KINESIOL 1Y03 Chapter Notes - Chapter 12: General Anaesthetic, Intestinal Permeability, Hyperkalemia
22 Jun 2018
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Department
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Professor
Ascites
= excess fluid in the peritoneal cavity due to an overwhelmed capacity of the lymphatic
system clearance
80% due to decomensated liver disease (along with oesophageal varices, jaundice and
encephalopathy)
50% of cirrhotics develop ascites over 10 years
50% mortality after 2 years
patients presenting should be admitted for urgent USS and paracentesis
Occurs when wedged hepatic venous pressure / portal pressure gradient (hepatic venous
pressure gradient - HVPG) <12mmHg
Causes of ascites
Cirrhosis and portal HTN
Alcoholic hepatitis
Pancreatitis
Peritoneal TB
Carcinomatosis
Budd-Chiari / portal vein
obstruction
Cardiac failure
Nephritic syndrome
Mechanism
1. Cirrhosis involves the deposition of collagen fibres by activated stellate cells; this
blocks the fenestrae lining capillaries thus “arterializes” them i.e. increases pressure
in them
2. Hence sinusoidal portal HTN
3. Hence splanchic artery vasodilatation (in response to increase in pressure)
4. This leads to decreased effective plasma volume (EPV) i.e. systemic hypovolaemia
5. Hence the sympathetic nervous system and renin-angiotensin-aldosterone system
(RAS) is activated release of ADH
6. Renal retention of Na+ and water under the action of ADH, as Na+ excretion in the
proximal and distal tubules is reduced
EITHER:
7. resulting increase in EPV leads to de-activation of RAS
OR:
8. there is persistence of low EPV as splanchic As remain dilated, leading to further Na+
and water retention worsening portal HTN excess interstitial fluid produced
across sinusoidal vascular bed when this can no longer be drained by regional
lymph nodes ascites
N.B. despite causation being high Na+, patients’ bloods will actually show up as low Na+
because of a dilutional hyponatraemia
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Document Summary
= excess fluid in the peritoneal cavity due to an overwhelmed capacity of the lymphatic system clearance. 80% due to decomensated liver disease (along with oesophageal varices, jaundice and encephalopathy) 50% of cirrhotics develop ascites over 10 years. 50% mortality after 2 years patients presenting should be admitted for urgent uss and paracentesis. Occurs when wedged hepatic venous pressure / portal pressure gradient (hepatic venous pressure gradient - hvpg) <12mmhg. N. b. despite causation being high na+, patients" bloods will actually show up as low na+ because of a dilutional hyponatraemia. N. b. definitions of transudate and exudate are unhelpful because in patients with liver disease exudates may not have as high protein contents as expected due to liver failure, hence comparison with serum is required. This cut off of 11g/l predicts the presence of portal htn with 97% accuracy. Management: treat primary cause, salt (and fluid) restriction.
