Obstructive Jaundice

What is Obstructive Jaundice?

All types of obstructive jaundice, like other violations of the flow of bile into the intestine, lead to a drastic weakening or cessation of the absorption of vitamin K and the steadily progressive deficiency of factors VII, X, II and IX.

In the laboratory, this depression begins to be clearly detected already on the 5-7th day after the complete cessation of bile post-chilliness in the intestine. The tendency to bleeding becomes noticeable after 1218 days.

Directly obstructive jaundice leads to progressive damage to the liver parenchyma, which in the later stages causes an additional decrease in the level of factors V, VIII.

Symptoms of Obstructive Jaundice

This type of bleeding occurs in 7-39% of patients. Their frequency steadily increases with the lengthening of the icteric period and in advanced cases reaches 100% of cases.

The first bleeding usually occurs when the prothrombin time lengthens by 2.5-3 times. There are hemorrhages at the injection site, in places of scratching the skin, nasal, gingival and gastrointestinal bleeding, blood in the urine. Hemorrhages in the intestinal wall, in the peritoneum, retroperitoneal tissue, intracranial hemorrhages are possible.

Diagnosis is based on the identification of deficiency of K-vitamin-dependent factors. In the future, there may be a shortage of the remaining components of the blood coagulation system, depending on liver function, as well as platelet dysfunction.

Treatment of Obstructive Jaundice

Intravenous administration of sufficiently large doses of vitamin K preparations (vikasol) and surgical restoration of bile secretion in the first 3 weeks of jaundice. If necessary, urgent correction of hemocoagulation prescribed jet transfusion of plasma and the introduction of PPSB.

In severe liver disease and the ineffectiveness of vitamin K supplements, somatotropin is additionally prescribed, which improves the synthesis of factors VII, II, X and IX.

Liver parenchyma lesions are accompanied by a regular, more or less pronounced deficit of K-vitamin-dependent coagulation factors, often masked by secondary hypercoagulation.

This defect can be exacerbated by a violation of the absorption of vitamin K from the intestine due to insufficient flow of bile into it. Some factors of the considered group can be spent also owing to the disseminated intravascular coagulation. In addition, in hepatic diseases, synthesis in hepatocytes and other coagulation factors may be impaired.

In contrast, the level of factor VIII is not significantly reduced, and even with particularly severe liver lesions it increases dramatically.