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PE & DVT

Up Acute coronary syn. Air embolism Aortic dissection Arrhythmia AV fistula Atheromatous emboli Cardiac arrest in adults Cardiac transplant Cardiogenic shock Cardiomyopathy CCF Endocarditis IABP Monitoring Myocarditis Post-op PE & DVT Pul. hypertension Sudden death Valvular disease Vascular surgery


Updated May 2009 by Charles Gomersall

Thromboembolic disease

  • 70% of patients with confirmed PE have DVT
  • 40% of patients with DVT have silent PE
  • DVT limited to calf veins (distal DVT) seldom results in clinically obvious PE
  • similarity in clinical outcome of patients with DVT or with PE during long-term follow up
  • PE and DVT should probably be regarded as a single clinicopathological entity

Risk

  • ~6.5% of patients have DVT on admission to ICU
  • further 20-30% develop DVT during ICU stay
  • risk highest amongst patients who have suffered major trauma (40-70%) and spinal cord injury (60-80%)

Mechanism of risk

Changes in blood flow

  • venous stasis
    • immobilization
    • raised CVP
    • valvular damage due to previous thromboembolic disease

Changes in properties of blood

  • increased coagulation and/or platelet activity eg lupus anticoagulant
  • decrease in physiological anticoagulants and/or fibrinolytic activity common in critically ill patients
    • antithrombin III, protein S and protein C deficiencies
    • acquired activated protein C resistance
    • high levels plasminogen activator inhibitor I

Changes in vessel wall

  • endothelial damage triggers coagulation
    • trauma
    • central venous catheters

Risk factors

Strong predisposition

  • lower limb fracture or joint replacement
  • major vascular surgery
  • major trauma
  • acute spinal cord injury (<1 month)
  • stroke (<1 month)

Moderate predisposition

  • critical illness
  • arthroscopic knee surgery
  • CVC
  • chemotherapy
  • malignancy
  • pregnancy: post-partum
  • previous venous thromboembolism
  • thrombophilia
    • antithrombin III deficiency
    • protein C & S deficiencies
    • inherited abnormalities of fibrinogen and plasminogen

Weak predisposition

  • bed rest >3 days
  • immobility due to sitting (eg prolonged car or air travel)
  • increased age
  • laparoscopic surgery
  • obesity
  • varicose veins
  • acute myocardial infarction
  • chronic heart or respiratory failure
  • hormone replacement therapy or oral contraceptive

Pathophysiology

  • massive PE increases RV afterload, enlarges RV and deviates septum to left thus decreasing LV volume and compliance
  • cardiac output and coronary blood flow (especially to right heart) are diminished resulting in decreased ventricular contractility and a cycle of cardiac decompensation. Death is usually due to right heart failure not refractory hypoxia.
  • neurogenic and humoral influences may result in catastrophic pulmonary hypertension with occlusion of as little as 30% of the pulmonary vascular bed
  • critically ill patients often have reduced cardiorespiratory reserve and small pulmonary emboli which would be well tolerated by less sick patients may be poorly tolerated by ICU patients
  • hypoxia is due to a combination of:
    • decreased cardiac output resulting in a fall in oxygen delivery and hence mixed venous oxygen saturation
    • zones of reduced flow in obstructed areas and zones of luxury perfusion of non-obstructed areas resulting in shunting
    • right to left shunt through patent foramen ovale resulting from raised right heart pressures

Clinical features

Small "heraldic" emboli commonly precede a major embolus and 90% of fatal emboli are recurrent emboli

Symptoms

  • dyspnoea or tachypnoea in 91% of patients; dyspnoea, tachypnoea or pleuritic pain present in 97% of patients with acute PE. Pleuritic pain is more common in patients with pulmonary infarction which is more common in patients with peripheral PE
  • non-productive cough
  • haemoptysis only occurs if infarction has occurred
  • syncope (suggests massive PE though may occur following minor PE)

Physical signs

RS

  • tachypnoea common
  • cyanosis usually only occurs after massive PE
  • pleural effusion
  • pleural rub (in patients with pulmonary infarction)
  • wheeze and crackles

CVS

  • HR: usually increased, bradycardia ominous
  • +/- signs of pulmonary hypertension (eg loud P2, gallop rhythm and parasternal heave, especially following massive PE
  • +/- raised JVP with prominent "a" waves
  • +/- shock after massive PE. Small sharp peripheral pulse may be palpated

Lower limbs

  • clinical evidence of DVT found in only 30%. DVT found in "normal" leg in 36%

Others

  • sweating and fever infrequent

Clinical prediction rules

  Revised Geneva score Wells score
Predisposing factors Age>65
Previous DVT or PE
Surgery or fracture within 1 month
Active malignancy
+1
+3
+2
+2
Previous DVT or PE
Recent surgery or immobilization
Cancer
+1.5
+1.5
+1
Symptoms Unilateral lower limb pain
Haemoptysis
+3
+2
Haemoptysis +1
Clinical signs & judgement Heart rate 75-94/min
Heart rate ≥95/min
Pain over lower limb deep vein on palpation and unilateral oedema
+3
+5
+4
Heart rate >100/min
Clinical signs of DVT
Alternative diagnosis less likely than PE
+1.5
+3
+3
Clinical probability
Low
Intermediate
High
Total
0-3
4-10
≥11

Low
Intermediate
High
Total
0-1
2-6
≥7

Differential diagnosis

  • MI
  • LVF
  • aspiration pneumonitis
  • pleural effusion
  • pneumonia
  • fat embolism
  • pneumothorax
  • aortic dissection

Investigations

Most screening tests have not been adequately validated for use in ICU patients and comments on sensitivity and specificity are based on studies in other groups of patients

To diagnose DVT

  • Compression ultrasonography
    • Sensitivity >90%, specificity ~95% for proximal DVT
    • Examination of common femoral and popliteal vessels only appears to be adequate
  • Impedence plethysmography: low sensitivity and specificity
  • MRI: accuracy of 96% in detecting pelvic thromboses

To diagnose PE

  • blood tests: raised WCC, raised D-dimer (non specific but sensitive; sensitivity varies from 80-99% depending on assay used)
  • CXR
    • changes neither sensitive nor specific.
    • localized infiltrates, consolidation, atelectasis in 2/3
    • pleural effusion in 1/2
    • classical "plump" pulmonary arteries with peripheral pruning relatively rare and non-specific. Tends to be associated with massive PE
  • ECG
    • normal in 30%.
    • changes of R heart strain most common
    • S1Q3T3 pattern infrequent
    • LAD > RAD
    • P pulmonale, RBBB, atrial arrhythmias occasionally present. Persistent if PE massive
  • ABG
    • hypoxaemia frequent but PaO2 >10.6 in 1/4 and A-a gradient may be normal
    • metabolic acidosis in shocked patients
  • Multi-detector CT angiography (MDCT)
    • imaging method of choice
       
      Clinical probability Negative predictive value Positive predictive value
      Low 96% 58%
      Intermediate 89% 92%
      High 60% 96%

     

    • negative MDCT adequate criterion for excluding PE in patients with low or intermediate clinical probability of PE
    • MDCT showing segmental or more proximal PE adequate proof of PE in patient with intermediate or high probability of PE
  • echo:
    • not recommended as part of elective diagnostic strategy in haemodynamically stable patients
    • may be useful in haemodynamically unstable patient
      • absence of echo signs of RV overload or dysfunction practically excludes PE as cause ro haemodynamic instability
      • unequivocal signs of RV pressure overload and dysfunction in patient with suspected PE are highly suggestive of PE
      • In patients who are too unstable to undergo CT some advocate treatment of PE for those with:
        • high clinical probability
        • shock index (HR/SBP) ≥1
        • RV dysfunction on echo
    • transoesophageal echo may demonstrate central PE or right heart thrombus
  • ventilation perfusion scintigraphy
    • use currently restricted to those without a high risk of death and who have a contraindication to CT arteriography or if multi-detector CT is unavailable

Management of pulmonary embolus

Appropriate management requires assessment of risk of death

  • high risk:
    • shock or
    • SBP <90 mmHg or pressure drop ≥40 mmHg for 15 mins, not due to new onset arrhythmia, hypovolaemia or sepsis
  • intermediate risk
    • not shocked AND
    • right ventricular dysfunction and/or myocardial injury

Supportive

  • Cautious fluid loading – marked rise in RVEDP will result in a marked decrease in right sided coronary perfusion pressure and a shift of the interventricular septum to the left, reducing LV preload
  • Norepinephrine ± dobutamine may be best combination of vasoactive drugs.
    • Isoproterenol is arrhythmogenic and a systemic vasodilator and is detrimental.
    • Nitroprusside decreases RV coronary perfusion
  • hypoxaemia can usually be reversed with supplemental oxygen. If mechanical ventilation is required care should be taken to avoid exacerbating RV failure

Definitive therapy

Thrombolytic therapy

  • recommended for patients with high risk of death. Note that absolute contra-indications to thrombolysis in acute myocardial infarction (eg GI bleeding within 1 month) may be considered only a relative contra-indication in a patient with an immediately life threatening PE
  • contraindicated in pregnancy
  • regimes:
    • streptokinase: 1.5 million IU over 2h
    • urokinase: 3 million IU over 2h
    • rtPA: 100 mg over 2 h
  • check APTT after infusion of thrombolytic is complete. Start heparin without loading dose when APTT <2 times upper limit of normal. If APTT is above this level repeat measurement every 4 h until safe to start heparin.

Catheter extraction of clot

  • requires technical expertise
  • limited case series suggest that this is a useful technique in those in whom thrombolysis is contraindicated or fails to improve haemodynamics

Surgical embolectomy

  • Rarely indicated
  • Mortality approaches 40%
  • Consider if thrombolysis contraindicated or unsuccessful and there is persistent hypotension, oliguria, hypoxia and metabolic acidosis with radiological confirmation of >50% occlusion

Anticoagulation with heparin and then warfarin.

  • Heparin should be started as soon as the diagnosis is suspected in the absence of specific contraindications
  • Heparin should be continued for 5 days after the start of warfarin even if INR is in therapeutic range. This is because warfarin not only inhibits vitamin K dependent clotting factors, it also reduces protein C levels. Thus a hypercoagulable state may exist during early stages of warfarin therapy, before the longer half-life factors (II, IX, X) are inhibited.
  • Low molecular weight heparin is as least as effective as unfractionated heparin in preventing recurrent venous thromboembolism and at least as safe with respect to major bleeding. Agent of choice for intermediate or low risk PE.
  • Unfractionated heparin indicated for patients with renal failure. There is a wide discrepancy in recommended unfractionated heparin dosage regimes. The American College of Chest Physicians recommend an initial bolus of 80 U/kg followed by 18 U/kg/h. Subsequent changes in infusion rate are based on APTT (see table 1).
    APTT (sec) APTT (x control) Adjustment
    <35 <1.2 80 U/kg bolus & ­ infusion by 4 U/kg/h
    35-45 1.2-1.5 40 U/kg bolus & ­ infusion by 2 U/kg/h
    46-70 1.5-2.3 No change
    71-90 2.3-3 ¯ infusion by 2 U/kg
    >90 >3 Stop infusion for 1 h then ¯ infusion by 3 U/kg/h

    Table 1. Heparin dose adjustment

Secondary prevention

IVC filter

Indications:

  • absolute contra-indication to anti-coagulation and high risk of recurrent venous thromboembolism
  • consider in pregnant women who develop extensive venous thrombosis in weeks before delivery

No data to support routine use of filters in patients with free-floating proximal DVT (risk of PE with adequate anticoagulation ~3%)

Thromboembolic disease and pregnancy

  • PE causes 15-25% of maternal deaths
  • pregnancy associated with 6-fold increase in thromboembolism as a result of venous stasis, a hypercoagulable state and vascular injury associated with delivery
  • dose of radiation delivered to fetus by chest CT is lower than that of perfusion scintigraphy
  • warfarin should not be used before delivery
  • heparin continued until labour begins and is restarted in postpartum period when bleeding has stopped
  • streptokinase (and probably other thrombolytics) does not cross the placenta and has been used for pregnant patients at high risk of death from PE

Prevention of DVT

  • low molecular weight heparin or low dose unfractionated heparin
  • graduated compression stockings ±intermittent pneumatic compression device for those in whom anticoagulation is contra-indicated. (Note that the efficacy of mechanical prophylaxis has never been tested in ICU patients).
Risk of DVT or PE Risk of bleeding Recommendations
++ + Heparin 5000U subcutaneously twice daily
+++ + Low molecular weight heparin
++ ++ Mechanical prophylaxis initially. Heparin 5000U SC bd when bleeding risk decreases
+++ ++ Mechanical prophylaxis initially. LMW heparin when bleeding risk decreases

 

Further reading

The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology. Guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J, 2008; 29:2276-2315


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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