Increased systemic venous pressure from any cause leads to hepatic congestion. The liver becomes enlarged, pulsatile, and tender. Transaminases, alkaline phosphatase, and conjugated (direct) bilirubin become moderately elevated. Occasionally, jaundice and an elevated prothrombin time occur.
Hepatic venous congestion (Passive Hepatic Congestion):
Congestive hepatopathy is diffuse venous congestion within the liver that results from right-sided heart failure (usually due to cardiomyopathy, tricuspid regurgitation, mitral insufficiency, cor pulmonale, or constrictive pericarditis).
Pathology Etiology Congestive hepatopathy resulting from passive hepatic congestion is caused by stasis of blood within the liver parenchyma due to compromise of hepatic venous drainage. Prolonged exposure to elevated hepatic venous pressure may lead to liver fibrosis and cirrhosis.
Underlying conditions include:
Pulmonary hypertension
Tricuspid regurgitation
Constrictive pericarditis
Restrictive cardiomyopathy
Congenital heart disease, especially those treated with a Fontan procedure
Markers:
If paracentesis is performed, the serum ascites albumin gradient (SAAG) will be equal to or above 1.1 g/dL, which is consistent with ascites due to portal hypertension. Elevation of total serum bilirubin levels can occur up to 70% of patients with congestive hepatopathy.
Radiographic features:
The majority (80%) of patients will have hepatomegaly, and in severe cases have peripheral edema, ascites, and/or pleural effusions.
CT:
Reticular enhancement pattern, similar to nutmeg liver in Budd-Chiari syndrome.
Zonal enhancement pattern.
Arterial-enhancing (i.e. hypervascular) nodules, which may represent focal nodular hyperplasia (more commonly) or hepatocellular carcinoma (especially in the setting of cirrhosis).
Ultrasound:
Sonographic findings are generally non-specific when used in isolation, but may contribute to a clinical picture when putative cause and effect (i.e. heart failure and liver disease) are shown to co-exist. 2D/B-mode ultrasound may reveal the following features:
1. Cirrhosis with portal hypertension:
Decreased hepatic size with nodularity and altered echogenicity.
Portosystemic shunts.
Color flow: Doppler of the portal vein extending to the hepatic edge may suggest recanalization of the umbilical vein.
a): Venous dilation:
Left renal vein diameter >1.5 cm
Portal vein diameter >1.3 cm
Superior mesenteric vein >1.0 cm
c): Splenomegaly
d): Ascites
2. Cardiac chamber enlargement and/or dysfunction:
Left ventricular systolic or diastolic dysfunction,
Decreased cardiac index,
Right ventricular dysfunction,
Right and/or left atrial enlargement,
Pleural effusion,
Valvular stenosis or regurgitation,
3. Sonographic pulmonary edema.
4. Dilated (>2.1 cm) inferior vena cava:
More specific for elevated filling pressures when lacking respiratory variation (<50%).
Elevated filling pressures in the absence of structural cardiac disease may (rarely) imply constrictive pericarditis.
5. Doppler studies may demonstrate:
a): Increased hepatic arterial resistance (RI >0.7):
Resistive index (RI) normally between 0.55 and 0.7.
This change may be obfuscated by portal hypertension-related shunting, which classically results in a decreased RI.
b): Pulsatility of the hepatic venous Doppler waveform:
Prominent a wave and v wave.
Tricuspid regurgitation may diminish or reverse the S wave.
Pure right ventricular dysfunction will have a preserved S/D relationship with the amplitude of the S wave > D wave.
c): elevated cardiac filling pressures:
Pulsed-wave Doppler of the tricuspid regurgitant jet showing an elevated right ventricular systolic pressure (RVSP).
Pulsed wave doppler of the right upper pulmonary vein showing high-velocity AR (atrial reversal) waves with a low S/D ratio.
Pulsed wave doppler of the mitral valve inflow showing restrictive filling.
Differential diagnosis:
For CT appearances of a nutmeg liver, consider:
Budd-Chiari syndrome.
Hepatic veno-occlusive disease (sinusoidal obstruction syndrome).
Portal venous emboli.
Shunting through vascular malformations - e.g. hereditary hemorrhagic telangiectasia.
Medication:
Abhayarist, Kumaryasav, Lohasav, Rohitkarist, Arogya Vardhini Vati, Mandoor Bhasma, Shankh Bhasma, Tamra Bhasma, Praval Panchamrit Ras (M.Y.), Navayas Loha, Yakrit Plihari Loha.
Declaration:
The information on this page is not intended to be a substitute for professional medical advice. These are only based on the study and practical performances. We do not recommend any of the above medicines to directly intake or to do not use this information to diagnose or ayurvedic treatment of kids-health and/or colic pain without consulting the doctor. Consult your physician before beginning an exercise regime.
Reference (as per modern aspects):
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