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Adverse event reporting can be found at the bottom of the page
Prescribing information for Fragmin® (dalteparin sodium) can be found here. Adverse event reporting can be found at the bottom of the page.
In addition to cancer, patients who also have thrombocytopenia, acute kidney injury and liver disease are at an increased risk of bleeding which can be fatal. In patients with significant bleeding risk, treating cancer-related venous thromboembolism (VTE) with an anticoagulant must outweigh risks of fatal bleeding.1-13
Each patient and their risks should, therefore, be assessed on a case-by-case basis.
Thrombocytopenia is a common problem in cancer patients. It can result either from chemotherapy or radiation treatment, or from an underlying disease itself.1
Patients with low platelet counts are at risk of bleeding, in combination with cancer as a risk factor for bleeding, thrombocytopenia in this circumstance can be especially dangerous.1
Thrombocytopenia generally arises from an imbalance of platelet production from the bone marrow vs destruction in circulation.2
It may be that your patients’ cancer treatment is, in fact, contributing to this imbalance (causes of imbalance highlighted in table below) but pausing chemotherapy or radiation treatment is not always possible only to restore the platelet count.2
Bone marrow suppression due to tumour involvement
Treatment-related bone marrow suppression
In thrombocytopenic patients, additional risk factors may occur. For example, a reduction in haematological parameters due to cancer-related bone marrow dysfunction which induce coagulation, (erythrocytes or leukocytes) may lead to bleeding.3
In patients who are already at high risk of bleeding, and with low platelet counts, anticoagulation treatment will reduce their clotting capability, and further increase their risk of bleeding.3
Choosing the right anticoagulant, monitoring patients on an individual basis and adapting treatment is key to positive treatment outcomes.1
Renal failure is a risk factor for bleeding.4,5
In addition to any pre-existing chronic renal insufficiency, patients with cancer are at risk of developing acute kidney injury (AKI) as a result of their disease or treatment.6
AKI in patients with cancer can be caused either by pre-renal (abnormalities in the blood before it reaches the kidney), intrinsic (within the kidney tissue) or post-renal (obstruction in urinary tract) factors which should be monitored regularly through biochemical assays.7
While many of the symptoms of AKI are present in combination or association with other diseases, some of these, such as dehydration and intravascular coagulation are related to the malignancy itself or to treatment.7
It is important to be aware of asymptomatic kidney disease which may lead to renal failure.
Abnormalities in kidney function can alter plasma volume, resulting in renal toxicity or dysregulation of coagulation factors, leading to bleeding or thromboses.6,8-11
Sepsis
Extracellular dehydration (diarrhoea, mucitis, vomiting)
Sinusoidal obstruction syndrome (formerly called hepatic veno-occlusive disease)
Drugs (e.g., ACE inhibitors, NSAIDs, cyclosporine)
Capillary-leak syndrome (IL2)
Intra-renal obstruction (e.g., urate crystals, light chain, and some medications)
Extra-renal obstruction (e.g., retroperitoneal fibrosis, ureteral or bladder outlet obstruction by tumour)
Patients with liver disease are at an increased risk for both bleeding and thrombosis.12
The liver synthesises coagulation factors, anticoagulants, proteins involved in fibrinolysis and the platelet production regulator, thrombopoietin. Importantly, hepatic dysfunction perturbs the clotting process.12
Cancer itself increases the risk of bleeding and thrombosis. Therefore, combined with liver disease, hepatic insufficiency can put patients at further risk.
Chemotherapeutic agents, radiotherapy and other drugs can be associated with mild to severe hepatotoxicity thus having detrimental effects on liver function and lead to bleeding.13
Thrombopoietin is the major regulator of platelet production.9 Thrombopoietin dysregulation as a result of cancer-related liver damage can cause decreased platelet production.12
Patients with liver disease have dysregulated levels of clotting factors and natural anticoagulants.12
Liver dysfunction can result in dysregulation of fibrinolytic factors, creating significant challenges in thrombosis and haemostasis.12
Molecules released by the liver in response to hepatotoxicity (such as nitric oxide) can alter platelet signalling and function.9,12
Cancer is a highly complex, multifactorial disease. As clinicians you should be monitoring several factors in your patients to ensure they are receiving the most suitable cancer and anticoagulant treatment, minimising risks associated with thrombosis and haemostasis.
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PP-UNP-GBR-7812. January 2024