INTERSTING CASE OF ASCITES PROF. DR.P.VIJAYARAGHAVAN’S UNIT DR.C.R.RAJKUMAR
INTERSTING CASE OF ASCITES
PROF. DR.P.VIJAYARAGHAVAN’S UNIT DR.C.R.RAJKUMAR
63yrs old male admitted with C/O Abdominal distension - 1
month Bilateral leg swelling -15
days
History of present illness:
◦ Abdominal distension -1month duration, -slowly progressive, uniform
◦ Bilateral legs swelling – 15 days duration,
-insidious, progressive◦ Shortness of breath – 15 days
◦ Abdominal pain – past few days -diffuse, dull aching
◦ Decreased urine output – past few days
No H/O jaundice, hematemesis, melena
No H/O Loose stools
No H/O fever
H/O Loss of appetite +
H/O Loss of weight +
PAST HISTORY
H/O jaundice present - 6yrs back -details not
knownNot a known SHT / DM / PT
PERSONAL HISTORY
Mixed dietKnown chronic alcoholic ->10yrs -180 – 270ml /105 gm /
dayChronic smoker
EXAMINATIONGeneral examinationConsciousOrientedAfebrileDyspneicMild pedal edema Pallor+An icteric No clubbingNo cyanosis Few lymph-nodes in left cervical
region 0.5 to 1cm in size.
SYSTEMIC EXAMINATIONCVS – S1, S2 Heard no murmursRS – NVBS Heard no added soundsP/A –Soft distended firm to hard liver palpable irregular surface free fluid + fluid thrill+,
few dilated veins flow below upwards
CNS –NFND
IMPRESSIONEthanol related DCLD with
ascites? Malignant transformation
INVESTIGATIONSCBCHb -9 gm / dlTC - 5400DC - P-60 L-30 E-10ESR - 10 / 22mmMCV - 88 fl MCH – 29pgRBC – 5000 millionsPLATELETS – 80000
RFT Blood sugar - 81 mg/dlUrea - 30mg /dlCreatinine - 0.9mg /dl
USG ABDOMENLiver – 9.5 cm , altered texture , nodular surface Free fluid +GB – Apparent GB wall thickening+Pancreas – 10 * 9 cm hetero echoic lesion in the para aortic area displacing the pancreasSpleen – 11.7 cmKidney – RT -10* 5.3 cm, left 9.9 * 4.5 cm
increased echo , 1.8 * 2 cm cystic lesion in the upper pole of RT kidney multiple lesion in the LT kidney
IMPRESSION Parenchymal liver disease with ascites. Para aortic lymphadenopathy+ Bilateral renal cortical cyst.
ASCITIC FLUID ANALYSIS
Appearance – milky (chylous) Total WBCs – 3000 cells/cummNeutrophils – 6-8 / hpfSugar – 87 mg/dlTotal protein 2.9 gm /dlAlbumin 1.4 gm / dlSAAG 1.2
Amylase - 271 u/ lCytology –
◦plenty of lymphocytes along with reactive mesothelial cells on eosinophilic backgrounds
Adenosine deaminase - 42.4 u/lAscitic fluid TGL: 210mg%
SP 3Hb -8.3 gm /dlTC - 6900cells/cummDC - P-63 , L-26 , E -11Platelets – 16000PCV -34.8MCV - 91.9MCH - 29.6MCHC- 32,5ESR - 38 mm/hrPT -14 secINR - 1APTT - 26
Blood sugar 81mg/dlUrea 26.16 mg/dlCreatinine -1.12 mg/dlTotal bilirubin -0.52 mg/dlDirect - 0.2mg/dlAST - 47u/lALT - 25 UGGT - 30 USAP -249Total protein -6.3 g/dlAlbumin -2.6 /dlGlobulin - 3.7 g/dlNa+ -131.7 meq/lk+ - 4.33 meq/lCl- 98.4meq/l
SEROLOGYHIV Antibody - negativeHBSAg - negativeAnti HCV - negativeURINE complete analysisColour - yellowishAppearance - turbid PH -6.0Specific gravity -1.030Albumin +Sugar , blood , ketone - negativeNitrite - negativeBilirubin +Urobilinogen - +
Urine microscopyleucocytes 5-6 cells/hpfEP cells – 2-3/ hpf
Chest physician opinion: - RT pleural effusionOGD SCOPY: -Erosive gastritis - No esophageal
varices
Pleural fluid analysis:Sugar – 93Protein – 2.8
With the above investigations what are the possibilities?
Comment
Causes of Chylous Ascites:
Points favouring TB ◦↑ ascitic fluid ADA◦↑ proteins exudate◦Right pleural effusion◦Para-aortic nodes
Points against – ◦High SAAG
How to proceed?
CT abdomenMultiple para-aortic nodes+.
Ascites with right pleural effusion.
CT being inconclusive, what to do next??
The small cervical nodes started becoming more conspicuous
FNAC -CERVICAL LYMPH NODE
possibility of chronic lymphoid leukemia / small lymphocytic lymphoma
INGUINAL NODE BIOBSYDiffuse effacement of lymphnode architecture
by monotonous population of neoplastic cells [lymphocytes]. The cells are small with scant cytoplasm noncleved centrally placed nucleus with open chromatin. The neoplastic cells are seen to infiltrate the adjacent perinodal pad of fat. Blood vessels are interspread with in neoplastic cells.
Impression Non Hodgkin lymphoma/
chronic lymphoid leukemia / small lymphocytic lymphoma
Patient had trouble with crossmatching possible Auto Immune Hemolytic Anemia
Hematology opinion
SuggestedLDH HematocritTo do Direct Coomb’s Test to r/o
AIHA
Plan to start chemotherapy after blood investigation
But before we could start chemotherapy pt deteriorated and died of cardio respiratory arrest
Final diagnosisSmall cell lymphoma infiltrating
the liver causing portal hypertension and chylous ascites with possibly autoimmune hemolytic anemia.
CHYLOUS ASCITES
Chylous ascites is an uncommon clinical condition that occurs as a result of disruption of the abdominal lymphatics.
CAUSESAbdominal surgeryAbdominal traumaMalignant neoplasms hepatoma, small
cell lymphoma, retro peritoneal lymphoma
Spontaneous bacterial peritonitis [SBP]Cirrhosis – upto 1%Peritoneal dialysisAbdominal tuberculosisCarcinoid syndrome Congenital defects of lacteal formation
classificationTrue chylous ascites: fluid with
high triglyceride content (>200mg%)
Chyliform ascites: fluid with a lecithin- globulin complex due to fatty degeneration of cells.
Pseudo chylous ascites: fluid that is milky appearance due to the pus
Chylous ascites diagnosed by-The ascitic fluid triglyceride level is
elevated in all pts with chylous ascites.
-TGL >110 mg/dl, >200 definite-Elevated ascites : plasma
triglyceride ratio [between 2.1 and 8.1]
ComplicationSepsisSudden death
TREATMENTChylous ascites is a manifestation
rather then a disease depends on the treatment of the underlying disease or cause
Supportive measures can relieve the symptoms such as repeated paracentesis, diuretic therapy, salt and water restriction
Low-fat diet with medium chain triglyceride
Octreotide is most likely effective
Non-hodgkin's Lymphoma of the LiverLymphomatous infiltration of the liver
is more common in non-Hodgkin's lymphoma (NHL) than in Hodgkin's
disease. Hepatic involvement with NHL has
been described in liver biopsy specimens in up to 53% of cases (and an even higher percentage at autopsy), is more common with small-cell varieties than with large- cell types.
Liver biochemical test results may be abnormal (primarily an increase in serum alkaline phosphatase), and hepatomegaly may be detected.
Rarely, NHL can present as a primary hepatic lymphoma.
Apart from human immunodeficiency virus–associated lymphomas, primary hepatic lymphoma has a better prognosis than NHL because of the possibility of cure with successful resection.
Jaundice is rare in patients with NHL and in the past was considered a terminal occurrence.
Jaundice secondary to extrahepatic biliary obstruction is more common in NHL (1.2%) than in Hodgkin's disease (0.3%), and biliary obstruction occurs most commonly at the porta hepatis, although primary lymphomatous involvement of the bile ducts has been reported in rare cases.
In patients with NHL and jaundice, gallstones and pancreatic adenocarcinoma must be excluded.
Treatment Hepatic resection/Orthotopic liver
transplant for primary hepatic NHL.
Chemotherapy for CLL/SLL with secondary hepatic involvement:◦Fludarabine/cladribine is usually
combined with an alkylating agent such as cyclophosphamide.
◦Alemtuzumab – a monoclonal antibody against CD52 is tried in refractory cases.
Thank you