Patient comes in with rounded abdomen, you will see umbilical hernia and caput

medusa. The prognosis is grim if you do not do anything. Compensated vs

decompensated cirrhosis. Portal hypertensive bleeding, ascites and hepatic
encephalopathy are what you see in decompensated cirrhosis. Cirrhosis is the most
common cause of ascites. Ovarian cancer can cause malignant ascites, but cirrhosis
is the big one. Portal hypertension has to be there for ascites to form, baroreceptor,
and aldosterone activation. Portal hypertension can lead to splanchnic arterial
vasodilation and leads to decreased arterial blood volume which will activate the
renin angiotensin system. Extreme vasodilation leads to hepatorenal syndrome
where there is renal vasoconstriction. HPVG above 12 mmHg is necessary for
ascites to develop and is associated with low sodium excretion. If you have portal
vein obstruction you wont see ascites, but with hepatic vein obstruction you can see
ascites. Diagnosis via physical exam with abdominal distension, bulging flanks, nonspecific and insensitive. Ultrasonogram is used to confirm suspicion. Diagnostic
paracentesis to check out the fluids. PMN count and culture at the bedside, protein
albumin gradient to see if it is hepatic or cirrhotic in origin. Anyone that has ascites,
you want to see why via a diagnostic paracentesis. Abdominal paracentesis is via
midline so that you are not going thru the bladder. Percuss out and see if there is
any dullness which shows fluid. You can do laterally or midline.
Drain the bladder before you do it. Z technique you would push down and put
pressure, and you will see a zigzag which prevents any fluid from going out.
Albumin, protein, pmn cell count, and cultures at BEDSIDE!!. SAAG is equal to serum
albumin ascites albumin, it is more than 1.1 then it is portal hypertension and if
the value is less than 1.1 then it is not portal hypertension. Look at the total protein,
high total protein almost always is cardiac ascites (post hepatic problem), high
protein means more than 2.5. If the total protein is less than 2.5 it is sinusoidal in
nature. Cirrhotic is low protein, cardiac is high protein. High SAAG is cirrhotic-portal
hypertension, and low SAAG is mainly peritoneal. If you are doing a paracentesis
you will do a culture with it.
If you do the blood culture at the bedside, the yield is 91% which is very good.
Portal hypertension with no ascites, you want to increase sodium intake.
Uncomplicated ascites- salt restriction + diruretics. Tense ascites can affect
breathing- you want to do a large volume paracentesis to reduce it. Diuretics you
will start with spirolactone and gradually include furosemide (for inadequate weight
loss or if hyperkalemia develops). Weight is going to be one of the best ways to
determine how you are diuresing the patient. Too much weight loss- you want to
lessen the diuretics. Gynecomastia is a side-effect of spironolactone. You want to
start low, but you will eventually go up in dosage to take care of the high urine
sodium present. Combined therapy- every 3-4 days while assessing the weights.
Consider ascites to be refractory- if there is no significant weight loss with combined
spironolactone and furosemide therapy. Large volume paracentesis can be used in
patients with no kidney disease, no edema. It is a second line therapy when
compared to diuretics. Large volume paracentesis every 2-4 weeks.
Peritoneal jugular shunts are not used that often. High complication rate associated
with it, and you can get a thrombosis associated with it. If you do nothing against

refractory ascites it can lead to hepatorenal syndrome. Diuretic resistant is when

you dont have any effect with the highest dose of diuretics. Shunt that goes into
the jugular vein, you can pump the ascites back into the jugular. Works for someone
that is not a transplant candidate and it is more of a last resort. TIPS works well with
patients that have mobile ascites. They dont have to be too strict with the sodium
intake. Had ascites, and sent to TIPS procedure, and if they have a recurrent ascites
then it is due to a TIP malfunction. You have to reassess the TIPS. Complications of
TIPS is stent stenosis and hepatic encephalopathy. Someone that has refractory
ascites, you want to get them evaluated and listed for a transplant.
TIPS is going to decrease the sinusoidal pressures. Secondary infections or
spontaneous infections can happen with ascites. Fluid present can allow for that
infection. Tense ascites with respiratory distress that can take place due to
increased intra-abdominal pressure. Umbilical hernia rupture is a surgical
emergency. Treatment is to control the ascites. SBP- acute bacterial infection that
occurs in the absence of infection elsewhere in body. Diagnosis is PMNs over 250
AND/OR culture positive, it is one or the other or both. Most common organism is E.
coli, gram mostly with some gram +. Most common type of infection in cirrhotic
patients is SBP- fever, abdominal pain, confusion, tenderness and hypertension.
Some may have no signs or symptoms and these are the people that you have to
watch, and do paracentesis. Variceal bleeding- treat with IV antibiotics to prevent
SBP. If you dont take care of the ascites there is a recurrence rate of 70-80% in one
year. High protein ascites- with cardiac ascites.
Diagnosis is PMN over 250 and/or culture positive. Avoid the aminoglycosides,
repeat paracentesis in 48 hours to assess the PMNs. Quinolones are used to
decrease the recurrence rate. Ceftaxime and ampicillin for 5 days.
Diagnosis and management of Spontaneous Bacterial Peritonitis- do a diagnostic
paracentesis and see if the PMN count is less than or more than 250. If it is less than
250 and the culture is not positive then no treatment is indicated. If the culture is
positive you would do a repeat paracentesis.
Oral olfloxacin for uncomplicated SBP. Avoid aminoglycosides. You want to eliminate
the ascites. Prevent official episode or recurrence via IV antibiotics. Bacterial
translocation does not increase in pre hepatic portal hypertension. Recover from
SBP requires daily quinolone therapy. Norfloxacin reduces the recurrence of
Spontaneous bacterial peritonitis. Hepatorenal syndrome can complicate ascites
and lead to renal dysfunction. Glucosee and ADH can differentiate a secondary
(anything from infection elsewhere in the body can affect it)- low glucose high
protein greater than 1. Marked dilation in extra renal circulation that is causing the
issue in hepatorenal syndrome. Type 1 is rapidly progressive renal failure, creatinine
doubles to more than 2.5. Marked renal vasoconstriction leading to reduced
glomerular filtration rate. Type 1 do poorly, and transplant is the recommended
choice. Type 2 should go to transplant center, but they dont do as poorly as type 1.
Type 2 is associated with refractory ascites. Creatinine greater than 1.5 or the
clearance less than 40 is used for diagnosis, you also should have advanced hepatic
failure and portal hypertension. Ascites and hyponatremia is always present with

hepato-renal syndrome!!! BOTH NEED TO BE PRESENT. Benefits of vasoconstrictors

and albumin together (octreotide and midodrine). Hepatorenal syndrome will
improve in 60% of patients. Low recurrence upon discontinuation of therapy with
type 2, but mortality remains high for type 1. One way to reverse and get back renal
function is via liver transplant. Hemodialysis does NOT work with hepato-renal
syndrome. Treatment- liver transplant, vasoconstrictors and albumin, TIPS, ECAD.
Low GFR, high plasma Norepi. Late complication of cirrhosis. It should be mobilized
to prevent complications. The more refractory the ascites the more advanced the
liver disease and the poorer the prognosis. Secondary bacterial peritonitis requires
more than 1 bacterial species, it is extra-hepatic in nature. Secondary can be due to
bowel perforation. ADH, glucose and protein levels.