Prothrombin defects – congenitial (Haemorrhagic disease of the new-born)
This is due to an exaggeration of the temporary physiological fall of prothrombin that occurs between the 1 st and 5th day of life, occurring in about 1% of new-born infants. At birth the baby has no reserve of vitamin K and its formation by bacterial synthesis in the baby’s intestine takes time until a bacterial flora has been established in it. Haematemesis, melaena and bleeding from umbilicus and elsewhere coincide with this period of temporary physiological Hypoprothrombinaemia. Transfusion of fresh (Rh negative) citrated blood at once supplies prothrombin and its accelerators of all types. Coagulation time and prothrombin time are prolonged.
Prothrombin defect – acquired. The acquired Hypoprothrombinaemia in adult occurs when (1) there is defective absorption of vitamin K after its normal synthesis by the intestinal bacteria or (2) defective formation of prothrombin in the liver as a result of the diseases of that organ. Vitamin K being fat soluble, absorption of this vitamin can occur only when fat digestion and absorption occur normally. In fatty diarrhea or sprue, a huge amount of fat is lost from the intestine, and along with this the fat soluble vitamin K. in biliary obstruction or fistula bile salt cannot reach the intestine to facilitate fat digestion and absorption, hence fat soluble vitamin K is not adequately absorbed from the intestine. In cirrhosis, the hepatic cells lose their power of producing prothrombin with the help of vitamin K. Dicoumarol and salicylates administered by mouth, compete metabolically with vitamin K, and thus production of prothrombin by liver is hampered, causing hypoprothrombinaemia. Treatment lies in the removal of the specific cause of hypoprothrombinaemia where possible, together with parenteral administration of vitamin K.
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