ASCITIS

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ASCITIS

• PRESENTED BY
• DR.SUJAPILLAI
• II MD
  REPERTORY
• GHMC CALICUT

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DEFINITION

• The word ascites is of Greek origin (askos) and
  means bag or sac.
• Ascites (also known as peritoneal cavity fluid,
  peritoneal fluid excess, hydroperitoneum or more
  archaically as abdominal dropsy) is an
  accumulation of fluid in the peritoneal cavity.

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• Healthy men have little or no intraperitoneal
  fluid, but women may normally have as much as 20
  mL, depending on the phase of their menstrual
  cycle.

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CLASSIFICATION

• Grade 1 mild, only visible on ultrasound
• Grade 2 detectable with flank bulging and
  shifting dullness
• Grade 3 directly visible, confirmed with fluid
  thrill.

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PATHOPHYSIOLOGY

• The accumulation of ascitic fluid represents a
  state of total-body sodium and water excess, but
  the event that initiates the unbalance is
  unclear.
• Three theories of ascites formation have been
  proposed underfilling, overflow, and peripheral
  arterial vasodilation.

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• The underfilling theory suggests that the primary
  abnormality is inappropriate sequestration of
  fluid within the splanchnic vascular bed due to
  portal hypertension and a consequent decrease in
  effective circulating blood volume.
• This activates the plasma renin, aldosterone, and
  sympathetic nervous system, resulting in renal
  sodium and water retention

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• The overflow theory suggests that the primary
  abnormality is inappropriate renal retention of
  sodium and water in the absence of volume
  depletion.
• This theory was developed in accordance with the
  observation that patients with cirrhosis have
  intravascular hypervolemia rather than
  hypovolemia.

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• The most recent theory, the peripheral arterial
  vasodilation hypothesis, includes components of
  both of the other theories.
• It suggests that portal hypertension leads to
  vasodilation, which causes decreased effective
  arterial blood volume.
• As the natural history of the disease progresses,
  neurohumoral excitation increases, more renal
  sodium is retained, and plasma volume expands.
• This leads to overflow of fluid into the
  peritoneal cavity.
• The vasodilation theory proposes that
  underfilling is operative early and overflow is
  operative late in the natural history of
  cirrhosis.

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• Ascitic fluid can accumulate as a transudate or
  an exudate. Amounts of up to 25 liters are
  possible.
• Roughly, transudates are a result of increased
  pressure in the portal vein (gt8 mmHg, usually
  around 20 mmHg e.g. due to cirrhosis
• Transudates have low protein (lt30g/L), low LDH,
  high pH, normal glucose, and fewer than 1 white
  cell per 1000 mm³.

• while exudates are actively secreted fluid due to
  inflammation or malignancy.
• As a result, exudates are high in protein, high
  in lactate dehydrogenase, have a low pH (lt7.30),
  a low glucose level, and more white blood cells.

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Etiology based upon serum - ascites albumin
gradient.

• High albumin gradient(gt1.1 g/dl)
• Cirrhosis
• Alcoholic hepatitis
• Cardiac ascites
• Massive liverMetastases
• Fulminant hepatic failure
• Hepatic vein thrombosis (Budd-Chiari syndrome)
• Portal vein thrombosis
• Veno-occlusive disease
• Acute fatty liver of pregnancy
• Myxedema

• Low albumin gradient(lt1.1 g/dl).
• Peritoneal carcinomatosis
• Tuberculosis
• Biliary ascites without cirrhosis
• Nephrotic syndromeAscites associated with
  connective tissue disease
• Ascites associated with bowel ischemia/infarction.

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SYMPTOMS

• Mild ascites is hard to notice, but severe
  ascites leads to abdominal distension.
• Patients with ascites generally will complain of
  progressive abdominal heaviness and pressure as
  well as shortness of breath due to mechanical
  impingement on the diaphragm.

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• Other signs of ascites may be present due to its
  underlying etiology, in portal hypertension ( due
  to cirrhosis or fibrosis of the liver) patients
  may also complain of leg swelling, bruising,
  gynecomastia, hematemesis, or mental changes due
  to encephalopathy.
• Those with ascites due to cancer (peritoneal
  carcinomatosis) may complain of chronic fatigue
  or weight loss.
• Those with ascites due to heart failure may also
  complain of shortness of breath as well as
  wheezing and exercise intolerance

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EXAMINATION

• Look at the patient, both lying down and standing
  up. The shape of the abdomen often suggests
  fluid. On lying down, the flanks are full but on
  standing the fluid accumulates in the lower
  abdomen.

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SIGNS

• Ascites is detected on physical examination of
  the abdomen by visible bulging of the flanks in
  the reclining patient ("flank bulging")
• "shifting dullness" (difference in percussion
  note in the flanks that shifts when the patient
  is turned on the side)
• "fluid thrill" or "fluid wave" (tapping or
  pushing on one side will generate a wave-like
  effect through the fluid that can be felt in the
  opposite side of the abdomen)

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• The liver may be difficult to palpate if a large
  amount of ascites is present, but if palpable,
  the liver is often found to be enlarged.
• Elevated jugular venous pressure may suggest a
  cardiac origin of ascites.
• A firm nodule in the umbilicus, the so-called
  Sister Mary Joseph nodule, is not common but
  suggests peritoneal carcinomatosis originating
  from gastric, pancreatic, or hepatic primary
  malignancy.
• A pathologic left-sided supraclavicular node
  (Virchow node) suggests the presence of upper
  abdominal malignancy.
• Patients with cardiac disease or nephrotic
  syndrome may have anasarca.

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INVESTIGATIONS

• LABORATORY STUDIES
• In patients with new-onset ascites of unknown
  origin, peritoneal fluid should be sent for cell
  count, albumin level, culture, total protein,
  Gram stain, and cytology.

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• CHEST AND PLAIN ABDOMINAL X-RAY
• . In 80 of patients with ascites, the lateral
  liver edge is medially displaced from the
  thoracoabdominal wall (Hellmer sign).
• . In the pelvis, fluid accumulates in the
  rectovesical pouch and then spills into the
  paravesical fossa. The fluid produces symmetric
  densities on both sides of the bladder, which is
  termed a "dog's ear" or "Mickey Mouse"
  appearance.

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• Ultrasonography
• Real-time ultrasonography is the easiest and
  most sensitive technique for the detection of
  ascitic fluid. Volumes as small as 5-10 mL can
  routinely be visualized.

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• Computed tomography (CT) scanning
• Ascites is demonstrated well on CT scan images.

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Other Tests

• Laparoscopy may be valuable for the diagnosis
  of otherwise unexplained cases, especially if
  malignant ascites is suspected.

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• Abdominal paracentesis
• Abdominal paracentesis is the most rapid and
  perhaps the most cost-effective method of
  diagnosing the cause of ascites formation.

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Differential Diagnosis

• The obese patient with a lax anterior abdominal
  wall may have a protuberant umbilicus (everted
  umbilicus sign)
• Metastases to the liver - in this case the firm
  liver holds the abdomen outward.
• Gaseous distention due to bowel obstruction
• Large pelvic mass
• Massive hepatosplenomegaly as in
  lympho-proliferative conditions.

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• Abdominal distention from the above causes can
  usually be distinguished from ascites by
  examination and percussion of the flanks.
• In ascites, the fluid falls into the lateral and
  lower peritoneal spaces when the patient is
  supine, giving bulging flanks and flank dullness.
• The absence of flank dullness on careful
  examination of a patient with abdominal
  distention excludes ascites with 90 accuracy.

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MANAGEMENT

• Salt restriction
• Salt restriction is the initial treatment, which
  allows diuresis (production of urine) since the
  patient now has more fluid than salt
  concentration. Salt restriction is effective in
  about 15 of patients. A no added salt diet
  restricted to lt90 mmol/day (5.2 g of salt/day) is
  useful, especially in cirrhosis but is unlikely
  to be effective in other aetiologies such as
  malignancy

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• Diuretics
• Monitoring diuresis Diuresis can be monitored by
  weighing the patient daily. The goal is weight
  loss of no more than 1.0 kg/day for patients with
  both ascites and peripheral edema and no more
  than 0.5 kg/day for patients with ascites
  alone.If daily weights cannot be obtained,
  diuretics can also be guided by the urinary
  sodium concentration.

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• Serum sodium 126-135 mmol/l with normal serum
  creatinine continue diuretics but watch
  electrolytes regularly (do not fluid restrict).
• Serum sodium 121-125 mmol/l with normal serum
  creatinine stop diuretics or continue diuretics
  cautiously at lower dose and watch electrolytes
  frequently.
• Serum sodium 121-125 mmol/l with elevated serum
  creatinine (gt150µmmol/l or gt120 µmmol/l and
  rising) stop diuretics and give volume
  expansion.

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• Only fluid restrict patients who are not
  dehydrated, not receiving diuretics and in whom
  creatinine is normal.

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• Avoiding alcohol is important in pancreatitis and
  cirrhosis of any aetiology, not just alcoholic.

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• Bed rest is not recommended for uncomplicated
  ascites. Theoretically, the upright position in
  those with ascites will aggravate
  renin-angiotensin-aldosterone/sympathetic nervous
  system activation, reducing glomerular filtration
  rate and sodium excretion and response to
  diuretics.
• Bed rest leads to muscle atrophy and other
  complications and may have the paradoxical
  opposite effect, actually extending stays in
  hospital.

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Therapeutic paracentesis

• Patients with large ascites generally benefit
  from therapeutic paracentesis.
• This needs to be a sterile procedure.
• Paracentesis of lt5 litres of uncomplicated
  ascites should be followed by plasma expansion
  with synthetic plasma expander i.e. 150-200 ml of
  gelofusine or haemacce.
• Larger volume paracenteses should be be followed
  by volume expansion, using 8 g albumin per litre
  of ascitic fluid removed.

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SURGICAL MANAGEMENT

• Surgical treatment may be required for malignancy
  and some patients may be suitable for liver
  transplantation.
• Transjugular intrahepatic portosystemic shunt
  (TIPS) can be used in patients with refractory
  ascites needing frequent paracentesis (gt3/month).

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PROGNOSIS

• Ambulatory patients with an episode of cirrhotic
  ascites have a 3-year mortality rate of 50.
• The development of refractory ascites carries a
  poor prognosis, with a 1-year survival rate of
  less than 50.
• Whilst therapeutic paracentesis and TIPS are not
  thought to improve long term survival without
  transplantation significantly for most patients
  with cirrhosis.
• In malignancy ascites tends to suggest widespread
  disease and a poor prognosis.

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REFERENCES

• Harrisons Textbook of Medicine.
• Hutchisons Clinical Methods.
• Davidsons Textbook of Medicine.
• www.emedicine.com
• www.mdlinx.com

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THANK YOU