Deep vein thrombosis
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.
Epidemiology
An average incidence of Deep-vein thrombosis of 24 percent was found among 474 untreated control neurosurgical patients 1).
However, based on the current literature, the incidence of Deep-vein thrombosis varies in patients with different diseases. For example, the incidence of Deep-vein thrombosis is 1.5–18% and 32% in patients with a subarachnoid hemorrhage and in patients with a brain tumor, respectively 2) 3).
In addition, the incidence of Deep-vein thrombosis after craniotomy has been reported to be as high as 50%, and using a threshold of 2 mg/L, D-dimer levels indicate venous thromboembolism with a high degree of sensitivity and specificity in patients who have undergone craniotomy 4).
In a study lower extremity Deep-vein thrombosis was a common complication following craniotomy in the enrolled Chinese neurosurgical patients. Multiple factors were identified as predictive of Deep-vein thrombosis in neurosurgical patients, including the presence of a tumor, an age greater than 50 years, hypertension, and immobility 5).
Taniguchi et al. reported an incidence of PE in neurosurgical patients with Deep-vein thrombosis of 60% 6) moreover, Deep-vein thrombosis may lead to a PE, which is lethal in up to 50% of affected neurosurgical patients 7) 8).
The rate of lower extremity Deep-vein thrombosis after neurosurgery was 31.1% in the series of Guo et al 9).
Risk factors
Diagnosis
Prophylaxis
Treatment
Complications
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.
Case series
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 10).
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 11).
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 12)