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324
There has been a recent push for transplanting patients with acute alcoholic
hepatitis. What are your thoughts?
Those studies were done in France, where there is a national healthcare program
and patients got close follow-up and rehabilitation for their alcoholism. In those
studies, the results of transplant were excellent and alcohol recidivism low.
However, in this country, we are not good at treating the major disease, which is
alcoholism. We may be good at treating liver problems, but our approach to alcohol
rehabilitation is poor.
In centers in the USA, where transplant for acute alcoholic hepatitis has been
more successful, there have been four qualiers that are essential: (1) this is the rst
episode of acute alcoholic hepatitis, (2) the patient has no history of relapse from
sobriety, (3) there is strong family support, and (4) the patient has no history of
psychological problems. Under these conditions, there is a much higher likelihood
of success without relapse.
F. D u r a z o
https://t.me/medicina_free
325© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
W. H. Sobin et al. (eds.), Managing Complex Cases in Gastroenterology,
https://doi.org/10.1007/978-3-031-48949-5_70
Chapter 70
Fatty Liver onUltrasound withNormal
LFTs
FranciscoDurazo
A 43-year-old male was having mid-abdominal pain, and an ultrasound was
obtained to rule out gallbladder disease. This showed a normal gallbladder but
some fatty steatosis. The patient drinks two glasses of wine a week. His liver enzymes
are totally normal. His BMI is 26.
In this case, does the nding of steatosis with normal liver enzymes merit
further workup?
All patients with fatty liver deserve a workup for chronic hepatitis. Some patients
with autoimmune hepatitis will present with fatty liver, some patients with Wilson’s
disease will present with fatty liver, and some patients with hepatitis C, particularly
those with genotype 3, will present with fatty liver. We also want to look for signs
of metabolic syndrome.
It would be appropriate to send off labs but not necessarily to perform liver
biopsy. In terms of liver biopsy, there is not enough manpower to do liver biopsies
on the huge number of people with fatty liver. We want to select those patients who
are most at risk of having NASH, those patients who demonstrate more components
of the metabolic syndrome. I personally use the NAFLD brosis score to help me
decide whether to perform a liver biopsy in these patients.
F. Durazo (*)
Division of Gastroenterology and Hepatology, Department of Medicine,
Medical College of Wisconsin, Milwaukee, WI, USA
e-mail: fdurazo@mcw.edu
https://t.me/medicina_free
327© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
W. H. Sobin et al. (eds.), Managing Complex Cases in Gastroenterology,
https://doi.org/10.1007/978-3-031-48949-5_71
Chapter 71
Evaluation forLiver Damage
fromChronic ETOH Use
FranciscoDurazo
A 52-year-old male is concerned about his drinking history. He has 3–4 glasses of
wine or 2–3 hard drinks a day. He is concerned that this could be causing liver dam-
age. His liver enzymes are normal as is his ultrasound.
Is there any role for FibroScan
®
? Has FibroScan
®
become a basic compo-
nent of the exam and evaluation of most patients with liver problems?
The jury is still out on how useful the FibroScan
®
is. Some practitioners nd it
very useful while others believe that a good history, physical exam, and a basic
ultrasound will give you the same information. They point out that FibroScan
®
is
most accurate in detecting extremes– full-blown cirrhosis or a normal liver. These
clinicians feel that the basic workup will yield the same information. For those in-
between cases, they believe there is too much discrepancy between the FibroScan
®
results and liver biopsy, or MR elastography.
What are some factors that can confound FibroScan
®
results?
Factors that can blur FibroScan
®
results include hepatic congestion, biliary
obstruction, and obesity. Some believe that FibroScan
®
is very unreliable in patients
with NAFLD; it is most accurate in patients with viral hepatitis.
F. Durazo (*)
Division of Gastroenterology and Hepatology, Department of Medicine,
Medical College of Wisconsin, Milwaukee, WI, USA
e-mail: fdurazo@mcw.edu
https://t.me/medicina_free
329© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
W. H. Sobin et al. (eds.), Managing Complex Cases in Gastroenterology,
https://doi.org/10.1007/978-3-031-48949-5_72
Chapter 72
Ascites inaPatient Without Obvious
Cirrhosis
JoseFranco
The patient is a 60-year-old male who presents with a complaint of abdominal dis-
tension. There is no history of heavy alcohol abuse; he has 1–2 drinks a day on
weekends only. The patient does have a strong family history of heart disease. He
has very mild dyspnea on exertion. On exam, there is moderate abdominal ascites;
his liver is not palpable. There is mild peripheral edema. Lungs are clear. There is
no S3. However, he has a BNP of 400. His albumin is 3.2, AST is 30, ALT is 45, alk
phos is 140 (Nl < 80), INR is 1.2, Hgb is 12.8, and platelet count is 140,000.
Hepatitis serology, autoimmune markers, and Fe/TIBC are all negative. An ultra-
sound of the liver does not show any liver nodularity, but there is some dilation of
the IVC and hepatic vein, and moderate ascites is present. EF is 30% on echocar-
diogram. The patient is started on diuretics for mild peripheral edema, and a para-
centesis is performed to evaluate the ascites. The SAAG is 1.2 with ascites albumin
of 2.0 and ascites total protein of 3.2. Cytology and AFB are negative. Cell count is
20 PMNs. FibroScan® shows 8kPa.
What is your differential diagnosis for patients who present with ascites but
do not have obvious cirrhosis?
I always tell students that cirrhosis is the leading cause of ascites, but it’s cer-
tainly not the only cause. When we do a paracentesis, we send an ascites albumin
and serum albumin to determine the SAAG (serum albumin-ascites albumin gradi-
ent) as well as an ascites total protein (TP). These results help us determine the eti-
ology of the ascites.
We break the ndings into four categories:
Category 1: SAAG >1.1g/dL and ascites TP< 2.5 g/dL.Most cases of cirrhosis,
also seen in fulminant liver disease.
J. Franco (*)
Department of Medicine-Division of Gastroenterology and Hepatology, Medical College of
Wisconsin, Milwaukee, WI, USA
e-mail: jfranco@mcw.edu
https://t.me/medicina_free
330
Category 2: SAAG >1.1g/dL and TP> 2.5 g/dL.Patients with CHF, constrictive
pericarditis, Budd-Chiari, and veno-occlusive disease.
Category 3: SAAG <1.1g/dL and TP<2.5g/dL.Patients with nephrotic syndrome,
peritoneal carcinomatosis (where the TP is usually high but on occasion low).
Category 4: SAAG <1.1g/dL and TP>2.5g/dL.Patients with peritoneal carcino-
matosis, TB, pancreatic ascites, and chylous ascites.
This patient has a SAAG of 1.2. The high SAAG indicates portal hypertension.
If we look at the differential diagnosis for high SAAG ascites uid, we have cirrho-
sis, fulminant liver disease, CHF, constrictive pericarditis, Budd-Chiari syndrome,
and veno-occlusive disease (VOD) or sinusoidal obstruction syndrome (SOS).
Occasionally, in advanced CHF, you will see a low SAAG.In a patient like this with
mild CHF, you would expect to see a high SAAG.
This patient has an elevated ascites uid total protein of 3.2, which is usually not
seen in cirrhosis by itself. It is seen in cases of CHF, constrictive pericarditis and
Budd-Chiari. The reason for the high total protein in these cases is that hepatic syn-
thetic function is usually preserved. In this case, the patient’s serum albumin of 3.2
and INR of 1.2 demonstrates good functional reserve. This is quite different from
the cirrhotic patient who presents with a serum albumin of 2.3 or 2.5. It is more
similar to patients with portal vein thrombosis, who have preserved synthetic func-
tion and a high total ascites protein.
This patient received some diuretics prior to paracentesis. Will this have any
effect on the SAAG or total protein?
Usually, you don’t see any change but occasionally the total protein will increase
due to volume contraction.
In cases where ascites is due to CHF, how often do they have cardiac
cirrhosis?
Most patients with ascites due to heart failure do not have cirrhosis. Most of the
time, they have congestive hepatopathy, with associated portal hypertension. This
congestion is veried by the nding of a dilated IVC and hepatic veins on ultra-
sound. Patients who have severe, long-standing CHF, however, may get end-stage
cardiac cirrhosis after many years of complications.
Is there any role for doing an EGD looking for varices in a patient like this?
Yes, to me, this is no different than evaluating a patient with portal vein throm-
bosis. These patients can get esophageal and gastric varices from non-cirrhotic por-
tal hypertension. If you ask what the most feared complication is in a patient like
this it is bleeding varices. Ascites uid could get infected, but the highest mortality
would be bleeding varices, and you don’t want to miss these. So, you do need to
do an EGD.
Another thing we look at in deciding whether to do an EGD is the platelet count.
If the platelet count is <150,000, they are more likely to have varices. In this case, it
is 140,000.
J. Franco
https://t.me/medicina_free
331© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
W. H. Sobin et al. (eds.), Managing Complex Cases in Gastroenterology,
https://doi.org/10.1007/978-3-031-48949-5_73
Chapter 73
Ascites inCirrhosis of Unclear Etiology
withIncreased Mononuclear Cells
JoseFranco
A 57-year-old female with a normal BMI is found to have marked ascites. There is
no history of signicant alcohol use. Ultrasound shows a mildly nodular liver. The
AST is 34, ALT is 47, Alk phos is 90, bilirubin 1.3, and albumin is 2.9. Hepatitis
panel and autoimmune markers– including ANA, ASMA, and AMA– are negative.
A paracentesis is performed, which reveals 300 wbc/hpf, and 80% are mononuclear
cells. The Aa gradient is 1.0.
There is no obvious cause for her apparently cirrhotic liver, what are some
possible etiologies for this?
You’ve ruled out viral hepatitis. PBC is unlikely with the normal alkaline phos-
phatase and negative AMA.The patient could have late-stage PSC– but there is no
history of IBD here. I always check for alpha-1 antitrypsin deciency and Wilson’s.
You know, alpha-1 antitrypsin deciency is the leading indication for metabolic
liver transplant, in the pediatric population. But while we always check for alpha-1
and Wilson’s, it would be very unusual for the rst presentation to be at age 57.
Another consideration is hemochromatosis. A 57-year-old female is now post-
menopausal. It is possible for hemochromatosis to rst manifest itself at this age in
a woman. Remember, men will present much earlier than women. Women tend to
present when they are 50, 60, and 70. When they are younger, they are auto-
phlebotomizing through menstruation. So, it is a diagnosis worth considering.
The most common cause of cirrhosis, however, in a 57-year-old female would be
nonalcoholic fatty liver disease. Patients don’t have to be obese; they just have to
have insulin resistance and/or elevated triglycerides, those by themselves are risk
J. Franco (*)
Department of Medicine-Division of Gastroenterology and Hepatology, Medical College of
Wisconsin, Milwaukee, WI, USA
e-mail: jfranco@mcw.edu
https://t.me/medicina_free
332
factors. Obviously, there are no blood tests to diagnose nonalcoholic fatty liver dis-
ease; you diagnose it by ruling out other possible causes, and then, consider doing a
liver biopsy. So that’s how I would approach it.
In this case, the tests are all negative, yet I know she has cirrhosis. If my sero-
logic workup remains negative, I would consider doing a liver biopsy to see if it
helps me establish an etiology.
What would be causing the increase in mononuclear cells?
An increase in mononuclear cells on paracentesis is not something we commonly
see. You have to think about atypical things, like fungal infections or tuberculosis.
But it is also possible that they might represent cancer cells. Could the patient have
peritoneal carcinomatosis? If the uid looked milky, we’d consider chylous ascites,
which could involve the lymphatics leading to ascites uid with increased
lymphocytes.
J. Franco
https://t.me/medicina_free
333© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
W. H. Sobin et al. (eds.), Managing Complex Cases in Gastroenterology,
https://doi.org/10.1007/978-3-031-48949-5_74
Chapter 74
Low SAAG Ascites
JoseFranco
A 67-year-old male who drinks alcohol on a daily basis is being seen for moderate
ascites. He has anorexia and has lost 20 lbs. over the past month. Ultrasound shows
a nodular liver, with marked ascites and no obvious masses. His AST is 40, ALT is
25, alk phos is 120, and bilirubin is 1.4. A paracentesis is performed and reveals an
Aa gradient of 0.8. The ascites total protein is 2.3. Fluid cell count is 20 wbc.
Cytology is negative. UA is negative for protein. Because the patient’s creatinine is
1.8, you are reluctant to do a contrast-enhanced CT scan. An MR abdomen shows
no obvious cancer.
Normally, if it were just alcoholic cirrhosis, you would expect a high Aa
gradient. What might be causing a low gradient here? What further investiga-
tions would you do?
So, the patient has a nodular liver and normally you would expect to see a high
SAAG, but here it is low. Let’s review our categories again:
Category 1: SAAG >1.1g/dL and ascites TP< 2.5 g/dL.Most cases of cirrhosis,
also seen in fulminant liver disease.
Category 2: SAAG >1.1g/dL and TP> 2.5 g/dL.Patients with CHF, constrictive
pericarditis, Budd-Chiari, and veno-occlusive disease.
Category 3: SAAG <1.1g/dL and TP<2.5g/dL.Patients with nephrotic syndrome,
peritoneal carcinomatosis (in which the TP is usually high but on occasion low).
Category 4: SAAG <1.1g/dL and TP>2.5g/dL.Patients with TB, pancreatic asci-
tes, and chylous ascites.
J. Franco (*)
Department of Medicine-Division of Gastroenterology and Hepatology, Medical College of
Wisconsin, Milwaukee, WI, USA
e-mail: jfranco@mcw.edu
https://t.me/medicina_free
334
In this case, I am concerned that the low SAAG may represent peritoneal carci-
nomatosis. The negative cytology does not rule this out. That’s because cytology of
ascites uid is a poor test, less than a quarter of cases will actually be positive. It’s
great for diagnosing infection, but if you’re trying to nd malignant cells, it is not a
very good test.
I believe that this patient has cancer, and we just haven’t found it. In terms of the
other diagnoses for a low SAAG ascites, I don’t think he has pancreatic ascites,
because you would’ve seen something on an MRI.He doesn’t have chylous ascites,
because you obviously would have seen milky-looking uid. There’s nothing to
suggest nephrotic syndrome or TB.So, to me, this patient has a primary with peri-
toneal metastases causing ascites, and we just haven’t found the primary. So, he
might need a laparoscopy, to look at what is going on in his peritoneal lining.
J. Franco
https://t.me/medicina_free
335© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
W. H. Sobin et al. (eds.), Managing Complex Cases in Gastroenterology,
https://doi.org/10.1007/978-3-031-48949-5_75
Chapter 75
Banding Esophageal Varices
KiaSaeian
A 43-year-old male with a long history of alcoholism presented to your ER a week
earlier. One of the newer gastroenterologists on staff did an EGD and found grade
3 esophageal varices with stigmata of prior hemorrhage but were not actively
bleeding. He placed a total of 10 bands on the varices. The patient was discharged
and now presents again to the ER with torrential UGI bleeding. Endoscopy reveals
several post-banding ulcers, one of which is actively bleeding.
How do you stop bleeding from these ulcers? Can it be done endoscopically
or do you need IR?
In general, we think that banding ulcers resulting in bleeding occur in less than
5% of the cases, and while most of these bleeding episodes are minor, some of them
can be signicant, and fatal cases have been reported. Ulceration itself is almost
universal and typically occurs 3–7days after the banding with healing expected
within the rst 2–3weeks. While the thought is that it is often the perforating veins
as opposed to the main varix that is bleeding in the setting of post-banding ulcer-
ation resulting in lower volume bleeding, they are often very difcult to control if
they bleed signicantly.
It may seem ippant to answer in this way, but the short answer is that you pretty
much do whatever it takes to stop the bleeding. There are reports of attempting
almost anything you can think of to try to stop them from bleeding, including repeat
band ligation, cyanoacrylate glue injection, proceeding with TIPS or other portal
decompressive procedures, or even esophageal stents and Hemospray
®
. In my expe-
rience, I start with band ligation and then in a couple of cases have used glue
K. Saeian (*)
Division of Gastroenterology & Hepatology, Medical College of Wisconsin,
Milwaukee, WI, USA
e-mail: ksaeian@mcw.edu
https://t.me/medicina_free
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