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Thrombocytopenia

Essentials

  • Discontinue drugs that influence the functioning of platelets, as necessary.
  • If the thrombocytopenic patient has symptoms of bleeding, hospitalization is advisable.

Basic rules

  • The pathophysiological mechanism of thrombocytopenia (blood platelet count < 150 × 109 /l) may be
    • decreased production in the bone marrow
    • increasedconsumption
    • increased sequestration in the spleen.
  • When blood thrombocyte level < 100 × 109 /l is detected in a patient for the first time, examining blood smear or taking a sample in a citrate tube is recommended (investigation of pseudothrombocytopenia)..
  • Thrombocytopenia is a symptom, the cause of which should be clarified.
  • Typical manifestations of thrombocytopenia are skin bruising and petechiae and mucous membrane bleeding.
    • In particular, gum and nasal bleeding is common. Bleeding may also take place in the gastrointestinal and urinary tracts after surgery of the prostate gland or urinary tract.
    • Menorrhagia is also common.
  • A tendency towards bleeding is uncommon if the platelet count is 50-100 × 109 /l. Platelet concentrations of 10-50 × 109 /l are frequently associated with spontaneous bleeding and haemorrhages may be severe with platelet counts of < 10 × 109 /l. Drugs that affect the platelet function (ASA and ADP receptor blockers, e.g. clopidogrel, ticagrelor, prasugrel) increase bleeding tendency already in a rather moderate thrombocytopenia. Concurrent anticoagulation therapy also increases bleeding risk in a patient with thrombocytopenia.

Causes of thrombocytopenia

Decreased production

Increased consumption

  • Inborn causes
    • Non-immunological (haemolytic disease of the newborn, prematurity, maternal pre-eclampsia, infections)
    • Immunological alloimmune neonatal thrombocytopenia, maternal idiopathic thrombocytopenia purpura (ITP)
  • Acquired causes
    • Non-immunological (infections, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, haemolytic-uraemic syndrome, drug-induced over-consumption of platelets)
    • Immunological (drug-induced, following blood transfusion, chronic and acute ITP Bruises and Purpura in Children)

Platelet sequestration

  • Hypersplenism

Loss of platelets

  • Acute haemorrhage
  • Haemoperfusion

Clinical approach

Symptomless patient, platelet count 100-150 × 109 /l

  • The general practitioner can safely follow the situation, initially at intervals of a few months, if the blood picture otherwise is normal (no anaemia, no neutropenia etc.). If no underlying disease becomes evident and thrombocytopenia remains stable, no further follow-up is required. All drugs causing thrombocytopenia should be avoided if possible. Alcohol consumption habits should be discussed.
  • Many drugs cause thrombocytopenia relatively frequentlyhttp://www.ouhsc.edu/platelets/. These include heparin, quinidine, chloroquine, salicylates, sulphonamides, thiazides, allopurinol, phenytoin, carbamazepine and trimethoprim.
    • NSAIDs (especially acetosalicylic acid) and some other medicines (clopidrogel, ticagrelor, prasugrel) frequently impair platelet function and bring about a bleeding tendency. This tendency is disproportionately strong among thrombocytopenic patients.
    • Paracetamol does not to impair platelet function.

Symptomless patient, platelet count < 100 × 109 /l

  • Besides assessing the medication used by the patient, basic investigations are performed: complete blood count and, at discretion, bone marrow examination.
  • If the situation does not improve, referral to a specialist in haematology is advisable.

If a thrombocytopenia patient has symptoms of bleeding

  • He/she needs specialist care
  • It is important to detect the possible cause. Remember that the list of drugs possibly causing thrombocytopenia is very long. All these drugs should be avoided.

ITP

  • Treatment is planned by a haematologist, a specialist in internal medicine or a paediatrician.
  • In adults, prednisone or prednisolone is the first-line therapy. The starting dose is 1-2 mg/kg/day orally. Dexamethasone 40 mg/day for 4 days may be used as an alternative.
    • With a glucocorticoid, response to treatment is often achieved in 1-4 weeks. A partial response to treatment is achieved in 70-90% of cases, but a good one in only 30-50% of the patients.
    • After a response is observed, the drug is tapered to the smallest dose possible; the objective is a platelet count > 50 × 109 /l, with no symptoms of bleeding.
  • ITP in children is often a self-limited postinfectious condition Bruises and Purpura in Children.
  • Fibrinolysis inhibitors (tranexamic acid) may be used to reduce menorrhagia, severe nasal bleeding, and bleeding in the gastrointestinal or urinary tracts. Massive bleeding is compensated with red cells, fresh-frozen plasma and platelet concentrates.
  • In hospital care, intravenous gammaglobulin infusions may induce a response faster than glucocorticoids. This is well suited for situations when it is necessary to normalize the platelet count quickly. As second-line treatment, non-responders are often treated with rituximab; splenectomy can also be considered. Thrombopoietin-receptor agonists (romiplostim, eltrombopag) represent one option for the management of chronic ITP. These treatments are decided by a physician well versed in haematology.