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