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REFERENCES

1.Wolf JM, Sturdivant RX, Owens BD. Incidence of de Quervain’s tenosynovitis in a young, active population. J Hand Surg Am. 2009;34(1):112–115.

2.Huisstede BM, Coert JH, Fridén J, et al; for European HANDGUIDE Group. Consensus on a multidisciplinary treatment guideline for de Quervain disease: results from the European HANDGUIDE study. Phys Ther. 2014;94(8):1095–1110.

3.Lee KH, Kang CN, Lee BG, et al. Ultrasonographic evaluation of the first extensor compartment of the wrist in de Quervain’s disease. J Orthop Sci. 2014;19(1):49–54.

4.Di Sante L, Martino M, Manganiello I, et al. Ultrasound-guided corticosteroid injection for the treatment of de Quervain’s tenosynovitis. Am J Phys Med Rehabil. 2013;92(7):637–638.

5.Kang HJ, Koh IH, Jang JW, et al. Endoscopic versus open release in patients with de Quervain’s tenosynovitis: a randomised trial. Bone Joint J. 2013;95- B(7):947–951.

ADDITIONALREADING

Ali M, Asim M, Danish SH, et al. Frequency of de Quervain’s tenosynovitis and its association with SMS texting. Muscles Ligaments Tendons J. 2014;4(1):74–78.

Ashraf MO, Devadoss VG. Systematic review and meta-analysis on steroid injection therapy for de Quervain’s tenosynovitis in adults. Eur J Orthop Surg Traumatol. 2014;24(2):149–157.

Cavaleri R, Schabrun SM, Te M, et al. Hand therapy versus corticosteroid injections in the treatment of de Quervain’s disease: a systematic review and meta-analysis. J Hand Ther. 2016;29(1):3–11.

Goel R, Abzug JM. de Quervain’s tenosynovitis: a review of the rehabilitative options. Hand (N Y). 2015;10(1):1–5.

Kume K, Amano K, Yamada S, et al. In de Quervain’s with a separate EPB compartment, ultrasound-guided steroid injection is more effective than a clinical injection technique: a prospective open-label study. J Hand Surg Eur Vol. 2012;37(6):523–527.

Kwon BC, Choi SJ, Koh SH, et al. Sonographic identification of the intracompartmental septum in de Quervain’s disease. Clin Orthop Relat Res. 2010;468(8):2129–2134.

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Orlandi D, Corazza A, Fabbro E, et al. Ultrasound-guided percutaneous injection to treat de Quervain’s disease using three different techniques: a randomized controlled trial. Eur Radiol. 2015;25(5):1512–1519.

Pagonis T, Ditsios K, Toli P, et al. Improved corticosteroid treatment of recalcitrant de Quervain tenosynovitis with a novel 4-point injection technique. Am J Sports Med. 2011;39(2):398–403.

Peters-Veluthamaningal C, van der Windt DA, Winters JC, et al. Corticosteroid injection for de Quervain’s tenosynovitis. Cochrane Database Syst Rev. 2009;(3):CD005616.

Rousset P, Vuillemin-Bodaghi V, Laredo JD, et al. Anatomic variations in the first extensor compartment of the wrist: accuracy of US. Radiology. 2010;257(2):427–433.

Scheller A, Schuh R, Hönle W, et al. Long-term results of surgical release of de Quervain’s stenosing tenosynovitis. Int Orthop. 2009;33(5):1301–1303.

SEE ALSO

Algorithm: Pain in Upper Extremity

CODES

ICD10

M65.4 Radial styloid tenosynovitis [de Quervain]

CLINICALPEARLS

Repetitive movements of the wrist and thumb, and activities that require forceful grasping are the most common causes of de Quervain tenosynovitis.

Initial treatment is typically conservative.

Corticosteroid injections are helpful and have lower complication rates if done under ultrasound guidance.

Combined orthosis/corticosteroid injection approaches are more effective than either intervention alone.

Surgery is helpful for recalcitrant cases.

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DEEPVEIN THROMBOPHLEBITIS

Jaine McKenzie, MD Patricia Martinez Quinones, MD

Keith O’Malley, MD, FACS

BASICS

DESCRIPTION

Development of blood clot within the deep veins, usually accompanied by inflammation of the vessel wall

Major clinical consequences are embolization (usually to the lung), recurrent thrombosis, and postphlebitic syndrome.

EPIDEMIOLOGY

Ageand gender-adjusted incidence of venous thromboembolism (VTE) is 100 times higher in the hospital than in the community. Almost half of all VTEs occur either during or soon after discharge from a hospital stay or surgery.

Of patients with VTE, 20% complicated with pulmonary embolism (PE). The 28-day deep venous thrombosis (DVT) fatality rate is 5.4%; at 1 year, 20%; at 3 years, 29%.

Incidence

In the United States, VTE incidence is 50.4/100,000 person per year.

Increased incidence in Caucasian and African American populations and with aging

Most common site: lower extremity DVT

Incidence in pregnancy: ~0.5 to 3/1,000 (1)

1–5% of central venous catheters are complicated by thrombosis (2).

Prevalence

Variable; depends on medical condition or procedure

At time of DVT diagnosis, as many as 40% of patients also have asymptomatic PE; conversely, 30% of patients diagnosed with PE do not a have demonstrable source.

Present in 11% of patients with acquired brain injury entering neurorehabilitation

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ETIOLOGYAND PATHOPHYSIOLOGY

Factors involved may include venous stasis, endothelial injury, and abnormalities of coagulation (Virchow triad).

Genetics

Factor V Leiden, the most common thrombophilia, is found in 5% of the population and in 10–65% of all VTE events and increases VTE risk 3- to 6- fold.

Prothrombin G20210Ais found in 3% of Caucasians; increases the risk of thrombosis ~3-fold

RISK FACTORS

Acquired: previous DVT, age, cancer, immobilization, trauma, obesity, major surgery, orthopedic surgery, medications (oral contraceptives, estrogens), antiphospholipid syndrome, cerebrovascular accident, acute infectious process, thrombocytosis, pregnancy/puerperium, central venous catheters

Inherited: deficiencies of protein C, protein S, or antithrombin III; factor V Leiden R506Q, prothrombin G20210A, dysfibrinogenemia

Mixed/unknown: hyperhomocysteinemia, high levels of factor VIII, high levels of thrombin activatable fibrinolysis inhibitor (TAFI), high levels of factor XI

GENERALPREVENTION

Mechanical thromboprophylaxis is recommended in patients with high bleeding risk and as adjunct to pharmacologic thromboprophylaxis.

For acutely ill and for critically ill hospitalized patients at increased risk of thrombosis, low-molecular-weight heparin (LMWH), low-dose unfractionated heparin, or fondaparinux are recommended (3)[C].

For most patients, prolonged secondary prophylaxis is not recommended.

DIAGNOSIS

Modified Wells criteria, a validated clinical prediction rule, is useful to determine pretest probability of having a DVT.

–Active cancer (+1 point)

–Calf swelling >3 cm compared to other leg (+1 point)

–Collateral superficial veins (+1 point)

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–Pitting edema to symptomatic leg (+1 point)

–Previous documented DVT (+1 point)

–Swelling of entire leg (+1 point)

–Localized tenderness along deep venous system (+1 point)

–Paralysis, paresis, or recent cast immobilization of lower extremities (+1 point)

–Recently bedridden >3 days or major surgery in past 4 weeks (+1 point)

–Alternative diagnosis at least as likely (−2 points)

Interpretation: Score of 0, DVT unlikely. Score of 1 to 2, moderate risk. Score of ≥3, DVT likely. D-dimer testing and/or ultrasound should follow based on Wells criteria score.

HISTORY

Higher clinical suspicion in patient with risk factors (See “Risk Factors” section.)

Wells criteria are used to determine pretest probability.

DVT is classified as provoked or idiopathic based on underlying risk factors.

Clinical assessment of bleeding risk (bleeding with previous history of anticoagulation, history of liver disease, recent surgeries, history of GI bleed) is important prior to initiating treatment.

PHYSICALEXAM

Symptoms may present as pain, swelling, or discoloration but may be nonspecific or absent.

Resistance to dorsiflexion of the foot (Homan sign) is unreliable and nonspecific.

Edema, due to swelling of collateral veins, is the most specific symptom.

Uncommonly, patients may have phlegmasia alba dolens (“milk leg”) or phlegmasia cerulean dolens due to arterial occlusion secondary to extensive DVTs.

DIFFERENTIALDIAGNOSIS

Cellulitis, fracture, ruptured synovial cyst (Baker cyst), lymphedema, muscle strain/tear, extrinsic compression of vein (e.g., by tumor/enlarged lymph nodes), compartment syndrome, and localized allergic reaction

DIAGNOSTIC TESTS & INTERPRETATION

Initial Tests (lab, imaging)

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D-dimer (sensitive but not specific; has high negative predictive value

[NPV]), indicated in patients with low pretest probability of DVT or PE but not indicated high pretest probability patients; false positives in liver disease, inflammation, malignancy, trauma, pregnancy, and recent surgery

Patients with a prior DVT and those with malignancy have higher rates of VTE, which decreases the NPV of Wells criteria.

CBC, platelet count, activated partial thromboplastin time (aPTT), prothrombin time (PT)/INR

Diagnostic imaging required in patients with high pretest probability (Wells criteria)

Compression ultrasound (CUS): first-line imaging for DVT due to noninvasive nature and ease of use; sensitive and specific for popliteal and femoral thrombi if experienced user; recommended in patients with moderate or high pretest probability

In patients with suspected DVT, the diagnosis process should be guided by the assessment of the pretest probability.

–Low pretest probability: high-sensitivity D-dimer assay sufficient to exclude DVT if negative. If positive, follow with CUS.

–Moderate to high pretest probability: CUS initial test; if positive, CUS then treat DVT. If negative, DVT is excluded but consider repeat CUS in 1 week.

Contrast venography: gold standard, technically difficult, requires pedal vein cannulation, risk of morbidity

Impedance plethysmography: sensitive and specific for proximal vein thrombosis

MR venography: as accurate as contrast venography; may be useful for patients with contraindications to IV contrast

125I-fibrinogen scan: detects only active clot formation; very good at detecting ongoing popliteal thrombi; takes 4 hours for results

Follow-Up Tests & Special Considerations

In young patients and/or those of concern or with idiopathic/recurrent VTE, consider thrombophilia testing (factor V Leiden mutation, prothrombin G20210Agenetic assay, ATIII functional assay, protein C functional assay, protein S antigen and functional assay and free S, phospholipid-dependent tests and anticardiolipin antibodies, lupus anticoagulant [drawn before heparin]).

Risk of an underlying malignancy is more likely if recurrent VTE, risk 3.2

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(95% CI 2.0–4.8). Unprovoked VTE, 4.6 times higher (vs. secondary); upper extremity DVT, not catheter associated; odds ratio (OR) 1.8, abdominal DVT; OR 2.2 (4), bilateral lower extremity DVT, OR 2.1 (4)

TREATMENT

MEDICATION

Consider starting therapy even before confirmation in patients with high pretest probability.

Anticoagulation is mainstay of therapy. Patients with PE or proximal DVT, long-term therapy (at least 3 months) is recommended. Duration of therapy after 3 months is case-by-case basis.

Indefinite anticoagulation is considered if there is low risk of bleeding, if index event is unprovoked PE, and/or if D-dimer is positive 1 month after stopping anticoagulation (5).

Direct oral anticoagulants (dabigatran, rivaroxaban, apixaban, or edoxaban) recommended instead of vitamin K antagonists for the first 3 months of treatment in patients with lower extremity DVT or PE and no cancer (4)[B] Use and choice of anticoagulation should be considered based on patient’s

history, bleeding risk, cost, and ease of compliance.

First Line

Unfractionated heparin

–IV drip: initial dose of 80 U/kg followed by continuous infusion of 18 U/kg/hr. Target aPTT ratio >1.5 times control. Monitor aPTT every 6 hours and adjust infusion rate accordingly until two successive values are within

therapeutic range. LMWH

–Enoxaparin (Lovenox): 1 mg/kg/dose SC q12h or 1.5 mg/kg daily

–Dalteparin (Fragmin): 200 U/kg SC q24h; off-label use for treatment of DVT/PE

Direct and indirect factor Xa inhibitors

–Fondaparinux (Arixtra): 5 mg (body weight <50 kg), 7.5 mg (body weight = 50 to 100 kg), or 10 mg (body weight >100 kg) SC once daily

–Rivaroxaban (Xarelto): 15 mg PO twice daily with food for the first 3 weeks then 20 mg PO qday

–Apixaban (Eliquis): 10 mg PO twice daily for 1 week followed by 2.5 to 5.0

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mg PO twice daily

– Edoxaban (Savaysa): 60 mg PO daily (>60 kg), 30 mg PO daily (≤60 kg) Thrombin inhibitors

–Dabigatran (Pradaxa): 150 mg PO twice daily for creatinine clearance >30 mL/min

Vitamin K antagonists

–Warfarin (Coumadin): Start with 2 to 5 mg/day. Adjust to a target INR of 2 to 3; overlap with parenteral anticoagulant for minimum of 5 days until therapeutic INR sustained ≥24 hours.

Adverse effects

–All anticoagulants increase risk of bleeding.

–Heparin and LMWH can also cause heparin-induced thrombocytopenia (HIT) (LMWH has lower risk) and injection site irritation.

–Warfarin is teratogenic.

–Dosage adjustments may be required for patients with decreased creatinine clearance.

Second Line

Heparin can be given by intermittent SC self-injection.

Pregnancy Considerations

Warfarin (Coumadin) is a teratogen. It is contraindicated in pregnancy but is safe during breastfeeding.

LMWH are recommended over unfractionated heparin for treatment of acute DVT and PE in pregnancy (1)[B].

Enoxaparin, dalteparin, fondaparinux, and apixaban are pregnancy Category B.

Dabigatran, rivaroxaban, edoxaban are pregnancy Category C.

SURGERY/OTHER PROCEDURES

In selected patients with proximal DVT (acute iliofemoral DVT <14 days, good functional status, >1 year of life expectancy), may consider catheterdirected thrombolysis/open thrombectomy (6)

Thrombolysis (systemic or catheter directed) reduces incidence of postthrombotic syndrome (PTS) after a proximal (iliofemoral or femoral) DVT by one-third.

Thrombectomy is recommended in patients with limb-threatening ischemia due to iliofemoral venous outflow obstruction (6).

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IVC filter

–Not routinely inserted in patients with acute DVT

–May be considered in patients with DVT or PE with absolute contraindication to anticoagulation, or recurrent embolism despite adequate anticoagulation

–Special considerations can be given to patients who are chronically immobile, such as spinal cord injury patients.

ADMISSION, INPATIENT, AND NURSING CONSIDERATIONS

Admission for respiratory distress, proximal VTE, candidate for thrombolysis, active bleeding, renal failure, phlegmasia alba dolens, phlegmasia cerulea dolens, history of HIT

Limb elevation and multilayered compression for symptomatic relief In medically stable and properly anticoagulated patients, overlap of anticoagulation and warfarin monitoring may be done as an outpatient.

ONGOING CARE

FOLLOW-UPRECOMMENDATIONS

Resumption of normal activity with avoidance of prolonged immobility

Compression stockings not routinely recommended for prevention of PTS after acute DVT (4)[B] but can be used for patients who already present with symptoms of PTS

Patient Monitoring

Monitor platelet count while on heparin, LMWH, and fondaparinux for HIT.

An anti-Xa activity level may help guide LMWH titration of therapy.

Serial D-dimer measurements can be used to identify patients in whom anticoagulation can be safely discontinued.

Investigate significant bleeding (e.g., hematuria or GI hemorrhage) because anticoagulant therapy may unmask a preexisting lesion (e.g., cancer, peptic ulcer disease, or arteriovenous [AV] malformation).

PATIENT EDUCATION

Dietary habits should be discussed when warfarin is initiated to ensure that intake of vitamin K–rich foods is monitored.

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PROGNOSIS

20% of untreated proximal (iliofemoral, femoral, or popliteal) lower extremity DVTs progress to PE, and 10–20% of those are fatal. However, with anticoagulant therapy, mortality is decreased 5- to 10-fold.

DVT confined to the infrapopliteal veins has a small risk of embolization but can propagate proximally.

Up to 75% of patients with symptomatic DVT present with PTS after 5 to 10 years.

COMPLICATIONS

PE (fatal in 10–20%), arterial embolism (paradoxical embolization) with AV shunting, chronic venous insufficiency, PTS, treatment-induced hemorrhage, soft tissue ischemia associated with massive clot and high venous pressures; phlegmasia cerulea dolens (rare but a surgical emergency)

REFERENCES

1.Dresang L, Fontaine P, Leeman L, et al. Venous thromboembolism during pregnancy. Am Fam Physician. 2008;77(12):1709–1716.

2.Baumann Kreuziger LB, Jaffray J, Carrier M. Epidemiology, diagnosis, prevention and treatment of catheter-related thrombosis in children and adults. Thromb Res. 2017;157:64–71.

3.Holbrook A, Schulman S, Witt DM, et al. Evidence-based management of anticoagulant therapy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141(Suppl 2):e152S–e184S.

4.Kearon C, Akl EA, Ornelas J, et al. Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report. Chest. 2016;149(2):315–352.

5.Kearon C, Akl E. Duration of anticoagulant therapy for deep vein thrombosis and pulmonary embolism. Blood. 2014;123(12):1794–1801.

6.Meissner M, Gloviczki P, Comerota A, et al. Early thrombus removal strategies for acute deep venous thrombosis: clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum. J Vas Surg. 2012;55(5):1449–1462.

ADDITIONALREADING

Agnelli G, Buller HR, Cohen A, et al; for AMPLIFYInvestigators. Oral

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