Deep Vein Thrombosis

(DVT)

Introduksi Deep Vein Thrombosis (DVT)Arteri-arteri mempunyai otot-otot yang tipis didalam dinding-dinding mereka supaya mampu untuk menahan tekanan darah yang dipompa jantung keseluruh tubuh. Vena-vena tidak mempunyai lapisan otot yang signifikan, dan disana tidak ada darah yang dipompa balik ke jantung kecuali fisiologi. Darah kembali ke jantung karena otot-otot tubuh yang besar menekan/memeras vena-vena ketika mereka berkontraksi dalam aktivitas normal dari gerakan tubuh. Aktivitas-aktivitas normal dari gerakan tubuh mengembalikan darah ke jantung.Ada dua tipe dari vena-vena di kaki; vena-vena superficial (dekat permukaan) dan vena-vena deep (yang dalam). Vena-vena superficial terletak tepat dibawah kulit dan dapat terlihat dengan mudah pada permukaan. Vena-vena deep, seperti yang disiratkan namanya, berlokasi dalam didalam otot-otot dari kaki. Darah mengalir dari vena-vena superficial kedalam sistim vena dalam melalui vena-vena perforatoryang kecil. Vena-vena superficial dan perforator mempunyai klep-klep (katup-katup) satu arah didalam mereka yang mengizinkan darah mengalir hanya dari arah jantung ketika vena-vena ditekan.Bekuan darah (thrombus) dalam sistim vena dalam dari kaki adalah sebenarnya tidak berbahaya. Situasi menjadi mengancam nyawa ketika sepotong dari bekuan darah terlepas (embolus, pleural=emboli), berjalan ke arah muara melalui jantung kedalam sistim peredaran paru, dan menyangkut dalam paru. Diagnosis dan perawatan dari deep venous thrombosis (DVT) dimaksudkan untuk mencegahpulmonary embolism.Bekuan-bekuan dalam vena-vena superficial tidak memaparkan bahaya yang menyebabkan pulmonary emboli karena klep-klep vena perforator bekerja sebagai saringan untuk mencegah bekuan-bekuan memasuki sistim vena dalam. Mereka biasanya tidak berisiko menyebabkan pulmonary embolism.

Penyebab-Penyebab Deep Vein Thrombosis

Darah dimaksudkan untuk mengalir; jika ia menjadi mandek ada potensi untuknya untuk membeku/menggumpal. Darah dalam vena-vena secara terus menerus membentuk bekuan-bekuan yang mikroskopik yang secara rutin diuraikan oleh tubuh. Jika keseimbangan dari pembentukan bekuan dan pemecahan dirubah, pembekuan/penggumpalan yang signifikan dapat terjadi. Thrombus dapat terbentuk jika satu, atau kombinasi dari situasi-situasi berikut hadir:

Imobilitas (Keadaan Tak Bergerak)

Perjalanan dan duduk yang berkepanjangan, seperti penerbangan-

penerbangan pesawat yang panjang ("economy class syndrome"), mobil,

atau perjalanan kereta api

Opname rumah sakit

Operasi

Trauma pada kaki bagian bawah dengan atau tanpa operasi atau gips

Kehamilan, termasuk 6-8 minggu setelah partum

Kegemukan

Hypercoagulability (Pembekuan darah lebih cepat daripada biasanya)

Obat-obat (contohnya, pil-pil pengontrol kelahiran, estrogen)

Merokok

Kecenderungan genetik

Polycythemia (jumlah yang meningkat dari sel-sel darah merah)

Kanker

Trauma pada vena

Patah tulang kaki

Kaki yang memar

Komplikasi dari prosedur yang invasif dari vena

Gejala-Gejala Deep Vein Thrombosis

Superficial thrombophlebitis

Bekuan-bekuan darah pada sistim vena superficial paling sering terjadi disebabkan oleh trauma (luka) pada vena yang menyebabkan terbentuknya bekuan darah kecil. Peradangan dari vena dan kulit sekelilingnya menyebabkan gejala dari segala tipe peradangan yang lain:

kemerahan,

kehangatan,

kepekaan, dan

pembengkakan.

Sering vena yang terpengaruh dapat dirasakan sebagai tali menebal yang kokoh. Mungkin ada peradangan yang menyertai sepanjang bagian dari vena.Meskipun ada peradangan, tidak ada infeksi.Varicosities dapat memberi kecenderungan pada superficial thrombophlebitis. Ketika klep-klep dari vena-vena yang lebih besar pada sistim superficial gagal (vena-vena saphenous yang lebih besar dan lebih berkurang), darah dapat mengalir balik dan menyebabkan vena-vena untuk membengkak dan menjadi menyimpang atau berliku-liku. Klep-klep gagal ketika vena-vena kehilangan kelenturan dan peregangannya. Ini dapat disebabkan oleh umur, berdiri yang berkepanjangan, kegemukan, kehamilan, dan faktor-faktor genetik.

Deep Venous Thrombosis

Gejala-gejala dari deep vein thrombosis berhubungan dengan rintangan dari darah yang kembali ke jantung dan menyebabkan aliran balik pada kaki. Secara klasik, gejala-gejala termasuk:

nyeri,

bengkak,

kehangatan, dan

kemerahan.

Tidak semua dari gejala-gejala ini harus terjadi; satu, seluruh, atau tidak ada mungkin hadir dengan deep vein thrombosis. Gejala-gejala mungkin meniru infeksi atau cellulitis dari kaki.Menurut sejarah, dokter-dokter akan mencoba menimbulkan sepasang penemuan-penemuan klinik untuk membuat diagnosis. Dorsiflexion dari kaki (menarik jari-jari kaki menuju ke hidung, atau Homans' sign) dan Pratt's sign (memencet betis untuk menghasilkan nyeri), telah ditemukan tidak efektif dalam membuat diagnosis.

Saat Untuk Mencari Perawatan Medis Untuk Deep Vein Thrombosis

Diagnosis dari thrombosis superficial atau deep sering bersandar pada ketrampilan klinik dari dokter. Tes-tes diagnostik perlu disesuaikan pada setiap situasi.Kaki yang bengkak, kemerahan, dan nyeri mungkin adalah indikator-indikator dari bekuan darah dan harus tidak diabaikan. Gejala-gejala ini mungkin disebabkan oleh penyebab-penyebab lain (contohnya, cellulitis atau infeksi), namun mungkin sulit untuk membuat diagnosis tanpa mencari nasehat medis.Jika ada nyeri dada atau sesak napas yang berhubungan, maka keprihatinan lebih jauh ada bahwa pulmonary embolus mungkin adalah penyebabnya. Sekali lagi, segera mencari nasehat adalah tepat.

Mendiagnosa Deep Vein Thrombosis

Diagnosis dari superficial thrombophlebitis dibuat secara klinik.Ultrasound sekarang adalah metode standar dari mendiagnosa kehadiran deep vein thrombosis. Teknisi ultrasound mungkin mampu untuk menentukan apakah ada bekuan, dimana ia berlokasi di kaki, dan berapa besarnya. Ultrasounds dapat dibandingkan melalui waktu untuk melihat apakah bekuan telah tumbuh atau menghilang. Ultrasound adalah lebih baik untuk "melihat" vena-vena diatas lutut dibanding pada vena-vena dibawah lutut.Venography, menyuntikan zat pewarna (dye) kedalam vena-vena untuk mencari thrombus, umumnya tidak dilakukan lagi dan telah lebih menjadi catatan kaki sejarah.

D-dimer adalah tes darah yang mungkin digunakan sebagai tes penyaringan (screening) untuk menentukan apakah ada bekuan darah. D-dimer adalah kimia yang dihasilkan ketika bekuan darah dalam tubuh secara berangsur-angsur larut/terurai. Tes digunakan sebagai indikator positif atau negatif. Jika hasilnya negatif, maka tidak ada bekuan darah. Jika tes D-dimer positif, itu tidak perlu berarti bahwa deep vein thrombosis hadir karena banyak situasi-situasi akan mempunyai hasil positif yang diharapkan (contohnya, dari operasi, jatuh, atau kehamilan). Untuk sebab itu, pengujian D-dimer harus digunakan secara selektif.Pengujian darah lainnya mungkin dipertimbangkan berdasarkan pada penyebab yang potensial untuk deep vein thrombosis.

Perawtan Untuk Deep Vein Thrombosis (DVT)

Superficial Thrombophlebitis

Perawatan untuk bekuan-bekuan darah superficial adalah simptomatik dengan:

kompres-kompres hangat,

pengompresan kaki, dan

obat-obat anti-peradangan seperti ibuprofen.

Jika thrombophlebitis terjadi dekat selangkangan kaki dimana sistim-sistim superficial dan dalam bergabung bersama, ada potensial bahwa thrombus dapat meluas kedalam sistim vena dalam. Pasien-pasien ini mungkin memerlukan terapi anticoagulation atau pengenceran darah (lihat bawah).

Deep venous thromboses

Deep venous thromboses atau thrombos-thrombos vena dalam yang terjadi dibawah lutut cenderung tidak embolisasi (terlepas). Mereka mungkin diamati dengan rentetan ultrasounds untuk memastikan mereka tidak meluas keatas lutut. Pada saat yang sama, penyebab dari deep vein thrombosis mungkin perlu ditujukan.Perawatan untuk deep venous thrombosis diatas lutut adalah antikoagulasi, kecuali ada kontraindikasi. Kontraindikasi-kontraindikasi termasuk operasi besar baru-baru ini (karena antikoagulasi akan mengencerkan semua darah dalam

tubuh, tidak hanya yang di kaki, menjurus pada persoalan-persoalan perdarahan yang signifikan), atau reaksi-reaksi abnormal ketika sebelumnya dipaparkan pada obat-obat pengencer darah.Antikoagulasi mencegah pertumbuhan yang lebih jauh dari bekuan darah dan mencegahnya dari pembentukan embolus yang dapat berjalan ke paru.Antikoagulasi adalah proses dua langkah. Warfarin (Coumadin) adalah obat pilihan untuk antikoagulasi. Ia segera dimulai, namun sayangnya mungkin memerlukan waktu satu minggu atau lebih untuk darahnya mengencer secara tepat. Oleh karenanya, heparin berat molekul rendah [enoxaparin (Lovenox)] dimasukan pada saat yang bersamaan. Ia mengencerkan darah melaui mekanisme yang berbeda dan digunakan sebagai terapi penghubung (jembatan) hingga warfarin telah mencapai tingkat therapeutiknya. Suntikan-suntikan enoxaparin dapat diberikan pada basis pasien rawat jalan.Untuk pasien-pasien yang mempunyai kontraindikasi-kontraindikasi pada penggunaan dari enoxaparin (contohnya, gagal ginjal tidak mengizinkan obatnya untuk dimetabolis), heparin intravena dapat digunakan sebagai tindakan pertama. Ini memerlukan opname di rumah sakit.Dosis dari warfarin dimonitor dengan tes-tes darah yang mengukur waktu prothrombin atau INR (international normalized ratio). Untuk deep vein thrombosis yang tidak rumit (menyulitkan), lamanya terapi dengan warfarin yang direkomendasikan adalah tiga sampai enam bulan.Beberapa pasien-pasien mungkin mempunyai kontraindikasi-kontraindikasi untuk terapi warfarin, contohnya seorang pasien dengan perdarahan di otak, trauma utama, atau operasi yang signifikan baru-baru ini. Satu alternatif mungkin adalah untuk menempatkan saringan (filter) di inferior vena cava (vena utama yang mengumpulkan darah dari kedua kaki-kaki) untuk mencegah emboli mencapai jantung dan paru-paru. Saringan-saringan ini mungkin efektif namun mungkin juga adalah sumber dari pembentukan bekuan yang baru.

Komplikasi-Komplikasi Deep Vein Thrombosis (DVT)

Pulmonary embolism adalah komplikasi utama dari deep vein thrombosis. Ia dapat hadir dengan nyeri dada dan sesak napas dan adalah kondisi yang mengancam nyawa. Lebih dari 90% dari pulmonary emboli timbulya dari kaki-kaki.Post-phlebitic syndrome dapat terjadi setelah deep vein thrombosis. Kaki yang terpengaruh dapat menjadi bengkak dan nyeri secara kronis dengan perubahan-

perubahan warna kulit dan pembentukan borok-borok (ulcer) disekitar kaki dan pergeangan kaki.

Pencegahan Deep Vein Thrombosis

Seperti kasusnya dengan kebanyakan penyakit medis, pencegahan adalah kepentingan utama. Mengecilkan faktor-faktor risiko adalah kunci pada pencegahan deep vein thrombosis.Pada tatacara rumah sakit, staff bekerja keras untuk mengecilkan potensial untuk pembentukan bekuan pada pasien-pasien yang lumpuh (tidak dapat bergerak). Compression stockings (kaos-kaki penekan) digunakan secara rutin. Pasien-pasien operasi berjalan keluar dari ranjang lebih dini dan dosis rendah heparin atau enoxaparin digunakan untuk deep vein thrombosis prophylaxis (langkah-langkah yang diambil untuk mencegah DVT).Untuk mereka yang berwisata, adalah direkomendasikan bahwa mereka berdiri dan berjalan setiap beberapa jam selama perjalanan yang jauh.Compression stockings mungkin bermanfaat dalam mencegah pembentukan deep vein thrombosis dimasa depan pada pasien-pasien dengan sejarah bekuan sebelumnya.

kaki yang bengkak satu sisi itu namanya Trombosis Vena Dalam a.k.a Deep Vein

Thrombosis

nah

keadaan ini terjadi karena adanya imobilitas pada mbak-mbak hamil, nenek, &

kakek yang mengakibatkan aliran darah jadi tidak lancar

tp tenang aja kok

insyaallah semua ada jalan

*hehe.. ustadz-ustadz mode on!!

a. Definisi

Obstruksi pada vena oleh bekuan darah tanpa didahului oleh reaksi inflamasi

pada dinding vena akibat adanya gangguan actor koagulan

b. Lokasi terjadinya

• DVT proksimal: proximal dari vena sentral

• DVT distal: iliaka, femoral, popliteal

c. Kondisi yang berhubungandengan DVT / etiologi:

• Operasi, x: umum, ortopedi

• Neoplasma

• Trauma/fraktur

• Imobilisasi, x: pasien CHF & lumpuh

• Kontrasepsi oral

• Estrogen, x: kontrasepsi & HRT

• Hamil

• Hiperkoagulatif faktor

• Venulitis

• Sepsis

• Obesitas

• Pernah DVT

• Artroskopi: inspeksi kavitas sendi melaui tindak operasi untuk tujuan biopsy

d. Faktor resiko:

pengguna indwelling vena central catether

e. Manifestasi klinis

Anamnesis:

• Kaki bengkak & nyeri

• RPD & RPK: pernah terdapat DVT atau thrombosis

• faktor resiko

Fisik:

• Edema tungkai unilateral: iliaka, femoral, popliteal. Banyak di lower extrimity

• Eritema

• Warmth/hangat

• cord/ tonjolan

• peningkatan turgor jaringan

• Distensi vena superfisial

• Vena kolateral

• Tanda houman (+): nyeri & peningkatan resistensi ketika kaki yang edema

dorsofleksi

• Kulit:

Phlegmasia cerculea dolens: sianotik/ biru2

Phlegmasia alba dolens: pallor di tunkai yang bengkak

Laboratorium:

• peningkatan D-dimer

• antitrombin

Tambahan:

Noninvasif

• Duplex Venous USG:

Untuk: mengetahui adanya vena kolaps dan kompresi vena

Negative pada wanita hamil pada daerah pelvis, iliaka, & v. cava

Lebih sensitif & spesifik pada DVT proximal

• USG Dppler:

Untuk: mengetahui kecepatan aliran darah

aliran darah menurun pada kondisi: gangguan respirasi & kompresi vena

Lebih sensitif & spesifik pada DVT proximal

• MRI:

Untuk: mengetahui thrombosis pada vena cava & vena pelvis

Untuk wanita hamil

Invasif

• Venografi/ phlebografi

Untuk: mengetahui defek atau tidak adaknya blood filling di vena tersebut

Pada DVT: betis, paha, ileofemoral

Kerugian: pasang kateter → syok, injeksi kontaras/ yodium→ alergi

f. Dd

• Ruptur otot

• Kista popliteal yang ruptur

• Trauma

• Hemoragi

• Limfedema

Identifikasi masalah

1. Edema kaki dan nyeri

2. anti-trombin menurun

Prioritas masalah

1. penurunan anti-trombin

Karena pada DVT , penurunan anti-trombin → emboli paru → gangguan perfusi

O2-darah-jaringan→ hipoxia→ iskemik→ nekrosis bahkan kematian

2. Edema kaki+nyeri

Karena tergantung etiologinya berbeda-beda dan organ-organ yang terlibat

seperti jantung (CHF), renal (sindroma nefrotik), hati(HCC), pembuluh darah

(emboli+trombosis), & wucheria bancrofti. Beda etiologi berakibat beda dampak +

tatalaksana

Analisis & sintesis

1. anti-trombinmenurun

a. etiologi:

- gangguan faktor koagulasi:

kongenital

• hemofiliaA

• hemophilia B

• vWD disease: < factor VIII→ anti-trombin

didapat

• defisiensi vit.K

vit. K adalah kofaktor karboxilasi untuk residu protein rotrombin kompleks.

Sehingga def vit.K → gangguan produksi factor II, VII, IX, X → anti-

trombinmenurun

• penyakit Hati

menyebabkan penurunan seluruh faktor kecuali factor IIIV (kan vWD gtu!!) →

anti-trombinpenurunan → peningkatan PT, (n)/ peningkatan PTT

- gangguan trombotik:

• thrombosis (dvt, superficial thrombosis vein, dll)

• hiperkoagulasi

antitrombin (n) namun pada penyakit ini lebih cenderung mudahterjadi bekuan

darah

• trombofilia

herediter/ primer: def anti-trombinIII, def protein C & S (untuk produksi factor II,

IX, X), fibrinolisis defek, mutasi factor v Leiden (→ inaktivasi factor C), dll

sekunder : imobilisasi, malignansi sisteik, MPD, terapi estrogen (penurunan AT-III

& tPA), sindroma antibody antifosfolipid

• trauma endothelial: memacu proses fisiologis hemostasis

• gangguan aliran darah. Pada gangguan jantung, aliran darah Cuma mengalir di 1

daerah cenderung membentuk emboli.misalny pada gangguan atrial fibrillation

b. dampak:

peningkatan fibrin & sel- sel darah → thrombosis

peningkatan degradasi fibrin → peningkatan D-dimer

Misalnya:

• Hipoxia, Iskemik, dan nekrosis

• SVT

• DVT

• Emboli paru

• stroke

c. mekanisme: tergantung di etiologi (liat di atas)

2. edema tungkai +nyeri

etiologi+mekanisme

• jantung

CHF: karena adanya gangguan venous return. pitting edema tanpa nyeri, warna

kulit normal

• renal (sindroma nefrotik)

hipoglobulin→ edema anasarka + pitting + (-) nyeri

• hati(HCC)

penurunan produksi lipoprotein yang berikatan dengan globulin → edema +

pitting + (-) nyeri

• pembuluh darah (emboli+trombosis)

stasis vena, peningkatan prokoagulan, Ganggguan dinding pembuluh darah →

obstruksi vena+ kompresi saraf → edema tungkai unilateral + kulit (ada bagian

yang pallor & sianotik)+ non pitting+ eritema+ warmth+nyeri

• wucheria bancrofti

edema tungkai bilateral

dampak:

• gangguan perfusi O2 ke jaringan

• distensi vena superficial

• turgor jaringan meningkat

Simpulan kasus

Mr. XXX / mrs. XXY (biasanya pada ibu hamil)mengalami edema tungkai + nyeri

karena anti-trombin menurun yang dipengaruhi oleh factor resiko (indwellin vein

catether)& keadaan pasien (pasca operasi ortopedi & umum, hamil, imobilisasi,

RPK-RPD pernah trombosis)

Tatalaksana

Tujuan terapi:

• Stop peningkatan thrombus

• Batasi progresivitas edema tumgkai

• Lisis & buang bekuan darah (trombektomi)

• Cegah: disfungsi vena, emboli paru & past-thrombotic syndrome

Medikamentosa & non medikamentosa:

• Antikoagulan

Unfractioned heparin/ low molecular weight heparin

i.v 18 IU/kg BB/ jam → cek trombosit, PTT, APTT meningkat 2x →heparin

subkutan

ESO: trombositopenia [heparin- induced thrombositopenia/ HIT], thrombosis

arterial, & iskemia

Warfarin [bareng heparin]

Efek: full antikoagulan

Beri di minggu pertama selama 4-5 hari, lalu stop warfarin. Karena efeknya akan

overlapping dengan heaparin dan warfarin tidak efektif lagi

• Trombolitik

Tujuan: lisis thrombus

x: streptokinase, urokinase & tPA

kurang efektif untuk cegah emboli paru

• Trombektomi

Bila terdapat:

1. Trombosis vena ileofemoral akut

2. Fistula arteriovena

• Filter vena kava

Untuk DVT Proksimal → cegah emboli paru

Jangan lupa!!!

1. Attitude

2. Komunkasi

3. Sistematika berpikir

i. Komplikasi

• Emboli paru

• Kematian

• Post-thrombotic syndrome

• Trombositopenia

j. Prognosis

Baik bila diagnosis & terapi cepat & tepat serta menggunakan profilaksis

Maaph klo terkesan ga lengkap n asal

Deep vein thrombosisFrom Wikipedia, the free encyclopedia"DVT" redirects here. For other uses, see DVT (disambiguation).

Deep vein thrombosis

Classification and external resources

A deep vein thrombosis in the right leg. Note the swelling and redness.

ICD-10 I 80.2

ICD-9 453.40

DiseasesDB 3498

MedlinePlus 000156

eMedicine med/2785

MeSH D020246

Deep vein thrombosis (DVT) is the formation of a blood clot (thrombus) in a deep vein, most commonly of the legs. A DVT can occur without symptoms, but in many cases the affected extremity will be painful, swollen, red, and warm, and the superficial veins may be engorged. The most serious complication of a DVT is that the clot could dislodge and travel to the lungs, which is called a pulmonary

embolism (PE). DVT and PE are the two manifestations of the disease venous thromboembolism (VTE). Untreated lower extremity DVT has a 3% PE-related mortality rate. Deaths associated with upper extremity DVT are extremely rare.[1] A late complication of DVT is the post-thrombotic syndrome (PTS), which can manifest itself as edema, pain or discomfort and skin problems.

According to Virchow's triad, venous thrombosis occurs due to three factors: decreased flow rate of the blood (venous stasis), damage or activation of theblood vessel wall and an increased tendency of the blood to clot (hypercoagulability). DVT formation can start inside of leg vein valves, where the blood is relatively oxygen deprived. Several medical conditions increase the risk for DVT, such as physical trauma, cancer and antiphospholipid syndrome. Otherrisk factors include older age (the strongest), surgery, immobilization (as with bed-rest, orthopedic casts, or during long-haul flights), oral contraceptivesand inborn tendencies to form clots known as thrombophilia (for example, in carriers of factor V Leiden). Women have an increased risk during pregnancy (due to altered blood protein levels) and in the postnatal period, partially due to substances released by the placenta. However, some of those who develop DVT have no recognized risk factors.

Individuals suspected of having a DVT may receive a probability assessment, such as the Wells score, and a D-dimer test, which may exclude the diagnosis or signal further testing is needed. Diagnosis of DVT is most commonly done with ultrasound of the affected veins. Treatment for DVT is dominated by anticoagulation (which prevents further coagulation) with a heparin and a vitamin K antagonist. If anticoagulation is not possible, management may involve inferior vena cava filter placement to presumably prevent PE. A complication of DVT, post-thrombotic syndrome, appears to be reduced by wearing graduated compression stockings (GCS). Prevention of DVT is advised in at-risk medical and surgical inpatients with options such as early and frequent walking, anticoagulants, GCS or intermittent pneumatic compression (IPC).

Contents

[hide]

1 Classification2 Signs and symptoms

3 Causeso 3.1 Risk factors

4 Pathophysiology5 Diagnosiso 5.1 Probability assessmento 5.2 D-dimero 5.3 Imaging

6 Preventiono 6.1 Surgery patientso 6.2 Pregnancyo 6.3 Travellerso 6.4 Medical inpatients

7 Treatmento 7.1 Anticoagulationo 7.2 Graduated compression stockingso 7.3 Inferior vena cava filtero 7.4 Home vs. hospitalo 7.5 Serial imagingo 7.6 Thrombolysis and thrombectomy

8 Prognosis9 Epidemiology10 History11 Research directions12 Notes13 References14 External links

[edit]Classification

The popliteal vein is at the top of the image.

DVT and pulmonary embolism (PE) are the two manifestations of venous thromboembolism (VTE), a term which represents a distinct disease state.[2] DVTs can be lower extremity (from the lower limbs), upper extremity, abdominal or pelvic in origin;[3] they can also occur in the neck.[4] DVTs in the legs are proximal (or iliofemoral)[5] when above the knee and distal when below the knee.[6] DVTs below the popliteal vein, a proximal vein behind the knee, are in distal calf veins.[7] An incident DVT is an initial episode and any subsequent DVTs are termed recurrent.[8] Bilateral DVT refers to its presence in both legs while unilateral specifies one leg.[9]

DVTs that have no symptoms, but are found only by screening, are labeled asymptomatic.[10] Pain and swelling are symptoms of acute DVT.[11] Acute DVTs are usuallyocclusive,[7] meaning they obstruct blood flow, whereas nonocclusive DVTs are more asymptomatic.[12] The label of chronic has been applied to symptomatic DVTs which persist longer than 10 or 14 days.[13] DVTs that develop in association with surgery are perioperative,[14] A DVT may also be called idiopathic when it "occurs in the absence of a known precipitating factor, such as oral contraceptives, surgery, trauma, or cancer."[15]

[edit]Signs and symptoms

Approximately half of people with DVT have symptoms. They include pain and tenderness in the leg, swelling, warmth in the leg that is swollen or painful, redness or discoloration, and dilation of surface veins.[16] However, signs and symptoms can not be used to diagnose DVT. When taken together with the risk factors (see below), they are useful in determining the likelihood of DVT,[7] but

most of those suspected of DVT do not have it after evaluation.[17] Most symptomatic individuals have another condition, and those possibilities include "cellulitis, Baker's cyst, musculoskeletal injury, [and] lymphedema".[18]

In phlegmasia alba dolens, which usually results from acute occlusion of the iliac and femoral veins, the leg is pale and cool with a diminished arterial pulse caused by spasm. A severe and uncommon form of DVT, phlegmasia cerulea dolens, often develops on top of a life-threatening illness.[12][19] It is characterized by an acute and nearly total venous occlusion of the entire extremity outflow, including the iliac and femoral veins. The leg is usually painful, cyanosed (blue from lack of oxygen) and edematous (filled with fluid). Venous gangrene may develop as a result.

In women, recurrent miscarriage may be a sign of DVT risk, as it is associated with antiphospholipid syndrome, a risk factor for DVT.[20]

[edit]Causes

Venous thrombi are recognized to be caused mainly by a combination of venous stasis and hypercoagulability—but to a lesser extent endothelial damage and activation.[21] The three factors of stasis, hypercoaguability, and alterations in the blood vessel wall represent Virchow's triad, and changes to the vessel wall are the least understood.[22] Various risk factors increase the likelihood of any one individual developing a thrombosis. Older age is the strongest risk factor;[22] after aging, blood composition favors clotting.[21] However, venous thrombosis can form without the presence of a risk factor, and many individuals with multiple risk factors never have a venous thrombosis.[23]

Inherited thrombophlias (deficiencies in the anticoagulation factors protein C, protein S, antithrombin, or mutations in the factor V and prothrombin genes) are present in about 30 to 50% of those with VTE.[24] Factor V Leiden and prothrombin G20210A, both predmoninantly expressed in Caucasians, are cited as the most commonly inherited risk factors;[21] they moderately increase risk, by factors of about 3 to 8 and 2 to 3, respectively.[25][24] Deficiencies in antithrombin, protein C and S are "rare but strong risk factors for venous thrombosis."[21] Relative risks estimates of the three vary. They have been estimated at 15- to 20-fold for all three,[23] down to 10 for antithrombin deficiency, and a maximum of 10 for protein C and S deficiencies.[24]

Different types of DVT can be influenced by different risk factors. In isolated distal DVT, the profile of risk factors appears to be different than proximal DVT; transient factors, such as surgery and immobilization, appear to dominate whereas thrombophilias and age do not seem to increase risk.[26] In upper extremity DVT, central venous catheters are a dominant risk factor.[27]

[edit]Risk factors

Acquired Older age[22]

Major surgery and orthopedic surgery[25]

Cancers, most particularly pancreatic, but not cancers of the lip, oral cavity, and pharynx[28]

Immobilization, as in orthopedic casts [25] the sitting position, and travel, particularly by air[21]

Pregnancy and the postpartum period[21][29]

Antiphospholipid syndrome [25] (such as lupus anticoagulant)[21][22]

Trauma [21] Previous VTE[1]

Oral contraceptives [25]

Inherited Antithrombin

deficiency [21] Protein C

deficiency [21] Protein S

deficiency (type I)[23]

Factor V Leiden[21]

Prothrombin G20210A[21]

Dysfibrinogenemi a [25]

Non O-blood type [25]

Mixed Low free protein S[23]

Activated protein C resistance [23]

High factor VIII levels[21]

Hyperhomocysteinemi a [21]

High fibrinogen levels[21]

High factor IX levels[21]

High factor XI levels[21]

The factor V protein is mutated in carriers of factor V Leiden, which is the most common inherited DVT risk factor.[31]

Hormonal replacement therapy [25]

Central venous catheters[25]

Some autoimmune diseases [30]

Nephrotic syndrome [23]

Obesity[25]

Infection[23]

HIV[23]

Polycythemia vera [25]

Chemotherapy [22] [edit]Pathophysiology

The femoral vein (in the thigh), the iliac veins (in the pelvis), and the inferior vena cava (in the abdomen) are places of potential DVT extension.

DVTs usually develop first in the calf veins, and when they extend, they "grow" in the direction of venous flow, towards the knees.[32] When DVTs do not grow, they can be cleared naturally and dissolved into the blood.[33] There is a strong tendency for DVT to develop in the left leg (about 70 to 90% of the time) "possibly because of exacerbation of the compressive effects on the left iliac vein due to its being crossed by the right iliac artery."[34] DVT commonly affects the leg veins of

the femoral vein, the popliteal vein, or the iliofemoral vein (as in May-Thurner syndrome) or the deep veins of the pelvis. Occasionally the veins of the arm are affected, as with Paget-Schrötter disease. Very extensive lower extremity DVTs can extend into the iliac veins or the inferior vena cava. Rarer DVTs can affect the upper extremities or the mesenteric (from the intestines) and pelvic veins.[3]

In contrast to the understanding for how arterial thromboses occur, as with heart attacks, venous thrombosis formation is not well understood.[35] With arterial thrombosis, blood vessel wall damage is required for thrombosis formation, as it initiates coagulation,[35] but the majority of venous thrombi form without any injured epithelium.[21] Red blood cells and fibrin are the main components of venous thrombi,[21] and the thrombi appear to attach to the blood vessel wallendothelium, normally a non-thrombogenic surface, with fibrin.[35] Platelets in venous thrombi attach to downstream fibrin, while in arterial thrombi, they compose the core.[35] As a whole, platelets constitute less of venous thrombi when compared to arterial ones.[21] The beginning of the process is thought to be initiated by tissue factor effected thrombin production, which leads to fibrin deposition.[22]

The valves of veins are a recognized site of VT initiation.[33] Due to the blood flow pattern, the base of the valve sinus is particularly deprived of oxygen (hypoxic). Stasis exacerbates hypoxia, and this state is linked to the activation of white blood cells (leukocytes) and the endothelium. Specifically, the two pathways of hypoxia-inducible factor-1 (HIF-1) and early growth response 1 (EGR-1) are activated by hypoxia, and they contribute to monocyte and endothelial activation. Hypoxia also causes reactive oxygen species (ROS) production that can activate HIF-1, EGR-1, and nuclear factor-κB (NF-κB), which regulates HIF-1 transcription.[22] HIF-1 and EGR-1 pathways lead to monocyte association with endothelial proteins, such as P-selectin, prompting monocytes to release tissue factor filledmicrovesicles, which presumably initiate fibrin deposition (via thrombin) after binding the endothelial surface.[22]

[edit]Diagnosis

Swelling in the leg from fluid (edema) can result in "pitting" after pressure is applied.

An ultrasound image demonstrating a blood clot in the left common femoral vein.

Abdominal CT scan showing a common iliac vein thrombosis. The arrow indicates the filling defect in the vein visualised usingradiocontrast.

Venograms of DVT.

In 2012, the American College of Chest Physicians (ACCP) released their 9th edition of clinical guidelines,[36] which included recommendations on VTE diagnosis.[17] The recommendations were given strengths with "grades", depending upon the evidence for them.

Grade Description of 2012 ACCP grade[37]

1A Strong recommendation, high-quality evidence

1B Strong recommendation, moderate-quality evidence

1C Strong recommendation, low- or very-low-quality evidence

2A Weak recommendation, high-quality evidence

2B Weak recommendation, moderate-quality evidence

2C Weak recommendation, low- or very-low-quality evidence[38]

This article cites 2012 ACCP recommendations, and includes the grade in parentheses in this section and the prevention and treatment sections below.

[edit]Probability assessment

In those with suspected DVT, a clinical assessment of probability can be useful to determine which tests to perform.[39] The most studied clinical prediction rule is the Wells score.[17]

Wells score or criteria: (Possible score −2 to 9)

1. Active cancer (treatment within last 6 months or palliative): +1 point2. Calf swelling ≥ 3 cm compared to asymptomatic calf (measured 10 cm

below tibial tuberosity): +1 point3. Swolen unilateral superficial veins (non-varicose, in symptomatic leg): +1

point4. Unilateral pitting edema (in symptomatic leg): +1 point5. Previous documented DVT: +1 point6. Swelling of entire leg: +1 point7. Localized tenderness along the deep venous system: +1 point8. Paralysis, paresis, or recent cast immobilization of lower extremities: +1

point9. Recently bedridden ≥ 3 days, or major surgery requiring regional or general

anesthetic in the past 12 weeks: +1 point10.Alternative diagnosis at least as likely: −2 points[18]

A Wells score can be interpreted in a binary (likely vs. unlikely) or ternary (low, moderate, or high probability) fashion. For a binary interpretation, scores of two or above are categorized as likely, while one and below means unlikely. For a ternary interpretation, scores of one and two are of moderate probability, while scores below or above are low and high probability, respectively.[18] When people are segregated into binary groups, DVT prevalence is about 6% versus 28%. Ternary groups stratify prevalences into groups of about 5%, 17%, and 53%.[17]

[edit]D-dimer

D-dimers are a fibrin degradation product, and a positive D-dimer test can result from the sensitive detection of a thrombosis being dissolved by plasmin. A positive test may also result from other conditions.[17] Thus, a positive D-dimer text means further diagnostic testing should be done to determine if a DVT is present, while a negative result can exclude a DVT diagnosis.[17] For suspected first lower extremity DVT in a low-probability situation, the typical next step is to test D-dimer levels with either moderate or high sensitivity.[40] In a moderate-probability scenario, a high-sensitivity D-dimer is recommended over ultrasound imaging (2C),[41] and in high-probability cases D-dimers are to be skipped in favor of diagnostic imaging.[42]

[edit]Imaging

Imaging studies are used to diagnose DVT. Ultrasound on the veins is the most common method, and the two standard options include proximal compression ultrasound or whole-leg ultrasound. Drawbacks to each method exist. A single proximal scan may miss a distal DVT, while whole-leg scanning can lead to distal DVT overtreatment.[17] Doppler ultrasound,[43] CT scan venography, MRI venography or MRI of the thrombosis are also possibilities.[17][40]The gold standard for judging imaging methods is contrast venography, which involves injecting a peripheral vein of the affected limb with a contrast agent and taking X-rays, to reveal whether the venous supply has been obstructed. Because of its cost, invasiveness, and other limitations this test is rarely performed.[17]

[edit]Prevention

Walking is an effective preventative measure.[44] Walking activates the body's muscle "pumps", increasing venous velocity and preventing low blood flow. In immobile hospital patients at risk of DVT, mechanical measures may instead be used to improve blood flow patterns. Long-term anticoagulation is warranted in patients with recurrent DVT,[citation needed] but is not recommended in asymptomatic individuals with thrombophilia (1C).[45] While an individual with the strong thrombophilia of antithrombin deficiency is at a 0.8 to 1.5% annual risk of VTE, long-term anticoagulation carries a 3% annual risk of major bleeding is not advised.[24]

[edit]Surgery patients

Surgery patients, particularly those who had major surgery, are at an increased risk of forming a DVT. In patients who have undergone non-orthopedic surgery, early ambulation (walking), mechanical prophylaxis (intermittent pneumatic compression [IPC] or graduated compression stockings [GCS]), and drugs (low-molecular-weight heparin [LMWH], low-dose-unfractionated heparin [LDUH]) are potential recommended treatments depending upon the risk of VTE, risk of major bleeding, and patient preferences.[46] In major orthopedic surgery patients—those undergoing total hip replacement, total knee replacement, and hip fracture surgery—additional drug options, such as fondaparinux andaspirin, are recommended (1B), though LMWH is preferred (2B or 2C).[47] IPC is an option (1C).[47][48]

[edit]Pregnancy

See also: Hypercoagulability in pregnancy

Warfarin, a common VKA, is only recommended postpartum (after childbirth) in at risk women.

The risk of VTE is increased in pregnancy by about 4-fold[34] due to a more hypercoaguable state, a likely adaptation against fatal postpartum hemorrhage.[29] Additionally, pregnant women with genetic susceptibility to blood coagulation are subject to a further and approximate 3- to 30-fold increased risk for VTE, depending upon the risk factor(s).[20]

The 2012 ACCP clinical guidelines suggested that specific groups of at-risk pregnant women receive targeted (INR of 2 to 3) preventative measures. Homozygous carriers of factor V Leiden or prothrombin G20210A with a family history of VTE were recommended to receive antepartum LMWH and either LMWH or a vitamin K antagonist (VKA) for the 6 weeks following childbirth (2B); those with another thrombophlia and a family history but no previous VTE were recommended to be subject to clinical vigilance during pregnancy and LMWH or

(for those without protein C or S deficiency) a VKA (2C); homozygous carriers with no personal or family history of VTE were recommended to be subject to clinical vigilance during pregnancy and LMWH or a VKA for 6 weeks after childbirth (2B); and those with another thrombophilia but no family or personal history of VTE were suggested to receive clinical vigilance (2C).[20] Warfarin , a common VKA, is known to have teratogenic effects on the fetus if administered in early pregnancy[49][50] and is not advised in pregnant women.

[edit]Travellers

In the 2012 ACCP clinical guidelines, grade 2C recommendations were offered. For at risk long-haul travelers—those with "previous VTE, recent surgery or trauma, active malignancy, pregnancy, estrogen use, advanced age, limited mobility, severe obesity, or known thrombophilic disorder"—recommendations for prevention included frequent walking, calf exercises, and aisle seating in airplanes to ease walking.[51][52] The use of "properly fitted, below-knee GCS providing 15 to 30 mm Hg of pressure at the ankle during travel" was recommended though use of aspirin or anticoagulants were not.[53] Compression stockings have sharply reduced the levels of asymptomatic DVT in airline passengers, but the effect on symptomatic VTE is unknown as no individuals studied developed symptomatic VTE.[54]

[edit]Medical inpatients

Graduated compression stockings are recommended in some at-risk hospital patients

Clinical practice guidelines state:

American College of Physicians (ACP) in 2011:[2][55]

"ACP recommends assessment of the risk for thromboembolism and bleeding in medical (including stroke) patients prior to initiation of

prophylaxis of venous thromboembolism (Grade: strong recommendation, moderate-quality evidence)."

"ACP recommends pharmacologic prophylaxis with heparin or a related drug for venous thromboembolism in medical (including stroke) patients unless the assessed risk for bleeding outweighs the likely benefits (Grade: strong recommendation, moderate-quality evidence)."

"ACP recommends against the use of mechanical prophylaxis with graduated compression stockings for prevention of venous thromboembolism (Grade: strong recommendation, moderate-quality evidence)."

"ACP does not support the application of performance measures in medical (including stroke) patients that promotes universal venous thromboembolism prophylaxis regardless of risk."

The summary of the 2012 ACCP guidelines state: "For acutely ill hospitalized medical patients at increased risk of

thrombosis, we recommend anticoagulant thromboprophylaxis with [LMWH], [LDUH] bid, LDUH tid, or fondaparinux (Grade 1B) and suggest against extending the duration of thromboprophylaxis beyond the period of patient immobilization or acute hospital stay (Grade 2B). For acutely ill hospitalized medical patients at low risk of thrombosis, we recommend against the use of pharmacologic prophylaxis or mechanical prophylaxis (Grade 1B). For acutely ill hospitalized medical patients at increased risk of thrombosis who are bleeding or are at high risk for major bleeding, we suggest mechanical thromboprophylaxis with [GCS] (Grade 2C) or [IPC] (Grade 2C). For critically ill patients, we suggest using LMWH or LDUH thromboprophylaxis (Grade 2C). For critically ill patients who are bleeding or are at high risk for major bleeding, we suggest mechanical thromboprophylaxis with GCS and/or IPC at least until the bleeding risk decreases (Grade 2C). In outpatients with cancer who have no additional risk factors for VTE we suggest against routine prophylaxis with LMWH or LDUH (Grade 2B) and recommend against the prophylactic use of vitamin K antagonists (Grade 1B)."[56]

[edit]Treatment

[edit]Anticoagulation

Structural representations of the backbone of heparins (left), which vary in the size of their chain, and the synthetic pentasaccaride (five-sugar) fondaparinux (right)

Anticoagulation, which prevents further coagulation, is the standard treatment for acute DVT of the leg. Patients are recommended to receive a parenteral anticoagulant (such as LMWH, fondapariniux or unfractionated heparin) for at least five days and to start vitamin K antagonist (VKA) treatment the same day (1B). The parenteral anticoagulant is recommended until the international normalized ratio(INR) is ≥ 2.0 for 24 hours minimum (1B); or, if the INR is > 3.0, the parental anticoagulant treatment can stop early.[57][58] LMWH andfondaparinux are recommended over unfractionated heparin (2B or C),[59] but unfractionated heparin does not present clearance issues in those with compromised kidney function.[58] The VKA may be taken for a minimum of 3 months to maintain an INR of 2 to 3,[60] but the benefit of taking a VKA declines as the duration of treatment extends, while the risk of bleeding remains.[61] In patients who have had recurrent DVTs, anticoagulation is generally life-long.[citation

needed] Guidelines for anticoagulant management have been published, but many facets are understudied.[62] In those who have a positive D-dimer level after the end of VKA treatment for idiopathic VTE, there is an increased risk of recurrent VTE (about 9% vs. about 4% for negative results) and this result may be used in clinical decision making.[63]

A methodologically sound randomized controlled trial of anticoagulation versus placebo in the treatment of VTE has never been done, but it is unlikely to be performed due to ethical constraints. Evidence for clinical practice is derived from secondary evidence, such as "trials comparing anticoagulation versus placebo after initial anticoagulation."[64]

[edit]Graduated compression stockings

In addition to anticoagulation treatment, graduated compression stockings (GCSs)—which apply higher pressure (30–40 mm Hg) at the ankles and a lower pressure around the knees[58]—are recommended for those with symptomatic DVT (2B).[65] Use should begin as soon as possible after anticoagulation.[58] Randomized controlled trials indicate GCSs reduce the risk of post-thrombotic syndrome (PTS), although the "evidence is of moderate quality".[58][66] Trials do not indicate a reduction in recurrent VTE.[58] The number needed to treat is relatively high, at 4 to 5 patients needing to have been treated to prevent one case of PTS.[67] The recommended duration of use is for two years, though inconvenience and discomfort can reduce patient compliance.[65]

[edit]Inferior vena cava filter

An IVC filter

Inferior vena cava filters (IVC filters) are used on the presumption that they reduce pulmonary embolism, though their effectiveness and safety profile is not well established.[4]In general, they are recommended "to be restricted to certain high-risk situations until more information becomes available";[4] they are recommended in those with a contraindication to anticoagulant treatment (1B), but not in addition to anticoagulation (1B) unless an individual with an IVC filter, but without a risk for bleeding, develops acute proximal DVT (2B).[68] While IVC filters are "associated with an increased risk of DVT in the longer term"[4] they are not considered to be reason enough to maintain extended anticoagulation.[69]

[edit]Home vs. hospital

Home treatment is recommended for the initial treatment of those with acute leg DVT (1B) who feel "well enough to be treated at home (eg, [those without] severe leg symptoms or comorbidity)" as long as there is an adequate home environment, which is described as "well-maintained living conditions, strong support from family or friends, phone access, and ability to quickly return to the hospital if there is deterioration."[70]

[edit]Serial imaging

A follow-up imaging test (typically ultrasound) about one week post-diagnosis is an option for those with an acute isolated distal DVT without a high risk for extension (2C); if the thrombosis does not extend, no anticoagulation is recommended (1B).[58][71] This technique can benefit those at a high risk for bleeding. However, "patients who place a high value on avoiding the inconvenience of repeat imaging and a low value on the inconvenience of treatment and on the potential for bleeding are likely to choose initial anticoagulation over serial imaging."[71] When applied to symptomatic patients with a negative initial ultrasound result, serial testing is inefficient and "not cost effective."[7]

[edit]Thrombolysis and thrombectomy

Thrombolysis can be systemic or, depending upon medical capabilities, catheter-directed, but anticoagulation alone is preferred (2C). Although, those "who are most likely to benefit" from thrombolysis—"who attach a high value to prevention of postthrombotic syndrome (PTS), and a lower value to the initial complexity, cost, and risk of bleeding"—"are likely to choose [it] over anticoagulation alone."[72]

A mechanical thrombectomy device can remove a thrombus. However, it is only recommended as an option when the following conditions apply: "iliofemoral DVT, symptoms for < 7 days (criterion used in the single randomized trial), good functional status, life expectancy of ≥ 1 year, and both resources and expertise are available."[58] In general, anticoagulation alone is preferred (2C).[73]

[edit]Prognosis

Main article: Post-thrombotic syndrome

Distal DVT itself "is seldom if ever associated" with PTS or PE.[17] For those with proximal DVT, the risk of PE is higher in the presence of more extensive clots. After the one to two year period after the initial development of symptoms of DVT, PTS occurs in between as few as a fifth, and as many as half of cases. A "severe" PTS likewise varies in frequency between a twentieth and a tenth of individuals diagnosed with DVT. This malady is sometimes characterized by varicose ulceration.[74]

[edit]Epidemiology

DVTs occur in about 1 per 1000 adults per year.[75] It is estimated that approximately 300,000 to 600,000 Americans each year suffer from VTE with about 60,000 to 100,000 deaths attributable to PE.[76] Venous thrombosis is rare in the pediatric population. Children have an incidence of about 1 in 100,000 per year. From childhood to old age, the incidence increases by a factor of about 1000; almost 1 in 100 in the elderly population experience a venous thrombosis per year.[77]

In studies on pregnancy-associated acute VTE where "either all or most patients underwent accurate diagnostic testing", VTE incidence "ranges from 0.6 to 1.7 episodes per 1,000 deliveries."[20] VTE develops after knee- and hip-surgery patients who receive preventative measures at rates of about 1 per 100 after total or partial knee replacements and about 1 per 200 after total or partial hip replacements.[78]

[edit]History

Rudolf Virchow

The first known case of DVT occurred in the 13th century, "in the right leg of a 20-year-old man."[23] At some point, the increased incidence of DVT in women after childbirth was noticed. In the late 1700s, a public health recommendation was issued to encourage breast feeding as a means to prevent this phenomenon; the DVT was called "milk leg" as it was thought to result from milk building up in the leg.[79]

In 1856, German physician and pathologist Rudolf Virchow published what is referred to as Virchow's triad, the three major causes of thrombosis.[23][79] The triad provides the framework for how venous thrombosis formation is currently

explained.[23] Virchow also noted that more deep venous thrombosis occurred in the left leg than in the right and proposed compression of the left common iliac vein by the overlying right common iliac artery as the underlying cause (see May-Thurner syndrome).[citation needed]

Pharmacological therapies for DVT were introduced in the 20th century. Oral anticoagulants were introduced in the 1940s, subcutaneous LDUH in 1962, and subcutaneous LMWH in 1982. A RCT demonstrating the effectiveness of oral anticoagulation was done in 1959 and for subcutaneous LDUH, 1972.[80] Diagnoses were commonly performed by impedance plethysmography in the 1970s and 1980s, but Doppler ultrasound largely superseded the method with its increased accuracy.[81]