Case conference

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Case conference

• 98-6-8
• PGY ???

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• ??x
• 58Y, woman
• Past history
• 1) Liver cirrhosis, HCV, with massive ascites,
  Child C, f/u at GI OPD, liver transplantation
  waiting list, admitted on April 2009 due to SBP
• 2) Vertebro-basilar artery insufficency
• 3) Right transudative pleural effusion, s/p
  pig-tail drainage
• Admission since 98-5-18now

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• C.C. Abdominal pain and fullness in recent days.
  
• P.I.
• 98-5-14
• She had abdominal pain and fullness in recent
  days. The pain was diffuse, dull, persistent, and
  cannot relieved by postural change. Some
  insomnia, poor intake and decreased urine output
  and leg edema was noted.
• There were no fever with chills, productive
  cough, cold sweating, nausea with vomiting,
  diarrhea or dysuria. So she was taken to our ER
  for help.

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• Personal history
• No smoking, alcohol drinking, allergy, travel
  history

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Physical examination

• Vital signsT 37.6 ?C   P 80 /min   R 20 /min
    BP175/93 mmHg
• General appearanceModerate development and
  nutrition, chronic ill looking, GCSE4V5M6, clear
  , well verbal communication , no disorientation.
  Peripheral warm limbs and no cyanosis.
• SkinNormal skin turgor, no easy bruising, no
  patechiae, no ecchymosis, no spider angioma over
  upper chest wall.
• HEENTpink conjunctiva, icteric sclera.
• Neck Supple, no lymphadenopathy, Jugular veinNo
  engorgement, ThyroidNo enlargement. TracheaNo
  stridor, no deviation.Carotid arteryNo bruit.

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Physical examination

• Chest      a. InspectionSymmetric expansion of
  chest wall, no barrel shape chest,  no cynosis,
  no respiratory accessory muscle use,  no
  hyperventilation.      b.PalpationNo deviation
  of trachea, normal of tactile voice fremitus.
       c.PercussionBilateral symmetric resonance.
       d.Auscultationno wheezing
• Heart PMI 5th ICS of 1't midclavicular line,
  regular heart beat without murmurs, no thrill ,
  no fraction rubs
• Abdomen a. Inspection distended, no
  operation scar. b. Auscultation normactive
  bowel sound c. Palpation tenderness, no
  muscle gurading, no rebounding pain, no tympanic,
  No Murphy's sign, no hepatomegaly, no
  splenomegaly. No bil flank knocking pain.
  d. Percussion shifting dullness  
• Extremities      no clubbing fingers, no
  deformity, freely movable, pitting edema 3
• Nervous system No muscle power decreasing,
  normal DTR, Barbinski's sign-/-

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Lab data at ER

• 98-05-14WBC 2,7, RBC 2.39, Hb 7.7, Hct 22.4,
  MCV 93.5, MCH. 32.2, MCHC 34.4, RDW 19.5,
  PLT. 50, MPV 9.1, Band. 1, Seg. 50, Lym.
  32, Eosin.3, Baso.0, Myelocyte. 1.Lipase
  316, Glucose (Random) 108, Na 134.8, K 6.01,
  BUN 58, Cr 2.61, S-GOT(AST) 45, S-GPT(ALT) 8,
  Ammonia 22, Bili Total 2.75Pro. time(INR)
  1.2, Pro.T.Control 9.7, P.T. 12.9,
  A.P.T.T.Control 29.0, A.P.T.T. 35.8
• 98-05-15K 6.41-gt K 4.94, Hb 9.1
• Ascites routine AppearanceCloudy,ColorReddish
  ,RBC31000,WBC80,Lymphocyte71,Neutrophil4,M
  esothelial cell5,Histocyte0,Malignant cell0
• 98-05-17WBC 4.0, RBC 2.60, Hb 8.4, Hct 23.9,
  MCV 92.0, MCH. 32.3, MCHC 35.0, RDW 19.8,
  PLT. 45, MPV 8.2, Band. 1, Seg. 55, Lym.
  28, Mono. 14, Eosin.1, Baso.0, Myelocyte.
  1, BUN 71, Cr 2.59, K 4.28.

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• CXR

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• Impression1) Liver cirrhosis, Child C, with
  massive ascites2) SBP

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• Plans1) Flumarin 1g, q12h2) FFP 3U qd and
  Lasix 40mg qd3) Check body weight and abdominal
  waist4) Arrange abdominal ultrasound 5)
  Abdominal tapping if needed

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5/18-5/20 Flumarin
5/23-5/27 Zinacef
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5/19 75.5kg
5/24 76.5kg
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5/30 77kg
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(No Transcript)
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• Consult Nephrologist for progressive renal
  dysfunction.
• Reply 1) Check urine Na, K if maximal doses of
  diuretics is reached. (Aldactone 400mg/day, lasix
  160mg/day)2) If ascites is refractory to
  diuretics, large volume paracentesis or ascites
  ultrafiltration is considered if patient agrees

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6/671kg

• 98-6-4Ascites ultrafiltration -5.92kg

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• Treatment of diuretics-resistant ascites in
  patients with cirrhosis.
• From uptodate.

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INTRODUCTION 

• Ascites due to cirrhosis can be mobilized in
  approximately 90 percent of patients with a
  treatment regimen consisting of dietary sodium
  restriction (usually 88 meq 2000 mg/day) and
  oral diuretics (usually consisting of
  spironolactone and furosemide).

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DEFINITION

• Diuretic-resistant ascites in patients with
  cirrhosis is considered to be present when one or
  both of the following two criteria is present in
  the absence of therapy with a nonsteroidal
  antiinflammatory drug (NSAID), which can induce
  renal vasoconstriction and diminish diuretic
  responsiveness
• An inability to mobilize ascites despite
  compliance with dietary sodium restriction 78 meq
  of sodium or urine sodium lt urine potassium on a
  random sample) and the administration of maximum
  tolerable doses of oral diuretics (400 mg/day of
  spironolactone and 160 mg/day of furosemide) .
• The development of prohibitive diuretic-related
  complications, such as progressive azotemia,
  hepatic encephalopathy or progressive electrolyte
  imbalance.

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Differential diagnosis

• Resistant ascites in patients with cirrhosis must
  be differentiated from malignant ascites due to
  peritoneal carcinomatosis or from chylous
  malignant ascites. These disorders are typically
  refractory to diuretic therapy because of an
  inability to mobilize the ascitic fluid. In
  contrast, massive hepatic metastases, another
  cause of malignant ascites, is due to
  intrahepatic hypertension and can be treated in a
  similar fashion to patients with cirrhosis.
• Another form of diuretic-resistant ascites,
  called nephrogenic ascites, occurs in patients
  with end-stage renal disease who are usually
  being treated with maintenance dialysis. The
  pathogenesis of this disorder may be related to
  an increase in peritoneal capillary permeability
  induced in part by inadequate dialysis.
• Patients with Budd-Chiari syndrome (hepatic vein
  thrombosis) may be unusually diuretic-resistant.
  Doppler ultrasound frequently provides
  information about hepatic venous patency.

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PATHOGENESIS

• True diuretic-resistant ascites is usually
  associated with advanced cirrhosis, marked
  neurohumoral activation (of the sympathetic and
  renin-angiotensin-aldosterone systems), and very
  low urinary excretion of sodium, frequently less
  than 10 meq/day despite maximal tolerated doses
  of diuretics.
• Neurohumoral activation results in renal
  vasoconstriction and enhanced sodium reabsorption
  in the proximal tubule (under the influence of
  angiotensin II and norepinephrine) and collecting
  tubules (under the influence of aldosterone).
  Even among patients with nonazotemic cirrhosis,
  those with a greater degree of neurohumoral
  activation show diminished diuretic
  responsiveness.
• The development of true diuretic resistance in a
  previously diuretic-sensitive patient is most
  often due to progression of the liver disease.
  However, it can also be due to two other
  complications of cirrhosis hepatocellular
  carcinoma and/or portal vein thrombosis. A liver
  and spleen ultrasound with Doppler or CT scan and
  measurement of serum alpha fetoprotein can help
  diagnose or exclude these complications.

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PATHOGENESIS

• Progression to diuretic-resistance is generally
  an irreversible process unless there is a
  reversible component to the liver disease (eg,
  alcoholic hepatitis) or the patient undergoes a
  successful liver transplant, transjugular
  intrahepatic portosystemic stent shunt (TIPS), or
  peritoneovenous shunt. As urinary sodium
  excretion dwindles despite diuretics, progressive
  azotemia and electrolyte imbalance (eg,
  hyponatremia) are expected. Diuretics are
  generally discontinued in such patients.

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THERAPEUTIC OPTIONS 

• Patients with diuretic-resistant ascites have
  pre-hepatorenal syndrome and a very poor
  prognosis.
• The two-year survival rate of all patients with
  cirrhosis after the development of ascites is
  approximately 50 percent.
• In comparison, survival in patients with
  diuretic-resistant ascites is 50 percent at six
  months and 25 percent at one year.
• Similar prognostic stratification can be achieved
  using baseline urinary sodium excretion. In one
  series, for example, patients with ascites and
  urinary sodium excretion below 10 meq/day had a
  mean survival rate of five to six months.
• There are three major therapeutic options in
  patients with diuretic-resistant cirrhotic
  ascites
• Liver transplantation
• Serial therapeutic paracentesis approximately
  every two weeks with Colloid replacement. 
• Transjugular intrahepatic portosystemic stent
  shunt (TIPS)
• Other modalities such as a peritoneovenous
  (LeVeen or Denver) shunt have very limited
  indications.
• Oral midodrine has shown some promise in the
  treatment of refractory ascites, especially in
  unusually hypotensive patients.

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• Thanks for your attention!