Symptoms and signs of liver

disease
• Fever • Pallor, Jaundice
• Vomiting/nausea • Hepatomegaly
• Pain RUQ • Splenomegaly
• Yellowish • Edema/ascites*
• Disorientation • Purpuric rashes*
• Hematemesis*
• Malena*
• Abnormal higher
function*
 Evaluation of Patients with
Possible Liver Dysfunction
• Biochemical Tests:
– serum aminotransferase,
– bilirubin (total and fractionated),
– alkaline phosphatase (AP) levels,
– prothrombin time (PT) or international
normalized ratio (INR)
– albumin level.
 Severity of liver disease
• Clinical signs
– encephalopathy, variceal hemorrhage,
worsening jaundice, apparent shrinkage of liver
mass, or ascites.
• Biochemical alterations
– hypoglycemia, acidosis, hyperammonemia,
electrolyte imbalance, continued
hyperbilirubinemia, marked hypoalbuminemia,
or a prolonged PT or INR that is unresponsive
to parenteral administration of vitamin K.
 Interpretation of biochemical tests
• Raised AST and ALT levels
– acute hepatocellular injury;
– In chronic liver disease or
– in intrahepatic and extrahepatic biliary obstruction,
(elevations may be less marked).
– in nonalcoholic fatty liver disease (NAFLD).
• High gamma-globulin levels
– autoimmune hepatitis (anti–smooth muscle,
antinuclear, and anti–liver-kidney-microsome
antibodies).
• Antimitochondrial antibodies
– autoimmune hepatitis.
• α-fetoprotein levels
– hepatoma, hepatoblastoma, or hereditary
tyrosinemia
• Hypoalbuminemia (severe liver disease)
• Deficiencies of factor V and of the vitamin
K–dependent factors (II, VII, IX, and X)
severe liver disease or fulminant hepatic
failure.
 Evaluation of Patients with Possible Liver Dysfunction Contd…..

• Liver Biopsy
• Hepatic Imaging Procedures
– plain x-ray study
– US
– CT/MRI
– Radionuclide scanning
• technetium 99m-labeled sulfur colloid, which
undergoes phagocytosis by Kupffer cells; 99mTc-
iminodiacetic acid agents, which are taken up by
hepatocytes and excreted into bile in a fashion similar
to bilirubin
 Evaluation of Patients with Possible Liver Dysfunction

Contd …..
• Cholangiography
• Endoscopic retrograde
cholangiopancreatography (ERCP)
• Selective angiography
• Upper GI endoscopy
• Barium swallow
 Case History
• A ten year old female child presented in the
emergency because of vomiting of blood in the
morning. She has similar episode one year back
and was transfused two units of blood.
• She was delivered normally at KMC at term
having birth weight of 2500g. She was
discharged on second day. She is exclusively
breast fed up to 4 months.
• On seventh day of life she had umbilical
infection for which she was treated with IV
antibiotics
A ten year old female child presented in the emergency
because of vomiting of blood

• Further information:
– No pain, no history of recurrent vomiting,
no use of drug, no history of rash or
bleeding from other sites.
– Past history of umbilical infection during
neonatal period and treated with IV
antibiotics
– No history of jaundice in the past.
– Complete immunization including Hep.B
and A.
– No history of seizure.
A ten year old female child presented in the emergency
because of vomiting of blood

• On examination:
– Pulse: 120/min, apyrexial,
resp. rate: 28/min.
BP: 80/50 mm of Hg.
– Moderate pallor, no jaundice,
no oedema
– No organomegaly.
– No ascites.
A ten year old female child presented in the
emergency because of vomiting of blood

• Investigations:
– Hb: 7G
– Platelets adequate, normal peripheral smear
– Liver function: normal
– Ultrasound: minimal fluid in the peritoneal
cavity.
• What further investigation confirms the
diagnosis?
A ten year old female child presented in the emergency because of
vomiting of blood

• A ten year old female child • Lower oesophageal erosion

presented in the emergency – Vomiting
– reflux
because of vomiting of blood in • Bleeding disorders:
the morning. She has similar – DIC
episode one year back and – Thrombocytopenia
was transfused two units of • Ulcer
blood. – Stress
• She was delivered normally at – H. Pylori
KMC at term having birth • Drug
– Steroid
weight of 2500g. She was – Anti-inflammatory
discharged on second day. • Vascular
She is exclusively breast fed – Hemangioma
up to 4 months. • Traumatic
• On seventh day of life she had – Corrosives
umbilical infection for which • Portal hypertension
she was treated with IV – Umbilical sepsis
antibiotics – Acute or chronic liver infection
– Metabolic diseases
 A ten year old female child presented in the
emergency because of vomiting of blood
• Further information: • Lower oesophageal erosion
– No pain, no history of recurrent – Vomiting
vomiting, no use of drug, no history of – reflux
rash or bleeding from other sites.
• Bleeding disorders:
– Past history of umbilical infection
during neonatal period and treated with – DIC
IV antibiotics – Thrombocytopenia
– No history of jaundice in the past. • Ulcer
– Complete immunization including – Stress
Hep.B and A. – H. Pylori
– No history of seizure. • Drug
– Steroid
– Anti-inflammatory
• Vascular
– Hemangioma
• Traumatic
– Corrosives
• Portal hypertension
– Umbilical sepsis
– Acute or chronic liver infection
– Metabolic diseases
 A ten year old female child presented in the
emergency because of vomiting of blood
• On examination: • Lower oesophageal erosion
– Vomiting
– Pulse: 120/min, apyrexial, – reflux
resp. rate: 28/min. • Bleeding disorders:
BP: 80/50 mm of Hg. – DIC
– Thrombocytopenia
– Moderate pallor, no
• Ulcer
jaundice, no oedema – Stress
– No organomegaly. – H. Pylori
– No ascites. • Drug
– Steroid
– Anti-inflammatory
• Vascular
– Hemangioma
• Traumatic
– Corrosives
• Portal hypertension
– Umbilical sepsis
– Acute or chronic liver infection
– Metabolic diseases
 A ten year old female child presented in the
emergency because of vomiting of blood
• Investigations: • Lower oesophageal erosion
– Vomiting
– Hb: 7G – reflux
– Platelets adequate, normal • Bleeding disorders:
peripheral smear – DIC
– Thrombocytopenia
– Liver function: normal
• Ulcer
– Ultrasound: minimal fluid in – Stress
the peritoneal cavity. – H. Pylori
• Drug
– Steroid
– Anti-inflammatory
• Vascular
– Hemangioma
• Traumatic
– Corrosives
• Portal hypertension
– Umbilical sepsis
– Acute or chronic liver infection
– Metabolic diseases
Causes of Hematemesis
• Lower oesophageal erosion
– Vomiting
– reflux
• Bleeding disorders:
– DIC
– Thrombocytopenia
• Ulcer
– Stress
– H. Pylori
• Drug
– Steroid
– Anti-inflammatory
• Vascular
– Hemangioma
• Traumatic
– Corrosives
• Portal hypertension
– Umbilical sepsis
– Acute or chronic liver infection
– Metabolic diseases
– Congestive: hepatic vein thrombosis
 Portal Hypertension
Portal pressure: >5-10 mm Hg

Post-hepatic

Hepatic

Pre-hepatic
 Portal hypertension
• The portal vein may be obstructed by
infective or thrombotic disorders or by a
congenital abnormality.
• The presenting features are asymptomatic
splenomegaly, alimentary bleeding with
portal hypertension at any age throughout
childhood or adult life, and ascites and
failure to thrive.
 Portal hypertension
• The diagnosis is suspected by the finding
of portal hypertension or esophageal
varices in a patient with splenomegaly and
no clinical or biochemical evidence of liver
disease.
• The diagnosis is confirmed by
ultrasonography or angiographyd or Upper
GI endoscopy.
 Portal hypertension
• The treatment is that of bleeding
esophageal or rectal varices.
• There is an increased frequency of
bleeding during adolescence.Hepatic
encephalopathy may occur in adult life.
 Portal hypertension
• Treatment:
– Blood transfusion
– Vitamin K
– Vasopressin
– Propranolol
– Spironolactone
– Surgical?
– Treatment of primary cause.
 Chronic Liver Disease
In children, up to <2 cm below the right costal
margin.
In a newborn infant, <3.5 cm below the costal
margin
1.Hepatomegaly
– Storage: Wilson’s disease
– Inflammation: Hep B, autoimmune hepatitis
– Infiltration: Non alcoholic fatty liver disease,
Tumors
 Chronic Liver Disease
• Jaundice (Icterus) • Variceal Hemorrhage
– decreased
• Encephalopathy
biotransformation
(conjugation) • Variceal Hemorrhage
– Cholestasis • Endocrine
– Pruritus
Abnormalities
• Spider Angiomas
• Renal Dysfunction
• Palmar Erythema
• Pulmonary
• Xanthomas
Involvement
• Portal Hypertension
• Ascites
 Fulminant Hepatic Failure
• definition in children includes
– biochemical evidence of acute liver injury (usually <8 wk
duration);
– no evidence of chronic liver disease;
– and hepatic-based coagulopathy prothrombin time (PT)
>15 sec or international normalized ratio (INR) >1.5 not
corrected by vitamin K
in the presence of clinical hepatic encephalopathy,
• or a PT >20 sec or INR >2 regardless of the
presence of clinical hepatic encephalopathy.
 Etiology
• viral hepatitis (A, B, D, E), Epstein-Barr virus, herpes simplex
virus (HSV), adenovirus, enteroviruses, cytomegalovirus,
parvovirus B19, human herpesvirus-6, and varicella-zoster
infections
• autoimmune hepatitis
• hemophagocytic lymphohistocytosis (HLH)
• hepatotoxic drugs
• severe heart failure, cyanotic congenital heart disease, or
circulatory shock
• Metabolic disorders
– Wilson disease,, galactosemia, hereditary tyrosinemia,
 Hepatitis B
• Spread via blood, saliva, sexual contact,
perinatal
• Chronic: asymptomatic, eventually worsening
liver function, cirrhosis, increased risk of
hepatocellular ca
• Perinatal transmission: newborns MUCH
likely to get chronic disease (85-90%) versus
newly affected adults.
• HBIG, early vaccination within 12 hrs of life.
 Hepatitis C
• yaTransmitted via blood, feces, saliva,
parinatally
• Acute infection often symptomatic
• 60-80% will develop chronic infection in
which 20-30% will have liver failure/ cirrhosis.
• Chronic infection may cause malaise,
arthralgia, myalgia, anorexia, nausea.
• Diagnosis: anti HCV antibody, HCV RNA.
 Autoimmune hepatitis
• All ages.
• May be asymptomatic to presenting with
fulminant hepatic failure.
• Type 1: + ANA or + ASMA
Type 2: + anti-ALKM1
• May have extraintestinal manifiestation or
other autoimmune
 Wilson’s Disease
• Inherited disorder of copper transport, copper
accumulates in liver, CNS.
• Autosomal recessive.
• Can see effectts virtually every organ, system.
• Average age: 9-13 years
• Symptoms: hepatitis, personality changes.
Neurological symptoms: dysarthria, dystonia, tremor.
Hemolysis.
• Diagnosis: low ceruloplasmin, Kayser-Fleisher rings, liver
biopsy
 Clinical Manifestations
• Progressive jaundice, fetor hepaticus,
fever, anorexia, vomiting, and abdominal
pain.
• A rapid decrease in liver size without
clinical improvement.
• A hemorrhagic diathesis and ascites.
• hepatic encephalopathy.
 Treatment
• Curative: N-acetylcysteine
(acetaminophen), acyclovir (HSV), penicillin
(Amanita mushrooms), lamivudine (HBV),
prednisone (autoimmune hepatitis), and
pleconaril (enteroviruses).
• Symptomatic:
– Hypovolemia, Coagulopathy, infection,
Cerebral edema, Endotracheal intubation,
Orthotopic liver transplantation (OLT)
 Which of the following is not a
sign of severe liver disease?

a) Jaundice
b) Ascites
c) Purpuric rash
d) Altered sensation
 Which of the following is a sign
of Fulminant Hepatic Failure?

a) Hypoglycemia
b) Acidosis,
c) Hyperammonemia,
d) prolonged PT or INR that is
unresponsive to parenteral administration
of vitamin K.
This presentation is available on

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