Heparin is a blood anticoagulant that increases the activity of antithrombin. It is used in the treatment of heart attacks and unstable angina. Heparin is an anticoagulant medication that is used every day in every hospital in the United States and is administered by IV (intravenously) or by injection under the skin. It is used to decrease the clotting ability of the blood and to help prevent harmful clots from forming in blood vessels. Heparin is commonly called a “blood thinner”, although it does not actually thin the blood.

In cases of heparin‐induced thrombocytopenia and thrombosis (HIT or HITT), the medication causes the exact opposite effect for which it is designed. Rather than prevent blood from clotting, the administration of heparin actually causes the formation of significant and harmful blood clots!

A blood clot is essentially an accumulation of blood that clumps together in the patient’s vessels or vascular system (veins or arteries). While heparin is administered to prevent clots, every so often, heparin can sometimes trigger a reaction that causes the blood to clot excessively instead of preventing clots. It causes the patient’s immune system to make antibodies that activate platelets. Platelets are blood cells that cause your blood to clot. In the presence of heparin, excessive blood clotting puts the patient at risk of developing life-threatening blood clots (thrombosis). The reaction also causes platelet levels to drop (thrombocytopenia).

Heparin-induced thrombocytopenia is fairly common from a medical statistical standard:  approximately 5% of people who take heparin for more than four days develop HIT. This means that one (1) out of every twenty (20) patients administered heparin for more than 96 hours may suffer this adverse reaction or “allergy” to heparin.

Low levels of platelets may be an indication of HIT. About half of people with HIT develop a new blood clot, such as a deep vein thrombosis (DVT) or pulmonary embolism (PE).

Early-onset HIT appears one to three days after the patient starts taking heparin. This early form of HIT occurs when the patient has taken heparin in the past (usually within the last three months). When this happens, the body “remembers” heparin because it has already physiologically been exposed to it. The patient has essentially already created antibodies to heparin that are ready to react.

Refractory or “persistent” HIT appears and then continues in the patient even weeks after heparin has
been discontinued.

Delayed onset HIT doesn’t appear until the patient has stopped taking heparin. It starts five or more days after
heparin cessation.

In patients with an intermediate or high pretest probability of HIT, an enzyme-linked immunosorbent assay (ELISA) to detect heparin-platelet factor 4 (PF4) immunoglobulin G (IgG) antibodies is the first diagnostic step. This is commonly called the HIT 4 T's score.

Medical professionals possess a duty to recognize the 4 T's of heparin-induced thrombocytopenia.  The “4 T's” (Thrombocytopenia, Timing of platelet count fall, Thrombosis or other sequelae, and other causes for thrombocytopenia) enable the calculation of a pretest clinical score for the diagnosis of heparin-induced thrombocytopenia.

When you are hospitalized for any reason, please be aware of this potential adverse reaction to heparin.

And feel free to contact us at MANEY | GORDON Trial Lawyers should you suspect that a patient has died, or suffered amputation, or lost portions of a limb because this condition was not properly and timely recognized by hospital, medical, or nursing staff.

Contact MANEY | GORDON Trial Lawyers Today for a Heparin‐Induced Thrombocytopenia and Thrombosis Case Evaluation to determine if you qualify to file a heparin lawsuit.