A blood clot in the lung, known medically as a Pulmonary Embolism (PE), occurs when a thrombus, typically originating from a deep vein in the leg, travels through the bloodstream and lodges in a pulmonary artery. This blockage restricts blood flow, impacting the lung’s ability to oxygenate the blood, which can rapidly become a life-threatening event. Individuals with a cancer diagnosis face a significantly elevated risk of developing these blood clots, a condition clinically termed Cancer-Associated Thrombosis (CAT). The development of CAT is a serious complication, and the resulting PE is recognized as the second leading cause of death in cancer patients, behind the progression of the cancer itself.
Mechanisms Behind Increased Risk
Cancer creates a biological environment that strongly favors the formation of blood clots, a state known as hypercoagulability. Tumor cells directly contribute to this by releasing microscopic substances that activate the body’s clotting cascade. Specifically, malignant cells express and shed Tissue Factor (TF), a potent trigger that initiates the extrinsic pathway of coagulation, leading to the formation of a fibrin clot.
The presence of cancer also triggers a systemic inflammatory response throughout the body, further promoting a pro-clotting environment. This inflammation involves the release of various signaling molecules, such as cytokines, which stimulate the liver to produce more clotting factors. This action simultaneously suppresses the body’s natural anticoagulant mechanisms, shifting the delicate balance toward thrombosis.
Beyond these molecular changes, physical and treatment-related factors also elevate the risk. A large tumor mass can press directly against nearby veins, causing blood flow to slow or pool, a phenomenon called stasis. Certain cancer therapies, including specific chemotherapy agents like cisplatin, hormonal therapies, and major surgery, can damage the inner lining of blood vessels (endothelium). Damage to the endothelium exposes underlying tissue, which acts as a powerful signal for platelets to aggregate and begin the clotting process.
Identifying Signs and Confirming Diagnosis
Recognizing the signs of a PE in a cancer patient can be challenging because the symptoms often overlap with the effects of the underlying disease or its treatments. Sudden shortness of breath, which may be new or dramatically worsened, is a common symptom that requires immediate attention. Patients may also experience sharp chest pain that is often more intense when taking a deep breath or coughing, along with a rapid heart rate or an unexplained, persistent cough.
A significant portion of PEs in cancer patients are found incidentally on imaging scans performed for other reasons, with some research suggesting up to 31% may be asymptomatic. This highlights the need for a high level of clinical suspicion, especially when a patient reports subtle changes like new lightheadedness or fatigue. When a PE is suspected, the initial step often involves a blood test for D-dimer, a product released when a blood clot breaks down.
The D-dimer test is often less definitive in cancer patients. Systemic inflammation and the malignancy itself can cause persistently elevated D-dimer levels, limiting its usefulness for ruling out a clot. The most reliable method for confirming a PE is a CT Pulmonary Angiography (CTPA), which uses an injected contrast dye and a CT scanner to visualize the blood vessels in the lungs. If a CTPA is not feasible, such as in patients with kidney impairment or a severe contrast allergy, a Ventilation/Perfusion (V/Q) scan is an alternative imaging technique.
Specialized Treatment Protocols
The treatment for CAT, particularly a confirmed PE, centers on the use of anticoagulants. These medications are designed to thin the blood and prevent the clot from growing while also reducing the risk of new clots forming. Historically, Low Molecular Weight Heparin (LMWH), administered via daily injections, was considered the standard of care for long-term treatment.
More recently, Direct Oral Anticoagulants (DOACs), such as apixaban and rivaroxaban, have emerged as alternatives. DOACs offer the convenience of a pill and demonstrate similar or superior efficacy in reducing clot recurrence in many cancer patients. However, the choice between LMWH and a DOAC is often individualized and depends on the specific type of cancer a patient has.
LMWH may still be preferred for patients with active cancers of the upper gastrointestinal or genitourinary tracts, where DOACs have been associated with a potentially higher rate of major bleeding. The complex nature of cancer treatment necessitates careful consideration of drug interactions between the anticoagulant and the patient’s chemotherapy regimen. Treatment duration for CAT is typically extended, often continuing for at least six months or as long as the cancer remains active.
In rare situations where a patient cannot safely receive any anticoagulant due to an extremely high bleeding risk, a temporary Inferior Vena Cava (IVC) filter may be considered. This device physically traps clots before they can reach the lungs.