BIOCHEMICAL AND CLINICAL PROFILE OF CIRRHOTIC PATIENTS BY- ultra sonographical parameters,type of anemia picture and spleen diameter ratio

Volume : VII, Issue : V, May - 2018

Dr Ajay Kumar Nandmer, Dr Vijay Kumar Nandmer

Cause of cirrhosis, the pathologic features consist of the development of fiosis to the point that there is architectural distortion

with the formation of regenerative nodules. This results in a decrease in hepatocellular mass, and thus function, and an alteration

of blood flow. The induction of fiosis occurs with activation of hepatic stellate cells, resulting in the formation of increased

1 amounts of collagen and other components of the extracellular matrix.

Portal hypertension is a significant complicating feature of decompensated cirrhosis and is responsible for the development of

ascites and bleeding from esophagogastric varices, two complications that signify decompensated cirrhosis. Portal hypertension is

defined as the elevation of the hepatic venous pressure gradient (HVPG) to >5 mmHg. Portal hypertension is caused by a

combination of two simultaneously occurring hemodynamic processes: (1) increased intrahepatic resistance to the passage of

blood flow through the liver due to cirrhosis and regenerative nodules, and (2) increased splanchnic blood flow secondary to

vasodilatation within the splanchnic vascular bed. Portal hypertension is directly responsible for the two major complications of

cirrhosis, variceal hemorrhage and ascites. Variceal hemorrhage is an immediate life–threatening problem with a 2030%

1 mortality associated with each episode of bleeding.

Cirrhosis is the most common cause of portal hypertension and clinically significant portal hypertension is present in >60% of

patients with cirrhosis. Approximately 515% of cirrhotic per year develop varices, and it is estimated that the majority of patients

with cirrhosis will develop varices over their lifetime. In patients with cirrhosis who are being followed chronically, the

development of portal hypertension is usually revealed by the presence of thrombocytopenia; the appearance of an enlarged

1 spleen; or the development of ascites, encephalopathy and/or esophageal varices with or without bleeding.

Congestive splenomegaly is common in patients with portal hypertension. Clinical features include the presence of an enlarged

spleen on physical examination and the development of thrombocytopenia and leucopenia in patients who have cirrhosis. Some

patients will have fairly significant left–sided and left upper quadrant abdominal pain related to an enlarged and engorged spleen.

Splenomegaly itself usually requires no specific treatment, although splenectomy can be successfully performed under very

special circumstances. Hypersplenism with the development of thrombocytopenia is a common feature of patients with cirrhosis

1 and is usually the first indication of portal hypertension.

In our study, we are analyzed the simple biochemical and ultrasonographical parameters which can predict the esophageal varices

which may be cost effective. And we are used contrast CD echo to identify the intrapulmonary vascular dilation hence, making the

diagnosis of hepatopulmonary syndrome.