Deep vein thrombosis is a condition in which a blood clot forms most often in the deep veins of the leg, groin, or arm (known as Deep-Vein Thrombosis) and travels in the circulation, lodging in the lungs (known as pulmonary embolism, PE).
The main hazard of Deep-vein thrombosis is acute stage thrombus shedding, which can cause a pulmonary embolism (PE) and acute respiratory distress syndrome when the blood flow blocks the pulmonary artery
Contributes significantly to the morbidity and mortality of neurosurgical patients.
Symptomatic Deep-Vein Thrombosis or pulmonary embolism.
Non-specific signs may include pain, swelling, redness, warmness, and engorged superficial veins. Pulmonary embolism, a potentially life-threatening complication, is caused by the detachment (embolization) of a clot that travels to the lungs.
Together, Deep-vein thrombosis and pulmonary embolism constitute a single disease process known as venous thromboembolism. Post-thrombotic syndrome, another complication, significantly contributes to the health-care cost of Deep-vein thrombosis. Prevention options for at-risk individuals include early and frequent walking, calf exercises, anticoagulants, aspirin, graduated compression stockings, and intermittent pneumatic compression.
In 1856, German pathologist Rudolf Virchow postulated the interplay of three processes resulting in venous thrombosis, now known as Virchow's triad: a decreased blood flow rate (venous stasis), increased tendency to clot (hypercoagulability), and changes to the blood vessel wall. Deep-vein thrombosis formation typically begins inside the valves of the calf veins, where the blood is relatively oxygen deprived, which activates certain biochemical pathways. Several medical conditions increase the risk for Deep-vein thrombosis, including cancer, trauma, and antiphospholipid syndrome. Other risk factors include older age, surgery, immobilization (as with bed rest, orthopedic casts, and sitting on long flights), combined oral contraceptives, pregnancy, the postnatal period, and genetic factors such as a non-O blood type. The frequency of occurrence (incidence) increases dramatically from childhood to old age; in adulthood, about 1 in 1000 adults develops Deep-vein thrombosis annually.
Medical records of Japanese adult patients with craniotomy for brain tumor were reviewed. In addition to clinical variables including patients' age, sex, body mass index, previous history of Deep-vein thrombosis, leg paresis, medications, tumor histology, surgical factors, adjuvant therapy, infection, and duration of post-operative immobilization and hospitalization, plasma D-dimer levels were measured at pre-surgery (baseline), on post-operative day (POD) one to 30 and during adjuvant therapy, and were compared between patients with and without Deep-vein thrombosis.
Thirteen of 61 patients (21.3%) had Deep-vein thrombosis after surgery with mechanical prophylaxis. All Deep-vein thrombosiss were asymptomatic. Multivariate analyses found post-operative infection (odds ratio, 12.15; 95% confidence interval, 1.09-134.98; P = 0.03) to be a sole independent risk factor for Deep-vein thrombosis. D-dimer levels were not significantly different between patients with and without Deep-vein thrombosis at baseline and POD 1-30, but were significantly elevated during adjuvant therapy in patients with Deep-vein thrombosis (P = 0.03).
Not a few Japanese patients developed Deep-vein thrombosis after brain tumor surgery with mechanical prophylaxis, and patients with infection should be carefully monitored for post-operative Deep-vein thrombosis 1).
There is a common belief that the administration of anticoagulants to patients with brain tumors is contraindicated. Between 1982 and 1986, 50 patients with deep venous thrombosis and pulmonary emboli and brain tumors were examined and treated. Twenty-four patients received an inferior vena cava Greenfield filter and 25 patients were treated with anticoagulants. One patient was terminal and received no therapy. Patients in each group were similar with regard to age, sex, primary tumor, computed tomographic findings, and ultimate outcome. At the time of diagnosis, all patients had a residual tumor and most had significant cerebral edema and midline shift. There were no complications in the group receiving Greenfield filters. One patient had a pulmonary embolus after the filter was placed and later required anticoagulant therapy. In the group receiving anticoagulants, one patient had focal intraventricular bleeding observed incidentally on computed tomographic scan one month after beginning anticoagulant therapy and was totally asymptomatic. One patient had gastrointestinal tract bleeding five days after beginning anticoagulant therapy with heparin sodium, and the therapy was therefore discontinued. No other patient had significant bleeding. In view of these findings, a reevaluation of anticoagulant therapy in patients with central nervous system tumors is warranted 2).
Kaufman HH, Satterwhite T, McConnell BJ, Costin B, Borit A, Gould L, Pruessner J, Bernstein D, Gildenberg PL. Deep-Vein Thrombosis and pulmonary embolism in head injured patients. Angiology. 1983 Oct;34(10):627-38. PubMed PMID: 6226216 3)