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78
Budd-Chiari syndrome
Management depends on etiology, the severity of the liver derangement, the degree of IVC patency,
and the patient’s clinical status
A. H. Sohail et al.
Management
Survival Liver transplantation is associated with a long-term survival of 65% to 85%
The primary goals are to relieve hepatic engorgement and prevent recurrence
Case scenario Management
Focal hepatic web Thrombolysis and angioplasty
Reversible liver damage+ patent IVC Portosystemic shunts (TIPS) to preserve hepatic
function and control ascites
Acute onset Budd-Chiari Catheter directed thrombolysis
Chronic Budd-Chiari TIPS
Irreversible liver decompensation Liver transplantation
Splenic vein thrombosis
Etiology Usually secondary to pancreatitis
Causes isolated gastric varices (fundus; through short gastrics) in the absence of esophageal varices
Presentation
Most common presentation: Upper gastrointestinal bleeding from gastric varices
Management Splenectomy in patients with bleeding gastric varices
Portal vein thrombosis (PVT)
Risk factors Hypercoagulability, cirrhosis, myeloproliferative disorders
Often an incidental nding on imaging
Presentation
Diagnosis Contrast-enhanced CT of abdomen
Management
May present with abdominal pain
Bowel ischemia and infarction can occur, especially if superior mesenteric vein is thrombosed
Ascites without liver failure
Esophageal varices develop later
Acute PVT➔Heparin
3 Liver
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Liver Failure
Hepatic failure and hepatorenal syndrome
Acute liver failure (ALF): Massive hepatocyte necrosis with resulting hyperammonemia and
Denition
Causes
coagulopathy for <26weeks
Chronic liver failure: Lasts >26weeks
Acetaminophen use (50%): Dose dependent; characterized by high aminotransferase levels (>3500)
Idiosyncratic drug-induced liver injury (13%): Dose independent; occurs within 6months of
starting a medication (antibiotics, NSAIDs, anticonvulsants)
Viral hepatitis (12%) caused by hepatitis A, B, D, and E (hepatitis C➔rarely causes ALF), herpes
simplex virus, varicella zoster virus, Epstein-Barr virus, adenovirus, cytomegalovirus
Hypoperfusion (1–2.5%): Caused by systemic hypotension (such as congestive heart failure,
sepsis), venous obstruction (Budd-Chiari syndrome), arterial vasoconstriction (cocaine,
methamphetamines)
Wilson disease (5% ALF): Coombs-negative hemolytic anemia; ocular slit-lamp exam➔KayserFleischer ring, low ceruloplasmin level
Autoimmune hepatitis (2–3% ALF): Positive antinuclear antibody test, anti-smooth muscle
antibody
Acute fatty liver of pregnancy/HELLP syndrome (rare): Hemolysis, elevated liver enzymes, low
platelets
Toxins (rare): primarily Amanita phalloides mushroom or carbon tetrachloride
79
Diagnosis
Staging
ALF can be conrmed if symptoms occur for less than 26weeks and all of the following criteria
are met:
• Elevated transaminases and bilirubin
• Encephalopathy
• INR>1.5
• No cirrhosis or prior liver disease by history, physical exam, or imaging
Best indicator of synthetic function in patients with cirrhosis➔prothrombin time
Child-Pugh classication is based on assessment of the synthetic function of the liver (albumin,
bilirubin, and prothrombin time) and clinical signs of liver decompensation (ascites and
encephalopathy)
Child-Turcotte-Pugh scoring is on a scale from 5 to 15
Child-Turcotte-Pugh class Score Prognosis
Class A 5–6 points Can undergo elective surgery
Class B 7–9 points Can undergo elective surgery with caution
Class C 10–15 points Very high risk
MELD was developed due to the failings of child-Pugh (subjective parameters such as degree of
ascites and encephalopathy)
MELD system classies liver disease severity for the purposes of liver transplant allocation based
on serum INR, Cr, and bilirubin
MELD scoring is on a scale from 6 to 40
MELD score=0.957*ln(creatinine mg/dL)+0.378*ln(bilirubin mg/dL)+1.120*log(INR)+0.643
80
Hepatic failure and hepatorenal syndrome
Hepatic encephalopathy grading
Grade Symptoms
Grade I Mild confusion, slurred speech, disordered sleep
Grade II Lethargy, moderate confusion
Grade III Marked confusion, incoherent, arousable
Grade IV Comatose
Grading
King’s College criteria for liver transplantation in patients with ALF
Acetaminophen toxicity pH<7.3 or
Grade III or IV encephalopathy and
Prothrombin time>100seconds (INR>6.5) and
Serum creatinine >3.4mg/dL
All other causes: Prothrombin time >100s
Or any three of the following:
Age<10years or>40years
Etiology: Non-A/non-B hepatitis, idiosyncratic drug reactions,
halothane hepatitis
Duration of jaundice before encephalopathy onset >7days
Prothrombin time >50s
Serum bilirubin >18mg/dL
A. H. Sohail et al.
Management
Prognosis
ICU admission
Early liver transplant evaluation or transfer to a transplant center
Serial liver function tests, INR, arterial pH, lactate
N-acetylcysteine for acetaminophen toxicity
Serial neurologic exams
Intubation for airway protection for grade III–IV encephalopathy
ICP monitoring may be used for intubated patients: 30% of ALF patients will develop intracranial
hypertension (cerebral edema is a major cause for mortality; CPP>60mmHg; ICP<25mmHg)
Mannitol, hypertonic saline, barbiturate coma, and hypothermia are used to optimize ICP
Maintain MAP >75mmHg with IV hydration as needed for CPP>60mmHg
No role for antimicrobial prophylaxis
Early enteral nutrition, GI prophylaxis
Coagulopathy is treated only if the patient is bleeding
Steroids for autoimmune hepatitis
Acute liver failure has 80% mortality
Condition Outcome
High grade encephalopathy Associated with a higher risk of mortality
Low-grade encephalopathy is a predictor of recovery from ALF
Hepatitis B, drug-induced
hepatitis, autoimmune
hepatitis, or Wilson’s disease
Hepatitis A, ischemia, or
pregnancy
ALF due to acetaminophen
overdose
Lower likelihood of survival without a liver transplant versus
other causes
Recover spontaneously
60% recover spontaneously
3 Liver
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Research
Reference Findings
81
H.C.Cho, H.Y.Jung, D.H.Sinn, etal. Mortality after
surgery in patients with liver cirrhosis: comparison of
Child-Turcotte-Pugh, MELD and MELDNa score. Eur
J Gastroenterol Hepatol. 2011;23:51–9
Hepatorenal syndrome
Type 1: Creatinine doubles within 2weeks and reaches at least 2.5mg/dL
Types
Pathophysiology
Diagnosis
Management
Type 2: Renal impairment and ascites that do not respond to diuretics
Portal hypertension➔splanchnic vasodilation➔decreases effective arterial blood volume
and renal perfusion
Splanchnic vasodilatation occurs due to an increase in nitric oxide➔causes vasodilation and a
decrease in systemic vascular resistance
The renin-angiotensin system and sympathetic nervous systems are activated by
hypotension➔further reduces the glomerular ltration rate and limits sodium excretion
Cirrhosis, ascites, and acute kidney injury
No response to volume expansion with IV uids over 48-period
Absence of shock, absence of nephrotoxic drugs
Normal renal ultrasound
Octreotide (somatostatin) causes splanchnic vasoconstriction
Terlipressin (vasopressin analog) causes splanchnic vasoconstriction (not FDA approved)
MELD-Na score is validated as the best predictor of
perioperative mortality in cirrhotic patients
MELD-Na is superior to MELD especially for patients
with lower MELD values
Midodrine (α-adrenergic agonist) causes systemic vasoconstriction
Refractory hepatorenal syndrome➔dialysis
>6weeks of renal replacement therapy➔combined liver–kidney transplant evaluation
Outcome Patients with hepatorenal syndrome often die within weeks of onset
Patient survival is dependent on successful treatment of liver failure
Ascites
Most common cause is cirrhosis
Etiology
Pathophysiology
Diagnosis
Management
Ascites can be due to portal hypertension (cirrhosis, Budd- Chiari syndrome),
hypoalbuminemia, or peritoneal disease
Cirrhosis leads to portal hypertension➔arterial vasodilation, arterial hypotension, and
hypervolemia➔high arterial inow into the splanchnic microcirculation increases hydrostatic
pressures➔excessive production of splanchnic lymph
Serum ascites albumin gradient (SAAG): Subtract the albumin value from the serum albumin
value
Portal hypertensive ascites: SAAG >1.1g/dL
Nonportal hypertensive ascites: SAAG <1.1g/dL
Water restriction
Decrease sodium intake
Spironolactone—Counteracts hyperaldosteronism seen in liver failure
Paracentesis
82
A. H. Sohail et al.
Transjugular intrahepatic portosystemic shunt (TIPS)
Mechanism TIPS is used to reduce portal venous pressures by creating a low resistance channel
between hepatic vein and the portal vein
TIPS is used as rescue therapy for patients with:
Indications
Contraindications
• Active variceal bleeding and failure of endoscopic and pharmacologic treatment
• Portal hypertensive gastropathy
• Refractory ascites
• Budd-Chiari syndrome
• Congestive heart failure
• Biliary obstruction
• Severe tricuspid regurgitation
• Severe pulmonary hypertension
• Polycystic liver disease
Complications
• Hepatic encephalopathy
• 50% occlude by 1year
• Cardiac failure
• Liver failure
Research
Reference Findings
Kerlan RK Jr, Haskal LJ, Ring EJ:
Transjugular portosystemic shunts, in
Ernst CB, Stanley JC (eds): Current
Therapy in Vascular Surgery. St.
Louis, Mosby-Year Book Inc, 1995,
pp751-754
Most TIPS procedures are performed using the Wallstent to maintain
patency of the hepatic parenchymal tract between the portal and systemic
venous circuits. This particular stent’s exibility allows the acute
intrahepatic venous angles to be easily negotiated
Hepatic encephalopathy
Liver failure leads to inability to metabolize ammonia➔buildup of
Etiology
Management
ammonia➔impairment of cognitive and neuromuscular function
• Identify and correct the etiology of elevated ammonia
• Lower ammonia levels (lactulose➔rst line, non-absorbable oral
antibiotics➔neomycin)
Spontaneous bacterial peritonitis (SBP)
Characteristics Most often seen in patients with prolonged cirrhosis
Renal failure develops in 30–40% of patients with SBP
Presentation Fever, abdominal pain, mental status changes
Diagnosis Ascitic uid PMN>250 cells/mm
Etiology Most commonly caused by E. coli
Management 3rd generation cephalosporin (Cefotaxime)
Recurrence 40–70%
3
3 Liver
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Research
83
Reference Findings
Piessen G, Muscari F, Rivkine E, etal. Prevalence of and
risk factors for morbidity after elective left colectomy:
cancer vs. noncomplicated diverticular disease. Arch Surg.
2011;146(10):1149–55
Varices
Distal esophagus and proximal stomach leading to the gastroesophageal
variceal complex
Rectum➔inferior mesenteric vein and the superior hemorrhoidal veins
connect with the pudendal vein and inferior hemorrhoidal veins➔leading to
Common locations
Esophageal varices
hemorrhoids
Periumbilical area➔vestigial umbilical vein communicates with the left
branch of the portal vein and the epigastric veins➔leading to caput medusa
Retroperitoneum in women➔mesenteric veins communicate with the ovarian
veins
Due to portal hypertension➔high resistance to blood ow through the
liver➔resistance increases pressure in the hepatic portal venous
system➔dilates varices and increases active angiogenesis➔blood ows from
the left gastric vein to the inferior vena cava (gastroesophageal junction
cephalad)
Small asymptomatic varices➔nonselective beta-blocker (decrease portal ow,
decrease cardiac output, splanchnic vasoconstriction, increase portal resistance,
and decrease portal pressure)
Before an elective colectomy, any ascites should be
controlled and resolved since ascites is a major
predictor of postoperative morbidity after colectomy
Upper gastrointestinal bleeding
from ruptured varices
Intravenous somatostatin or octreotide
Octreotide➔mesenteric arterial vasoconstriction reduces portal pressure
Somatostatin➔splanchnic arterial vasoconstriction reduces portal pressure
Large varices+ history of bleeding➔endoscopic variceal banding/
sclerotherapy (every 2–8weeks until varices are obliterated)+nonselective
beta blocker
If rebleeding➔repeat endoscopy
If bleeding is refractory to medical and endoscopic management➔arrange
portal decompression versus variceal devascularization
TIPS is needed for refractory variceal bleeding
If portal vein thrombosis➔devascularization (leads to ascites)
84
Research
A. H. Sohail et al.
Reference Findings
Triantos C.Endoscopic treatment of
esophageal varices in patients with liver
cirrhosis. World J Gastroenterol.
2014;20(36):13015–26
Early rebleeding after endoscopic treatment of esophageal varices
should be managed with repeat endoscopy and re-intervention
Umbilical hernia with ascites
Incidence Cirrhosis patients with ascites have 40% lifetime risk of developing umbilical hernia
Management Hernia repair is the standard of care
Use of mesh is not contraindicated
Optimal timing of surgery is crucial and outcomes depend on aggressive control of
ascites before elective surgery
Case scenario Management
Strangulated hernia+ ascites Urgent repair
Reducible hernia+ ascites Medical correction of ascites before repairing
Hernia+ ascites refractory to medial
management
A patent umbilical vein should not be ligated if encountered (a portion of the patient’s
splanchnic ow may be diverted through the umbilical vein➔ligation can cause
decompensation)
TIPS rst➔then repair
Research
Reference Findings
Gaba RC, Parvinian A, Casadaban LC, etal.
Survival benet of TIPS versus serial paracentesis in
patients with refractory ascites: a single institution
case-control propensity score analysis. Clin Radiol.
2015;70(5):e51–7
Telem DA, Schiano T, Divino CM.Complicated
hernia presentation in patients with advanced
cirrhosis and refractory ascites: Management and
outcome. Surgery. 2010;148(3):538–43
Transjugular intrahepatic portosystemic shunt improves
intermediate and long-term survival compared with
repeated paracentesis in patients with refractory ascites
TIPS followed by semi-elective repair of umbilical hernia
appears to be associated with improved outcomes,
especially wound complications, in patients with
umbilical hernias and refractory ascites
3 Liver
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Hepatic Ultrasound
Hepatic ultrasound
Penetration of pulses is inversely related to ultrasound frequency
Resolution of images is directly related to ultrasound frequency
With extracorporeal scanning, usually use 3–5mHz transducers
General
information
Intraoperative
ultrasound
With intracorporeal scanning, transducer is in contact with tissue, may be 5–10mHz, and thus
have better resolution
Lower frequencies: Higher tissue penetration; lower resolution
Higher frequencies: Lower tissue penetration; higher resolution
Ultrasound probe: T-probe versus nger probe
High-frequency probes in the 7- to 10-MHz range using solid state linear array transducers are
optimal
Intraoperative ultrasound of the biliary tree provides real-time information regarding anatomical
structures and can demonstrate CBD stones
85
Sonographic features that differentiate portal veins from hepatic veins
Hepatic veins
Orientation Vertically oriented Horizontally oriented
Echogenicity Low level wall echoes Periportal brofatty tissue produces brighter
Location Hepatic veins are a landmark separating the
liver segments➔INTERSEGMENTAL
vessels
Flow Drain blood into IVC (hepatofugal ow) Hepatopetal ow (carry blood towards liver)
Radiology
Gray-scale ultrasound image demonstrates
normal trifurcation of the three main hepatic
veins converging into the IVC (star)
Run through the middle of the liver
segments➔INTRASEGMENTAL vessels
Gray-scale ultrasound images of the liver
demonstrate the portal vein (arrow). Note the
CBD anterior to the portal vein
Portal veins
echoes around the portal veins
86
Liver Biopsy
A. H. Sohail et al.
Percutaneous liver
biopsy
Risks Bleeding, bile leak,
transient bacteremia,
pneumothorax
Patient inability to
cooperate
Contraindications
Key steps
Inability to identify an
adequate biopsy site
Identify the lesion with
ultrasound
Create a small skin
incision
Pass the needle through
the skin into the lesion
under ultrasound
guidance
Obtain the biopsy while
the patient is holding
breath
Laparoscopic liver
biopsy
Bleeding, bile leak,
iatrogenic solid organ
injury
Inaccessible location:
• Hepatic dome lesions
due to proximity of
diaphragm, pleural
space, lung
parenchyma, cardia, or
vertebral column
posteriorly
• Small lesions adjacent
to large vessels or bile
ducts, particularly the
hepatic veins
• Small lesions in the
caudate lobe
Place a camera port plus
one to two additional
ports in the subcostal
and epigastric area
Biopsy with a Tru-Cut
or core needle
Open liver biopsy
Bleeding, bile leak, infection
(subphrenic abscess),
diaphragm injury
Coagulopathy,
thrombocytopenia (<50,000/
μL)
Right subcostal or upper
midline laparotomy incision
The round and falciform
ligaments are taken down
Divide triangular and coronary
ligaments to aid in exposure,
if needed
Biopsy with a Tru-Cut or core
needle or perform a wedge
resection
Postoperative complication of liver biopsy
Signs and symptoms
Tachycardia, hypotension, increasing
Hemorrhage
Bile leak
right upper quadrant pain, decreasing
hemoglobin, and high sanguineous
drain output
Nausea, emesis, fever, right upper
quadrant pain, jaundice, elevated liver
enzymes, and increasing bilious drain
output
Management
Minor hemorrhage➔cautery, argon laser, or
hepatorrhaphy with #1 chromic or topical sealants
Major hemorrhage➔packing and pringle maneuver
(gain access to the lesser sac and apply a Rummel
tourniquet)
Drainage➔if leak doesn’t resolve➔may require
reoperation
3 Liver
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Hepatic Infections
87
Characteristics
Management
Pyogenic abscess Amebic abscess Fungal abscess
Most commonly caused by
direct spread from biliary
system or portal venous
spread from intestines
Polymicrobial (mixed
enteric facultative and
anaerobic species)
Culture➔antibiotics
Antibiotics coverage (gram
negative, gram positive
cocci, and anaerobes)
Antibiotic duration:
2–6weeks
<3cm abscess➔antibiotics only
>3cm abscess➔antibiotics+percutaneous
drainage
Most common
extraintestinal
complication of
Entamoeba
histolytica infection
Metronidazole for
10days or tinidazole
for 5days
Surgical indications:
Peritonitis from
rupture, inconclusive
serology, bacterial
superinfection,
persistent symptoms
despite antiamebic
therapy
Percutaneous catheter
drainage superior to
needle aspiration in
amebic abscesses
(>10cm)
Common in
immunosuppressed
patients
Can occur as
superinfection in
pyogenic abscess
Systemic treatment
for fungus
Echinococcal
cyst
Caused by infection
with metacestodes
(larval stage) of the
Echinococcus
granulosus tapeworm
Cyst
<5cm➔albendazole
Large or complex
multicystic
lesions➔punctureaspiration- injectionreaspiration (PAIR)
Periprocedural
albendazole or
mebendazole
administered 4hours
before PAIR and for
at least 28days
post-procedure
Research
Reference Finding
Mazza OM, De Santibañes E.Pyogenic liver
abscess. In: Jarnagin WR, ed. Blumgart’s surgery of
the liver, biliary tract and pancreas, 5th ed.
Philadelphia, PA: Elsevier; 2012:1006–16
For liver abscess, the most common reasons for recurrent
symptoms after percutaneous drain placement are drain
clogging and migration. Drain study is warranted with
recurrent symptoms
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