Photoclinic

Ovarian Malignancy With a Deceptively Elevated Serum-Ascites Albumin Gradient

Gerard Chaaya, MD
Mahmoud Farhoud, MD
Esteban Janolo, Jr., MD
Sayed K. Ali, MD, FACP
Volume 55 - Issue 12 - December 2015

A 58-year-old woman with a past medical history of type 2 diabetes mellitus and hypothyroidism was admitted to a hospital for chronic, worsening abdominal pain. 

She had a 2-month history of constant lower abdominal pain, which she described as 3 of 10 in severity. She denied nausea, vomiting, constipation, and diarrhea. She also denied fevers or changes in bowel movements. She had noticed a significant weight gain along with increased abdominal girth, asthenia, anorexia, bilateral leg edema, and shortness of breath on exertion. She denied alcohol or tobacco use. 

Both of her parents had died from coronary artery disease, but the rest of her family history was noncontributory. 

Results of a screening colonoscopy 3 years prior had been reported as normal. Her husband had died many years ago, and she had been sexually inactive since then. She denied any travel history and spent most of her day at home tending to household chores.

Physical examination. The patient  was afebrile on presentation, with normal vital signs. She appeared to be comfortable and was able to converse in full sentences. She denied orthopnea. Cardiac examination revealed a normal S1 and S2 with no murmurs, rubs, or gallops. Her lungs were clear to auscultation bilaterally. She had a distended abdomen with shifting dullness, slightly tender to palpation below her umbilicus, but without any rebound or guarding. She had 2+ pitting edema in her lower extremities, which hindered her ability to wear close-fitted shoes.

Diagnostic tests. Results of a complete blood count and a comprehensive metabolic panel including liver function and thyroid function were within normal range. Prothrombin time, international normalized ratio, and partial thromboplastin time results also were normal. Results of a CA-125 test and carcinoembryonic antigen test were within normal range. Her serum albumin level was low at 2.9 g/dL.


Figure 1. Computed tomography showed a right ovarian mass.

 

Abdominal ultrasonography confirmed the presence of moderate ascites. Ultrasound-guided large-volume paracentesis showed an albumin level of 1.2 g/dL and protein level of 3.3 g/L. The fluid cytology showed no evidence of malignant cells. The ascetic amylase level was normal, and cultures eventually were reported as negative. Results of 2-dimensional echocardiography demonstrated a normal ejection fraction with no wall abnormalities. A computed tomography scan of the abdomen with contrast revealed a large, right ovarian and upper pelvic, complex, cystic mass (14 × 29 × 25 cm) with faintly visualized septations (Figure 1).

Discussion. Ascites is a frequently encountered problem in both the outpatient and inpatient settings. The movement across a capillary membrane is controlled by the balance of hydrostatic and colloid osmotic pressures, with albumin being a key player.1 

The serum-ascites albumin gradient (SAAG) has been shown to be extremely helpful in determining the etiology of ascites. Some studies suggest that the SAAG is superior to the total-protein–based exudate/transudate analysis.2,3 The SAAG often is used to discriminate between ascites caused by liver disease and those caused by a neoplasm.1 The measurement is calculated by subtracting the value of the ascetic fluid albumin from the value of the serum albumin, usually obtained on the same day.3,4

A SAAG value of 1.1 g/dL or greater strongly suggests portal hypertension (97% accuracy) as the cause of the ascites buildup.2 The differential diagnosis includes but is not limited to cirrhosis, alcohol hepatitis, hepatocellular carcinoma, massive liver metastases, fulminant hepatic failure, cardiac ascites, myxedema, and Budd-Chiari syndrome.3,4 A SAAG of less than 1.1 g/dL is suggestive of other causes such as peritoneal tuberculosis, pancreatitis, nephrotic syndrome, peritoneal carcinomatosis, chlamydia peritonitis, biliary ascites, serositis, nephrotic syndrome, or bowel perforation or infarction.3,4 Malignancy-related ascites often produces a low SAAG value.5

Our patient’s SAAG (2.9 g/L -1.2 g/L = 1.7 g/L) suggested portal hypertension as the probable cause. However, the clinical absence of liver stigmata and normal results of liver function tests and imaging suggested otherwise. Only 13% of patients with malignancy-related ascites are found to have a high SAAG without coexisting cirrhosis.5-7 This usually is seen with massive liver metastases or portal venous involvement,5,7 both of which were not present in our patient.

The reason for the elevated SAAG associated with this rather large ovarian tumor is unclear. However, 3 possible hypotheses may help explain it: This case is among the 3% in which the SAAG is unreliable; the ascites contained fluid from the cystic ovarian mass, which affected the SAAG; or the borderline nonmalignant nature of the ovarian tumor made the SAAG unreliable.


Figure 2. Gross pathology of the ovarian tumor.

 

Outcome of the case. The patient underwent urgent exploratory laparotomy. The right ovarian mass was resected; in addition, a total abdominal hysterectomy and bilateral salpingo-oophorectomy were performed. Results of histopathology tests revealed a stage 1, well-differentiated, mucinous, borderline ovarian tumor, intestinal type, measuring 35 × 35 × 14 cm (Figure 2), with no evidence of invasion.

The patient elected to have surgery to remove the mass and had no postsurgical complications. She was discharged a week later and was doing well at her 6-month follow-up visit. Her case is being followed diligently by the gynecologic oncology service.

The SAAG has a high accuracy rate and should be always calculated as part of the workup of patients presenting with ascites.  However, this case highlights a rare scenario in which the SAAG was not reflective of the ongoing process.

References:

  1. Paré P, Talbot J, Hoefs JC. Serum-ascites albumin concentration gradient: a physiologic approach to the differential diagnosis of ascites. Gastroenterology. 1983;85(2):240-244.
  2. Runyon BA, Montano AA, Akriviadis EA, Antillon MR, Irving MA, McHutchison JG. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Ann Intern Med. 1992;117(3):215-220.
  3. Hou W, Sanyal AJ. Ascites: diagnosis and management. Med Clin North Am. 2009;93(4):801-817.
  4. Gordon FD. Ascities. Clin Liver Dis. 2012;16(2):285-299.
  5. Fincher RK, Green RH. High serum albumin ascites gradient ascites—an atypical presentation of metastatic pancreatic cancer. Mil Med. 2012; 177(9):1117-1118.
  6. Gupta R, Misra SP, Dwivedi M, Misra V, Kumar S, Gupta SC. Diagnosing ascites: value of ascitic fluid total protein, albumin, cholesterol, their ratios, serum-ascites albumin and cholesterol gradient. J Gastroenterol Hepatol. 1995;10(3):295-299.
  7. Runyon BA, Hoefs JC, Morgan TR. Ascitic fluid analysis in malignancy-related ascites Hepatology. 1988;8(5):1104-1109.