الفهرس 
Magnitude of the Problem
Potential Application of Risk AssessmentOnly 14 pages are availabe for public view
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Abstract
Venous thromboembolism (VTE), includes both
deep vein thrombosis (DVT) and pulmonary embolism
(PE), is the second-leading causes of death in hospitalized
and ambulatory cancer patients. The risk of VTE in cancer
patients is increased three- to five fold for those who are
undergoing surgery and 5-6 folds for those who are
receiving chemotherapy.
In the 19th century, the association between
thrombosis and malignancy was described in 1823 by
Bouillaud and then in 1865 by Armand Trousseau and is
now often referred to as Trousseau syndrome. A few years
later, in 1878, histological evidence for tumor cells within a
thrombus was founded by Theodor Billroth.
This rate of venous thromboembolism (VTE) in
patients with cancer is greater than that in patients without
cancer and chemotherapy increases the risk to a greater
fold.
The mechanism of the so-called ―Trousseau‘s
syndrome‖ probably includes all aspects of Virchow’s triad:
stasis of blood, trauma or pathology of the endothelium and
hypercoagulability of the blood itself. The pathogenesis of VTE in cancer patients is
complex and involves the interplay of multiple factors –
related to the tumor itself, patient and anticancer therapies.
Several biomarkers were identified as potential
predictors of VTE events. These include elevated platelet
and leukocyte counts, decreased hemoglobin, elevated Ddimer, elevated prothrombin activation products, elevated
soluble P-selectin, peak thrombin generation and elevated
levels of TF bearing microparticles.
Risk assessment includes 5 parameters known as
―Khorana-Score‖ include:
1. Site of cancer (Very high risk (stomach, pancreas) -
High risk (lung, lymphoma, gynecologic, bladder,
testicular)),
2. Platelet count (≥350,000/μL),
3. Hemoglobin (<10 g/dL) and/or use of erythropoiesisstimulating agents,
4. Leukocyte count (>11,000/μL), and
5. Body mass index (BMI) (35 kg/m² or more) to predict
chemotherapy-associated thrombosis in cancer patients.This risk scoring model expanded by inclusion of two
further biomarkers, sP-selectin (>53.1 ng/mL) and D-dimer
(>1.44ug/ml).
The diagnosis of VTE is done through:
1- Clinical presentation (including sign, symptoms &
differential diagnosis),
2- Clinical likelihood assessment (through well’s score &
revised Geneva score),
3- Laboratory testing (including Plasma D-dimer, imaging
duplex ultrasound, chest CT, Magnetic Resonance
angiography).
The typical symptoms of DVT include pain,
heaviness, cramps in the lower extremity, particularly in the
calf, which may progress slowly or may suddenly
accelerate more rapidly leading to swelling and blue-red or
cyanotic discoloration.
Signs of DVT include Low grade pyrexia, increase in
heart rate, tenderness of the veins in the popliteal region,
calf or over the distribution of the deep veins, because
soreness and pain is the most common.
Typical presentations of PE comprise acute dyspnea,
chest pain, or coughing with or without hemoptysis. It is important to consider syncope as a characteristic, albeit
infrequent presentation of PE.
Characteristic signs of pulmonary embolism include
tachycardia and tachypnea. On auscultation, there is typical
pleural leather rub and crackles. Pain is often caused by
pleural inflammation due to peripheral emboli causing
pulmonary infarction, alveolar hemorrhage, hemoptysis.
ECG changes are describes and arterial blood gas analysis
typically shows hypoxia, hypocapnia and respiratory
alkalosis, but sometimes show normal values.
VTE may result in the debilitating long-term
complications of post-thrombotic syndrome of the legs and
chronic thromboembolic pulmonary hypertension which
can be fatal where there is sudden cardiac death during
exertion.
Treatment and prophylaxis of venous thromboembolism is
maintained through:
1. Pharmacological agents including include:
Parenteral anticoagulants (Unfractionated heparin,
low molecular weight heparin, Fondaparinux),
Oral antithrombotics: (Warfarin (VKA), New oral anticoagulants including (dabigatran,
rivaroxaban),
Oral antiplatelet drug (aspirin).
2. Mechanical methods include elastic stockings and
intermittent pneumatic compression.
3. Vena Cava filter are the main ways of preventing
thrombosis and the central venous catheter thrombosis.