Obstructive Sleep Apnea and Deep Vein Thrombosis

Although obesity is a risk factor for OSA studies have indicated that most Asian patients with OSA are not obese.1 Also, Asians exihibit more craniofacial bone restriction. Caucasians are more obese than Asians.

Nocturnal symptoms of OSA mainly include loud and habitual snoring, choking, restless sleep, dry throat and nocturia. In elderly, nocturia and cognitive impairment are prominent symptoms. During daytime, OSA patients mainly experience fatigue, sleepiness and inability to concentrate. In fact, OSA patient may present with daytime symptoms only, as nocturnal symptoms are observed by the partner sharing the bedroom; who may consider snoring as a normal phenomenon. There is poor awareness of OSA in society at large.

Venous return from legs is dependent upon the skeletal muscles, which act as a pump. This is effective while the subject is walking and running. The changes in venous pressure coupled with normal functioning valves help the blood to go caudally. While standing the postural muscles in legs alternately contract and relax to keep the body in balance. This muscle activity also promotes venous return, maintains central venous pressure, lowers venous and capillary pressure in feet and lower limbs. It must also be appreciated that respiratory activity also contributes to venous return by following mechanisms-(a) Increasing the rate and depth of respiration promotes venous return and therefore enhances cardiac output. (b) Intrapleural pressure becomes more negative during inspiration which leads to the expansion of lungs, cardiac chambers (right atrium and right ventricle) and superior and inferior vena cava. The resultant fall in the intravascular and intracardiac pressure leads to increased venous return, increased preload and stroke volume. During expiration, opposite events occur.

The breathing abnormalities during sleep have effects on venous return. Varicose veins may develop. Pooling of blood in legs which occurs during apnea and hypopnea, coupled with hemodynamic changes and pathological cascades, favour thrombosis in legs and subsequent thromboembolism. OSA has possible implications in vascular endothelial injury, stagnant blood flow, increased coagulability (Virchow's triad) and Trousseau's syndrome. OSA suspicion must be high in all patients with venous thrombosis, particularly in those who have recurrent episodes of this disorder. These events pave the way for thrombosis against a background of pro-thrombotic state. Patients with OSA can present with idiopathic pitting oedema of legs as a result of venous pooling.

Peng et al2 stated that patients with OSA exhibit a higher risk of subsequent deep vein thrombosis and pulmonary embolism. The specific underlying mechanism explaining the association between OSA and venous thromboembolism remains unclear. However, three mechanisms operate (1). Vascular endothelial injury (2). Stagnant blood flow (3). Increased coagulability (Virchow's triad). It should be appreciated that elevated platelet activity, fibrinogen levels, plasminogen activator inhibitor -1 levels, erythrocyte adhesiveness and aggregation but reduced fibrinolytic capacity contribute to this hypercoagulable state.(3,4)

OSA is an independent risk factor for deep vein thrombosis.(5) Alonso-Fernandez et al (6) reported that after the first episode of pulmonary embolism, OSA is an independent risk factor for pulmonary embolism recurrence or restarting oral anticoagulants for a new thromboembolic event. We reported the first case of Schamberg's disease in a patient of severe OSA. (7)

The path taken by nocturnal events in OSA culminating in a pro-thrombotic state and various cardiovascular consequences is highlighted in a flow diagram.(8)

The most accepted mode of treatment of OSA is by using Continuous Positive Airway Pressure while sleeping. This stabilizes respiration and restores proper venous flow from legs.

There is evidence to show that OSA is a risk factor for venous thrombosis which can affect any system. Venous flow from legs is dependent upon respiration also. Deep venous thrombosis can occur as a consequence of OSA. Recognition and treatment of OSA in patients with deep vein thrombosis can be highly rewarding. Recognition and treatment of OSA routinely in clinical practice can prevent several consequences including venous thrombosis.