o Chylous ascites – in patients with malignant
lymphoma appears to be caused by lymph node
Block IV - Alterations in Gastrointestinal Function
Module Abdominal Enlargement
Tutor Dr. F. Sabaten
Topic Abdominal Enlargement
ASCITES: Bag or Sack
CIRRHOTIC ASCITES
o PORTAL HYPERTENSION
o Portal pressure increases above a critical threshold and
circulating nitric oxide levels increases which leads to
vasodilation.
o As a state of vasodilation worsens, plasma levels of
vasoconstrictor, sodium-retentive and ascetic fluid
forms – state of decompensation.
o Paradox of volume overload with neurohormonal
excitation characteristic of volume depletion
o An organism’s ability to detect changes in intravascular
volume is limited, however, and is linked to pressure
receptors.
NON-CIRRHOTIC
o Malignancy-related ascites
o Peritoneal carcinomatosis – results from production
of proteinaceous fluid by tumor cells lining the
peritoneum; extracellular fluid enters the peritoneal
cavity to reestbalish oncotic balance or in attempt to re-
establish fluid balance
o Fluid accumulates in patients with massive liver
metastasis because of portal hypertension caused by
stenosis or acclusion of portal vein by tumor nodules or
tumor emboli.
obstruction by the tumor and rupture of chyle-containing
lymphatics.
o Cardiac cirrhosis and nephrotic syndrome
o Effective arterial blood volume appears to be decreased
and the vasopressin, renin-aldosterone and sympathetic
nervous systems are activated; these changes lead to
renal vasoconstriction and sodium and water retention.
o Tuberculous or chlamydia infection
o Mechanism is similar to peritoneal carcinomatosis
o Pancreatic and biliary ascites
o Fluid accumulates by leakage of pancreatic juices or bile
into the peritoneal cavity or forms secondary to a
“chemical burn” of the peritoneum
o Post abdominal surgery
o Caused by lymphatic leak similar to chylous ascites
CLINICAL FEATURES
o CIRRHOSIS: most common cause of ascites, usually from
alcohol, hepatitis C, and NASH (US data) in the Philippines,
it’s hepatitis B that is endemic
o Ascites can develop early in alcoholic liver disease in the
precirrhotic, alcoholic hepatitis stage; at this stage, portal
hypertension and the resulting predisposition to sodium
retention are reversible with abstinence from alcohol.
o Patients with a long history of stable cirrhosis and the
sudden development of ascites should be suspected
of harbouring a hepatocellular carcinoma that has
precipitated the decompensation.
o Malignancy-related ascites frequently is painful,
whereas cirrhotic ascites usually is not, unless bacterial
peritonitis or alcoholic hepatitis is superimposed
o Tuberculous pertitonitis usually manifest as a fever and
abdominal pain
o Ascites may occur in patients with acute pancreatitis with
necrosis or ruptured pancreatic duct from the chronic
pancreatitis or trauma.
o Fitz-hugh-curtis syndrome caused by chlamydia or
gonorrhoea may cause inflammatory ascites in sexually
active women.
o Patients in whom ascites and anasarca develop in the
setting of diabetes mellitus should be suspected of
having nephrotic ascites.
o Serositis in patients with connective tissue disease may
be complicated by ascites. Classic example; SLE in young
females, marfan’s: check abdominal girth
PHYSICAL EXAMINATION
Diagnosis of ascites is readily suspected and usually confirmed
easily on PE.
o The presence of full, bulging abdomen should lead to
percussion of the flanks, check for shifting if the degree of
flank dullness is greater than the usual (i.e. if the percussed
air-fluid level is higher than that of the normally found on the
IV ABDOMINAL ENLARGEMENT
lateral aspect of the abdomen with the patient in supine) if
flank dullness is absent, checking for shifting is unnecessary.
o Approx. 1500 ml of fluid must be present before dullness is
detected. (lesser amount thru UTZ)
o Ascites is difficult to assess in patients with ovarian
masses, gaseous distention and who are obese; may
need ultrasound to confirm
o Some clues in the determining etiology of ascites:
o Portal hypertension from cirrhosis: presence of
palmar erythema, large pulsatile spider angioma
(atleast 6), large abdominal wall collateral veins, or
fector hepaticus.
o Peritoneal carcinomatosis: an immobile mass in the
umbilicus , the sister mary joseph nodules.
o Cardiac cirrhosis: neck vein engorgement.
DIAGNOSIS: PARACENTESIS
INDICATIONS
 All inpatients and outpatients with new onset ascites
 Because of the possibility of ascetic fluid infection in a
cirrhotic patient admitted to the hospital, a surveillance
paracentesis performed on admission may detect
unexpected infection
 Not all patients with ascetic fluid infection are symptomatic;
may have subtle symptom, such as mild confusion
noticed only by the family
 Early detection of infection at the asymptomatic stage may
reduce mortality
CONTRAINDICATIONS
 Coagulopathy should preclude paracentesis only when
clinically evident fibrinolysis or disseminated
intravascular coagulation (DIC) is present; rare
 No deaths or infection caused by paracentesis; no episodes
of hemoperitoneum or entry of the paracentesis needle into
the bowel
 Complications have included only abdominal wall hematomas
in approx. 2% of paracentesis
 Transfusion of blood products (fresh frozen plasma or
platelet) routinely before paracentesis in cirrhotic patients
with coagulopathy is not supported by the data
PATIENT POSITION AND CHOICE OF ENTRY OFNEEDLE
SITE
 Large volume of ascites and thin abdominal wall: supine
position with the head of the bed or examining table
elevated slightly
 Less fluid: lateral decubitus position and tapped in the
midline or in the right or left lower quadrant while supine
 Small amounts of fluid: face-down position or with
ultrasound guidance
 Obese: (with abdominal wall usually is substantially thicker
in the midline than in the lower quadrant): ultrasound
examination is helpful in confirming the presence of fluid and
guiding the paracentesis needle
 Avoid tapping in the site of surgical scars: ultrasound
guidance may be required in patients with multiple
 Recommended site: left lower quadrant (LLQ) two
finger breadths (3cm) cephalad and two finger breadth
medial to the anterior superior iliac spine
 Material: standard metal 1.5 in, 22- gauge needle,
obese patients require the use of longer needle, inches and
gauge 22
 Steel needles: are preferable to plastic-sheathed cannulas
because plastic sheath may shear off to the peritoneal cavity
with the potential to kink and obstruct the flow of fluid
after the metal cannula is removed; metal needles do not
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puncture the bowel unless the bowel is adherent to a scar or
severe gaseous distention is present
TECHNIQUE: DIAGNOSTIC PARACENTESIS (diagnosing
portal hypertension)
 Asepsis (aseptic technique) – minimum requirement is the
use of sterile gloves
 Z tract ( old term, confusing) – technique of needle insertion
is accomplished by displacing one gloved hand the skin
approx.. 2cm downward and then slowly inserting the needle
mounted on the syringe held in the other hand
o The hand holding the syringe stabilizes the syringe and
retracts its plunger simultaneously; a steady hand and
experience are needed. Skin is released only after the
needle has penetrated the peritoneum and fluid flows
o When the needle is ultimately removed, the skin
resumes its original position and seals the needle
pathway
 Needles should be advanced slowly through the abdominal
wall approx. 5 mm increments
o Allows the operator to see blood if a vessel is entered
and allows the bowel to move away from the needle
o Slow insertion also allows time for the elastic peritoneum
to “tent” over the end of the needle and be pierced by
it.
 Approx. 30 ml of fluid is obtained
 Use of 5- to 10- ml syringe for the initial portion of a
diagnostic tap and then twist this syringe off the needle and
replace it with 20-to 30- ml syringe to obtain the remainder
of the sample
 The initial use of small syringe allows the operator to have a
better control and to see the fluid more easily as it
enters the hub of the syringe
 A sterile needle is then placed on a larger syringe, and
an appropriate amount of fluid is inoculated into each of a
pair of prepared blood culture bottles.
 Usually 5-10 ml is inoculated into 50-ml bottles and 10-
20 ml into 100-ml bottles
 The next aliquot is placed into a “purple-top” or
ethylenediaminetetraacetic acid tube for a cell count.
And the final aliquot is placed into “red-top” plane tube for
chemistries
 Inoculating the culture bottles with the sterile needle
minimizes contamination
TECHNIQUE: THERAPEUTIC PARACENTESIS
 Similar process but using a large bore needle to remove
larger amount of fluid
 Preferred size: use a standard metal 1.5 inch, 16-18 gauge
 Obese patients may require a larger needle: 3.5 inches
and 18 gauge
 A set of 15-gauge five-hole needles has been produced
specifically for therapeutic abdominal paracentesis: these
needle may replace the spinal needles used currently for
paracentesis in obese patients
 The 15-gauge needle have a removable sharpd inner
component and a blunt outer cannula; they range in length
from 3.25 to 5.9 inches
 A tiny scalpel nick is required to permit the large needle to
enter the skin
 Use of vaccum bottles (1-2 L) connected to the needle
with noncollapsible tubing is much faster; use of a pump is
even faster than the vaccum bottles
 With respiratory movement, the needle may gradually works
its way out of the peritoneal cavity and into the soft tissue,
and some serosanguineous fluid may appear in the needle
hub or tubing; when this happens, the pump should be
2
IV ABDOMINAL ENLARGEMENT

turned off or a clamp placed on the tubing connected to the Tuberculous, secs
vaccum bottle Peritoneal
carcinomatos
ASCITIC FLUID ANALYSIS (refer at the back pages) is:
predominance
of
lymphocytes
Leakage of 1 PMN is
blood into the subtracted
peritoneal from the
cavity leads to absolute
RBC
an elevated ascetic fluid
ascetic fluid PMN count
WBC count for every 250
RBC
SAAG >1.1 SAAG does
g/dl (11 g/L): not explain
portal the
hypertension pathogenes
with an is of ascites
accuracy of formation,
approx. 97%: nor does not
because of the explain
FINDINGS/R ascetic fluid where the
ITEM NORMAL REMARKS
ESULT abumin conc. albumin
ANC <1000/ cannot be came from
mm³ greater than – that is, liver
(1.0x109/L): the ascetic or bowel;
clear fluid total simply gives
Transparent,
ANC >5000/ protein conc. the dr. an
sl yellow,
mm³ <1.1 g/dl: indirect but
PMN’s
(5.0x109/L): unlikely to accurate
<250/mm³
cloudy have portal index of
[0.25 x
ANC >50,000/ hypertension portal
109/L]
mm³ Serum pressure
(50.0x109/L): hyperglobuline The accuracy
resembles mia (serum of the SAAG
mayonnaise globulin is also
SERUM
RBC count greater than reduced
ASCITES
GROSS about 10,000/ 5g/dl) leads to when
ALBUMIN
APPEARAN mm³ (10.0x a high ascetic specimens of
GRADIENT
CE 109/L): pink fluid globulin serum and
RBC
appearance conc. and can ascites are
>20,000/ mm³ narrow the not obtained
(20.0x109/L) albumin nearly
distinctly red gradient by simultaneousl
>200-1000 contributin to y; specimens
mg/dl (2.26- the oncotic should be
11.3 mmol/L) forces: to obtained on
opaque, correct the same
milky Corrected day,
LIPID
>100-200 SAAG = preferably
mg/dl )1.13- uncorrected within the
2.26 mmol/L) SAAG x 0.16 same hour
dilute skim x (serum Arterial
milk globulin in hypertension
Spontaneous Dipstick g/dl 2.5) may result in
bacterial count can a decrease in
peritonitis detect an portal
PMN’s <250/ (SBP) most ascetic fluid pressure and
CELL a narrowing
mm³ common cause PMN count
COUNT of the SAAG.
(0.25x109/L) of elevated greater than
WBC of 70% 250/ mm³ The SAAG
PMNs (0.25x109/L) needs to be
in 90-120 determined

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IV ABDOMINAL ENLARGEMENT

only on the SBP: ascetic Ascetic fluid

first fluid level rises concentration
paracentesis because of the of LDH is
specimen in a release of LDH usually is less
given patient from than one half
neutrophils of the serum
SBP: SBP is like and the ascetic level in
monomicrobi bacteremia in fluid uncomplicate
al, low terms of the concentration d cirrhotic
bacterial number of LACTATE is greater than ascites.
concentration, bacteria DEHYDRO that of serum.
median colony present: GENASE Secondary
count of only 1 culturing (LDH) peritonitis:
organism/mL ascetic fluid LDH level is
as if it were even higher
blood has a than that seen
CULTURE No organism in SBP and
high yield
Bedside may be several
inoculation fold higher
is superior to than that of
delayed the serum LDH
laboratory level
inoculation of Likely surgical peritonitis and merit immediate radiologic
blood culture evaluation:
bottles in the o total protein greater than 1 g/dl ( g/L)
laboratory o glucose less than 50 mg/dL (2.8 mmol/L)
Cirrhosis:prot The protein o LDH greater than the upper limit of the normal serum
ein concentration In
concentration in ascetic uncomplic Acute
greater than fluid in the ated pancreatitis
2.5 g/dl setting of ascites, or intestinal
(25g/L) cirrhosis is amylase perforation:
Malignant determined concentrat fluid amylase
ascites, the almost AMYLASE ion usually concentration
ascites is entirely by is one half usually >2000
TOTAL
caused by the serum that of the /L and approx.
PROTEIN serum five fold greater
massive liver protein
metastases concentration value, than
or and portal approx.. simultaneous
hepatocellula pressure 50U/L serum values
r carcinoma Gram stain
that is low SBP: median of the body
ascetic fluid ascetic fluid
protein concentration of demonstrat
concentration bacteria in 1 e a bacteria
Low: SBP Concentratio organism/mL only when
detected late n of glucose similar to the more than
in its course in ascetic colony count in 10,000
(as well as in fluid is similar bacteremia bacteria/m
the setting of to that of L are
intestinal serum, present.
perforation unless Gram stain
into the ascetic glucose is GRAM STAIN of ascetic
fluid), the being fluid is
GLUCOSE ascetic fluid consumed most
glucose by the helpful in
concentration ascetic fluid the
is usually drops WBCs or diagnosis
to 0 mg/dl bacteria of free
because of perforation
large numbers of the
of stimulated intestine
neutrophils into ascetic
and bacteria fluid where
sheets of

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IV ABDOMINAL ENLARGEMENT

multiple perforation: fluid is

different an ascetic fluid dark
bacteria bilirubin level brown
are found. greater than
Laparosco 6mg/dL
One 50-mL py with (102umol/L)
aliquot fluid is histology and greater
centrifuged and and than the serum
the pellet is culture of level
cultured (50% peritoneal
SMEAR AND sensitivity) biopsies
CULTURE OF has a
TB sensitivity
approachin
g 100% for
detecting
tuberculo
us
peritonitis
Peritoneal Not all
No carcinmatosis malignanc
malignant : expected to y-related
cells detect ascites
CYTOLOGIC malignancy only are
EXAMINATIO when tumor peritoneal
N cells line the carcinmat
peritoneal cavity osis (Figure 91.3)
and exfoliate
into the ascetic COMPLICATIONS OF ASCITIC FLUID INFECTION
fluid  SPONTANEOUS BACTERIAL PERITONITIS
Chylous Should be - postive ascitic fluid culture and an elevated ascitic fluid
ascites: measured if absolute of PMN count w/o evidence of an intra
trigluceride ascetic fluid abdominal surgically treatable source of infection
conc. > is  MONOMICROBIAL NONNEUTROCYTIC
200mg/dL opalescent, BACTERASCITES (MNB)
(2.26 mmol/L) milky o Positive ascetic fluid culture for a single organism
and greater o An ascetic fluid PMN count lower than 250 cell/
than the serum mm³
level, greater o No evidence of an intra-abdominal surgically
than 1000 treatable source of infection
mg/dL
(11.30mmol/L)  CULTURE-NEGATIVE NEUTROCYTIC ASCITES (CNNA)
o The ascetic fluid culture grows no bacteria
Sterile ascetic o PMN count is 250 cell/ mm³ or greater
fluid in the o No antibiotics have been given (not even a single dose)
TRIGLYCERID o No other explanation for an elevated ascetic fluid PMN
setting of
E count (eg. Haemorrhage into ascites, peritoneal
cirrhosis that
are slightly carcinomatosis, tuberculosis, pancreatitis) can be
cloudy, w/o an defined
elevated cell  SECONDARY BACTERIAL PERITONITIS
count: >64+/- o The ascetic fluid culture is positive (usually for multiple
40 mg/dL (0.72 organisms)
+/- 0.45 o The PMN count is 250 cells/ mm³ or greater
mmol/L) o The intra-abdominal surgically treatable primary source
compared with of infection (eg. Perforated intestines, perinephric
18 +/- 9 mg/dL abcess) has been identified
(0.20 +/- 0.10
mmol/L) for  POLYMICROBIAL BACTERASCITES
clear ascites in o Multiple organisms are seen on gram stain or cultured
the setting of from the ascetic fluid
cirrhosis o The PMN count is lower than 250 cells/ mm³
Biliary or Should be - The diagnosis should be suspected when the
proximal measured paracentesis is traumatic or unusually difficult because
BILIRUBIN of ileus or when stool or an air is aspirated into the
small of the
intestinal ascetic paracentesis syringe.

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IV ABDOMINAL ENLARGEMENT
ASCITIC FLUID INFECTION: CLINICAL SETTING
 The spontaneous variant – SBP, CNNA, MNB occur almost
exclusively in the setting of cirrhosis
 Essentially all patients with SBP have elevated bilirubin level
and abnormal prothrombin time
 Peritonitis is unlikely to precede the development of ascites
 Infection usually develops when the volume of ascites is at
its maximum
 SBP and polymicrobial bacterascites can develop with any
kind of ascites and requires that an intra-abdominal source of
infection is present.
ASCITIC FLUID INFECTION: PATHOGENESIS
 Spontaneous forms of infection results from overgrowth of a
specific organism in the intestines which undergoes
translocation of the microbe from the intestines to
the mesenteric lymph nodes
 Low protein ascetic fluid (protein content less than 1 g/dL
[10g/L] is susceptible to SBP
 Patients with deficient ascitic fluid opsonic activity are
predisposed
 Infection usually develops when the volume of ascites is at
its maximum
ASCITIC FLUID INFECTION: SIGNS AND SYMPTOMS
 87% of patients with SBP are symptomatic but the s/sx are
often subtle such as slight change in mental status
 E. coli, streptococci, Klebsiella: cause most of episodes of
SBP and MNB
 Spontaneous: monomicrobial
 Secondary: polymicrobial
(Refer Table 91.6 and 91.7)
ASCITIC FLUID INFECTION: RISK FACTORS AND
DIAGNOSIS
 Risk factors: cirrhosis, low ascitic fluid protein, phagocytic
dysfunction, paracentesis (theoretical risk), GI bleeding
(hematemesis from esophageal varices) (peak is 48h after
onset haemorrhage), UTI
 Fever and abdominal pain raise the suspicion; for high
ascitic fluid PMN, ascitic fluid infection should be the working
impression until proven otherwise (common cause elevated
WBC in cirrhotic is SBP)
 Difficult to distinguish secondary from spontaneous bacterial
peritonitis
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 Brown ascitic fluid within a bilirubin conc >6mg/dL
(102umol/L) and greater than serum level is indicative of
biliary or proximal small intestinal perforation
 Within the minutes of detection of neurocytic ascitic fluid,
patients should undergo imaging studies to confirm and
localize site or rupture: antibiotics alone is unsuccessful in
secondary bacterial perforation from ruptured viscus
 If no free air is seen, continue antibiotic and repeat
paracentesis after 48 hours; culture remains positive in
secondary and becomes negative in spontaneous
ASCITIC FLUID INFECTION: TREATMENT
 Empiric antibiotics should be started if ascitic fluid
PMN is >250cels/mm3 (1.25x109/L)
 Patients with haemorrhage into ascitic fluid, peritoneal
carcinomatosis, pancreatic ascites or tuberculous peritonitis
may have elevated ascitic PMN unrelated to SBP and don’t
require antibiotic; stop antibiotics once culture is negative
 MNB: decision to begin antibiotics should be individualized;
begin if with persistent symptoms
 CNNA: start antibiotics; repeat paracentesis after 48 hours;
drop in PMN documents response to treatment; persistently
high PMN suggests a nonbacterial cause
 Gram stain is helpful in detecting secondary peritonitis; if
gram stain is positive, coverage for aerobic (metronidazole)
 Co-amoxiclav has been shown to be as effective as
cefotaxime (if can tolerate oral antibiotics)
 Oral antibiotics: Ofloxacin 400mg/tab BID,
Ciprofloxacin 500mg/tab BID following a 2-day course of
IV Ciprofloxacin
 Duration of treatment: 10-14 days for life-
threatening infection is recommended by ID specialists but
nonsupporting data; and RCT demonstrated effectivity of 5-
day course of treatment for SBP and CCNA
 Albumin is effective in increasing intravascular volume,
decrease vasodilation, reduce risk of renal failure, improve
survival
 Repeat paracentesis is not needed if the setting (ie. advance
cirrhosis with s/sx of infection), bacterial isolate
(monomicrobial), and response to treatment (dramatic
reduction s/sx of infection is typical; repeat paracentesis
after 48 hours if course is a typical
6
IV ABDOMINAL ENLARGEMENT
 Ceftriaxone 1g daily for 7 days is given in the setting of GI
bleeding
 Co-trimoxazole has been proven to be effective in animal
models
(Refer Table 91.10)
TYPES DESCRIPTION
Cellulitis Risk factors include obesity, homelessness,
greater degree of edema
Tense “Total ascites”, even more than 22L appears to
ascites be safe
Pleural Usually unilateral and right-sided, but may be
effusion bilateral and larger on the left
Unilateral pleural effusion suggests
tuberculosis
Hepatic hydrothorax: a large effusion in a
patient with cirrhotic ascites usually presenting
with shortness of breath
The fluid analysis is similar but not
identical; total protein conc is higher (by
approx. 1 g/dL (10g/L) in the pleural fluid
Treatment of hepatic hydrothorax: Na
restriction + diuretics, TIPS, liver transplant;
chest tube with pleurodesis, peritoneovenous
shunt and direct surgical repair are ineffective
Abdominal Usually umbilical or Incisional
wall Elective surgical treatment should be
hernias considered; ascitic fluid should be removed
preoperatively because hernias recur in up to
73% of cases
Laparoscopic surgery is done usually with TIPS
or liver transplant
Surgery is done urgently if with skin ulceration,
crusting or black discoloration and emergently for
refractory incarceration or rupture
TREATMENT OF ASCITES
 Low-Albumin-Gradient Ascites
 Peripheral edema is managed with diuretics
 Non-ovarian peritoneal carcinomatosis is managed with
outpatient therapeutic paracentesis
 Tuberculous peritonitis: anti-TB medications
 Pancreatic ascites may resolve spontaneously but may
require endoscopic placement of PD or may respond to
Somatostatin
 Post-op lymphatic leak may resolve spontaneously but
may require surgical intervention or placement of
peritoneovenous shunt
 Chlamydia peritonitis is cured by tetracycline
 Lupus serositis responds to steroids
 Dialysis-related ascites respond to aggressive dialysis
Hospitalization Large volume ascites and those who
are resistant to outpatient treatment
usually require hospitalization
Precipitation Correct the underlying cause: saline
cause infusion, Na bicarbonate infusion
Diet education Recommended: 2g/day (88mmol);
severely sodium restricted diet, ie,
500mg/day (22mmol) is not palatable
Protein is not restricted unless patient has
hepatic encephalopathy refractory to two
drug and on a vegetable protein diet
Fluid Restrict Na not fluids
restriction Attempts to correct hyponatremia rapidly
can lead to more complications; symptoms
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of hyponatremia does not develop in
cirrhotic patients until Serum Na
<110mmol/L
Bed rest Not necessary
Strict bed rest may lead to decubitis
ulcer formation in emaciated patients
Crea is checked to assess adequacy
of the collection: men 15-20mg/kg/day,
women 10-15mg/kg/day
Urine A suboptimal decline in body weight may
examination be a result of inadequate natriuresis,
failure to restrict Na or both
Patients who are adherent to an
88mmol/day Na restricted diet and
excretes more than 78mmol/day should
lose weight; if weight is increasing despite
urinary losses, patient is consuming more
Na than prescribed
Random urine Na > K: 24 hour urine
specimen will reveal Na excretion >
Urine Na to K 78mmol per day in 90% cases
ratio Random urine Na:K > 1 predicts that
patient should lose weight; if patient does
not lose weight with a Random Urine Na:K
>1, then he is not adherent to diet
Avoidance of May lead to cystitis and bacteremia
Urinary Should be inserted only in ICU setting and
Bladder only for a short period of time
Catheters
Spironolactone: mainstay of
treatment but increases natriuresis
slowly
Recommendations: Spironolactone
100mg, Furosemide 40mg; dose may be
increases to as high as Spironolactone
Diuretics 400mg, Furosemide 160mg
Amiloride 10mg/day has a more rapid
effect and does not cause gynecomastia
IV diuretics can cause acute decrease in
GFR and should be avoided
Paracentesis is done if rapid weight
loss is desired:
Target: 0.5kg/day weight loss
Discontinue if: encephalopathic, Serum
Na <120mmol/day, Serum Crea > 2mg/dL
(180mmol/L), significant drop in blood
pressure from baseline WITH confusion or
azotemia
Patients who have demonstrated response
to regimen may be discharged
Role of Na Usually used in mild renal tubular
Bicarbonate acidosis
Na bicarbonate is recommended but
should not be routinely used
Used to increase urinary water
Aquaretics excretion and increase serum Na
concentration
No clear benefit
Monitor: body weight, orthostatic
symptoms, serum electrolytes, urea,
Outpatient creatinine
management 24-hour urine collection may be done if
needed
Diuretic doses and dietary Na intake
may be titrated to achieve weight
7
IV ABDOMINAL ENLARGEMENT
loss and negative Na balance
Monitoring of urine Na conc provide insight
to adhere to diet
TREATMENT OF REFRACTORY ASCITES
 Definition: ascites unresponsive to Na-restricted diet
and high-dose diuretic treatment; may manifest as no
weight loss and development of complications
Should be considered even if still diuretic-
Liver transplant sensitive
Surgery in the RUQ causes adhesions that
become vascularized and difficult to
remove during transplant
One of the older methods
Serial First-line treatment in patients with
paracentesis tense ascites and second-line for
patients with refractory ascites
World record for volume of fluid removed:
4L
Paracentesis-induced circulatory
dysfunction: rise in plasma renin levels
Colloid after paracentesis
replacement Albumin infusion: recommended but
no study has demonstrated survival
benefit; very expensive
Terlipressin is an alternative but no
evidence
Never give hetastarch which accumulate
in Kupffer cells
Transjugular Side to side portocaval shunt initially used
intrahepatic for refractory variceal bleeding
portosystemic TIPS dysfunction has been seen when
shunt (TIPS) uncovered shunts were used
Also used in the treatment of hepatic
hydrothorax and umbilical hernia
Peritoneovenous Inferior to TIPS (even with uncoated
shunt shunts)
HEPATIC ENCEPHALOPATHY
 Transient and reversible neurologic and psychiatric
manifestations
 Develops 50-70 % of patients with cirrhosis and is a poor
prognostic indicator
 Triggered by an inciting event that results in a rise in
serum ammonia not necessary to hep. Enceph. diagnosis
PATHOPHYSIOLOGY
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 Production of neurotoxins, altered permeability of the
BBB, altered neurotransmission
 Ammonia: best known neurotoxin; produced in the
colon where bacteria metabolize proteins and other
Nitrogenous products into ammonia which enters the portal
circulation then metabolized and cleared by the liver
 Arterial hyperammonemia is seen in up to 90% of
patients with HE, although serum level is either sensitive nor
specific
 HE affects neuronal membrane fluidity, CNS
neurotransmitter expression, neurotransmitter receptor
expression and activation
 GABA-benzodiazepine system is the most well-studied
 Increased sensitivity of the astrocyte BZD receptor
enhance activation of the GABA-BZD system
 Activated by nuerosteroids: allopregnenalone and
tetrahydrodeoxycorticosterone
CLINICAL FEATURES
 Portosystemic encephalopathy syndrome test (PSET)
evaluates the attention , concentration, fine motor skills,
orientation; led to the recognition of the syndrome of
minimal HE (not readily available)
 Magnetic resonance spectrometry has been used to
measure brain concentration of choline and glutamine
(Refer Table 92.2)
TREATMENT
 Primary treatment is to eliminate or correct precipitating
factors, reduce blood ammonia levels and avoid the toxic
effect of ammonia on the CNS
 Protein restriction is not recommended; vegetable and
dairy proteins are preferred because of more favourable
calorie-to-nitrogen ration
 Branched chain amino acids may improve symptoms but
benefit does not justify its routine use
 Lactulose or lactitol: nonabsorbable disaccharides are
metabolized by the colonic bacteria to by products that
induce catharsis decreasing intestinal pH inhibiting ammonia
absorption; improve symptoms but has not been shown to
improve test performance or mortality
o Side effects: abdominal cramping, flatulence, diarrhea,
electrolyte imbalance
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o May be administered per rectum although efficiency

has not been evaluated
 Oral antibiotics modify the intestinal flora lowering stool
pH and enhance the excretion of ammonia
 Second line treatment for HE
 Neomycin 1-3g q6 PO for 6 days in acute HE; 0.5-1g q12 PO
for chronic HE
 Efficacy has not been established
 Ototoxicity and nephrotoxicity in seen in renal patients
 Rifaximin 400mg TID PO
 Other antibiotics: metronidazole, vancomycin
 Other agents that modify intestinal flora:
 Acarbose: intestinal a-glocosidae inhibitor which inhibits
intestinal absorption of carbohydrates and glucose
 Probiotics: diminish ammonia generation
 Other agents that enhance ammonia clearance:
 Na benzoate , Na phenylbutyrate, Na phenylacetate:
enhance ammonia excretion and urine
 Zinc
 Extracorporeal albumin dialysis
 L-ornithine L-aspartate: activates the urea cycle and
enhances ammonia clearance

HEPATORENAL SYNDROME
 Part of a cascade of events associated with intense dilatation
of the splanchnic arterial vasculature in the setting of
cirrhosis or acute liver injury resulting in profound renal
arterial vasoconstriction and progressive renal failure
 Appears to be an extension of the pathophysiology prerenal
azotemia and is potentially reversible
 HRS develops in ~30% of cirrhotic patients who are admitted
with SBP or other infection, 25% who are hospitalized for
severe alcoholic hepatitis, 10% who require large-volume
paracentesis

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