Introduction 

Thrombophilia is a medical disorder that increases the likelihood of developing abnormal blood clots. The condition can be inherited as a result of genetic abnormalities or acquired. While blood clot formation is a normal physiological process that avoids excessive bleeding, patients with thrombophilia exhibit an increased clotting response, which can result in life-threatening problems such as deep vein thrombosis (DVT) and pulmonary embolisms (PE).¹

Surgical operations change the body's haemostatic equilibrium, which increases the risk of clot formation as a result of vascular injury, inflammatory reactions, and prolonged immobilisation As thrombophilia already increases the risk of blood clot formation, surgery being conducted on these individuals will only exacerbate this, demanding an organised strategy of risk management prior to, during, and following surgery. Post-operative management entails thorough risk categorisation, anticoagulant therapy modifications, mechanical prophylaxis, and close postoperative monitoring.¹

Types and causes of thrombophilia

Thrombophilia can be categorised as either hereditary (genetic) or acquired. Both categories influence blood coagulation pathways, increasing the risk of venous thromboembolism (VTE).²

Inherited thrombophilia

Inherited (genetic) thrombophilia is triggered by gene mutations that control coagulation proteins. The most prevalent inherited thrombophilic diseases are: 

• Factor V Leiden Mutation - The most common hereditary thrombophilia. It is caused by a mutation in the F5 gene that renders Factor V, a coagulation protein, resistant to deactivation by activated Protein C, resulting in sustained clotting activity²
• Prothrombin G20210A Mutation - A mutation that causes enhanced production of prothrombin, a critical clotting agent, and so enhances the clot formation process²
• Protein C and Protein S Deficits - These proteins control anticoagulation processes. Their insufficiency causes abnormal clotting²
• Antithrombin III Deficiency - A rare but severe illness in which the absence of antithrombin, a natural thrombin inhibitor, raises the risk of thrombosis²

Acquired thrombophilia

Instead of hereditary mutations, acquired thrombophilia can be caused by lifestyle factors and other diseases. The most frequent causes are: 

• Antiphospholipid Syndrome (APS) - An autoimmune condition in which the body creates antibodies that cause clot formation, resulting in recurrent miscarriages and VTE³
• Cancer-Associated Thrombophilia - Malignancies, particularly pancreatic and ovarian malignancies, can cause hypercoagulability due to higher yields of procoagulant substances³
• Long-term immobilisation, such as post-surgical bed rest, promotes venous stasis and increases the likelihood of thrombosis³
• Hormone Therapy and Pregnancy - Oestrogen-containing oral contraceptives and pregnancy can cause hypercoagulability by boosting clotting factor synthesis and decreasing fibrinolysis⁴

Understanding the kind of thrombophilia is critical for surgical planning, since each thrombophilic disorder necessitates distinct anticoagulation methods.

Surgical risk stratification and preoperative management

Assessing thrombotic risk

A preoperative risk assessment is critical for determining the optimal anticoagulation regimen. The Caprini Risk Score is a commonly used instrument for determining particular thrombotic risk based on medical history, the type of surgery being performed, and concurrent comorbidities.⁵

Patients are classified as follows:

• Low-risk (0-1 points) - Minimal thromboprophylaxis is necessary
• Moderate risk (2-4 points) - Entails mechanical or pharmacologic prevention
• High-risk (5+ points or a history of VTE) - Intensive anticoagulation and long-term thromboprophylaxis are required

Individuals having a history of VTE or high-risk thrombophilia (for example, homozygous Factor V Leiden mutation, APS) are considered extremely susceptible and require individualised perioperative anticoagulation programs.⁵

Perioperative anticoagulation strategies

The perioperative (time around the surgery) treatment of anticoagulation requires a balance between thrombosis prevention and bleeding risk.

Patients on long-term anticoagulants, such as warfarin or direct oral anticoagulants (DOACs), may need bridging treatment with low molecular weight heparin (LMWH) or unfractionated heparin (UFH).⁶

Warfarin is routinely discontinued 5 days before surgery, with INR monitored to ensure it falls below 1.5 before the procedure. In high-risk individuals, LMWH is used as a bridge.⁶

Direct oral anticoagulants (DOACs) such as apixaban and rivaroxaban are typically discontinued 24-48 hours before surgery, based on renal function and bleeding risk.⁶ Prophylactic LMWH is begun before surgery in patients who are not on chronic anticoagulation but have a significant thrombotic risk, particularly in orthopaedic and large abdominal procedures.⁶

Intraoperative considerations

Throughout surgery, mechanical prophylaxis such as intermittent pneumatic compression (IPC) devices and graded compression stockings are utilised to decrease venous stasis⁷.Anaesthetic procedures also have an impact on thrombotic risk; for example, regional anaesthesia is linked with a reduced incidence of VTE than general anaesthesia.⁷

Haemodynamic stability is critical because hypotension and hypoxia might predispose individuals to thrombosis. To limit prothrombotic stimuli, surgical teams should also shorten operating times and avoid excessive tissue stress.⁷

Postoperative thromboprophylaxis

Postoperative care is essential for avoiding thrombosis. Early ambulation (patient’s ability to move independently or with assistance) dramatically lowers the incidence of VTE by enhancing venous circulation. Mechanical prophylaxis (IPC devices, compression stockings) must be used for high-risk individuals until complete mobility is restored.⁸

Pharmaceutical prophylaxis, the choice to restart anticoagulation after surgery is based on the risk of bleeding. In most cases: 

• LMWH is restarted 12-24 hours after surgery, if there are no ongoing bleeding issues⁹
• DOACs or warfarin are continued within 48-72 hours, typically concurrently with LMWH, until therapeutic levels are reached⁹

For orthopaedic procedures, LMWH or DOACs should be used for up to 35 days of thromboprophylaxis. Cancer patients having surgery also require extended prophylaxis due to their prothrombotic status.⁹

Monitoring for postoperative complications

Despite prevention, some individuals may still experience thrombotic problems. 

Symptoms such as leg swelling, dyspnoea (difficulty breathing), and chest discomfort should be investigated immediately for DVT or PE. D-dimer tests, Doppler ultrasonography, and CT pulmonary angiography are all useful diagnostic tools for these concerns.¹⁰ 

Immediate anticoagulation is begun in patients of suspected PE unless contraindicated. Thrombolytic treatment is only used for haemodynamically unstable individuals with large PE.¹⁰

Summary

To avoid thrombotic problems, surgical patients with thrombophilia must be carefully assessed and managed during the procedure. Individualised anticoagulation programs, mechanical prophylaxis, early mobilisation, and close postoperative monitoring are among the strategies used. The anticoagulant used, the period of prophylaxis, and the mode of administration are all determined by the patient's risk factors, the kind of operation, and probable bleeding hazards. The risks of surgery in thrombophilic individuals can be successfully minimised with a complete multidisciplinary approach, leading to better patient outcomes.