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PE & DVT
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VQ scan

Thromboembolic disease

Mechanism of risk

Risk factors

Pathophysiology

Clinical features

Differential diagnosis

Investigations

Management

Prognosis

Pregnancy

Further reading

 

 

  • 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

  • prolonged immobilization
  • increased age
  • surgery & trauma
  • coagulation abnormalities:
    • polycythaemia
    • platelet abnormalities
    • antithrombin III deficiency
    • protein C & S deficiencies
    • inherited abnormalities of fibrinogen and plasminogen
    • previous venous thrombosis
    • smoking
  • medical conditions, especially those associated with low cardiac output or prolonged bed rest:
    • CCF, MI
    • shock syndromes
    • CVA
    • obesity
    • malignancy, especially pancreas, stomach, lung, GU tract, breast
    • vasculitis
    • dysproteinaemias
    • hyperlipidaemia
    • inflammatory bowel disease
    • paroxysmal nocturnal haemoglobinuria
    • Behcets
    • sickle cell anaemia
  • drugs, eg oral contraceptive/oestrogen
  • pregnancy

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

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
  • 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 and rub
  • wheeze and crackles

CVS

  • HR: usually increased, bradycardia ominous
  • +/- signs of pulmonary hypertension, 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

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

  • US. Doppler US notoriously insensitive in detecting proximal vein thrombi in asymptomatic patients (even those at high risk) although sensitivity in symptomatic patients is 91%. High specificity in both groups of patients. Examination of common femoral and popliteal vessels only appears to be adequate
  • impedence plethysmography: low sensitivity and specificity
  • contrast venography: visualization of external and common iliac veins is inadequate. Complications include pain, hypersensitivity reactions, phlebitis, DVT
  • MRI: accuracy of 96% in detecting pelvic thromboses

To diagnose PE

  • blood tests: raised WCC, raised D-dimer (non specific but very sensitive; D-dimer <500 mg/L virtually excludes PE)
  • 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
  • VQ scan
    • probability of PE based on clinical suspicion and results of VQ scan. High clinical suspicion based on presence of one or more predisposing factors, appropriate clinical presentation and absence of other diseases to account for presentation while low suspicion based on absence of underlying risk factors and the presence of other diseases to account for presentation.

Clinical suspicion

Low

Intermediate

High

Normal/very low probability scan

2

6

0

Low probability scan

4

16

40

Intermediate probability scan

16

28

66

High probability scan

56

88

96

  • pulmonary angiography
    • "gold standard". Indicated in those patients in whom probability of PE based on clinical suspicion and VQ scan does not allow confident diagnosis or exclusion of PE. Contrast may cause catastrophic vasodilatation and resuscitation facilities should be available
    • if pulmonary angiography is not available:- patients with low or intermediate probability scans in whom clinical suspicion of PE is intermediate or high should have Doppler US of legs. If this is normal the probability of a thromboembolic event is < 5%. In patients without cardiorespiratory disease it is probably reasonable not to treat at this level of risk. However patients with underlying cardiorespiratory disease require a more aggressive approach as PE appears to be more dangerous in this group.
  • echocardiographic features associated with PE:
    • decreased mitral valve opening
    • thromboemboli in R heart or PA
    • RV dilatation
    • RV hypokinesis
    • abnormal septal position/paradoxical systolic movement
    • reduced LV size
    • increased RV:LV diameter ratio
    • PA dilatation
    • tricuspid or pulmonary regurgitation
  • CT angiography

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

Management of pulmonary embolus

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.
  • 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. There is a wide discrepancy in recommended 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

Definitive therapy

Thrombolytic therapy

  • improves outcome in patients with massive PE although when given to all patients with PE no evidence of benefit in terms of outcome has been demonstrated. Should probably be reserved for those patients with diagnosis proven by a well established imaging method (ie pulmonary angiography or CT angiography).
  • may also be used for patients with significant swelling associated with proximal DVT in absence of contraindications (rare in ICU patients).
  • contraindicated in pregnancy
  • recommended regimes:
    • streptokinase: 250000 U over 30 min then 100000 U/h for 24 h
    • urokinase: 900U/kg over 10 min then 900U/kg/h for 24 h
    • rtPA: 100 mg over 2 h

rtPA may produce more rapid improvement than streptokinase and is probably the agent of choice as deaths from massive pulmonary embolus tend to occur early and result from acute right heart failure

  • 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

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

Secondary prevention

IVC filter

Indications:

  • recurrent PE despite adequate anticoagulation
  • anticoagulant intolerance
  • large free-floating thrombus in ileo-femoral veins
  • immediately following embolectomy

Prognosis

  • initial mortality following PE is 2.5%, mostly due to recurrent PE
  • in 399 patients with well-documented PE, 1 year mortality was 24% (19.2% of those treated with heparin followed by oral anticoagulation). Cardiac disease, recurrent PE and cancer caused 3/4 of deaths (cancer 1/3 of them). Recurrences of PE were usually seen in first 2 weeks of follow-up and accounted for only about 10% of deaths
  • mortality of in-hospital DVT 5%

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
  • venography after the first trimester and ventilation perfusion scans should not be avoided if indicated
  • warfarin should not be used before delivery
  • heparin continued until labour begins and is restarted in postpartum period when bleeding has stopped

Further reading

Curzen, N., Haque, R., and Timmis, A. Applications of thrombolytic therapy. Intens.Care Med. 24:756-768, 1998.

Fennerty T. The diagnosis of pulmonary embolism. BMJ 1997; 314:425-9

Freebairn RC, Oh TE. Pulmonary embolism. In Oh TE. Intensive Care Manual, 4th ed.

Geerts W, Cook D, Selby R, Etchells E. J Crit Care, 2002; 17:95-104

Tapson VF. Strategies for the prevention and treatment of acute venous thromboembolism. http://www.chestnet.org/pccu/lesson7-12.html


©Charles Gomersall, September, 2008 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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