03-13 Portal HTN/Ascites Flashcards
• Define Portal hypertension • Discuss the major causes of portal hypertension. Compare and contrast pre-hepatic, intra-hepatic and post-hepatic etiologies • Describe the major pathophysiologic consequences and complications of portal hypertension • Describe the various theories of how ascites is formed • Discuss the principles of treatment and prevention of bleeding varices and ascites • Describe a Transjugular intrahepatic portosystemic shunt (TIPS) procedure and explain how
<p>OBJECTIVE: Define portal HTN</p>
<p>Increased P in portal venous system</p>
<ul>
<li>due to either increased flow into the liver or increased resistance (either before, within, or after the liver)</li>
<li>resulting in an <strong>imbalance of vasoconstriction and vasodilatation</strong></li>
<li>Can be just a part (<strong>segmental portal HTN</strong>)</li>
</ul>
<p>WHVPG</p>
<p>Wedge hepatic vein pressure gradient = WHVP - F(ree)HVP</p>
<ul>
<li>increases proportional to degree of cirrhosis</li>
</ul>
<p>OBJECTIVE: What are major causes of portal HTN. (Compare and contrast pre-, intra-, and post-hepatic etiologies)</p>
<p>Pre-Hepatic <em>(bad vessels, good liver)</em></p>
<ul>
<li>thrombus (or less commonly tumor) blocking portal v.</li>
<li>excess flow due to splenomegaly (myelofibrosis, e.g.) or A-V shunt</li>
</ul>
<p>Intra-Hepatic <em>(good vessels, bad liver)</em></p>
<ul>
<li>EtOH</li>
<li>Viral Hep</li>
<li>Schistosomiasis</li>
<li>Other cirrhotic liver dzs</li>
<li>Non-Cirrhotic portal HTN (distinct more vascular dz, mainly India, Japan)</li>
</ul>
<p>Post-Hepatic <em>(bad vessels, good liver)</em></p>
<ul>
<li>hepatic v. thrombosis</li>
</ul>
<p>Vasoconstriction/Vasodilatation Paradox</p>
<p>Vasodilatation</p>
<ul>
<li>well perfused skin</li>
<li>NO production in liver is fucked by portal HTN
<ul>
<li>low in liver → incr resistance</li>
<li>high in splanchnic (sheer stress) /periph circ → vasodilatation
<ul>
<li>this increases flow rate into liver exacerbating sheer stress on liver endothelium</li>
</ul>
</li>
</ul>
</li>
</ul>
<p>Vasoconstriction</p>
<ul>
<li>low arterial BP</li>
<li>incr activity of endogenous vasoconstrictors in the liver of cirrhotics</li>
<li>go systemically → hepatorenal syndrome, portal-systemic encephalopathy, hepatopulmonary syndrome (lung shunting, bubble test)</li>
</ul>
<p>Child Score components</p>
<ul>
<li>Ascites</li>
<li>Encephalopathy</li>
<li>Albumin</li>
<li>Bilirubin</li>
<li>PT/INR</li>
</ul>
<p>OBJECTIVE: Describe the major pathophysiologic consequences and complications of portal hypertension</p>
<ul>
<li>varices/bleeding</li>
<li>h2o/salt retention → ascites/edema</li>
<li>encephalopathy from impaired detox ability</li>
<li>multi-organ system failure (lungs, kidneys, brain, heart)</li>
</ul>
<p>OBJECTIVE: Describe the various theories of how ascites is formed</p>
<p>Two theories</p>
<ul>
<li>Older "Underfill" Theory: low alb → decr oncotic P → fluid leaks into peritoneal cavity → low effective circ volume → RAAS system activated → salt/water retention → incr hydrostatic P → more ascites</li>
<li>Newer "Overfill" Theory: portal HTN → imbalance of vasodilatation in splanchnic vv. e.g. and vasoconstriction periph including <u>renal vasoconstriction</u> → RAAS activated b/c kidney "sees" low ECV → salt/water retention → incr hydrostatic P + low oncotic P of low albumin → ascites</li>
</ul>
<p>DDx for ascites</p>
<p>Always do a diagnostic paracentesis the first time someone presents with ascites OR in cases of decompensating liver dz</p>
<p>Think Peritoneal vs. Non-Peritoneal</p>
<ul>
<li>Peritoneal
<ul>
<li>malignancy</li>
<li>inflamm</li>
</ul>
</li>
<li>Non-Peritoneal
<ul>
<li>Portal HTN</li>
<li>Other Diseases
<ul>
<li>hypoalbuminemia</li>
<li>myxedema (get TSH)</li>
<li>overian syndromes</li>
<li>pancreaic problem, bile leak (e.g. s/p liver bx), chyle, etc.</li>
</ul>
</li>
</ul>
</li>
</ul>
<p>OBJECTIVE: Describe a TIPS procedure and explain how it can correct the consequences of portal hypertension</p>
<p>TIPS = Transjugular intrahepatic portosystemic shunt</p>
<ul>
<li>Punch a hole through liver parenchyma to place a shunt between branch of portal v. and branch of hepatic v.</li>
<li>Decreases the pressure built up in the portal system and prevents development of complications of portal HTN:
<ul>
<li>varices, ascites, imbalance of systemic vasoconstriction/local vasodilatation and splenomegaly</li>
</ul>
</li>
</ul>
<p>OBJECTIVE Discuss the principles of treatment and prevention of bleeding varices</p>
<p>Acute Tx</p>
<ul>
<li>banding</li>
<li>sclerotherapy</li>
<li>meds</li>
<li>TIPS or surgical shunt</li>
</ul>
<p>Prevention</p>
<ul>
<li>Treat liver dz</li>
<li>Prescribe non-selective β-blockers (nadolol, propranolol)</li>
<li>Band/sclerose non-bleeding varices</li>
<li>consider transplant (unfortunately not part of MELD score)</li>
</ul>
<p>OBJECTIVE: Discuss the principles of treatment and prevention of ascites</p>
<p>Prevention/Treatment of Treatable Ascites</p>
<ul>
<li>reduce salt</li>
<li>add spironolactone/amiloride</li>
<li>add furosemide
<ul>
<li>This low salt + diuretic regimen is 90% effective in new osnet ascites</li>
</ul>
</li>
</ul>
<p>Treatment of Diuretic-Resistance Ascites</p>
<ul>
<li>d/c NSAIDs</li>
<li>LVP (up to 12 L)</li>
<li>TIPS</li>
<li>Liver transplant</li>
</ul>
<p>OBJECTIVE: Describe the clinical features and pathophysiology of hepatic encephalopathy</p>
<p>[All WIKI, not in either slides or notes]</p>
<p>CLINICAL FEATURES: like being drunk</p>
<ul>
<li>First Stage: inverted sleep pattern (awake at night, sleep during day), slight neuropsych ∆s, e.g. forgetfulness, mild confusion, and irritability</li>
<li>Second Stage: lethargy, personality ∆s, <strong>asterixis</strong></li>
<li>Third Stage: worsened confusion, clonus/Babinski on neuro exam</li>
<li>Fourth Stage: progression to coma</li>
</ul>
<p>PATHOPHYSIOLOGY</p>
<ul>
<li>NH3 crosses BBB → astrocytes it ammonia when synthesising glutamine from glutamate</li>
<li>↑ [glutamine] → ↑<span> osmotic P in astrocytes </span>→<span> swollen</span></li>
<li>↑ <span>GABA activity, and the energy supply to other brain cells is decreased. This can be thought of as an example of brain eedema of the "cytotoxic" type</span></li>
</ul>
<p>OBJECTIVE: Describe the fluid and electrolyte disturbances of cirrhosis and hepatorenal syndrome</p>
<ul>
<li>hyponatremia/fluid overload</li>
<li>hypoalbuminemia</li>
<li>increased 3rd spacing</li>
</ul>
<p>Budd-Chiari syndrome</p>
<ul>
<li>Cause</li>
<li>DDx</li>
</ul>
<p>Cause</p>
<ul>
<li>obliterative disease of hepatic veins (large vessel thrombosis)</li>
<li>In severe acute disease the liver can be massively congested w/ impressive jaundice ascites . In a number of</li>
<li>sometimes part of the liver separately drains into the ICV.</li>
<li>prevents damage due to impaired outflow that is absent in this part of the liver (cellular compression and death)
<ul>
<li>hypertrophies, may feel likea liver tumor on palpation</li>
</ul>
</li>
</ul>
<p>DDx</p>
<ul>
<li>compression of hepatic veins by benign processes (hydatid cyst), malignant tumor, or by so-called vascular webs.</li>
<li> impaired inflow into the heart (right HF, tricuspid insuff, constrictive pericarditis).</li>
</ul>
<p><em>There is a tendency to call all types of hepatic outflow obstruction “Budd Chiari” syndrome.</em></p>
<p>What tests do you run on ascites fluid?</p>
<ul>
<li>WBC count: infection (if very high: think perf or malig)</li>
<li>Total Prot (TP): raised in infx, malig, HF, ?hypothyroidims</li>
<li>RBCs: ?HF</li>
<li>Serum albumin-ascites gradient (SAAG): > 1.1gm/dL means ascites are likely decompensated liver disease</li>
</ul>
