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Pulmonary embolism (PE)

Doctor drawing a heart

What is Pulmonary embolism (PE)

Pulmonary embolism occurs in the lungs. The lung, as well as containing airways, also contain blood vessels, which are derived from the pulmonary arteries. The pulmonary arteries (which receive blood from the right side of the heart) break up into progressively smaller and smaller branches until they form small capillaries. PE’s start off as clots that may from in leg, pelvic, or abdominal veins, or even occasionally in the right side of the heart. These clots then travel through the bloodstream to lodge (embolise) in the lung arteries, cutting off further blood flow through that artery. This means that the region of lung normally supplied by this artery is no long able to function, as inspired air does not come into contact with the circulation. Pulmonary embolism may involve one or many clots, which may be small or large.

Statistics on Pulmonary embolism (PE)

Post-mortem studies show that pulmonary embolism in fact occurs very commonly, but is not diagnosed this often in life, partly because very small emboli often don’t cause any problems. Symptomatic pulmonary embolism occurs in 20 to 25 per 100 000 hospitalised patients, and much less often in non-hospitalised patients.

Risk Factors for Pulmonary embolism (PE)

Many factors may predispose to pulmonary embolus. The most important predisposing factors are:

  • recent surgery, especially pelvic and abdominal surgery,
  • prolonged bed rest, pelvic and leg fractures.
  • pregnancy and childbirth,
  • advanced age,
  • smoking,
  • inherited clotting diseases, and
  • any severe, debilitating illness (for example heart disease, cancer).
  • Increased oestrogen in the body can increase the likelihood of clot formation, and thus of pulmonary embolism. The commonest cause of increased oestrogen is the oral contraceptive pill. Studies have shown, however, that only women over the age of 40, who smoke, and take the pill, have an increased risk of clot formation.

The link between air travel and pulmonary embolism is a weak one. Research suggests so far that long-haul air travel causes a very slight increase in risk of deep vein thrombosis, or leg clots. This increase is mainly in those with pre-existing illness or other predisposing factors. If the increased risk of DVT on long flights is slight, then the risk of pulmonary embolism arising from such DVTs is even lower. One French study found the incidence of pulmonary embolism to be 0.5 per million passengers landing in Paris per year; it is debatable how many of these were due to the air travel. , Many factors may predispose to pulmonary embolus. The most important predisposing factors are:

  • recent surgery, especially pelvic and abdominal surgery,
  • prolonged bed rest, pelvic and leg fractures.
  • pregnancy and childbirth,
  • advanced age,
  • smoking,
  • inherited clotting diseases, and
  • any severe, debilitating illness (for example heart disease, cancer).
  • Increased oestrogen in the body can increase the likelihood of clot formation, and thus of pulmonary embolism. The commonest cause of increased oestrogen is the oral contraceptive pill. Studies have shown, however, that only women over the age of 40, who smoke, and take the pill, have an increased risk of clot formation.

The link between air travel and pulmonary embolism is a weak one. Research suggests so far that long-haul air travel causes a very slight increase in risk of deep vein thrombosis, or leg clots. This increase is mainly in those with pre-existing illness or other predisposing factors. If the increased risk of DVT on long flights is slight, then the risk of pulmonary embolism arising from such DVTs is even lower. One French study found the incidence of pulmonary embolism to be 0.5 per million passengers landing in Paris per year; it is debatable how many of these were due to the air travel.

Progression of Pulmonary embolism (PE)

The course of events depends on the size of the clot causing pulmonary embolism.

  • Small to medium pulmonary embolism: cut off the circulation to a part of the lung, and cause shortness of breath due to hypoxia. In 10% of cases, the region of lung supplied by the blocked artery dies due to inadequate blood flow. This will eventually heal with a fibrous scar.
  • Massive pulmonary embolism: If a very large clot forms, usually in one of the pelvic or large abdominal veins, it may embolise in the main pulmonary artery, blocking off almost all blood flow to the lungs. This causes back-pressure on the right side of the heart, causing a reduction in the amount of blood pumped from the heart into the lungs, and right heart failure. These changes to the heart may happen suddenly (massive pulmonary embolism), or gradually, due to recurrent pulmonary emboli.

Clinical Examination of Pulmonary embolism (PE)

1. Small to medium pulmonary embolism may present with the following signs:

  • Tachypnoea, tachycardia, fever (if infarction has occurred).
  • Crackles over involved area.
  • Localised plural rub (with infarction).
  • Cardiovascular examination may show atrial fibrillation or other tachyarrhythmia.
  • Clinical evidence of leg thrombosis (pain, swelling, redness, engorged superficial veins) is present in less than 50% of patients.

2. Massive pulmonary embolism:

  • Pale, sweaty, cool peripheries, slow capillary return.
  • Tachypnoeic, tachycardic, hypotensive.
  • Raised jugular venous pulse.
  • Right ventricular heave, gallop rhythm, widely split second heart sound may occur.

3. Multiple, recurrent pulmonary emboli:

  • Right ventricular heave.
  • Loud pulmonary component of second heart sound.

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How is Pulmonary embolism (PE) Diagnosed?

  • Arterial blood gas analysis will show decreased oxygen (hypoxia) and decreased carbon dioxide (hypocapnoea).
  • Chest x-ray – pulmonary embolism is difficult to diagnose on X-ray; findings are often normal. CXR is useful to rule out alternate causes for the presentation.
  • ECG – this is an important investigation; it may cause non-specific changes or sometime characteristic changes.

Prognosis of Pulmonary embolism (PE)

Around 10% of clinical pulmonary emboli are fatal. Importantly, 30% of patients with pulmonary embolism will suffer a second, thus, secondary prevention is important. In the long term PE may cause decompensated right heart failure which also has significant morbidity and mortality.

How is Pulmonary embolism (PE) Treated?

There are two categories in pulmonary embolism treatment: acute (emergency) treatment, and the prevention of further emboli. Acute treatment involves supporting the patient in providing oxygen to the blood; either by high-flow oxygen, or treatment at the intensive care unit for massive emboli. Drugs (such as streptokinase) which dissolve clots may be given in massive embolism. Occasionally, again in severe, massive embolism, surgery to remove the clot is necessary. The prevention of further emboli involves:

  1. reducing predisposing factors – e.g. quitting smoking, and
  2. medications to thin the blood. These blood thinners are commenced immediately, in the form of heparin or clexane injections, and changed to warfarin tablets over the following days. Warfarin therapy continues for six weeks to six months, depending on the patient and their risk of further embolism. Some patients require warfarin therapy for life. Warfarin therapy has significant adverse effects, relating to the propensity to bleed, and this must be monitored by regular blood tests.
  3. Occasionally, blood thinning medications are not adequate, or not appropriate, and an operation to place a filter in the main abdominal vein leading up to the heart, the inferior vena cava, is required.

Pulmonary embolism (PE) References

  1. Clerel M. Caillard G. Thromboembolic syndrome from prolonged sitting and flights of long duration: experience of the Emergency Medical Service of the Paris Airports. Bulletin de l”Academie Nationale de Medecine. 183(5):985-97; 1999.
  2. Cotran RS, Kumar V, Collins T. Robbins Pathological Basis of Disease Sixth Ed. WB Saunders Company 1999. pp703-04.
  3. Kumar P, Clark M. Clinical Medicine. Fourth Ed. WB Saunders, 1998. pp. 719-722.
  4. Talley NJ, O’Connor S. Clinical examination. Third Ed. MacClennan & Petty, 1996. p126.

Dates

Posted On: 23 May, 2003
Modified On: 13 May, 2008

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