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Case Study #8: Deep Vein Thrombosis (DVT)

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9 Deep Vein Thrombosis Nursing Care Plans

Deep vein thrombosis ( DVT ) is a common and potentially life-threatening condition that requires prompt medical attention. As a nurse , understanding the nursing care plans and nursing diagnosis for DVT is essential to providing the best care for clients. This guide provides a comprehensive overview of DVT nursing care plans and nursing diagnoses , including common symptoms, nursing interventions , nursing management , and treatment options.

Table of Contents

What is deep vein thrombosis, nursing problem priorities, nursing assessment, nursing diagnosis, nursing goals, 1. promoting effective gas exchange, 2. enhancing peripheral tissue perfusion, 3. managing acute pain, 4. preventing bleeding risk and injury, 5. initiating health teaching and patient education, 6. assessing and monitoring for potential complications, 7. administering medications and pharmacologic support, 8. monitoring laboratory and diagnostic procedures, 9. providing perioperative care, recommended resources, references and sources.

Thrombophlebitis is the inflammation of the vein wall resulting in the formation of a thrombosis ( blood clot) that may interfere with the normal blood flow through the vessel.

Typically, venous thrombophlebitis occurs in the lower extremities. It may also occur in superficial veins such as cephalic, basilic, and greater saphenous veins, which usually is not life-threatening and does not necessitate hospitalization, or it may happen in a deep vein, which can be life-threatening because clots may travel to the bloodstream and cause a pulmonary embolism .

Three contributing factors (known as Virchow’s triad) can lead to the development of deep vein thrombosis (DVT), which includes venous stasis, hypercoagulability, and vessel wall injury .

Venous stasis occurs when blood flow is decreased, as in immobility, medication therapies, and in heart failure. Hypercoagulability occurs most commonly in clients with deficient fluid volume , pregnancy, oral contraceptive use, smoking, and some blood dyscrasias. Venous wall damage may occur secondary to venipuncture, certain medications, trauma , and surgery . The objective of treatment of DVT involves preventing the clot from dislodgement (risking pulmonary embolism) and reducing the risk of post-thrombotic syndrome.

DVT is a common venous thromboembolic (VTE) disorder with an incidence of 1.6 per 1000 annually. Even in clients who do not get pulmonary emboli , recurrent thrombosis and “post-thrombotic syndrome” are major causes of morbidity. DVT is a major medical problem accounting for most cases of pulmonary embolism. Only through early diagnosis and treatment can the morbidity be reduced (Schick, 2023).

Nursing Care Plans and Management

Nursing care management for patients with deep vein thrombosis (DVT) involves thorough assessment of the patient’s history and symptoms, administering anticoagulant medications, managing pain , promoting circulation through compression therapy and activity, educating the patient about DVT and self-care measures, providing psychosocial support, collaborating with the healthcare team, and closely monitoring the patient’s condition.

The following are the nursing priorities for patients with deep vein thrombosis:

• Preventing pulmonary embolism.
• Management of pain .
• Promotion of circulation and prevention of complications.
• Patient education and health teachings.
• Anticoagulant therapy.

Assess for the following subjective and objective data :

• Apprehension
• Hypercapnia
• Restlessness
• Asymptomatic
• Increased leg warmth
• Edema (Unilateral)
• Pain during palpation of a calf muscle

Following a thorough assessment , a nursing diagnosis is formulated to specifically address the challenges associated with deep vein thrombosis based on the nurse’s clinical judgement and understanding of the patient’s unique health condition. While nursing diagnoses serve as a framework for organizing care, their usefulness may vary in different clinical situations. In real-life clinical settings, it is important to note that the use of specific nursing diagnostic labels may not be as prominent or commonly utilized as other components of the care plan. It is ultimately the nurse’s clinical expertise and judgment that shape the care plan to meet the unique needs of each patient, prioritizing their health concerns and priorities.

Goals and expected outcomes may include:

• The client will demonstrate adequate ventilation and oxygenation, as evidenced by ABGs within the normal range.
• The client will report or display resolution or absence of symptoms of respiratory distress.
• The client will maintain optimal peripheral tissue perfusion in the affected extremity, as evidenced by strong palpable pulses, reduction in and/or absence of pain , warm and dry extremities, and adequate capillary refill.
• The client will not experience pulmonary embolism, as evidenced by normal breathing, heart rate , and absence of dyspnea and chest pain .
• The client will report that pain or discomfort is alleviated or controlled, and verbalize methods that provide relief.
• The client will display a relaxed manner, be able to sleep or rest, and engage in desired activities.

Nursing Interventions and Actions

Therapeutic interventions and nursing actions for patients with deep vein thrombosis may include:

Clients with deep vein thrombosis (DVT) can experience impaired gas exchange due to altered blood flow to the alveoli and changes in the alveolar-capillary membrane. DVT can obstruct blood flow to the lungs , reducing the amount of blood that reaches the alveoli, where gas exchange takes place. Additionally, changes in the alveolar-capillary membrane, such as inflammation and increased permeability, can further impair gas exchange by reducing the diffusion of oxygen and carbon dioxide between the lungs and the bloodstream. To ensure optimal gas exchange, healthcare providers focus on interventions to improve lung function. Regular monitoring of respiratory status allows for early detection of complications.

1. Assess the level of consciousness and changes in mentation. Initial signs of systemic hypoxemia include restlessness and irritability, followed by progressively decreased mentation. Reduced oxygenation is a risk factor for thrombosis since the incidence of thrombosis is increased under systemic or local hypoxia. Hypoxia occurs when oxygen demand is greater than oxygen supply, for example, when blood flow is reduced by immobility or reduced by trauma (Gupta et al., 2019).

2. Auscultate lungs for areas of decreased and absent breath sounds and the presence of adventitious sounds (crackles). Non-ventilated areas may be identified by the absence of breath sounds. Crackles may be seen in fluid-filled tissues and the airway or may indicate cardiac decompensation. A client with a developing pulmonary embolism (PE) may exhibit dyspnea. Dyspnea may be acute and severe in central PE, whereas it is often mild and transient in small peripheral PE (Vyas & Goyal, 2022).

3. Monitor vital signs. Observe changes in cardiac rhythm . Tachycardia, tachypnea , and BP changes are associated with progressing hypoxemia and acidosis. Alterations in heart rhythm and extra heart sounds may indicate increased cardiac workload related to worsening ventilation imbalance. PE may become apparent when the client exhibits hypotension (systolic blood pressure less than 90 mm Hg or a drop in SBP of 40 mm Hg or more from baseline) (Vyas & Goyal, 2022).

4. Assess respiratory rate and rhythm. Observe for use of accessory muscles, nasal flaring, and pursed lip breathing. Tachypnea and dyspnea are indicative of pulmonary obstruction. Dyspnea and increased work of breathing may be the first or only signs of subacute pulmonary embolism. Severe respiratory distress and failure accompany moderate to a severe loss of functional lung units. Shock and right ventricular dysfunction confer a poor prognosis and predict mortality. Clients with PE and a coexisting DVT are also at an increased risk for death (Vyas & Goyal, 2022).

5. Observe for generalized duskiness and cyanosis in the earlobes, lips, tongue, and buccal membranes. This is suggestive of systemic hypoxemia. Late signs of hypoxia include bluish discoloration of the skin and mucous membranes, where vasoconstriction of the peripheral vessels causes cyanosis. Cyanosis is most easily seen around the lips and in the oral mucosa. However, the nurse should never assume the absence of cyanosis means adequate oxygenation (Doyle & McCutcheon, 2015).

6. Assess activity tolerance , such as reports of weakness and fatigue , vital sign changes, or increased dyspnea during exertion. Encourage rest periods, and limit activities to client tolerance. These guidelines help in determining the response of the client to resume activities and the ability to engage in self-care. The nurse may use the six-minute walk test to assess the response of oxyhemoglobin saturation to exercise or activities, as well as the total distance the client can walk in six minutes on a ground level (Bhutta et al., 2022).

7. Monitor ABGs or pulse oximetry. Hypoxemia is present in varying degrees, depending on the degree of airway obstruction , cardiopulmonary status, and presence and degree of shock. Respiratory alkalosis and metabolic acidosis may also be present. Arterial oxygen saturation refers to the amount of oxygen bound to hemoglobin in arterial blood. ABGs are useful tools to evaluate hypoxia because they can also shed light on the etiology of the disease process (Bhutta et al., 2022).

8. Evaluate sleep patterns, noting reports of difficulties and whether the client feels well-rested. The client may have difficulty sleeping due to the feeling of dyspnea. Nocturnal trend oximetry provides information about oxyhemoglobin saturation over a period (usually overnight). This test is primarily used to assess the adequacy or need for oxygen supplementation at night. The use of overnight trend oximetry as a surrogate for a diagnostic sleep study is possible, however, a formal sleep study should be used whenever possible (Bhutta et al., 2022).

9. Check the client frequently and arrange for someone to stay with the client, as indicated. This assures that changes in condition will be noted and that assistance is readily available. The client may manifest neurological symptoms such as restlessness, headache, and confusion with moderate hypoxia, therefore, the client must be assessed and checked as frequently as possible to avoid further deterioration of the client’s condition (Bhutta et al., 2022).

10. Assist with frequent changes of position, and encourage ambulation as tolerated. Turning and ambulation enhance the aeration of different lung segments, thereby improving oxygenation. The ACCP Consensus Conference on Antithrombotic and Thrombolytic Therapy for venous thromboembolism recommended ambulation as tolerated for clients with DVT. Therefore, early ambulation on day 2 after initiation of outpatient anticoagulant therapy, in addition to effective compression, is strongly recommended. Early ambulation without ECS is not recommended (Patel, 2019).

11. Encourage coughing , deep breathing exercises, and suctioning as indicated. Increases oxygen delivery to the lungs by mobilizing secretions and enhancing ventilation. Deep breathing exercises are used to decrease the incidence and severity of pulmonary complications such as pneumonia , atelectasis , and hypoxemia. During exercise education, the nurse explains and demonstrates how to take a deep, slow breath, and how to exhale slowly, three to five times every one to two hours. Clients who performed deep breathing exercises had better pulmonary function compared to the performing no exercise group (Unver et al., 2018).

12. Keep the head of the bed elevated. This promotes maximal chest expansion, making it easier to breathe and enhancing physiological and psychological comfort . A prone position should be avoided. In COVID-19 acute respiratory distress syndrome (ARDS), a prone position is frequently applied. During prone ventilation, the client’s position remains nearly unchanged, with minimal movements limited to the head and limbs. Therefore, the prone position can be a potential contributor to blood flow changes in these clients (Gebhard et al., 2021).

See also: Patient Positioning: Complete Guide and Cheat Sheet for Nurses

13. Assist with chest physiotherapies, such as postural drainage and percussion of the non-affected area, and with an incentive spirometer . This facilitates deeper respiratory effort and promotes drainage of secretions from lung segments into bronchi , where they may more readily be removed by coughing or suctioning. Pulmonary rehabilitation can significantly improve dyspnea, overall health, and exercise endurance in clients with PE. The existing evidence suggests that pulmonary rehabilitation is a potential treatment for alleviating post-PE syndrome, which improves the quality of life and prognosis of clients with PE (Yu et al., 2022).

14. Provide supplemental humidification, such as ultrasonic nebulizers. Nebulization gives moisture to mucous membranes and helps liquefy secretions to facilitate airway clearance. Dry nasal mucosa occurs when the flow is greater than or equal to 4 L/minute, therefore humidification is necessary for clients using low-flow oxygen devices (Bhutta et al., 2022).

15. Provide oxygen therapy with an appropriate method as ordered. Oxygen therapy can help increase oxygen levels and enhance tissue perfusion, decreasing the risk of hypoxia and other related complications. Oxygen therapy may be indicated for clients with low PaO2 that is less than 60 or SaO2 less than 90, and this can be achieved by increasing the percentage of oxygen in the inspired air that reaches the alveoli (Bhutta et al., 2022).

16. Provide adequate hydration, either oral (PO) or IV, as indicated. Increased fluids may be given to decrease the hyperviscosity of blood, which can potentiate thrombus formation, or support circulating volume and tissue perfusion. A low fluid volume state can lead to hemoconcentration and low venous flow. Clients who experienced a VTE were found to have elevated biochemical indices of dehydration , in comparison to clients who had not (Keiter et al., 2015).

17. Administer medications, as indicated . See Pharmacologic Management

18. Prepare the client for a lung scan. This may reveal the pattern of abnormal perfusion in areas of ventilation, reflecting ventilation and perfusion mismatch, confirming the diagnosis of pulmonary embolism and the degree of obstruction. The absence of both ventilation and perfusion reflects alveolar congestion or airway obstruction. The planar ventilation/perfusion scan is an established diagnostic test for suspected PE. V/Q scanning is mostly performed for clients in whom computed tomographic pulmonary angiography (CTPA) is contraindicated or inconclusive, or when additional testing is needed (Vyas & Goyal, 2022).

19. Prepare for and assist with bronchoscopy . The purpose of this procedure is to remove blood clots and clear the airway. During flexible bronchoscopy, clots can be removed piecemeal by biopsy forceps, dislodged using a Fogarty catheter, or removed en bloc using either suctioning or a cryoprobe (Sehgal et al., 2017).

20. Prepare for surgical intervention , if indicated. Vena caval ligation or insertion of an intracaval umbrella is intended for clients with recurrent emboli despite adequate anticoagulation, when anticoagulation is contraindicated, or when septic emboli arising from below the renal veins unresponsive to treatment; Pulmonary embolectomy is often done as a last resort treatment of PE. Traditional venous thrombectomy is performed by surgically exposing the common femoral vein and saphenofemoral junction through a longitudinal skin incision. Care must be taken to avoid dislodging the clot or breaking it into small fragments because pulmonary embolus will result (Patel, 2019).

21. Assist the client to deal with fear and anxiety that may be present. Feelings of fear and severe anxiety are associated with the inability to breathe and may actually increase oxygen consumption and demand. Encourage the client to express their feelings so that the client may regain some sense of control over emotions. Provide the client with brief explanations of what is happening and the expected effects of outcomes. This may allay anxiety related to the unknown and help reduce fears concerning personal safety.

Deep vein thrombosis (DVT) can lead to ineffective tissue perfusion due to several factors. The increased blood coagulability makes it more likely for a blood clot to form in the deep veins, leading to restricted blood flow. Venous stasis, caused by reduced blood flow and muscle contractions, can also contribute to DVT, while vessel wall injury can cause inflammation and clot formation, further impeding blood flow. All these factors combined can result in ineffective tissue perfusion, which can lead to a range of complications. Healthcare providers employ various interventions to improve tissue perfusion in these patients.

1. Assess for contributing factors such as a family history of blood clots or inherited blood clotting disorders, prolonged immobility, trauma to the veins, such as from surgery , injury, or infection , use of hormonal birth control or hormone replacement therapy, obesity, sedentary lifestyle , smoking, and alcohol consumption. Most clients with DVT are asymptomatic. Knowledge of high-risk situations helps in early detection. Genetic mutations within the blood’s coagulation cascade represent those at the highest risk for the development of venous thrombosis. Genetic thrombophilia is identified in 30% of clients with idiopathic venous thrombosis. Immobility can be as transient as that occurring during a transcontinental airplane flight or an operation under general anesthesia (Patel, 2019).

2. Assess for the signs and symptoms of deep vein thrombosis (DVT). The signs and symptoms that occur in the leg affected by the deep vein clot include swelling , pain or tenderness, increased warmth, and changes in skin color (redness). Edema is the most specific symptom of DVT. Thrombus that involves the iliac bifurcation, the pelvic veins, or the vena cava produces leg edema that is usually bilateral rather than unilateral. Superficial thrombophlebitis is characterized by the finding of a palpable, indurated, cordlike, tender, subcutaneous venous segment (Patel, 2019).

3. Measure the circumference of the affected leg with a tape measure. Unilateral leg and thigh swelling can be assessed by measuring the circumference of the affected leg 10 cm below the tibial tuberosity and 10 cm to 15 cm above the upper edge of the patella. Deep vein thrombosis is suspected if there is a difference of >3 cm between the extremities. High partial obstruction often produces mild bilateral edema that is mistaken for the dependent edema of right-sided heart failure, fluid overload , or hepatic or renal insufficiency (Patel, 2019).

4. Monitor the results of diagnostic tests . See Laboratory and Diagnostic Procedures

5. Monitor the following coagulation profile: international normalized ratio (INR), prothrombin time (PT), and partial thromboplastin time (PTT) results . These are used to measure the effectiveness of anticoagulant therapy. The PT/INR is used for clients receiving warfarin . Baseline values are obtained before the first dose of anticoagulant is administered. Repeated tests are done at prescribed intervals to adjust drug dosages to achieve desired changes in coagulation. A prolonged prothrombin time or activated partial thromboplastin time does not imply a lower risk of new thrombosis. Progression of DVT and PE can occur despite full therapeutic anticoagulation in 13% of clients (Patel, 2019).

6. Assess the client’s level of pain. Leg pain occurs in 50% of clients, but this is entirely nonspecific. Pain can occur on dorsiflexion of the foot (Homan sign). Tenderness occurs in 75% of clients but is also found in 50% of clients without objectively confirmed DVT. When tenderness is present, it is usually confined to the calf muscles or along the course of the deep veins in the medial thigh (Patel, 2019).

7. Maintain adequate hydration. Hydration prevents an increased viscosity of blood, which contributes to venous stasis and clotting. A low fluid volume state can lead to hemoconcentration and low venous flow. In a prospective study, dehydration was independently linked to VTE in those clients who had previously had an acute ischemic stroke (Keiter et al., 2015).

8. Encourage bed rest and keep the affected leg elevated (depending on the size and location of the clot) as indicated. Clients usually require bed rest until symptoms are relieved. The affected leg should be elevated to a position above the heart to decrease swelling. Leg elevation is a simple intraoperative and postoperative technique for improving venous drainage from the lower extremities, which minimizes venous stasis (Keiter et al., 2015).

9. Provide warm, moist heat to the affected site. Heat promotes comfort and reduces inflammation. Vascular boot warming, also known as Rooke boot warming, helps to vasodilate the distal arterial bed, improves perfusion, raises tissue pressure, and increases venous blood return from the lower extremities, thus improving clinical outcomes for DVT. Compared to other mechanical methods, such as intermittent compression stockings, the vascular boot is relatively more comfortable to wear as it has less pressure on the heel and other bony areas (Zhang et al., 2021).

10. Apply below-knee compression stockings as prescribed. Ensure that the stockings are the correct size and are applied correctly. Compression stockings enhance circulation by providing graduated pressure on the affected leg to help return the venous blood to the heart. Inaccurately applied stockings can serve as a tourniquet and can promote clot formation. Below-the-knee elastic compression stockings (ECS) assist the calf muscle pump and reduce venous hypertension and venous valvular reflux. This reduces leg edema, aids in microcirculation, and prevents venous ischemia . Graduated compression stockings, on the other hand, with ankle pressures of 30 to 40 mm Hg reduced the incidence of PTS by 50% (Patel, 2019).

11. Administer analgesics as prescribed. Analgesics relieve pain and promote comfort . Acetaminophen is the safest pain reliever while taking an anticoagulant, but the daily dose recommended must not be exceeded. NSAIDs should be avoided for clients taking anticoagulants because they are associated with an increased risk of bleeding (The North American Thrombosis Forum, 2022).

12. Administer anticoagulants ( heparin / warfarin ) as prescribed. Treatment with anticoagulant is used primarily to prevent the formation of new clots by decreasing the normal activity of the clotting mechanism. Heparin IV or subcutaneous low-molecular-weight heparin is started initially. Oral anticoagulant therapy ( warfarin ) will be initiated while the client is still receiving heparin because the onset of action for warfarin can be up to 72 hours. Heparin will be discontinued once the warfarin reaches therapeutic levels.

13. With a massive DVT severely comprising tissue perfusion, anticipate thrombolytic therapy. Thrombolytic therapy is used only in severe embolism that significantly comprises blood flow to the tissues since they can cause sudden bleeding . For maximum effectiveness, therapy must be started soon after the onset of symptoms (within 5 days). Accordingly, careful assessment of the indications for lysis against the possibility of bleeding must be carried out before pharmacologic thrombolysis is attempted (Patel, 2019).

14. For clients who are unresponsive to anticoagulant therapy, anticipate the following surgical treatment . See Preoperative Care

15. Encourage the client to ambulate as tolerated. In Europe, early ambulation and compression have been the mainstay of adjunctive therapy for DVT. In North America, the unsubstantiated fear of dislodging clots by ambulation led clinicians to recommend bed rest and leg elevation to their clients. The authors explained that bed rest promotes venous stasis, which is a major risk factor for DVT, and therefore, may actually enhance thrombus propagation and the risk of subsequent PE (Patel, 2019).

Clients with deep vein thrombosis (DVT) can experience acute pain due to several factors. The presence of a blood clot in the affected vein can lead to diminished arterial circulation and oxygenation of tissues, causing the accumulation of lactic acid and triggering pain receptors. Additionally, the inflammation response in the affected vein can further exacerbate pain by sensitizing pain receptors and causing tissue damage. Healthcare providers employ various strategies to manage acute pain in these patients.

1. Assess the degree and characteristics of discomfort and pain. The degree of pain depends on the extent of circulatory deficit, the inflammatory process, the degree of tissue ischemia , and the extent of edema associated with thrombus development. Changes in the characteristics of pain may indicate the development of complications. Leg pain can occur in 50% of clients, but it can be entirely unspecific. Pain can occur on dorsiflexion of the foot (Homan sign) (Patel, 2019).

2. Investigate reports of sudden or sharp chest pain , accompanied by dyspnea, tachycardia, and apprehension, or the development of new pain with signs of another site of vascular involvement. These signs and symptoms suggest the presence of pulmonary embolism as a complication of DVT or peripheral arterial occlusion associated with heparin‐induced thrombocytopenia with thrombosis syndrome (HITT). Both conditions require immediate medical treatment. Pleuritic chest pain without other symptoms or risk factors may be a presentation of pulmonary embolism. Pleuritic or respirophasic chest pain is a particularly worrisome symptom. Its presence suggests that the embolus is located more peripherally and thus may be smaller (Ouellette & Mosenifar, 2020).

3. Monitor vital signs, noting increased temperature. Elevations in heart rate may indicate increased discomfort or may occur in response to fever and inflammatory processes. Fever can also increase the client’s discomfort. Fever of less than 39℃ (102.2℉) may be present in 14% of clients; however, a temperature higher than 39.5℃ (103.1℉) is not from pulmonary embolism (Ouellette & Mosenifar, 2020).

4. Maintain bed rest during the acute phase, then start early ambulation gradually as tolerated. This decreases discomfort associated with muscle contraction and movement. However, the concept of immobilizing DVT clients is outdated, since early mobilization has been demonstrated not to increase the risk of embolization, and large cohort studies have clearly proven that outpatient DVT treatment is feasible and safe for the majority of clients being diagnosed with DVT outside of hospitals. Admitted clients with DVT may be safely mobilized, provided that adequate anticoagulation is immediately initiated (Endig et al., 2016).

5. Encourage the client to change position frequently. This reduces muscle fatigue, helps minimize muscle spasms, and maximizes circulation to tissues. Position changes can help reduce pain in DVT by improving blood flow and reducing pressure on the affected vein. When the client changes their position, this helps prevent blood from pooling in the affected area and decreases the risk of further developing blood clots.

6. Provide a foot cradle. The cradle keeps the pressure of bedclothes off the affected leg, thereby reducing pressure discomfort. Additionally, a foot cradle supports the foot and the ankle in a neutral position, which can help improve blood flow and reduce the risk of further blood clots. However, this measure should be used in conjunction with other strategies to prevent DVT, such as regular exercise, position changes, and the use of compression stockings.

7. Elevate affected extremity. This encourages a venous return to facilitate circulation, reducing stasis and edema formation. Virchow’s triad states that venous stasis is a predisposing factor for DVT. Leg elevation is a simple intraoperative and postoperative technique for improving venous drainage from the lower extremities, which minimizes venous stasis (Keiter et al., 2015).

8. Apply a warm compress to the affected leg using a 2-hour-on, 2-hour-off schedule around the clock. Moist heat may be applied to the affected region to relieve pain and improve circulation through vasodilation. Heat therapy produces increased collagen extensibility, increased blood flow, metabolic rate, and inflammation resolution. Decreased joint stiffness, muscle spasm, and pain are also positive effects of heat therapy. Heat raises the pain threshold and acts directly on the muscle spindle, decreasing spindle excitability (El-Tallawy et al., 2021).

9. Teach the client non-pharmacological pain management techniques, such as deep breathing exercises, guided imagery, or relaxation techniques. These techniques can help alleviate pain and decrease the need for opioids or other pain medications, which may have adverse effects. These therapies may also help clients to feel more in control of pain management , improve overall well-being, and promote better compliance with the prescribed treatment plan.

10. Administer medications, as indicated . See Pharmacologic Management

11. Recommend the use of a vascular warming boot or Rooke boot. A study evaluated the safety, efficacy, and impact of vascular boot warming on post-thrombotic syndrome in DVT. Pain and swelling are two critical concerns for clients and are closely correlated to their quality of life. Results suggest that vascular boot warming can reduce pain and swell much faster than the standard of care, and it does not increase bleeding (Zhang et al., 2021). 

12. Encourage therapeutic exercise as tolerated. When the pain decreases, mobilization should be regained gradually. The best treatment in such cases is combined gradual stretching and strengthening exercises. Client education is mandatory about a therapeutic exercise regimen at home once therapeutic sessions have ceased. Therapeutic exercise consists of passive movements, active-assistive exercises, active exercises, stretching, and relaxation exercises (El-Tallawy et al., 2021).

13. Ensure proper wearing of compression stockings. The more a DVT client is affected by pain and leg swelling, the more likely they will benefit from compression therapy (stockings or bandages), provided that the compression device is fitted correctly. Clients receiving compression therapy need to be educated on proper use and the risk of developing pressure injuries , which is a significant risk. Daily skin inspections are necessary during compression therapy (Endig et al., 2016).

Clients with deep vein thrombosis (DVT) are at risk for bleeding due to several factors. Abnormal blood profile, such as low platelet counts or coagulopathy, can increase the risk of bleeding. Additionally, anticoagulation therapy, which is commonly used to prevent new blood clots in DVT, can also increase the risk of bleeding by reducing the blood’s ability to clot. This can result in bleeding or hemorrhage , especially in patients who are also taking other medications that can further increase the risk of bleeding, such as aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs). Healthcare providers utilize several strategies to prevent bleeding and injury in these patients.

1. Assess for the signs and symptoms of bleeding. Bruises, epistaxis, and gum bleeding are early signs of spontaneous bleeding. Significant bleeding, such as hematemesis, hematuria , or GI hemorrhage should be thoroughly investigated because anticoagulant therapy may unmask a pre-existing disease like cancer , peptic ulcer disease , or an arteriovenous malformation (Patel, 2019).

2. Monitor platelet counts and coagulation test results (INR, PT, PTT). The effects of anticoagulation therapy must be closely monitored to reduce the risk of bleeding. The clotting time is the time it takes for plasma to clot after the addition of different substrates in vitro under standard conditions using the capillary method. PT/INR is the initial test used to identify defects in secondary hemostasis . It is the time taken for blood to clot and generates thrombin. A delay in the PT or aPTT indicates the presence of either a deficiency or inhibitor of the clotting factor (Umerah & Momodu, 2022).

3. Monitor platelets and the heparin-induced platelet aggregation (HIPA) status. A sudden decrease in the platelet count can occur with heparin use and is known as heparin-induced thrombocytopenia (HIT). HIT is less commonly seen with the use of low-molecular-weight heparin. HIT typically presents as a steady drop in platelet counts (no fluctuations), while hemoglobin and hematocrit counts remain relatively stable. The most common symptom of HIT is the enlargement or extension of a blood clot or the development of a new blood clot. In clients receiving IV heparin, they may experience chills, fever, hypertension , tachycardia, shortness of breath, and chest pain (Nicolas et al., 2023).

4. Administer anticoagulant therapy as prescribed (continuous IV heparin/subcutaneous low-molecular-weight heparin; oral warfarin). Anticoagulants are given to prevent further clot formation. The type of medication varies per protocol and severity of the clot. First-line therapy for non-high-risk VTE or PE consists of direct oral anticoagulants over vitamin K antagonists. There are also possibilities for advances in anticoagulant delivery systems including the expansion of new oral agents and their antidotes, reducing the size of heparins, developing oral or topical heparins, and modifying physical or chemical formulations. Ita suggests that transdermal delivery may potentially bypass known issues with heparin use (Patel, 2019).

5. If bleeding occurs while on IV heparin: terminate the infusion then recheck the PTT level stat, and reevaluate the dose of heparin based on the PTT result. Laboratory data guide further treatment. The guide for the PTT level is 1.5 to 2 times normal. Anticoagulation-related major bleeding is associated with an increased risk of death and thrombotic events, independent of the class of anticoagulant used. With the increasing use of non-vitamin K antagonists or oral anticoagulants, the number of clients who require reversal of their anticoagulant effects can be expected to rise (Patel, 2019).

6. Avoid the use of invasive procedures, such as injections or venipuncture, if possible, and use caution during any necessary procedures to minimize the risk of bleeding. If an invasive procedure is necessary, nurses should take appropriate precautions, such as using a smaller gauge needle or applying pressure to the puncture site, to reduce the risk of bleeding. The management of anticoagulation in clients undergoing surgical procedures is challenging since interrupting anticoagulation for a procedure transiently increases the risk of thromboembolism. At the same time, surgery and invasive procedures have associated bleeding risks that are increased by anticoagulants. A balance between reducing the risk of thromboembolism and preventing excessive bleeding must be reached for each client (Douketis, 2023).

7. Teach the client the importance of complying with the prescribed medication regimen and report any signs of bleeding, such as unusual bruising, nosebleeds, or blood in the stool or urine . Adhering to the medication regimen prevents the formation of new blood clots and decreases the risk of serious complications, such as pulmonary embolism. Anticoagulants need to be taken regularly and as prescribed by the physician to ensure that the blood’s clotting parameters are within the therapeutic range. Long-term anticoagulation is necessary to prevent the high frequency of recurrent venous thrombosis or thromboembolic events. Interruption of anticoagulation within the first 12 weeks of therapy appears to result in a 25% incidence of recurrent thrombosis (Schreiber & Brenner, 2020).

8. Convert from IV anticoagulation to oral anticoagulation after the appropriate length of therapy. Monitor INR, PT, and PTT levels. PT or INR levels should be in a therapeutic range for anticoagulation before discontinuing heparin. Oral vitamin K antagonists (VKAs) remain the preferred approach for long-term treatment, which allows for single-dosing oral therapy that can be continued on an outpatient basis. The American College of Chest Physicians (ACCP) recommends cessation of anticoagulant therapy after 3 months of treatment in those with surgery -associated acute proximal DVT, an acute proximal DVT or PE provoked by a nonsurgical transient risk factor, and a first unprovoked VTE and a high risk of bleeding (Schreiber & Brenner, 2020).

9. If HIPA is positive, stop all heparin products and anticipate a hematology consult. The continuation of heparin products further complicates the situation. Specialty expertise is needed. Laboratory confirmation of HIT is of crucial importance and remains challenging and relies on platelet functional assays highlighting the presence of heparin-dependent platelet-activating antibodies in the client’s serum or plasma. Platelet functional assays using washed platelets include the C-serotonin release assay (SRA), usually described as the gold standard, and HIPA (Gonthier et al., 2021).

10. Keep reversal agents for different anticoagulants within easy access. The initial step for any condition requiring urgent reversal of anticoagulation is always to discontinue the anticoagulant. Protamine sulfate counteracts the activity of unfractionated heparin. It is also indicated for bleeding in clients on LMWH, although it is not as effective as with bleeding associated with UFH. Idarucizumab is an anti-dabigatran monoclonal antibody fragment used in clients treated with dabigatran presenting with life-threatening bleeding. Andexanet alfa can be given to clients receiving apixaban, betrixaban, edoxaban, and rivaroxaban (Umerah & Momodu, 2022).

11. Avoid administering platelet transfusions to clients with confirmed HIT in the acute phase. Platelet transfusions are contraindicated during the acute phase, as transfused platelets can bind to IgG and become activated and release PF4, thus worsening the hypercoagulable state. Activated platelets release prothrombotic substances and PF4, creating a continuous cycle that can only be broken when heparin is discontinued and appropriate treatment is initiated (Nicolas et al., 2023).

Lack of knowledge can be a common issue for clients with deep vein thrombosis (DVT) due to unfamiliarity with the disease and its management. This can result in a lack of understanding about the importance of adherence to treatment and lifestyle modifications that can help prevent future occurrences of DVT. Initiating health teaching and patient education is an essential component of caring for patients with deep vein thrombosis (DVT). Education plays a vital role in empowering patients to actively participate in their own care and make informed decisions regarding their health. Healthcare providers provide comprehensive information to patients about DVT, its risk factors, signs and symptoms, and the importance of adherence to the prescribed treatment plan. Patients are educated about the rationale and potential side effects of anticoagulant medications, as well as the importance of regular monitoring and follow-up appointments.

1. Assess the client’s understanding of the causes, treatment, and prevention plan for deep vein thrombosis. This information gives an important starting point in education. DVT requires preventive effort to reduce the risk of reoccurrence. DVT is one of the most prevalent medical problems today, with an annual incidence of 80 cases per 100,000. Early recognition and appropriate treatment of DVT and its complications can save many lives (Patel, 2019).

2. Assess the following signs of pulmonary embolus such as shortness of breath, chest pain that worsens with deep breathing or coughing, palpitations, clammy skin, lightheadedness, and cough . These symptoms can be caused by a blood clot that breaks off from the original clot in the leg and travels to the lung. The challenge in dealing with pulmonary embolism is that clients rarely display the classic presentation of this problem, that is, the abrupt onset of pleuritic chest pain, shortness of breath, and hypoxia. The presentation of PE may vary from sudden catastrophic hemodynamic collapse to gradually progressive dyspnea (Ouellette & Mosenifar, 2020).

3. Instruct the client to take medications as indicated, explaining their actions, dosages, and side effects. Correct knowledge decreases future complications. Analgesics and anti-inflammatory medications are indicated for short-term symptom relief. Clients may require anticoagulation for weeks or long term, depending on the risks. The immediate symptoms of DVT often resolve with anticoagulation alone, and the rationale for intervention is often the reduction of the 75% long-term risk of PTS. Systemic IV thrombolysis is no longer recommended because of an elevated incidence of bleeding complications, a slightly increased risk of death, and insignificant improvement in PTS (Patel, 2019).

4. Inform the client of the need for regular laboratory testing while on oral anticoagulation. Routine coagulation monitoring is necessary to ensure that a therapeutic response is obtained and prevent reoccurrences of clots. For admitted clients with unfractionated heparin (UFH), the aPTT or heparin activity level must be monitored every six hours while the client is taking IV heparin until the dose is stabilized in the therapeutic range. Clients treated with LMWH or fondaparinux do not require monitoring of the aPTT (Patel, 2019).

5. Discuss and give the client a list of signs and symptoms of excessive anticoagulation. Clients need to self-manage their condition. The early assessment facilitates prompt treatment. Hemorrhagic complications are the most common adverse effects of anticoagulant therapy. Anticoagulation therapy for three to six months results in major bleeding complications. Significant bleeding, such as hematemesis, hematuria, or GI hemorrhage, should be thoroughly investigated because anticoagulant therapy may unmask a preexisting disease (Patel, 2019).

6. Provide teaching regarding the safety measures while on anticoagulant therapy such as the use of an electric razor, and the use of a soft toothbrush. These precautionary measures help reduce the risk of bleeding. The use of a soft-bristled toothbrush prevents trauma to the oral mucous membranes and the risk of bleeding from the gums. Toothpicks and dental floss should also be avoided, as they can injure the gums when used vigorously (Wayne, 2023).

7. Instruct the client to avoid rubbing or massaging the calf. This will prevent breaking off the clot, which may travel into the circulation as an embolus. Massaging lower extremities using forceful techniques and for prolonged periods where a client has been diagnosed with DVT in the leg veins is associated with complications. Massage can dislodge an already established thrombus, embolus, or blood clot and predispose the client to develop PE and cause sudden death (Behera et al., 2017).

8. Instruct the client on the correct application of compression stockings. Stockings applied inaccurately can serve as a tourniquet and promote clot formation. The incorrect use of compression stockings can be unsafe; thigh-length stockings that are fitted incorrectly or that roll down the leg can create a tourniquet effect, which can potentially damage the skin and reduce venous outflow. Additionally, one length of stocking may be more appropriate than the other in certain clients; knee-length stockings may be more likely to induce wound complications in clients undergoing knee replacement surgery as the elastic support lies over the wound, creating unwanted localized pressure (Wade et al., 2016).

9. Educate the client about the following measures to prevent reoccurrence:

• 9.1. Avoid constricting garters or socks with tight bands Wearing constricting clothing decreases normal blood flow and promotes clotting. Constricting socks or garters work by applying pressure to the lower extremities which helps to improve blood flow and prevent blood clots from forming. However, if the pressure is too high or the socks are too tight, it can restrict blood flow, increasing the risk of blood clots.
• 9.2. Avoid staying in one position for long periods; get up and move around every hour or so on a long flight. This will avoid the occurrence of venous stasis. The concept of immobilizing DVT clients is outdated, since early mobilization has been demonstrated not to increase the risk of embolization, and large cohort studies have proven that outpatient DVT treatment is feasible and safe for the majority of clients being diagnosed with DVT outside of hospitals (Endig et al., 2016).
• 9.3. Maintain adequate hydration. Sufficient hydration prevents hypercoagulability. A low-volume state can lead to hemoconcentration and low venous flow. A study found that clients who experienced VTE have elevated biochemical indices of dehydration , in comparison to clients who had not (Keiter et al., 2015).
• 9.4. Maintaining a healthy body weight Obesity contributes to venous insufficiency and venous hypertension through the compression of the main veins in the pelvic region. It has been shown that the risk of VTE increases with increasing BMI . the risk is higher when obesity interacts with other thrombotic risk factors (Hotoleanu, 2020).
• 9.5. Not sitting with the legs crossed The client should refrain from any position that promotes vein compression. When the client crosses their legs or thighs, they obstruct some of the veins in the legs, slowing down blood flow. As a result, blood can pool in the veins, which may slightly increase the risk of blood clots in the legs (Triffin & Ketchum, 2020).
• 9.6. Participating in an exercise program Walking, swimming, and cycling help promote venous return through the contraction of the calf and thigh muscles. These muscles act as a pump to compress veins and support the column of blood returning to the heart. A narrative summary of the included studies related to DVT shows that exercise sessions with a target intensity of 70% peak heart rate significantly improved cardiorespiratory fitness. Additionally, exercise training also improved leg strength and flexibility, as well as calf pump function (Xu et al., 2021).
• 9.7. Quitting smoking Cigarettes contain nicotine which is a vasoconstrictor that affects blood clotting and circulation. Researchers described through their research that the mechanism of smoking impacts on blood is very dangerous because in smokers the activities of platelet predispose them to blood clots. Platelets regulate clot formation, which is a primary cause of heart attacks (Aslam et al., 2017).
• 9.8. Wearing properly sized, correctly applied compression stockings as indicated. Clients with DVT are at high risk for redevelopment and may need to wear stockings over the long term. The regular use of graduated elastic compression stockings reduced the incidence of PTS by 50%. Authors strongly recommend the early use and widespread implementation of graduated elastic stockings with adequate anticoagulant therapy for symptomatic proximal DVT to prevent the development of PTS (Patel, 2019).

10. Explain the purpose of activity restrictions and the need for balance between activity and rest. Rest reduces the oxygen and nutrient needs of compromised tissues and decreases the risk of fragmentation of thrombosis. Balancing rest with activity prevents exhaustion and further impairment of cellular perfusion. A systematic review found that in clients with acute DVT, early walking exercise is safe and may help to reduce acute symptoms and that in clients with previous DVT, exercise training does not increase leg symptoms acutely and may help to prevent or improve the postthrombotic syndrome (Patel, 2019).

11. Educate women about the possible effect of hormonal contraceptives on the risk of developing DVT. Hormonal contraceptives are widely used throughout the world and have been associated with blood clots in the legs and lungs. Users of hormonal contraceptives have a significantly increased risk of DVT compared to non-users. Women should be informed of these risks and offered education in fertility-awareness-based methods with comparable efficacy for family planning (Keenan et al., 2019).

12. Instruct in meticulous skin care of the lower extremities. Instruct the client to prevent or promptly treat breaks in the skin and report the development of ulcers or changes in skin color. Chronic venous congestion and post-phlebitis syndrome may develop, especially in the presence of severe vascular involvement and recurrent DVT, potentiating the risk of stasis ulcers.

13. Review the client’s usual medications and foods when on oral anticoagulant therapy. Warfarin interacts with many foods and drugs either increasing or decreasing the anticoagulant effect. Salicylates and excess alcohol decrease prothrombin activity, whereas vitamin K (multivitamins, bananas, leafy green vegetables) increases prothrombin activity and can cause a higher or lower INR, possibly outside the therapeutic range. Barbiturates increase the metabolism of coumadin drugs; antibiotics alter intestinal flora and may interfere with vitamin K synthesis.

Assessing and monitoring for potential complications is an integral part of the care provided to patients with deep vein thrombosis (DVT). Healthcare providers play a crucial role in assessing and monitoring patients for these potential complications to ensure timely intervention and optimal outcomes. Through vigilant assessment, including regular evaluation of vital signs, monitoring of coagulation profiles, and examination for signs and symptoms of complications such as pulmonary embolism or post-thrombotic syndrome, healthcare providers can identify any changes or developments that may require immediate attention.

1. Assess vital signs frequently. Vital signs provide baseline data and can indicate changes in the patient’s condition. Elevated temperature, increased heart rate, and decreased blood pressure may suggest infection or other complications associated with DVT.

2. Assess and document the location, size, and characteristics of the thrombus. This information helps evaluate the severity of the clot, the potential for migration or obstruction, and the effectiveness of treatment. It also serves as a baseline for comparison in subsequent assessments.

3. Monitor and document peripheral pulses. Diminished or absent pulses distal to the clot site may indicate compromised circulation due to clot extension or obstruction. Prompt recognition of reduced peripheral pulses is crucial for early intervention.

4. Assess for signs of pulmonary embolism (PE). DVT can lead to PE, a potentially life-threatening complication. Monitor for signs such as sudden dyspnea, tachypnea , chest pain, hemoptysis, anxiety, or changes in mental status. Early detection and treatment of PE are essential.

5. Observe for signs of compartment syndrome . Extensive or massive DVT can cause compartment syndrome due to increased pressure within the affected limb. Monitor for signs such as severe pain, swelling, paresthesia, pallor, and loss of pulse distal to the clot. Timely intervention can prevent tissue damage.

6. Perform regular neurological assessments. Neurological changes may indicate complications associated with DVT, such as stroke or cerebral venous thrombosis. Assess for changes in level of consciousness, motor or sensory deficits, visual disturbances, or sudden severe headaches.

7. Monitor laboratory values. Regularly assess coagulation studies, including prothrombin time (PT), activated partial thromboplastin time (aPTT), international normalized ratio (INR), and D-dimer levels. Abnormal results may indicate the progression or resolution of DVT or the effectiveness of anticoagulant therapy.

8. Evaluate for signs of bleeding or hemorrhage. Anticoagulant therapy increases the risk of bleeding. Monitor for signs such as tachycardia, hypotension , melena, hematemesis, hematuria, ecchymosis, or bleeding from invasive lines or puncture sites. Early recognition and intervention can prevent complications.

9. Assess for skin changes and potential ulceration. Chronic DVT can cause venous stasis ulcers. Monitor for skin discoloration, edema, increased warmth, or breakdown in the affected limb. Prompt identification and management of ulcers can prevent infection and further tissue damage.

10. Educate the patient on signs and symptoms to report. Providing education empowers the patient to recognize and report any changes or symptoms promptly. Reinforce the importance of reporting pain, swelling, redness, warmth, shortness of breath, chest pain, or any other concerning symptoms.

Administering medications and providing pharmacologic support are essential components of the comprehensive management of patients with deep vein thrombosis (DVT). Pharmacologic support in patients with DVT requires close monitoring of medication effectiveness, adverse effects, and potential drug interactions. Regular laboratory assessments, including coagulation studies and complete blood counts, are essential to ensure appropriate dosing and therapeutic efficacy while minimizing the risk of bleeding complications. Nursing professionals play a crucial role in administering medications, monitoring patient response , and educating patients about the importance of adherence and potential side effects.

1. Thrombolytic agents , such as alteplase, anistreplase, reteplase, streptokinase, tenecteplase, and urokinase These agents are intended to bring about clot lysis (breakdown of the clot) and immediate normalization of venous blood flow. The use of thrombolytic medications to lyse DVT can cause intracranial bleeding, though this is infrequent, and death or impairment can result. The need should be compelling when thrombolysis is considered in a setting of known contraindications (Patel, 2019).

2. Morphine sulfate and anti-anxiety agents These are given to decrease pain or anxiety and improve the work of breathing, maximizing gas exchange. However, caution should be practiced when giving morphine because current morphine use is associated with PE in DVT clients. The risk of PE increased with augmented morphine dosage only in clients treated with morphine within the past 30 days, according to a study (Lee et al., 2014).

3. Anticoagulants The mainstay of medical therapy has been anticoagulation since the introduction of heparin in the 1930s. Other anticoagulation drugs have subsequently been added to the treatment armamentarium over the years, such as vitamin K antagonists and low-molecular-weight heparin (LMWH). Long-term coagulation is necessary to prevent the high frequency of recurrent venous thrombosis or thromboembolic events (Patel, 2019).

4. Opioid and nonopioid analgesics This relieves pain and decreases muscle tension. Opioids produce their effect by acting as agonists at opioid receptors, which are found in the brain , spinal cord , and sites outside the CNS. Most opioids have a similar spectrum of adverse effects, such as respiratory depression , sedation, nausea / vomiting , and constipation (El-Tallawy et al., 2021).

5. Antipyretics (Acetaminophen) This reduces fever and inflammation. Since NSAIDs are not recommended for clients with DVT, acetaminophen may be appropriate for short-term use. Regular monitoring for hepatotoxicity is required for clients who receive acetaminophen regularly and beyond the maximum dosage of 3 g daily (El-Tallawy et al., 2021).

Laboratory and diagnostic tests provide valuable information about the patient’s clotting status, the severity of the thrombus, and the effectiveness of treatment interventions. Monitoring laboratory and diagnostic procedures in patients with DVT allows healthcare providers to assess the effectiveness of treatment, detect potential complications, and adjust the management plan accordingly. Close collaboration between nursing professionals, laboratory personnel, and radiologists is crucial to ensure timely and accurate testing, interpretation of results, and appropriate interventions.

1. Ultrasonography Ultrasonography is currently the first-line imaging examination for DVT because of its relative ease of use, absence of irradiation or contrast material, and high sensitivity and specificity in institutions with experienced sonographers. Compression ultrasonography entails imaging the calf to the groin in the axial plane. Some protocols use gray-scale ultrasonography alone, whereas others include Doppler interrogation (Hoffer & Cho, 2022).

2. D-dimer assay D-dimer is a marker for clot lysis. This test can also be used to check the effectiveness of the treatment. D-dimer levels remain elevated in DVT for about seven days. Clients presenting late in the course, after clot organization and adherence have occurred, may have low levels of D-dimer. Current evidence strongly supports using a D-dimer assay in the setting of suspected DVT (Patel, 2019).

3. Impedance plethysmography (IPG) This test uses an inflated cuff for blocking the venous flow and monitoring the blood volume increase in the limb. In some countries, IPG has been the initial non-invasive diagnostic test of choice and is sensitive and specific for proximal vein thrombosis. However, IPG also has several limitations; among them is insensitivity for calf vein thrombosis, non-occluding proximal vein thrombus, and iliofemoral vein thrombosis above the inguinal ligament (Patel, 2019).

4. Contrast venography This test uses radiopaque contrast media injected through a foot vein to localize thrombi in the deep venous system. The criterion standard for diagnostic imaging for DVT remains venography with pedal vein cannulation, intravenous contrast injection, and serial limb radiographs (Patel, 2019).

Providing perioperative care for patients with deep vein thrombosis (DVT) requires a comprehensive and tailored approach to ensure optimal outcomes. Individualized treatment plans are essential when providing perioperative care for patients with DVT. The management approach should be based on a thorough assessment of the patient’s medical history , clot characteristics, and overall risk profile.

1. Placement of a vena cava filter The filter is inserted inside the vena cava. The filter catches blood clots before they travel to the lungs, which prevents pulmonary embolism. Inferior vena cava filters are not recommended in clients with acute VTE on anticoagulant therapy. An inferior vena cava filter is a mechanical barrier to the flow of emboli larger than 4 mm (Patel, 2019).

2. Thrombectomy The most severe cases of DVT may require the surgical removal of the blood clot from the vein (thrombectomy). Surgical thrombus removal has traditionally been used in clients with massive swelling and phlegmasia cerulea dolens. When thrombosis is extensive, fibrinolysis alone may be inadequate to dissolve the volume of the thrombus present (Patel, 2019).

3. Replacement of venous valves Percutaneously placed bioprosthetic venous valves are under development and may provide a minimally invasive therapy for the long-term complication of postthrombotic syndrome (PTS) due to valve destruction. Effective therapy should diminish one of the primary indications for aggressive thrombolytic therapy for acute DVT (Patel, 2019).

Recommended nursing diagnosis and nursing care plan books and resources.

Disclosure: Included below are affiliate links from Amazon at no additional cost from you. We may earn a small commission from your purchase. For more information, check out our privacy policy .

Ackley and Ladwig’s Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care We love this book because of its evidence-based approach to nursing interventions. This care plan handbook uses an easy, three-step system to guide you through client assessment, nursing diagnosis, and care planning. Includes step-by-step instructions showing how to implement care and evaluate outcomes, and help you build skills in diagnostic reasoning and critical thinking.

Nursing Care Plans – Nursing Diagnosis & Intervention (10th Edition) Includes over two hundred care plans that reflect the most recent evidence-based guidelines. New to this edition are ICNP diagnoses, care plans on LGBTQ health issues, and on electrolytes and acid-base balance.

Nurse’s Pocket Guide: Diagnoses, Prioritized Interventions, and Rationales Quick-reference tool includes all you need to identify the correct diagnoses for efficient patient care planning. The sixteenth edition includes the most recent nursing diagnoses and interventions and an alphabetized listing of nursing diagnoses covering more than 400 disorders.

Nursing Diagnosis Manual: Planning, Individualizing, and Documenting Client Care  Identify interventions to plan, individualize, and document care for more than 800 diseases and disorders. Only in the Nursing Diagnosis Manual will you find for each diagnosis subjectively and objectively – sample clinical applications, prioritized action/interventions with rationales – a documentation section, and much more!

All-in-One Nursing Care Planning Resource – E-Book: Medical-Surgical, Pediatric, Maternity, and Psychiatric-Mental Health   Includes over 100 care plans for medical-surgical, maternity/OB, pediatrics, and psychiatric and mental health. Interprofessional “patient problems” focus familiarizes you with how to speak to patients.

Other recommended site resources for this nursing care plan:

• Nursing Care Plans (NCP): Ultimate Guide and Database MUST READ! Over 150+ nursing care plans for different diseases and conditions. Includes our easy-to-follow guide on how to create nursing care plans from scratch.
• Nursing Diagnosis Guide and List: All You Need to Know to Master Diagnosing Our comprehensive guide on how to create and write diagnostic labels. Includes detailed nursing care plan guides for common nursing diagnostic labels.

Other care plans for hematologic and lymphatic system disorders:

• Anaphylactic Shock
• Aortic Aneurysm
• Bleeding Risk & Hemophilia
• Deep Vein Thrombosis
• Disseminated Intravascular Coagulation
• Sepsis and Septicemia
• Sickle Cell Anemia Crisis

Recommended journals, books, and other interesting materials to help you learn more about deep vein thrombosis nursing care plans and nursing diagnosis:

• Aslam, S., Mirza, R., & Shaukat, H. (2017). Obesity and Smoking are Risk Factors for Deep Vein Thrombosis in general population – a comparative clinical study. Pakistan Journal of Medical & Health Sciences , 11 (4).
• Behera, C., Devassy, S., & Gupta, S. K. (2017). Leg massage by mother resulting in fatal pulmonary thromboembolism. Medico-Legal Journal , 86 (3).
• Bhutta, B. S., Alghoula, F., & Berim, I. (2022). Hypoxia – StatPearls . NCBI. Retrieved March 27, 2023.
• Douketis, J. D. (2023). Perioperative management of patients receiving anticoagulants. UpToDate .
• Doyle, G. R., & McCutcheon, J. A. (2015). Clinical Procedures for Safer Patient Care . BC Open Textbook Project.
• El-Tallawy, S. N., Nalamasu, R., Salem, G. I., LeQuang, J. A. K., Pergolizzi, J. V., & Christo, P. J. (2021). Management of Musculoskeletal Pain: An Update with Emphasis on Chronic Musculoskeletal Pain. Pain and Therapy , 10 .
• Endig, H., Michalski, F., & Beyer-Westendorf, J. (2016). Deep Vein Thrombosis – Current Management Strategies. Clinical Medicine Insights: Therapeutics .
• Gebhard, C. E., Zellweger, N., Gebhard, C., Hollinger, A., Chrobok, L., Stahli, D., Schönenberger, C. M., Todorov, A., Aschwanden, M., & Siegemund, M. (2021, December 25). Prone Positioning as a Potential Risk Factor for Deep Vein Thrombosis in COVID-19 Patients: A Hypothesis Generating Observation . NCBI. Retrieved March 27, 2023.
• Gonthier, M.-C., Gendron, N., Eloy, P., Bourrienne, M.-C., Alhenc-Gelas, M., Pouplard, C., Tardy, B., Szymezak, J., Burdet, C., Gkalea, V., Faille, D., & Ajzenberg, N. (2021, September 24). Heparin-induced Thrombocytopenia Diagnosis: A Retrospective Study Comparing Heparin-induced Platelet Activation Test to 14 C-serotonin Release Assay . NCBI. Retrieved March 29, 2023.
• Gupta, N., Zhao, Y.-Y., & Evans, C. E. (2019, September). The stimulation of thrombosis by hypoxia. Thrombosis Research , 181 .
• Hoffer, E. K., & Cho, K. J. (2022, August 15). Imaging in Deep Venous Thrombosis of the Lower Extremity: Practice Essentials, Computed Tomography, Magnetic Resonance Imaging . Medscape Reference. Retrieved March 27, 2023.
• Hotoleanu, C. (2020, April). Association between obesity and venous thromboembolism. Medicine Pharmacy Reports , 93 (2).
• Keenan, L., Kerr, T., Duane, M., & Van Gundy, K. (2019, January). Systematic Review of Hormonal Contraception and Risk of Venous Thrombosis. The Linacre Quarterly , 85 (4).
• Keiter, J. E., Johns, D., & Rockwell, W. B. (2015). Importance of Postoperative Hydration and Lower Extremity Elevation in Preventing Deep Venous Thrombosis in Full Abdominoplasty: A Report on 450 Consecutive Cases Over a 37-Year Period. Aesthetic Surgery Journal , 35 (7).
• Klaiber, U., Stephan-Paulsen, L. M., Bruckner, T., Müller, G., Auer, S., Farrenkopf, I., Fink, C., Dörr-Harim, C., Diener, M. K., Büchler, M. W., & Knebel, P. (2018). Impact of preoperative patient education on the prevention of postoperative complications after major visceral surgery: the cluster randomized controlled PEDUCAT trial. Trials , 19 (288).
• Lee, C. W.-S., Muo, C.-H., Liang, J.-A., Sung, F.-C., Kao, C.-H., & Yeh, J.-J. (2014, March). Pulmonary embolism is associated with current morphine treatment in patients with deep vein thrombosis. The Clinical Respiratory Journal , 9 (2).
• Nicolas, D., Nicolas, S., Hodgens, A., & Reed, M. (2023, March). Heparin Induced Thrombocytopenia – StatPearls . NCBI. Retrieved March 29, 2023, from
• The North American Thrombosis Forum. (2022, February 17). Patient Pulse: Pain Relievers and Anticoagulation – What’s the Story? North American Thrombosis Forum. Retrieved March 27, 2023.
• Ouellette, D. R., & Mosenifar, Z. (2020, September 18). Pulmonary Embolism (PE) Clinical Presentation: History, Physical Examination, Complications . Medscape Reference. Retrieved March 28, 2023.
• Patel, K. (2019, June 5). Deep Venous Thrombosis (DVT): Practice Essentials, Background, Anatomy . Medscape Reference. Retrieved March 27, 2023.
• Schick, M. (2023, January 19). Deep Vein Thrombosis – StatPearls . NCBI. Retrieved March 27, 2023.
• Schreiber, D., & Brenner, B. E. (2020, October 30). Anticoagulation in Deep Venous Thrombosis: Advantages of Anticoagulant Therapy, Initial Anticoagulation Therapy, Long-Term Anticoagulation . Medscape Reference. Retrieved March 29, 2023.
• Sehgal, I. S., Dhooria, S., Agarwal, R., & Behera, D. (2017, December 30). Use of a Flexible Cryoprobe for Removal of Tracheobronchial Blood Clots . Respiratory Care. Retrieved March 27, 2023.
• Triffin, M., & Ketchum, D. (2020, May 18). Is Sitting With Your Legs Crossed Bad for You? Here’s What to Know | livestrong. Livestrong.com .
• Umerah, C. O., & Momodu, I. I. (2022, July). Anticoagulation – StatPearls . NCBI. Retrieved March 29, 2023.
• Unver, S., Kivanc, G., & Aiptekin, H. M. (2018). Deep breathing exercise education receiving and performing status of patients undergoing abdominal surgery . NCBI. Retrieved March 27, 2023.
• Vyas, V., & Goyal, A. (2022). Acute Pulmonary Embolism – StatPearls . NCBI. Retrieved March 27, 2023.
• Wade, R., Paton, F., & Woolacott, N. (2016). Systematic review of patient preference and adherence to the correct use of graduated compression stockings to prevent deep vein thrombosis in surgical patients. Journal of Advanced Nursing , 73 (2).
• Wayne, G. (2023, March 18). Risk for Bleeding – Nursing Diagnosis & Care Plan . Nurseslabs. Retrieved March 28, 2023.
• Xu, L., Fu, C., Zhang, Q., He, C., & Wei, Q. (2021). The effectiveness of exercise training in treating venous thromboembolism: a systematic review. The Physician and Sportsmedicine , 49 (1).
• Yu, A., Ding, W., Lin, W., Cai, J., & Huang, W. (2022, January). Application of pulmonary rehabilitation in patients with pulmonary embolism (Review). Experimental and Therapeutic Medicine , 23 (1).
• Zhang, Y., Jin, J., Song, B., Wang, Y., & Liang, M. (2021, April 15). Vascular boot warming improves clinical outcomes of patients with deep vein thrombosis in lower extremities . NCBI. Retrieved March 27, 2023.

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Deep vein thrombosis

Investigating DVT

An approach to symptoms suggestive of lower deep vein thrombosis (DVT)

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This article has a correction. Please see:

• Deep vein thrombosis - March 21, 2018
• M J Stubbs , clinical research fellow and haematology registrar 1 ,
• Maria Mouyis , consultant rheumatologist 2 ,
• Mari Thomas , consultant haematologist 1
• 1 University College London Hospital, London, UK
• 2 North West London Hospitals NHS Trust, London, UK
• Correspondence to M Stubbs m.stubbs{at}doctors.org.uk

What you need to know

Pain, swelling, and redness of the affected limb are common symptoms of deep vein thrombosis (DVT)

Assess patients’ clinical risk of DVT using the Wells score

Refer urgently patients with suspected DVT for D-dimer test and/or proximal leg ultrasound

Anticoagulation to prevent clot extension and embolisation is initiated in secondary care, ideally within four hours of presentation

A direct oral anticoagulant is now first line for anticoagulation in patients with DVT not associated with cancer

Deep vein thrombosis (DVT) commonly affects the lower limb, with clot formation beginning in a deep calf vein and propagating proximally. 1 It is a common venous thromboembolic (VTE) disorder with an incidence of nearly 1.6 per 1000 inhabitants a year. 2 3 4 The rate of involvement of particular sites varies: distal veins 40%, popliteal 16%, femoral 20%, common femoral 20%, and iliac veins 4%. 1 Certain medical conditions listed in box 1 increase the likelihood of clot formation in the deep veins. Upper limb DVT represents less than 10% of all DVT, and central venous catheters are the main risk factor. 7 Venocaval thromboses are rare and are associated with malignancy, compression, and vascular abnormalities. 8 This article provides an overview for non-specialists on initial approach to patients with suspected DVT.

DVT risk factors 5 6

Transient risk factors.

Surgery with general anaesthetic (increased if >30 minutes)*

Hospitalisation (increased if >3 days with “bed rest”)*

Caesarean section*

Oestrogen therapy

Pregnancy or puerperium

Leg injury with reduced mobility for at least three days

Persistent risk factors

Active cancer

Medical condition with increased risk of recurrent VTE (inflammatory bowel disease, systemic lupus erythematosus)

Unprovoked VTE

If the above “Transient” and “Persistent” criteria are not met

*10 fold increase in VTE risk

Sources and selection criteria

We searched Medline and Cochrane databases for clinical trials, systematic reviews, and meta-analyses relevant to the diagnosis and management of DVT. Search terms included “deep vein thrombosis,” “venous thromboembolism,” “direct oral anticoagulants,” “thrombolysis,” and “post-thrombotic syndrome.” We reviewed guidelines from the British Society of Haematology, American College of Chest Physicians, and National Institute for Health and Care Excellence (NICE).

How do patients present?

Early recognition and referral for further investigation of DVT is likely to happen in primary care, however, diagnosis and initiation of anticoagulant treatment usually takes place in secondary care or hospital settings.

Pain, swelling, and redness in the affected limb are common symptoms. Pain is typically throbbing in nature, and comes on while walking or bearing weight. Skin changes include erythema, warmth, and oedema ( fig 1 ). 9 10 Some patients are asymptomatic, having had investigation for other conditions such as pulmonary embolism or malignancy 11 (although data on how many is unavailable). Alternative diagnoses to consider include cellulitis, ruptured Baker’s cyst, chronic venous insufficiency, and lymphoedema. 2 3 4

Deep vein thrombosis in the right leg of a patient, with leg swelling and erythema visible

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How is it diagnosed?

Refer patients with symptoms suggestive of DVT to acute/emergency services for further evaluation. 12 Diagnosis is based on clinical assessment and investigations (ultrasound or D-dimer) being conducted ideally within four hours of presentation as per NICE recommendations. 12 If a delay is expected, interim anticoagulation can be offered in hospital or a secondary care setting (discussed below under ‘How is it treated?’ ) to avoid clot progression and the risk of pulmonary embolism. 12 Ultrasound investigation is recommended within 24 hours in suspected cases. 12

Clinical score

The pre-test probability of DVT can be calculated using a validated score, such as the Wells score ( box 2 ), which combines assessment for risk factors and clinical features of DVT. 12 NICE recommends using the modified two-tier Wells score, whereas the American College of Chest Physicians (ACCP) guidelines cite the three-tiered Wells score. 9 10 Both scores are clinically acceptable, and local departmental guidance determines which is used in practice. 12 14

Pre-test probability scores for DVT 10 13

Wells score (1997).

Active cancer (treatment ongoing or within 6 months, or palliative) +1 point

Paralysis, paresis, recent immobilisation of the lower limbs +1 point

Recently bedridden for >3 days, or major surgery within 4 weeks +1 point

Localised tenderness along distribution of deep venous system +1 point

Entire leg swelling +1 point

Calf swelling, >3 cm, compared with asymptomatic leg +1 point

Pitting oedema (greater in symptomatic leg) +1 point

Collateral superficial veins (non-varicose) +1 point

Alternative diagnosis as likely, or more likely, than DVT −2 points

Modified Wells score (2003)

Scoring criteria as for Wells Score, with the addition of

Previous documented DVT +1 point

Interpretation

Wells score ≥3 high, 1-2 moderate, 0 low probability

Modified Wells score ≥2 likely DVT, <2 DVT unlikely

In clinical trials, 10 13 the Wells score has shown a high negative predictive value in patients with a low probability score for DVT (negative predictive value 99.7%, 95% confidence interval 98.3% to 100%). It is thus effective to exclude DVT in these patients. However, the score had a lower negative predictive value in high risk patients (82%, 95% confidence interval 98.3% to 100%), and should not be used to rule out DVT in these patients. 10 13 Patients were excluded if they were under 18, had less than three months’ life expectancy, were pregnant, or had already started anticoagulant treatment. The score is not appropriate in these groups. Investigation with D-dimer or ultrasound is required after calculating the pre-test probability in all patients, but the investigation pathway varies (infographic). 14

D-dimer test

The D-dimer blood test measures degraded fibrinogen, which is raised in patients with a clot. The reference range varies and is set by the laboratory. This test is recommended in patients with a low or moderate clinical probability of DVT, as calculated by the Wells score. 13 Patients with a high clinical probability of DVT need not undergo the D-dimer test and should directly have ultrasonography. 13 The test is easy to perform and readily available in secondary care. It has high sensitivity but is not very specific. Thus, a negative D-dimer can be used to exclude DVT in patients with a low clinical probability of DVT. However, it cannot confirm DVT, as D-dimer can be raised in other conditions including malignancy, infection, pregnancy, post-surgery, inflammation/trauma, disseminated intravascular coagulopathy, and renal impairment. 14 15 An ultrasound is needed to confirm DVT. 14

Ultrasonography

Request an ultrasound scan of the leg in patients with a high pre-test probability of DVT or with a low/moderate probability and a positive D-dimer test ( fig 2 ). Guidelines recommend performing an ultrasound (when indicated) within four hours of presentation, otherwise interim anticoagulation should be initiated. If not possible within four hours, ultrasound should be performed within 24 hours. In practice, substantial delays in ultrasound scanning for DVT should not occur.

Ultrasound image of the lower limb veins. (A) Normal deep vein, with patent vessel visible. (B) Thrombosed deep vein, with occluded vein apparent within dashed line

Proximal, above knee ultrasound is recommended in low risk cases, and either proximal or whole leg in high risk cases. 12 14 Rarely, a repeat scan after one week might be required to ensure DVT is not missed, for example in patients with a moderate/high probability and an initial negative ultrasound scan. Initiate anticoagulation during this window period. 12 14

Alternative imaging modalities, such as venography (computed tomography or magnetic resonance imaging, where radio-opaque contrast is injected to visualise the patency of vasculature) can be used if there is diagnostic uncertainty (eg, an inconclusive ultrasound report that might be caused by chronic venous scarring) or if ultrasound is impractical (eg, plaster cast). 14 These modalities are not routinely recommended, and should be discussed with a specialist before requesting them. 14

What additional investigations might be considered?

Cancer is a recognised risk factor for developing DVT. Up to 10% of DVT patients are subsequently diagnosed with a malignancy. 16 17 However, recent trials have found a low yield from screening for occult malignancy in patients with unprovoked DVT. 18 19 20 21 NICE now recommends only a limited cancer screen in patients with unprovoked DVT (ie, history, examination, basic blood tests, and age appropriate national cancer screening investigation, eg, in UK, mammography in women who are 50 to 70). 12

Inherited and acquired thrombophilias contribute to DVT. There is conflicting guidance on the role of thrombophilia testing, 22 and this should be discussed with a haematologist. 23

What are the complications?

Common chronic complications after DVT include post-thrombotic syndrome (25%-38%) and venous ulceration (9.8%), whereas pulmonary embolism (6%-32%) is more acute and can be fatal in 5%-10% of cases. 1 24 25 26 27 Complications can occur immediately following an acute DVT or several months to years later.

Patients with post-thrombotic syndrome might present with pain, swelling/oedema, leg heaviness, aching, skin discolouration, or venous ulceration. Venous ulcers are typically located medially above the ankle, with an irregular outline, and can be discoloured, oedematous, and exudative. The main risk factors include recurrent ipsilateral DVT and non-therapeutic international normalised ratio (>50% of the time). 28 Other risks include advanced age, increased body mass index, female sex, and size and location of thrombosis. 28 29

Rarer complications include chronic thromboembolic pulmonary hypertension, sudden death, and loss of limb. 1

How is it treated?

Anticoagulation to prevent clot extension and embolisation is the standard treatment, where bleeding risk permits. It is started in hospital or secondary care settings after a diagnosis of DVT is established, preferably within four hours of presentation. 12 30

Direct oral anticoagulants

Guidelines from NICE and ACCP recommend direct oral anticoagulants (DOACs) as first line treatment for DVT. 12 14 DOACs include direct factor Xa inhibitors apixaban, rivaroxaban, and edoxaban, and a direct thrombin inhibitor, dabigatran. Randomised controlled trials have shown DOACs to be at least as effective as vitamin K antagonists in treating thromboembolic events (see supplemental file for details of these trials). 31 32 33 34 Dabigatran and edoxaban require initial treatment with low molecular weight heparin (LMWH) (>5 days) before commencement of the DOAC, whereas rivaroxaban and apixaban do not 31 32 33 34 35 36 (see supplementary file). Typically patients are anticoagulated between five and 17 hours of taking these drugs. Caution is advised, however, in patients with chronic renal impairment, particularly with a glomerular filtration rate <30 ml/min, and in patients taking other drugs that have possible risk of interaction. 37

Low molecular weight heparin and warfarin

These are established anticoagulants that are preferred in certain people, such as those with liver and renal dysfunction, extremes of body weight (<50 kg or >120 kg), and DVT associated with cancer.

Warfarin, a vitamin K antagonist, is an effective and cheap oral anticoagulant. However, it requires frequent monitoring with blood tests, and has a narrow therapeutic window, with bleeding events being not uncommon. 30 LMWH is delivered daily or twice daily as a subcutaneous injection. It has a rapid onset of action, predictable anticoagulation effect, and does not require routine monitoring. 30

LMWH is recommended in patients with cancer-associated VTE, because VTE recurrence rates are lower than in patients taking vitamin K antagonists. 18 38 39 40 41 However, in a randomised controlled trial (1050 patients with cancer-associated VTE) oral edoxaban was shown to be non-inferior to daltaparin in terms of VTE recurrence (non-inferiority P=0.006, 95% confidence interval 0.70 to 1.36), but with a higher rate of major bleeding (P=0.04, 95% confidence interval 1.03 to 3.04). 42 More investigation is needed before recommending DOACs in cancer-associated VTE.

How long is anticoagulation continued?

The optimal duration of anticoagulation depends on what provoked the DVT, bleeding risk, patient preference, and thrombophilia status. Consensus expert opinion is to offer three months of anticoagulation treatment for patients with a DVT provoked by surgery or with a non-surgical transient risk factor. 38 Patients with a proximal DVT and a persistent risk factor or high risk of DVT recurrence might be offered lifelong anticoagulation. 43 Scoring systems such as the DASH prediction score and HERD002 score (in women) help predict recurrence after an unprovoked VTE event. 43 44 These might be used for risk stratification of patients to guide duration of anticoagulation.

What other treatments are available?

Some patients, such as those with extensive DVT, might require escalation of treatment beyond simple anticoagulation to reduce complications and recurrence of DVT. Box 3 lists other treatment options for DVT clot dissolution. These might be offered in specialist settings.

Other treatment options for patients with DVT 45

Percutaneous endovascular venous thrombolysis

Endovascular mechanical thrombectomy

Ultrasonic destruction of thrombus (+ thrombolysis)

Endovascular stenting (including iliac vein stenting)

Systemic thrombolysis (rarely used)

Surgical thrombectomy (rarely used, reserved for failed thrombolysis)

Inferior vena cava filter (rarely used and with limited/controversial evidence)

A Cochrane review (17 trials, 1103 patients) found that thrombolysis with anticoagulation reduced the incidence of post-thrombotic syndrome by a third compared with anticoagulation alone in patients with lower limb DVT. 46 47 On follow-up at >5 years, the rate of post-thrombotic syndrome was 390/1000 in the thrombolysis group, compared with 658/1000 in the control group (relative risk 0.58, 95% confidence interval 0.45 to 0.77; P<0.0001). No difference in mortality was observed between the two groups. Bleeding complications were increased in the thrombolysis group compared with controls (relative risk 2.23; 95% confidence interval 1.41 to 3.52, P=0.0006). There is limited data on the effect of thrombolysis in preventing leg ulceration, pulmonary embolism, and recurrence.

NICE guidelines suggest thrombolysis can be considered in an acute proximal DVT (<14 days) in a patient with low bleeding risk, with good performance status, and life expectancy >1 year. 47 Selection of patients must be guided by a multidisciplinary approach, with inputs from a vascular surgeon and interventional radiologist, and must consider patient preferences. 28 45 46 47 48

Results from the large multicentre ATTRACT study comparing catheter-directed thrombolysis with standard anticoagulation treatment in 692 DVT patients are expected soon, and will further inform thrombolysis decisions. 41

Is there a role for compression stockings?

Historically, it was believed that wearing compression stockings after DVT could reduce the risk of developing post-thrombotic syndrome. However, trials and meta-analyses have found no evidence of this, 49 50 51 and it is no longer recommended to wear compression stockings to prevent post-thrombotic syndrome. 38

How does management of superficial vein thrombosis differ?

Patients with superficial vein thrombosis can present with leg pain, erythema, and swelling, which are often indistinguishable from DVT. Patients with a recent superficial vein thrombosis have a four- to sixfold increased risk for DVT/pulmonary embolism. Risk factors for extension of superficial vein thrombosis into DVT include a superficial vein thrombosis <10 cm from the saphenofemoral junction, male sex, history of VTE, cancer, absence of varicose veins, and severe venous insufficiency. 8 Management is directed at reducing the risk of DVT, and has been discussed in depth elsewhere. 52

Questions for future research

What is the efficacy and safety of DOACs for treatment of DVT in patients with cancer?

Additional educational resources

British Society of Haematology haemostasis guidelines ( www.b-s-h.org.uk/guidelines )

Royal College of Obstetricians and Gynaecologists guidelines ( www.rcog.org.uk/guidelines )

American College of Chest Physicians ( www.chestnet.org/Guidelines-and-Resources )

BMJ review—BMJ clinical review. Diagnosis and management of heritable thrombophilias 14

BMJ Practice Pointer—Superficial vein thrombosis: http://www.bmj.com/content/350/bmj.h2039

Information resources for patients

Thrombosis UK Charity: www.thrombosisuk.org

Education into practice

Describe how you would investigate a patient with suspected DVT

How would you draw up a protocol for management of DVT in hospital?

What are the different treatment options for DVT, including indications for bridging therapy and duration of treatment?

How patients were involved in the creation of this article

A patient and carer kindly reviewed an earlier draft of this article. The patient highlighted the importance of making a timely diagnosis of DVT. Based on his suggestion, we have included the timescales suggested by NICE for urgent investigations and initiation of treatment.

Contributors M J Stubbs, M Mouyis, M Thomas

We have read and understood The BMJ policy on declaration of interests and declare that we have no competing interests.

Patients were not involved in the creation of this article.

Provenance and peer review: Commissioned; externally peer reviewed.

• Strijkers RH ,
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• ↵ Behravesh S, Hoang P, Nanda A, et al. Pathogenesis of thromboembolism and endovascular management. Thrombosis 2017;2017:3039713.
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• ↵ National Institute for Health and Care Excellence. Guidelines on ultrasound-enhanced, catheter-directed thrombolysis for deep vein thrombosis. 2015. https://www.nice.org.uk/guidance/ipg523
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9.1: Learning Objectives

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Case 8 describes a patient’s experience with Deep Vein Thrombosis (DVT) that develops as a complication of her hospitalization.

Learners reviewing this case have an opportunity to explore how DVT develops, treatment options and prevention. The interprofessional collaboration is role modelled between nursing, ultrasound, nuclear medicine and medical residents.

Learning Objectives

In this case, learners have an opportunity to:

• Review etiological factors (i.e., risk factors, prevalence, co­morbidities) associated with DVT
• Build knowledge related to the patient’s experience of DVT, specifically related to compromised communication
• Continue to develop comprehensive assessment, and monitoring skills and abilities (e.g., assessment, diagnostic studies, laboratory data)
• Consider the links between evidence-based knowledge and practice in the care of patients with DVT
• Recommend interventions based on the risk factors, status, and progression of DVT
• Define the roles of healthcare professionals and the contributions they make to the healthcare team (or describe your own role and the roles of those in other professions)

Introduction

Conclusions, acknowledgments, statement of ethics, conflict of interest statement, funding sources, author contributions, data availability statement, deep medullary vein thrombosis in newborns: a systematic literature review.

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Jacopo Norberto Pin , Letizia Leonardi , Margherita Nosadini , Maria Federica Pelizza , Luca Capato , Luca Piretti , Maria Elena Cavicchiolo , Paolo Simioni , Eugenio Baraldi , Giorgio Perilongo , Matteo Luciani , Stefano Sartori; Deep Medullary Vein Thrombosis in Newborns: A Systematic Literature Review. Neonatology 2 October 2023; 120 (5): 539–547. https://doi.org/10.1159/000530647

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Background: Deep medullary vein (DMV) thrombosis is a rare cause of brain damage in both preterm and full-term neonates. In this study, we aimed to collect data on clinical and radiological presentation, treatment, and outcome of neonatal DMV thrombosis. Methods: Systematic literature review on neonatal DMV thrombosis was carried out in PubMed, ClinicalTrial.gov, Scopus, and Web of Science up to December 2022. Results: Seventy-five published cases of DMV thrombosis were identified and analysed (preterm newborns were 46%). Neonatal distress, respiratory resuscitation, or need for inotropes were present in 34/75 (45%) of patients. Signs and symptoms at presentation included seizures (38/75, 48%), apnoea (27/75, 36%), lethargy or irritability (26/75, 35%). At magnetic resonance imaging (MRI), fan-shaped linear T2 hypointense lesions were documented in all cases. All had ischaemic injuries, most often involving the frontal (62/74, 84%) and parietal lobes (56/74, 76%). Signs of haemorrhagic infarction were present in 53/54 (98%). Antithrombotic treatment was not mentioned in any of the studies included. Although mortality was low (2/75, 2.6%), a large proportion of patients developed neurological sequelae (intellectual disability in 19/51 [37%] and epilepsy in 9/51 [18%] cases). Conclusions: DMV thrombosis is rarely identified in the literature, even if it is possibly under-recognized or under-reported. Presentation in neonatal age is with seizures and non-specific systemic signs/symptoms that often cause diagnostic delay, despite the pathognomonic MRI picture. The high rate of morbidity, which determines significant social and health costs, requires further in-depth studies aimed at earlier diagnosis and evidence-based prevention and therapeutic strategies.

The deep medullary veins (DMVs) belong to the deep cerebral venous system. They are located in the subcortical white matter and drain the deep white matter and the striate body. The DMVs show a radial pattern in the superior lateral corner of the lateral ventricles. Through the subependymal veins, they are tributaries of the internal cerebral vein, the basal vein of Rosenthal, and the vein of Galen [ 1‒3 ] (Table 1 ). Recently, DMV engorgement and/or thrombosis have been recognized as an important cause of brain damage both in preterm and full-term neonates [ 4, 5 ], although their incidence in children is not known. DMV thrombosis can occur isolated or in association with cerebral sinovenous thrombosis (CSVT), a more frequent condition with estimated incidence of 0.67 cases per 100,000 newborns per year [ 6 ] and multifactorial aetiology in neonates, including maternal factors (such as pre-eclampsia, diabetes), placental factors (chorioamnionitis), and/or perinatal causes (i.e., birth asphyxia, sepsis, cardiac defects, inherited prothrombotic abnormalities) [ 6, 7 ]. CSVT is recognized as an important cause of neurodevelopmental disabilities; affected children suffer intellectual disabilities, disorders of speech and language, cerebral palsy, or epilepsy in 23–79% of cases [ 6 , 8‒10 ], whereas limited data exist regarding the aetiology and the neurological sequelae of neonatal DMV thrombosis [ 11, 12 ]. Brain magnetic resonance imaging (MRI) is the gold standard for the diagnosis of DMV thrombosis, and recent technical innovations have contributed to improve its diagnostic sensitivity [ 1, 11, 12 ]. DMV involvement on MRI can be an indirect sign of CSVT or it can independently be a direct sign of DMV thrombosis [ 1, 13 ]. The spectrum of parenchymal radiological findings in DMV thrombosis includes vasogenic or cytotoxic oedema and haemorrhage of variable extent (from petechial haemorrhages to larger haematomas) [ 5, 13 ]. No clinical trials or definite treatment algorithms are available for DMV thrombosis in neonates. The choice of antithrombotic therapy is therefore based on the experience of the single centres or on indications extrapolated from available guidelines on CSVT [ 14‒18 ]. The aim of this study was to review the available pertinent literature in order to provide an up-to-date summary of the available evidence on clinical-radiological presentation, treatment, and outcome of DMV thrombosis in neonates.

Anatomical and pathological details of DMV

We performed a systematic literature review of neonatal DMV thrombosis, complying with the PRISMA guidelines. The search was carried out in PubMed, ClinicalTrial.gov, Scopus, and Web of Science by three independent researchers (L.L., L.C., and J.N.P.) from databases inception up to December 2022. The search terms used were ([deep medullary vein] and [stroke or infarction or ischaemia or ischaemic or thrombosis] and [neonatal or neonate or newborn or perinatal]). We also considered clinicaltrial.gov for ongoing trials. Articles in all languages were included. The available articles were filtered manually for patients of neonatal age (≤28 days of life) with DMV thrombosis. Demographics, clinical, radiological, and treatment data were collected. Studies where DMV thrombosis was a collateral finding or consequent to other cerebral thrombotic and/or haemorrhagic conditions were excluded. We also excluded articles involving medullary vein malformations or mixed populations (children and adults) without a clear division by age groups. A narrative synthesis of included studies was then conducted because the study designs (case reports and case series) did not allow meaningful meta-analysis to be performed.

The literature search yielded a total of 45 results (Fig. 1 ). Twenty-eight records were excluded because they were duplicates. Three additional records were excluded: 1 study included only adults [ 19 ], and 2 studies reported outcomes different from those of interest [ 20, 21 ]. A total of 14 full-text articles were assessed for eligibility. After full-text examination, 8 more studies were excluded: 2 reviews not reporting any data on DMV thrombosis [ 3, 5 ], 5 articles reporting neonatal patients studied for other conditions in which DMV thrombosis was a collateral finding [ 12 , 22‒25 ], and 1 article including infants where DMV thrombosis was a collateral finding of secondary interest [ 26 ]. A final number of 6 studies were included [ 1 , 4 , 11 , 27‒29 ], reporting a total of 75 cases of DMV thrombosis in neonates. The articles were analysed and described below and in Table 2 .

Identification of studies.

Summary of evidence on DMV thrombosis in neonates

11/24 (46%) were born preterm; 13/24 (54%) were born at term. Of the remaining 51/75, described by Benninger et al., mean gestational age (only data mentioned) was equal to 37 ± 2.2 weeks [ 4, 11 ]. We observed a prevalence of male newborns (50/74, 68%); in 1 case report, sex was not mentioned [ 28 ]. 3/75 (4%) neonates were born from twin pregnancies. Risk factors identified included maternal factors [ 4 ], such as pre-eclampsia or hypertension (17/51, 33%), gestational diabetes (6/51, 12%), prothrombotic disorders (3/51, 6%). Perinatal history of neonatal distress, respiratory resuscitation, or need for inotropes during the first week of life was present in 34/75 (45%) of patients. Neonatal comorbidities included hypoglycaemia (18/51, 35%), neonatal infection (9/51, 18%), complex congenital heart disease (4/51, 8%), meningitis (4/51, 8%), prothrombotic disorders (4/51, 8%). Arrigoni et al. [ 1 ] reported a preterm baby with a mitochondrial disease. At clinical presentation, signs and symptoms included seizures (38/75, 48%), apnoea (27/75, 36%), lethargy or irritability (26/75, 35%), poor feeding and weight loss (19/75, 25%). Onset of symptoms occurred during the first week of life for all patients described (Table 3 ). Diagnosis was made with brain MRI, which was performed between 0 and 48 days after birth. Fan-shaped linear T2 hypointense lesions were documented in all cases; in 53/54 cases, associated signs of haemorrhagic infarction were present (98%). Lesion distribution was highest in the frontal (62/74, 84%) and parietal areas (56/74, 76%). Temporal (30/74) and occipital (6/74) lobes were less often involved (41% and 8%, respectively). Collateral MRI findings were often described, in particular oedema or ischaemia of the corpus callosum (58/75, 77%), periventricular subependymal cysts (9/75, 12%), germinal matrix and intraventricular haemorrhage (8/75, 11%), parenchymal haematoma (4/75, 7%). None had associated CSVT. Brain MRI was repeated in 10/75 cases (13%) during the first 4 months of life; in 6/75 cases (8%), it was repeated after 9 months of life. Of the 10 cases where MRI was repeated during the first 4 months of life, 5/10 (50%) had stable lesions, whereas the other 5/10 cases showed an evolution to periventricular cysts. After 9 months of life, in 5/6 (83%) cases, MRI showed progression to periventricular leukomalacia (PVL)-like lesions, while in 1/6 (17%) case, MRI was normal. 2/75 (3%) patients underwent cranial ultrasound, which in one case highlighted the presence of periventricular bilateral hyperechogenicity, and in the other hyperechogenic areas on the right hemisphere and left frontal pole. Neurological outcomes of DMV thrombosis are described by Benninger et al. [ 4 ], who reported that at 2–17 years of age, patients with neonatal DMV thrombosis developed major neurodevelopmental impairment (defined as any of the following: a Bayley-III, Wechsler Preschool and Primary Scale of Intelligence – Fourth Edition [WPPSI-IV], or Wechsler Intelligence Scale for Children – Fifth Edition [WISC-V] score more than 2 standard deviations below the mean) in 37% of cases, intellectual disabilities (32%), motor disorders or cerebral palsy (27%), behavioural problems (22%), visual impairment (20%), language impairment (20%), epilepsy (18%), hearing impairment (4%). In 1 case report, the child had hemiparesis [ 28 ]. Death was described in 2 cases [ 1, 27 ]. The first case died at 3 days of life due to continuing seizures and raised intracranial pressure, while the latter died at 2 years of age because of complications of the underlying mitochondrial disease. Antithrombotic treatments for DMV thrombosis were not mentioned in any of the articles.

Clinical characteristics of neonates with DMV thrombosis

DMV thrombosis is a rarely reported aetiology of neonatal stroke. We have carried out a systematic literature review with the aim of clarifying risk factors, clinical-radiological characteristics, treatment, and outcomes of this condition. Our main results, derived from pooling together the 75 patients identified in the literature, show that more than half of neonates were healthy at birth. The great majority presented with seizures, accompanied by systemic signs and symptoms such as respiratory distress, lethargy or irritability, poor feeding during the first week of life. Gold standard for diagnosis was brain MRI, which showed fan-shaped white matter lesions (T2 hypointense) with associated haemorrhage in nearly all patients. Antithrombotic treatment was not mentioned in any of the included studies.

The incidence of DMV thrombosis cannot be precisely estimated. However, included articles have all been published after 2011, possibly reflecting an increasing interest in this topic, in particular following the innovations in neuroimaging that have allowed recognition of the characteristic patterns of DMV thrombosis. Engorgement and thrombosis of the DMVs can be isolated or associated with other conditions such as CSVT, vascular malformations, and Sturge-Weber syndrome [ 1 , 30‒32 ]. Specifically, CSVT is a more widely known entity that shares some clinical and diagnostic aspects with DMV thrombosis. With respect to the general characteristics of our cohort, we identified several risk factors in infants with DMV thrombosis, even if, in more than half of cases, neonates were healthy at birth [ 4 ]. Risk factors, as well as those in CSVT, can be divided into maternal factors, including pre-eclampsia or hypertension (33%), gestational diabetes (12%), prothrombotic disorders (6%), and perinatal factors such as neonatal distress, respiratory resuscitation at birth or need for inotropes during the first week of life (45%). However, only gestational diabetes and a low Apgar score at 1 min have been found to be significantly related to severe white matter injury due to DMV thrombosis [ 12 ]. Placental risk factors were not mentioned in any of the studies included. These data are comparable to CSVT, where similar risk factors and comorbidities can be identified in ca. 60% of cases [ 6, 10, 33, 34 ]. In CSVT, preterm neonates often present with more extensive white matter damage, whereas full-term neonates usually present with punctate white matter lesions [ 34 ]. The rapid development of the nervous system during the preterm period makes the brain highly vulnerable to hypoxic insults; the combination of destructive insults and developmental changes may result in extensive white matter injury [ 35‒37 ]. However, even if white matter injury is usually more extensive in preterm babies, prematurity does not appear to be itself a risk factor for CSVT [ 37 ]. In line with these data, we did not notice a clear prevalence of preterm versus full-term babies among the cases with DMV thrombosis included. Neonates with DMV thrombosis are predominantly male (68%). Male prevalence has also been noted in CSVT, where babies are male in 2/3 of cases [ 33, 38, 39 ]. Of the neonates included, 4% were born from twin pregnancies. This prevalence is higher than what is expected in the general population (2.4%) [ 40 ]. The reasons for this higher prevalence are unknown, but we hypothesize that it may be due to placental insufficiency and a more frequently complicated delivery. Patients usually present during the first week of life with seizures (48%), apnoea (36%), lethargy or irritability (35%), poor feeding and weight loss (25%). In 51/75 cases, the onset of symptoms occurred at 4.5 ± 5.3 days of life [ 4, 11 ]. A similar non-specific clinical presentation is typical of CSVT [ 6, 33, 39, 41 ]. The timing of presentation and the absence of clear risk factors at birth in most cases suggest that DMV thrombosis might be the result of an insult occurring during the perinatal period, in particular at the moment of delivery.

The gold standard for diagnosis is brain MRI. Although symptoms often occur during the first week of life, we noticed that the first MRI is usually performed later on in the neonatal period, on average around the 11th day of life (with a wide range spanning between 0 and 48 days of life). This highlights a diagnostic delay and suggests that DMV thrombosis may be an under-recognized condition due to the lack of specificity of clinical presentation. On brain MRI, DMV thrombosis is defined as linear T2 hypointense/T1 hyperintense lesions of the periventricular white matter spreading in a radial pattern from the lateral surface of the ventricles, reflecting the anatomic distribution of the deep white matter venous drainage [ 1, 4, 5, 11 ]. Technical advances in brain MRI have recently allowed for better characterization of the typical lesions related to DMV thrombosis, which can now be recognized with a higher sensitivity. This has also enabled better understanding of pathophysiological mechanisms and definition of the severity of the lesions. All patients presented symptomatic ischaemic strokes, suggesting that minor injuries with paucisymptomatic clinical presentation may be under-recognized [ 13, 41 ]. We noted a higher prevalence of lesion distribution in the fronto-parietal areas of the brain compared to temporo-occipital areas, which appear to be less affected in all studies considered. In this regard, the lower width of white matter and the shorter length of the DMVs in the temporo-occipital areas than in fronto-parietal areas appear to be protective factors against prothrombotic mechanisms. Besides, in the temporal and occipital regions, there is a higher presence of transcerebral veins which relieve venous stasis in these areas [ 1 ]. Other associated radiological findings were often described, both at first examination and when MRI was repeated later on. Oedema of the corpus callosum was the main associated finding (77% of cases). Veins draining the corpus callosum are tributaries of the subependymal veins, where DMVs also converge, highlighting a common pathogenetic mechanism. Contrary to what reports on CSVT suggest, signs of intracranial hypertension were not found in any of the cases included. CSVT determines a delay in venous emptying and an increase in capillary hydrostatic pressure. This in the end alters cerebrospinal fluid absorption and thereby results in an increase of intracranial pressure [ 42 ]. It has been hypothesized that during the first month of life, lesions are mostly stable and, afterwards, evolve towards necrosis and formation of periventricular cysts [ 1 ]. After 9 months of life, in 5/6 cases, MRI showed progression to PVL-like lesions, while in 1/6 case, MRI was normal [ 1 ]. Against that, Chen et al. found that in 3/5 cases, when MRI was repeated 15–21 days after birth, PVL-like lesions had already developed [ 9 ]. No signs of progression or recurrence of the ischaemic lesions have been reported. This should be carefully taken into account when considering the risk-benefit ratio of repeating neuroimaging in these infants, in particular given the sedation-related risks. Due to incomplete data, we were not able to draw out any significant differences on MRI between preterm and full-term babies, but several hypotheses have been put forward regarding pathophysiological mechanisms. In premature neonates, who still have poorly developed draining venous systems, DMV thrombosis could be a complication of parenchymal or intraventricular haemorrhage that could cause mechanical obstruction and/or congestion of the vessels. This can induce an increase in the upstream draining venous pressures, that ultimately result in congestion and thrombosis of the DMV [ 1, 5, 22 ]. In full-term neonates, this appears to happen less often, and DMV thrombosis occurs usually as the result of direct involvement of DMVs due to thrombotic or prolonged hypoperfusive events. Cerebral venous hypertension and immaturity of coagulation systems of neonates can also contribute to these mechanisms [ 1 ]. Cranial ultrasound was performed only in 2 cases [ 1, 28 ]. In both cases, areas of hyperechogenicity were noticed, consistent with an ischaemic injury [ 43‒45 ]. However, this is a highly non-specific and frequent finding, which is usually further investigated only in the presence of other warning signs. Thus, to date, brain MRI remains the gold standard for the diagnosis of DMV thrombosis. Benninger et al. [ 11 ] developed a score to assess the severity of MRI lesions. Cavitary lesions accounted for more severe brain damage and were given higher scoring points. A global severity score of 16/102 appeared to be the optimal cut-off to identify infants at higher risk for long-term neurodevelopmental impairment, even if sensitivity and specificity reported were 66% and 58%, respectively. They observed no difference between the severity score and perinatal risk factors. We could not collect data on outcomes for all the patients included. Benninger et al. found that in 37% of cases, patients with neonatal DMV thrombosis had neurodevelopmental impairment, consistent with reports on the incidence of adverse neurological or developmental sequelae in neonates with CSVT, that ranges between 23 and 79% [ 4, 6, 10, 37, 39, 41 ]. At follow-up at 2–17 years old, patients developed intellectual disabilities and behavioural problems (32% and 22%, respectively), motor disorders or cerebral palsy (27%), visual and hearing impairment (20% and 4%, respectively), language disabilities (20%) [ 4 ]. Epilepsy occurred in 18% of cases, similarly to what has been previously reported after CSVT [ 4, 10, 46 ]. Patients with severe neurodevelopmental impairment had a higher grade of severity of brain damage compared to patients with little or no impairment, whereas gestational age, birth weight, socioeconomic status were not different between the two groups [ 4 ]. Similarly, in neonates with CSVT, outcomes appear to be related to the extent and the bilateral localization of the infarction associated with thrombosis [ 6, 39, 47, 48 ]. Given the high rate of morbidity, social and health costs related to DMV thrombosis appear to be significant. Among included cases, death in the immediate neonatal period was reported only in 1 case (1.3%) [ 27 ]. Another patient died at the age of 2 years due to unspecified complication of mitochondrial disease [ 1 ]. Mortality as an early outcome is reported to be higher in CSVT, with death rate that ranges between 6 and 19% [ 10, 37 ].

No articles mentioned the treatment used for DMV thrombosis. Currently, treatment is guided by the clinical experience of the single physicians, usually in accordance with the latest guidelines on the treatment of cerebral venous thrombosis [ 14, 15 ], even if randomized controlled trials are still lacking. However, existing evidence suggests that anticoagulation can be used in neonates with CSVT, especially in the absence of a brain haemorrhage [ 15 ]. Typically, in neonates without significant intracranial haemorrhage, anticoagulation should be initiated with unfractionated heparin (and subsequently with low molecular weight heparin) or low molecular weight heparin alone, and then continued for a total duration of 6 weeks to 3 months [ 14 ]. For neonates with CSVT with significant haemorrhage, guidelines suggest the possibility of radiological monitoring of the thrombosis at 5–7 days, with initiation of anticoagulation if thrombotic extension is noted [ 14 ]. Treatment decision-making in this condition should take into account that anticoagulant therapy can be associated with adverse events in a significant proportion of cases [ 10, 15 ].

Limitations to this study included the heterogeneity of the data collected from selected articles, which did not allow for a meta-analysis to be performed. In some cases, it was not possible to ascertain the individual patient’s data. Due to the low presumed incidence, the population of this study was small.

To the best of our knowledge, this is the first systematic literature review on stroke associated with DMV thrombosis in neonates. Despite the above-mentioned limitations, in the present study, we sought to collect data on DMV thrombosis, in order to better characterize and understand it. However, there is still poor acknowledgement of underlying primary mechanisms and risk factors, which represents an important limitation for prevention, recognition, and acute management of this condition. DMV thrombosis is rare in neonates, even if probably underdiagnosed and possibly associated with maternal or foetal risk factors; its clinical presentation is often non-specific with seizures and systemic signs/symptoms, and it causes severe neurological sequelae. These factors should aid in a timely clinical suspicion of this rare condition, also considering the burden of the diagnostic delay. Our study highlights a knowledge gap in the treatment strategies for DMV thrombosis as regards the potential indication for anticoagulation treatment, the efficacy and safety of which in this clinical setting are yet to be properly assessed in randomized clinical trials and larger studies. The high rate of morbidity and the associated social and health costs require in-depth studies aimed at defining an earlier diagnosis and at developing evidence-based prevention and therapeutic strategies.

This work was carried out within the project Pediatric Thrombosis (DOR2211211); PI: Prof. Stefano Sartori, University of Padua, Italy.

An ethics statement is not applicable because this study is based exclusively on published literature. Ethical approval and consent were not required as this study was based on publicly available data.

The authors have no conflicts of interest to declare.

This research did not receive grants from any funding agency in the public, commercial, or not-for-profit sectors.

Letizia Leonardi, Luca Capato, and Jacopo Norberto Pin carried out the literature review and drafted the paper. Margherita Nosadini contributed to the last version of the manuscript. Stefano Sartori and Matteo Luciani provided senior support for the article conceptualization and contributed to the last version of the manuscript. Maria Federica Pelizza, Luca Piretti, Maria Elena Cavicchiolo, Eugenio Baraldi, Giorgio Perilongo, and Paolo Simioni supervised the literature review and contributed to the critical revision of the manuscript.

The data that support the findings of this study are openly available in PubMed Central (PMC) at http://doi.org/10.3174/ajnr.A2687 , reference number [1]; http://doi.org/10.1177/0883073820967161 , reference number [4]; http://doi.org/10.3174/ajnr.A5940 , reference number [11]; http://doi.org/10.1212/WNL.0000000000001719 , reference number [27]; http://doi.org/10.1016/j.jpeds.2018.03.051.Epub 2018, reference number [28]; and http://doi.org/10.1212/WNL.0000000000011502 , reference number [29]. Further enquiries can be directed to the corresponding authors.

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• v.7(Suppl 3); 2017 Dec

Deep vein thrombosis: pathogenesis, diagnosis, and medical management

Jonathan stone.

1 Division of Interventional Radiology, Mayo Clinic, Phoenix, AZ, USA

Patrick Hangge

Hassan albadawi, alex wallace, fadi shamoun.

2 Division of Cardiovascular Diseases, Mayo Clinic, Phoenix, AZ, USA

M. Grace Knuttien

Sailendra naidu.

Deep vein thrombosis (DVT) is a major preventable cause of morbidity and mortality worldwide. Venous thromboembolism (VTE), which includes DVT and pulmonary embolism (PE), affects an estimated 1 per 1,000 people and contributes to 60,000–100,000 deaths annually. Normal blood physiology hinges on a delicate balance between pro- and anti-coagulant factors. Virchow’s Triad distills the multitude of risk factors for DVT into three basic elements favoring thrombus formation: venous stasis, vascular injury, and hypercoagulability. Clinical, biochemical, and radiological tests are used to increase the sensitivity and specificity for diagnosing DVT. Anticoagulation therapy is essential for the treatment of DVT. With few exceptions, the standard therapy for DVT has been vitamin K-antagonists (VKAs) such as warfarin with heparin or fractionated heparin bridging. More recently, a number of large-scale clinical trials have validated the use of direct oral anticoagulants (DOACs) in place of warfarin in select cases. In this review, we summarize the pathogenesis, diagnosis, and medical management of DVT, with particular emphasis on anticoagulation therapy and the role of DOACs in the current treatment algorithm.

Introduction

Deep vein thrombosis (DVT), a subset of venous thromboembolism (VTE), is a major preventable cause of morbidity and mortality worldwide. The incidence of VTE is estimated to be 1 per 1,000 people annually ( 1 , 2 ), with DVT accounting for approximately two-thirds of these events ( 3 ). Pulmonary embolism (PE), a dreaded complication of DVT, occurs in up to one-third of cases and is the primary contributor to mortality ( 4 ). Much of the morbidity of DVT results from the development of post-thrombotic syndrome, which occurs in up to 50% of patients within 2 years of DVT and encompasses a number of symptoms including leg pain, swelling, and in severe cases, venous ulcers ( 5 , 6 ). Anticoagulation is the mainstay of therapy for DVT, with the goal of preventing progression to PE and recurrence of thrombosis. The 30-day mortality rate exceeds 3% in patients with DVT who are not anticoagulated, and this mortality risk increases 10-fold in patients who develop PE ( 7 ). The advent of direct oral anticoagulants (DOACs) has generated a need to compare these newer agents with the more conventional vitamin K-antagonists (VKAs) for the treatment of DVT. Several recent clinical trials have addressed this question and demonstrated a similar safety and efficacy profile between the two drug classes. With more therapeutic options, clinicians are now better able to incorporate disease- and patient-specific considerations into the medical management of DVT.

Pathogenesis

Virchow’s Triad, first described in 1856, implicates three contributing factors in the formation of thrombosis: venous stasis, vascular injury, and hypercoagulability. Venous stasis is the most consequential of the three factors, but stasis alone appears to be insufficient to cause thrombus formation ( 8 ). However, the concurrent presence of venous stasis and vascular injury or hypercoagulability greatly increases the risk for clot formation ( 9 ). The clinical conditions most closely associated with DVT are fundamentally related to the elements of Virchow’s Triad; these include surgery or trauma, malignancy, prolonged immobility, pregnancy, congestive heart failure, varicose veins, obesity, advancing age, and a history of DVT ( 10 ).

Venous thrombosis tends to occur in areas with decreased or mechanically altered blood flow such as the pockets adjacent to valves in the deep veins of the leg ( 11 ). While valves help to promote blood flow through the venous circulation, they are also potential locations for venous stasis and hypoxia. Multiple postmortem studies have demonstrated the propensity for venous thrombi to form in the sinuses adjacent to venous valves ( 12 - 14 ). As blood flow slows, oxygen tension declines with a coincident increase in hematocrit ( 15 ). The hypercoagulable micro-environment that ensues may downregulate certain antithrombotic proteins that are preferentially expressed on venous valves including thrombomodulin and endothelial protein C receptor (EPCR) ( 16 ). In addition to reducing important anticoagulant proteins, hypoxia drives the expression of certain procoagulants. Among these is P-selectin, an adhesion molecule which attracts immunologic cells containing tissue factor to the endothelium ( 17 , 18 ). Debate remains regarding the precise location of tissue factor in this process, whether expressed on the endothelium or by cells within the extravascular tissue, but there is general agreement that tissue factor serves as the primary nidus for thrombus formation ( 19 ). Thrombus formation appears to require both tissue factor and P-selectin ( 17 , 18 ).

A venous thrombus has essentially two components, an inner platelet rich white thrombus forming the so-called lines of Zahn surrounded by an outer red cell dense fibrin clot ( 12 ). Fibrin and extracellular DNA complexed with histone proteins forms the outer scaffold, which may be important in determining thrombus susceptibility to tissue plasminogen activator (TPA) and thrombolysis ( 20 ). As the ratio of procoagulants to anticoagulants increases, so does the risk of thrombus formation. The proportion of proteins is in part determined by the ratio of endothelial cell surface to blood volume. A decreased cell surface to blood volume ratio (i.e., large vessels) favors procoagulants ( 21 ). Factor VIII, von Willebrand factor, factor VII and prothrombin seem to be particularly influential in tipping the scale towards coagulation ( 22 ). In addition to promoting thrombin generation, prothrombin inhibits the anticoagulant properties of activated protein C, thereby dampening a natural anticoagulant pathway. There are three such pathways: the protein C anticoagulant pathway (protein C, protein S, thrombomodulin, and perhaps EPCR), heparin-antithrombin pathway, and tissue factor inhibitor pathway. Defects in these pathways are associated with an increased risk for thrombus formation. In humans, less is known regarding the role of tissue factor inhibitor pathway ( 19 , 22 , 23 ). There are also a number of familial variants that predispose to thrombus formation by increasing the levels of factor VII, VIII, IX, von Willebrand factor, and prothrombin. In factor V Leiden, which affects up to 5% of Caucasians and increases the risk of thrombosis 7-fold, activated factor Va is resistant to the inhibitory influence of protein C ( 19 ). Other risk factors for clot formation include cancer, oral contraceptives, obesity, and advancing age. Malignancy can exert a compressive effect on veins contributing to stasis. It also leads to shedding of procoagulants such as tissue factor on membrane particles that promotes thrombosis ( 24 ). Obesity and oral contraceptive use are independent risk factors for thrombosis. Together, they increase thrombosis risk synergistically ( 25 ). Finally, advancing age is associated with an increased risk for thrombosis. While the cause for this remains unsettled, several factors related to aging have been observed: greater prevalence of obesity, increased frequency of illness and periods of prolonged immobility, comorbid medical conditions, and an increase in the level of procoagulants without a commensurate increase in anticoagulants such as protein C ( 19 ). Taken together, thrombosis formation is a dynamic, multicausal process that hinges on a fine balance of physical and biochemical factors.

The clinical presentation of DVT varies with the extent and location of a thrombus. The cardinal signs and symptoms of DVT include asymmetrical swelling, warmth, or pain in an extremity, and a high index of suspicion should be present in patients with the aforementioned risk factors. A number of scoring systems have been devised to estimate the pre-test probability of DVT. In the United States, the most widely used scoring system is the Wells criteria ( 26 ). In its original form, patients were stratified into three categories, high, intermediate, or low risk, based on the presence or absence of 9 clinical criteria. DVT prevalence was estimated to be 5% and 53% in the low- and high-risk groups, respectively ( 27 ). Several years later, the Wells scoring system was revised to include a “previously documented DVT” criterion and extend the post-operative duration from 4 to 12 weeks. The risk categories were also trimmed to “unlikely” or “likely”, with the prevalence of DVT estimated to be 6% and 28%, respectively ( 28 ). In 2012, the National Institute for Health and Care Excellence (NICE) guidelines estimated the sensitivity and specificity for DVT of the Wells criteria to be 77–98% and 38–58%, respectively ( 29 ). While the sensitivity of the Wells criteria can be quite high, it is clear from this data that the scoring system cannot be used as the sole diagnostic modality for DVT. Nevertheless, it is clinically useful in stratifying patients and determining the most appropriate sequence for further testing.

Like the Wells scoring criteria, the D-dimer assay has a high sensitivity and relatively lower specificity for the diagnosis of DVT, estimated by the NICE guidelines to be 75–100% and 26–83%, respectively ( 29 ). The test measures D-dimer, a prominent fibrin degradation product, which is generated by the fibrinolytic response to thrombus formation in the body. Elevation in D-dimer is not unique to thrombosis however, as it can be increased in a variety of pathologic states including malignancy, inflammatory conditions, pregnancy, and liver disease. It is also increased during the post-operative period and after trauma. Given its high sensitivity, the D-dimer assay can help to rule out DVT in low-risk patients, particularly when combined with the Wells scoring criteria or ultrasound (US).

Diagnostic imaging is often employed to confirm the presence of DVT. US is the first-line imaging modality for diagnosis of proximal DVT because it is safe, easily accessible, cost-effective, and reliable ( 30 - 32 ). It can accurately determine the size, chronicity, and degree of occlusion of a thrombus and therefore better inform the decision to pursue medical management or interventional techniques. During the examination, an US probe is used to gently compress the vein of interest. Inability to compress the vein is considered diagnostic for DVT. The clot can be further characterized with real-time imaging such as duplex and color-flow Doppler ( Figure 1 ). The primary limitation of US is its diminished ability to detect distal DVT. A meta-analysis by Goodacre et al. estimated the pooled sensitivity of US for proximal and distal DVT to be 94.2% and 63.5%, respectively ( 33 ). However, proximal compressive US examinations are often favored over whole-leg US in the clinical setting because distal DVT rarely results in clinically significant sequelae ( 34 ). US is augmented by the Wells scoring criteria and D-dimer assay. In patients with a negative D-dimer who are “unlikely” to have DVT, US is not necessary. In similarly stratified patients with a positive D-dimer, US is recommended. Finally, in patients with a comorbid condition associated with an elevated D-dimer, US is preferred in place of D-dimer ( 34 ). Other diagnostic imaging modalities used for DVT include conventional contrast venography, computed tomography (CT) venography, and magnetic resonance (MR) venography. Contrast venography is the gold standard for lower extremity DVT, but it is limited by a number of factors including availability, patient discomfort, user-dependence, inadequate visualization, and patient-specific variables such as contrast allergy and renal insufficiency ( 32 , 34 ). The exam is performed by cannulating a dorsal vein in the foot and applying a compression tourniquet to the proximal thigh. Contrast media is injected and serial radiographs are taken to visualize the deep venous system of the leg. A persistent filling defect in multiple views is considered diagnostic for DVT ( 35 ) ( Figure 2 ). In CT venography, contrast media is injected into the arm and imaging is timed with opacification of the deep venous system in the lower extremities ( Figure 3 ). The exam is non-invasive, readily available, highly sensitive and specific for DVT, and provides the added benefit of cross-sectional imaging. It may be particularly useful for identifying proximal DVT in patients with suspected PE ( 36 ). Like conventional venography, it carries the same exposure to ionizing radiation and contrast media and is limited by renal insufficiency and severe contrast allergy. MR venography provides many of the same benefits as CT venography without the need for ionizing radiation. It has a similar sensitivity and specificity for DVT ( 37 ) ( Figure 4 ) . In addition, a variety of pulse sequences can be applied to visualize the deep venous system without the need for contrast media. The disadvantages of MR venography are similar to other MR exams, namely patient intolerability, increased cost, and incompatible hardware. Although not yet well studied, MR venography is becoming an increasingly viable option when US is not feasible in cases of suspected DVT ( 37 ).

Venous color-flow Doppler. US Doppler imaging of the left femoral vein showing complete occlusion by a heterogeneous thrombus with dilatation of the vein at the site of thrombosis. No significant waveform is present. The adjacent artery is also shown for reference. US, ultrasound.

Contrast venography. Angiogram imaging of the left popliteal vein demonstrating a partially occlusive thrombus with irregular margins and diminished contrast flow. This thrombus was subsequently treated with catheter directed therapy.

CT venography. CT imaging demonstrating bilateral common iliac vein thrombi as hypodense occlusive masses with vein wall enhancement and dilatation. This thrombus extended far into the inferior vena cava. CT, computed tomography.

MR venography. MR imaging demonstrating a focal thrombus in the left common iliac vein that was seen extending superiorly to the inferior vena cava. No thrombus is seen on the contralateral side. MR, magnetic resonance.

Medical management

Anticoagulation is an essential component of therapy for DVT. With a few notable exceptions, patients with DVT can be treated with oral anticoagulants alone. In cases of extensive thrombus burden involving proximal deep veins, mechanical- and catheter-directed thrombolysis (CDT) may be indicated in the acute phase to rapidly induce clot lysis and reduce the risk of post-thrombotic syndrome ( 38 , 39 ). These techniques are also being employed for the treatment of acute limb ischemia secondary to arterial thrombosis, although there is an increased risk for ischemia-reperfusion injury ( 40 , 41 ). However, thrombolytic therapy is associated with an increased risk of major bleeding and has shown no mortality benefit in patients with DVT ( 42 - 45 ). Further studies are underway to determine the proper patient selection and potential short- and long-term benefits of CDT as compared to systemic thrombolysis and/or anticoagulation therapy ( 45 ). In patients with an increased risk of bleeding or absolute contraindication to anticoagulation therapy, an inferior vena cava filter can be placed to prevent progression to PE.

Unfractionated heparin (UFH)/low molecular weight heparin (LMWH)

During the acute phase, which corresponds to the first 5–10 days of therapy, UFH or LMWH is utilized as a bridging agent when a VKA is planned. Rapid initiation of treatment helps to curb fibrin clot formation and augment the body’s fibrinolytic response, thereby reducing symptoms and risk of further thrombus formation or progression to PE. These agents are particularly useful in the hospital setting given their short half-life and relative convenience for perioperative management. UFH has several advantages over LMWH; it has a shorter elimination half-life (~1 hour); it is fully reversible, and it is preferred in patients with body mass index (BMI) >40 kg/m 2 or weight <50 kg, or those who have creatinine clearance <30 mL/min ( 46 ). However, optimal therapeutic levels are difficult to achieve given substantial differences in dosing requirements among individuals ( 47 ), and UFH carries an 8–10-fold increased risk for heparin-induced thrombocytopenia (HIT) when compared to LMWH ( 48 ). For these reasons, LMWH such as enoxaparin is often the bridging therapy of choice. Fondaparinux, a synthetic pentasaccharide, can also be used for bridging purposes. Similar to UFH and LMWH, its anticoagulant effect is mediated through activation of antithrombin III, but it is selective for factor Xa and has no affinity for PF-4, conferring a substantial reduction in incidence of HIT. In clinical practice, fondaparinux is limited by its long half-life (17–21 hours with normal renal function) and lack of a reversal agent ( 48 , 49 ). Once therapeutic levels are achieved, as determined by activated partial thromboplastin time (aPTT) or anti-Xa levels, VKA therapy should begin. Parenteral anticoagulation with UFH or LMWH should be continued for at least 5 days and until the international normalized ratio (INR) is sustained >2 for 24 hours. In most circumstances, LMWH/VKA therapy is recommended for at least 3 months and can safely be completed on an outpatient basis ( 46 , 49 - 52 ).

VKAs versus DOACs

DOACs are an attractive alternative to VKAs such as warfarin for a number of reasons; they have fewer drug-drug interactions; they can be taken orally and in some cases do not require bridging; they do not require frequent laboratory monitoring, and they have been shown to be as effective as VKA therapy for DVT ( 46 , 50 , 52 ) ( Table 1 ). The primary disadvantages of DOACs relate to their long half-life, making them less suitable for inpatient treatment and also contraindicated in patients with poor liver and/or renal function. Also, DOACs have not been well studied in all patient populations and therefore are not recommended in cases of active malignancy, thrombocytopenia, or high bleeding risk ( 46 , 50 ).

*, RE-LY trial studied patients with atrial fibrillation; **, increased risk of ACS and MI demonstrated in several additional studies when used for reasons other than DVT. VKA, vitamin K-antagonist; MI, myocardial infarction; ACS, acute coronary syndrome; GI, gastrointestinal; RCTs, randomized controlled trials; DVT, deep vein thrombosis.

The effectiveness of dabigatran for treatment of DVT has been confirmed in three recent double-blind randomized controlled trials: RE-COVER, REMEDY, and RESONATE. In the RE-COVER trial, more than 2,500 patients with documented proximal DVT were assigned to either dabigatran or standard LMWH/warfarin for the duration of therapy. There was no difference in mortality, major bleeding, acute coronary events, or recurrence of VTE ( 53 ). These results were confirmed in the RE-COVER II trial, with pooled data from both studies showing a hazard ratio of recurrent VTE of 1.09 (95% CI, 0.76–1.57) and major bleeding of 0.73 (95% CI, 0.48–1.11) ( 52 ). In the RE-LY study, there did appear to be an increased risk of gastrointestinal (GI) bleeding in patients with atrial fibrillation who were treated with dabigatran as compared to warfarin ( 54 ). This risk was not corroborated by the RE-COVER, RE-COVER II, or REMEDY trials, likely owing to differences in the patient population between the studies. In particular, patients with atrial fibrillation tend to be older, have other comorbid conditions, and are more likely to be on concomitant anti-platelet agents such as aspirin or Plavix. In a large meta-analysis that included the RE-LY and RE-COVER trials, as well as several other studies comparing the efficacy of dabigatran to warfarin for stroke prophylaxis, acute coronary syndrome, and DVT prophylaxis in joint replacement, dabigatran was associated with an increased risk of myocardial infarction or acute coronary syndrome with a pooled odds ratio of 1.33 (95% CI, 1.03–1.77) ( 55 , 56 ). Taken together, dabigatran appears to be as effective as warfarin in the short- and long-term treatment for DVT. Until further studies are conducted, caution should be used when prescribing dabigatran to elderly patients with atrial fibrillation or other cardiac risk factors.

Rivaroxaban

Rivaroxaban, a direct factor Xa inhibitor, has been shown to be as effective as warfarin for DVT in randomized controlled trials. In the EINSTEIN DVT trial, patients were randomized to either rivaroxaban or LMWH/VKA therapy within 48 hours of diagnosis. The hazard ratio for recurrent VTE was 0.68 (95% CI, 0.44–1.04), major bleeding was 0.65 (95% CI, 0.33–1.30), and non-major bleeding was 0.97 (95% CI, 0.76–1.22) ( 57 ). The EINSTEIN PE trial yielded similar results in terms of safety when rivaroxaban was compared to warfarin for treatment of symptomatic PE ( 58 ). However, based on a recent meta-analysis of 12 randomized controlled trials (RCTs) and a population-based cohort study, rivaroxaban does appear to be associated with an increased risk of GI bleeding in patients over the age of 75 ( 59 , 60 ). Therefore, it should be used judiciously in these patients.

Apixaban was compared to warfarin therapy for DVT in the AMPLIFY trial. Patients were randomized to either apixaban or LMWH/VKA therapy within 36 hours of diagnosis. There was no statistical difference in all-cause mortality or recurrent VTE. Major bleeding and clinically-relevant non-major bleeding was lower in the apixaban group compared to the warfarin group with a relative risk of 0.31 (95% CI, 0.17–0.55) and 0.44 (95% CI, 0.36–0.55), respectively ( 61 ). Apixaban has not been associated with an increased risk of GI bleeding or acute coronary syndrome in other studies ( 44 , 62 ). Therefore, apixaban is an attractive alternative to conventional therapy for DVT in appropriately selected patients.

The HOKUSAI-VTE study compared edoxaban, an oral direct thrombin inhibitor, to warfarin for treatment of VTE. This large, randomized double-blind non-inferiority study included more than 8,200 patients from 37 countries across the world. Patients with DVT or PE were randomized to edoxaban or warfarin treatment arms after a median of 7 days of parenteral anticoagulant therapy. The hazard ratio for edoxaban (60 mg once daily) compared to warfarin for recurrent VTE was 0.89 (95% CI, 0.70–1.13), major bleeding was 0.84 (95% CI, 0.59–1.21), and clinically-relevant non-major bleeding was 0.81 (95% CI, 0.71–0.94). Similar to apixaban, there was no difference in all-cause mortality or major bleeding, and edoxaban was associated with a decreased risk of clinically-relevant non-major bleeding compared to warfarin ( 63 ). Based on these study results, edoxaban appears to be as effective as warfarin with a lower risk of non-major bleeding after an initial 5–10-day course of parenteral anticoagulant therapy.

DVT is a prevalent and vexing problem for clinicians. Normal blood physiology allows for coagulation in the appropriate setting, but a variety of disease states can alter the balance of pro- and anti-coagulant factors leading to pathologic thrombus formation. DVT is diagnosed with increasing precision using the Wells criteria, D-dimer assay, and an expanding array of imaging modalities including US, CT, and MR venography. The treatment of DVT has traditionally included VKAs such as warfarin with heparin or fractionated heparin bridging ( 47 , 50 - 52 ). With the arrival of DOACs came hope for more therapeutic options for DVT, but the safety and efficacy profile of these newer agents compared to conventional therapy has been of paramount importance. After more than a decade of research, multiple large-scale clinical trials have demonstrated comparable efficacy between the two drug classes ( 46 , 50 , 52 , 57 , 58 , 61 , 63 ). Although the safety profile for DOACs has been quite favorable, dabigatran and rivaroxaban have been associated with an increased risk of GI bleeding in select patients ( 54 , 59 , 60 ). Conversely, apixaban and edoxaban were associated with a lower risk of non-major bleeding in the AMPLIFY and HOKUSAI-VTE trials, respectively ( 61 , 63 ). In patients receiving dabigatran for other reasons including stroke and DVT prophylaxis, as well as acute coronary syndrome (ACS), there may be an increased risk of myocardial infarction ( 55 , 56 ). Taken together, DOACs are as effective as warfarin for treatment of DVT. DOACs should be used with caution in select patient populations including those of advanced age, with atrial fibrillation or other cardiac risk factors, or who have an increased risk of GI bleeding.

Acknowledgements

Funding : R Oklu gratefully acknowledges funding from the National Institutes of Health (EB021148, CA172738, EB024403, HL137193) and the Mayo Clinic.

Conflicts of Interest : The authors have no conflicts of interest to declare.