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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Use of a protocol for pharmacist determination of heparin sodium dosages administered by continuous i.v. infusion was evaluated by retrospective chart review in a California hospital. Charts of adult medical-surgical patients who received heparin infusions between June 1982 and December 1983 were reviewed for the following information: patient sex, age, and reason for receiving heparin; times, dates, numbers, and values of coagulation tests before and during heparin therapy; times, dates, and values of prothrombin time determinations during conversion to warfarin therapy; and times, number, and costs of heparin infusions. Charts were divided into two groups: those of patients for whom physicians prescribed heparin doses empirically and those of patients for whom physicians requested heparin dosing by the pharmacy department. Data were evaluated for 62 patients in the physician-dosed group and 26 patients in the pharmacy protocol group. Pulmonary embolism was the reason for heparin therapy in 34% of the physician-dosed patients and only 15% of the pharmacist-dosed patients. Pharmacists using the protocol ordered fewer anticoagulation tests and fewer heparin infusions per patient. Time from the start of heparin therapy to therapeutic anticoagulation was shorter in patients whose heparin dose was determined by the protocol, and values in the therapeutic range were achieved in a greater percentage of these patients than in the empirically dosed patients. Pharmacists using a standard dosing protocol effectively initiated and maintained heparin therapy that compared favorably with physician-dosed empiric therapy.
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PMID:Pharmacist-directed heparin therapy using a standard dosing and monitoring protocol. 405 Aug 13

Eight patients with massive pulmonary thromboembolism documented by angiography were treated with Urokinase (UK) 4.400 IU/Kg/hr for 12 hours. UK i.v. infusion was started immediately after angiographic evaluation (Miller index) and was followed by anticoagulant therapy with heparin and sodium warfarin. All patients survived even though 4 pts. were in shock before treatment. Significant reduction of pulmonary obstruction (reduction of Miller index) was obtained in 7 patients with 48 hours from withdrawal of the drug. Mild superficial bleedings which did not influence the clinical course were the only complication recorded. Neither bleedings nor angiographic improvement showed a correlation with thrombin time prolongation. Indications for thrombolytic therapy of pulmonary embolism and particularly prevention of the major haemorrhagic complications are briefly discussed. It is concluded that the high doses of UK suggested by Food and Drug Administration may be used safely in patients affected by massive pulmonary thromboembolism with or without shock, if patients are adequately selected and prevention of major haemorrhagic complications is continued throughout treatment.
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PMID:[Thrombolytic therapy with urokinase in 8 patients with massive pulmonary thromboembolism]. 409 13

Low-dose heparin prophylaxis against fatal pulmonary embolism has been studied in a random and prospective trial in 300 patients over the age of 50 who underwent major surgery. A dose of 5,000 IU mucous heparin sodium given two hours preoperatively and for five days post operatively prevented fatal pulmonary embolism in all 156 patients so treated, whereas out of 144 patients in the unheparinized group 6 (4.2%) died of pulmonary embolism. This difference is statistically significant. There was no increase in operative or post-operative bleeding or in the formation of wound haematomas in the heparinized group.
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PMID:Heparin prophylaxis against fatal postoperative pulmonary embolism. 482 14

Fibrinogen degradation, fibrin polymerisation, and the insertion of cross links into fibrin by fibrin stabilising factor lead to the appearance of new antigenic determinants. Antibodies against these antigenic sites may react specifically with the derivatives but not with the parent molecules. We have utilised a monoclonal antibody, which interacts with the cross linked fragment D dimer and related high molecular weight fibrin derivatives, to develop an enzyme immunoassay which measures cross linked fibrin derivatives in plasma and serum using D dimer as standard. Mean concentration in plasma from normal subjects was 75 ng/ml with an upper limit of about 144 ng/ml. Concentrations in patients with pulmonary embolism, deep venous thrombosis, arterial thromboembolism, and disseminated intravascular coagulation were raised in all cases. Confirmation of the specific increase of cross linked fibrin derivatives in patients with disseminated intravascular coagulation was obtained by parallel monitoring of their fibrin degradation products in serum using affinity chromatography and sodium dodecyl sulphate (SDS) polyacrylamide gel electrophoresis. In many patients the plasma concentrations greatly exceeded the serum values of cross linked fibrin degradation products, suggesting that the procedure can measure fibrin derivatives in plasma which are absent from serum.
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PMID:Measurement of cross linked fibrin derivatives in plasma: an immunoassay using monoclonal antibodies. 620 97

A prospective study was performed in 120 patients undergoing total hip arthroplasty. The patients were randomly allocated to four groups. The first two groups had nitroprusside-induced hypotensive anesthesia with either a fixed combination of sodium heparin and dihydroergotamine mesylate (HDHE) or dextran 70. The other two groups had normotensive halothane anesthesia with either HDHE or preoperative hemodilution with dextran 70. Hypotensive anesthesia reduced surgical bleeding. Blood loss was increased in patients undergoing preoperative hemodilution as compared to thromboprophylaxis with HDHE, whereas no difference was found between conventional administration of dextran and HDHE. Deep vein thrombosis, diagnosed with ascending phlebography of the operated leg, was registered in 48% of the patients. There was no difference between the techniques of anesthesia and thromboprophylaxis. Pulmonary embolism, studied with perfusion-ventilation scintigraphy, was diagnosed in 19% of the patients. No significant difference was found between hypotensive and normotensive anesthesia, or between thromboprophylaxis with conventional dextran and HDHE. There was a lower incidence of pulmonary embolism in patients with HDHE and normotensive anesthesia. Major wound hematomas were noted postoperatively in 12% of the patients receiving HDHE, whereas no major hematomas developed following dextran prophylaxis. No anaphylactic reaction was noted from dextran 70, using hapten-dextran prophylaxis.
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PMID:Hypotensive anesthesia, thromboprophylaxis and postoperative thromboembolism in total hip arthroplasty. 620 42

Postoperative pulmonary embolism continues to be a problem in patient care, especially in high-risk patients. This study was designed to evaluate a combined pharmacologic approach to the prophylaxis of postoperative deep venous thrombosis (DVT) by mediating at least two and probably three of Virchow's predisposing factors. Patients 40 years of age and older undergoing operations greater than 45 minutes under general anesthesia were placed in one of five treatment groups and studied by a prospective randomized, double-blind protocol. Study drugs were the following: (1) 0.5 mg of dihydroergotamine plus 5000 IU of sodium heparin (DHE 5000), (2) 0.5 mg DHE plus 2500 IU heparin (DHE 2500), (3) 5000 IU of HEP (HEP 5000), (4) 0.5 mg of DHE (DHE 0.5), and (5) a placebo. Study medications were administered 2 hours preoperatively and continuously thereafter every 12 hours postoperatively subcutaneously in the anterior abdominal wall for 5 to 7 days or until a positive radiofibrinogen uptake test (RFUT). The RFUT was performed according to standardized technique and was used to establish the presence or absence of DVT. This report is an analysis of the major subgroup of patients undergoing intra-abdominal operations. Results showed a highly statistically significant prophylactic benefit from DHE 5000 compared with the placebo (p less than 0.003) and all other treatment groups (p less than 0.05). There was no significant benefit from DHE 2500, HEP 5000 (p greater than 0.13), and DHE 0.5 (p greater than 0.3). All patients who entered the study had two or more risk factors for postoperative DVT, and high-risk patients were distributed equally throughout all treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prophylactic efficacy of low-dose dihydroergotamine and heparin in postoperative deep venous thrombosis following intra-abdominal operations. 638 9

From 1957 to 1982, 115 patients underwent radical vulvectomy and bilateral inguinal lymphadenectomy for invasive squamous carcinoma of the vulva. From 1957 to 1971, 57 patients received perioperative prophylactic sodium warfarin (Coumadin) as prophylaxis against pulmonary embolism. From 1971 to 1976, 27 consecutive patients received dextran-40 as prophylaxis for pulmonary embolism and to improve the microcirculation to the inguinal skin flaps. Because of the report that dextran-40 is a cause of acute renal failure, this study was terminated and the subsequent 19 patients were treated with mini-dose heparin because of the reported benefit as prophylaxis against thromboembolic disease. During the 25-year period, 12 patients received no prophylactic anticoagulants. Mini-dose heparin resulted in a significant morbidity not previously reported in patients undergoing inguinal lymphadenectomy: 43% (8/19) of the mini-dose heparin patients, 7% (2/27) of the dextran-40 patients, 0% (0/57) of the sodium warfarin patients, and none of the 12 patients not receiving perioperative prophylaxis developed inguinal lymphocysts (P less than .001). There was no significant difference in the prevention of pulmonary embolism between the mini-dose heparin (0/19), dextran-40 (0/27), and no treatment groups (0/12) as compared to the 5% (3/57) incidence in the sodium warfarin patients (.10 less than P less than .50). The significant relationship between prophylactic heparin and the subsequent development of inguinal lymphocysts and the need to reassess its role in prevention of pulmonary embolism in patients undergoing lymphadenectomy is discussed.
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PMID:Prophylactic anticoagulation as a possible cause of inguinal lymphocyst after radical vulvectomy and inguinal lymphadenectomy. 685 17

One hundred thirty-four patients with venous thrombosis or pulmonary embolism, confirmed by radiological techniques, received continuous-pump heparin therapy while their responses were monitored by the activated coagulation time (ACT). The suggested protocol was as follows: (1) give an intravenous bolus of about 50 units/kg; (2) follow with 15 to 25 units/kg/hr; (3) modify infusion rate to maintain ACT of 150 to 190 s; (4) after two or three days with ACT in target range, start oral warfarin sodium therapy; (5) after three to five days of warfarin therapy, if prothrombin time is two to 2 1/2 times the control value, discontinue heparin administration. One hundred thirty-two patients responded, with no heparin failures. Dangerous bleeding occurred in two who received excessive amounts of heparin. Some patients, mostly with short ACTs, responded slowly; some, many with long ACTs, had minor bleeding. The protocol proved successful and safe when followed closely.
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PMID:Heparin therapy for thromboembolic disorders. A prospective evaluation of 134 cases monitored by the activated coagulation time. 688 62

The records of 32 cancer patients who were treated with heparin sodium and warfarin sodium for thromboembolic disease were reviewed. Standard techniques for anticoagulation were neither safe nor effective. Sixteen patients experienced 21 different hemorrhagic complications. Eight patients had major hemorrhages that led to cessation of therapy or death. Six of 32 patients had pulmonary embolisms while receiving anticoagulants. It is suggested that venous interruption may be a safer and more effective method of prophylaxis against pulmonary embolism in cancer patients.
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PMID:Anticoagulants, venous thromboembolism, and the cancer patient. 697 Oct 83

A case study report is presented of a 20 year old black woman with a past history of oral contraceptive (OC) use who developed Budd-Chiari syndrome (hepatic vein thrombosis) associated with decreased levels of antithrombin 3. This combination has not been previously reported. The woman presented on December 28, 1979 with midepigastric pain. She had no previous illnesses, but OCs had been used up to 2 years prior to admission. Shortly after admission the patient became hypotensive, developed oliguric renal failure, and began to rapidly accumulate ascites. During this admission, the patient's transaminase levels abruptly declined. A percutaneous liver biopsy obtained on January 9, 1980 showed centrilobular hemorrhagic necrosis of a severe degree. An inferior vena cavagram was repeated on January 14, 1980 demonstrating hepatic vein thrombosis. Streptokinase, followed by heparinization, was given in an effort to lyse the thrombi, but repeat inferior cavagram on January 24th proved this to be unsuccessful. Thrombosis of the left iliac and left femoral vein then appeared. Because of her apparent "hypercoagulable state," the antithrombin 3 level was measured on January 31st and found to be 27%. A simultaneous serum fibrinogen was 255 mg/dl. Family members (father, mother, and 4 children) were studied. All had normal antithrombin 3 levels, thus excluding a familial defect. The patient gradually improved and was discharged on February 25, 1980 on Coumadin, diuretics, and a 3 g sodium diet. Because of ascites and peripheral edema, a LeVeen shunt was placed on March 25, 1980. At surgery, she was noted to have obstruction of the right internal jugular and right cephalic veins. Because of possible thrombosis in the superior inferior vena cava branches, venography was performed on March 31st and demonstrated thrombosis of the right subclavian, inferior vena cava, and internal iliac veins. Despite the therapy, patient again began to reaccumulate ascites and was readmitted on May 17th. The then nonfunctioning shunt was repositioned in the patient's right atrium. Postoperatively, the patient's course was complicated by DIC. Because heparin induced thromboycytopenia was suspected, heparin was discontinued and Coumadin begun. On June 6th the patient became suddenly short of breath. A lung scan was consistent with pulmonary embolism. She could not be adequately ventilated and died on June 8th. Although the patient discontinued OC use 2 years prior to initial presentation of the disease, the morphologic features of the venous thrombosis and hepatic damage were indicative of a chronic, ongoing process of longer than 6 months' duration, thus raising the possibility of a cause-effect relationship between the OC and thrombotic process. Prospective studies are needed to substantiate the view of a relationship between OC use, antithrombin 3 deficiency, and the Budd-Chiari syndrome.
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PMID:Budd-Chiari Syndrome and antithrombin III deficiency. 710 23


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