitis media , Viral
infection (especially rubella, parvovirus)
SUPRACLAVICULAR -Malignancy or infection in
the mediastinum (right) , Metastatic malignancy
from the abdomen (left) , Lymphoma,
Tuberculosis
EPITROCHLEAR - Hand infection, arm infection,
Lymphoma, Sarcoid, Syphilis

39. INGUINAL- Urinary tract infection ,Venereal disease,
Lower extremity suppurative infection, Plague
HILAR- Tuberculosis , Histoplasmosis, Blastomycosis,
Coccidioidomycosis, Leukemia/lymphoma, Hodgkin
disease, Metastatic malignancy,Sarcoidosis ,
Castleman disease
AXILLARY - Cat-scratch disease, Arm or chest wall
infection, Malignancy of chest wall ,
Leukemia/lymphoma ,Brucellosis
ABDOMINAL -Malignancies ,Mesenteric adenitis
(measles, tuberculosis,Yersinia, group A

40. Hepatosplenomegaly
with
Lymphadenopathy

41. Hepatosplenomegaly with
Generalised Lymphadenopathy
Differential diagnosis
1 Infections
Bacterial
Typhoid , brucellosis , miliary tuberculosis ,
syphils
Viral
Infectious mononucleosis
Parasitic
toxoplasmosis

42. 2 Haematological
Lymphoma , leukaemia
3 Metabolic
Niemann-Picks disease , Hurler’s disease
4Rheumatological
Rheumatoid arthritis , SLE
5Drugs
Phenytoin
6Others
Langerhan cell histiocytosis

43. Is there any history of recent infection? (eg: rash, pharyngitis, cough, SOB, fever,
exposure, poorfeeding, malaise etc)
Has the child consumed any contaminated food or experienced any diarrhea and/or
vomiting?
Is there any history of loss of consciousness or seizures?
 Are there any constitutional symptoms such as fever, night sweats, or weight loss?
Is there any abnormal bruising, bone pain, or history of frequent infections?
Does the child have any preexisting liver diseases, lung diseases, or congenital heart
diseases?
Were there any complications during pregnancy, delivery, and after delivery?
 Are there any growth (weight gain) and developmental concerns?
Was there persistent, unresolved jaundice following delivery?
Is there any maternal history of hepatitis B or C, CMV, EBV or HIV?
 Does the child have any history of surgeries or transfusions?
Is there any family history of cystic fibrosis, alpha-1 antitrypsin deficiency, storage
diseases, liver diseases, heart diseases, autoimmune diseases or malignancy?
Has the child had any change in stool color?What color are his/her stools?
Is there any history of drug or toxin ingestion? Is there any exposure to radiation?
Is the child on any medications right now?
Is there any recent travel,trauma?
Questions to Ask

44. SKIN: Petechiae and purpura (thrombocytopenia, autoimmune
disorder, malignancy); jaundice (hemolytic anemia or liver disease);
rashes (infection, lupus, RA, infective endocarditis)
EYE: Icterus, uveitis, iritis (sarcoidosis or rheumatoid arthritis), cherry
red retinal spots or cloudy cornea (lipid storage disease) Kayser-Fleischer
(Wilson’s disease)
CVS/ RESPIPATORY SYSTEM:
Murmur, SOB, fatigue (anemia or heart failure) , abnormal heart sounds
(S3, S4) (congenital heart diseases), SOB/ abnormal breath sounds
(alpha-1 antitrypsin deficiency)
GIT:
tenderness, distension, ascites, hepatosplenomegaly
MSK:
joint tenderness (RA, lupus, hepatitis), bone pain (malignancy)
NEUROLOGICAL: Poor vision (osteopetrosis), loss of developmental
milestones (storage diseases, chronic infection, or immunodeficiency)
General Physical examination

45. Examine this patient who may have chronic liver disease
SIGNS OF CHRONIC LIVER DISEASE
1Examine the fingers for white nails (leukonychia) with loss of the
lunula (half-moons at the nail base) and ankle oedema - all due to
hypoalbuminaemia.
2Look for spider naevi (upper half of the body), palmar erythema,
gynaecomastia and testicular atrophy - all due to oestrogen excess.
3Look for bruising due to:
• Thrombocytopenia (hypersplenism)
• Reduced hepatic synthesis of coagulation factors (II, VII, IX and
X)
• Multiple falls due to alcohol intoxication.
4Look for muscle wasting from malnutrition and/or liver synthetic failure.
5Examine for signs of liver failure:
• Look for a coarse flap of the outstretched hands (asterixis) due to
metabolic brainstem dysfunction (other causes include heart,
renal and respiratory failure)
• Smell the patient's breath to detect fetor hepaticus (a sweetish,
musty smell) due to accumulation of the volatile amine, methyl
mercaptan
• Check for signs of hepatic encephalopathy (grade 1-4) due to the
metabolic changes affecting cerebral function.

46. LIVER EXAMINATION
Palpation
 Start in the right iliac fossa. Place your hand flat on the
abdomen with your fingers pointing upwards and
sensing fingers (index and middle) lateral to the rectus
muscle, so that your finger tips lie parallel to rectus
sheath

Keep your hand stationary. Ask the patient to breathe
in deeply through the mouth. Feel for the liver edge as
it descends on inspiration.

Move your hand progressively up the abdomen, 1 cm at
a time, between each breath the patient takes, until
you reach the costal margin or detect the liver edge.

47.  Right lobe is palpable in the right
hypochondrium or lumber region depending
on extent of enlargement
 Left lobe is palpable in the epigastrium.it
indicates chronic hepatomegaly.

48. Palpation of liver

49. Percussion:
 Liver span is determined better by percussion than by palpation
in children.
 Percuss along the midclavicular line to find the upper margin of
the liver.The transition from resonance to dullness indicates the
upper liver border.It usually lies in 4th intercostal
space. Resonance below the 5th intercostal space suggests
emphysema or occasionally the interposition of the transverse
colon between the liver and the diaphragm (Chilaiditi's sign).
Measure the distance in centimetres below the costal margin in
the midclavicular line or from the upper border of dullness to the
palpable liver edge.
 Continue percussion down the subcostal region keeping fingers
parallel to the ribs.The note turns resonant beyond the lower
margin of liver

50. Scratch test
Place the diaphragm of your stethoscope just
above the right costal margin at the midclavicular
line.
Lightly scratch the skin of the abdomen with the
fingertip along the midclavicular line, starting from
below the umbilicus towards the costal margin.
 A change in sound indicates the liver edge.

51. The scratch test to determine the liver’s edge

52. Liver Size
Liver is usually described in cm palpable below the
right costal margin in the mid clavicular line
Liver span is distance b/w upper & lower border of
liver..
Note the size ,surface,consistency, margins,
tenderness, or the presence of any masses or
bruits

53. Normal liver size estimations are based on age-
related clinical indices, such as:
~ the degree of extension of the liver edge below
the costal margin;
~ the span of dullness to percussion;
~or the length of the vertical axis of the liver,as
estimated from imaging techniques.
The liver span increases linearly with body
weight and age in both sexes, ranging from
≈4.5–5.0 cm at 1 wk of age to ≈7–8 cm in boys
and 6.0–6.5 cm in girls by 12 yr of age.
Normal liver span in adults 10 – 15 cm

55. Pattern of liver enlargement

56. ~Downward displacement of the liver by the
diaphragm (pneumothorax ,emphysema or
respiratory distress) or thoracic organs can
create an erroneous impression of
hepatomegaly.But total liver span is normal.
~Sometimes liver may be palpable below
costal margin but total span is reduced
suggesting cirrhosis
NOTE
~The lower edge of the right lobe of the liver
extends downward (Riedel lobe) and is
palpable as a broad mass in some normal
people

57. Surface
 Gently roll the fingers over the surface of liver
 Nodular in cirrhosis & malignancy
Consistency
 Hard as a bone in hepatic malignancy
 Firm as tip of nose in chronic conditions,like
obstructive jaundice,cirrhosis or haemolytic
anaemias
 Soft in acute viral hepatitis or CCF

58. Margins
 Smooth in normal liver
 Sharp and leafy in cirrhosis or malignancy
Tenderness
 While palpating the liver see if pt winces or
not
 Liver is tender in acute viral hepatitis , CCF ,
hepatic amoebiasis , pyaemic abscess of liver
,hepatoma,actinomycosis,weil’s disease

59. Bruits over liver
May be heard in hepatoma,AV malformation,
hepatocellular cancer & alcoholic hepatitis
Pulsatile liver
Indicates tricuspid regurgitation

60. Palpation:
Patient should be supine and relaxed
Relaxation is improved if legs and neck are
slightly flexed
Start palpating from lower left quadrant in
infants, as the spleen tends to enlarge inferiorly
towards the left iliac fossa.
 Palpation should be started from the right
lower quadrant in older children.
Splenic Examinaion

61.  Start from the umbilicus. Keep your hand stationary
and ask the patient to breathe in deeply through the
mouth. Feel for the splenic edge as it descends on
inspiration (Fig. A).

Move your hand diagonally upwards towards the left
hypochondrium 1 cm at a time between each breath
the patient takes.

Feel the costal margin along its length, as the
position of the spleen tip is variable.

If you cannot feel the splenic edge, ask the patient to
roll towards you and on to his right side; repeat the
above. Palpate with your right hand, placing your left
hand behind the patient's left lower ribs, pulling the
ribcage forward (Fig. B).

62. Palpation of the spleen.

63. Palpation of the spleen
 With the patient in the right lateral position,
minimal splenic enlargement can be detected
by examining either from in front or in back of
the patient

64. Palpation
The Hooking maneuver of Middleton
o place the patient’s Left fist under their Left
posterior chest
o position yourself on the patient’s Left side,
facing the patient’s feet
o using both hands, curl your fingers under the
patient’s Left costal margin
o ask the patient to take a long, deep breath à
attempt to palpate the spleen with your
fingertips

66. Castell’s method:
 percuss the lowest intercostal space in the
left anterior axillary line.
In normal cases dull note is present only on
inspiration
In splenomegaly dull note is present both in
inspiration and expiration
More useful in infectious mononucleosis
where direct palpation can cause rupture
Percussion

68. Traube’s space:
bound superiorly by the 6th rib; laterally
by the mid-axillary line and inferiorly by
the costal margin.
Dullness to percussion indicates
splenomegaly

71. Percussion by Nixon’s method
o place the patient in Right lateral decubitus
o begin percussion midway along the Left
costal margin
o proceed in a line perpendicular to the Left
costal margin
o if the upper limit of dullness extends >8 cm
above the Left costal margin, in adults, this
indicates possible splenomegaly

72. The landmarks used in Nixon’s
Method

73. Spleen size
~The size of spleen is measured from the left
subcostal margin in the midclavicular line to
the tip along the direction of enlargement
~It is also described in cm below the subcostal
margin
Mild splenomegaly
Only tip is palpable
or it is palpable just 1-2 cm below costal margin
Moderate splenomegaly
Easily palpable,but not reaching umbilicus
or if it is palpable 3-7 cm below the costal margin
Massive splenomegaly
Extending upto umbilicus or beyond
Or if it is palpable >7cm below the costal margin

74. Pattern of spleen enlargement

75. Hackett’s classification of
splenomegaly
GRADE STAGE EXAMINATION
0 Not palpable
MILD 1 Just palpable
MODERATE 2 Midway between costal margin
&umbilicus
MODERATE 3 Upto umbilicus
SEVERE 4 b/w umbilicus & pubic symphysis
SEVERE 5 Upto pubic symphysis

77. Consistency
Soft in enteric fever
Firm in hemolytic anaemia
A moderate to severely enlarged spleen is
usually Firm
Splenic notch
Felt as an indentation on the lower medial
border of spleen

78. Auscultation
 Friction rub
(inflammation, tumor, infarction)
 systolic murmur over spleen
- massive splenomegaly (dilated, tortuous
splenic artery)

79. D/D
 Left kidney mass
 Left adrenal mass
 Left colonic mass
 Retroperitoneal mass

80. Distinguishing feature Spleen Left Kidney
Mass is smooth and
regular in shape
More likely Polycystic kidneys are
bilateral irregular
masses
Mass descends in
inspiration
Yes, travels
superficially and
diagonally
Yes, moves deeply and
vertically
Able to feel deep to the
mass
Yes No
Palpable notch on the
medial surface
Yes No
Bilateral masses
palpable
No Sometimes (e.g.
polycystic kidneys)
Percussion resonant
over the mass
No Sometimes
Mass extends beyond
the midline
Sometimes No (except with horse-
shoe kidney)

81. SPLEEN MALIGNANT
GROWTH OF
STOMACH/
PANCREAS
EDGE,NOTCH present absent
CROSSINGTO
RIGHT SIDE
If splenic
enlargement is
severe,it crosses
the midline at or
below the
umbilicus
In pancreatic
enlargement the
tumour crosses
the midline above
umbilicus

82. SPLEEN CA SPLENIC
FLEXURE OF
COLON
DIRECTON OF
ENLARGEMENT
More forwards and
inwards
transverse
EDGE,NOTCH present absent
PERCUSSION dull resonant
INTESTINAL
SYMPTOMS
abdominal Blood,fullness,mucus
in stools,alternating
diarrhea and
constipation
BARIUM STUDIES normal Show pathological
lesion

83. Pseudosplenomegaly.
 Abnormally enlarged mesenteric connections may
produce a wandering or ptotic spleen.
 An enlarged left lobe of the liver, a left upper quadrant
mass, or a splenic hematoma may be mistaken for
splenomegaly.
 Splenic cysts may contribute to splenomegaly or mimic
it; these may be congenital (epidermoid) or acquired
(pseudocyst) after trauma or infarction. Cysts are
usually asymptomatic and are found on radiologic
evaluation.
 Splenosis after splenic rupture or an accessory spleen
(present in 10% of normal individuals) may also mimic
splenomegaly; most are not palpable.
 The syndrome of congenital polysplenism includes
cardiac defects, left-sided organ anomalies, bilobed
lungs, biliary atresia, and pseudosplenomegaly

84. Hypersplenism.
 Increased splenic function (sequestration or destruction of
circulating cells) results in peripheral blood cytopenia,
increased bone marrow activity, and splenomegaly. It is
usually secondary to another disease and may be cured by
treatment of the underlying condition or, if absolutely
necessary, moderated by splenectomy.
Congestive Splenomegaly (Banti
Syndrome).
 Splenomegaly may result from obstruction in the hepatic,
portal, or splenic veins .
 Septic omphalitis or thrombophlebitis may be spontaneous
or may occur as a result of umbilical venous catheterization
in neonates and may also result in secondary obliteration of
these vessels.
 Splenic venous flow may be obstructed by masses of sickled
erythrocytes.
 When the spleen is the site of vascular obstruction,
splenectomy cures hypersplenism.

85. Tropical Splenomegaly Syndrome
 “Big spleen”
 defined as hyperreactive malarial syndrome
(HMS)

86. Visceroptosis
 Visceroptosis is a prolapse or a sinking of
the abdominal viscera (internal organs)
below their natural position. Any or all of
the organs may be displaced downward
 May give false impression of
hepatomegaly or splenomegaly

87. Lymph nodes
General principles
•Inspect for visible
lymphadenopathy.
•Palpate one side at a time using the fingers
of each hand in turn.
•Compare with the nodes on the
contralateral side.

88.  Assess:
 Site
 Size
 Consistency
 Tenderness.
 Determine whether the node is fixed to:
 Surrounding and deep structures
 Skin.
 Measure the main nodes.

89. Cervical nodes
 From behind, examine the submental, submandibular,
preauricular, tonsillar, supraclavicular and deep cervical nodes in
the anterior triangle of the neck
 Palpate for the scalene nodes by placing the index finger
between the sternocleidomastoid muscle and clavicle. Ask the
patient to tilt his head to the same side and press firmly down
towards the first rib.
 From the front of the patient, palpate the posterior triangles, up
the back of the neck and the posterior auricular and occipital

90. Axillary nodes
 From the patient's front or
side, palpate the right axilla
with the left hand and vice
versa
 Gently place the finger tips
into the apex of the axilla and
then draw them downwards,
feeling the medial, anterior
and posterior axillary walls in
turn. Keep the nails short to
avoid causing discomfort.

91. Epitrochlear nodes
 Support the patient's
right wrist with the left
hand, grasp his partially
flexed elbow with the
right hand, and use the
thumb to feel for the
epitrochlear node.
Examine the left
epitrochlear node with
the left thumb

92. Inguinal nodes
 Examine for the inguinal
and popliteal nodes with
the patient lying down.
 Palpate over the
horizontal chain, which
lies just below the
inguinal ligament, and
then over the vertical
chain along the line of
the saphenous vein

93. Laboratory Investigations
•Complete blood count, peripheral blood smear, ESR
AST, ALT, GGT, alkaline phosphatase, bilirubin, total
protein, albumin, prothrombin time
Serum electrolytes and BUN
Urinalysis
CBC with differential and peripheral blood smear
Fasting blood glucose
Hepatitis serology
Additional investigations based on clinical suspicion: EKG,
total and direct bilirubin, lipid profile, ceruloplasmin, alpha-
1-antitrypsin (AAT), blood culture, autoantibodies, alpha
fetoprotein, Viral serology (EBV, CMV, Parvovirus B19, HIV
etc.), acid beta-glucosidase (↓ in Gaucher disease), ANA (for
SLE), bone marrow aspirate and biopsy

94. Lactate Free Fatty
Acids
B-
Hydroxybutyra
te
Glucose
Glycogen Storage
Diseases
↓ N N N
Defect in
Gluconeogenesis
↓ ↑ N ↓/N
Defect in Fatty Acid
metabolism
↓ N ↑ ↓
Common laboratory findings in storage
diseases

95. Abdominal ultrasound with Doppler
Hyperechogenic hepatic parenchyma can be seen
with metabolic disease (glycogen storage disease
Abdominal CT or MRI (hepatic masses, biliary tree,
anatomical obstructions)
Echocardiogram (congenital heart defects)
ERCP (stones)
Liver Imaging
Liver Biopsy

96. Hepatomegaly.The right lobe of the liver extends well below the lower pole of the right kidney
(K) and measures 20 cm (between cursors, +), well exceeding the normal limit of 15.5 cm

97. Splenic Imaging (not
routinely done)
Ultrasound (for identifying space occupying
lesions such as cysts or abcess and
differentiating between kidney vs splenic
abnormalities)
CT scan or MRI: (for ruling out disseminated
malignancy and liver diseases)
Radioactive (Tc-99m) sulfur colloid
scintigraphy (the only radiological modality
that provides functional information)

98. Splenomegaly - In this picture we can see the affinity between spleen
and left kidney.
We can not measure just from such picture, but spleen is undoubtedly
enlarged.

99. Lymph nodes
 Fine-needle aspiration
 Cutting needle biopsies
 Excisional biopsy,
If pus is present, it may be aspirated, with
CT or ultrasound guidance, or if it is
extensive, it will require incision and
drainage. Gram stain and culture of the
pus should be obtained. Surgical drainage
is required for an abscess.

100. Imaging Studies
•Chest X-ray - Mediastinal
adenopathy and underlying
pulmonary diseases.
•Ultrasound of the lymph node
•Nuclear medicine scanning -
lymphomas.
•Lymphangiography -
assessment of the lower
abdominal lymph nodes &
response to therapy.
•CT or US guided lymph node
biopsy

101. Some common causes of
hepatosplenomegaly c LAP
CAUSE CLINICAL FEATURES DIAGNOSTIC
INVESTIGATION
TYPHOID Stepladder rise of fever , relative
bradycardia, rose spots , pea soup
stools, HSM , LAP
PCR , Widal test , blood
culture , leukopenia
MILIARY TB High fever , failure to thrive , may
be CNS lesions , HSM , LAP
H/OTB , +ve Mantoux
test , miliary mottling on
chest X ray
BRUCELLOSI
S
High fever , sweating , jaundice ,
HSM , LAP
H/O of association with
cattle , Brucella
agglutination test,
culture
CONGENITAL
SYPHILIS
LBW , prolonged physiological
jaundice , codyloma , snuffles ,
maculopapular rash , bullous
lesion , pseudoparalysis of parrot
H/O repeated abortions ,
still birth , child born
with syphilitic
stigmata,VDRL , FTA-

102. CAUSE CLINICAL FEATURES DIAGNOSTIC
INVESTIGATION
INFECTIOUS
MONONUCLEOSIS
Sore throat , fever , rash , LAP
, HSM
P/S Downey cells , Paul
Bunnel test
MALARIA Fever , chills & rigors
,sweating, anaemia,HSM
QBC , thick & thin smear
KALA AZAR Fever , anaemia , ashen grey
colour , jaundice
,cachexia,HSM
Endemic area ,P/S LD
bodies , Montenegro
test
HAEMOLYTIC
ANAEMIA
Anaemia 4-6 months after
birth
Jaundice , progessive
enlargement of skull bones,
malar prominence,HSM,LAP
P/S , osmotic fragility
test, Na metabisulphite
,electrophoresis , RBC
survival time
LEUKAEMIA Pallor , pyrexia , purpura , pain
, HSM ,LAP
FNAC, bone marrow
aspiration
LYMPHOMA Advanced stage: HSM, LAP Gland biopsy , Reed
Sternberg cell