Pulmonary embolism fatal

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. 

Hull RD, Hirsh J, Sackett DL, et al. Cost-effectiveness of primary and secondary prevention of fatal pulmonary embolism in high-risk surgical patients. CMAf 1982 127 990-5. 

Venous stasis resulting from prolonged bed rest, cardiac failure, or pelvic, abdominal, or hip surgery may precipitate thrombus formation in the deep veins of the leg or calf and may lead to fatal pulmonary embolism. Heparin may also be used prophylactically following surgery. 

Thrombotic (blood clot) events, and subsequent complications, are a leading cause of morbidity and mortality in the general population.1 In 2005, it was estimated that there were more than 900,000 total venous thromboembolism events in the United States,2 two thirds of which were acquired in hospital. More than 600,000 of those were nonfatal venous thromboembolism events. Nearly 300,000 were fatal events, including more than 2,200 cases of deep venous thrombosis and 294,000 cases of pulmonary embolism. The majority deaths (93%) were due to sudden fatal pulmonary embolism, or were a consequence of undiagnosed venous thromboembolism. It was estimated that 340,000 patients developed complications from venous thromboembolism, including 336,000 with postthrombotic syndrome and 3,300 with chronic thromboembolic pulmonary hypertension. 

As of 31 December 1993, there were 18 cases of fatal pulmonary embolism in association with clozapine therapy in users aged 10-54 years. Based on the extent of use recorded in the Clozapine National Registry, the mortality rate associated with pulmonary embolism was 1 death per 3450 person years of use. This rate was about 28 times higher than that in the general population of a similar age and sex (95% Cl = 17,42). Whether pulmonary embolism can be attributed to clozapine or some characteristic(s) of its users is not clear (53). 

Fatal pulmonary embolism occurred in a 29-year-old man who was not obese, did not smoke, and had not had recent surgery, after he had taken clozapine 300 mg/day... 

Collins R,Scrimgeour A, Yusuf S,PetoR. Reduction in fatal pulmonary embolism and venous thrombosis... 

Grimm W, Schwieder G, Wagner T. Todliche Lungenembolie bei Bein-Beckenvenenthrombose unter Lysetherapie. [Fatal pulmonary embolism in venous thrombosis of the leg and pelvis during lysis therapy.] Dtsch Med Wochenschr 1990 115(31-32) 183-7. 

Typical barium suspensions range from 31) to more than 120% weight/volume (w/v). and because they are eolloidal suspensions, they cannot be given intruvaseularly the colloidal particles would produce fatal pulmonary embolism. Tlie barium suspensions used for UGI or BE studies are too dense to be u.sed for gut opacification during CT studies of the abdomen, because they produce unacceptable radiographic artifacts. Instead, commercial barium preparations are diluted to I to 4% w/v. 

I Databases can be linked by computer, e.g. people exposed to a particular product, and people admitted to hospital with a particular problem. Linking a national registry of clozapine recipients to national death records found that clozapine increased the risk of fatal pulmonary embolism and respiratory disorders but reduced the risk of stticide. 

A number of drugs have been developed that inhibit the blood coagulation cascade. Snch drngs are nseful in cases in which patients develop sponta-neons thrombi, which, if left untreated, wonld result in a fatal pulmonary embolism. There are three major classes of snch drngs the heparins, vitamin K antagonists, and specific inhibitors of thrombin. 

It was possible to reduce fatal pulmonary embolism with Dextran 70 infusion by more than 20%. In 2011 patients under dextran prophylaxis, 8 cases of fatal complications were found, as opposed to 1797 controls with 36 exitus, where pulmonary embolism was diagnosed by post-mortem examination (29 ). 

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. 

Cl 0.08-0.96) and symptomatic pulmonary embolism (PE) (OR 0.34, 95% Cl 0.17-0.69), but an increase in major extracranial hemorrhage when compared to placebo (OR 2.17, 95% Cl 1.10. 28). Nonsignificant reductions in combined death and disability, as well as increases in case fatality and sICH were also observed. The authors concluded that insufficient evidence existed to support the routine use of LMWH in the management of patients with ischemic stroke. 

Hedenmalm K, Samuelsson E, Spigset O. Pulmonary embolism associated with combined oral contraceptives reporting incidences and potential risk factors for a fatal outcome. Acta Obstet Gynecol Scand 2004 83 576-85. 

The goal in the treatment of deep venous thrombosis and pulmonary embolism is the prevention of recurrent, fatal embolism. 

In a placebo-controlled study of severely anemic patients with low-grade non-Hodgkin s lymphoma, chronic lymphocytic leukemia, or multiple myeloma, a fatal case of pulmonary embolism was thought to have been related to treatment with epoetin beta (95). Thrombotic events, such as vascular access thrombosis, venous thrombosis, and pulmonary embolism, have occurred after treatment with epoetin or darbepoetin alfa (96). It is therefore recommended that a rapid rise in the hemoglobin concentration be avoided and that care should be taken that the hemoglobin concentration does not exceed 12.1 g/dl (7.5 mmol/1) (97). 

Several reviews of the adverse effects of vitamin E have been published (3,4), especially relating to premature infants (5), in whom high doses have been associated with infectious complications and fatal hepatic failure. In adults, thrombophlebitis, thromboembolism, pulmonary embolism, hypertension, fatigue, gynecomastia, and breast tumors have been described as particularly serious effects of vitamin E, but there is little evidence about their frequency. Diarrhea and abdominal pain can occur. For some of these effects there seems to be a dose relation. A dose of 800 mg/day for 30 days had no reported adverse effects in healthy elderly subjects (6). Table 1 shows reported adverse effects related to dosage in a review of about 50 publications on vitamin E (7). 

Niacin in the CDP significantly reduced definite, nonfatal MI as compared with placebo (10.1% versus 13.9%), whereas clofibrate did not reduce death from any cause or nonfatal or fatal MI at the 5-year follow-up period. Clofibrate did increase the rate of definite or suspected fatal or nonfatal pulmonary embolism or thrombophlebitis compared with placebo (5.8% versus 3.6%) after adjusting for baseline characteristics for total follow-up. Other findings with clofibrate that occurred more frequently than with placebo included intermittent claudication, arrhythmias, palpable spleen, cholelithiasis (including cholecystectomy), and more frequent use of anticoagulants. Skin reactions, gastrointestinal complaints, and the use of gout... 

Heydrich s clinical course does not explain his death. Although infection was likely to accompany his injury, his sudden deterioration and death do not conform to the usual expression of fatal sepsis. It is noteworthy that infection was not a prominent finding at autopsy. Heydrich s death is actually much more suggestive of a massive pulmonary embolism, yet his heart and lungs were said to be normal.1... 

A therapeutic regimen that usually controls haemorrhage involves discontinuation of enzyme treatment, administration of e-aminocaproic acid in a dose of 100 mg/kg body weight by slow intravenous injection, and blood transfusion (F). It is important to remember that the risk of thrombolytic therapy is not only haemorrhage but also thromboembolism. In one group of 93 patients with deep vein thrombosis treated by streptokinase infusion, a patient died of pulmonary embolism 8% of the patients in all experienced a less serious embolism (11 ). Eight cases of embolism, 4 of them with a fatal outcome, were seen in a series of 80 treated with streptokinase (18 ). 

Dextran 70 has proved its effectiveness in preventing pulmonary embolism and, in particular, has reduced mortality from this cause. In a comparative double-blind trial of prophylaxis of thromboembolism in surgical patients, 435 received saline infusions, out of which 13 developed pulmonary embolism and 7 were fatal. In the Dextran 70 series, 396 were treated, 3 developed embolism, 1 died. The incidence of deep vein thrombosis was similar in the 2 groups (28 ). 

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