- Stop drugs possibly causing thrombocytopenia unless vitally indicated.
- If the thrombocytopenic patient has symptoms of bleeding, immediate hospitalization is advisable.
- Remember the possibility of so-called pseudothrombocytopenia.
- The pathophysiological mechanism of thrombocytopenia (blood platelet count < 150 × 109/l, in late pregnancy < 120 × 109/l) may be
- decreased production in the bone marrow
- increased sequestration in the spleen.
- Artificially low platelet counts are occasionally obtained when counted from EDTA-anticoagulated blood (pseudothrombocytopenia). When thrombocytopenia (< 100 × 109/l) is detected in a patient for the first time, the same blood sample should be checked manually for the presence of thrombocyte aggregates.
- 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.
- 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 are often severe with platelet counts of < 10 × 109/l. Drugs that affect the platelet function (ASA, clopidogrel) increase bleeding tendency already in a rather moderate thrombocytopenia.
Causes of thrombocytopenia
- Inborn causes
- Inherited thrombocytopenias (rare)
- Fanconi's anaemia
- Acquired causes
- Aplastic anaemia
- Bone marrow infiltrates (carcinoma, leukaemia, myelofibrosis, myelodysplasia, tuberculosis)
- Ionizing radiation, other causes of myelosuppression (cytotoxic chemotherapy)
- Drugs (trimethoprim-sulfamethoxazole, gold, thiazide diuretics, oestrogens, interferons)
- Deficiency of vitamins and other essential trace elements or nutrients (B12, folate, iron)
- Viral infections
- Heavy drinking
Platelet sequestrationLoss of platelets
- 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 )
- Acute haemorrhage
Symptomless patient, platelet count 100–150 × 109/l
Symptomless patient, platelet count < 100 × 109/l
- The general practitioner can safely follow the situation, initially at intervals of a few months. 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 frequently[C]. These include heparin, quinidine, chloroquine, gold, salicylates, sulphonamides, thiazides, allopurinol, phenytoin, carbamazepine and trimethoprim.
- NSAIDs (especially acetosalicylic acid) and some other medicines (clopidrogel) 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.
If a thrombocytopenia patient has symptoms of bleeding
- Besides assessing the medication used by the patient, basic investigations are performed: haemoglobin, leucocyte count and differential, platelet count and bone marrow examination.
- If the situation does not improve, referral to a specialist in internal medicine or haematology is advisable.
- 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.
- Treatment is planned by a specialist in internal medicine, a paediatrician or haematologist.
- In adults, predniso(lo)ne continues to be the first-line therapy. The starting dose is 1–2 mg/kg/day. Response to treatment is often achieved in 1–4 weeks. At least a partial response is observed in 70–90% of cases, but a good one (i.e. platelet count > 100 × 109/l) in only 30–50% of the patients. After a maximal response is observed, the drug is slowly (over weeks) tapered to the smallest dose resulting in an acceptable clinical situation, say a platelet count > 50 × 109/l, with no symptoms of bleeding. ITP in children is often a self-limited postinfectious condition .
- Intravenous gammaglobulin infusions may induce a response faster than corticosteroids. Non-responders are treated with immunosuppressants or splenectomy.
- Fibrinolysis inhibitors may be used to reduce excessive mucous membrane haemorrhages, such as nasal, gastrointestinal and urinary tract bleeding and menorrhagia. Platelet transfusions are effective if no platelet antibodies are present. Massive bleeding is compensated with red cells, fresh-frozen plasma and platelet concentrates.
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