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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

Slide 3

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 4

Hepatic Failure

Major Reasons for ICU Admission

• Variceal hemorrhage

• Encephalopathy

• Refractory ascites

• Spontaneous bacterial peritonitis

• Hepatorenal syndrome

Slide 5

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 6

Causes of Portal Hypertension

LIVER

Pre-sinusoidal PV thrombosis PV extrinsic comp. Schistosomiasis Sarcoidosis PBC

Sinusoidal Cirrhosis Alcoholic hepatitis

Post Sinusoidal Budd – Chiari Veno-occlusive dis. Severe CHF Restrictive heart dis.

BLOOD FLOW

Slide 7

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 8

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 9

Hierarchical Treatment for Variceal Bleeding

Pharmacologic

Endoscopic

Radiologic shuntTIPSS

Surgical Shunt

Balloon Tamponade

Pharmacologic and endoscopic therapyare the usual 1st and

2nd interventions

Slide 10

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 11

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., alpha-adrenergic 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 12

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 13

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 14

Banding of Esophageal Varix

Slide 15

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 post-banding 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 16

Acute Variceal HemorrhageBalloon 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 17

Sengstaken – Blakemore Tube

Gastric balloon

Esophageal balloon

Gastric aspiration port

Slide 18

Minnesota Tube

Gastric balloon

Esophageal balloon

Gastric aspiration port

Esophageal aspiration port

Slide 19

Tube Positioning and Gastric Balloon Inflation

1. Tube inserted to 50 cm

2. Auscultate in stomach

3. Inflate gastric balloon with 50 cc

4. Stat portable film

1. Re-confirm proximal position2. Inflate GB 300-400 cc air3. Pull to insure anchorage4. Recheck film 5. 1-2 lbs of pulley traction

Slide 20

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

– ulcer

– perforation

– stricture

Slide 21

Malposition of the Gastric Balloon

Slide 22

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 23

Summary of Trials Comparing TIPSS to Endoscopic Therapy for Variceal Bleeding

Stanley AJ, Hayes PC. Lancet. 1997;350:1235-1239.

Generally, higher rates of rebleeding were more common after endoscopy treatment, while encephalopathy rates were higher in the TIPSS groups

Slide 24

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 25

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 26

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 27

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 28

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 29

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 30

Hepatic Encephalopathy

• Hepatic encephalopathy reflects a spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction after exclusion of other known brain disease.

Slide 31

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 2– Lethargy or apathy– Minimal disorientation for time

or place– Subtle personality change– Inappropriate behavior– Impaired performance of

subtraction– Asterixis

• Grade 3

– Somnolence to semi-stupor but responsive to verbal stimuli

– Confusion

– Gross disorientation

• Grade 4

– Coma, unresponsive to verbal or noxious stimuli

Slide 32

Hepatic Encephalopathy: Differential Diagnosis

• Metabolic encephalopathies

– Hypoglycemia

– Hypoxia

– Uremia

– Electrolyte abnormalities

• Toxic encephalopathies

– Alcohol

– Barbiturates, other CNS depressants

– Heavy metals

• Intracranial lesions

– Subarachnoid, subdural, or intracerebral hemorrhage

– Stroke

– Intracranial tumor

– Intracranial abscess

– Epilepsy

• Neuropsychiatric disorders

Slide 33

Hepatic Encephalopathy: Precipitating Factors

• Increased ammonia production

– Gastrointestinal hemorrhage

– Excess dietary protein

– Azotemia

– Infection, including SBP

– Blood transfusion

– Hypokalemia

– Systemic alkalosis

– Constipation

• Portosystemic shunts

– Spontaneous

– TIPSS

– Surgical

• Progressive hepatic parenchymal damage

• Hepatoma

• Use of benzodiazepines or other psychoactive drugsRiordan SM, Williams R. N Engl J Med. 1997; 337:473-479.

Slide 34

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 35

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 urea-splitting 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 36

Flumazenil in Hepatic Encephalopathy

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.

Flumazenil

N = 265

Placebo

N = 262

Neurologic

improvement

17.5% (Gr3)

14.7% (Gr4)

3.8% (Gr3)

2.7% (Gr4)

EEG

improvement

27.8% (Gr3)

21.5% (Gr4)

5.0% (Gr3)

3.3% (Gr4)

Barbaro G, et al. Hepatology. 1998;28:374-378.

Slide 37

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 peritonitisRunyon BA. Hepatology. 2004;39:841-856.

Slide 38

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 39

Ascites - Classification

High SAAG 1.1 g/dL

Cirrhosis (75% cases)

Alcoholic hepatitis

Portal vein thrombosis

Budd-Chiari syndrome

Cardiac failure

Veno-occlusive disease

Low SAAG 1.1 g/dL

Peritoneal carcinomatosis

Pancreatic ascites

Biliary ascites

Nephrotic syndrome

Tuberculous peritonitis

Krige J, et al. BMJ. 2001;322.

Slide 40

Spontaneous Bacterial Peritonitis

• Spontaneous infection of ascitic fluid in the absence of a secondary intra-abdominal 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 41

Spontaneous Bacterial PeritonitisDiagnosis

• 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 42

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 43

Spontaneous Bacterial PeritonitisAASLD 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 44

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 0.06-0.28)

– 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 45

Tc -Labeled Sulfur Colloid Showing Fluid Passage From Peritoneal to Pleural Space

99

Bhattacharya A, et al. J Gastroenterol Hepatol. 2001;16:317-321.

Slide 46

Right Hydrothorax Managed with Pleural Catheter Drainage

Before After

Slide 47

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 48

Hepatorenal Syndrome

Ginès P, et al. N Engl J Med. 2004;350:1646-1654.

Slide 49

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 50

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 51

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

TOTAL 165 104 (63%) 73 (44%) 30 (18%)Or – orlipressin NE – norepinephrineTe - terlipressin OC - octreotide Mi - midodrine A - albumin

These results, although encouraging, need to be validated by a large, prospective randomized trial.

Slide 52

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 53

Other Pulmonary Complications of Chronic Liver Disease

• 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.

Hoeper MM et al. Lancet. 2004;363(9419):1461-1468.

Slide 54

Other Pulmonary Complications of Chronic Liver Disease

• 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 non-randomized, 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.

Hoeper MM et al. Lancet. 2004;363(9419):1461-1468.

Slide 55

Pathophysiology of Hypoxemia in Hepatopulmonary Syndrome

Hoeper MM et al. Lancet. 2004;363(9419):1461-1468.

Slide 56

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.

• 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.

Murray K, Carithers R. AASLD Practice Guidelines: evaluation of the patient for liver transplantation. Hepatology. 2005;41:1407-1432.

Slide 57

Liver Transplantation

Slide 58

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

Case Studies with Questions

The following are case studies that can be used for review of this presentation.

Review Cases

End

Slide 60

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

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Slide 62

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

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Slide 64

Conclusion

• This concludes the Hepatic Failure presentation.