Platelet administration, thrombocytopenia

Other adverse reactions associated with penicillin are hematopoietic changes such as anemia, thrombocytopenia (low platelet count), leukopenia (low white blood cell count), and bone marrow depression. When penicillin is given orally, glossitis (inflammation of the tongue), stomatitis (inflammation of die mouth), dry mouth, gastritis, nausea, vomiting, and abdominal pain occur. When penicillin is given intramuscularly (IM), there may be pain at die injection site Irritation of the vein and phlebitis (inflammation of a vein) may occur witii intravenous (IV) administration. 

More than half of the patients receiving this drug by the parenteral route experience some adverse reaction. Severe and sometimes life-threatening reactions include leukopenia (low white blood cell count), hypoglycemia (low blood sugar), thrombocytopenia (low platelet count), and hypotension (low blood pressure). Moderate or less severe reactions include changes in some laboratory tests, such as the serum creatinine and liver function tests. Other adverse reactions include anxiety, headache, hypotension, chills, nausea, and anorexia Aerosol administration may result in fatigue a metallic taste in the mouth, shortness of breath, and anorexia... 

A complete blood count, platelets, and stools for occult blood may be ordered periodically throughout therapy. Thrombocytopenia may occur during heparin administration. A mild, transient thrombocytopenia may occur 2 to 3 days after heparin therapy is begun. This early development of thrombocytopenia tends to resolve itself despite continued tiierapy. The nurse reports a platelet count of less than 100,000 mm3 immediately because die primary care provider may choose to discontinue die heparin therapy. 

Heparin, which has an anticoagulation action, may give rise to heparin-induced thrombocytopenia, which is an immune-mediated condition that usually develops 5-10 days after the administration of the drug. When heparin is used, a platelet count should be measured before treatment and if administration is repeated, platelet counts should be monitored regularly. Signs of thrombocytopenia include a reduction in platelet count. It may present with spontaneous haemorrhage and heparin should be stopped. Factor VIII is used in the treatment and prophylaxis of haemorrhage in patients with haemophilia. 

TPO should alleviate thrombocytopenia in most instances by encouraging platelet production. Currently, the standard therapy for the condition entails administration of 5 units of platelets to the sulferer (1 unit equals the quantity of platelets derived in one sitting from a single blood donor). TPO therapy is a particularly attractive potential alternative because ... 

The following points should be considered in all patients receiving heparin Platelet counts should be performed frequently thrombocytopenia appearing in a time frame consistent with an immune response to heparin should be considered suspicious for HIT and any new thrombus occurring in a patient receiving heparin therapy should raise suspicion of HIT. Patients who develop HIT are treated by discontinuance of heparin and administration of a direct thrombin inhibitor or fondaparinux (see below). 

In four patients with von Willebrand disease, desmopressin caused a significant but transient reduction in platelet count without an increase in plasma glycocalicin concentrations nor enhanced expression of P selectin, suggesting that acute thrombocytopenia after the administration of desmopressin in type 2B von Willebrand disease is not related to platelet activation and consumption (68). 

The bleeding potential is similar among the agents. However, thrombocytopenia, particularly profound thrombocytopenia (platelet count <50,000 mrrT3) occurs with a two-to four-fold higher frequency with abciximab (0.4— 1.0%) compared with eptifibatide (0-0.2%) or tirofiban (0,1 —0.3%) (6), The exact mechanism of this difference is not clear, However, immune complex-mediated reaction (due to an anamnestic response to the humanized chimeric antibody) may contribute to rapid precipitation of thrombocytopenia with abciximab (6), Platelet counts should, therefore, be measured early (within the first one to four hours) after administration of these agents and followed for the duration of therapy. Platelet transfusion should be considered for profound thrombocytopenia with or without serious bleeding (6). 

ASPIRIN SSRIs Possible t risk of bleeding with SSRIs Uncertain. Possible additive effects including inhibition of serotonin release by platelets, SSRI-induced thrombocytopenia, and 1 platelet aggregation Avoid co-administration with high-dose aspirin... 

Positive human anti-chimeric antibodies have been detected in 6% of patients (generally in low titers) but were not associated with hypersensitivity or allergic reactions. Preliminary data indicate that abciximab can be safety readministered, although a greater incidence of thrombocytopenia after administration has been reported with a lesser efficacy of platelet transfusion (12). 

Type I heparin-induced thrombocytopenia is common and is characterized by a mild transient thrombocytopenia (with platelet counts that usually do not fall below 50 X 10 /1) the thrombocytopenia occurs on the first few days of heparin administration (usually 1-5 days) and requires careful monitoring but not usually withdrawal of heparin. Type I thrombocytopenia is generally harmless and very probably results from direct heparin-induced platelet aggregation. Thrombocjdopenia is most common when large doses of heparin are used, or in some particular circumstances, such as after thrombolytic therapy (35) or in the early orthopedic postoperative period (36) it can abate in spite of continued therapy. Tjrpe I thrombocytopenia is a non-immune reaction, probably due to a direct activating effect of heparin on platelets. 

Although inhibition of stem-cell proliferation is the most likely mechanism of hematological toxicity, increased platelet hepatic uptake has been suggested to account for thrombocytopenia (227). Raised serum thrombopoietin concentrations were found in patients with interferon alfa-induced thrombocytopenia (228). However, there is evidence that serum thrombopoietin concentrations in patients who have had thrombocytopenia during interferon alfa treatment for chronic viral hepatitis C either do not increase (in patients with compensated cirrhosis) or increase only moderately and less than expected (in non-cirrhotic patients) (229). The authors proposed that interferon alfa impairs liver production of thrombopoietin, raising the possibility of testing thrombopoietin administration in patients with severe thrombocytopenia before or during treatment with interferon alfa (230). 

Interferon alfa-induced immune-mediated thrombocytopenia shares many features with idiopathic thrombocytopenic purpuras and may be therefore coincidental (SED-13, 1094) (SEDA-20, 328) (SEDA-21, 371), but recurrence of thrombocytopenia on interferon alfa readministration strongly supports a causal role of interferon alfa (232). Cross reaction with interferon beta was not found in an isolated report (SEDA-20, 329). Even though severe and even fatal worsening of idiopathic thrombocjdopenic purpura has been observed after administration of interferon alfa (SED-13, 1094) (SEDA-20, 328), interferon alfa was not considered harmful in patients with chronic hepatitis C who were previously positive for platelet-associated immunoglobulin G (233). 

Hematological abnormalities have been found to be associated with prolonged administration of intravenous fat emulsion in children on a program of long-term cyclic parenteral nutrition. Recurrent thrombocytopenia is common and platelet lifespan is reduced. In one study (80), thrombocytopenia occurred in 66% of patients, but most of these had taken drugs that might have interfered with platelet function. Hypercoagulability was not found in the majority of cases. 

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