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2. TRANSAMNINASES
ALANINE TRANSFERASE (A. L. T.) N. V.=8-20 u/l
ASPARTATE TRANSFERASE (A. S. T.) N. V.-10-30 u/l
causes of >transaminase
-acute viral or alcoholic hepatitis
A. L.T. >200 U/L
-chronic hepatitis or liver
cirrhosis
3. PROTHROMBIN TIME ( P. T.) (N. V.=18-22"); Prothrombin index
>90%)
(is influenced by the level of prothrombin, cloting factors: V, VII,
IX, fibrinogen)
-causes of < P. T.
-liver cirrhosis
-vitamine K deficiency
4. PROTEIN ELECTROPHORESIS
-serum albumine (35-50 gr/l) decresed in liver cirrhosis
-serum globulines (ă=8-16 gr/l) incresed in chronic hepatitis,
liver cirrhosis
5.TESTS FOR VIRAL INFECTION
6. HEMATOLOLOGY
7. LIVER BIOPSY
8. IMAGING TEHNIQUE (ULTRASONOGRAPHY, COMPUTER
TOMOGRAPHY, SCINTIGRAPHY, ARTERIOGRAPHY
Imaging techniques
Ultrasonography
»
Imaging techniques
CT
MRI
scintigraphy (Tc99).
» Laparoscopy
RADIOLOGY
– Hepatic arteriography
– Splenoportography
– ERCP
other
» Endoscopy
» paracentesis
Physical exam
Nutrition
Physical exam
INSPECTION
Physical exam
PALPATION
Physical exam
LIVER PALPATION
Physical exam
PERCUTION
-UPPER MARGIN
- V ic space - mid axilar line
-VII ic space- anterior axilar line
-X ic – space scapular line.
Physical exam
ASCULTATION – hepatic artery murmer in
liver cancer
Hepatomegaly
Def lower margin mid clavicular line :
costal rib
upper margin : percusion 5th
intercostal space mdi clavicular line; 8th ic
space mid axila
Hepatomegaly
Inflammation – acute hepatitis, chronic hepatitis
autoimune hepatitis, alcoholic liver disease, tuberculosis,
liver abces, liver cirrhosis,
Metabolic disorders – steatosis,
Biliarry diseases primary billiary cholangitis, biliarry
obstruction
Vascular disorders heart failure, chronic pericarditis
Tumors, liver metastasis
Congenital disorders hemocromatosis, Wilson disease,
glicogenosis
Hematological disorders chornic leukemia, lymphomas
Hepatomegaly
Liver cirrhosis; not painful, high
consistency, nodular
Liver tumors; painful, irregular
Heart failure: painful, regular, mobile,
hepato-jugular reflex
JAUNDICE
DEFINITION
hepatitis A, B, C, E
Autoimune hepatitis
Alcohol (toxic)
Hepatic cirrhosis
Wilson D
Dubin-Johnson sdr
Rotor sdr
Primary biliary cirrhosis
toxic
Posthepatic gallstones
Cancer of head pancreas
PREHEPATIC JAUNDICE
Simptoms LAB
•Unconjugated bilirubin
• No itching
•stercobilinogen
•urobilinogenurie
• Hipercromic feces
•Normal liver tests
• normal hipercromic urines
•Elevated reticule cell count,
• palor
•Normocrom normocitic anemia,
• splenomegaly.
HEPATOCELULAR JAUNDICE
Simptoms Lab
• variable jaundice • Unconjugated and conjugated Bilirubin
• ± signs of liver disease • ± citolysis
• • ± Hipocolesterolemia, hipoalbuminemia ,
hipergamaglobulinemia
POSTHEPATIC JAUNDICE
Lab
Conjugated hyperbilirubine,
hipercolesterolemia,
Alcaline Phosphatase , GGT
Normal liver tests at the bigining
Tablou clinic P index -corected with K1
itching
jaundice
acolic feces
hipercromic urines
!!!
diareea (steatoree);
US
Liposoluble vitamines malabsortions
MRI
ERCP
ASCITES
BACKGROUND
The word ascites is of Greek origin (askos)
and means bag or sac.
Ascites describes the condition of
pathologic fluid accumulation within the
abdominal cavity.
Healthy men have little or no
intraperitoneal fluid, but women may
normally have as much as 20 mL
depending on the phase of the menstrual
cycle.
PATHOPHYSIOLOGY
The pathogenesis of ascites in patients with cirrhosis
involves several mechanisms.
Portal hypertension results in decreased perfusion of
hepatocytes with portal blood. This leads to increased
reabsorption of sodium and water by the kidney resulting in
increased plasma volume and increased portal flow.
Portal inflow increases but resistance within the liver is relatively
fixed secondary to underlying hepatic fibrosis. This too results in
portal hypertension.
Hepatic fibrosis also results in sinusoidal hypertension altering starling
forces and driving fluid into the Space of Disse. Recall that the Space
of Disse is a perisinusoidal space into which microvilli of the
hepatocytes protrude.
Patients with cirrhosis are often hypoalbuminemic and
hypoalbuminemia also works to promote this
movement of fluid into the Space of Disse. This fluid
is removed by hepatic lymphatics.
PATHOPHYSIOLOGY
Hepatic lymph flow increases dramatically in
response to tissue edema.
Normal thoracic duct lymph flow is 800-1000 cc per day. In
patients with cirrhosis, hepatic lymph flow may approach 20
liters per day exceeding the capacity of the thoracic duct and
percolate from the liver capsule into the peritoneal cavity.
Also as a result of decreased perfusion of
hepatocytes, splanchnic vasodilation occurs.
This triggers the release of sympathetic
neurotransmitters further activating the renin-
angiotensin-aldosterone axis. This further stimulates
sodium and water retention by the kidney. It is
important to note that renal function in patients with
cirrhosis is disturbed long before ascites forms.
PATHOPHYSIOLOGY
Portal Hypertension
Portosystemic Collaterals
Nitric Oxide Stimulation
7 Direct Reflex
Hyperdynamic State
Underfill Physiology, ↓ SVR
Compensatory Pathways
Lymphatics Overwhelmed
(Hepatic, Planchnic, and Peritoneal)
Ascites
7 Trigger
Portal Hypertension
Hepatorenal Syndrome
Facilitating and
opposing forces in
Ambulatory patients with an episode of
cirrhotic ascites have a 3-year mortality rate
of 50%. The development of refractory
ascites carries a poor prognosis, with a 1-year
survival rate of less than 50%.
HISTORY
Most cases of ascites are due to liver disease. Patients often state that their
increasing abdominal girth has been noted for a short period.
Patients with ascites should be asked about risk factors for liver diseases. These
include the following:
› Alcohol use and duration of use
› Chronic viral hepatitis or jaundice
› Intravenous drug use
› Sexual promiscuity
› Sexual orientation
› Transfusions: Hepatitis C has been linked to transfusions occurring before 1980.
› Tattoos
› Habitation or origination from an area endemic for hepatitis
Patients with alcoholic liver disease who intermittently cease or reduce alcohol
consumption may experience ascites in a cyclic fashion. When the patient has a
very long history of stable cirrhosis and then develops ascites, the possibility of
superimposed hepatocellular carcinoma should be considered.
Obesity, hypercholesterolemia, and type 2 diabetes mellitus are now recognized
causes of nonalcoholic steatohepatitis, which can progress to cirrhosis.
Patients with a history of cancer, especially gastrointestinal cancer, are at risk for
malignant ascites. Malignancy-related ascites is frequently painful, whereas
cirrhotic ascites is usually painless.
Patients who develop ascites in the setting of known diabetes or nephrotic
syndrome may have nephrotic ascites.
PHYSICAL EXAMINATION
The physical examination should focus on the signs of portal
hypertension and chronic liver disease.
Physical findings suggestive of liver disease include jaundice, palmar
erythema, and spider angiomas.
The liver may be difficult to palpate if a large amount of ascites is
present, but often, the liver is enlarged. The puddle sign indicates that as
little as 120 mL of fluid is present. When peritoneal fluid exceeds 500
mL, ascites may be demonstrated by the presence of shifting dullness or
bulging flanks. A fluid-wave sign is notoriously inaccurate.
Elevated jugular venous pressure may suggest a cardiac origin of ascites.
A firm nodule in the umbilicus, the so-called Sister Mary Joseph nodule,
is not common but suggests peritoneal carcinomatosis originating from
gastric, pancreatic, or hepatic primary malignancy.
A pathologic left-sided supraclavicular node (Virchow node) suggests
the presence of upper abdominal malignancy.
Patients with cardiac disease or nephrotic syndrome may have anasarca.
•
CAUSES OF ASCITES
Normal peritoneum
› Portal hypertension (serum-ascites albumin gradient [SAAG]
>1.1 g/dL)
Hepatic congestion, congestive heart failure, constrictive
pericarditis, tricuspid insufficiency, Budd-Chiari syndrome
Liver disease, cirrhosis, alcoholic hepatitis, fulminant hepatic
failure, massive hepatic metastases
› Hypoalbuminemia (SAAG <1.1 g/dL)
Nephrotic syndrome
Protein-losing enteropathy
Severe malnutrition with anasarca
› Miscellaneous conditions (SAAG <1.1 g/dL)
Chylous ascites
Pancreatic ascites
Bile ascites
Nephrogenic ascites
Urine ascites
Ovarian disease
CAUSES OF ASCITES
› Diseased peritoneum (SAAG <1.1 g/dL)
› Infections
Bacterial peritonitis
Tuberculous peritonitis
Fungal peritonitis
HIV-associated peritonitis
› Malignant conditions
Peritoneal carcinomatosis
Primary mesothelioma
Pseudomyxoma peritonei
Hepatocellular carcinoma
› Other rare conditions
Familial Mediterranean fever
Vasculitis
Granulomatous peritonitis
Eosinophilic peritonitis
IN VARIOUS DISEASE STATES
Condition Gross Protein, Serum- Cell Count Other
Appearanc g/L Ascites Red Blood White Blood Tests
e Albumin Cells, Cells, per L
Gradient, >10,000/L
Cirrhosis Straw-colored <25 (95%) g/dL
>1.1 1% <250 (90%)a;
or bile-stained predominantly
mesothelial
Neoplasm Straw-colored, >25 (75%) <1.1 20% >1000 (50%); Cytology, cell
hemorrhagic, variable cell block,
mucinous, or types peritoneal
Tuberculous chylous
Clear, turbid, >25 (50%) <1.1 7% >1000 (70%); biopsy
Peritoneal
peritonitis hemorrhagic, usually >70% biopsy, stain
chylous lymphocytes and culture for
Pyogenic Turbid or If purulent, <1.1 Unusual Predominantly acid-fast
Positive
peritonitis purulent >25 polymorphonu bacilli
Gram's stain,
clear culture
Congestive Straw-colored Variable, 15– >1.1 10% leukocytes
<1000 (90%);
heart failure 53 usually
mesothelial,
Nephrosis Straw-colored <25 (100%) <1.1 Unusual mononuclear
<250; If chylous,
or chylous mesothelial, ether
mononuclear extraction,
Pancreatic Turbid, Variable, often <1.1 Variable, may Variable Increased
Sudan staining
ascites hemorrhagic, >25 be blood- amylase in
(pancreatitis, or chylous stained ascitic fluid
DIFFERENTIAL DIAGNOSES
ASCITIC LIQUID
paracentesis
LABORATORY STUDIES
› Total protein:
› In the past, ascitic fluid has been classified as an exudate if the protein
level is greater than or equal to 2.5 g/dL. However, the accuracy is only
approximately 56% for detecting exudative causes. The total protein
level may provide additional clues when used with the SAAG. An
elevated SAAG and a high protein level are observed in most cases of
ascites due to hepatic congestion. Those patients with malignant ascites
have a low SAAG and a high protein level
› Culture/Gram stain:
› The sensitivity with bedside inoculation of blood culture bottles with
ascites results in 92% detection of bacterial growth in neutrocytic
ascites. Gram stain is only 10% sensitive for helping visualize bacteria
in early-detected spontaneous bacterial peritonitis. Approximately
10,000 bacteria/mL are required for detection by Gram stain; the median
concentration of bacteria in spontaneous bacterial peritonitis is 1
organism/mL.
› Cytology:
› Cytology smear results are reported to be 58-75% sensitive for helping
detect malignant ascites.
IMAGING STUDIES
Chest and plain abdominal films
› Elevation of the diaphragm, with or without sympathetic
pleural effusions (hepatic hydrothorax), is visible in the
presence of massive ascites. More than 500 mL of fluid
is usually required for ascites to be diagnosed based on
findings from abdominal films.
› Many nonspecific signs indicate ascites, such as diffuse
abdominal haziness, bulging of the flanks, indistinct
psoas margins, poor definition of the intra-abdominal
organs, erect position density increase, separation of
small bowel loops, and centralization of floating gas
containing small bowel.
Abdominal ultrasound
IMAGING STUDIES
Ultrasound
› Real-time sonography is the easiest and most sensitive
technique for the detection of ascitic fluid.. Free ascites does
not displace organs but typically situates itself between them,
contouring to organ margins and demonstrating acute angles
at the point at which the fluid borders the organ.
› The smallest amounts of fluid tend to collect in the Morison
pouch and around the liver as a sonolucent band. With
massive ascites, the small bowel loops have a characteristic
polycyclic, "lollipop," or arcuate appearance because they
are arrayed on either side of the vertically floating
mesentery.
› Certain sonographic findings suggest that the ascites may be
infected, inflammatory, or malignant...
› Most patients (95%) with carcinomatous peritonitis have a
gallbladder wall that is less than 3 mm thick. The thickening
of the gallbladder is primarily a reflection of cirrhosis and
portal hypertension.
IMAGING STUDIES
CT scan:
Ascites is demonstrated well on CT scan images. Small amounts
of ascitic fluid localize in the right perihepatic space, the
posterior subhepatic space (Morison pouch), and the Douglas
pouch. A number of CT features suggest neoplasia. Hepatic,
adrenal, splenic, or lymph node lesions associated with masses
arising from the gut, ovary, or pancreas are suggestive of
malignant ascites. Patients with malignant ascites tend to have
proportional fluid collections in the greater and lesser sacs;
whereas, in patients with benign ascites, the fluid is observed
primarily in the greater sac and not in the lesser omental bursae.
PROCEDURES
Abdominal paracentesis: Abdominal paracentesis is
the most rapid and perhaps the most cost-effective
method of diagnosing the cause of ascites
formation. Therapeutic paracentesis may be
performed for refractory or tense ascites. The
removal of 5 L of fluid is considered large-volume
paracentesis. Total paracentesis, ie, removal of all
ascites (even >20 L), can usually be performed
safely. Recent studies demonstrate that
supplementing 5 g of albumin per each liter over 5
L decreases complications of paracentesis, such as
electrolyte imbalances, and increases in serum
creatinine secondary to large shifts of intravascular
volume.
STAGING
Ascites may be semiquantified using the
following system:
– Stage 1+ is detectable only after careful
examination.
– Stage 2+ is easily detectable but of relatively
small volume.
– Stage 3+ is obvious ascites but not tense ascites.
– Stage 4+ is tense ascites.
Paracentesis
Introduction
Diagnostic tap
– New onset ascites: Evaluate fluid to help determine
etiology, to differentiate transudate versus exudate,
to detect the presence of cancerous cells, or to
address other considerations.
– Suspected spontaneous or secondary bacterial
peritonitis
Therapeutic tap
– Respiratory distress secondary to ascites
– Abdominal pain or pressure secondary to ascites
Contraindications
Absolute
Acute abdomen that requires surgery
Relative Severe thrombocytopenia (platelet count <20 X 103/μL),
coagulopathy (international normalized ratio [INR] >2.0), or both
– Patients with an INR greater than 2.0 should receive fresh frozen plasma (FFP) prior
to the procedure. One strategy is to infuse one unit of fresh frozen plasma before the
procedure and then perform the procedure while the second unit is infusing.
– Patients with platelet counts less than 20 X 103/μL should receive an infusion of
platelets prior to performing the procedure.
In patients without clinical evidence of active bleeding, routine labs such
as prothrombin time (PT), activated partial thromboplastin time (aPTT),
and platelet counts may not be needed prior to the procedure.5 In these
patients, pretreatment with FFP, platelets, or both before the paracentesis is
also probably not needed.
Pregnancy
Distended urinary bladder
Abdominal wall cellulitis
Distended bowel
Intra-abdominal adhesions
Treatment and Medication
Anesthesia
Local anesthesia is used.
Equipment
Disposable paracentesis/thoracentesis kits
Antiseptic swab sticks
Fenestrated drape
Lidocaine 1%, 5-mL ampule
Syringe, 10 mL
Injection needles, 22 gauge (ga), 2
Injection needle, 25 ga
Scalpel, No. 11 blade
Eight-French catheter over 18 ga x 7 1/2" needle with 3-way stopcock, self-sealing
valve, and a 5-mL Luer-Lock syringe
Syringe, 60 mL
Introducer needle, 20 ga
Tubing set with roller clamp
Drainage bag or vacuum container
Specimen vials or collection bottles, 3
Gauze, 4 x 4 inch
Adhesive dressing
Positioning
The two recommended areas of
abdominal wall entry for paracentesis
are as follows (see photo):
– Two centimeters below the umbilicus in
the midline (through the linea alba)
– Five centimeters superior and medial to
the anterior superior iliac spines on either
side
Recommended routine use of
ultrasonography to verify the presence
of a fluid pocket under the selected
entry site in order to increase the rate
of success.6 The ultrasound also helps
the physician avoid a distended • Patients with severe ascites can be
urinary bladder or small bowel positioned supine. Patients with mild
adhesions below the selected entry
point. To minimize complications, ascites may need to be positioned in the
avoid areas of prominent veins (caput lateral decubitus position, with the skin
medusa), infected skin, or scar tissue. entry site near the gurney. The lateral
decubitus position is advantageous because
air-filled loops of bowel tend to float in a
distended abdominal cavity.
Technique
Apply a sterile fenestrated drape to create a sterile
field.
Autoimmune hepatitis
Wilson's disease
Outcomes of drug metabolism
Clinical manifestations of hereditary hemochromatosis
Common physical findings in hereditary hemochromatosis
Findings Occurrence, %
Hepatomegaly 60–85
Cirrhosis 50–95
Skin pigmentation 40–80
Arthritis (second and third metacarpophalangeal joints) 40–60
Clinical diabetes 10–60
Splenomegaly 10–40
Loss of body hair 10–30
Testicular atrophy 10–30
Dilated cardiomyopathy 0–30
Wilson's disease pathophysiology
Chromosome 13
Copper transport protein
Membrane-spanning p-type ATPase protein
Decreased hepatic excretion of copper into bile
Clinical manifestations of Wilson's disease
Diagnosis of wilson's disease
Serum ceruloplasmin
Urinary copper
Hepatic copper
Hepatic histology
Glucosuria, hemolysis
LIVER CIRRHOSIS
-Definition:
Necrosis of liver cells followed by fibrosis, nodular regeneration
-Causes:
-Toxins: - Alcohol
- Drugs (metil dopa, tuberculostatic drugs)
-Infection- Hepatic virus B, C
-Autoimune reaction
- Primary biliary cirrhosis
-Metabolic- Haemochromatosis: iron deposits in liver
cirrhosis+ diabetes+ pigmentation
- Wilson Disease: copper deposits in liver
cirrhosis + neurological abnormalities+ Kayser
Fleyscher ring
-Congestive change
- Right heart failure
-Obstruction
- Secundary biliary cirrhosis
Simptoms & Signs
1. Enlargement of liver: -pain
-revealed at physical exam
2. Portal hypertension:
-bleeding varices + hemoroids
-splenomegaly + hipersplenism
-ascites
-colateral superior abdominal circulation
-hepatic encephalopaty
personality change, stupor, coma
3. Hepatocelular failure
- ↓ serum albumine →ascites, edema
- ↓ excretion of bilirubine →jaundice
- ↓ fibriongen, store vitamine K →bleeding
- ↓ detoxication:
oestrogen → spider naevi
palmar erythema
gynecomastia
loss of body hair
testicular athrophy
aldosterone → edema
nitroso products from the gut
→ neurological abnormalities
Development of ascites
Early signs of ascites
Abdominal ultrasound
Indications for diagnostic paracentesis
At first presentation of ascites
Alteration of the patient's clinical state
Sudden increase in ascites
Worsening of hepatic encephalopathy
Presence of fever
Differential diagnosis of ascites
Cirrhosis Constrictive pericarditis
1.GALLSTONES
-90% ASYMPTOMATIC
-biliary colic
-pain in right upper quadrat
-nausea
-vomit
-Murphy sign
-diagnosis
-ultrasonography
2. ACUTE COLECISTITIS
-biliary colic +
-fever + chills +
-jaundice +
-tendernes
Figure 1.13 - The gallbladder
TABLE 7-34. CLINI CAL RISK FACTORS FOR CHOLESTEROL GALLSTO NE FORMATION
Estrogens:
Age
Hypertriglyceridemia
Gallbladder Stasis:
Radiopaque on CT scan
Figure 8.10 - Typical black pigment stones are
irregular in contour
-ULTRASONOGRAPHY EXAMINATION
-COMPUTER TOMOGRAPHY
Diagnosis of acute pancreatitis
Acute pancreatitis.
Percutaneous pancreatography
performed by direct puncture
under ultrasound guidance.
Dilated duct in chronic
pancreatitis.
Alcohol-induced chronic
pancreatitis.