Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2948_Библиотеки_им_академика_М_И_Перельмана
.pdf
347© 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_79
Chapter 79
Portal Vein Thrombosis in Cirrhosis
JamesEsteban
A 56-year-old male was diagnosed with alcohol-associated cirrhosis 2years ago
and stopped drinking at that time. He has been undergoing abdominal ultrasound
every 6months for hepatocellular cancer screening. On his last ultrasound, a portal
vein thrombus was seen. The last ultrasound 6months ago did not show PVT.
Would you anticoagulate this patient?
Portal vein thrombosis (PVT) is a known complication of cirrhosis. It appears
paradoxical that patients with cirrhosis, who often have prolonged prothrombin
time and thrombocytopenia, would develop PVT.However, cirrhosis is a state of
rebalanced hemostasis, where patients experience simultaneous changes in both
pro- and anticoagulant factors [1]. Decisions on anticoagulation for patients with
PVT, who may have varices, bleeding portal hypertensive gastropathy, or GAVE,
can be challenging.
The rst thing I would do is obtain contrast-enhanced CT or MRI, to conrm the
PVT; determine the presence of collaterals (or cavernoma), which indicate chronic-
ity, determine the extent of the clot, in terms of being partially or totally occlusive
and extension into superior mesenteric vein (SMV) or splenic veins; and make sure
it is not a malignant thrombus. My decision about anticoagulation will be based on
chronicity of the clot, extent of the clot and the presence of symptoms of intestinal
ischemia, and the patient’s potential liver transplant candidacy [2, 3].
If the clot is chronic, with well-established collaterals and cavernoma, there is no
established benet with anticoagulation. We would be continuing medical manage-
ment and surveillance of portal hypertension.
J. Esteban (*)
Division of Gastroenterology and Hepatology, Department of Medicine, Medical College of
Wisconsin, Milwaukee, WI, USA
e-mail: jesteban@mcw.edu
https://t.me/medicina_free
348
If the clot is recent (<6months) but involves only intrahepatic PV branches or
only partially occludes the main PV, I would offer either anticoagulation or surveil-
lance imaging with expectant management. It is reasonable to repeat abdominal
imaging after 2–3months, and anticoagulate only if the clot progresses.
If the clot is recent and extensive, which is to say that it totally occludes the main
PV or extends into the SMV, particularly if the patient is a liver transplant candidate
or has symptoms of intestinal ischemia, I would anticoagulate as soon as possible. I
would go as far as discussing with interventional radiology and transplant surgery
whether we should consider portal vein recanalization and transjugular intrahepatic
portosystemic shunt (TIPS), especially if the patient has another indication for TIPS
(e.g., ascites or variceal bleeding) or if clot extension threatens portal anastomosis
during transplant.
In this case, the patient is felt to have a recent clot, which is totally occluding the
main portal vein. He does not have abdominal pain or bloody diarrhea. The patient’s
last EGD was 2years earlier, and at that time, there were no varices present. The
decision is made to repeat EGD, and this reveals two grade 2 varices and one grade
3 varix, with a red mark.
How do you want to manage this?
Since the patient has high-risk esophageal varices and needs anticoagulation, I
would pursue band ligation.
If you band, how long will you wait before starting anticoagulation?
It is debatable if anticoagulation should be delayed until varices are eradicated. I
feel that cirrhotic patients with totally occlusive clots of the main PV and/or SMV
should be anticoagulated without delay, while patients with less extensive clots may
hold off anticoagulation until varices are banded or eradicated. Early anticoagula-
tion of PVT is important for clot recanalization and prevention of clot progression
[4, 5]. The AASLD does recommend initiating anticoagulation as soon as possible
and not delaying until varices are eradicated [3]. Available data do not suggest
higher risk of bleeding with this practice. Moreover, the data suggest that anticoagu-
lation can continue uninterrupted through band ligation without risk of bleeding [6].
I treat patients with small and low-risk varices with nonselective beta-blockers
such as carvedilol (my preference), propranolol, or nadolol instead of band ligation,
with the goal of preventing the growth and rupture of varices. I prefer carvedilol
over propranolol because studies show that it more effectively lowers portal pres-
sure [7] as a result of its additional effect on alpha-1 adrenergic receptors, which
reduce intrahepatic vascular resistance in addition to reducing portal blood ow.
I also use carvedilol in patients even after large varices are eradicated by band
ligation because studies show that carvedilol not only reduces the risk of variceal
bleeding but also hepatic decompensation events such as ascites [8].
What anticoagulant agents do you use and how long do you anticoagulate
patients?
I have used warfarin and direct oral anticoagulants as rst-line agents for antico-
agulation in PVT.Warfarin probably has the most data on efcacy and safety, and it
is also cheaper and more easily reversible if the patient develops a bleeding compli-
cation, but it requires normal baseline INR – which many cirrhotics don’t
J. Esteban
https://t.me/medicina_free
349
have– and also frequent INR monitoring. Direct oral anticoagulants (DOAC) do not
require INR monitoring and are thus easier to use. Many recent studies show
DOAC’s success in PVT, but it is unclear if they are safe to use in patients with more
advanced stages of liver disease (i.e., Child’s C). I would request hematology con-
sultation in more complicated cases, such as patients with progressive clot despite
anticoagulation or underlying thrombophilia.
I anticoagulate patients for at least 6months. I obtain cross-sectional abdominal
imaging after 2–3months to check if the clot resolves, improves, or progresses. If
the clot completely resolves, I will discontinue anticoagulation, but continue routine
surveillance with doppler ultrasound or cross-sectional imaging every 6months. If
the clot progresses, assuming the patient is being adherent, my options are changing
anticoagulants with the guidance of hematology or interventional radiology consul-
tation for intravascular procedures or TIPS.
References
1. Lisman T, Caldwell SH, Intagliata NM.Haemostatic alterations and management of haemosta-
sis in patients with cirrhosis. J Hepatol. 2022;76(6):1291–305.
2. De Franchis R, Bosch J, Garcia-Tsao G, Reiberger T, Ripoll C, Abraldes JG, Albillos A, Baiges
A, Bajaj J, Bañares R, Barrufet M.Baveno VII–renewing consensus in portal hypertension. J
Hepatol. 2022;76(4):959–74.
3. Northup PG, Garcia-Pagan JC, Garcia-Tsao G, Intagliata NM, Superina RA, Roberts LN,
Lisman T, Valla DC.Vascular liver disorders, portal vein thrombosis, and procedural bleed-
ing in patients with liver disease: 2020 practice guidance by the American Association for the
Study of Liver Diseases. Hepatology. 2021;73(1):366–413.
4. Loffredo L, Pastori D, Farcomeni A, Violi F.Effects of anticoagulants in patients with cir-
rhosis and portal vein thrombosis: a systematic review and meta-analysis. Gastroenterology.
2017;153(2):480–7.
5. Delgado MG, Seijo S, Yepes I, Achécar L, Catalina MV, García-Criado Á, Abraldes JG, de la
Peña J, Bañares R, Albillos A, Bosch J.Efcacy and safety of anticoagulation on patients with
cirrhosis and portal vein thrombosis. Clin Gastroenterol Hepatol. 2012;10(7):776–83.
6. Guillaume M, Christol C, Plessier A, Corbic M, Péron JM, Sommet A, Rautou PE, Consigny
Y, Vinel JP, Valla CD, Bureau C.Bleeding risk of variceal band ligation in extrahepatic por-
tal vein obstruction is not increased by oral anticoagulation. Eur J Gastroenterol Hepatol.
2018;30(5):563–8.
7. Jachs M, Hartl L, Simbrunner B, Bauer D, Paternostro R, Balcar L, Hofer B, Psterer N,
Schwarz M, Scheiner B, Stättermayer AF.Carvedilol achieves higher hemodynamic response
and lower rebleeding rates than propranolol in secondary prophylaxis. Clin Gastroenterol
Hepatol. 2022;21(9):2318–2326.e7.
8. Villanueva C, Albillos A, Genescà J, Garcia-Pagan JC, Calleja JL, Aracil C, Bañares R,
Morillas RM, Poca M, Peñas B, Augustin S. β blockers to prevent decompensation of cirrhosis
in patients with clinically signicant portal hypertension (PREDESCI): a randomized, double-
blind, placebo-controlled, multicentre trial. Lancet. 2019;393(10181):1597–608.
79 Portal Vein Thrombosis in Cirrhosis
https://t.me/medicina_free
351© 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_80
Chapter 80
PVT andBudd Chiari as aComplication
ofUC
KiaSaeian
The patient is a 28-year-old female with a history of ulcerative colitis that was well
controlled on mesalamine. She presents with increased diarrhea and rectal bleeding
but also has marked abdominal distension. An US of the abdomen conrms the pres-
ence of a large amount of ascites. There is no history of liver disease, alcohol use,
etc. Her labs show AST of 120, ALT of 140, AP of 100, and bilirubin of 1.4. Hepatitis
panel and autoimmune panel are negative. A CT is obtained, which shows thrombus
in the hepatic vein, IVC, and portal vein. There is a suggestion of gastroesophageal
varices. There is hepatomegaly but no suggestion of cirrhosis. She has a combined
EGD/colon, and while on EGD there are grade 2 esophageal varices, on colon
there is evidence for moderately severe ulcerative colitis. The patient is placed on
IV steroids and beta-blockers. Anticoagulation is started (IV heparin), and the next
day the patient starts having more active rectal bleeding. Her abdominal distension
is getting worse. Heparin is put on hold.
How would you manage the presumed Budd-Chiari and portal vein
thrombosis?
First, I’m not sure I would have started her on beta-blockers in the rst place,
particularly in the setting of a large amount of ascites, where the use of beta- blockers
is controversial. And with grade 2 varices, I don’t think you have to jump in and
immediately do anything about her varices.
But, of course, we do have to address the thromboses. Here, it’s a little unusual,
it’s not only Budd-Chiari, and it’s also portal vein thrombosis and extension into the
IVC, which makes it a pretty extensive thrombus. She’s very young, so I’m not as
concerned about malignancy. But while the IBD could be a trigger for her
K. Saeian (*)
Division of Gastroenterology & Hepatology, Medical College of Wisconsin,
Milwaukee, WI, USA
e-mail: ksaeian@mcw.edu
https://t.me/medicina_free
352
hypercoagulable state, it seems a little out of proportion. Since it’s very extensive, I
would look for other causes of hypercoagulable state, even though IBD might
remain the sole explanation. I’d want to make sure that there is nothing else going
on with her bone marrow. These days, it is almost mandatory, when you have some-
one who presents with Budd-Chiari, to rule out polycythemia vera, or some of the
other myeloproliferative disorders that can certainly trigger this. That would be on
my radar as well.
Looking at the bigger picture, we have to decide how to manage this very com-
plex patient who is bleeding but needs treatment for thrombosis. In this setting, we
have really discovered that TIPS is the way to go. I would get interventional radiol-
ogy and transplant surgery involved. While TIPS is generally feasible in Budd-
Chiari, the portal vein thrombus in this case presents an increased level of complexity
for performing a successful TIPS.And, if you are successful in placing a TIPS, you
want to anticoagulate afterward to prevent shunt thrombosis. So, in this case you
should notify colorectal surgery as well, because even though I’m not recommend-
ing a colectomy at the time, that’s where you may end up heading if rectal bleeding
becomes intractable.
Even though she is young, I would get an echocardiogram, to see whether she
has any pulmonary hypertension and whether she is a suitable candidate for TIPS,
and get IR involved to see if it’s feasible to place a TIPS and maintain its patency.
In most cases of Budd-Chiari, the thrombus is fairly new and the radiologist can
get a wire through it. In this case, however, the clot is more extensive, and it goes
into the IVC, and so the question is whether there are other channels that IR can get
into. In some of these cases, it might require DIPS to be successful.
If you only have hepatic vein thrombosis, is stenting the vein ever an option?
You could consider it, but in almost all cases, the thrombus in Budd-Chiari
involves multiple small venous tributaries, almost like a spider web conguration.
If you have the classic Asian type of Budd-Chiari, where there is an IVC web, then
a stent is a very good option for those patients. But in the patients we tend to see
who have involvement of all the little venous radicals, you really do need TIPS
decompression. There’s good evidence that if you intervene early with TIPS, you
can help prevent some of these patients from needing a liver transplant. But if you
don’t act quickly and aggressively, cirrhosis can develop pretty quickly.
K. Saeian
https://t.me/medicina_free
353© 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_81
Chapter 81
HCC Management, Solitary Lesion
inaChild’s ACirrhosis
FranciscoDurazo
A 63-year-old man with chronic HCV is sent to you with Child’s A cirrhosis and a
3-cm mass in the liver with characteristics of an HCC.The patient’s overall health
is otherwise quite good.
Can you ever consider surgical resection of a hepatoma in a patient with
cirrhosis? Is there anything that would make you want to put this patient on a
transplant track?
Our current guidelines state that if a patient with Child’s A cirrhosis has a single
resectable lesion, surgery is the treatment of choice. There is a 50% chance of recur-
rence after surgical resection, but that means 50% of patients may be cured.
If, instead, you recommend liver transplant, the patient needs to undergo trans-
plant evaluation, go on a waiting list, and will require locoregional therapy as a
temporizing bridge to transplant. If he gets transplanted, the patient will be con-
demned to lifelong immunosuppression.
This patient is a male, and it should be noted that HCC is much more common in
males; the management is the same in males and females.
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
355© 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_82
Chapter 82
Management ofUnresectable HCC
inaCirrhotic
FranciscoDurazo
A 59-year-old male with alcoholic cirrhosis has been abstinent for 5 years and
presents with a 6cm HCC and portal vein thrombosis. The AFP is 400. You had last
seen him 3years ago, at which time ultrasound showed no lesion in the liver. He was
subsequently lost to follow-up, until now.
What do you recommend for HCC surveillance?
For patients with cirrhosis, we get an ultrasound and AFP every 6 months. If
there is an abnormality on ultrasound, we order a CT or MRI.
Is AFP still recommended for surveillance?
Actually, the American Association for the Study of Liver Diseases (AASLD)
“red” the AFP a while back, but the 2018 recommendations had a soft reintroduc-
tion, with the recommendation of surveillance using ultrasound, with or without
AFP, every 6months. However, we still nd the AFP to be helpful. There are occa-
sional patients who have a normal ultrasound but an AFP of 1000, so we order an
MRI.On MRI, we see the hepatoma that was missed on US.I think that most hepa-
tologists still follow the AFP.
How would you manage this patient if there was no portal vein thrombosis?
We think about possible liver transplant to cure the HCC and cirrhosis, but
according to Milan criteria the lesion is too large. Therefore, we would try to down-
size the lesion. For lesions under 4 cm in size, ablation with radiofrequency or
microwave is effective. For lesions larger than 4cm, transarterial catheterization
and chemoembolization (TACE) or radioembolization, with Yttrium 90 (TARE), are
recommended for downsizing, with TARE causing fewer side effects than TACE,
although the two modalities have not been compared head-to-head for efcacy.
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
356
Do you ever see cures with locoregional therapies?
Yes, the lesions may disappear and be absent in the liver explant. In spite of this,
transplant is still recommended, because new tumors will form in the cirrhotic liver;
you treat one tumor and a new one pops up.
This patient has portal vein thrombosis. In patients with HCC, are the por-
tal vein thrombi assumed to be malignant?
No, benign portal vein thrombosis is common in cirrhotics. Malignant portal
vein thrombi are generally easy to differentiate from benign PVT.They are usually
contiguous with the HCC, and they take up contrast on CT and MRI, so usually they
are easily discernible. The distinction between malignant and benign portal vein
thrombosis is important because malignant PVT closes the door on transplant.
How do you manage benign PVT in a transplant candidate?
Some centers will anticoagulate these patients, usually with coumadin. Other
centers will take the patient to transplant with a PVT and do thrombectomy at the
time of transplant, as long as the PVT does not extend to the SMV (in which case
anticoagulation is necessary).
This patient gets therapy with TACE and the lesion shrinks to 3cm. AFP is 500.
Can you list the patient for transplant now?
Not yet. Once the lesion is downsized and the AFP is under 500, you then have
to wait 6months before giving exception points to the patient. It was found that
delaying transplant leads to better outcomes by weeding out those tumors that have
the most unfavorable biology. In addition, it was found that hepatomas with an
AFP >1000 had a very unfavorable prognosis, leading to the requirement that
patients had to have an AFP under 500 to be listed.
F. D u r a z o
https://t.me/medicina_free
357© 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_83
Chapter 83
HCC inNAFLD Without Cirrhosis
FranciscoDurazo
A 57-year-old, obese female is seen in the community and referred for elevated
LFTs and a mass in the liver. Her labs include ALT of 220, AST of 150, Alk phos of
170, and platelets of 180,000. US reveals diffuse steatosis and a 4-cm mass in the
liver. All viral and autoimmune serology is negative. CT scan shows a lesion that
has characteristic ndings of hepatocellular carcinoma and no evidence of cirrho-
sis. There is no liver nodularity or enlarged spleen nor suggestion of varices.
Do some patients with NAFLD develop HCC without rst having cirrhosis?
Over the past 10years, there have been cases of HCC in patients with NASH
without cirrhosis, although it remains uncommon. This is called steatohepatitic
hepatocellular carcinoma, a kind of noncirrhotic HCC in patients with underlying
fatty liver. Many of these patients have a single-nucleotide polymorphism. We’ve
seen a couple of cases like this at our institution.
How should we be screening for this possibility?
In the absence of warning signals, we continue to screen patients with NAFLD
and cirrhosis for HCC every 6months, but now I am also screening patients with
fatty liver without cirrhosis every 12months with ultrasound and AFP.A number of
our colleagues are doing the same thing, to help us all sleep better at night.
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
359© 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_84
Chapter 84
Managing Primary Biliary Cholangitis
JuanTrivella
The patient is a 45-year-old female who’s referred for abnormal liver enzymes. She
has an alkaline phosphatase of 240 (nl<80), and her AST is 25, ALT is 30, and bili-
rubin is 1.0. Her GGTP is three times normal. Her anti-mitochondrial antibody is
positive at 1:80, ANA is negative, anti-smooth-muscle antibody is negative, albumin
is 3.6, platelets are 210,000, and ultrasound of the liver is normal. The patient
doesn’t drink alcohol and is on no medications.
Are you comfortable making the diagnosis of primary biliary cholangitis?
Do you need a liver biopsy?
Yes, I am comfortable making the diagnosis. This female patient has cholestasis
and a clearly positive AMA, with no risk factors for other chronic liver disorders.
No liver biopsy is needed in this case. If you are considering a superimposed diag-
nosis or are unable to stage the degree of brosis via noninvasive methods, then I
would perform a liver biopsy [1].
It appears that the majority of patients with PBC are asymptomatic at the
time of diagnosis. Is that your experience?
Yes, this has been my experience, and although most patients are asymptomatic
at diagnosis, almost everyone with PBC will experience symptoms within two
decades [2]. The presence or absence of symptoms at diagnosis or on follow-up
does not correlate well with the stage of the disease and has shown no difference in
survival outcomes.
J. Trivella (*)
Division of Gastroenterology and Hepatology, Department of Medicine, Medical College of
Wisconsin, Milwaukee, WI, USA
e-mail: jtrivella@mcw.edu
https://t.me/medicina_free
Соседние файлы в папке Библиотека им академика М.И. Перельмана