Massive Pulmonary Embolism

Massive Pulmonary Embolism

A 48 year old lady was admitted to critical care whilst suffering from sepsis secondary to severe cellulitis of her leg. She was obese with a BMI of 38 and was managed with insulin and oral anti-hyperglycaemics for type 2 diabetes mellitus. A doppler scan was unable to exclude a DVT. She had a further deterioration 30 hours later. Her sinus tachycardia accelerated to 130 bpm, along with a drop in blood pressure to 100/40. Arterial blood gas demonstrated an increasing A-a gradient as his FiO2 increased. Although such changes can occur in sepsis, the acute onset led to concerns regarding venous thromboembolism and pulmonary emboli.

What are the options for prevention of venous thromboembolism and pulmonary embolism?

Duncan Chambler

A pulmonary embolism (PE) can be life threatening and acute, but due to the highly variable presentation the diagnosis and subsequent management can be difficult. In the critically ill patient, many of the common symptoms and signs are masked or already present due to concurrent disease.

Deep vein thromboses (DVT) and pulmonary emboli (PE) are common in patients admitted to hospital. Reviewed studies (1) have shown the DVT incidence in critically ill patients to be between 13 and 31%, whilst the PE incidence at postmortem of such patients as high as 27%.

Rudolf Virchow published his description of the pathophysiology behind pulmonary emboli in 1856, but the eponymous Virchow’s Triad of hypercoagulability, haemodynamic change such as stasis, and endothelial activation was not described until after his death. It is now established that proximal venous thrombo-emboli (VTE) are the source for pulmonary thrombo-emboli, traversing the right heart to enter the lungs. Prevention of PE therefore lies with preventing peripheral VTE, the majority of which occur in lower limb veins. Methods can be divided into mechanical and pharmacological.

The primary mechanical method utilised is graduated compression stockings (GCS), known commonly as Thrombo Embolus Deterrent Stockings or T.E.D.S.™. In 1975, Sigel (2) demonstrated in 7 healthy volunteers that graduated pressure (18mmHg at the ankles, reducing to 8mmHg at the upper thigh) was effective at increasing blood flow at the femoral vein to 1.38 times baseline. Additionally, by preventing venous over-distension, endothelial tears and tissue factor activation is reduced. Comparison of knee-length GCS against thigh-length GCS has shown no significant difference, and NICE Clinical Guidance 92 (3) emphasises the importance of choosing length with the individual patient in mind. In this particular case, the patient had broken skin around both ankles from diabetes related ulceration, and therefore GCS were contraindicated and not applied.

An alternative mechanical method is intermittent pneumatic compression devices (IPCD), such as Flowtron™. Although there is no evidence that these offer better prevention than GCS, they can be applied when GCS are contraindicated. The patient described here did have an IPCD applied to his non-infected leg.

Pharmacological prophylaxis is heparin, of which there is no evidence to say that LMW heparin is better or worse than unfractionated heparin. When comparing mechanical and pharmacological prophylaxis, despite many small randomised control trials, there is no clear advantage of one over the other. NICE suggest that any high risk patient, which would include all critical care patients, receive some form of mechanical prophylaxis in addition to a pharmacological agent at the discretion of each Trust. This patient received 40mg enoxaparin once daily subcutaneously. Although no dose adjustment for body weight is suggested by the manufacture of Clexane™, it is possible this represents an under-dosing for this obese patient.

When pharmacological and mechanical prophylaxis are contraindicated, for example in cases of poly-trauma, or if the risk of embolisation from existing DVTs is high, inferior vena
cava filters can be placed.

Diagnosis of PE is difficult in critically ill patients: many clinical features are masked by concurrent pathophysiological changes present already; scoring systems such as that described by Wells cannot be applied with any specificity; D-dimer tests are of minimal use in critically ill patients; and V/Q scans are difficult to interpret in the presence of abnormal lung function. The PIOPED II randomised control trial (4) demonstrated the specificity and sensitivity of CT Angiogram studies for diagnosing PEs, albeit in a non-critically ill population. Sensible extrapolation of this study, along with the limited practical alternatives, makes CTPA the primary tool for diagnosing PEs in critically ill patients. When the risks related to transferring a patient are deemed too great, bedside echocardiogram is an alternative diagnostic option, as highlighted in a recent review (5). The role of lower limb venous ultrasonography is unclear.

Therapy for established pulmonary embolism includes anticoagulation, thrombolysis, surgical thrombectomy or radiologically guided percutaneous thrombectomy. Considering the pharmacological options, trials have not established a clear benefit of thrombolysis over anticoagulation with heparin in unselected patients (6). Patients at high risk of death, usually defined as those with shock (systolic BP < 90mmHg) may benefit from thrombolysis if the risk of catastrophic haemorrhage is low. Sub-massive PE (without shock) with right ventricular (RV) strain on echocardiogram may also benefit from thrombolysis. In the absence of shock or RV strain, anticoagulation should be commenced. Surgical or radiological intervention should be considered in massive or submassive PEs when thrombolysis and anticoagulation is likely to cause excessive haemorrhage.

1 Geerts W, et al. Venous Thromboembolism and Its Prevention in Critical Care. Journal of Critical Care. 2002; 17(2): 95-104. Doi: 10.1053/jcrc.2002.33941
2 Sigel B et al. Type of Compression for Reducing Venous Stasis: A Study of Lower Extremities During Inactive Recumbency. Arch Surg. 1975; 110(2): 171-175. Doi: 10.1001/archsurg.1975.01360080037005
3 National Clinical Guideline Centre – Acute and Chronic Conditions. Venous thromboembolism: reducing the risk of thromboembolism (deep vein thrombosis and pulmonary embolism) in patients admitted to hospital. 2010
4 Stein PD, et al, for the PIOPED II Study Group. Multidetector Computed Tomography for Acute Pulmonary Embolism. NEMJ 2006; 354: 2317-27.
5 Zochios VA, and Keeshan A. Pulmonary embolism in the mechanically-ventilated critically ill patient: is it different? Journal of the Intensive Care Society 2013; 14(1): 36-44.
6 Wan S, et al. Thrombolysis Compared With Heparin for the Initial Treatment of Pulmonary Embolism: A Meta-Analysis of the Randomised Controlled Trials. Circulation 2004; 110: 744-749. Doi: 10.1161/01.CIR. 0000137826.09715.9C


One thought on “Massive Pulmonary Embolism

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s