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Critical Care Aspects of
Chronic Hepatic Failure
Aditya N. Dubey, MD
Peter K. Linden, MD
University of Pittsburgh Medical Center
Department Critical Care Medicine
Learning Objectives
• After reviewing this topic, the learner will be able to:
• Recognize complications of chronic liver failure requiring critical care
support
• Verbalize the pathophysiology and clinical sequelae of portal
hypertension
• Explain the urgent treatments and management for variceal
hemorrhage
• Demonstrate strategies to treat diuretic refractory ascites
• Describe the diagnosis, treatment, and prevention of spontaneous
bacterial peritonitis
• Identify the indications for referral for liver transplantation
Slide 3
Hepatic Failure
Major Reasons for ICU Admission
• Variceal hemorrhage
• Encephalopathy
• Refractory ascites
• Spontaneous bacterial peritonitis
• Hepatorenal syndrome
Slide 4
Portal Hypertension
Terminology
• Portal pressure = PV inflow x outflow resistance
• The transhepatic gradient (THG) can be measured by the difference
between the free hepatic vein pressure and wedge pressure in the
hepatic vein (estimated PV pressure)
• THG = free HVP – wedged HVP
– Normal gradient <5 mm Hg
– Increased risk of bleeding >12 mm Hg
• Portal hypertension may be elevated without intrinsic liver disease
due to pre- and post-sinusoidal pathology (see next slide).
Slide 5
Causes of Portal Hypertension
BLOOD FLOW
LIVER
Pre-sinusoidal
PV thrombosis
PV extrinsic comp.
Schistosomiasis
Sarcoidosis
PBC
Post Sinusoidal
Sinusoidal
Cirrhosis
Alcoholic hepatitis
Budd – Chiari
Veno-occlusive dis.
Severe CHF
Restrictive heart dis.
Slide 6
Variceal Hemorrhage
Incidence and Outcome
• Gastroesophageal varices in 40%-60% cirrhotics
• Variceal hemorrhage occurs in 25%-35% cirrhotics
• 30% of the initial bleeding episodes are fatal
• 70% have recurrent bleeding with a 1-year survival
ranging from 30% to 80%
• Non-variceal pathology (ulcers, gastritis, mucosal tear)
may cause bleeding in patients with known liver disease
and portal hypertension. Sharara AI, Rockey DC. N Engl J
Med. 2001;345; 669-681.
Slide 7
Variceal Hemorrhage
Initial evaluation and stabilization
•
Assessment of intravascular volume status
– Blood pressure is unreliable indicator of volume status
– Hematocrit does not reflect acute blood losses
•
Fluid resuscitation
– Place two large bore IVs and/or a central venous catheter
– Colloid or crystalloid titrated to parameters of perfusion
– Cross-matched or O-negative blood can be used
•
Endotracheal intubation prior to endoscopy for:
– Uncontrolled bleeding
– Altered mental status, severe agitation
– Respiratory distress or depression
Slide 8
Hierarchical Treatment for
Variceal Bleeding
Pharmacologic and
endoscopic therapy
are the usual 1st and
2nd interventions
Pharmacologic
Endoscopic
Balloon
Tamponade
Radiologic shunt
TIPSS
Surgical Shunt
Slide 9
Acute Variceal Hemorrhage:
Pharmacotherapy
•
Octreotide
– Synthetic analogue of somatostatin
– Decreases portal pressure and azygos blood flow
– Stops variceal bleeding in 80% of the cases
– Efficacy is similar to endoscopic sclerotherapy and better than vasopressin
– 5-day course reduces bleeding after endoscopic therapy
– Can cause mild hyperglycemia and abdominal cramping
•
Vasopressin
– Reduces portal pressure but causes myocardial and mesenteric ischemia
•
Terlipressin
– Efficacy similar to endoscopic sclerotherapy and as effective as balloon
tamponade when used with nitroglycerin
– Not approved for use in U.S.
Corley DA. Gastroenterology. 2001;120:946-954; Harry
R. Curr Opin Crit Care. 2002;8:164-170; Sharara AI,
Rockey DC. N Engl J Med. 2001;345:669-681.
Slide 10
Possible Targets for Therapeutic
Intervention in Variceal Hemorrhage
1. Reduction of cardiac output by
beta-1 blockade to prevent
bleeding
2. Reduction of splanchnic blood
flow by beta-2 blockade or
vasoconstrictors (e.g., alphaadrenergic agonists or
vasopressin analogues)
3. Reduction of intrahepatic
resistance by vasodilators
4. Reduction of variceal or
collateral flow by beta-2
blockade, balloon tamponade,
or endoscopic therapy
Slide 11
Esophageal vs. Gastric Varices
Esophageal varices
• Primary approach is endoscopic
banding or sclerotherapy
• TIPSS, surgical shunts are
alternatives
Gastric varices
• Diffuse, deep submucosal
anatomy
• Endoscopic tx difficult,
dangerous
• Primary approach is TIPSS or
surgery
Slide 12
Variceal Hemorrhage: Endoscopic
Therapy
• Endoscopic Band Ligation (see next slide)
– Controls bleeding in 80%-90% of cases
– Lower complication rates than sclerotherapy
• Endoscopic Sclerotherapy
– Intravariceal or paravariceal injection of a sclerosing agent
– Stops bleeding in 80%-90% of the cases
– Complications include perforation, ulceration, and stricture
• Cyanoacrylate Injection
– Used to control bleeding from gastric varices
– Superior to EBL for treatment of bleeding gastric varices
– Not available in U.S.
Laine L. Ann Intern Med. 1995;123:280-287;
Lo GH. Hepatology. 2001;33:421-427.
Slide 13
Banding of Esophageal Varix
Slide 14
Post-Endoscopy Problems Include…
• Abdominal distension: From endoscopic air insufflation, retained
luminal blood, and increased ascites from resuscitation. This can
even progress to abdominal compartment syndrome with associated
respiratory compromise, hypotension, oliguria, and acidosis.
Nasogastric decompression may partially alleviate this problem.
• Worsening encephalopathy: This may occur due to
gastrointestinal passage of blood, hepatic hypoperfusion (“shock
liver), and accumulation of sedative medication.
• Recurrent bleeding: More likely to recur in advanced cirrhosis.
Incidence can be reduced with a 5-day course of octreotide postbanding and long-term use of a non-selective beta-blocker
(propranolol, nadolol).
• Infection: Spontaneous bacterial peritonitis is 3-5x higher following
variceal hemorrhage due to occult bacteremia and ascites seeding.
Antimicrobial prophylaxis (quinolone, beta-lactam) reduces the
incidence of SBP significantly.
Slide 15
Acute Variceal Hemorrhage
Balloon Tamponade
• Effectively controls bleeding in 90% of patients but is
only a temporizing measure in massive uncontrolled
variceal hemorrhage when initial endoscopic treatment is
delayed or unsuccessful.
– Can cause aspiration, esophageal ulceration,
perforation with mediastinitis
– Balloon-related mortality is 3%-5%
– Gastric balloon inflation is usually sufficient
– Esophageal balloon inflation should only be used
when gastric balloon is unsuccessful as it is
associated with higher morbidity.
Slide 16
Sengstaken – Blakemore Tube
 Gastric balloon
 Esophageal balloon
 Gastric aspiration port
Slide 17
Minnesota Tube
 Gastric balloon
 Esophageal balloon
 Gastric aspiration port
 Esophageal aspiration port
Slide 18
Tube Positioning and Gastric Balloon
Inflation
1.
2.
3.
4.
1.
2.
3.
4.
5.
Tube inserted to 50 cm
Auscultate in stomach
Inflate gastric balloon with 50 cc
Stat portable film
Slide 19
Re-confirm proximal position
Inflate GB 300-400 cc air
Pull to insure anchorage
Recheck film
1-2 lbs of pulley traction
Gastric and Esophageal Balloon
Inflation
Esophageal Balloon inflated
to 30 mm Hg
1. Last resort
2. Deflate periodically
3. Use minimum effective
pressure
4. Complication
Slide 20
–
ulcer
–
perforation
–
stricture
Malposition of the Gastric Balloon
Slide 21
Transjugular Intrahepatic
Portosystemic Shunt (TIPSS)
Major Indications
• Refractory variceal bleeding
• Refractory ascites, hydrothorax
• Radiologic insertion of a metallic shunt
(8-12 mm diameter) that joins the
hepatic and portal veins
• Target gradient (HV-PV) <12 mm Hg
• Restores hepatopedal flow
• Decompression of varices
Slide 22
Summary of Trials Comparing TIPSS to
Endoscopic Therapy for Variceal Bleeding
Generally, higher rates of rebleeding were more common after endoscopy
treatment, while encephalopathy rates were higher in the TIPSS groups
Stanley AJ, Hayes PC. Lancet. 1997;350:1235-1239.
Slide 23
Complications of TIPSS
• Peri-procedure mortality of 1%-2%
– Intraperitoneal bleeding due to perforation of the
hepatic capsule, hepatic or portal veins
– TIPSS embolization
– Acute right heart failure due to increased venous
return to right heart
• Later complications include recurrent bleeding due to
TIPSS stenosis or thrombosis, infection, and hepatic
encephalopathy.
Slide 24
Conditions That May Contraindicate
TIPSS
This venogram shows an occlusive thrombus
of the portal vein, which may make safe TIPSS
placement impossible.
This abdominal CT demonstrates a large
hypodense hepatic lesion due to
hepatocellular carcinoma in a very
shrunken cirrhotic liver. Other contraindications
include hepatic vein occlusion, heart failure or
pulmonary hypertension, biliary obstruction,
and poorly controlled systemic infection.
Slide 25
TIPSS Thrombosis/Stenosis
• Incidence 12%-74%
• Most likely within the first month
• Symptoms - recurrent bleeding, ascites
• Detection - Doppler ultrasound angiography (shows
velocity gradient)
• Treatment
– Balloon dilatation
– Placement of TIPSS
Slide 26
Trans-TIPSS Embolization of
Persistent Varices
Persistent variceal bleeding due to high-flow collaterals despite a patent TIPSS
may be coil-embolized radiologically via the TIPSS itself.
Slide 27
Acute Variceal Hemorrhage: Surgery
• The distal splenorenal shunt (Warren shunt) procedure is
generally reserved for Child’s A or B cirrhotics.
• Consider in patients with bleeding refractory to
pharmacologic, endoscopic, and radiologic treatment.
• Complications include shunt thrombosis, infection, and
worsening encephalopathy.
• 30-day mortality is close to 80% in Child’s C patients
requiring emergency shunt surgery.
Slide 28
Relative Effectiveness of Available Therapies for
the Prevention of Recurrent Variceal Bleeding
Beta-blockers are the single
most effective and safest
strategy to prevent the
recurrence of variceal
bleeding.
More aggressive strategies,
such as banding, TIPSS, or
shunt surgery, may decrease
bleeding but are associated with
higher risks and costs.
Sharara AI, Rockey DC. N Engl J Med.
2001;345:669-681.
Slide 29
Hepatic Encephalopathy
• Hepatic encephalopathy reflects a spectrum of
neuropsychiatric abnormalities seen in patients with liver
dysfunction after exclusion of other known brain disease.
Slide 30
Hepatic Encephalopathy – West Haven
Criteria for Grading Mental State
•
•
•
Grade 1
– Trivial lack of awareness
– Euphoria or anxiety
– Shortened attention span
– Impaired performance of
addition
Grade 3
– Somnolence to semi-stupor
but responsive to verbal
stimuli
– Confusion
Grade 2
– Lethargy or apathy
– Minimal disorientation for time
or place
– Subtle personality change
– Inappropriate behavior
– Impaired performance of
subtraction
– Asterixis
– Gross disorientation
•
Slide 31
Grade 4
– Coma, unresponsive to verbal
or noxious stimuli
Hepatic Encephalopathy: Differential
Diagnosis
•
Metabolic encephalopathies
•
– Hypoglycemia
– Subarachnoid, subdural, or
intracerebral hemorrhage
– Hypoxia
– Stroke
– Uremia
– Intracranial tumor
– Electrolyte abnormalities
•
– Intracranial abscess
Toxic encephalopathies
– Epilepsy
– Alcohol
– Barbiturates, other CNS
depressants
Intracranial lesions
•
– Heavy metals
Slide 32
Neuropsychiatric disorders
Hepatic Encephalopathy:
Precipitating Factors
• Increased ammonia production
• Portosystemic shunts
– Gastrointestinal
hemorrhage
– Spontaneous
– TIPSS
– Excess dietary protein
– Azotemia
– Surgical
– Infection, including SBP
• Progressive hepatic
parenchymal damage
– Blood transfusion
• Hepatoma
– Hypokalemia
• Use of benzodiazepines or
other psychoactive drugs
– Systemic alkalosis
Riordan SM, Williams R. N Engl J Med. 1997;
337:473-479.
– Constipation
Slide 33
Why does the ammonia level correlate
poorly with encephalopathy?
•
Venous ammonia levels < arterial
•
Time lag from ↑NH3 and CNS
•
Blood-brain permeability is variable
•
Balance of NH3 / NH4+
•
Processing (must be on ice, <20 min)
Slide 34
Management of Hepatic
Encephalopathy
•
First and foremost control the underlying precipitant(s).
•
Medical therapy - optimal agent is controversial (see meta-analysis)
•
Lactulose - has multiple actions including cathartic, acidification of the
colon to “ion-trap” ammonia as NH4+, and reduction of inoculum of ureasplitting bacteria. Drawbacks include osmotic diarrhea with hypernatremia
due to free water loss and gaseous bowel distension.
•
Neomycin - non-absorbed aminoglycoside that reduces colon bacterial
burden. Dosed at 2-6 grams orally per day. Small incidence of ototoxicity
and nephrotoxicity with prolonged usage.
•
Rifaximin - non-absorbed antimicrobial 400 mg q 8 hours orally
•
Metronidazole - oral dosing at 800 mg/day. No large scale reported
experience. Agent is associated with neurotoxicity in hepatic failure due to
accumulation.
•
Flumazenil - benzodiazepine receptor (GABA) antagonist.
Slide 35
Flumazenil in Hepatic
Encephalopathy
Flumazenil
Placebo
N = 265
N = 262
Neurologic
17.5% (Gr3)
3.8% (Gr3)
improvement
14.7% (Gr4)
2.7% (Gr4)
EEG
27.8% (Gr3)
5.0% (Gr3)
improvement
21.5% (Gr4)
3.3% (Gr4)
In this double-blind, placebo-controlled, randomized trial, flumazenil showed
transient benefit in higher grades of encephalopathy. The role of flumazenil for
all degrees of encephalopathy or as a longer term agent in critically ill patients
has not been determined.
Barbaro G, et al. Hepatology. 1998;28:374-378.
Slide 36
Ascites - Critical Care Aspects
•
Complicated ascites may be the principal reason for critical care admission
but is frequently associated with hemorrhage, renal failure, and/or hepatic
encephalopathy.
•
Common complications of ascites include:
– Diuretic-refractory ascites - defined as unresponsiveness to sodium
restriction and high-dose diuretics (400 mg/day spironolactone and 160
mg/day furosemide) OR rapid recurrence after therapeutic paracentesis
– Tense ascites - this may result in the development of:
• Abdominal compartment syndrome with impaired venous return causing
hypotension, impaired renal perfusion causing oliguria, and reduced
hepatosplanchnic perfusion
• Respiratory compromise may occur due to impaired diaphragmatic
contractility and/or hydrothorax due to the passage of ascites into the pleural
space
– Infection - spontaneous bacterial peritonitis
Runyon BA. Hepatology. 2004;39:841-856.
Slide 37
Paracentesis
• Abdominal paracentesis is the most rapid and cost-effective
technique to diagnose the cause of ascites.
– An area of percussion dullness in the left lower quadrant (2 cm
cephalad and anterior to the anterior superior iliac spine) has a
greater likelihood of ascites present than the midline.
– Ultrasound guidance should be utilized if ascites is difficult to
localize and to avoid venous collaterals, intestine.
– Since bleeding is sufficiently uncommon, the prophylactic use of
plasma or platelets before paracentesis is not recommended.
– An indwelling drainage catheter can be left for 3-5 days if
therapeutic drainage is required.
Runyon BA. Hepatology. 2004;39:841-856.
Slide 38
Ascites - Classification
High SAAG 1.1 g/dL
Low SAAG 1.1 g/dL
 Cirrhosis (75% cases)
 Peritoneal carcinomatosis
 Alcoholic hepatitis
 Pancreatic ascites
 Portal vein thrombosis
 Biliary ascites
 Budd-Chiari syndrome
 Nephrotic syndrome
 Cardiac failure
 Tuberculous peritonitis
 Veno-occlusive disease
Krige J, et al. BMJ. 2001;322.
Slide 39
Spontaneous Bacterial Peritonitis
•
Spontaneous infection of ascitic fluid in the absence of a secondary intraabdominal source of infection
•
Translocation of intestinal bacteria or hematogenous seeding of ascites
•
Mainly a complication of cirrhotic ascites
•
Incidence is 15%-20% of cirrhotics with the highest incidence in Child’s
class C cirrhosis and following upper gastrointestinal bleeding
•
E. coli, Klebsiella sp., S. pneumoniae most common
•
Clinical manifestations include fever, abdominal pain, unexplained
encephalopathy, although asymptomatic presentations are not uncommon
•
Mortality per episode = 20%-30%
•
One year follow-up mortality = 50%
Slide 40
Spontaneous Bacterial Peritonitis
Diagnosis
• Ascites should be processed for the following:
– Total cell count and differential
– Bacterial cultures in blood culture bottles
– Other tests (protein, albumin, LDH, glucose, special cultures)
may be indicated based upon clinical judgment
• A diagnosis of SBP is established by any one of the following:
– >250 polymorphonuclear cells per cubic mm of ascitic fluid, and
a positive ascitic fluid culture is diagnostic.
– Patients with 250 PMNs/mm3 but negative cultures (neutrocytic
ascites)
– Positive ascites cultures and <250 PMNs/mm3 (monomicrobial
non-neutrocytic ascites)
Runyon BA. Hepatology. 2004;39:841-856.
Slide 41
Spontaneous Bacterial Peritonitis
• Suspected secondary bacterial peritonitis
– PMN count 250 cells/mm3
– Multiple organisms on Gram’s stain and culture
– Anaerobes cultured
– Two of the following ascites criteria:
• Total protein >1g/dL
• LDH > upper limit of normal for serum
• Glucose <50 mg/dL
– Treatment – third-generation cephalosporin, consider CT scan of
abdomen and pelvis, and possible laparotomy
Slide 42
Spontaneous Bacterial Peritonitis
AASLD Guidelines
• Patients with ascitic fluid PMNs 250/mm3 should receive empiric
antibiotic therapy, e.g., cefotaxime, 2 g every 8 hours (I).
• Patients with ascitic fluid PMNs <250/mm3 with signs or symptoms
of infection should receive empiric antibiotics pending culture results
(II-B).
• Oral ofloxacin can be considered in patients without vomiting, shock,
grade 2 hepatic encephalopathy, or serum creatinine >3 mg/dL.
• Prevention of SBP:
– Short-term (7 days) inpatient norfloxacin or Bactrim prophylaxis
in patients with gastrointestinal hemorrhage
– Patients with prior SBP should receive long-term prophylaxis
with daily norfloxacin or Bactrim (SBP recurs in up to 70% of
cases within one year).
Slide 43
Refractory Ascites: Management
•
Serial paracentesis every 2 to 4 weeks and/or transjugular intrahepatic
portosystemic shunts:
– Post-paracentesis volume expansion is controversial but may be
considered when 5 L or more of fluid is removed. Albumin (6-8 g per liter
of fluid removed), dextran 70 or Hemaccel may be used.
•
A recent meta-analysis comparing TIPSS vs. paracentesis showed:
– 30-day mortality - no difference, OR 1.0 (CI 0.1-10.06)
– 24-month mortality - no difference, OR 1.17 (CI 0.52-2.66)
– 12-month ascitic fluid reaccumulation - less in TIPSS, OR 0.14 (CI 0.060.28)
– Hepatic encephalopathy - more with TIPSS, OR 2.11 (CI 1.22-3.66)
– No difference in the incidence of GI bleed, infections, or acute renal
failure.
Sheagren JN, et al. J Clin Gastroenterol. 1996;22:207-210;
Saab S. Cochrane Hepato-Biliary Group. 2005.
Slide 44
Tc 99 -Labeled Sulfur Colloid Showing Fluid
Passage From Peritoneal to Pleural Space
Bhattacharya A, et al. J
Gastroenterol Hepatol.
2001;16:317-321.
Slide 45
Right Hydrothorax Managed with
Pleural Catheter Drainage
Before
After
Slide 46
Hepatorenal Syndrome
• Type 1 HRS:
– Acute impairment in renal function defined by
doubling of initial serum creatinine above 2.5 mg/dL
or a 50% reduction of the initial 24-hour creatinine
clearance to a level lower than 20 mL/min in less than
2 weeks. Mortality is as high as 90% after 2-4 weeks
• Type 2 HRS:
– Stable or slowly progressive impairment in renal
function not meeting the above criteria. Associated
with better survival than Type 1 HRS.
Slide 47
Hepatorenal Syndrome
Slide 48
Ginès P, et al. N Engl J Med. 2004;350:1646-1654.
Hepatorenal Syndrome
• Criteria for Diagnosis of HRS:
– Serum creatinine >1.5 mg/dL or 24-hr creatinine clearance <40
mL/min
– Absence of shock, ongoing bacterial infection or fluid loss, and
no current treatment with nephrotoxic drugs
– Absence of sustained improvement in renal function (decrease in
serum creatinine to 1.5 mg/dL) after discontinuation of diuretics
and trial of plasma expansion
– Absence of proteinuria (<500 mg/d) or hematuria (<50 RBCs per
HPF)
– Absence of ultrasonographic evidence of obstructive uropathy or
parenchymal renal disease
– Urinary sodium concentration <10 mmol/L
Slide 49
Hepatorenal Syndrome: Treatment
• Administration of one of the following drugs or drug combinations
can be considered:
– Norepinephrine 0.5-3.0 mg/h intravenously
– Midodrine 7.5 mg three times daily increased to 12.5 mg three
times daily if needed in combination with octreotide 100 g
subcutaneously three times daily, increased to 200 g three
times daily if needed
• Concomitant administration of albumin 1 g/kg intravenously on day
one, followed by 20-40 g daily
• Treatment is given for 5-15 days.
• End point of the treatment is reduction of serum creatinine to <1.5
mg/dL
Slide 50
Vasoconstrictor Studies in HRS
STUDY
Treatment
# Pts
HRS Reversal
Survival
Liver Tx
Guevara
Or + A
8
4
5
-
Uriz
Te + A
9
7
5
3
Gulberg
Or, D, A
7
4
4
2
Mulkay
Te + A
12
7
4
2
Ortega
Te ± A
13
10
9
5
Angeli
Mi,Oc,A
5
4
4
2
Duvoux
NE + A
12
10
6
3
Moreau
Te ± A
99
58
36
13
165
104 (63%)
TOTAL
Or – orlipressin NE – norepinephrine
Te - terlipressin OC - octreotide
Mi - midodrine
A - albumin
73 (44%) 30 (18%)
These results, although encouraging, need to be
validated by a large, prospective randomized trial.
Slide 51
Hepatorenal Syndrome: Treatment
• Hemodialysis or continuous venovenous hemofiltration
may be required as a bridge to liver transplantation.
• Liver transplantation offers the best survival rate of 70%
at 2 years.
• Kidney function may return to normal post-successful
liver transplant.
Slide 52
Other Pulmonary Complications of
Chronic Liver Disease
•
Hoeper MM et al. Lancet.
2004;363(9419):1461-1468.
Hepatopulmonary syndrome
– Incidence of 4%-29%
– Diagnosis requires demonstration of hypoxemia due to abnormal
intrapulmonary vascular dilatations causing shunting or severe
ventilation:perfusion mismatching.
– Vascular dilatations demonstrable by either agitated saline
echocardiography or macro-aggregated albumin scanning.
– Orthodeoxia (desaturation with upright posture) and platypnea
(dyspnea with upright posture) may be seen.
– Management includes supplemental oxygen to maintain SaO2.
– Mortality rate of 41% at 2.5 years reported.
– Severe HPS may slowly remit after successful liver
transplantation although supplemental oxygen required.
Slide 53
Other Pulmonary Complications of
Chronic Liver Disease
•
Hoeper MM et al. Lancet.
2004;363(9419):1461-1468.
Portopulmonary hypertension
– Incidence of 2%-10% (as high as 16% in those referred for liver
transplant).
– Mean PA pressure >25 mm Hg, PVR >250 dyne s-1 cm-5, PA occlusion
(wedge) <15 mm Hg.
– Pathogenesis unclear but may include pulmonary arterial plexopathy in
medium pulmonary arteries due to shear stress, high output state, or
humoral influences.
– Suspect in patients with progressive dyspnea and signs of right heart
failure.
– Continuous prostacyclin (PGI2) infusion has shown benefit in nonrandomized, open-label experience but may not improve long-term
survival without liver transplantation.
– Severe case (mean PA >45 mm Hg) or poor right heart function
contraindicates liver transplantation.
Slide 54
Pathophysiology of Hypoxemia in
Hepatopulmonary Syndrome
Hoeper MM et al. Lancet. 2004;363(9419):1461-1468.
Slide 55
Considerations for Liver
Transplantation in Critically Ill
• Liver transplantation is the most
effective treatment for chronic liver
failure, with overall 1-year 88%
patient survival.
Murray K, Carithers R. AASLD Practice
Guidelines: evaluation of the patient for
liver transplantation. Hepatology.
2005;41:1407-1432.
• Patients with cirrhosis should be referred for transplantation when
evidence of hepatic dysfunction or major complications develop.
• Patients with type I HRS should have an expedited referral for liver
transplantation.
• The prognostic model for end-stage liver disease (MELD score)
predicts liver-related mortality based on the serum Cr, serum
bilirubin, and INR.
Slide 56
Liver Transplantation
Slide 57
Summary
• Complications of cirrhosis requiring critical care
management require prompt diagnostic and therapeutic
intervention to minimize morbidity and mortality
• Critical care physicians need to be familiar with specific
interventions for variceal hemorrhage, hepatic
encephalopathy, refractory ascites, spontaneous
peritonitis, and hepatorenal syndrome
• Early referral to a liver transplant center is indicated
when the patient is stable for transport
Slide 58
Case Studies with Questions
The following are case studies that can be used for review
of this presentation.
Review Cases
End
Case Presentation
• 60-year-old man with documented cirrhosis due to hepatitis C.
Medications – lactulose, Lasix, aldactone, tmp/smx, nadolol
• Admitted directly to ICU with progressive lethargy, oliguria, melena
• BP 90/40, P 60, R 24/min, T 36.8, oriented x 1, somnolent, asterixis
jaundice, spider angiomas, abdominal venous collaterals,
splenomegaly, abdomen distended, dull to percussion, no
tenderness/rebound
• Hct 18%, WBC 14,500, 12% bands, platelets 42,000, INR 3.2, AST
85, ALT 100, bilirubin 6.5, BUN 55, Cr 1.5, glucose 115 mg/dL,
ammonia 110, chest film – poor inspiration, subsegmental
atelectasis
Slide 60
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Case Presentation Follow-Up
• TIPSS placed with HV-PV gradient decrease from 24 mm Hg to 8
mm Hg
• Post-TIPSS day 3 – fever, WBC 18,000, worsening encephalopathy
• Ascites tap: WBC 5,200, 90% PMN
Serum albumin 2.5
Ascites albumin 2.2
Ascites amylase 850
Ascites cultures – enterococcus, B. fragilis, E. coli
Slide 62
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Conclusion
• This concludes the Hepatic Failure presentation.
Slide 64