scholarly journals Pulmonary Septic Emboli due to Azygos Vein Septic Thrombosis

2013 ◽  
Vol 2013 ◽  
pp. 1-3 ◽  
Author(s):  
Ginius Pradhan ◽  
Khaldoon Shaheen ◽  
Mary Muoneke ◽  
Basel Altaqi
Keyword(s):  
Pulmonary Embolism ◽  
Epidural Abscess ◽  
Azygos Vein ◽  
Pulmonary Emboli ◽  
Septic Emboli ◽  
Vein Thrombosis ◽  
History Of ◽  
Septic Pulmonary Embolism ◽  
And Control ◽  
Infectious Source

The triad of extrapulmonary infection, contiguous septic vein thrombosis, and septic pulmonary embolism is a rare complex but associated with significant morbidity and mortality. Septic azygos vein thrombosis is extremely rare and potentially serious since it may also cause pulmonary emboli and sudden death. We report a case of a 32-year-old woman with history of IV drug abuse who presented with epidural abscess and methicillin-resistantS. aureus(MRSA) bacteremia. Later she developed signs of septic pulmonary embolism secondary to septic azygos vein thrombosis. With early diagnosis, appropriate antimicrobial therapy, and control of the infectious source, resolution of the illness can be expected for most patients with avoidance of potential complications.

Familial thrombophilia associated with fibrinogen Paris V: Dusart syndrome

Blood ◽  
2000 ◽  
Vol 96 (3) ◽  
pp. 1191-1193 ◽  
Author(s):  
Takashi Tarumi ◽  
Danko Martincic ◽  
Anne Thomas ◽  
Robert Janco ◽  
Mary Hudson ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Venous Thromboembolism ◽  
Early Onset ◽  
Family Members ◽  
Initial Presentation ◽  
Pulmonary Emboli ◽  
Common Cause ◽  
History Of ◽  
Prophylactic Anticoagulation ◽  
Fibrin Clots

Abstract We report on a family with a history of venous thromboembolism associated with fibrinogen Paris V (fibrinogen A-Arg554→Cys). Ten members experienced thrombotic events, including 4 with fatal pulmonary emboli. Pulmonary embolism was the presenting feature in 4. Those with the mutation and a history of thrombosis had somewhat higher fibrinogen concentrations than those with the mutation and no thrombosis (294 ± 70 mg/dL vs 217 ± 37 mg/dL, respectively). The Paris V mutation consistently caused a prolongation of the reptilase time, and fibrin clots containing the abnormal fibrinogen were more translucent than normal clots. Given the early onset of symptoms and the initial presentation with pulmonary embolism in some family members, it was justifiable to offer prophylactic anticoagulation with warfarin to carriers of the mutation. Fibrinogen Paris V has now been reported in 4 apparently unrelated families, indicating that it is a relatively common cause of dysfibrinogenemia-associated thrombosis.

scholarly journals Renal Vein Thrombosis and Pulmonary Embolism Secondary to Vaccine-induced Thrombotic Thrombocytopenia (VITT)

2021 ◽  
Author(s):  
Nikita Cliff-Patel ◽  
Lindsay Moncrieff ◽  
Veqas Ziauddin
Keyword(s):  
Pulmonary Embolism ◽  
General Hospital ◽  
Regulatory Agency ◽  
Renal Vein ◽  
District General Hospital ◽  
Renal Vein Thrombosis ◽  
The Other ◽  
Pulmonary Emboli ◽  
Vein Thrombosis ◽  
The Uk

The Medicines and Healthcare products Regulatory Agency (MHRA) of the UK has approved the use of three vaccines to combat COVID-19 (SARS-CoV-2). There have been rare reports of thrombosis after vaccination with the AstraZeneca vaccine. We present three cases of vaccine-induced thrombotic thrombocytopenia (VITT) in one UK district general hospital following administration of this vaccine. Two of the patients had asymptomatic pulmonary emboli, while the other is the first known case of both renal vein thrombosis and pulmonary embolism.

Therapie der tiefen Venenthrombose mit niedermolekularem Heparin, Beinkompression und sofortigem Gehen

VASA ◽  
2001 ◽  
Vol 30 (3) ◽  
pp. 195-204 ◽  
Author(s):  
H. Partsch
Keyword(s):  
Pulmonary Embolism ◽  
Bed Rest ◽  
Lower Leg ◽  
Bleeding Complications ◽  
Pulmonary Emboli ◽  
Malignant Diseases ◽  
Vein Thrombosis ◽  
Fatal Bleeding ◽  
Lung Scan ◽  
Low Incidence

Background: Traditionally, patients with acute deep vein thrombosis (DVT) are treated with strict bed rest for several days to avoid clots from breaking off and causing pulmonary emboli. The purpose of this study is to give a precise estimate of short term complications like pulmonary embolism, bleeding, heparin-induced thrombocytopenia (HIT) and death in a cohort of consecutive patients who were admitted because of acute symptomatic DVT, all treated by compression and walking exercises instead of conventional bed-rest and nearly all by low-molecular-weight heparin. Patients and methods: In 1289 consecutive patients the following five endpoints were registered for the period of hospital-stay: 1. Frequency of pulmonary embolism (PE ) at admission (V/Q lung scan), 2. Frequency of new PE’s after 10 days (second lung scan), 3. Fatal events (autopsy), 4. Frequency of malignant disease, 5. Bleeding complications and HIT. Results: 1. 190/356 (53.4% of iliofemoral, 355/675 (52.6%) of femoral and 84/239 (35.1%) of lower leg vein thrombosis showed PE (difference iliofemoral and femoral versus lower leg DVT p < 0.001). Two thirds of these PE were asymptomatic. 2. New PE after 10 days in comparison to the baseline scan occurred in 7.4%, 6.4% and 3.4% respectively. 3. Fatal events, all investigated by autopsy, were caused by PE in 3 patients aged over 76 years (0.23%), by malignant diseases in 12 (0.9%) and due to other causes in 2 (0.15%). 4. 232 patients (18%) had associated malignant diseases, from which 33% were detected by our screening. 5. Non-fatal bleeding complications were seen in 3.3%, including 5 patients (0.4%) with major bleeding. Three patients (0,2%) suffered from HIT II. Conclusion: The low incidence of recurrent and fatal pulmonary emboli in this series affirms the value of early ambulation with heavy leg compression in patients with symptomatic acute leg deep venous thrombosis. In addition, the presence of pulmonary emboli in one-third of those with calf vein thrombi emphasizes the importance of fully diagnosing and treating calf clots.

scholarly journals Septic Pulmonary Embolism Secondary to Klebsiella pneumoniae Epididymitis: Case Report and Literature Review

2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Juan Sebastián Alonso Ojeda Gómez ◽  
Jorge Alberto Carrillo Bayona ◽  
Laura Cristina Morales Cifuentes
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Circulation ◽  
Respiratory Symptoms ◽  
Unusual Complication ◽  
Chest Imaging ◽  
Case Presentation ◽  
History Of ◽  
Septic Pulmonary Embolism ◽  
Uncommon Condition ◽  
Acute Epididymitis

Background. Septic pulmonary embolism (SPE) is defined as the occurrence of septic thrombi in the pulmonary circulation. We report a case of SPE secondary to K. pneumoniae epididymitis. Case Presentation. A 74-year-old male with a history of diabetes mellitus experienced SPE secondary to epididymitis, with isolation of K. pneumoniae in blood and presence of lung nodules, with a chest computed tomography showing the halo and reversed halo signs. Discussion. SPE is characterized by the presence of septic thrombi in the pulmonary circulation coming from an extrapulmonary infective focus. SPE secondary to K. pneumoniae epididymitis is an uncommon condition that is characterized by the presence of multiple bilateral nodules of peripheral distribution. Conclusion. SPE is an unusual complication of acute epididymitis. Suspicion of SPE should be considered in patients with a diagnosis of epididymitis, respiratory symptoms, and multiple nodules in chest imaging assessments.

scholarly journals Metastatic Spreading of Community AcquiredStaphylococcus aureusBacteraemia

2011 ◽  
Vol 2011 ◽  
pp. 1-5
Author(s):  
Giovanna Fabio ◽  
Maria Carrabba ◽  
Luca Mellace ◽  
Cinzia Hu ◽  
Diego Spagnoli ◽  
...  
Keyword(s):  
Risk Factors ◽  
Epidural Abscess ◽  
Tertiary Care ◽  
Skin Lesions ◽  
University Hospital ◽  
Serious Infection ◽  
History Of ◽  
Associated Risk Factors ◽  
Healthcare Associated ◽  
And Control

A 29-year-old woman presented to the Fondazione IRCCS “Cà Granda” Ospedale Maggiore, a tertiary care university hospital in Milan (Italy), with skin lesions, fever, myalgia, joint pain and swelling, and a one-week history of low back pain. The diagnosis wasStaphylococcus aureus(S. aureus) bacteraemia spreading to skin, bones, and joints and a lumbosacral epidural abscess L5-S2. Neither initial focus nor predisposing conditions were apparent. The antibiotic therapy was prolonged for six-weeks with the resolution of fever, skin lesions, articular inflammation, and the epidural abscess. Community-acquiredS. aureusinfections can affect patients without traditional healthcare-associated risk factors, and community acquisition is a risk-factor for the development of complications. Raised awareness ofS. aureusbacteraemia, also in patients without healthcare-associated risk factors, is important in the diagnosis, management, and control of this infection, because failure to recognise patients with serious infection and lack of understanding of empirical antimicrobial selection are associated with a high mortality rate in otherwise healthy people.

Familial thrombophilia associated with fibrinogen Paris V: Dusart syndrome

Blood ◽  
2000 ◽  
Vol 96 (3) ◽  
pp. 1191-1193
Author(s):  
Takashi Tarumi ◽  
Danko Martincic ◽  
Anne Thomas ◽  
Robert Janco ◽  
Mary Hudson ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Venous Thromboembolism ◽  
Early Onset ◽  
Family Members ◽  
Initial Presentation ◽  
Pulmonary Emboli ◽  
Common Cause ◽  
History Of ◽  
Prophylactic Anticoagulation ◽  
Fibrin Clots

We report on a family with a history of venous thromboembolism associated with fibrinogen Paris V (fibrinogen A-Arg554→Cys). Ten members experienced thrombotic events, including 4 with fatal pulmonary emboli. Pulmonary embolism was the presenting feature in 4. Those with the mutation and a history of thrombosis had somewhat higher fibrinogen concentrations than those with the mutation and no thrombosis (294 ± 70 mg/dL vs 217 ± 37 mg/dL, respectively). The Paris V mutation consistently caused a prolongation of the reptilase time, and fibrin clots containing the abnormal fibrinogen were more translucent than normal clots. Given the early onset of symptoms and the initial presentation with pulmonary embolism in some family members, it was justifiable to offer prophylactic anticoagulation with warfarin to carriers of the mutation. Fibrinogen Paris V has now been reported in 4 apparently unrelated families, indicating that it is a relatively common cause of dysfibrinogenemia-associated thrombosis.

scholarly journals Case Report: Unprovoked venous thromboembolism in a young adult

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 182
Author(s):  
Jeyhan Dhabhar ◽  
Varshil Mehta ◽  
Nimit Desai ◽  
Sameer Dawoodi ◽  
Sojib Bin Zaman
Keyword(s):  
Pulmonary Embolism ◽  
Venous Thromboembolism ◽  
Trauma Surgery ◽  
Sudden Onset ◽  
Vein Thrombosis ◽  
Doppler Study ◽  
Pulmonary Angiogram ◽  
Co Morbidity ◽  
History Of ◽  
Prolonged Immobilization

A 24-year-old male was presented to us with sudden onset of chest pain and dyspnea for the past one hour. There was no history of calf pain, trauma, surgery, prolonged immobilization, long-haul air travel, bleeding diathesis or any other co-morbidity. The patient denied any addiction history. The Electrocardiogram showed tachycardia with S1Q3T3 pattern. The left arterio-venous Doppler study was suggestive of a thrombus in popliteal vein and sapheno-popliteal junction. The CT-Pulmonary Angiogram scan was suggestive of a massive pulmonary thromboembolism. The patient was thrombolysed with Intravenous Alteplase immediately and was put on tab Rivaroxaban for maintenance. He was later discharged after being stable. Unprovoked venous thromboembolism (VTE) is very rare and has the potential to lead to pulmonary embolism which could be disastrous, especially in young adults. We present such a case where unprovoked VTE was diagnosed and treated. This case suggests that high clinical suspicion is the key for the diagnosis of acute pulmonary embolism, especially in the absence of history suggestive of deep vein thrombosis.

Hypofibrinolysis in Patients with a History of Idiopathic Deep Vein Thrombosis and/or Pulmonary Embolism

1992 ◽  
Vol 67 (04) ◽  
pp. 397-401 ◽  
Author(s):  
Vito Grimaudo ◽  
Fedor Bachmann ◽  
Jacques Hauert ◽  
Maria-Adele Christe ◽  
Egbert K O Kruithof
Keyword(s):  
Pulmonary Embolism ◽  
Deep Vein Thrombosis ◽  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Venous Occlusion ◽  
Vein Thrombosis ◽  
Molar Excess ◽  
History Of ◽  
Deep Vein ◽  
Pai 1

SummaryAn impaired fibrinolytic activity after a venous occlusion test is the most common abnormality associated with thomboembolic disease. To better characterize the causes of abnormal responses we have measured different fibrinolytic parameters, before and after 10 and 20 min of venous occlusion, in 77 patients with a history of idiopathic deep vein thrombosis and/or pulmonary embolism and in 38 healthy volunteers.The patients had a lower mean fibrinolytic response to venous occlusion than the controls and higher antigen levels of tissue-type plasminogen activator (t-PA: Ag) and plasminogen activator inhibitor type 1 (PAI-1:Ag). Before venous occlusion, PAI-1 levels were at a molar excess over those of t-PA in all patients and controls. After 20 min of venous occlusion, the release of t-PA from the vascular endothelium resulted in a molar excess of t-PA over PAI-1 in the majority of controls (72%) but only in a minority of patients (39%).To identify patients with fibrinolytic abnormalities, reference intervals (RI) for fibrinolytic activity, t-PA:Ag and PAI-1:Ag were established in healthy controls. None of the patients had low levels of t-PA:Ag, but 17 (22%) had elevated PAI-1:Ag levels before venous occlusion and 12 (16%) exhibited low fibrinolytic activity after 20 min of venous occlusion. Ten of these were among the 17 subjects with high PAI-1: Ag levels before venous occlusion. Thus, the measurement of PAI-1:Ag levels before venous occlusion (i.e. in samples taken without any stimulation) is a sensitive (83%) and specific (89%) assay for the detection of patients with an impaired fibrinolytic response to venous occlusion.

ACUTE PYELONEPHRITIS AND SEPTIC RENAL VEIN THROMBOSIS LEADING TO SEPTIC PULMONARY EMBOLISM

CHEST Journal ◽  
2019 ◽  
Vol 156 (4) ◽  
pp. A525
Author(s):  
Galo Sanchez Palacios ◽  
Stephen Sexauer ◽  
Joseph Carrington ◽  
Brian Boer
Keyword(s):  
Pulmonary Embolism ◽  
Acute Pyelonephritis ◽  
Renal Vein ◽  
Renal Vein Thrombosis ◽  
Vein Thrombosis ◽  
Septic Pulmonary Embolism

scholarly journals Septic pulmonary emboli from mitral valve endocarditis in a patient with repaired tetralogy of fallot

2016 ◽  
Vol 3 (3) ◽  
pp. 7
Author(s):  
Aniket S. Rali ◽  
Arun Iyer ◽  
Claire Sullivan ◽  
James Strainic ◽  
Brian Hoit
Keyword(s):  
Mitral Valve ◽  
Septal Defect ◽  
Pulmonary Emboli ◽  
Transesophageal Echocardiogram ◽  
Bronchial Arteries ◽  
Lower Extremity Weakness ◽  
Septic Emboli ◽  
Multiple Organs ◽  
Computed Tomography Images ◽  
History Of

A 37-year-old woman with a past medical history significant for congenital deafness and surgically repaired Tetralogy ofFallot presented with three day history of nausea, vomiting, fever, chills, dyspnea, and lower extremity weakness and physicalexamination notable for Janeway lesions. Peripheral blood and urine cultures were positive for methicillin sensitive Staphlococcusaureus. Transesophageal echocardiogram was consistent with mitral valve endocarditis. Computed tomography images of thechest, abdomen and pelvis demonstrated septic emboli to multiple organs including lungs, liver, spleen and kidneys. Salinecontrast study was negative for a patent foramen ovale, or residual ventricular septal defect. Thus, effectively ruling out left toright intracardiac shunt as the cause of pulmonary septic emboli from mitral valve endocarditis. Moreover, cardiac MRI did notshow any evidence of right sided endocarditis. Therefore, we believe the source of septic pulmonary emboli from mitral valveendocarditis to be through the bronchial arteries. The extent of septic emboli to various organs and the precise mechanism ofpulmonary emboli from left sided endocarditis in a patient with surgically altered cardiac anatomy make this case unique.

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