Under normal conditions, about 90% of the venous return in the lower extremities is via deep veins, mainly facilitated through compartmental muscular contraction of the foot, calf, and thigh against tight fascia. The highest pressure is generated by the calf muscle and is estimated to be about 65%, in comparison to 15% generated by the thigh muscles [4]. As the muscle contracts, the pressure raises within the compartment which allows antegrade flow to the heart. In the meantime, valve closure prevents reverse venous flow or refluxing to the superficial system. As the muscle relaxes, the pressure within the compartment decreases and allows antegrade flow of venous blood from the superficial to the deep system (Figs. 36.2 and 36.3).

There are many methods to classify venous diseases, depending on factors such as distribution and severity; however, the most effective method is to assess severity based on clinical, etiological, anatomical, and pathophysiological aspects. This international classification is not only an efficient description, but useful in determining appropriate management. Understanding the new terminology is crucial, not only to keep up with the American venous forum update, but also to serve as a common language among venous specialists.

Superficial thrombophlebitis (STP) is an inflammatory condition associated with thrombus formation within the superficial veins. It commonly occurs in the lower extremity; however, the incidence in the upper extremity is increasing, secondary to intravenous instrumentation. It usually has a benign and self-limited course. Clinical presentations include pain, redness, and swelling along the course of the affected vein. Fever and malaise are not uncommon. The pathophysiology can be explained in light of Virchows’s triad consisting of blood stasis, endothelial injury, and hypercoagulability. Therefore, a history of minor trauma or long travel may be the initial nidus for STP. Proper diagnosis and appropriate treatment is crucial to alleviate the pain and discomfort. A venous duplex scan will delineate the distribution of the STP and rule out the presence of DVT [7, 8]. The incidence of DVT is estimated to be as high as 40% in patients with STP. Migratory STP should raise the suspicion for underlying malignancy or other thrombophilias. Some diseases, such as Buerger’s disease, may be associated with migratory STP. Treatment is usually conservative and includes graduated compression stockings (30–40 mmHg), ambulation, and nonsteroidal antiinflammatory medications (Ibuprofen). Antibiotics are not recommended unless there is surrounding cellulitis. Special attention should be paid to a free-floating GSV thrombus at the SFJ, which should be treated with anticoagulation, or an IVC filter in those who have a contraindication to anticoagulation. Patients with iliofemoral DVT that meet the free-floating criteria are at significant risk for a pulmonary embolism, despite the administration of heparin [9].

Venous thromboembolism (VTE) is the fourth leading cause of death in Western countries. It is a common cause of morbidity and mortality. Although it is a preventable disease, the incidence of VTE exceeds 1/1,000 persons, with almost 400,000 new cases annually in the United States. Of patients who survive the initial event of VTE, 30% will have some kind of recurrence and 30% will develop postphlebitic syndrome within 10 years. Despite overwhelming evidence for the effectiveness of regimens [10–13], the concern over bedside prophylaxis and management often dissuades physicians from complying with guidelines.

The Virchow triad is often used to explain the development of perioperative DVT. Vascular stasis occurs primarily in the great veins of the body, which act as a reservoir system for circulation. At any given moment, approximately 70% of the total blood is contained in the venous system. Stagnation of venous blood is more likely when the patient is lying flat under the effect of anesthesia, particularly during laparoscopic surgery. The second component, hypercoagulability, occurs as a consequence of decreased clearance of the procoagulant factors (as seen in Table 36.3), or depletion of the lytic system (with or without underlying coagulopathies). The third component, endothelial damage, results from direct trauma to the vessel or by placement of a prosthetic graft. The combined influence of these factors promotes the development of venous thrombi in low-flow areas (e.g., subadjacent to the venous valves or adjacent to foci of intimal disruption). The propagation of thrombus leads to the development of overt DVT [14–20].

Leg swelling causes passive muscle engorgement and dilation of the muscle fibrils. These, in turn, activate pain receptors located in the muscle spindle and account for muscle discomfort. Stretching of the muscle aggravates the discomfort; this is the physiologic basis for the Homan’s sign (calf tenderness on dorsiflexion of the foot).

Additional factors that contribute to the pain are the inflammatory mediators released from stable clots that can contribute to the redness and leg swelling. DVT can be caused by numerous etiologies, including traumatic, vasculitic, hematologic, and drug-induced (Figs. 36.4 and 36.5).

Pulmonary embolism (PE) is one of the most dreaded complications of DVT. The true prevalence of perioperative PE is unknown; it varies according to the type of surgery, the use and type of prophylaxis, and the mode of diagnosis. Estimates indicate that without prophylaxis, fatal PE occurs in 0.1–0.8% of patients undergoing elective general surgery, 2–3% of those undergoing elective hip replacement, and up to 4–7% of those undergoing surgery for a fractured hip. The incidence of VTE increases after the age of 60 [10, 11].

Secondary to a potential lethal outcome of PE, early diagnosis is imperative for prompt therapy. Clinical presentation (shortness of breath, chest pain, and hemoptysis) and certain clinical criteria have been validated in the literature. The most commonly used validated criteria are the Wells score, which has been modified from year 1995 to 2001.

Score: