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PE DVT and Thee

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					PE, DVT, and Thee

          By
 Paul Rega, MD, FACEP
  OMNI Health Services

    (You know…the docs
      who work the ER)
                 VTE
Definition: Spectrum of diseases that
includes DVT and PE
              Introduction
2 million diagnosed with DVT annually
 – Maybe 80-117/100,000 persons occur
   annually.
    900/100,000 by age 85
– ~ 1 person in 20 will develop a DVT in his/her
  lifetime.
– ~ 600,000 hospitalizations per year occur for
  DVT in the United States.
– In hospitalized patients, the incidence of
  venous thrombosis is considerably higher and
  varies from 20-70%.
         More Introduction
600,000 diagnosed with PE annually
 – Death from DVT is attributed to massive PE
 – Causes 200,000 deaths annually in the United
   States.
Prospective studies in patients with proven DVT
but without any signs or symptoms to suggest
PE find that roughly half of these "asymptomatic"
patients have experienced undiagnosed PE.
              Interesting…
Prospective studies show that in the absence of
prophylaxis acute DVT may be demonstrated in
any of the following:
– General medical patients placed at bed rest for a
  week (10-13%)
– Patients in medical intensive care units (29-33%)
– Patients with pulmonary disease kept in bed for 3 or
  more days (20-26%)
– Patients admitted to a coronary care unit after
  myocardial infarction (27-33%)
– Patients who are asymptomatic after coronary artery
  bypass graft (48%)
 What is the Virchow Triad?
Not a type of Kishka
– Blood sausage from Poland
    For you WASPS out there.
           Virchow Triad
All recognized risk factors for VTE arise
from the 3 underlying components of the
Virchow triad:
– Venous stasis,
– Hypercoagulability, and
– Vessel intimal injury.
                     Risk Factors
General                                Medical
 – Age                                  – Cancer
 – Immobilization longer than 3 days    – Previous DVT
 – Pregnancy and the postpartum                5x
   period
                                        – Stroke
       Impaired fibrinolysis
                                               50% in 5d post-stroke
 – Major surgery in previous 4
   weeks                                – Acute myocardial infarction
                                          (AMI)
       General anesthesia (500x)
                                        – Congestive heart failure (CHF)
       Impaired fibrinolysis
                                        – Sepsis
 – Long plane or car trips (>4 h) in
   previous 4 weeks                     – Nephrotic syndrome
 – Obesity?                             – Ulcerative colitis
Trauma                                         Fibrinogen/VIII up
 – Multiple trauma                             Antithrombin III down
 – CNS/spinal cord injury               – Hyperlipidemia
       40% in post-op
 – Burns
 – Lower extremity fractures
        Risk Factors (continued)
Vasculitis                            Hematologic
– Systemic lupus erythematosus        – Polycythemia rubra vera
  (SLE) and the lupus anticoagulant
                                      – Thrombocytosis
       9%                             – Inherited disorders of
– Behçet syndrome                       coagulation/fibrinolysis
– Homocystinuria
                                      – Antithrombin III (anticoag)
                                        deficiency
Drugs/medications                           Liver disease
– Intravenous drug abuse              – Protein C (anticoag) deficiency
– Oral contraceptives                       Natural/acquired
       Impaired fibrinolysis          – Protein S (anticoag) deficiency
       3-12 x higher                  – Prothrombin 20210A mutation
– Estrogens                           – Factor V Leyden
– Heparin-induced                           7% of general population
  thrombocytopenia                          50% of idiopathic DVT
– ChemoRx
                                      – Dysfibrinogenemias and
       Reduce anticoag/increase         disorders of plasminogen
       procoag                          activation
                                      – Type A in reproductive women
          What about…
The upper extremity (UE)?
        Upper Extremity DVT
Growing incidence
– Due to indwelling catheters and dialysis .
PE from UE DVT ~ as frequent as PE from LE DVT.
– Sounds like a cryptic message from al-Qaeda, doesn’t it?


512 patients with arm DVT (Chest. 2008;133:143-8.)
– 196 patients (38%) had cancer and 228 patients (45%) had
  catheter-related DVT.
– Patients with arm DVT have less often clinically overt PE than
  those with lower-limb DVT, but their 3-month outcome is similar.
– Among patients with arm DVT, those with cancer have the worse
  outcome.
What are the signs and symptoms
            of DVT?
Lower extremity (LE)
 – Proximal
 – Distal
Most clinical PEs come from
 – Popliteal v.
 – Femoral v.
 – Iliac v.
              A Dilemma
Even when a patient has a swollen, painful,
congested leg that appears to be clinically
obvious DVT, the chance that DVT is the correct
diagnosis is only 50%.
Most cases of DVT lack classic signs or
symptoms
Thus, diagnostic tests must be performed
whenever the diagnosis of DVT is being
considered.
           Propagation
10-30% of distal clots propagate to
proximal legs.
The single largest autopsy series ever
performed to specifically to look for the
source of fatal PE was performed by Havig
in 1977, who found that one third of the
fatal emboli arose directly from the calf
veins.
  Wells’ Clinical model for predicting pretest
    probability of deep-vein thrombosis
Active CA (Rx ongoing, given within previous 6 mos. or palliative):    1
Paralysis, paresis, or recent plaster immobilization of lower limbs:    1
Recently bedridden >3d or major surgery within previous 12 wk requiring
general or regional anesthesia:                                         1
Localized tenderness along deep venous system:                          1
Swelling of entire leg:                                                 1
Calf swelling >3cm more than uninvolved leg (10 cm below tibial
tuberosity):                                                            1
Pitting edema confined to symptomatic leg:                              1
Collateral superficial veins (nonvaricose):                             1
Previously documented DVT:                                              1
Alternative diagnosis at least as likely as DVT:                       -2


Score: 2 or more = DVT                  High probability: ≥ 3 (>65%)
probability likely;                     Moderate probability: 1-2
Score < 2 = DVT probability             Low probability: 0 or less (<10%)
unlikely.
              Case 1
35 YO Female
Left leg pain
What do you want to know?
              Case 1
Present Hx
Past Hx
Family Hx
Medications
       Case 1: The Exam
Examining the leg
               Case 1
Probability?
               Case 2
85 YO Male
Deep ache in right leg just above ankle.
What do you want to know?
               Case 2
Probability?
               Case 3
50 YO Female
Pain and swelling left leg.
What do you want to know?
               Case 3
Probability?
Now the test…
In the days of King Arthur…IPG
Records changes in blood volume of an
extremity, which are directly related to
venous outflow.
Sensitive and specific for proximal vein
thrombosis
Insensitive for calf vein thrombosis.
Insensitive for UE DVT
                  IPG
Noninvasive             Operator dependent
Inexpensive             Insensitive (false neg.)
Safe                    – Calf DVT
                        – Non-obstructing thrombi
No radiation
Portable                Nonspecific (false pos.)
                        – Increased intra-abdominal
Accurate                  pressure
– Proximal DVT          – Increased CVP
– Recurrent DVT         – Decreased blood flow to
                          legs
                        – Nonthrombotic venous
                          outflow obstruction
               Venogram
Sensitive                Invasive
– ~100% (Proximal)       Expensive
Specific                 Not portable
– ~100% (Proximal)       Contraindications
Acute vs Chronic         – Renal insufficiency
Less operator            – Contrast allergy
dependent                Painful
Most accurate for calf   Cause DVT
DVT
                 Venogram
Gold standard?
– Radiologists
    Uncomfortable/unwilling
     – With non-expert radiologists
           Up to 30% are technically inadequate
    Phlebitis
    Allergic reaction
Largely replaced by Doppler US.
                            US
Compressibility of veins
– Doppler
     Flow characteristics
Sensitivity of duplex ultrasonography
– Proximal vein DVT: 97%
– Calf vein DVT: 73%
Specific
– 95%
               US
Noninvasive         Operator dependent
Safe                Less accurate
Portable            – Chronic DVT
Relatively          – Calf DVT
inexpensive         – Pelvic DVT

Available           Difficult
                    – Obesity
No radiation
                    – Edema
UE DVT
                   US
In U.S., 500,000 patients evaluated for
DVT
– 80% normal at 1st US
– Only 2% abnormal 5-7 days later
– Spending a lot of $$$$ when most of the tests
  come back negative.
                    US
Negative at Day 0
– 50%: Positive at Day 1
– 50%: Positive by day 7
                        MRI
In limited studies, accuracy approaches that of
venography.
The diagnostic test of choice for suspected iliac vein or
inferior vena caval thrombosis when CT venography is
contraindicated or technically inadequate.
In the second and third trimester of pregnancy, MRI is
more accurate than duplex ultrasonography because the
gravid uterus alters Doppler venous flow characteristics.
Said to be as sensitive as US in detecting calf and pelvic
DVTs.
                   MRI
Sensitive            Claustrophobic
Specific             Expensive
Safe                 Not portable
Pelvic/IVC DVT       Metallic devices
No radiation         Insensitive
Acute vs chronic         – Calf DVT
                       D-Dimer
Fibrin degradation product
Value increases with clots, surgery, trauma, CA,
infection, Gabby Hays.
Many types
– Most accurate: Quantitative
– ELISA (Enzyme-linked immunosorbent assay)
– STA Liatest immunoturbidimetric D-dimer assay
      Cut-off: 0.21 µg/mL
Low risk patients + normal D-dimer = <1% probability of
DVT.
D-dimer: Not to be used alone to r/o DVT in patients with
moderate or high probability of DVT
– Sensitivity is always lower for calf DVT
            Bottom Line
A positive D-dimer needs further testing.
             Determination of pretest probability of DVT


  DVT unlikely (score ≤1)                 DVT likely (score >1)

      Good D-Dimer test
                _                         Good D-Dimer test
       +                                                _
                                              +
Ultrasound        No DVT          Ultrasound       Ultrasound
              _                                                   _
 +                                _                 +
                                          +
Treat with                  Repeat US     Treat with        No DVT
                  No
                            in
anticoagulants    DVT                     anticoagulants
                            1 week
                              _           +
                         No DVT


                           One Guideline
Importance of Proper/Prompt DVT
            Therapy
Decreases risk of recurrent DVT to 5%
Decreases risk of fatal PE to <1%
                Leg DVT
Heparin/Lovenox: OK
Fibrinolysis
– Unclear
– If Limb-threatening
– Remember: Thrombolytic therapy increases
  the risk of major bleeding 1.5-fold to threefold
  in patients with acute venous
  thromboembolism
                       Heparin
Binds to Antithrombin
Accelerates ability of Antithrombin to inactivate
Thrombin, factor Xa, & Factor IXa.
1/2 –life: 60”
Bioavailability
– Variable due to protein binding.
Bleeding complication
– The risk of bleeding associated with IV unfractionated heparin
  (UFH) in patients with acute venous thromboembolism is < 3% in
  recent trials.
– Bleeding risk may increase with increasing heparin dosages and
  age (> 70 years).
  Low-Molecular-Weight Heparin

Derived from heparin
Result of depolymerization
1/3rd the size of heparin
Research on thousands
– Safe
– Effective
– Convenient
                     LMWH
Enoxaparin (Lovenox), dalteparin (Fragmin), and
tinzaparin (Innohep) have received US Food and Drug
Administration (FDA) approval for the treatment of DVT
in the United States.
Enoxaparin: Approved for inpatient and outpatient
treatment of DVT.
No monitoring
 – >90% bioavailable
 – Minimal protein binding
 – Levels are predictable
No heparin-induced thrombocytopenia (1%)
No anti-heparin antibodies
In plasma for 12-16h
 – Allows for BID dosing
Associated with less major bleeding compared with UFH
in acute venous thromboembolism.
     Fondaparinux (Arixtra)
New
A synthetic pentasaccharide
Catalyzes the inhibition of factor Xa, but not
thrombin, in an antithrombin-dependent fashion
Binds only to antithrombin
– therefore, HIT and osteoporosis are unlikely to occur.
Excellent bioavailability when administered
subcutaneously
– Has a longer half-life than LMWHs.
– Given once daily by subcutaneous injection in fixed
  doses, without anticoagulant monitoring.
  Direct Thrombin Inhibitors
Hirudin
Bivalirudin
Argatroban
Melagatran

Parenteral
         Greenfield Filter
When anticoagulation has failed or
Risk of serious hemorrhage
May double risk of recurrent DVT
 Proven Clinically Significant DVT

   Any reason for hospitalization ?
            Comorbidity?
       Compliance concerns?
          Logistical issues?
      Yes                  No


Hospitalize              1) LMWH
                         2) Coumadin 5mg q day
                         3) VNA for BID
                              injections
                         4) Evaluate
                         discontinuation of LMWH
                         5) Evaluate q 5-7d
                    PE
300,000/annually
2% die within 1st day
10% get recurrent PE
– Death rate: 45%
    PE: A Difficult Diagnosis
2 Studies
– Univ. of Toronto
     44 die from PE
       – 30 (68%) diagnosed at autopsy
– Henry Ford
     20 die from PE
       – 14 (70%) diagnosed at autopsy
2/3rd of patients with proven PE have no DVT
symptoms, and
1/3rd of patients: Impossible to find the original
site of DVT without an autopsy.
  What are the S&S of PE?
Come on…. “What are the signs and
symptoms of PE?”
              A Conundrum
Hemoptysis, dyspnea, chest pain occur in fewer than
20% of patients in whom the diagnosis of PE is made
Most patients with those symptoms are found to have
some etiology other than PE to account for them.
Of patients who go on to die from massive PE
– 60% have dyspnea
– 17% have chest pain
– 3% have hemoptysis
PE has been diagnosed in 21% of young, active patients
who come to the ED complaining only of pleuritic chest
pain.
  Signs Seen in Massive PE
96%: Tachypnea          32%: Clinical signs
(respiratory rate       and symptoms
>16/min)                suggesting
58%: Rales              thrombophlebitis
44%: Tachycardia        24%: Lower extremity
(heart rate >100/min)   edema
43%: Fever              23%: Cardiac murmur
(temperature            19%: Cyanosis
>37.8° C)
36%: Diaphoresis
      Atypical Presentations
Patients with PE may present with atypical symptoms,
where strong suspicion in a high-risk patient often leads
to consideration of PE in the differential diagnosis:
Seizures
Syncope
Abdominal pain
Fever
Productive cough
Wheezing
Decreasing level of consciousness
New onset of atrial fibrillation
        Wells’ Clinical Prediction Rule for PE

Clinical symptoms of DVT                                  3
Other dx less likely than PE                              3
Heart rate >100 bpm                                       1.5
Immobilization/surgery within past 4 wks                  1.5
Previous DVT/PE                                           1.5
Hemoptysis                                                1
Malignancy                                                 1


Risk Score: > 6: High risk (78.4%); 2-6: Moderate risk (27.8%); <2: Low risk (3.4%).
What non-imaging tests can help
            you?
Come on…“ What non-imaging tests can
help you?”
                    What tests?
EKG?
– Nonspecific changes or tachycardia usually
– S1-Q3-T3 pattern: In only 20% of patients with proven PE.
ABGs?
–   Nonspecific
–   Moderately sensitive
–   pO2; may be normal with minor PE
–   ↓ pO2 and ↓pCO2
       Seen in conditions other than PE
D-dimers?
– Depends
Others?
               CXR?
What would you expect to find?
                           CXR
Virtually always normal.
Rarely the Westermark sign
 – A dilatation of the pulmonary vessels proximal to an embolism
     along with collapse of distal vessels, sometimes with a sharp
     cutoff.
Over time, an initially normal CXR often begins to show atelectasis,
which may progress to cause a small pleural effusion and an
elevated hemidiaphragm.
After 24-72 hours, one third of patients with proven PE develop focal
infiltrates that are indistinguishable from an infectious pneumonia.
A rare late finding of pulmonary infarction
 – The Hampton hump, a triangular or rounded pleural-based
     infiltrate with the apex pointed toward the hilum, frequently
     located adjacent to the diaphragm.
                          V-Q Scan
Scan                           Clinical Probability

                   80 – 100%            20 - 79%       0 - 19%

High                 82-99%            78-94%         21-86%


Intermediate         49-80%           22-34%          8-27%

Low                  16-68%           11-22%          1-11%

Normal               0-52%             2-16%%         0-9%

       Bottom line: Only use scans with “high probability” or
               “normal” for clinical decision-making.
         N.B. Only 40% of scans in PE patients are “high
                            probability.”
                      MDCTA
High-resolution multidetector computed
tomographic angiography
– Has sensitivity and specificity comparable to that of
  contrast pulmonary angiography
– Accepted both as the preferred primary diagnostic
  modality and as the criterion standard for making or
  excluding the diagnosis of pulmonary embolism.
     Caution: Multiple small emboli that have lodged in distal
     vessels
Overall negative predictive value of MDCTA for
pulmonary embolism is greater than 99%.
Future: Simultaneous MDCTA + Below-the-
pelvis CT venography without added contrast
    Pulmonary Angiography
Complications: 3-4%
– Arrhythmias, cardiac perforation, cardiac arrest,
  hypersensitivity
Gold standard
– A positive pulmonary angiogram provides virtually
  100% certainty that an obstruction to pulmonary
  arterial blood flow does exist.
– A negative pulmonary angiogram provides greater
  than 90% certainty in the exclusion of PE.
Being replaced by MDCTA
Transthoracic Echocardiography
             (TTE)
TTE alone is not sensitive or specific
enough for detecting PE
New study: The ratio of right ventricular to
left ventricular (RV/LV) end diastolic
dimension was the most accurate
predictor for PE, with a sensitivity and
specificity of 66% and 77%, respectively.
– Might lead cardiologist in the right direction
    Echocardiography 2008; 25: 584-590
                                          S&S of PE


                                   Pre-test PE probability score


                                   CT pulmonary angiography


              Treat PE      Positive                         Negative


                                                         Doppler US of legs


                                                  Negative                  Positive       Treat VTE


                                   Pre-test PE probability score


                           Low            Intermediate             High




                                 D-dimer or serial US               Angiography




                                       Negative                           Positive     Treat PE




                          Follow-up for alternative dx




Diagnosing PE with CT (adapted from Am Fam Phys 2004; 69 [12])
                                                                  S&S of PE


                                                           Pre-test PE probability score


                                                                 V-Q Scan


             Low/Intermediate Probability                       High Probability                  Normal   Follow-up for alternative dx


                                                             Pre-test PE probability score
Follow US protocol from prior slide
                                                       Low            Intermediate         High



                                                Angiography



                                            Negative          Positive             Treat PE




                            Follow-up for alternative dx




 Diagnosing PE with V/Q Scanning (adapted from Am Fam Phys 2004; 69 [12])
                  Case 1
35 YO Female
Mom 2 days ago
“I feel a little shaky, a little short of…
breath.”
              Case 1
What do you want to know?
              Case 1
What do you want to do?
                Case 2
85 YO Male
Admitted for cellulitis of the left leg
“My damn heart is doing flippity-flops,
Cutie.”
              Case 2
What do you want to know?
              Case 2
What do you want to do?
               Case 3
50 YO Female
Being worked up for spread of breast CA.
“I can’t breathe all of a sudden.”
              Case 3
What do you want to know?
              Case 3
What do you want to do?
          The Drugs
UFH
LMWH
Arixtra
                 Heparin (UFH)
5000U or 80 U/kg IV to start
Heparin-Induced Thrombocytopenia (HIT)
– 9/332 (2.7%)
– Consider
      Thrombotic syndrome
      Platelets fall >50%
– Especially if treated within 2 weeks
      Usually between 5-14 days of heparin initiation
        – May not be on heparin at the time
Bleeding
– The risk of major bleeding associated with IV unfractionated
  heparin (UFH) in patients with acute venous thromboembolism is
  < 3% in recent trials. This bleeding risk may increase with
  increasing heparin dosages and age (> 70 years).
      35/1853 (1.9%)
    Suspected or Confirmed HIT?
            What to do?
An alternative, nonheparin anticoagulant
–   Danaparoid
–   Lepirudin (Refludan)
–   Argatroban
–   Fondaparinux (Arixtra) or
–   Bivalirudin (Angiomax) over the further use of unfractionated
    heparin (UFH) or low-molecular-weight heparin (LMWH) therapy
    or initiation/continuation of vitamin K antagonists (VKAs)
For patients receiving Coumadin at the time of diagnosis
of HIT, vitamin K (10 mg po or 5 to 10 mg IV) is
recommended
– When to re-start? Controversial.
        LMWH Dosages
Lovenox: 1 mg/kg q 12h or 1.5 mg/kg/d SC
– Max.: 180 mg/d
Fragmin: 100U/kg q 12h or 200 U/kg/d SC
– Max.: 18,000U/d
Innohep: 175U/kg/d SC
– Max.: 18,000U/d
     Fondaparinux (Arixtra)
A synthetic pentasaccharide
Catalyzes the inhibition of factor Xa, but not
thrombin, in an antithrombin-dependent fashion
Binds only to antithrombin
– therefore, HIT and osteoporosis are unlikely to occur.
Excellent bioavailability when administered
subcutaneously,
– Has a longer half-life than LMWHs.
– Given once daily by subcutaneous injection in fixed
  doses, without anticoagulant monitoring.
Recent Recommendations for VTE
      Therapy (Confirmed)
Patients with objectively confirmed deep vein
thrombosis (DVT) or pulmonary embolism (PE)
 – subcutaneous (SC) low-molecular-weight heparin
   (LMWH),
 – monitored IV, or SC unfractionated heparin (UFH),
 – unmonitored weight-based SC UFH, or
 – SC Fondaparinux
At least 5 days
 – With Coumadin
Recent Recommendations for VTE
      Therapy (Suspected)
Patients with a high clinical suspicion of
DVT or PE
 – Treatment with anticoagulants while awaiting
   the outcome of diagnostic tests.
  Recent Recommendations for PE
      Thrombolytic Therapy
Confirmed PE
 – Early evaluation of the risks to benefits of thrombolytic
   therapy.
      Thrombolytic therapy increases the risk of major
      bleeding 1.5-fold to threefold in patients with acute
      venous thromboembolism
 – Hemodynamic compromise
      Short-course thrombolytic therapy
 – Nonmassive PE
      Use of thrombolytic therapy not recommended
              Thrombolytics
Reteplase (Retavase): Preferred (fast)
Alteplase/t-PA (Activase): Preferred (fast)
Urokinase (Abbokinase)
Streptokinase (Kabikinase, Streptase)
 – Least desirable of the 4: Antigenic problems and
   other adverse reactions force the cessation of therapy
   in a large number of cases.

Total pulmonary resistance (along with pulmonary artery
pressure and cardiac index) improved significantly after
just 0.5 hours in the reteplase group as compared to 2
hours in the alteplase group.
Surgical Thromboembolectomy
Reserved for patients in whom fibrinolysis
has failed or cannot be tolerated.
             Disposition
PE
– Admit
DVT
– Another story
A Word about Special Cases
                   Pregnancy
Pulmonary embolism (PE): Leading cause of maternal
mortality during pregnancy and up to 6 weeks
postpartum.
– Most common nontraumatic cause of maternal death in
  pregnancy
Compared with nonpregnant women, pregnant women
have a 5-fold increased risk for VTE.
– Prevalence is even higher in the postpartum period.
LMWH over UFH for the prevention and treatment of
VTE
– Throughout pregnancy & 6 weeks post-partum
Thrombolytics (same dosage) if condition warrants.
       Imaging in Pregnancy
Helical computed axial tomographic pulmonary
angiography (HCTPA ) vs. V/Q vs. MRI?
HCTPA is associated with lower radiation doses when
compared with V/Q scanning during all trimesters of
pregnancy.
MRI
– Fetus is not exposed to ionizing radiation or intravenous contrast
  material.
– Sensitivity and specificity of MRI have been reported in ranges
  comparable to HCTPA for the diagnosis of PE.
– Disadvantages: Long acquisition times, with the need for
  respiratory and cardiac gating.
What does X-Ray do here?????
                 Kids
Anticoagulant therapy with either
unfractionated heparin (UFH) or low-
molecular-weight heparin (LMWH)
         In Conclusion
Ahhh……hhhh………..hhh, finally!
  VTE Prophylaxis in Hospital
No to aspirin alone as thromboprophylaxis for any patient group
Mechanical methods of thromboprophylaxis OK for patients at high bleeding
risk or possibly as an adjunct to anticoagulant thromboprophylaxis
Major general surgery, thromboprophylaxis with a low-molecular-weight
heparin (LMWH), low-dose unfractionated heparin (LDUH), or Fondaparinux
Routine thromboprophylaxis for all patients undergoing major gynecologic
surgery or major, open urologic procedures with LMWH, LDUH,
Fondaparinux, or intermittent pneumatic compression (IPC).
Elective hip or knee arthroplasty, one of the following three anticoagulant
agents is recommended: LMWH, Fondaparinux, or a vitamin K antagonist
(VKA)
Hip fracture surgery (HFS), the routine use of Fondaparinux, LMWH, a VKA
or LDUH is recommended
All major trauma and all spinal cord injury (SCI) patients should receive
thromboprophylaxis
Acute medical illness, thromboprophylaxis with LMWH, LDUH, or
Fondaparinux is recommended
All ICU patients be assessed for their risk of VTE, and that most receive
thromboprophylaxis on admission
               References
Clinical Policy: Critical Issues in the Evaluation
and Management of Adult Patients Presenting
with Suspected Lower-Extremity Deep Venous
Thrombosis. Ann Emerg Med: 2003; 42: 124-
135.
Bates SM, Ginsberg JS. Treatment of Deep-
Vein Thrombosis. NEJM 2004; 351: 268-277.
Linken LA, Choi PT, et al. Clinical Impact of
Bleeding in Patients Taking Oral Anticoagulant
Therapy for Venous Thromboembolism. Ann
Intern Med 2003; 139: 893-900.
             References
Kearon C, Hirsh J. Venous Thromboembolism.
www.acpmedicine.com/sam/chapters/ch0118.ht
m. Accessed 1/5/05.
Ramzl DW, Leeper KV. DVT and Pulmonary
Embolism: Diagnosis. Am Fam Physician
2004;69:2829-2836.
Kyrte PA, Eichinger S. Deep Vein Thrombosis.
Lancet 2005; 365: 1163-1174.
Ho WK, Hankey GJ, et al. Venous
Thromboembolism: Diagnosis and Management
of Deep Venous Thrombosis. MJA 2005; 182:
476-481.
              References
Kearon C, Ginsberg JS, et al. A randomized
Trial for Diagnostic Strategies after Normal
Proximal Vein Ultrasonography for Suspected
Deep Venous Thrombosis: D-Dimer Testing
Compared with Repeated Ultrasonography. Ann
Intern Med 2005; 142: 490-496.
Scarvelis D, Wells PS. Diagnosis and
Treatment of Deep-Vein Thrombosis. CMAJ
2006; 175: 1087-1091.
Stein PD, Hull RD, et al. Tracking the Uptake of
Evidence (Two decades of hospital practice
Trends for diagnosing deep vein thrombosis and
pulmonary embolism). Arch Intern Med 2003;
163: 1213-1219.
              References
Schreiber D. Deep Venous Thrombosis and
Thrombophlebitis
http://www.emedicine.com/emerg/topic122.htm.
Accessed 6/14/08.
Feied C. Deep Venous Thrombosis
http://www.emedicine.com/MED/topic2785.htm.
Accessed 6/14/08.
Muñoz FJ, Mismetti P, Poggio R, et al. Clinical
outcome of patients with upper-extremity deep
vein thrombosis: results from the RIETE
Registry. Chest. 2008 Jan;133(1):143-8.
             References
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