Bleeding is a frequent and serious complication for individuals with cancer, ranging from minor bruising to severe, life-threatening hemorrhage. The cause is multifactorial, depending heavily on the specific cancer type, its stage, and the treatment regimen. Understanding these different mechanisms is crucial for prevention and management.
Systemic Causes: Low Platelets and Coagulation Defects
The most common systemic driver of generalized bleeding is thrombocytopenia, a deficiency in the blood’s ability to clot due to low platelet counts. Platelets form the initial plug at a vascular injury site; a low count drastically impairs this hemostatic function. This reduction often stems from myelosuppression, where chemotherapy or radiation therapy damages the bone marrow cells that produce platelets.
The cancer itself can also directly suppress the marrow, such as when malignant cells from breast, lung, or prostate cancer infiltrate the bone marrow space. Some chemotherapeutic agents, including platinum-based regimens, can trigger an immune-mediated destruction of circulating platelets, accelerating their clearance. The resulting platelet deficit makes the patient susceptible to spontaneous bleeding, particularly when counts fall below 10,000 per microliter of blood.
A second systemic cause involves defects in the plasma-based coagulation cascade, which provides the fibrin mesh to stabilize the initial platelet plug. Cancers that metastasize to the liver can impair the organ’s function, reducing its ability to synthesize necessary clotting factors (Factor II, VII, IX, and X). A severe complication is Disseminated Intravascular Coagulation (DIC), a paradoxical disorder where the cancer triggers widespread, inappropriate activation of the clotting system.
In DIC, the body rapidly consumes platelets and clotting factors across numerous small vessels, leading to exhaustion where the blood cannot clot when injury occurs. This consumptive coagulopathy results in a high risk of both internal bleeding and microvascular thrombosis simultaneously. Specific hematologic malignancies, such as acute promyelocytic leukemia, are known to trigger this life-threatening systemic malfunction.
Localized Causes: Direct Tumor Erosion
While systemic failure often causes minor, generalized bleeding, localized tumor erosion is responsible for many severe, acute hemorrhagic episodes. Malignant tumors are highly aggressive, growing into and destroying the surrounding healthy tissue and blood vessel infrastructure. As the tumor mass expands, it can erode the wall of a major artery or vein, leading to sudden, catastrophic bleeding.
The blood vessels within the tumor mass itself are also a source of fragility, often exhibiting abnormal and disorganized structures due to rapid, unregulated angiogenesis. These structurally compromised vessels lack the integrity of normal blood vessels and are prone to rupture or chronic oozing. Tumors in certain anatomical locations carry a high risk of localized bleeding due to their proximity to highly vascularized areas.
Tumors in the gastrointestinal tract, such as those in the stomach or colon, are frequent sources of bleeding, presenting as blood in the stool or vomit. Lung tumors near the central airways or major pulmonary vessels can cause hemoptysis (coughing up blood). In these cases, the bleeding is a direct mechanical consequence of the tumor mass breaching the vascular network.
Secondary and Iatrogenic Risk Factors
Beyond the direct effects of the cancer, various secondary factors and treatments can significantly increase a patient’s risk of hemorrhage. The high rate of venous thromboembolism (VTE) in cancer patients necessitates the use of anticoagulants, which inherently elevates the risk of bleeding. Patients on drugs like warfarin or direct oral anticoagulants (DOACs) have a higher incidence of bleeding complications compared to non-cancer patients receiving the same medications.
Certain non-chemotherapy cancer drugs directly interfere with vessel maintenance and healing. Anti-angiogenic agents, such as bevacizumab, inhibit the formation of new blood vessels, which also disrupts the integrity of existing vasculature, making them susceptible to rupture. Infections and sepsis also compound the problem, as severe systemic infection can exacerbate existing coagulopathies like DIC or damage the endothelial lining of blood vessels, leading to leakage.
Treatments like chemotherapy and radiation can cause damage to the mucosal linings throughout the body, leading to bleeding distinct from clotting failure. Mucosal damage in the gastrointestinal tract or bladder, termed mucositis, creates raw, ulcerated surfaces that bleed easily. This treatment-induced injury is independent of the platelet count and provides an open portal for blood loss.