A 47YearOld Woman With Ascites Chapter 16

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A 47-Year-Old Woman With Ascites Chapter 16
Eugene G. Martin, Ph.D. Associate Professor of
Pathology Laboratory Medicine

• Based upon LABORATORY MEDICINE CASEBOOK. An
  introduction to clinical reasoning
• Jana Raskova, MD Professor of Pathology
  Laboratory MedicineStephen Shea, MD
  Professor of Pathology Laboratory
  MedicineFrederick Skvara, MD Associate
  Professor of Pathology Laboratory MedicineNagy
  Mikhail, MD Assistant Professor of Pathology
  Laboratory MedicineUMDNJ-Robert Wood Johnson
  Medical SchoolPiscataway, NJ

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History and Presentation

• A 47-year-old woman admitted to hospital
• Chief Complaint (CC)
• Increasing Shortness of breath (SOB)
• Extreme Fatigue
• Medical History
• Unspecified cardiac arrythmias
• 20 year history of heavy consumption of alcohol

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Physical Examination

• Alert, oriented woman
• BP 100/65 HR 96 bpm RR 23/min
• Temp. 97.5 oF
• Findings
• Distended jugular veins
• Protuberant abdomen with ascites
• Liver and spleen NOT palpable
• Pitting edema lower extremities

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Chest x-rays
ADMISSION
THREE YEARS EARLIER
Pulmonary vascular congestionPulmonary edema
Lung Fields Clear
Cardiac shadow Normal
Cardiac shadow Enlarged
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Chest Films - CHF
Congestive Heart Failure
Normal Chest Film

• Cardiomegaly
• Prominence of pulmonary vasculature
• Increased density small vasculature
• Kerely B lines Hallmark of the seepage of
  fluid into the interstitium Short straight
  lines in the periphery of the llug lying
  perpendicular to the pleural surface.

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HEMATOLOGY - Admission
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CHEMISTRY - Admission
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Electrolytes - Admission
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Clinical Course

• Patient developed severe hypotension and
  bradycardia (HR35).
• Following stabilization a bedside EKG showed
• Left atrial and right ventricular hypokinesis
• The next morning the patient again developed
  severe hypotension and bradycardia ? asystole.
• Resucitation efforts failed
• Patient expired.

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Liver at autopsy

• Liver wt. 1440 gm (Normal 1300 gms)
• Acute, passive centrilobular congestion
  necrosis
• Fatty change

Alcoholic Liver Disease

• Foci of inflammation and hepatocyte degeneration
• Mallory bodies amorphous, eosinophilic
  inclusions

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Histopathology

• Uniform, unremarkable nuclei
• No inflammation or fatty infiltration

Normal x78

• Fine fibrosis with thinning of the myocytes
• Some enlarged nuclei
• Fatty change

Patient X 31
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Summary

• Dilated cardiomyopathy
• Alcoholic liver disease
• Presenting findings
• Ascites
• Pitting Edema
• -? Could be because of congestive heart failure
  or alcoholic liver disease or both

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Alcoholism and lab profile

• ? GGTP a microsomal enzyme induced by alcohol.
  Highest levels in patients with 5-20 yr. hx.
• ? ? ? AST Markedly increased in alcholic
  hepatitis
• ALT Usually normal
• When AST 1 suggestive of
  alcholic liver disease
• ? Serum Albumin usually decreased in severe
  disease due to poor nutrition may indicate
  cirrhosis often assoc. with polyclonal ? in
  immunoglobulins
• ? WBC 1/3 of alocholic patients, WBC
  15,000/µl with left shift
• ? MCV Macrocytosis occurs in 50 of chronic
  alcoholics

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ALBUMIN

• Hypoalbuminemia
• Liver
• ? liver synthesis
• Hemodilution
• ? renal loss of albumin
• ? albumin without ? total protein think
  inflammatory stimulation of immunoglobulin
  synthesis
• ? Ca in a hypoalbuminemic patient may be due to
  decreased transport not ? Ca

• Synthesis liver
• Half-Life 20 days
• Role transports substances bilirubin, fatty
  acids, metal ions (Ca), hormones, drugs
• Hypoalbuminemia is more frequent in older adult
  patients who are institutionalized.

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Hypoalbuminemia

• Albumin levels mortality
• Albumin, globulin and fibrinogen compose total
  protein albumin (60)

• Inflammatory factors TNF, IL-1 and IL-6 all ?
  albumin synthesis.
• Roles of albumin
• Maintenance of oncotic pressure
• Drug transport
• Total protein ? colloid osmotic pressure holds
  fluid in circulation