Update Management in Hepatic...

Update

Management in

Hepatic Cirrhosis RINI R. BACHTIAR

STAF ILMU PENYAKIT DALAM SUBDIVISI GASTROENTEROHEPATOLOGY

FAKULTAS KEDOKTERAN UNIVERSITAS HASANUDDIN

MAKASSAR

Hepatic Cirrhosis

Hepatic Cirrhosis

Cirrhosis may be entirely asymptomatic with no clinical signs.

Routine laboratory tests that may suggest underlying cirrhosis include: thrombocytopenia,

hyperbilirubinemia, and hypoalbuminemia.

Non - invasive tests (serum panels and transient elastography) are valuable to rule

in or rule out cirrhosis.

Decompensation of cirrhosis is often precipitated by infection, medications, and

medical procedures (especially surgery).

Child – Pugh – Turcotte Score and MELD score are used to assess prognosis in cirrhotic

patients regardless of etiology.

All patients with cirrhosis require screening for esophageal varices and ultrasound

surveillance for hepatoma.

Control of the underlying cause of liver disease may lead to fibrosis regression

with “ resolution ” of cirrhosis; however, risk of hepatocellular carcinoma (HCC)

persists.

Practice points:

optimizing medical therapy for cirrhotic patients going for surgery

Any operation in a cirrhotic patient carries an increased risk of mortality: Child ’ s C > B > A, mostly as a consequence of hypotension.

Medical optimization:

• Avoid any surgery in patients with acute severe hepatitis or Child ’ s C cirrhosis.

• Replace fluid loss with colloids (blood/albumin), minimal normal saline should be given as this will immediately lead to the formation of ascites.

Practice points:



• Avoid benzodiazepines, aminoglycosides, and NSAIDs (use acetaminophen).

Proton pump inhibitors should only be used if necessary because of the associated increased risk of infection in this population.

Practice points:



• All patients need treatment of any infection as soon as it is

suspected.

• Electrolyte abnormalities, particularly hypokalemia and

metabolic alkalosis, should be corrected to reduce the

chance of cardiac arrhythmias and hepatic encephalopathy.

Practice points:



• Reduce chance of hepatic encephalopathy by preventing

constipation and carefully monitoring the use of opioids.

• Evaluate and monitor renal function throughout hospital

stay; i.v. furosemide should be avoided.

Complication

Asites Pathogenesis

Portal Hypertension:

Transjugular Intrahepatic

Portosystemic Shunt

Portal Hypertension: Transjugular

Intrahepatic Portosystemic Shunt

Portal Hypertension:

Transjugular Intrahepatic

Portosystemic Shunt

Renal Complication of Liver Disease

Renal Complications of Liver Disease

Hepatic Encephalopathy

Hepatic Encephalopathy

Management

Management

The clinical practice guidelines on cirrhosis were

released by

the European Association for the Study of the

Liver

on April 10, 2018.

Management

the etiologic factor, should be removed,

particularly alcohol consumption and hepatitis B or C virus

infection,

as this strategy is associated with decreased risk of

decompensation and increased survival.

Management

potential benefit to decrease cirrhosis progression in patients with

decompensated cirrhosis :

Strategies based on targeting abnormalities in gut-liver axis by antibiotic

administration (ie, rifaximin),

improving the disturbed systemic circulatory function (ie, long-term

albumin administration),

decreasing the inflammatory state (ie, statins)

Reducing portal hypertension (ie, beta blockers)

Management

HMG-coA reductase inhibitors (statins), independent of cholesterol-

lowering effects,

Statin are beneficial in liver diseases by reducing endothelial

dysfunction, intrahepatic vasoconstriction, inflammation and fibrosis,

and can reduce portal vein blood pressure.

Clinically significant portal hypertension (hepatic vein wedge

pressure greater than or equal to 10mmHg) is the most important

predictor of decompensation and death in patients with cirrhosis.

Management

A diagnostic paracentesis is recommended:

all patients with new onset grade 2 or 3 ascites

Ascites those hospitalized for worsening of ascites or any complication

of cirrhosis.

Management

Neutrophil count and culture of ascitic fluid culture should be

performed to exclude bacterial peritonitis.

A neutrophil count above 250 cells/µl is required to diagnose

spontaneous bacterial peritonitis (SBP).

Management

Ascitic total protein concentration should be performed to identify

patients at higher risk of developing SBP.

Management

The serum ascites albumin gradient (SAAG) should be calculated

when the cause of ascites is not immediately evident, and/or when

conditions other than cirrhosis are suspected.

SAAG Interpretation

SAAG = serum albumin – ascites albumin

A high gradient (SAAG >1.1 g/dL) indicates

portal hypertension and suggests a

nonperitoneal cause of ascites.

A low gradient (SAAG < 1.1 g/dL)

indicates nonportal hypertension and

suggests a peritoneal cause of ascites.

Management

Cytology should be performed to differentiate malignancy-related

from non-malignant ascites.

Management

Liver transplantation (LT) should be considered as a potential

treatment option.

Since the development of grade 2 or 3 ascites in patients with cirrhosis is

associated with reduced survival,

Management

A moderate restriction of sodium intake (80–120 mmol/day,

corresponding to 4.6–6.9 g of salt) is recommended in patients with

moderate, uncomplicated ascites.

This is generally equivalent to a no-added-salt diet with avoidance of pre-prepared meals.

Adequate nutritional education of patients on how to manage

dietary sodium is also recommended.

Management

Diets with a very low sodium content (<40 mmol/day) should be

avoided, as they favor diuretic-induced complications and can

endanger a patient's nutritional status.

Management

Patients with the first episode of grade 2 (moderate) ascites should

receive an anti-mineralocorticoid drug alone, starting at 100 mg/day with stepwise increases every 72 hr (in 100 mg steps) to

a maximum of 400 mg/day if there is no response to lower doses.

Management

In patients who do not respond to anti-mineralocorticoids, as defined by a body weight reduction of less than 2 kg/wk, or in

patients who develop hyperkalemia,

furosemide should be added at an increasing stepwise dose from 40 mg/day to a maximum of 160 mg/day (in 40 mg steps).

Management

Patients with long-standing or recurrent ascites should be treated

with a combination of an anti-mineralocorticoid drug and

furosemide, the dose of which should be increased sequentially

according to the response.

Torasemide can be given in patients exhibiting a weak response to

furosemide.

During diuretic therapy, a maximum weight loss of 0.5 kg/day in

patients without edema and 1 kg/day in patients with edema is

recommended.

Once ascites has largely resolved, the dose of diuretics should be reduced to the lowest effective dose.

Management

In patients presenting with GI hemorrhage, renal impairment,

hepatic encephalopathy, hyponatremia, or alterations in serum

potassium concentration,

these abnormalities should be corrected before starting diuretic therapy. In these patients, cautious initiation of diuretic therapy and

frequent clinical and biochemical assessments should be

performed.

Diuretic therapy is generally not recommended in patients with

persistent overt hepatic encephalopathy.

Management

Diuretics should be discontinued if severe hyponatremia (serum sodium concentration <125 mmol/L), acute kidney injury (AKI),

worsening hepatic encephalopathy, or incapacitating muscle

cramps develop.

Management

Furosemide should be stopped if severe hypokalemia occurs (<3 mmol/L). Anti-mineralocorticoids should be stopped if severe

hyperkalemia occurs (>6 mmol/L).

Management

Albumin infusion or baclofen administration (10 mg/day, with a

weekly increase of 10 mg/day up to 30 mg/day) is recommended in

patients with muscle cramps.

Management

Large volume paracentesis (LVP) is the first-line therapy in patients

with large ascites (grade 3 ascites), which should be completely

removed in a single session. LVP should be followed with plasma

volume expansion to prevent post-paracentesis circulatory dysfunction (PPCD).

Management

In patients undergoing LVP greater than 5 L of ascites, plasma

volume expansion should be performed by infusing albumin (8 g/L

of ascites removed), as it is more effective than other plasma

expanders, which are not recommended for this setting.

Management

In patients undergoing LVP less than 5 L of ascites, the risk of

developing PPCD is low. However, it is generally agreed that these

patients should still be treated with albumin because of concerns

about use of alternative plasma expanders.

Management

Non-steroidal anti-inflammatory drugs should not be used in patients

with ascites because of the high risk of developing further sodium

retention, hyponatremia, and AKI.

Management

Repeated LVP plus albumin (8 g/L of ascites removed) is

recommended as first-line treatment for refractory ascites.

Management

Diuretics should be discontinued in patients with refractory ascites who do not excrete >30 mmol/day of sodium under diuretic

treatment.

Management

Antibiotic prophylaxis is recommended in cirrhotic patients with

acute GI bleeding because it reduces the incidence of infections

and improves control of bleeding and survival.

Treatment should be initiated on presentation of bleeding and continued for up to 7 days. Ceftriaxone (1 g/24 hr) is the first choice

in patients with decompensated cirrhosis, those already on

quinolone prophylaxis, and in hospital settings with high prevalence

of quinolone-resistant bacterial infections.

Oral quinolones (norfloxacin 400 mg bid) should be used in the

remaining patients.

Management

The clinical practice guidelines on cirrhosis were released by the

European Association for the Study of the Liver on April 10, 2018.

Prognosis

Prognosis

The prognosis of cirrhosis is highly variable, depending on the

etiology of liver disease, presence of complications, and comorbid

diseases.

Predictive models have been developed to help estimate the survival of patients with cirrhosis.

Child–Turcotte–Pugh score

Model for end - stage l iver d isease ( MELD )

Clinical stages of cirrhosis


The minimum score is 5

• Grade A (well compensated): score of 5 – 6

• Grade B (signifi cant functional compromise): score of 7 – 9

• Grade C (decompensated disease): score of 10 – 15.


The Child – Pugh grade is predictive of 1 - and 2 - year survival:

• Grade A: 100% 1 - year, 85% 2 - year survival

• Grade B: 80% 1 - year, 60% 2 - year survival

• Grade C: 45% 1 - year, 35% 2 - year survival.

The Child – Pugh score is also predictive of mortality with abdominal surgery:

Grade A 10%, Grade B 30%, and Grade C 82%.

Prognosis



diseases.



Model for end - stage liver disease ( MELD )


Model for end-stage liver disease

(MELD)

MELD has also been validated as a predictor of survival in the following conditions:

• alcoholic hepatitis

• hepatorenal syndrome (MELD > 20 predicts worse survival)

• acute variceal hemorrhage in cirrhotic patients

• sepsis in cirrhotic patients as long as unrelated to spontaneous bacterial

peritonitis

• abdominal, orthopedic, and cardiac surgery in known cirrhotic patients.

Model for end-stage liver disease

(MELD) Modifications have been proposed including:

• serum sodium concentration,

• serum albumin concentration, and different

• weighting of the bilirubin, INR, and creatinine.

These modifications may ultimately be adopted for organ allocation.

The MELD score is modified if HCC is present because patients may have poor

survival based on the presence of HCC despite relatively preserved liver

synthetic function, and thus low MELD scores.

Prognosis



diseases.



Model for end - stage l iver d isease ( MELD )


Clinical stages of cirrhosis The Baveno classification system categorizes patients with cirrhosis based on

clinical factors only, which have proven to be useful for prognostication at the

population level.

Stage 1: uncomplicated cirrhosis (no varices/ascites)

Stage 2: cirrhosis with varices (no ascites or bleeding)

Stage 3: cirrhosis with ascites with or without varices

Stage 4: cirrhosis with GI bleeding with or without ascites.

Stages 1 and 2 are compensated while Stages 3 and 4 have signs of

decompensation.

Update Management in Hepatic...

Documents

Transcript of Update Management in Hepatic...