Persistent ascites and low serum sodium identify patients with cirrhosis and low MELD scores who are at high risk for early death

[Guest guest]

An Expert Opinion on: Persistent ascites and low serum sodium identify

patients with cirrhosis and low MELD scores who are at high risk for early

death. Hepatology. 2004;40:802.

Ascites Returns to the Spotlight

Bruce A. Runyon MD

Chief, Liver Service, Loma University Medical Center, Loma ,

California

Posting Date: October 22, 2004

Ascites has been known to be associated with shortened life expectancy since

the time of the ancient Greeks. Both of the early systems developed to

predict survival in the setting of cirrhosis, the Child-Turcotte score

(1964) and the Pugh modification (Child-Pugh-Turcotte [CPT] score, 1973),

included ascites as a criterion. However, ascites can disappear with

appropriate treatment, and it can occasionally be transient and detected

only by imaging. In our current obesity epidemic, I have seen obesity

masquerade as ascites and lead to inappropriate treatment with diuretics.

These vagaries, as well as the prior " honor system " related to listing for

liver transplantation (and the frequent violations of the honor system based

on CPT score) led to adoption of the Model for End-stage Liver Disease

(MELD) system in 2002 for transplantation listing. MELD is objective, being

based only on serum creatinine, bilirubin, and international normalized

ratio.

In the " old days, " we classified patients as class A, B, or C. More

recently, we gave each patient a CPT score, a number from 5-15, and skipped

discussion of class. We are now rapidly transitioning into MELD, even in the

nontransplant candidate setting, and usually provide the CPT score and MELD

score during discussions of a patient. Both scores give a clearer " picture "

of the patient's status relative to survival and listing for transplant.

However, none of these scoring systems tells the whole story. There are

always exceptions. The paper by Heuman and colleagues provides data

suggesting that we should consider reinstating ascites and adding serum

sodium to the equation.[1]

Ascites has now returned to the spotlight. The key feature of ascites in

this context is its persistence. We know that development of ascites is an

important landmark in the natural history of cirrhosis. Unless there is a

major reversible component to the liver injury, such as alcohol use,

autoimmune disease, or replicating hepatitis B virus, development of ascites

predicts death in ~50% of patients within 2 years. Once ascites becomes

refractory, ~50% of patients are dead within 6 months.

Spontaneous (as opposed to diuretic-induced) hyponatremia was recognized as

a marker of poor prognosis in patients with cirrhosis as far back as

1973.[2] However, it has not received the " respect " that it deserves in this

regard. Free water clearance has been proposed as a more scientific way to

measure the patient's inability to regulate the amount of water excreted vs

retained, but this measurement has not caught on in the clinics or wards.

Why is hyponatremia useful for prognosis? It appears that the patient with

cirrhosis loses his ability to excrete sodium before he loses his ability to

excrete water; the inability to excrete water occurs only at the end of the

line. Diuretic-induced hyponatremia of a mild nature (130-135 mmol/L) is

expected and does not have such a sinister connotation. However, as serum

sodium drifts under 130 or under 125, even in the setting of judiciously

used diuretics, the situation is more ominous, in my experience.

It is tempting to restrict water in such circumstances, but this attempt

usually fails unless the patient is locked in a room without access to

water. Neither the nurses nor the dieticians can realistically enforce a

water restriction. The level of restriction is neither agreed upon nor

data-supported, nor is the policy to include or exclude fluids on the

hospital tray when calculating the level of restriction. I have seen great

variability in these regards from hospital to hospital. Years ago I had

approval to conduct a randomized trial of fluid restriction vs no fluid

restriction but gave up on this study, because patients would not consent to

an enforced fluid restriction. The first thing a patient wants, when you

tell her to restrict her fluid intake, is a drink of water--this is basic

human nature. When we order fluid restriction, we are treating ourselves,

rather than treating the patient. Because of the futility and time wasted

trying to enforce a water restriction, and the lack of data supporting the

need to correct this laboratory abnormality, I do not request fluid

restriction until the serum sodium is < 120 mmol/L; this happens very

seldom, in fewer than 1% of patients with ascites.[3]

Treating the hyponatremia per se should therefore not be the focus of

attention. Although hyponatremia carries a poor prognosis, there is no

evidence that improving serum sodium improves survival in the setting of

cirrhosis and ascites. Treating the underlying liver disease is the real

issue. Liver transplantation is the most aggressive option. However, having

one half of patients with a MELD score < 21 die within 180 days in the

absence of transplant is not an optimal situation.[1] Use of MELD scores

leads to transplantation of the sickest first; those with scores < 21 don't

get many offers. Since persistent ascites and hyponatremia were strong

independent predictors of mortality in patients with MELD < 21 in the study

by Heuman and colleagues, the United Network for Organ Sharing should

perhaps consider incorporating the results of this study in the next

iteration of listing criteria.

References

1. Heuman DM, Abou-Assi SG, Habib A, et al. Persistent ascites and low serum

sodium identify patients with cirrhosis and low MELD scores who are at high

risk for early death. Hepatology. 2004;40:801-810.

2. Arroyo V, Rodes J, Gutierrez-Lizarraga, MA, et al. Prognostic value of

spontaneous hyponatremia in cirrhosis with ascites. Dig Dis.

1976;21:249-255.

3. Runyon BA. Management of adult patients with ascites due to cirrhosis.

Hepatology. 2004;39:841-856.

http://clinicaloptions.com/hep/jopt/articles/article.asp?a=Heuman-Hepatol-2004-1\

0 & page=commentary

[Guest guest]

An Expert Opinion on: Persistent ascites and low serum sodium identify

patients with cirrhosis and low MELD scores who are at high risk for early

death. Hepatology. 2004;40:802.

Ascites Returns to the Spotlight

Bruce A. Runyon MD

Chief, Liver Service, Loma University Medical Center, Loma ,

California

Posting Date: October 22, 2004

Ascites has been known to be associated with shortened life expectancy since

the time of the ancient Greeks. Both of the early systems developed to

predict survival in the setting of cirrhosis, the Child-Turcotte score

(1964) and the Pugh modification (Child-Pugh-Turcotte [CPT] score, 1973),

included ascites as a criterion. However, ascites can disappear with

appropriate treatment, and it can occasionally be transient and detected

only by imaging. In our current obesity epidemic, I have seen obesity

masquerade as ascites and lead to inappropriate treatment with diuretics.

These vagaries, as well as the prior " honor system " related to listing for

liver transplantation (and the frequent violations of the honor system based

on CPT score) led to adoption of the Model for End-stage Liver Disease

(MELD) system in 2002 for transplantation listing. MELD is objective, being

based only on serum creatinine, bilirubin, and international normalized

ratio.

In the " old days, " we classified patients as class A, B, or C. More

recently, we gave each patient a CPT score, a number from 5-15, and skipped

discussion of class. We are now rapidly transitioning into MELD, even in the

nontransplant candidate setting, and usually provide the CPT score and MELD

score during discussions of a patient. Both scores give a clearer " picture "

of the patient's status relative to survival and listing for transplant.

However, none of these scoring systems tells the whole story. There are

always exceptions. The paper by Heuman and colleagues provides data

suggesting that we should consider reinstating ascites and adding serum

sodium to the equation.[1]

Ascites has now returned to the spotlight. The key feature of ascites in

this context is its persistence. We know that development of ascites is an

important landmark in the natural history of cirrhosis. Unless there is a

major reversible component to the liver injury, such as alcohol use,

autoimmune disease, or replicating hepatitis B virus, development of ascites

predicts death in ~50% of patients within 2 years. Once ascites becomes

refractory, ~50% of patients are dead within 6 months.

Spontaneous (as opposed to diuretic-induced) hyponatremia was recognized as

a marker of poor prognosis in patients with cirrhosis as far back as

1973.[2] However, it has not received the " respect " that it deserves in this

regard. Free water clearance has been proposed as a more scientific way to

measure the patient's inability to regulate the amount of water excreted vs

retained, but this measurement has not caught on in the clinics or wards.

Why is hyponatremia useful for prognosis? It appears that the patient with

cirrhosis loses his ability to excrete sodium before he loses his ability to

excrete water; the inability to excrete water occurs only at the end of the

line. Diuretic-induced hyponatremia of a mild nature (130-135 mmol/L) is

expected and does not have such a sinister connotation. However, as serum

sodium drifts under 130 or under 125, even in the setting of judiciously

used diuretics, the situation is more ominous, in my experience.

It is tempting to restrict water in such circumstances, but this attempt

usually fails unless the patient is locked in a room without access to

water. Neither the nurses nor the dieticians can realistically enforce a

water restriction. The level of restriction is neither agreed upon nor

data-supported, nor is the policy to include or exclude fluids on the

hospital tray when calculating the level of restriction. I have seen great

variability in these regards from hospital to hospital. Years ago I had

approval to conduct a randomized trial of fluid restriction vs no fluid

restriction but gave up on this study, because patients would not consent to

an enforced fluid restriction. The first thing a patient wants, when you

tell her to restrict her fluid intake, is a drink of water--this is basic

human nature. When we order fluid restriction, we are treating ourselves,

rather than treating the patient. Because of the futility and time wasted

trying to enforce a water restriction, and the lack of data supporting the

need to correct this laboratory abnormality, I do not request fluid

restriction until the serum sodium is < 120 mmol/L; this happens very

seldom, in fewer than 1% of patients with ascites.[3]

Treating the hyponatremia per se should therefore not be the focus of

attention. Although hyponatremia carries a poor prognosis, there is no

evidence that improving serum sodium improves survival in the setting of

cirrhosis and ascites. Treating the underlying liver disease is the real

issue. Liver transplantation is the most aggressive option. However, having

one half of patients with a MELD score < 21 die within 180 days in the

absence of transplant is not an optimal situation.[1] Use of MELD scores

leads to transplantation of the sickest first; those with scores < 21 don't

get many offers. Since persistent ascites and hyponatremia were strong

independent predictors of mortality in patients with MELD < 21 in the study

by Heuman and colleagues, the United Network for Organ Sharing should

perhaps consider incorporating the results of this study in the next

iteration of listing criteria.

References

1. Heuman DM, Abou-Assi SG, Habib A, et al. Persistent ascites and low serum

sodium identify patients with cirrhosis and low MELD scores who are at high

risk for early death. Hepatology. 2004;40:801-810.

2. Arroyo V, Rodes J, Gutierrez-Lizarraga, MA, et al. Prognostic value of

spontaneous hyponatremia in cirrhosis with ascites. Dig Dis.

1976;21:249-255.

3. Runyon BA. Management of adult patients with ascites due to cirrhosis.

Hepatology. 2004;39:841-856.

http://clinicaloptions.com/hep/jopt/articles/article.asp?a=Heuman-Hepatol-2004-1\

0 & page=commentary

[Guest guest]

An Expert Opinion on: Persistent ascites and low serum sodium identify

patients with cirrhosis and low MELD scores who are at high risk for early

death. Hepatology. 2004;40:802.

Ascites Returns to the Spotlight

Bruce A. Runyon MD

Chief, Liver Service, Loma University Medical Center, Loma ,

California

Posting Date: October 22, 2004

Ascites has been known to be associated with shortened life expectancy since

the time of the ancient Greeks. Both of the early systems developed to

predict survival in the setting of cirrhosis, the Child-Turcotte score

(1964) and the Pugh modification (Child-Pugh-Turcotte [CPT] score, 1973),

included ascites as a criterion. However, ascites can disappear with

appropriate treatment, and it can occasionally be transient and detected

only by imaging. In our current obesity epidemic, I have seen obesity

masquerade as ascites and lead to inappropriate treatment with diuretics.

These vagaries, as well as the prior " honor system " related to listing for

liver transplantation (and the frequent violations of the honor system based

on CPT score) led to adoption of the Model for End-stage Liver Disease

(MELD) system in 2002 for transplantation listing. MELD is objective, being

based only on serum creatinine, bilirubin, and international normalized

ratio.

In the " old days, " we classified patients as class A, B, or C. More

recently, we gave each patient a CPT score, a number from 5-15, and skipped

discussion of class. We are now rapidly transitioning into MELD, even in the

nontransplant candidate setting, and usually provide the CPT score and MELD

score during discussions of a patient. Both scores give a clearer " picture "

of the patient's status relative to survival and listing for transplant.

However, none of these scoring systems tells the whole story. There are

always exceptions. The paper by Heuman and colleagues provides data

suggesting that we should consider reinstating ascites and adding serum

sodium to the equation.[1]

Ascites has now returned to the spotlight. The key feature of ascites in

this context is its persistence. We know that development of ascites is an

important landmark in the natural history of cirrhosis. Unless there is a

major reversible component to the liver injury, such as alcohol use,

autoimmune disease, or replicating hepatitis B virus, development of ascites

predicts death in ~50% of patients within 2 years. Once ascites becomes

refractory, ~50% of patients are dead within 6 months.

Spontaneous (as opposed to diuretic-induced) hyponatremia was recognized as

a marker of poor prognosis in patients with cirrhosis as far back as

1973.[2] However, it has not received the " respect " that it deserves in this

regard. Free water clearance has been proposed as a more scientific way to

measure the patient's inability to regulate the amount of water excreted vs

retained, but this measurement has not caught on in the clinics or wards.

Why is hyponatremia useful for prognosis? It appears that the patient with

cirrhosis loses his ability to excrete sodium before he loses his ability to

excrete water; the inability to excrete water occurs only at the end of the

line. Diuretic-induced hyponatremia of a mild nature (130-135 mmol/L) is

expected and does not have such a sinister connotation. However, as serum

sodium drifts under 130 or under 125, even in the setting of judiciously

used diuretics, the situation is more ominous, in my experience.

It is tempting to restrict water in such circumstances, but this attempt

usually fails unless the patient is locked in a room without access to

water. Neither the nurses nor the dieticians can realistically enforce a

water restriction. The level of restriction is neither agreed upon nor

data-supported, nor is the policy to include or exclude fluids on the

hospital tray when calculating the level of restriction. I have seen great

variability in these regards from hospital to hospital. Years ago I had

approval to conduct a randomized trial of fluid restriction vs no fluid

restriction but gave up on this study, because patients would not consent to

an enforced fluid restriction. The first thing a patient wants, when you

tell her to restrict her fluid intake, is a drink of water--this is basic

human nature. When we order fluid restriction, we are treating ourselves,

rather than treating the patient. Because of the futility and time wasted

trying to enforce a water restriction, and the lack of data supporting the

need to correct this laboratory abnormality, I do not request fluid

restriction until the serum sodium is < 120 mmol/L; this happens very

seldom, in fewer than 1% of patients with ascites.[3]

Treating the hyponatremia per se should therefore not be the focus of

attention. Although hyponatremia carries a poor prognosis, there is no

evidence that improving serum sodium improves survival in the setting of

cirrhosis and ascites. Treating the underlying liver disease is the real

issue. Liver transplantation is the most aggressive option. However, having

one half of patients with a MELD score < 21 die within 180 days in the

absence of transplant is not an optimal situation.[1] Use of MELD scores

leads to transplantation of the sickest first; those with scores < 21 don't

get many offers. Since persistent ascites and hyponatremia were strong

independent predictors of mortality in patients with MELD < 21 in the study

by Heuman and colleagues, the United Network for Organ Sharing should

perhaps consider incorporating the results of this study in the next

iteration of listing criteria.

References

1. Heuman DM, Abou-Assi SG, Habib A, et al. Persistent ascites and low serum

sodium identify patients with cirrhosis and low MELD scores who are at high

risk for early death. Hepatology. 2004;40:801-810.

2. Arroyo V, Rodes J, Gutierrez-Lizarraga, MA, et al. Prognostic value of

spontaneous hyponatremia in cirrhosis with ascites. Dig Dis.

1976;21:249-255.

3. Runyon BA. Management of adult patients with ascites due to cirrhosis.

Hepatology. 2004;39:841-856.

http://clinicaloptions.com/hep/jopt/articles/article.asp?a=Heuman-Hepatol-2004-1\

0 & page=commentary

[Guest guest]

An Expert Opinion on: Persistent ascites and low serum sodium identify

patients with cirrhosis and low MELD scores who are at high risk for early

death. Hepatology. 2004;40:802.

Ascites Returns to the Spotlight

Bruce A. Runyon MD

Chief, Liver Service, Loma University Medical Center, Loma ,

California

Posting Date: October 22, 2004

Ascites has been known to be associated with shortened life expectancy since

the time of the ancient Greeks. Both of the early systems developed to

predict survival in the setting of cirrhosis, the Child-Turcotte score

(1964) and the Pugh modification (Child-Pugh-Turcotte [CPT] score, 1973),

included ascites as a criterion. However, ascites can disappear with

appropriate treatment, and it can occasionally be transient and detected

only by imaging. In our current obesity epidemic, I have seen obesity

masquerade as ascites and lead to inappropriate treatment with diuretics.

These vagaries, as well as the prior " honor system " related to listing for

liver transplantation (and the frequent violations of the honor system based

on CPT score) led to adoption of the Model for End-stage Liver Disease

(MELD) system in 2002 for transplantation listing. MELD is objective, being

based only on serum creatinine, bilirubin, and international normalized

ratio.

In the " old days, " we classified patients as class A, B, or C. More

recently, we gave each patient a CPT score, a number from 5-15, and skipped

discussion of class. We are now rapidly transitioning into MELD, even in the

nontransplant candidate setting, and usually provide the CPT score and MELD

score during discussions of a patient. Both scores give a clearer " picture "

of the patient's status relative to survival and listing for transplant.

However, none of these scoring systems tells the whole story. There are

always exceptions. The paper by Heuman and colleagues provides data

suggesting that we should consider reinstating ascites and adding serum

sodium to the equation.[1]

Ascites has now returned to the spotlight. The key feature of ascites in

this context is its persistence. We know that development of ascites is an

important landmark in the natural history of cirrhosis. Unless there is a

major reversible component to the liver injury, such as alcohol use,

autoimmune disease, or replicating hepatitis B virus, development of ascites

predicts death in ~50% of patients within 2 years. Once ascites becomes

refractory, ~50% of patients are dead within 6 months.

Spontaneous (as opposed to diuretic-induced) hyponatremia was recognized as

a marker of poor prognosis in patients with cirrhosis as far back as

1973.[2] However, it has not received the " respect " that it deserves in this

regard. Free water clearance has been proposed as a more scientific way to

measure the patient's inability to regulate the amount of water excreted vs

retained, but this measurement has not caught on in the clinics or wards.

Why is hyponatremia useful for prognosis? It appears that the patient with

cirrhosis loses his ability to excrete sodium before he loses his ability to

excrete water; the inability to excrete water occurs only at the end of the

line. Diuretic-induced hyponatremia of a mild nature (130-135 mmol/L) is

expected and does not have such a sinister connotation. However, as serum

sodium drifts under 130 or under 125, even in the setting of judiciously

used diuretics, the situation is more ominous, in my experience.

It is tempting to restrict water in such circumstances, but this attempt

usually fails unless the patient is locked in a room without access to

water. Neither the nurses nor the dieticians can realistically enforce a

water restriction. The level of restriction is neither agreed upon nor

data-supported, nor is the policy to include or exclude fluids on the

hospital tray when calculating the level of restriction. I have seen great

variability in these regards from hospital to hospital. Years ago I had

approval to conduct a randomized trial of fluid restriction vs no fluid

restriction but gave up on this study, because patients would not consent to

an enforced fluid restriction. The first thing a patient wants, when you

tell her to restrict her fluid intake, is a drink of water--this is basic

human nature. When we order fluid restriction, we are treating ourselves,

rather than treating the patient. Because of the futility and time wasted

trying to enforce a water restriction, and the lack of data supporting the

need to correct this laboratory abnormality, I do not request fluid

restriction until the serum sodium is < 120 mmol/L; this happens very

seldom, in fewer than 1% of patients with ascites.[3]

Treating the hyponatremia per se should therefore not be the focus of

attention. Although hyponatremia carries a poor prognosis, there is no

evidence that improving serum sodium improves survival in the setting of

cirrhosis and ascites. Treating the underlying liver disease is the real

issue. Liver transplantation is the most aggressive option. However, having

one half of patients with a MELD score < 21 die within 180 days in the

absence of transplant is not an optimal situation.[1] Use of MELD scores

leads to transplantation of the sickest first; those with scores < 21 don't

get many offers. Since persistent ascites and hyponatremia were strong

independent predictors of mortality in patients with MELD < 21 in the study

by Heuman and colleagues, the United Network for Organ Sharing should

perhaps consider incorporating the results of this study in the next

iteration of listing criteria.

References

1. Heuman DM, Abou-Assi SG, Habib A, et al. Persistent ascites and low serum

sodium identify patients with cirrhosis and low MELD scores who are at high

risk for early death. Hepatology. 2004;40:801-810.

2. Arroyo V, Rodes J, Gutierrez-Lizarraga, MA, et al. Prognostic value of

spontaneous hyponatremia in cirrhosis with ascites. Dig Dis.

1976;21:249-255.

3. Runyon BA. Management of adult patients with ascites due to cirrhosis.

Hepatology. 2004;39:841-856.

http://clinicaloptions.com/hep/jopt/articles/article.asp?a=Heuman-Hepatol-2004-1\

0 & page=commentary