Newsletter Summer 2003- Thromboembolism
Every physician who is involved in patient care encounters patients who are at risk for pulmonary embolism (PE). An estimated 700,000 Americans may suffer pulmonary embolism each year in the United States (350,000 nonfatal PE, and 250,000 fatal PE).1

Mortality rates are significant, as PE is the second most common cause of sudden natural death at any age, following coronary artery disease. Without prompt treatment, there is a 30% mortality rate, but that may drop to as low as 3% with rapid diagnosis and treatment. For patients with a massive PE, approximately 80% will die within the first two hours after onset, mainly from right-sided heart failure.2

While most PE typically arise from thrombi originating in the deep venous system of the lower extremities, they may also originate in the pelvic, renal, or upper extremity veins and the right heart chambers. After traveling to the lung, large thrombi lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise.1

The release of these thrombi is generally thought to be due to three main causes, referred to as the Virchow triad. These include: venostasis, hypercoagulability, and vessel wall inflammation. Associated risk factors include: immobility, obesity, surgery, fractures, trauma and chronic medical conditions. Pregnant women have a fivefold increased risk of venous thrombosis and women with C-sections are 7 times more likely to have a PE than vaginally delivered women.

Clinical presentation
Unfortunately, the correct diagnosis of PE is often missed because symptoms may be nonspecific and many of the initial diagnostic tests may be negative.3 Classic symptoms such as hemoptysis, dyspnea and chest pain are neither sensitive nor specific, occurring in fewer than 20% of patients in whom the diagnosis of PE is made. Of patients who die from massive PE, only 60% have dyspnea, 17% have chest pain, and 3% have hemoptysis.3

PE is generally categorized into four classes based on the acuity and severity of pulmonary arterial occlusion.1

1. Massive pulmonary embolism-- compromises sufficient pulmonary circulation to produce circulatory collapse and shock. The patient has hypotension; appears weak, pale, sweaty, and oliguric; and develops impaired mentation, tachycardia, and tachypnea.

2. Acute pulmonary infarction-- peripheral occlusion of a pulmonary artery causing parenchymal infarction. These patients present with acute onset of pleuritic chest pain, breathlessness, and hemoptysis.

3. Acute embolism without infarction-- nonspecific symptoms of unexplained dyspnea and/or substernal discomfort.

4. Multiple pulmonary emboli— either repeated documented episodes of pulmonary emboli over years, or those patients with no previously documented pulmonary emboli but have widespread obstruction of the pulmonary circulation with clot. Usually present with signs and symptoms of pulmonary hypertension and cor pulmonale.

Diagnostic testing

• Pulse oximetry- measures oxygen saturation level, is neither sensitive nor specific in the majority of patients with PE.

• A low PO2 on Arterial Blood Gases analysis (ABG) has a strongly positive predictive value for PE in select patients with a very high incidence of PE without a history of other respiratory ailments.

• Clotting studies may be normal initially. Prolonged prothrombin time (PT), activated partial thromboplastin time (aPTT), or clotting time have no prognostic value in the diagnosis of PE.

• D-dimer is not sensitive or specific enough to impact diagnostic evaluations or treatment for patients with suspected PE. The D-dimer study misses 10% of patients with positive pulmonary angiograms, while only 30% of those with a positive D-dimer will have a positive angiogram.7

• Chest x-rays are usually normal initially but subsequent x-rays may show atelectasis or pleural effusions.

• EKG abnormalities (tachycardia and nonspecific ST-T wave abnormalities) are nonspecific and insensitive for PE. The classic findings of right heart strain and acute cor pulmonale occur in only 20% of patients with proven PE.

• Lung ventilation-perfusion (V/Q) scans are the most important diagnostic tests for detecting PE. However, unless the scan shows normal perfusion, further definitive testing (pulmonary angiography) is needed to rule out PE or to prove an alternative diagnosis.

• Pulmonary angiography is the gold standard for the diagnosis of PE, providing virtually 100% certainty.

• High-resolution helical CT angiography may replace pulmonary angiography and the need for invasive pulmonary artery catheters.3

Therapy
Thrombolytic therapy with intravenous tissue plasminogen activator (t-PA), reteplase (r-PA), urokinase, or streptokinase typically has been reserved for patients with life threatening pulmonary embolism and has been the standard of care for all patients with massive or unstable PE since the 1970s.3,4

Fibrinolytic therapy dramatically reduces the mortality and morbidity rates, regardless of the size or type of PE at the time of presentation. These may be given empirically in unstable patients, particularly when the clinical likelihood of PE is overwhelming and the patient's condition is deteriorating, unless overwhelming contraindications are evident. The risk/benefit is considered low in these situations.

Early anticoagulation with heparin should also be started as soon as the diagnosis of pulmonary thromboembolism is considered seriously, as it prevents clot progression and reduces the risk of further embolism. Intervenous fluids should be used with caution in patients with PE because IV fluids may actually worsen the patient's condition of heart failure.

Vasopressor therapy to raise blood pressure does not eradicate the need for fibrinolysis. CPR and advanced cardiac life support (ACLS) protocols are of little value in patients whose cardiac arrest is due to PE. Oxygenated blood is obstructed in reaching the peripheral or cerebral circulation and closed chest compressions are unable to provide any blood flow to the cerebral circulation.

Sequential compression devices (SCD) or compression stockings that provide a 30-40 mm Hg compression gradient should be used as an adjunctive treatment to limit or prevent extension of thrombus. Anti-embolic stockings or "TED hose" produce a maximum compression of 18 mm Hg. and provide such limited compres-sion, they have no efficacy in the treatment of DVT and PE, nor have they been proven effective as prophylaxis against a recurrence.1

Airline litigation related to PE
“Coach class syndrome” is a name applied to travelers who develop venous thrombosis following travel as a result of cramped seating and sitting motionless for long periods of time, but does not exclude travelers in business, first-class or those using other forms of long distance travel. At least 200 cases of traveler's thrombosis worldwide have been reported in the last decade.5

Lawsuits are becoming more common, alleging failure to warn passengers about the risks associated with long air travel. Recently the U.S. District Court in San Francisco ruled that the plaintiffs are entitled to pursue their claims under the Warsaw Convention of 1929, which governs airline liability. The convention holds that an airline is liable if a passenger suffers death or bodily injury in an accident while on board an aircraft or while embarking or disembarking.

While there have been no epidemiological studies published which show a statistically significant increase in cases of DVT when traveling in the absence of preexisting risk factors. Some reports have documented elevated D-dimer levels, an indicator of clotting activity, in 10-12% of test subjects.6

This assumption has been challenged. The Aerospace Medical Association states “It is unlikely that hypoxia or hypobaric changes are responsible for venous thrombosis, as there is no reported increased incidence of VTE in populations living at high altitudes nor in patients with hypoxic lung disease. There is no evidence of any increased incidence of DVT among commercial airline pilots who spend their working lives sitting in a hypobaric environment.” 5

Malpractice related to PE
Pulmonary embolism is one of the most common causes of unexpected death in hospitalized patients and one of the top diseases leading to medical malpractice lawsuits.5

Studies that have reviewed malpractice cases involving PE found that failure to anticipate and reduce the chance of PE was the basis for claims.

Risk management for PE should focus on identifying those high-risk patients for deep vein thrombosis. Physicians should also consider documenting a concurring second opinion when making anticoagulant-related decisions.6 Hospitals are being mandated to develop formal strategies that address the prevention of thromboembolic complications including protocols for anticoagulation for patients at risk.

Conclusion
The correct diagnosis of PE is often missed because symptoms are variable and non-specific. This is associated with a high morbidity and mortality. Patients with unexplained dyspnea are dismissed as having anxiety or hyperventilation; those with unexplained chest pain are dismissed as being due to musculoskeletal pain.

The Legal Nurse Consultants at Century Consulting LLC are experienced in reviewing cases for PE and deep vein thrombosis. Call today to see how to put their expertise and experience to work on your next medically related case.

References
1.http://www.emedicine.com/MED/topic1958.htm

2. Almoosa K. Is thrombolytic therapy effective for pulmonary embolism? American Family Physician. 2002 Mar 15;65(6):1097-102.

3.http://www.emedicine.com/EMERG/topic490.htm

4.http://www.ahcpr.gov/clinic/epcsums/dvtsum.htm

5.http://www.asma.org/Publication/medguid.pdf

6.http://www.airhealth.org/news.htm

7. Tapson VF. Prophylaxis strategies for patients with acute venous thrombo-embolism. American Journal Managed Care. 2001 Nov;7(17 Suppl):S524-31

8. Fink S. Pulmonary embolism and malpractice claims Southern Medical Journal. 1998 Dec; 91(12):1149-52