What Is Pulmonary Embolism;Causes,Symptoms,Treatment And Prevention

Pulmonary embolism is a blockage of one or more arteries of the lungs caused by fat, air, blood clot or cancer cells.Because the lung has a dual blood supply, most pulmonary emboli do not lead to infarction.Pulmonary embolism can also lead to pulmonary hypertension, a condition in which blood pressure in the lungs and the right side of the heart is higher than normal. When there are obstructions in the arteries of the lungs, the heart has to work harder to push the blood through these vessels. This increases blood pressure within these vessels.

What Is Pulmonary Embolism;Causes,Symptoms,Treatment And Prevention

Etiology  of Pulmonary Embolism.

The predisposing factors can be grouped in the manner originally suggested by Virchow in 1856: stasis, vein injury, and hypercoagulability. Stasis occurs with immobilization, obesity, varicose veins, congestive heart failure, and pregnancy. Vein injury occurs with surgery, trauma, and bums. The exact definition of hypercoagulability is controversial; in a broad sense it is an altered state of the coagulation system predisposing to the development of thrombus. Hypercoagulability may exist with carcinoma, polycythemia rubra vera, hemolytic anemia, splenectomy with thrombocytosis, homocystinuria, and perhaps use of oral contraceptives.

Recurrent venous thromboembolism is known to occur with abnormalities of platelets, of the coagulation cascade, and of spontaneous fibrinolysis. Some patients have been reported to have increased platelet adhesiveness and decreased platelet survival. Increased venous thrombosis has occurred in association with large increases in factor V or VIII, abnormal fibrinogens, and antithrombin III deficiency. Recurrent venous thromboembolism has also been associated with both a decrease in plasminogen activator in venous endothelium and a decrease in the release of plasminogen activator with various stimuli. Increased inhibitors of plasmin or plasminogen activators as well as abnormal plasminogens are relatively rare predisposing factors.

CAUSES OF PULMONARY EMBOLISM

The main cause of pulmonary embolism is emboli originating from thromboses in the veins of the lower limbs, a condition called deep venous thrombosis (DVT). They are pieces of thrombus from the veins of the legs, thighs or pelvis that usually embolize to the lungs.

What Is Pulmonary Embolism;Causes,Symptoms,Treatment And Prevention

Consequently, the risk factors for DVT also end up being risk factors for pulmonary embolism. Are they:

  • Obesity.
  • Smoking
  • Varicose veins and venous insufficiency of the lower limbs
  • Cancer (read:
  • Advanced age.
  • Heart Failure
  • Nephrotic syndrome
  • Pregnancy.
  • Contraceptive pill
  • Hormone replacement.
  • Use of tamoxifen or raloxifene.
  • Thrombophilia (coagulation disorders such as antiphospholipid antibody).
  • Prolonged detention, such as in the case of people in bed or long plane trips
  • Surgeries, especially of the hip or lower limbs.

Symptoms of Pulmonary Embolism

Symptoms of pulmonary embolism usually vary, depending on the number of arterial blocks and what parts of the lung are involved. The main symptoms of pulmonary embolism are:

Pain under the sternum or on one side of this, which can:

  • Being sharp or penetrating
  • Being described as a burning sensation, pain, numbness or weight
  • Worse when the subject breathes deeply, coughs, eats or bows
  • Have the patient bend or hold his or her chest in response to pain.

In addition, the patient may present:

  • Sudden coughing, expectoration of blood or bloody sputum
  • Quick Breathing
  • High heart rate
  • Sudden respiratory failure.

Treatment of Pulmonary Embolism.

Anticoagulation with Heparin.

Without anticoagulation, recurrence rates of pulmonary embolism are between 30 and 50 per cent and up to half the recurrences are fatal. Therefore, a rapidly acting anticoagulant, intravenous heparin, is commonly utilized initially for ten days while starting an oral anticoagulant such as warfarin on the fifth day. Intermittent intravenous heparin has been reported to be associated with significantly more major bleeding complications (around 15 per cent) than has continuous intravenous heparin (around 1 per cent).

Whether these differences are due to the method of administration or the total daily dose is not clear, since larger doses of heparin are required to keep an activated partial thromboplastin time (APTT) or a I.ee-White clotting time in the range of 1.5 to 2.5 times normal by the intermittent route (approximately 36,000 units per day) than by the continuous route (approximately 25,000 units per day). However, a more recent study, which was restricted to patients with objective diagnostic tests confirming pulmonary embolism or deep venous thrombosis, has found a significantly higher recurrence rate with continuous heparin (27 per cent) than with intermittent heparin (3 per cent).

There are several important factors associated with increased risk for bleeding complications during therapy with intermittent heparin: (1) age greater than 60 years, (2) abnormal prothrombin time, APTT, or platelet count, (3) uremia, (4) alcoholic liver disease, (5) recent surgery (within two weeks), (6) previous gastrointestinal bleeding within six months, (7) severe systemic hypertension with diastolic pressure greater than 110, or (8) massive pulmonary embolism with severe pulmonary hypertension.

If a patient with a risk factor for bleeding is to be treated with intermittent heparin, it is wise to use a lower dose and to keep the APTT or Lee-White clotting time no more than 1.5 times normal just before the next dose is due. If continuous heparin is used, larger doses should probably be used to push the activated APTr or Lee-White clotting time closer to 2.5 times normal. Higher doses may reduce the recurrence rate with continuous heparin but unfortunately will likely produce more major bleeding complications. Continuous heparin in an average dose of 33,000 units per day has been reported to have a major bleeding complication rate of 15 per cent.

Long-Term Therapy Treatment of Pulmonary Embolism

There are no randomized prospective tnals comparing long-term anticoagulation with no anticoagu-lation following ten days of heparin therapy for pulmonary embolism. The best estimates are that orai anticoagulation produces its maximal benefit within the first six weeks, but is probably worthwhile for at least three months. Whether longterm anticoagulative regimens that are effective following acute deep venous thrombosis will be effective following acute pulmonary embolism is unknown. After 10 days of continuous intravenous heparin therapy of acute deep venous thrombosis, the following treatment regimens are effective with minimal bleeding complications: (1) Subcutaneous heparin every 12 hours with dose tailored to prolong APTT to 1.5 times normal six hours after injection. (2) Less intense oral warfann with therapeutic goal of a simplastin prothrombin time of about 15 seconds with a control of 12 seconds.

Oral anticoagulation with warfarin and the usual therapeutic goal of simplastin prothrombin time of about 20 seconds with control of 12 seconds is very effective in preventing recurrence of deep venous thrombosis but has major bleeding complications of about 4 to 12 per cent despite the best control possible. Low dose subcutaneous hepann in a dose of 5000 units every 12 hours following 10 days of continuing intravenous hepann for deep venous thrombosis has almost no bleeding complications but is associated with a recurrence rate of about 25 per cent. In recurrent deep venous thrombosis, low dose subcutaneous hepann and conventional oral anticoaguiation with warfann are frequently ineffective, with recurrence rates of over 25 per cent. In these patients antiplatelet drugs with aspirin* 1200 mg per day and dipyridamole* 100 mg per day significantly reduce recurrences. Whether the antiplatelet drug would be effective in recurrent pulmonary embolism despite oral anticoaguiation is unknown.

Prevention of Pulmonary Embolism.

Low dose subcutaneous heparin (5000 units twice per day) significantly reduces the incidence of deep venous thrombosis and deaths from pulmonary embolism associated with major surgery. Low dose heparin also appears to be effective following myocardial infarction, but not after operations that are more traumatic such as total hip replacement. Patients undergoing major surgery who are at high risk for developing venous thromboembolism should receive low dose heparin prophylactic. The high risk factors include age over 40 years, malignancy, marked obesity, varicose veins, and history of previous deep venous thrombosis or pulmonary embolism.

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