Pulmonary Embolism--A Silent Potential Killer
Don't let this happen to you ... a "public service" page for my family, friends, and colleagues.
New! Great article on PE!
New! UK court clears way for airline blood clots class action suit

Table of Contents


Hi all!

I posted this web page as a place to send people regarding this underreported and often misdiagnosed life-threatening malady.

I realize that PE and DVT (Deep Vein Thrombosis) are getting more attention with respect to long-distance flying but, actually, PE's can happen to anybody no matter how healthy or not and for even the most innocuous of reasons. It doesn't have to be only because of air travel.

And, more to the point, it doesn't HAVE to have life-threatening consequences if the likely situations are known along with a knowledge of symptoms. I might add that this lack of appreciation and knowledge applies not only to the public but even to the medical community as you can see in one of the articles below.

Because we are people and not merely something to be shoveled through openings, pressed into conveyances, fed, gouged, and insulted, I have used this web page to reveal something personal of myself, thus, hopefully, bringing it closer to home.

I would also like to say how much I appreciated the wonderful support I received from everybody. I could not have predicted this ... nor my reaction to it.

Thanks so much! :-)

I liberally internally linked this page to make it easier to navigate and also so you can quickly visit just the places of interest.

All the best to you!



What Happened to me (Where I stand 1 week after)

Dave hi!

Hope your hiking went very well.

Me, I just got out of the ICU at St. E's on Thur eve. Went 911 last Sunday eve breathing extremely hard and fast for air but not getting anywhere (it was like drowning in air instead of water).

After an intitial incorrect diagnosis of pneumonia, they ultimately discovered "many small clots and several big clots" in both lungs (pulmonary embolism)--life threatening. When I entered ER my blood O2 content was 83% (barely sustenance level).

Presently I'm at home, working on dissolving the clots with blood thinners and taking it easy so as not to break any off. Big ones will take months.

Docs are perplexed as to WHY this occurred as I apparently have NONE of the factors for this to happen except possibly my June flight to France and back. To help them in their diagnosis, I'm trying to get an accurate history since I first began noticing shortness of breath.

Anyway, I'm doing much better each day. I still have to take it easy though cuz there remains some danger of breaking off a clot under too much stress. But the small ones must be dissolving since I can breath SO MUCH better now. (Now when I take a breath, something actually happens!)

I spent several days padding about the house. Y'day I could go out in the yard and today I am allowed to walk down the street a couple blocks and the next day further, etc.

In preparation to seeing my own doc I've been doing a lot of reading up on PE and DVT (deep vein thormbosis). It's not so simple as first meets the eye. I have a list of questions, among them about the genetic thing. I also heard there was a recent cover story in Time mag on PE from air travel, so I'll probably make a trip to the library.

Apparently, 50% of people who got PE never had swelling or pain in their legs (I never did). Untreated acute PE means you die (almost always) and they only find out later with an autopsy. There's a surprising amount of un(mis)diagnosed and/or untreated PE and it is 3rd leading cause of death. I (and others in the medical field) find this a reprehensible failing of the medical community not to have much better methodology when an extensive knowledge exists on this condition.

I still keep wondering what exactly happened to so drastically change things over my HS reunion weekend a week ago from a mild to medium shortness of breath to near total failure. Could it be that this drastic change was one of the "big" clots that got into my lungs? I never saw the images but the ER doc said the Radiologist told him there were "many small clots and several big ones."

Anyway, one day at a time ...

I'll keep you posted.

Best regards,


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Where I'm Going From Here

Frankie hi

Thanks for your letter and for your thinking of me! I appreciate it! :-)

I've pasted down below fyi a little summary I made after my first visit to my doctor this last Friday. As you can see, there are a number of tests ahead for me.

I'm on Warfarin (rat poison) for 6-12 months. Still working on getting my coagulation time in range. Should be there in a couple days and he says I can then resume the same activities as I had before. I'm looking fwd to soon getting back on my bike, going golfing, doing my exercises, etc.

Presently, I'm feeling GREAT right now compared to the last 2 months. I can BREATH again! :-)

I'm doing more and more each day--gently raising my activity level because there is still some danger (much smaller now) that one could break away and damage my heart or enter my brain. But the blood thinner must be working since I feel so much better now than I did a week ago.

Of course I had a "couple" of questions to ask my doc about the WHY. My hospital docs were baffled, considering my background. It MIGHT have been my long flight home from France in June but that seems too far away from the time I first started feeling out of breath. We may never know, in which case I will be on blood thinners rest of my life. Probably not THAT big a deal actually.

Anyway, I was relieved to find that my doc also could not believe that I even could get clots when I was taking 2800 mg/day aspirin and that he wants to agressively go after the WHY--not just blow it away with the air flight thing. He doesn't think the clotting is a genetic problem cuz, at age 58, troubles should have shown up long ago and, anyway, there's nothing in my family that I know of. This would mean that the propensity for clotting was an acquired thing for me and we need to check those out.

Anyway, I feel I am on track towards doing something positive about my situation

Thanks again for thinking of me!


PS I now have official clearance for you to send something funny to me.



  • Dr. Hallett wants to agressively look for the cause (I'm happy for that).
  • He too was surprised there could be a clot while Iwas taking 2800 mg aspirin.
  • He showed me the StE's Angio CT report that they never told me about while in the hospital: a 2x3x3 cm feature at the bottom of the left lung that could be either a cancer or a pulmonary infarct. Total surprise to me, to say the least! Can't believe that is why the wanted the 1 month rescan but didn't tell me (erroneously assumed it was to check for clots).
  • In light of my melanoma 15 yrs ago he feels compelled to check out anything to do with cancer.
  • Prostate cancer (PSA) checks out OK
  • Plans are in works for following:
    • ultrasound calves 1st (unusual to have clots here with no symptoms) to look for clot sites
    • if ultra is neg, the pelvis CT (more likely clot source)
    • echocardiogram (my murmur is Grade 1)
    • appt with hemotologist/oncologist (Dr. Tony Phillips)
    • Followup Angio CT of lungs in a couple weeks
  • Doubts very much genetic (would have shown up long before age 58).
  • I can resume my normal activities (biz trips, bike, blading, crunches, golf, etc.) as soon as the Protime gets within range.



  • Ultrasound of legs revealed a deep venous thrombosis in left calf. Highly probable site for forming the clots that ended up in the lungs. This kind of clotting commonly happens with travel/prolonged sitting and is consistent with the long plane trip and bus ride (20 hours) back from France in late June.
  • Echocardiogram of heart showed no abnormalities or damage.
  • Still left with why did the blood clot in the first place, especially when taking 2800 aspirin/day.
  • Follow-up Angio CT of lungs (14 Sept) and blood hemotology still scheduled.


  • Dramatic reduction in pulmonary emboli from 1st Angio-CT
  • 2x3x2 "mass density" still there in lower left lung and unchanged from first Angio-CT.
  • Could have been there for a long time but no past chest XRAY available to prove that.
  • Appointment with Pulmonary Specialist 27 Sept 01--needle biopsy definitely, followed by much more invasive Video Assisted Thorasic Scope (VATS) if biopsy proved negative (20% false negative with needle).
  • Appointment with Hemotologist/Oncologist 4 Oct 01--ordered blood draws (11 vials!) on biopsy day when no anti-coagulants in blood. Testing for clotting chemistry.



  • Just before the needle biopsy was to begin (3 hrs prep time!), the two Theda Clark radiologists studying the last St E's low resolution CT films became suspicious whether the "mass density" was really a lobulated SPN (solitary pulmonary nodule)--previous diagnosis. An SPN can have a good chance of being cancerous)
  • Halted the needle biopsy procedure and ordered a high-res CT scan (1 mm thick slices instead of the 7 mm slices at St. E's) to carefully study the mass in various planes and orientations.
  • Size of mass from previous CT scan had reduced from 30 mm to 25 mm (significant with respect to cancer).
  • The "radiating bronchovascular bundles [in the high-res scan] strongly suggest Rounded Atelectasis." (NOT a cancer.)
  • Felt so confident of this diagnosis they cancelled the CT-guided pulmonary needle biopsy (they NEVER do this otherwise).
  • Return in 3-4 months to check on the mass (may even have disappeared by then).
  • Still have follow-up work (e.g., colonoscopy, complete belly CT, hemotology, etc.) to either find a cause for the clotting or somehow eliminate other adeno cancer (mysterious blood clotting can presage cancer by a year or more).
  • Needless to say, a high-res scan in the first place would have alleviated a LOT of consternation on my part over the 1-month time period!

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  • In the search for the fundamental cause of the blood clotting that led to my near-fatal pulmonary embolism, I just today discussed the results with my hemotologist/oncologist (cancer doctors need to know a LOT about blood).
  • 5 of 15 were out of normal range but not concerning to my doctor.
  • He found a mutation in my blood that I acquired from either my dad or mom. This mutation gives an increased propensity for heart disease, stroke, and clotting.
  • To put it into perspective, in the case of getting the mutation from only one parent (as is my case) as opposed to both parents, this mutation gives much less risk than, say, smoking or high blood pressure.
  • He said that I should pass this information on to my siblings and children because, with me having it, they may wish to get this blood test.
  • Having this mutation, I am to take a Folate pill every day to reduce the homocysteinemia and thus lower the risk for those things I mentioned above. This is an over the counter drug and is no big deal.
  • I will be on blood thinners for a long time, possibly for life, because of the combination of this blood chemistry mutation and my left leg surgery that causes a constriction in the blood flow (a thrombosis and blood clot was detected in my upper calf near the knee). Again, taking blood thinner is not a big deal really.
  • Next week I have a full belly CT scan and a colonoscopy to rule out cancers in those organs (considering the course of events that have transpired so far, he doesn't expect anything will be found, but, of course, prudence requires this)


  • Colonoscopy results AOK; "come back in 10 years"
  • Full Belly CT Scan--negative, no problems


  • PSA for prostate--normal
  • Lymph nodes--normal
  • Solitary Pulmonary Nodule found to be Rounded Actelectesis (non-cancerous)
  • Cancer ruled out as cause of PE (relief)
  • Likely cause for PE, according to my hemotologist/oncologist was combination of clotting factor, prior left calf surgery, and 20+ hr trip from France in June.


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Information from various medical sources on the WWW

Management of Deep Vein Thrombosis and Pulmonary Embolism

A Statement for Healthcare Professionals From the Council on Thrombosis (in Consultation With the Council on Cardiovascular Radiology), American Heart Association

Jack Hirsh, MD; John Hoak, MD

A clinical suspicion of venous thrombosis should always be confirmed by objective tests because patients with minimal leg symptoms may have extensive venous thrombosis, whereas the classic symptoms and signs of pain, tenderness, and swelling of the leg can be caused by nonthrombotic disorders.11

Despite the nonspecificity of clinical features, history and physical examination are important components of the diagnostic process because they may uncover an alternative cause of the patient's symptoms and because they allow patients to be classified as having a high, intermediate, or low probability for venous thrombosis.

Although a number of tests have been evaluated over the years, only three have been shown to be accurate for diagnosing venous thrombosis in symptomatic patients: venography,81-83 IPG,3,4,35,77,84-90 and venous ultrasonography.77

The diagnosis of clinically suspected recurrent venous thrombosis is often more difficult to establish than diagnosis of the first episode of venous thrombosis.

Patients may present with clinical features of minor or major PE. Patients with minor PE can have one or a combination of the following symptoms: transient shortness of breath, sharp localized chest pain aggravated by inspiration (pleuritic-type pain), and hemoptysis.

Patients with major PE usually have severe shortness of breath with or without associated right-heart failure. Patients who sustain a massive embolism or have impaired cardiorespiratory reserve and sustain a moderate-sized embolus may present with hypotension, syncope, and peripheral circulatory failure. Sometimes there is associated dull central chest pain.

The most reliable test for diagnosis of PE is pulmonary angiography, because a normal well-performed pulmonary angiogram excludes the diagnosis of PE, whereas demonstration of a constant intraluminal filling defect in a pulmonary artery establishes diagnosis.127

With PE, the ECG is often normal or shows nonspecific changes.135

The objectives of treating venous thrombosis and PE are to prevent local extension of the thrombus, prevent the thrombus from embolizing, and, in certain clinical circumstances, accelerate fibrinolysis. Anticoagulants are effective in most patients for preventing clinically important local extension of thrombosis, but they must be continued for weeks to months after the acute event and they may not prevent long-term complications of thrombosis.

In patients with venous thrombosis, PE can be prevented very effectively with anticoagulant therapy. Pulmonary emboli can also be prevented by inserting a filter into the vena cava, but this approach is used only if anticoagulant therapy is contraindicated because of bleeding or if PE has recurred despite adequate treatment with anticoagulants (see below for definition of adequate anticoagulant therapy).

There is good evidence that patients with PE have a high mortality and a high rate of recurrence if untreated.142 There is also good evidence that patients with symptomatic proximal143,144 or calf vein thrombosis145 have a high recurrence rate without treatment. Anticoagulation reduces mortality and recurrence in patients with acute PE and reduces recurrence in patients with DVT.143

Bleeding is by far the most important complication of anticoagulant therapy. The approach to bleeding depends on the severity of bleeding, the anticoagulant and dose used, results of laboratory tests at the time of bleeding, the length of time the patient has been treated with anticoagulants, and the seriousness of the thromboembolic event for which the patient is being treated.

The most important nonhemorrhagic side effect of warfarin is skin necrosis. This uncommon complication is usually observed on the third to eighth day of therapy353-373 and is caused by extensive thrombosis of the venules and capillaries within the subcutaneous fat.

Thrombophilia is defined as an increased tendency to thrombosis. It can be inherited or acquired.386

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Pulmonary Embolism

Authored by Craig Feied, MD, FACEP, FAAEM, Director of Informatics, Department of Emergency Medicine, Washington Hospital Center; Clinical Associate Professor, Department of Emergency Medicine, George Washington University; Director, National Center for Emergency Medicine Informatics

Coauthored by Jonathan A Handler, MD, Director of Informatics, Assistant Professor, Department of Emergency Medicine, Northwestern Memorial Hospital

Background: Pulmonary embolism (PE) is an extremely common and highly lethal condition that is a leading cause of death in all age groups. A good clinician actively seeks the diagnosis as soon as any suspicion of PE whatsoever is warranted, because prompt diagnosis and treatment can dramatically reduce the mortality rate and morbidity of the disease. Unfortunately, the diagnosis is missed far more often than it is made, because PE often causes only vague and nonspecific symptoms.

The most sobering lessons about PE are those obtained from a careful study of the autopsy literature. Deep vein thrombosis (DVT) and PE are much more common than usually realized. Most patients with DVT develop PE and the majority of cases are unrecognized clinically. Untreated, approximately one third of patients who survive an initial PE die of a future embolic episode. This is true whether the initial embolism is small or large.

Most patients who die of PE have not had any diagnostic workup, nor have they received any prophylaxis for the disease. In most cases, the diagnosis has not even been considered, even when classic signs and symptoms are documented in the medical chart. Sadly, appropriate diagnostic and therapeutic management often is withheld even when the potential diagnosis of PE has been considered explicitly and documented in the chart.

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Pathophysiology: Pulmonary thromboembolism is not a disease in and of itself. Rather, it is an often fatal complication of underlying venous thrombosis. Under normal conditions, microthrombi (tiny aggregates of red cells, platelets, and fibrin) are formed and lysed continually within the venous circulatory system. This dynamic equilibrium ensures local hemostasis in response to injury without permitting uncontrolled propagation of clot. Under pathological conditions, microthrombi may escape the normal fibrinolytic system to grow and propagate. PE occurs when these propagating clots break loose and embolize to block pulmonary blood vessels.

Thrombosis in the veins is triggered by venostasis, hypercoagulability, and vessel wall inflammation. These 3 underlying causes are known as the Virchow triad. All known clinical risk factors for DVT and PE have their basis in one or more of the triad.

Patients who have undergone gynecologic surgery, those with major trauma, and those with indwelling venous catheters may have DVTs that start at any location. For other patients, lower extremity venous thrombosis nearly always starts in the calf veins, which are involved in virtually 100% of all cases of symptomatic spontaneous lower extremity DVT. Although DVT starts in the calf veins, it already has propagated above the knee in 87% of symptomatic patients before the diagnosis is made.

Studies suggest that nearly every patient with thrombus in the upper leg or thigh will have a PE if a sensitive enough test is done to look for it. Current techniques allow us to demonstrate PE in 60-80% of these patients, even though about half have no clinical symptoms to suggest PE. Thrombus in the popliteal segment of the femoral vein (the segment behind the knee) is the cause of PE in more than 60% of cases.

PE can arise from DVT anywhere in the body. Fatal PE often results from thrombus that originates in the axillary or subclavian veins (deep veins of the arm or shoulder) or in veins of the pelvis. Thrombus that forms around indwelling central venous catheters is a common cause of fatal PE.

The belief that calf vein DVT is only a minor threat is outdated and inaccurate. DVT of the calf is a significant source of PE and often causes serious morbidity or death. In fact, one third of the cases of massive PE have their only identified source in the veins of the calf. One important autopsy study showed that more than 35% of patients who died from PE had isolated calf vein thrombosis. Other studies have shown that the overall frequency of PE from DVT isolated to the small deep veins of the calf is 33-46%. Most of the time, emboli from calf veins are of smaller caliber than those from more proximal venous segments, but not all emboli from calf veins are small. Even a very narrow vein can produce a long, sinuous clot that can cause hemodynamic collapse, and approximately 40% of PEs from calf veins produce perfusion scan defects that are large or massive.

Calf emboli that are very small carry their own special risks. In a 1993 study of patients with identifiable thrombi causing paradoxical embolization through a patent foramen ovale, the source was isolated to the calf veins in 15 of 24 cases.

Patients who survive an acute PE are at high risk for recurrent PE and for the development of pulmonary hypertension and chronic cor pulmonale, which occurs in up to 70% of patients and carries its own attendant mortality and morbidity.

Massive PE causes hypotension due to acute cor pulmonale, but the physical examination findings early in submassive PE may be completely normal. Initially, abnormal physical findings are absent in most patients with PE.
After 24-72 hours, loss of pulmonary surfactant often causes atelectasis and alveolar infiltrates that are indistinguishable from pneumonia on clinical examination and by x-ray.

New wheezing may be appreciated. If pleural lung surfaces are affected, a pulmonary rub may be heard.

The spontaneous onset of chest wall tenderness without a good history of trauma is always worrisome, because patients with PE may have chest wall tenderness as the only physical finding.
In patients with massive PE, the incidence of physical signs has been reported as follows:

96% have tachypnea (respiratory rate >16/min)
58% develop rales
53% have an accentuated second heart sound
44% have tachycardia (heart rate >100/min)
43% have fever (temperature >37.8° C)
36% have diaphoresis
34% have an S3 or S4 gallop
32% have clinical signs and symptoms suggesting thrombophlebitis
24% have lower extremity edema
23% have a cardiac murmur
19% have cyanosis

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Hypercoagulable states
Prolonged venous stasis or significant injury to the veins can provoke DVT and PE in any person, but increasing evidence suggests that spontaneous DVT and PE nearly always are related to some underlying hypercoagulable state. Other identified "causes" most likely serve only as triggers for a system that is already out of balance.

Hypercoagulable states may be acquired or congenital. An inborn resistance to activated protein C is the most common congenital risk factor for DVT that has been identified to date. Most patients with this syndrome have a genetic mutation in factor V known as "factor V Leyden," although other mechanisms also can produce a resistance to activated protein C.

Primary or acquired deficiencies in protein C, protein S, or antithrombin III are also common underlying causes of DVT and PE.

Risk markers: The most important clinically identifiable risk markers for DVT and PE are a prior history of DVT or PE, recent surgery or pregnancy, prolonged immobilization, or underlying malignancy. Many other recognized markers of risk for venous thromboembolic disease are listed here.
AIDS (lupus anticoagulant)

Antithrombin III deficiency
Behçet disease
Blood type A
Catheters (indwelling venous infusion catheters)
Congestive heart failure (CHF)
Drug abuse (intravenous [IV] drugs)
Drug-induced lupus anticoagulant
DVT in the past
Estrogen replacements (high dose only)
Fibrinogen abnormality
Hemolytic anemias
Heparin-associated thrombocytopenia
Myocardial infarction
Old age
Oral contraceptives
PE in the past
Plasminogen abnormality
Plasminogen activator abnormality
Postpartum period
Protein C deficiency
Protein S deficiency
Resistance to activated protein C
Systemic lupus erythematosus
Ulcerative colitis
Varicose veins
Venous pacemakers
Venous stasis
Warfarin (first few days of therapy)

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Imaging Studies:

The initial chest x-ray (CXR) findings of a patient with PE are virtually always normal.

On rare occasions they may show the Westermark sign, a dilatation of the pulmonary vessels proximal to an embolism along with collapse of distal vessels, sometimes with a sharp cutoff.

Over time, an initially normal CXR often begins to show atelectasis, which may progress to cause a small pleural effusion and an elevated hemidiaphragm.

After 24-72 hours, one third of patients with proven PE develop focal infiltrates that are indistinguishable from an infectious pneumonia.

A rare late finding of pulmonary infarction is the Hampton hump, a triangular or rounded pleural-based infiltrate with the apex pointed toward the hilum, frequently located adjacent to the diaphragm.

High-resolution helical (spiral) computed tomographic angiography (CTA) is a promising technique that soon may replace ordinary contrast pulmonary angiography. In many patients, helical CT scans with intravenous contrast can resolve third-order pulmonary vessels without the need for invasive pulmonary artery catheters.

The absolute sensitivity and specificity of CTA are evolving over time. Today we can say safely that in a patient with hemodynamic collapse due to a large PE, CTA is unlikely to miss the lesion. In a patient with pleuritic chest pain due to multiple small emboli that have lodged in distal vessels, CTA is more likely to miss the lesions, but these lesions also may be difficult to detect using conventional angiography.

Ongoing studies will determine whether the sensitivity and specificity of CTA are high enough to displace invasive angiography for the diagnosis of PE.

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Emergency Department Care:

Fibrinolytic therapy has been the standard of care for all patients with massive or unstable PE since the 1970s. Unless overwhelming contraindications are evident, a rapidly acting fibrinolytic agent should be administered immediately to every patient who has suffered any degree of hypotension or is significantly hypoxemic from PE.

Improvement of hypotension in response to hydration or pressors does not remove the indication for immediate fibrinolysis. The fact that hypotension has occurred at all is a sufficient indication that the patient has exhausted his or her cardiopulmonary reserves and is at high risk for sudden collapse and death.

Fibrinolysis also is strongly indicated for patients with PE who have any evidence of right heart strain, because substantial evidence indicates that the mortality rate can be cut in half by early fibrinolysis in this patient population.

Today, fibrinolysis should be considered for all patients with PE who lack specific contraindications to the therapy. Many centers now regard fibrinolysis as the primary treatment of choice for all patients with PE and even for all patients who have DVT without evidence of PE. Over the past 20 years, a large number of small studies and a small number of large studies have demonstrated consistently that fibrinolytic therapy dramatically reduces the mortality rate, morbidity, and rate of recurrence of PE regardless of the size or type of PE at the time of presentation.

Heparin reduces the mortality rate of PE because it slows or prevents clot progression and reduces the risk of further embolism. Heparin does nothing to dissolve clot that has developed already, but it is still the single most important treatment that can be provided, because the greatest contribution to the mortality rate is the ongoing embolization of new thrombi. Prompt effective anticoagulation has been shown to reduce the overall mortality rate from 30% to less than 10%.

Early heparin anticoagulation is so essential that heparin should be started as soon as the diagnosis of pulmonary thromboembolism is considered seriously. Anticoagulation should not wait for the results of diagnostic tests: if anticoagulation is delayed, venous thrombosis and PE may progress rapidly.

Oxygen should be administered to every patient with suspected PE, even when the arterial PO2 is perfectly normal, because increased alveolar oxygen may help to promote pulmonary vascular dilatation.

Compression stockings
Compression stockings that provide a 30-40 mm Hg compression gradient should be used, because they are a safe and effective adjunctive treatment that can limit or prevent extension of thrombus.

True gradient compression stockings (30-40 mm Hg or higher) are highly elastic, providing a gradient of compression that is highest at the toes and gradually decreases to the level of the thigh. This reduces capacitive venous volume by approximately 70% and increases the measured velocity of blood flow in the deep veins by a factor of 5 or more. Compression stockings of this type have been proven effective in the prophylaxis of thromboembolism and are also effective in preventing progression of thrombus in patients who already have DVT and PE.

A 1994 meta-analysis calculated a DVT risk odds ratio of 0.28 for gradient compression stockings (as compared to no prophylaxis) in patients undergoing abdominal surgery, gynecologic surgery, or neurosurgery.

Other studies have found that gradient compression stockings and low-molecular-weight heparin (LMWH) were the most effective modalities in reducing the incidence of DVT after hip surgery; they were more effective than subcutaneous unfractionated heparin, oral warfarin, dextran, or aspirin.

The ubiquitous white stockings known as "anti-embolic stockings" or "Ted hose" produce a maximum compression of 18 mm Hg. Ted hose rarely are fitted in such a way as to provide even that inadequate gradient compression. Because they provide such limited compression, they have no efficacy in the treatment of DVT and PE, nor have they been proven effective as prophylaxis against a recurrence.

True 30-40 mm Hg gradient compression pantyhose are available in sizes for pregnant women. They are recommended by many specialists for all pregnant women because they not only prevent DVT, but they also reduce or prevent the development of varicose veins during pregnancy.

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Medical/Legal Pitfalls:

Because PE is both extremely common and fairly difficult to diagnose, many patients are seen in the ED and later die from undiagnosed PE. In fact, respiratory complaints are the most common complaints in patients who are seen alive in the ED and later die unexpectedly.

A small number of often repeated mistakes in diagnosis and treatment are responsible for a large proportion of the bad outcomes with serious legal repercussions.

The most common and most serious of these errors are as follows:

  • Dismissing complaints of unexplained shortness of breath as anxiety or hyperventilation without an adequate workup
  • Dismissing complaints of unexplained chest pain as musculoskeletal pain without an adequate workup
  • Failure to properly diagnose and treat symptomatic DVT
  • Failure to recognize that DVT below the knee is just as serious as more proximal DVT
  • Failure to order a V/Q scan when a patient has symptoms consistent with PE
  • Failure to pursue the diagnosis after a V/Q scan that is not perfectly normal
  • Failure to start full-dose heparin at the first real suspicion of PE, before the V/Q scan
  • Failure to give fibrinolytic therapy immediately when a patient with PE becomes hemodynamically unstable

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Pulmonary embolism

Sudden lodgment of a blood clot in a pulmonary artery with subsequent obstruction of blood supply to the lung parenchyma.

Acute pulmonary embolism (PE) is a dynamic process. Thrombi (clots) begin to lyse immediately after reaching the lung. Usually, lysis is complete within several weeks in the absence of preexisting cardiopulmonary disease; in some instances, even large thrombi may lyse in a few days. The physiologic alterations lessen over hours or days as pulmonary circulation improves. However, massive emboli may cause death within minutes or hours, before infarction (dead blood vessel from clotting shutting off the flow) has time to develop. Infrequently, embolic events recur over a period of months or years, causing progressive pulmonary arterial obstruction with chronic pulmonary hypertension (inc blood pressure due to clot obstruction), increasing dyspnea, and cor pulmonale.

Symptoms and Signs

The clinical manifestations of PE are nonspecific and vary in frequency and intensity, depending on the extent of pulmonary vascular occlusion, preembolic cardiopulmonary function, and the development of PI (infarction). Small thromboemboli may be asymptomatic.

The manifestations of PE usually develop abruptly in minutes; those of PI, over a period of hours. They often last several days, depending on the rate of clot lysis and other factors, but usually decrease in intensity daily. In patients with chronic, recurrent small emboli, the symptoms and signs of chronic cor pulmonale tend to develop insidiously over weeks, months, or years.

Embolism without infarction causes breathlessness. Tachypnea is a consistent, often striking feature. Anxiety and restlessness may be prominent. (classic understatement in my opinion.)

Without infarction, the chest x-ray may be normal, or diminished pulmonary vascular markings in the embolized area may be noted. With infarction, the x-ray frequently shows a peripheral infiltrative lesion, often involving the costophrenic angle, with elevation of the diaphragm and pleural fluid on the affected side. Dilation of the pulmonary arteries in the hilar area, the superior vena cava, or the azygos vein signals pulmonary hypertension and right ventricular strain.

Anticoagulant therapy reduces the rate of recurrence to about 5%; only about 20% of these will be fatal.

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Links to other information on PE

Yahoo Health

Journal of American Medical Assoc (JAMA)

Controversies in PE

Mayo  Clinic


Virtual Hospital

XRAY Computed Tomgraphy of the Chest--the definitive diagnostic test (includes many beautiful images)

National Institute of Health

Google search on PE (type in pulmonary embolism)




Welcome to Airhealth.org Vacationing in Belize, Karen Perkins was in her scuba gear preparing for a dive, unaware that during her flight to Belize a blood clot had formed in her calf. As she kicked in the water, part of the clot passed through her heart, blocked her pulmonary artery, and she died. Her husband, Bradley Perkins, Vice President and General Counsel for Alliance Semiconductor Corporation, was on the dive boat but he could not save her; she had died almost instantly.

Really good website about PE from flying. Common misconceptions. Case histories. The dangers. How to avoid.

UK court clears way for airline blood clots action.

LONDON - A British court cleared the way Thursday for a class action suit against up to 30 airlines worldwide over blood clots suffered by passengers on long-haul flights, dubbed "economy class syndrome."

The airline industry, already in a financial tailspin from the global economic slowdown and the Sept. 11 attacks in the United States, could face millions of dollars in claims from hundreds of people around the world.

"We are delighted that the court has put in place the machinery to resolve this issue efficiently and effectively," said Des Collins, senior partner of the law firm representing the claimants.

Claimants argue that a combination of cramped flying conditions and long hours in the air give rise to the condition, formally known as deep vein thrombosis (DVT).

World airlines have said there is no definite proof linking DVT to air travel, but some have agreed to help a World Health Organization (WHO) study into whether a link exists.

The death of a 28-year-old woman after a flight from Australia to Britain in 2000 raised awareness of DVT and a number of incidents since have kept the issue in the headlines.

In July last year, Australian law firm Gordon & Slater launched suits against three international airlines -- KLM Royal Dutch Airlines, British Airways and Qantas Airways -- and Australia's air authority CASA.

At Thursday's hearing in London, lawyers representing both sides effectively agreed on a draft order to open the class action at England's High Court in London.

"The sooner we get this action properly constituted within the framework of a group litigation order the better," said Master Turner, a senior high court official.

The court will now seek approval of the draft order from the Lord Chief Justice of England before the legal battle begins later this year.

Lyn Walcott of Essex, whose husband died after a flight to Barbados in October 2000, will be the first claim in the class action to be served by Feb. 7, said Collins's lawyer Stuart Cakebread, adding that the number of claims was approaching 300.

The airlines will turn to the 1929 Warsaw Convention on air travel. The convention states that a carrier is only liable for damage to a passenger in an accident sustained while a passenger is aboard the aircraft or in the course of getting on or off the aircraft.

Robert Lawson, a lawyer for some of the airlines, told the court Thursday the "only true group issue" at the moment was whether DVT amounted to an accident under the convention.

But Colin Hall, the managing director of aviation analysts Avmark
International, said that several courts in the United States had overruled the convention on other issues.

"The Warsaw Convention is not a protection of all airlines' legal
liabilities. It helps but it's not a coverall," Hall said.

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