Pulmonary thrombosis

SuccessM treatment of PEA and asystole depends almost entirely on diagnosis of the underlying cause. Potentially reversible causes include (1) hypovolemia, (2) hypoxia, (3) preexisting acidosis, (4) hyperkalemia, (5) hypothermia, (6) hypoglycemia, (7) drug overdose, (8) cardiac tamponade, (9) tension pneumothorax, (10) coronary thrombosis, (11) pulmonary thrombosis, and (12) trauma. 

The use of BRMs to treat human disease has its origins in the use of bacterial toxins to treat cancer by William B. Coley.73 These early studies resulted in the use of microbi-ally-derived substances such as BCG, Picibanil, carbohydrates from plants or fungi such as Krestin and Lentinan, other products such as Biostim and Broncho-Vaxom, as well as thymic extracts (Table 9.4). However, the lot-to-lot variation in the manufacture of these drugs has dampened enthusiasm. Equally, the focus on MOAs in drug development strategies has also dampened developmental efforts. The particulate nature of some BRMs can also result in pulmonary thrombosis and respiratory distress following i.v. injection. However, BRMs are commonly used to treat bladder cancer and derivatives of natural products are routinely used clinically. 

Pulmonary thrombosis History, no pulse with CPR, distended neck veins Pulmonary arteriogram, surgical embolectomy, thrombolytics... 

Serotonin has been found to exert an intense vasoconstrictor effect on the pulmonary circulation 1 . Although the pulmonary vasoconstrictor effect of serotonin can be demonstrated easily by pharmacological methods, its physiological and pathophysiological roles have not been unequivocally demonstrated. In fact, the infusion of serotonin (1. 85 - 5. 5 mcg/kg/min) into the pulmonary artery of seven human subjects produced a definite rise in pulmonary artery pressure in only one instancel. Most of the serotonin found in whole blood is stored in platelets. This would imply that in the process of platelet aggregation to form a thrombus, serotonin would be available for release . Pulmonary vasoconstriction does occur as a result of pulmonary thrombosis. A further indication that serotonin could be implicated in the thrombosis-induced pulmonary vasoconstriction is the finding that 82 per cent of serotonin can be released from platelets by thrombin in five minutes. ... 

Pulmonary vascular hypertension Chronic pulmonary thrombosis Arteriovenous malformations Nonpuhnonary diseases Severe heart failure Hepatopulmonary syndrome... 

Deficiency of Factor VII is relatively rare and inherited as an autosomal recessive disorder. Deficiency of Factor VII has been reported to be associated with bond abnormal bleeding and thrombotic tendencies. Deep vein thrombosis and pulmonary emboli have been reported in affected individuals. There is a very high frequency of Factor VII deficiency in people with the Dubin-Johnson syndrome, which is a congenital disorder of Hver function. 

Indications for treatment with streptokinase include acute occlusion of arteries, deep vein thrombosis, and pulmonary embolism. Streptokinase therapy in coronary thrombosis, which is the usual cause of myocardial infarction (54,71,72), has proved to be valuable. In this frequently fatal condition, the enzyme is adrninistered intravenously at a dose of 1.5 million units over 60 min, or given by intracoronary infusion at a 20,000- to 50,000-unit bolus dose followed by 2000 to 4000 units/min for 60 min therapy must be instituted as soon as practicable after the diagnosis of heart attack is made. For deep vein thrombosis, pulmonary embolism, or arterial occlusion, streptokinase is infused at a loading dose of 250,000 units given over 30 min, followed by a maintenance dose of 100,000 units over a 60-min period. 

In general, arterial thrombi are platelet-rich ( white clots ) and form at ruptured atherosclerotic plaques, leading to intraluminal occlusion of arteries that can result in end-organ injury (e.g., myocardial infarction, stroke). In contrast, venous thrombi consist mainly of fibrin and red blood cells ( red clots ), and usually form in low-flow veins of the limbs, producing deep vein thrombosis (DVT) the major threat to life results when lower extremity (and, occasionally, upper extremity) venous thrombi embolize via the right heart chambers into the pulmonary arteries, i.e., pulmonary embolism (PE). 

Mild diarrhea and itching have been reported with the administration of vitamin B12. Other adverse reactions that may be seen include a marked increase in RBC production, acne, peripheral vascular thrombosis, congestive heart failure, and pulmonary edema... 

Many serious health problems result from abnormally located blood clots heart attacks (clots in coronary arteries), pulmonary embolism (clots in the lungs), and peripheral arterial occlusion and deep vein thrombosis (clots in the limbs). Each year heart attacks alone afflict over a million people in the United States, and almost half of them die as a result. 

Heparin and warfarin are widely used in the treatment of thrombotic and thromboembolic conditions, such as deep vein thrombosis and pulmonary embolus. Heparin is administered first, because of its prompt onset of action, whereas warfarin takes several days to reach full effect. Their effects are closely monitored by use of appropriate tests of coagulation (see below) because of the risk of producing hemorrhage. 

Streptokinase is administered by intravenous or intra-arterial infusion in the treatment of thrombo-embolic disorders, e g. pulmonary embolism, deep-vein thrombosis and arterial occlusiorrs. It is also used in acute myocardial irtfarclioa... 

Kamphuisen PW, Agnelli G. What is the optimal pharmacological prophylaxis for the prevention of deep-vein thrombosis and pulmonary embolism in patients with acute ischemic stroke Thromb Res 2007 119(3) 265-274. 

Management of Deep-Vein Thrombosis and Pulmonary Embolism... 

Monitor for evidence of cerebral edema, noncardiogenic (permeability) pulmonary edema, acute respiratory distress syndrome, hyperchloremic metabolic acidosis, and vascular thrombosis... 

Streptokinase + 35% +++/+ Infusion over 60 minutes 613 Pulmonary embolism, deep vein thrombosis, arterial thromboembol ism, clearance of an occluded arteriovenous catheter... 

Identify risk factors and signs and symptoms of deep vein thrombosis and pulmonary embolism. 

Venous thromboembolism (VTE) is one of the most common cardiovascular disorders in the United States. VTE is manifested as deep vein thrombosis (DVT) and pulmonary embolism (PE) resulting from thrombus formation in the venous circulation (Fig. 7-1).1 It is often provoked by prolonged immobility and vascular injury and is most frequently seen in patients who have been hospitalized for a serious medical illness, trauma, or major surgery. VTE can also occur with little or no provocation in patients who have an underlying hypercoagulable disorder. 

DVT, deep vein thrombosis HIT, heparin-induced thrombocytopenia PAI-I, plasminogen activator inhibitor PE, pulmonary embolism SERM, selective estrogen receptor modulator VTE, venous thromboembolism. 

Pulmonary hypertension develops late in the course of COPD, usually after the development of severe hypoxemia. It is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. Hypoxemia plays the primary role in the development of pulmonary hypertension by causing vasoconstriction of the pulmonary arteries and by promoting vessel wall remodeling. Destruction of the pulmonary capillary bed by emphysema further contributes by increasing the pressure required to perfuse the pulmonary vascular bed. Cor pulmonale is associated with venous stasis and thrombosis that may result in pulmonary embolism. Another important systemic effect is the progressive loss of skeletal muscle mass, which contributes to exercise limitations and declining health status. 

The WHI demonstrated an increased risk in venous thromboembolic disease in the HRT group (0.34%) compared with placebo (0.16%) (HR 2.11,95% Cl 1.58-2.82). This translates into an NNTH of approximately 555 and 18 more cases of venous thromboembolic events for every 10,000 women treated per year with HRT.3 The risk for deep vein thrombosis also was increased in the ERT arm of the WHI, but pulmonary embolism was not increased significantly.21... 

Lenalidomide was approved recently for the indication of myelodysplastic syndrome where the 5q deletion is present. Since lenalidomide is an analog of thalidomide, all the same precautions must be taken to prevent phocomelia. The time to maximum lenalidomide concentrations occurs 0.5 to 4 hours after the dose. The terminal half-life ranges from 3 to 9 hours. Approximately 65% of lenalidomide is eliminated unchanged in the urine, with clearance exceeding the glomerular filtration rate. To date, no pharmacokinetic studies have been done in patients with renal dysfunction. Lenalidomide is used in the treatment of myelodysplastic syndrome and multiple myeloma. Other side effects are neutropenia, thrombocytopenia, deep vein thrombosis, and pulmonary embolus. 

Lenalidomide (Revlimid) Possible birth defects (since analogue of thalidomide), neutropenia, thrombocytopenia, deep vein thrombosis, pulmonary embolism, pruritis, fatigue Dose is 10 mg orally taken with water once daily Women of childbearing age must use two forms of contraception Pregnancy test must be taken before and during use... 

By far the most widely measured marker of hemostatic activation is D-dimer, which is a product formed by the action of plasmin on cross-linked fibrin (95). D-dimer levels in plasma are generally elevated in DIC. The consumption of platelets and coagulation proteins as a result of thrombin generation leads to the deposition of fibrin thrombi at multiple organ sites. This triggers fibrinolysis with an increase in the formation of fibrin degradation products, which can cause bleeding at multiple sites. Because DIC can have a variety of causes and may coexist with systemic fibrinolysis, such as in pulmonary embolism or deep vein thrombosis, the d-Dimer test is not specific for DIC (95). 

Collins R., Scrimgeour A., Yusuf S Peto R. Reduction in fatal pulmonary embolism and venous thrombosis by perioperative administration of subcutaneous heparin Overview of results of randomized trials in general, orthopedic, and urologic surgery. N Engl J Med 1988 318, 1162-73. 

Eriksson B. I., Kalebo P Anthmyr B. A., et al. Prevention of deep-vein thrombosis and pulmonary embolism after total hip replacement. Comparison of low molecular weight heparin and unfractionated heparin. J Bone Joint Surg [Am] 1991 73A, 484-93. 

POEMS is an eponym applied to patients with a variety of plasma cell dyscrasias who present with polyneuropathy, organomegaly, endocrinopathy, an M protein and skin changes this disorder is also referred to as Crow-Fukase syndrome. Additional manifestations of this disorder are pulmonary hypertension, renal failure, a predisposition to thrombosis and congestive heart failure some of these features are likely to be attributable to vascular endothelial growth factor (VEGF) and matrix metalloproteinases, which are often elevated in the plasma of these patients [43]. 

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