D Asudani, D Manwani, D Arora
internal medicine, medicine
D Asudani, D Manwani, D Arora. Pulmonary Embolus: The Wrong Thing On The Wrong Journey. The Internet Journal of Internal Medicine. 2000 Volume 2 Number 2.
While it may not be possible to obtain the correct
figures worldwide, it certainly is a matter of grave concern that a large
number of people loose their lives cheaply. While majority emboli are small,
the larger ones have an acute course and may lead to cor pulmonale and
death. Pulmonary embolus, put simply, is "body friendly blood cells getting
together for some sort of a meeting and forming a thrombus; and this
thrombus suddenly decides to go out for a roller coaster ride in the
vasculature", which for 10% of people turns out to be fatal. Of the people
who survive, as many a third will have their thrombi going for a second
While it may not be possible to obtain the correct figures worldwide, it certainly is a matter of grave concern that a large number of people loose their lives cheaply. While majority emboli are small, the larger ones have an acute course and may lead to cor pulmonale and death. Pulmonary embolus, put simply, is
Pulmonary embolism put simply is the lodging of a thrombus in the pulmonary artery or its branches. Before considering the various aspects, it will be useful to deal with the differences between a clot and a thrombus. A clot is a cast, which sets in the vessel, post mortem due to the settling of blood constituents. A thrombus (which potentially can embolize), on the other hand is the deposition of the platelets and red cells in the vessel ante mortem. Currant jelly appearance of a clot is due to settling of red cells in the dependent parts of the vessel, while chicken fat comprises of the serum so separated. Lines of Zahn are the concentric entanglements of platelets in a thrombus. Clots do not adhere to the vessel wall, while thrombi do. It is such thrombi, which when become friable get dislodged and travel in the vasculature.
Pulmonary arteries (main or its peripheral branches) almost always get occluded following the lodging of embolus coming from the deep venous system of the lower extremities. An overwhelming majority (more than 95%) of the emboli have their origin in deep veins of lower extremities and peri pelvic plexus. The incidence of PE is highly variable with respect to whether general population or hospitalized population is being looked at. Autopsy findings suggest the incidence to be about 30% in patients with burns or major trauma. About two thirds of autopsies of patients who were hospitalized have shown to have PE. Prolonged hospitalization or convalescence is certainly a major cause of PE. Other causes include long hours of driving, hyper coagulable states, burns etc. One in ten victims loses his life to PE and of the surviving patients, a third get PE again.
As is evident a vast majority of emboli have their origin in the deep venous system, in the form of a thrombus,
Deficiency of Protein C or Protein S is one of the many reasons the blood goes disobedient. Autosomal Dominant in inheritance, this state prevents adequate inactivation of Factors Va and VIIIa.
Deficiency of anti thrombin III is also autosomal dominant. Anti thrombin III (ATIII) is responsible for keeping a check on thrombin and activated forms of Factor IX and X. When ATIII is inadequate quantitatively or qualitatively, the thrombus formation is promoted.
Disseminated cancers, paraneoplastic conditions, blood dyscrasias (polycythemia, thrombocytosis etc.) also cause hypercoagulability.
The use of Estrogens is also associated with Hypercoagulable State due to lowered ATIII concentrations and increased concentrations of coagulating factors.
Physiological states like pregnancy, smoking and advanced ages are also predisposing factors.
While formation of the embolus is the event, we are mainly concerned here, it is important to appreciate that thrombi are more likely to be cleared by the fibrinolytic activity. Other fates of thrombi are recanalization and propagation.
The course is primarily influenced by the size of the embolus and the site it occludes. Prior cardiopulmonary status also dictates the clinical course.
Clinically, the incidence of symptoms and signs of angiographically proven PE suggests the following distribution:
A large number of lives are lost due to delayed diagnosis and the acute course of large embolus. Unfortunately,
The most prudent diagnostic tool for a provisional diagnosis appears to be the history. However, history only contributes in making a diagnosis; a thorough work up is required for a final diagnosis. Knowledge about patient having undergone some surgery or being immobilized on some account is certainly desirable. Any family history of hypercoagulable states, history of long distance travels, cancers, pregnancy, use of contraceptive pills etc. contribute in arriving at a conclusion. Radiologic techniques remain the mainstays of diagnoses. . For the diagnosis of DVT, venography is the gold standard.
Prevention and Treatment
When a patient is identified to be at risk, appropriate antithrombotic measures should be instituted. Administration of heparin remains the mainstay of treatment, anticoagulation is desirable in appropriate patients.
For the prevention of PE, the risk factors need to be identified. As obesity & smoking are identified risk factors, weight loss and smoking cessation are recommended. An obese patient or a lady who is at risk of DVT should consider contraceptive methods other than Estrogen containing pills. It is important to emphasize role of frequent moving of immobilized patient. Early ambulation helps avert development of PE. Long journeys need to be interrupted to avoid stasis. If at increased risk, prophylactic low dose heparin is administered before surgery. Elastic stockings & isometric exercises are also recommended post op. Insertion of venous filter may be considered in appropriate candidates. However, PE continues to be a significant cause of mortality and it is desirable that an early diagnoses and emergent management be done. If hypercoagulable states or other risk factors are identified, it is extremely important to prevent blood cells to get rebellious and make thrombi which I due course can dictate cor pulmonale and death; which in many cases can be achieved with adequate prophylactic measures.
(DISCLAIMER: The authors do not intend to recommend any self-medication. The references made to medical or surgical interventions or any alterations in lifestyle are a part of this paper and should be resorted to only under supervision. Authors are not responsible for any damages whatsoever that might arise out of any injudicious step taken by the reader).
Dr. Deepak Asudani
3/9, Mahi Colony,
Dr. Arushi Manwani
B-30/2, East of Kailash,
Dr. Neha Arora
61 Type IV/Sector III,