User login
CHICAGO – Two laboratory measurements that are commonly used to assess the cause of symptomatic ascites before liver transplant may be deceptive when used to assess posttransplant ascites, a retrospective study of 15 patients suggested.
Before liver transplant, a serum-ascites albumin gradient (SAAG) greater than 1.1 g/dL differentiates ascites due to portal hypertension rather than other causes 97% of the time. An ascites total protein (aTP) measurement has a lower accuracy for portal hypertension of 57%, but when used in conjunction with SAAG, an aTP of 2.5 g/dL or greater suggests that the cause is cardiac ascites, tuberculous ascites, or peritoneal carcinomatosis, Dr. Jeffrey LaFond explained at the annual Digestive Disease Week.
He and his associates studied the records of 15 patients who developed symptomatic post-transplant ascites that had enough volume to require therapeutic paracentesis. The ascites occurred a mean of 515 days after transplantation (ranging from 14 to 2,744 days). In the work-up for ascites, the sensitivity of SAAG for portal hypertension was 82% and the sensitivity of aTP for portal hypertension was 50%.
Three of 12 patients who had a posttransplant SAAG had a gradient below 1.1 g/dL even though other tests found no evidence of another cause for ascites besides portal hypertension, and two of those three patients had confirmed portal hypertension, he reported. Five of 10 patients with an aTP had a value greater than 2.5 g/dL, even though they had confirmed portal hypertension and normal cardiac function, he reported.
"Assessment of ascites due to portal hypertension and/or vascular stricture in the posttransplant period using SAAG and aTP can be deceiving and cannot be relied upon to make diagnostic interventional decisions," said Dr. LaFond of the University of Virginia, Charlottesville. "A hepatic venogram should be performed early on in patients with posttransplant ascites to evaluate for strictures and portal hypertension.
Records showed that all patients in the study had ascites confirmed by imaging and/or paracenteses and had diagnostic studies to rule out heart failure, opportunistic infection, or malignancy as the source of ascites. Suspected portal hypertension was confirmed by pressure measurements or the presence of vascular strictures on venogram, with portal hypertension defined as a sinusoidal or portosystemic gradient greater than 5 or the presence of a stricture with a gradient of at least 3.
An estimated 3%-7% of patients develop ascites after liver transplant, which has been associated with an increased risk of renal impairment, prolonged hospitalization, and abdominal infections, he said.
Dr. LaFond reported having no financial disclosures.
On Twitter @sherryboschert
*This story was updated 6/3/2014.
CHICAGO – Two laboratory measurements that are commonly used to assess the cause of symptomatic ascites before liver transplant may be deceptive when used to assess posttransplant ascites, a retrospective study of 15 patients suggested.
Before liver transplant, a serum-ascites albumin gradient (SAAG) greater than 1.1 g/dL differentiates ascites due to portal hypertension rather than other causes 97% of the time. An ascites total protein (aTP) measurement has a lower accuracy for portal hypertension of 57%, but when used in conjunction with SAAG, an aTP of 2.5 g/dL or greater suggests that the cause is cardiac ascites, tuberculous ascites, or peritoneal carcinomatosis, Dr. Jeffrey LaFond explained at the annual Digestive Disease Week.
He and his associates studied the records of 15 patients who developed symptomatic post-transplant ascites that had enough volume to require therapeutic paracentesis. The ascites occurred a mean of 515 days after transplantation (ranging from 14 to 2,744 days). In the work-up for ascites, the sensitivity of SAAG for portal hypertension was 82% and the sensitivity of aTP for portal hypertension was 50%.
Three of 12 patients who had a posttransplant SAAG had a gradient below 1.1 g/dL even though other tests found no evidence of another cause for ascites besides portal hypertension, and two of those three patients had confirmed portal hypertension, he reported. Five of 10 patients with an aTP had a value greater than 2.5 g/dL, even though they had confirmed portal hypertension and normal cardiac function, he reported.
"Assessment of ascites due to portal hypertension and/or vascular stricture in the posttransplant period using SAAG and aTP can be deceiving and cannot be relied upon to make diagnostic interventional decisions," said Dr. LaFond of the University of Virginia, Charlottesville. "A hepatic venogram should be performed early on in patients with posttransplant ascites to evaluate for strictures and portal hypertension.
Records showed that all patients in the study had ascites confirmed by imaging and/or paracenteses and had diagnostic studies to rule out heart failure, opportunistic infection, or malignancy as the source of ascites. Suspected portal hypertension was confirmed by pressure measurements or the presence of vascular strictures on venogram, with portal hypertension defined as a sinusoidal or portosystemic gradient greater than 5 or the presence of a stricture with a gradient of at least 3.
An estimated 3%-7% of patients develop ascites after liver transplant, which has been associated with an increased risk of renal impairment, prolonged hospitalization, and abdominal infections, he said.
Dr. LaFond reported having no financial disclosures.
On Twitter @sherryboschert
*This story was updated 6/3/2014.
CHICAGO – Two laboratory measurements that are commonly used to assess the cause of symptomatic ascites before liver transplant may be deceptive when used to assess posttransplant ascites, a retrospective study of 15 patients suggested.
Before liver transplant, a serum-ascites albumin gradient (SAAG) greater than 1.1 g/dL differentiates ascites due to portal hypertension rather than other causes 97% of the time. An ascites total protein (aTP) measurement has a lower accuracy for portal hypertension of 57%, but when used in conjunction with SAAG, an aTP of 2.5 g/dL or greater suggests that the cause is cardiac ascites, tuberculous ascites, or peritoneal carcinomatosis, Dr. Jeffrey LaFond explained at the annual Digestive Disease Week.
He and his associates studied the records of 15 patients who developed symptomatic post-transplant ascites that had enough volume to require therapeutic paracentesis. The ascites occurred a mean of 515 days after transplantation (ranging from 14 to 2,744 days). In the work-up for ascites, the sensitivity of SAAG for portal hypertension was 82% and the sensitivity of aTP for portal hypertension was 50%.
Three of 12 patients who had a posttransplant SAAG had a gradient below 1.1 g/dL even though other tests found no evidence of another cause for ascites besides portal hypertension, and two of those three patients had confirmed portal hypertension, he reported. Five of 10 patients with an aTP had a value greater than 2.5 g/dL, even though they had confirmed portal hypertension and normal cardiac function, he reported.
"Assessment of ascites due to portal hypertension and/or vascular stricture in the posttransplant period using SAAG and aTP can be deceiving and cannot be relied upon to make diagnostic interventional decisions," said Dr. LaFond of the University of Virginia, Charlottesville. "A hepatic venogram should be performed early on in patients with posttransplant ascites to evaluate for strictures and portal hypertension.
Records showed that all patients in the study had ascites confirmed by imaging and/or paracenteses and had diagnostic studies to rule out heart failure, opportunistic infection, or malignancy as the source of ascites. Suspected portal hypertension was confirmed by pressure measurements or the presence of vascular strictures on venogram, with portal hypertension defined as a sinusoidal or portosystemic gradient greater than 5 or the presence of a stricture with a gradient of at least 3.
An estimated 3%-7% of patients develop ascites after liver transplant, which has been associated with an increased risk of renal impairment, prolonged hospitalization, and abdominal infections, he said.
Dr. LaFond reported having no financial disclosures.
On Twitter @sherryboschert
*This story was updated 6/3/2014.
AT DDW 2014
Key clinical point: Serum-ascites albumin gradient and ascites total protein cannot be relied upon to differentiate the cause of ascites after liver transplant.
Major finding: The sensitivity for portal hypertension as the cause of ascites after liver transplant was 82% for SAAG and 50% for aTP.
Data source: A retrospective study of 15 patients who developed symptomatic ascites after liver transplantation that required intervention.
Disclosures: Dr. LaFond reported having no financial disclosures.
