DEEP VENOUS THROMBOSIS

1
DEEP VENOUS THROMBOSIS

• DR.SHERAZ AHMED

2
Definition

• Deep vein thrombosis is the formation of a blood
  clot in one of the deep veins of the body,
  usually in the leg

3
ETIOLOGY

• DVT ususally originates in the lower extremity
  venous level ,starting at the calf vein level and
  progressing proximally to involve popliteal
  ,femoral ,or iliac system. .80 -90 pulmonary
  emboli originates here .

4
Virchow tried

• More than 100 years ago, Virchow described a
  triad of factors of
  
• venous stasis,
• endothelial damage, and
• hypercoagulable state

5
Venous stasis

• prolonged bed rest (4 days or more)
• A cast on the leg
• Limb paralysis from stroke or spinal cord injury
  
  
• extended travel in a vehicle

6
Hypercoagulability

• Surgery and trauma responsible for up to 40 of
  all thromboembolic disease
  
• Malignancy
• Increased estrogen (due to a fall in protein S)
  Increased estrogen occurs during
  
• all stages of pregnancy
• the first three months postpartum,
• after elective abortion, and
• during treatment with oral contraceptive pills

7
Inherited disorders of coagulation

• deficiencies of protein S,
• protein C, and
• antithrombin III.

8
Acquired disorders of coagulation

• nephrotic syndrome results in urinary loss of
  antithrombin III, this diagnosis should be
  considered in children presenting with
  thromboembolic disease
• Antiphospholipid antibodies accelerate
  coagulation and include the lupus anticoagulant
  and anticardiolipin antibodies.
  

9

• Inflammatory processes, such as
• systemic lupus erythematosus (SLE),
• sickle cell disease, and
• inflammatory bowel disease (IBD),
• also predispose to thrombosis, presumably due to
  hypercoagulability

10
Endothelial Injury

• Trauma,
• surgery, and
• invasive procedure may disrupt venous integrity
  
  
• Iatrogenic causes of venous thrombosis are
  increasing due to the widespread use of central
  venous catheters, particularly subclavian and
  internal jugular lines. These lines are an
  important cause of upper extremity DVT,
  particularly in children.

11
Clinical Pathophysiology

• The nidus for a clot is often an intimal defect
• When a clot forms on an intimal defect, the
  coagulation cascade promotes clot growth
  proximally. Thrombus can extend from the
  superficial veins into the deep system from which
  it can embolize to the lungs.

12

• Opposing the coagulation cascade is the
  endogenous fibrinolytic system. After the clot
  organizes or dissolves, most veins will
  recanalize in several weeks. Residual clots
  retract as fibroblasts and capillary development
  lead to intimal thickening.
• Venous hypertension and residual clot may
  destroy valves, leading to the postphlebitic
  syndrome, which develops within 5-10 years

13

• Edema, sclerosis, and ulceration characterize
  this syndrome, which develops in 40-80 of
  patients with DVT.
  
• patients also can suffer exacerbations of
  swelling and pain, probably as a result of venous
  dilatation and hypertension
  
•      Pulmonary embolism (PE) is a serious
  complication of DVT. Many episodes of pulmonary
  embolism go unrecognized, and at least 40 of
  patients with DVT have clinically silent PE on VQ
  scanning

14
Presentation and Physical Examination

• Calf pain or tenderness, or both
• Swelling with pitting oedema
• Swelling below knee in distal deep vein
  thrombosis and up to groin in proximal deep vein
  thrombosis
  
• Increased skin temperature
• Superficial venous dilatation
• Cyanosis can occur with severe obstruction

15

• Palpate distal pulses and evaluate capillary
  refill to assess limb perfusion.
  
• Move and palpate all joints to detect acute
  arthritis or other joint pathology.
  
• Neurologic evaluation may detect nerve root
  irritation sensory, motor, and reflex deficits
  should be noted
  
• Homans' sign pain in the posterior calf or knee
  with forced dorsiflexion of the foot

16

• Search for stigmata of PE such as tachycardia
  (common), tachypnea or chest findings (rare), and
  
  
• exam for signs suggestive of underlying
  predisposing factors.

17
(No Transcript)
18
Wells Clinical Prediction Guide

• The Wells clinical prediction guide incorporates
  risk factors, clinical signs, and the presence or
  absence of alternative diagnoses
  
• . Wells Clinical Prediction Guide for DVTClinical
  ParameterScore
  
• Active cancer (treatment ongoing, or within 6
  months or palliative)1
  
• Paralysis or recent plaster immobilization 1
• Recently bedridden for 3 days or major surgery
  

19

• Localized tenderness along the distribution of
  the deep venous system1
  
• Entire leg swelling1
• Calf swelling 3 cm compared to the asymptomatic
  leg 1
  
• Pitting edema (greater in the symptomatic leg)1
• Collateral superficial veins (nonvaricose)1
• Alternative diagnosis (as likely or that of
  DVT)
  

20

• Total of Above ScoreHigh probability Score
  ³3Moderate probability Score 1 or 2Low
  probability Score 0
  
• Adapted from Anand SS, et al. JAMA. 1998 279
  141094
  

21
Diagnostic Studies

• Clinical examination alone is able to confirm
  only 20-30 of cases of DVT
  
• Blood Tests
• the D-dimer
• INR.
• Current D-dimer assays have predictive value for
  DVT, and the
  
• INR is useful for guiding the management of
  patients with known DVT who are on warfarin
  (Coumadin)

22
D-dimer

• D-dimer is a specific degradation product of
  cross-linked fibrin. Because concurrent
  production and breakdown of clot characterize
  thrombosis, patients with thromboembolic disease
  have elevated levels of D-dimer
• three major approaches for measuring D-dimer
• ELISA
• latex agglutination
• blood agglutination test (SimpliRED

23

• False-positive D-dimers occur in patients with
• recent (within 10 days) surgery or trauma,
• recent myocardial infarction or stroke,
• acute infection,
• disseminated intravascular coagulation,
• pregnancy or recent delivery,
• active collagen vascular disease, or metastatic
  cancer

24
Imaging Studies

• Invasive
• venography,
• radiolabeled fibrinogen and.
• noninvasive
• ultrasound,
• plethysmography,
• MRI techniques

25
venography

• gold standard modality for the diagnosis of DVT
  
  
• Advantages
• Venography is also useful if the patient has a
  high clinical probability of thrombosis and a
  negative ultrasound,
  
• it is also valuable in symptomatic patients with
  a history of prior thrombosis in whom the
  ultrasound is non-diagnostic.

26
side effects

• phlebitis
• anaphylaxis

27
(No Transcript)
28
Nuclear Medicine Studies

• Because the radioactive isotope incorporates into
  a growing thrombus, this test can distinguish new
  clot from an old clot

29
Plethysmography

• Plethysmography measures change in lower
  extremity volume in response to certain stimuli.

30
Ultrasonography

• color-flow Duplex scanning is the imaging test of
  choice for patients with suspected DVT
  
• inexpensive,
• noninvasive,
• widely available
• Ultrasound can also distinguish other causes of
  leg swelling, such as tumor, popliteal cyst,
  abscess, aneurysm, or hematoma.     

31
clinical limitations

• expensive
• reader dependent
• Duplex scans are less likely to detect
  non-occluding thrombi.
  
• During the second half of pregnancy, ultrasound
  becomes less specific, because the gravid uterus
  compresses the inferior vena cava, thereby
  changing Doppler flow in the lower extremities

32
Magnetic Resonance Imaging

• It detects leg, pelvis, and pulmonary thrombi and
  is 97 sensitive and 95 specific for DVT.
  
• It distinguishes a mature from an immature
  clot.
  
• MRI is safe in all stages of pregnancy.

33
DIFFERENTIAL DIAGNOSIS

• Cellulitis Thrombophlebitis
• ArthritisAsymmetric peripheral edema secondary
  to CHF, liver disease, renal failure, or
  nephrotic syndrome lymphangitisExtrinsic
  compression of iliac vein secondary to tumor,
  hematoma, or abscessHematomaLymphedema

34

• Muscle or soft tissue injuryNeurogenic
  painPostphlebitic syndrome Prolonged
  immobilization or limb paralysisRuptured Baker
  cystStress fractures or other bony
  lesionsSuperficial thrombophlebitisVaricose
  veins

35
Management

• Using the pretest probability score calculated
  from the Wells Clinical Prediction rule, patients
  are stratified into 3 risk groupshigh, moderate,
  or low.
• The results from duplex ultrasound are
  incorporated as follows
  
• If the patient is high or moderate risk and the
  duplex ultrasound study is positive, treat for
  DVT.
  

36

• If the duplex study is negative and the patient
  is low risk, DVT has been ruled out.
  
• When discordance exists between the pretest
  probability and the duplex study result, further
  evaluation is required.
  
• If the patient is high risk but the ultrasound
  study was negative, the patient still has a
  significant probability of DVT

37

• a venogram to rule out a calf vein DVT
• surveillance with repeat clinical evaluation and
  ultrasound in 1 week.
  
• results of a D-dimer assay to guide management
• If the patient is low risk but the ultrasound
  study is positive, some authors recommend a
  second confirmatory study such as a venogram
  before treating for DVT

38
EMERGENCY DEPARTMANT CARE

• The primary objectives of the treatment of DVT
  are to
  
• prevent pulmonary embolism,
• reduce morbidity, and
• prevent or minimize the risk of developing the
  postphlebitic syndrome.

39

• Anticoagulation
• Thrombolytic therapy for DVT
• Surgery for DVT
• Filters for DVT
• Compression stockings

40
Anticoagulation

• Heparin prevents extension of the thrombus
• Heparin's anticoagulant effect is related
  directly to its activation of antithrombin III.
  Antithrombin III, the body's primary
  anticoagulant, inactivates thrombin and inhibits
  the activity of activated factor X in the
  coagulation process.

41

• Heparin is a heterogeneous mixture of
  polysaccharide fragments with varying molecular
  weights but with similar biological activity. The
  larger fragments primarily interact with
  antithrombin III to inhibit thrombin.
• The low molecular weight fragments exert their
  anticoagulant effect by inhibiting the activity
  of activated factor X. The hemorrhagic
  complications attributed to heparin are thought
  to arise from the larger higher molecular weight
  fragments.

42

• The optimal regimen for the treatment of DVT is
  anticoagulation with heparin or an LMWH followed
  by full anticoagulation with oral warfarin for
  3-6 months
• Warfarin therapy is overlapped with heparin for
  4-5 days until the INR is therapeutically
  elevated to between 2-3.

43

• After an initial bolus of 80 U/kg, a constant
  maintenance infusion of 18 U/kg is initiated. The
  aPTT is checked 6 hours after the bolus and
  adjusted accordingly. .
• The aPTT is repeated every 6 hours until 2
  successive aPTTs are therapeutic. Thereafter, the
  aPTT is monitored every 24 hours as well as the
  hematocrit and platelet count.

44
Advantages of Low-Molecular-Weight Heparin
OverStandard Unfractionated Heparin

• Superior bioavailability
• Superior or equivalent safety and efficacy
• Subcutaneous once- or twice-daily dosing
• No laboratory monitoring
• Less phlebotomy (no monitoring/no intravenous
  line)
  
• Less thrombocytopenia
• Earlier/facilitated

45

• At the present time, 3 LMWH preparations,
• Enoxaparin,
• Dalteparin, and
• Ardeparin

46
warfarin

• Interferes with hepatic synthesis of vitamin
  K-dependent coagulation factors
  
• Dose must be individualized and adjusted to
  maintain INR between 2-3
  
• 2-10 mg/d PO
• caution in active tuberculosis or diabetes
  patients with protein C or S deficiency are at
  risk of developing skin necrosis

47
Thrombolytic therapy for DVT

• Advantages include
• prompt resolution of symptoms,
• prevention of pulmonary embolism,
• restoration of normal venous circulation,
• preservation of venous valvular function,
• and prevention of postphlebitic syndrome.

48

• Thrombolytic therapy does not prevent
• clot propagation,
• rethrombosis, or
• subsequent embolization.
• Heparin therapy and oral anticoagulant therapy
  always must follow a course of thrombolysis.
  

49

• Thrombolytic therapy is also not effective once
  the thrombus is adherent and begins to organize
  
• The hemorrhagic complications of thrombolytic
  therapy are formidable (about 3 times higher),
  including the small but potentially fatal risk of
  intracerebral hemorrhage.
• The uncertainty regarding thrombolytic therapy
  likely will continue

50
Surgery for DVT

• indications
• when anticoagulant therapy is ineffective
• unsafe,
• contraindicated.
• The major surgical procedures for DVT are clot
  removal and partial interruption of the inferior
  vena cava to prevent pulmonary embolism.

51

• These pulmonary emboli removed at autopsy look
  like casts of the deep veins of the leg where
  they originated.
  

52
This patient underwent a thrombectomy. The
thrombus has been laid over the approximate
location in the leg veins where it developed.
53
Filters for DVT

• Indications for insertion of an inferior vena
  cava filter
  
• Pulmonary embolism with contraindication to
  anticoagulation
  
• Recurrent pulmonary embolism despite adequate
  anticoagulation
  

54

• Controversial indications
• Deep vein thrombosis with contraindication to
  anticoagulation
  
• Deep vein thrombosis in patients with
  pre-existing pulmonary hypertension
  
• Free floating thrombus in proximal vein
• Failure of existing filter device
• Post pulmonary embolectomy

55

• Inferior vena cava filters reduce the rate of
  pulmonary embolism but have no effect on the
  other complications of deep vein thrombosis.
  Thrombolysis should be considered in patients
  with major proximal vein thrombosis and
  threatened venous infarction

56
(No Transcript)
57
Compression stockings (routinely recommended
58
Further Inpatient Care

• Most patients with confirmed proximal vein DVT
  may be treated safely on an outpatient basis.
  Exclusion criteria for outpatient management are
  as follows
• Suspected or proven concomitant pulmonary
  embolism
  
• Significant cardiovascular or pulmonary
  comorbidity
  
• Morbid obesity
• Renal failure
• Unavailable or unable to arrange close follow-up
  care
  

59

• Patients are treated with a low molecular weight
  heparin and instructed to initiate therapy with
  warfarin 5 mg PO the next day. Low molecular
  weight heparin and warfarin are overlapped for
  about 5 days until the international normalized
  ratio (INR) is therapeutic.
• If inpatient treatment is necessary, low
  molecular weight heparin is effective and
  obviates the need for IV infusions or serial
  monitoring of the PTT.
• With the introduction of low molecular weight
  heparin, selected patients qualify for outpatient
  treatment only if adequate home care and close
  medical follow-up care can be arranged.

60

• Platelets also should be monitored and heparin
  discontinued if platelets fall below 75,000.
  
• While on warfarin, the prothrombin time (PT) must
  be monitored daily until target achieved, then
  weekly for several weeks. When the patient is
  stable, monitor monthly.
• Significant bleeding (ie, hematemesis, hematuria,
  gastrointestinal hemorrhage) should be
  investigated thoroughly since anticoagulant
  therapy may unmask a preexisting disease (eg,
  cancer, peptic ulcer disease, arteriovenous
  malformation).

61
Duration of anticoagulation in patients with deep
vein thrombosis

• Transient cause and no other risk factors
  3 months
  
• Idiopathic 3-6 months
• Ongoing risk for example, malignancy
  6 -12 months
  
• Recurrent pulmonary embolism or deep vein
  thrombosis 6-12 months
  
• Patients with high risk of recurrent thrombosis
  exceeding risk of anticoagulation indefinite
  duration (subject to review)
  

62
Further Outpatient Care

• Patients with suspected or diagnosed isolated
  calf vein DVT may be discharged safely on a
  nonsteroidal anti-inflammatory drug (NSAID) or
  aspirin with close follow-up care and repeat
  diagnostic studies in 3-7 days to detect proximal
  extension.
• At certain centers, patients with isolated calf
  vein DVT are admitted for full anticoagulant
  therapy.
  

63

• Patients with suspected DVT but negative
  noninvasive studies need to be reassessed by
  their primary care provider within 3-7 days.
  
• Patients with ongoing risk factors may need to be
  restudied at that time to detect proximal
  extension because of the limited accuracy of
  noninvasive tests for calf vein DVT.

64
Complications

• Acute pulmonary embolism
• Hemorrhagic complications
• Chronic venous insufficiency

65
Prognosis

• All patients with proximal vein DVT are at
  long-term risk of developing chronic venous
  insufficiency.
  
• About 20 of untreated proximal (above the calf)
  DVTs progress to pulmonary emboli, and 10-20 of
  these are fatal. With aggressive anticoagulant
  therapy, the mortality is decreased 5- to
  10-fold.
• DVT confined to the calf virtually never causes
  clinically significant emboli and thus does not
  require anticoagulation

66
Patient Education

• Advise women taking estrogen of the risks and
  common symptoms of thromboembolic disease.
  
• Discourage prolonged immobility, particularly on
  plane rides and long car trips

67
PROPHYLAXIS

• Ideidentify any patiant who is at risk.
• Prevent dehydration.
• During operation avoid prolonged calf
  compression.
  
• Passive leg exercises should be encourged whilst
  patient on bed.
  
• Foot of bed should be elevated to increase venous
  return.
  
• Early mobilization should be rule for all
  surgical patients.