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

A frequent condition affecting patients with stroke is venous thromboembolism (VTE), which consists of two components: deep vein thrombosis, and pulmonary embolism as its complication The main risk factors of VTE are: age over 65 years, motor deficit with immobilisation, heart failure, infection, obesity and coagulopathy Typical symptoms of deep vein thrombosis (pain, tenderness, swelling of calf and increased skin temperature) can be masked by sensory and autonomic deficits following brain ischaemia Diagnosis of VTE is based on clinical symptoms confirmed by biochemical and radiological findings The treatment of VTE consists of anticoagulation; prevention of VTE in stroke patients is based on use of low-molecular heparins and non-pharmacological methods.
Neurol Neurochir Pol
PMID:[Deep vein thrombosis in patients with stroke]. 1762 19

We present a case of an 80-year-old female admitted to hospital because of recurrent syncope. The echocardiogram revealed a large thrombus in the left and right atria, entrapped in the patent foramen ovale, right heart enlargement and pulmonary hypertension. Magnetic resonance confirmed significant pulmonary embolism. The patient was successfully treated with fractioned heparin.
Kardiol Pol 2007 Jul
PMID:[Thrombus entrapped in the foramen ovale in an 80-year-old woman with chronic pulmonary embolism manifested by recurrent syncope--a case report]. 1769 69

A 39 year old man with normal, stable blood pressure was admitted to the Cardio-Pulmonary Intensive Care Unit due to diagnosed spiral CT pulmonary embolism (PE) and deep venous thrombosis (DVT). In 1999, a hereditary antithrombin (AT) deficiency was confirmed in the presented case. In 2006, because of a knee injury, the patient was provided with a plaster cast and primary antithrombotic prophylaxis with low molecular weight heparin (LMWH) (80 mg of enoxaparin) was administered subcutaneously once a day (patient's weight was 80 kg). Despite prophylaxis PE and DVT occurred after 6 weeks of treatment. The patient was successfully treated with unfractioned heparin, repeated infusions of AT concentrate and oral anticoagulants (OA). Transient pulmonary hypertension documented by echocardiography and hemoptysis complicated course of PE. Secondary prophylaxis with OA, and INR maintenance between 2-3, was successfully continued.
Pneumonol Alergol Pol 2007
PMID:[The insufficiency of low molecular weight heparin (LMWH) prophylaxis in patients with hereditary antithrombin (AT) deficiency]. 1796 5

A case of a 48-year-old woman with a comminuted fracture of the left tibia and receiving prophylactic doses of nadroparin, with massive pulmonary embolism mimicking ST-elevation acute coronary syndrome and complicated by cardiogenic shock and cardiac arrest, is presented. Pulmonary angiography showed total right pulmonary artery occlusion. Intraarterial thrombolysis with reduced dose of alteplase (50 mg), platelet GP IIb/IIIa blockade with eptifibatide, endovascular embolus fragmentation with a pigtail rotation catheter, and rescue pulmonary balloon angioplasty were performed, after which complete recovery was achieved. On day 4 of hospitalisation the patient was transferred to the orthopaedic ward where she underwent uneventful tibial surgery.
Kardiol Pol 2007 Oct
PMID:[Massive pulmonary embolism mimicking ST-elevation acute coronary syndrome successfully treated with hybrid therapy in a trauma patient receiving nadroparin: diagnostic and therapeutic dilemmas]. 1797 54

The study presents the case of a 78-year-old woman with recurrent pulmonary embolism, treated with 2 courses of thrombolysis. In this patient, due to heparin-induced thrombocytopenia, fondaparinux therapy was used.
Pol Arch Med Wewn
PMID:[Recurrent pulmonary embolism in a patient with heparin-induced thrombocytopenia]. 1836 53

A 81-year-old woman was referred to the emergency department after having syncopal episode two days earlier. A chest computed tomography demonstrated a right main pulmonary artery embolism. The only prominent risk factor for thromboembolism was her poor response to activated protein C. Seven days later she demonstrated acute-onset chest pain with elevated troponin. Cardiac angiography showed stenosis of left anterior descending coronary artery which was successfully treated with angioplasty and stent implantation. This case illustrates the coincidence and the importance of clinical suspicion for the early diagnosis and treatment of acute coronary syndrome during massive pulmonary embolism.
Kardiol Pol 2008 May
PMID:[Acute coronary syndrome following massive pulmonary embolism in a 81-year-old woman with thrombophilia]. 1853 61

To discuss the evidence regarding the efficacy and safety of anticoagulant prophylaxis against deep vein thrombosis (DVT) in hospitalized medical patients; to understand barriers to implementation of prophylaxis and how they can be overcome; and to have a practical approach as to which patients should and should not receive anticoagulant prophylaxis. The frequency of DVT in hospitalized medical patients, in the absence of prophylaxis varies from 10-15%. Autopsy studies have shown that pulmonary embolism (PE) is associated with 5-10% of deaths in hospitalized patients. With appropriate use of anticoagulant prophylaxis, there is a 57% reduction in the risk for symptomatic PE (relative risk [RR] 0.43, 95% CI 0.26-0.71), a 62% reduction in the risk for fatal PE (RR 0.38, 95% CI 0.21-0.69), and a 53% reduction in the risk for symptomatic DVT (RR 0.47, 95% CI 0.22-1.00). Anticoagulant prophylaxis is also associated with a non-significant increased risk for major bleeding (RR 1.32, 95% CI 0.73-2.37). Risk factors for DVT and bleeding in medical patients may help to identify patients in whom anticoagulant prophylaxis is indicated or contraindicated but validated risk stratifications schemes are lacking. Among hospitalized medical patients, randomized trials have established an acceptable therapeutic benefit-to-risk ratio of anticoagulant prophylaxis to reduce the incidence of clinically silent and symptomatic venous thromboembolism, including a reduction in the incidence of fatal PE. Additional research is needed to develop a validated risk stratification model for hospitalized medical patients that can help identify patients who would benefit most from anticoagulant prophylaxis.
Pol Arch Med Wewn 2008 Apr
PMID:Prophylaxis against venous thromboembolism in hospitalized medical patients: an evidence-based and practical approach. 1857 20

We present a complication of the infected pacing system extraction by lobular pneumonia in a 73-year-old female patient. The pacing system involved DDD pacemaker, atrial and ventricular endocardial leads implanted 12 year beforehand. The defect of the atrial lead emerged during the pacemaker replacement 4 years ago. The diagnosis of the injury cause and its reparation were not undertaken at that time. An interruption of the atrial lead which resulted in the formation of a loop inside the cardiac chamber was found when purulant pacemaker pocket infection had been diagnosed. The patient was referred for the pacing system extraction after preoperative specific antibiotic treatment. After a long-lasting, difficult, two-step leads extraction procedure, pneumonia developed. An echocardiogram revealed enlargement of the right atrium and ventricle, with elevated pulmonary artery pressure up to 40 mmHg. An atypical chest X-ray with the presence of a large pleural liquid volume led to the work-up of hemorrhagic complications and postponed the antithrombotic therapy. With the delay of 1.5 month the pulmonary scintigraphy showed features of pulmonary embolism. The embolism was most likely caused by a vegetation mobilized from the endocardial lead and/or endocardium during the extraction maneuvers. Before the surgery, the vegetations attached to the leads or to the endocardium had not been visualized. Anticoagulant therapy with antivitamins K was successful, which resulted in the pulmonary pressure normalization. The patient has remained in a good condition for the next 3 months of follow-up.
Pol Arch Med Wewn 2008 May
PMID:Complications of permanent dual-chamber pacing such as late purulent pacemaker pocket infection with broken and looped atrial lead, complicated by pulmonary embolism after transvenous lead removal: a case report. 1861 85

Two cases of large, free-floating right heart thrombi in patients with massive pulmonary embolism and a history of deep vein thrombosis are presented. In a 30-year-old male with prominent obesity and a history of hypertension, disappearance of the thrombus at the end of alteplase infusion coexisted with onset of haemodynamic stabilization. In a 70-year-old female, the thrombus, which persisted despite streptokinase administration, translocated suddenly (during echocardiography) to the pulmonary artery, which resulted in a deterioration in her status. After alteplase administration following heparin infusion, steady clinical and echocardiographic improvement was observed.
Kardiol Pol 2008 Jun
PMID:[Thrombus in transit - two cases of patients with massive pulmonary embolism treated with thrombolysis]. 1862 37

Blood gas analysis is often performed in the initial diagnosis of acute pulmonary embolism (APE), and it is recognized that hypoxemia (H) strengthen its suspicion. However, the diagnostic power of hypoxemia is very week. Hypoxemia, usually deep, occurs in almost all patients with massive APE whereas moderate hypoxemia occurs in about 75% of unselected normotensive APE population without co-morbitides. H occurs also in most patients with chronic thromboembolic pulmonary hypertension (CTEPH). The patomechanism of H in pulmonary embolism is not completely known and is associated mainly with obstruction of pulmonary vasculature, pulmonary hypertension, and with co-morbitides. However, the secondary failure of ventilation followed by alveolar hypoxia can not be excluded in many cases of chronic pulmonary embolism. Hypoxemia seems to have moderate value in prognosis in APE and in CTEPH. H in massive APE requires oxygen therapy, and it can be speculated, whether long term oxygenation should be added to the anticoagulation in nonoperated, hypoxemic patients with CTEPH.
Pol Merkur Lekarski 2008 Jan
PMID:[Hypoxemia in pulmonary embolism--the occurrence, patomechanism and significance]. 1863 52


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