The parenteral or nonoral administration of heparin for the purpose of inhibiting blood coagulation is called heparinization. Either the less rapidly acting low-molecular-weight heparin is used for prophylaxis of thrombosis and embolism or the unfractionated heparin is used for treatment of thrombosis and embolism. The most common indications for the prophylactic use of the classic anticoagulant are surgery, atrial fibrillation, and artificial heart valves made of nonbiological material.
What is heparinization?
The parenteral or nonoral administration of heparin for the purpose of inhibiting blood coagulation is called heparinization. Heparins are polysaccharides belonging to the glycosaminoglycans with a variable number of aminosaccharides. Heparins with a chain length of more than five monosaccharides have an anticoagulant effect. With a chain length of 5 to 17 monosaccharides, they are called low-molecular-weight heparins (NMH), and with a chain length of 18 or more monosaccharides, they are called unfractionated heparins (UFH). NMH and UFH have the property of being very effective in binding certain thrombins, thus interrupting the coagulation cascade and explaining the anticoagulant properties of heparins. When heparin is administered, medical terminology usually distinguishes between full heparinization with UFH and heparinization with NMH. Full heparinization with UFH (optionally also with NMH) is used to treat acute embolism or thrombosis. Heparinization with the slower-acting NHM corresponds to a preventive safety measure in situations or conditions that could provoke the formation of blood clots. In laboratory medicine, the term full heparinization refers to the addition of heparin to whole blood samples and the wetting of blood-contact devices to preclude clotting.
Function, effect, and goals
Blood clotting is a complex process involving a number of clotting factors designed to prevent blood from clotting in the wrong place at the wrong time. For external injuries, the situation is still relatively simple because the presence of molecular oxygen in the air can accelerate clotting. In internal bleeding, controlling the necessary clotting is much more difficult to distinguish internal bleeding, where clotting is vital, from other situations where blood must flow through constricted vessels. Here, clotting that leads to thrombus formation might not be life-saving but life-threatening. Nevertheless, certain situations are predisposed to thrombus formation, which can cause thrombosis in situ or embolism by carryover elsewhere. In cases where there are known risks of thrombus formation, relatively low-dose heparinization with mostly low-molecular-weight heparin is used for prophylactic reasons. The anticoagulant effect is intended to counteract the formation of thrombi that could lead to thrombosis, embolism, myocardial infarction or stroke. The necessary heparin must not be administered orally because it cannot be absorbed by the digestive system. Therefore, heparin is usually injected subcutaneously or administered intravenously. Obviously, evolution has deemed this option not important because heparin is synthesized by the body itself in the amount needed – mainly by the mast cells of the immune system – but the blood plasma cannot naturally reach a concentration sufficient for prophylaxis. Typically, heparinization is performed before and after surgery and in cases of persistent atrial fibrillation. In the case of artificial heart valves that are not made of biological material, lifelong heparinization or another appropriate form of anticoagulation is recommended. In addition, there is another wide range of indications for which heparinization is recommended. Almost all other indications can be related to thrombosis, embolism, or local infarction that has already occurred and been treated. When full heparinization with unfractionated heparins is used, the partial thromboplastin time must be monitored to adjust a correct dosage.
Risks, Side Effects, and Hazards
Ultimately, full heparinization with UFH always involves a certain balancing act between overdosing and underdosing.An underdose ultimately offers too little preventive effect against the formation of thrombi and thus too little protection against thrombosis, embolisms, myocardial infarction and stroke, without the fact being noticed unless the thromboplastin time is monitored, which allows conclusions to be drawn about the coagulation protection. An overdose is immediately more problematic because it can lead to internal bleeding. With heparinization – especially with UFH – heparin-induced thrombocytopenia (HIT) type I or II may develop in rare cases. Type I HIT is associated with a transient reduction in platelet count, which usually increases again independently, so that no specific treatment is usually necessary. Type II HIT, which occurs when the immune system responds to heparinization with antibodies, is much more problematic. On the one hand, the platelet count drops to less than half the normal value and the heparinization effect is reversed. The tendency to blood clotting is not inhibited but increased, so that the risk of thrombosis or embolism increases. Long-term treatment with heparin may result in osteoporotic effects with measurably decreased bone density and vertebral fractures. If any of the serious side effects are noted, heparin must be discontinued and switched to another anticoagulant. A rare side effect of heparinization is a reversible increase in transaminases in the blood plasma, which is usually an indication of damage to the liver or heart. Transaminases play an important role in the metabolism of amino acids for the transfer of amino groups. Transaminases are normally found in the cytosol of cells rather than as free enzymes in the blood.
