Thromboembolism


Deep vein thrombosis (DVT) occurs in deep large veins of lower extremities and rarely in upper limbs. With the enlargement of thrombus, an embolus may get dislodged and be trapped in lungs resulting in pulmonary thromboembolism (PE). This leads to impaired perfusion but normal ventilation resulting in intrapulmonary shunting. The right ventricle, in turn, attempts to maintain the pulmonary perfusion by overcoming the elevated pulmonary vascular resistance. This results in right ventricular strain and in extreme cases right ventricular failure may ensue. The term venous thromboembolism (VTE) incorporates both DVT and PE.

Neurosurgical patients constitute a moderate risk group for development of deep venous thrombosis and pulmonary thromboembolism. In untreated neurosurgical patients, incidence of DVT is reported to be between 18% and 50%. Incidence of PE in neurosurgical patients varies between 8% and 25%. Mechanical prophylaxis reduces the risk of DVT by 10–20%. VTE after spine surgery varies between 8.3% and 19% with symptomatic PE in only 0.2% patients. The large variation in incidence reported is due to the heterogeneity in the method of diagnosis, inclusion of symptomatic or asymptomatic patients, and whether receiving any prophylaxis or not. While PE is the most commonly recognized in hospital consequence of DVT, venous incompetence and postthrombotic syndrome are a recognized source of morbidity in patients with a history of DVT. Postthrombotic syndrome is estimated to affect 23–60% of patients with DVT.

Risk factors for development of VTE in patients are enumerated in Table 1 .

Table 1
Risk Factors for VTE
Strong risk factors Moderate risk factors Weak risk factors
  • Fracture (hip or leg)

  • Hip or knee replacement

  • Major general surgery

  • Major trauma

  • Spinal cord injury

  • Arthroscopic knee surgery

  • Central venous lines

  • Chemotherapy

  • Congestive heart or respiratory failure

  • Hormone replacement therapy

  • Malignancy

  • Oral contraceptive therapy

  • Paralytic stroke

  • Pregnancy, postpartum

  • Previous VTE,

  • thrombophilia

  • Bed rest >3 days

  • Immobility due to sitting

  • Increasing age

  • Laparoscopic surgery

  • Obesity

  • Pregnancy, antepartum

  • Varicose veins

Brain is a rich source of tissue thromboplastin which is an initiator of the coagulation cascade. Patients with brain tumors have been found to have decreased plasmin activity, increased tissue factor, and raised platelet aggregatory action. This all leads to a procoagulant state, more so in malignant tumors. In an observational study by Sawaya et al., incidence of DVT in patients with meningiomas, malignant glioma, and metastatic disease was found to be 72%, 60%, and 20%, respectively. Moreover, restricted mobility or paralysis, osmotic dehydration, long surgical duration, and corticosteroids increase risk of VTE in these patients. In a study done on 4293 neurosurgical patients who were operated for intracranial tumor, 26 (3%) patients developed VTE. The authors found poorer functional status, older age, preoperative motor deficit, high grade glioma, and hypertension each independently increased the risk of perioperative VTE.

Patients with brain tumors, paralytic stroke, subarachnoid hemorrhage, spinal cord injury, or head trauma are thus prone to develop VTE. Genetic hypercoagulability syndromes like deficiency of antithrombin C, protein C, protein S, raised antiphospholipid antibodies, and factor V leiden mutation predispose patients to development of thrombosis.

Raslan M et al. suggest that surveillance for DVT should be undertaken in high-risk patients on a biweekly schedule, otherwise individualized surveillance is necessary.

Symptoms/Signs

Distal/calf vein DVT is usually clinically asymptomatic. Most of the times, it resolves on its own and rarely extends to proximal veins. Proximal (popliteal and thigh) DVT manifests as pain and tenderness, swelling, redness, warmth, and edema. Positive Homan sign (calf pain on dorsiflexion of foot with leg extended) has poor predictive value for DVT and is not relied upon these days.

PE may manifest as dyspnea, tachypnea, pleuritic chest pain, cough and hemoptysis, fever, and tachycardia. Under anesthesia, hemodynamic instability and sudden decrease in end tidal carbon dioxide should also alert toward PE.

Symptoms of postthrombosis syndrome include pain, venous congestion, edema, skin changes, and ulcers which are difficult to treat and have a significant negative impact on the patient’s quality of life.

Diagnosis of DVT

  • D-dimer : Cross-linked fibrin on degradation produces D-dimer which can be used for diagnosis of VTE. A negative test excludes DVT and no further testing is required. However, it is nonspecific and is also raised in cases of infection, trauma, recent surgery, malignancy, and pregnancy. Levels more than 0.5 mg/L indicate VTE with a sensitivity of 99.4% and specificity of 38.2%. In postcraniotomy patients, a threshold of 2 mg/L indicates VTE with a high degree of sensitivity and specificity in patients. If D-dimer is raised, next test done is ultrasonography of proximal veins.

  • Ultrasound : Inability to compress vein lumen, distended vessel lumen, and lack of flow are the features of DVT on ultrasonography. This technique is accurate, noninvasive, and readily available. If proximal ultrasound is positive for DVT, treatment is started and further tests are not required. However, it is difficult to perform in obese patients and cannot always differentiate acute and chronic DVT.

  • Contrast venograophy : Gold standard test for diagnosing DVT is ascending contrast venography. Presence of intraluminal filling defect, nonfilling of deep venous system, or presence of collateral flow indicate the presence of DVT. The drawbacks of this technique are it is invasive, requires contrast injection, and patient needs to be mobilized.

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