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Associations and outcomes of septic pulmonary embolism.

Goswami U, Brenes JA, Punjabi GV, LeClaire MM, Williams DN - Open Respir Med J (2014)

Bottom Line: Seven (17%) patients received systemic anticoagulants.Eight (20%) patients died due to various complications.Antibiotics, local drainage procedures and increasingly, anticoagulation are keys to successful outcomes.

View Article: PubMed Central - PubMed

Affiliation: Department of Pulmonary, Allergy, Critical Care and Sleep Medicine, University of Minnesota, Minneapolis, MN, USA.

ABSTRACT

Background: Septic pulmonary embolism is a serious but uncommon syndrome posing diagnostic challenges because of its broad range of clinical presentation and etiologies.

Objective: To understand the clinical and radiographic associations of septic pulmonary embolism in patients presenting to an acute care safety net hospital.

Methods: We conducted a retrospective analysis of imaging and electronic health records of all patients diagnosed with septic pulmonary embolism in our hospital between January 2000 and January 2013.

Results: 41 episodes of septic pulmonary embolism were identified in 40 patients aged 17 to 71 years (median 46); 29 (72%) were men. Presenting symptoms included: febrile illness (85%); pulmonary complaints (66%) including pleuritic chest pain (22%), cough (19%) and dyspnea (15%); and those related to the peripheral foci of infection (24%) and shock (19%). Sources of infection included: skin and soft tissue (44%); infective endocarditis (27%); and infected peripheral deep venous thrombosis (17%). 35/41 (85%) were bacteremic with staphylococcus aureus. All patients had peripheral nodular lesions on chest CT scan. Treatment included intravenous antibiotics in all patients. Twenty six (63%) patients required pleural drainage and/or drainage of peripheral abscesses. Seven (17%) patients received systemic anticoagulants. Eight (20%) patients died due to various complications.

Conclusion: The epidemiology of septic pulmonary embolism has broadened over the past decade with an increase in identified extrapulmonary, non-cardiac sources. In the context of an extrapulmonary infection, clinical features of persistent fever, bacteremia and pulmonary complaints should raise suspicion for this syndrome, and typical findings on the chest CT scans confirm the diagnosis. Antibiotics, local drainage procedures and increasingly, anticoagulation are keys to successful outcomes.

No MeSH data available.


Related in: MedlinePlus

Schematic of pathophysiology of SPE.
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Figure 2: Schematic of pathophysiology of SPE.

Mentions: SPE is an uncommon and serious disorder associated with significant morbidity and mortality. It remains a difficult diagnosis in part because of its varied etiology and clinical presentations. In this study we highlight the broad spectrum of etiologic causes that have changed over time. In one of the largest early studies reported by MacMillan et al. [1], 75% of cases of SPE were seen in the setting of right-sided infective endocarditis secondary to IV drug abuse, some with incidental superficial skin abscesses. More recently, Cook et al. [4] reported the role of infected IV catheters and devices as a source of SPE. The current series draws attention to the importance of skin, deep soft tissue and bone infections of the extremities as a key source. Infections with contiguous septic thrombophlebitis leading to SPE have been well established in pediatric populations [3] but have only recently been emphasized in adults by Brenes et al. [5]. Irrespective of the initial site of infection, there is a common sequence of events that triggers this syndrome (Fig. 2). An extrapulmonary site of infection can allow extravasation or translocation [7] of an organism, most commonly bacterial, into the systemic venous circulation. Once in the bloodstream, the pathogen can produce damage directly through toxins [8] and indirectly via inflammatory mediators [9], which may occasionally promote local thrombosis [10], which serves as an additional nidus for proliferation of the bacteria. Embolization of these thrombi into the pulmonary circulation allows for metastatic parenchymal infection of the lungs, even in the absence of cardiac valvular involvement. Special attention should be given to Staphylococcus aureus, which can provoke an intense inflammatory reaction, with direct endothelial damage via cytotoxins (e.g. Panton-Valentine leukocidin) and enzymatic mechanisms (e.g. Coagulase), culminating in septic pulmonary emboli, with concomitant septic thrombophlebitis in a minority of the cases [5].


Associations and outcomes of septic pulmonary embolism.

Goswami U, Brenes JA, Punjabi GV, LeClaire MM, Williams DN - Open Respir Med J (2014)

Schematic of pathophysiology of SPE.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4150379&req=5

Figure 2: Schematic of pathophysiology of SPE.
Mentions: SPE is an uncommon and serious disorder associated with significant morbidity and mortality. It remains a difficult diagnosis in part because of its varied etiology and clinical presentations. In this study we highlight the broad spectrum of etiologic causes that have changed over time. In one of the largest early studies reported by MacMillan et al. [1], 75% of cases of SPE were seen in the setting of right-sided infective endocarditis secondary to IV drug abuse, some with incidental superficial skin abscesses. More recently, Cook et al. [4] reported the role of infected IV catheters and devices as a source of SPE. The current series draws attention to the importance of skin, deep soft tissue and bone infections of the extremities as a key source. Infections with contiguous septic thrombophlebitis leading to SPE have been well established in pediatric populations [3] but have only recently been emphasized in adults by Brenes et al. [5]. Irrespective of the initial site of infection, there is a common sequence of events that triggers this syndrome (Fig. 2). An extrapulmonary site of infection can allow extravasation or translocation [7] of an organism, most commonly bacterial, into the systemic venous circulation. Once in the bloodstream, the pathogen can produce damage directly through toxins [8] and indirectly via inflammatory mediators [9], which may occasionally promote local thrombosis [10], which serves as an additional nidus for proliferation of the bacteria. Embolization of these thrombi into the pulmonary circulation allows for metastatic parenchymal infection of the lungs, even in the absence of cardiac valvular involvement. Special attention should be given to Staphylococcus aureus, which can provoke an intense inflammatory reaction, with direct endothelial damage via cytotoxins (e.g. Panton-Valentine leukocidin) and enzymatic mechanisms (e.g. Coagulase), culminating in septic pulmonary emboli, with concomitant septic thrombophlebitis in a minority of the cases [5].

Bottom Line: Seven (17%) patients received systemic anticoagulants.Eight (20%) patients died due to various complications.Antibiotics, local drainage procedures and increasingly, anticoagulation are keys to successful outcomes.

View Article: PubMed Central - PubMed

Affiliation: Department of Pulmonary, Allergy, Critical Care and Sleep Medicine, University of Minnesota, Minneapolis, MN, USA.

ABSTRACT

Background: Septic pulmonary embolism is a serious but uncommon syndrome posing diagnostic challenges because of its broad range of clinical presentation and etiologies.

Objective: To understand the clinical and radiographic associations of septic pulmonary embolism in patients presenting to an acute care safety net hospital.

Methods: We conducted a retrospective analysis of imaging and electronic health records of all patients diagnosed with septic pulmonary embolism in our hospital between January 2000 and January 2013.

Results: 41 episodes of septic pulmonary embolism were identified in 40 patients aged 17 to 71 years (median 46); 29 (72%) were men. Presenting symptoms included: febrile illness (85%); pulmonary complaints (66%) including pleuritic chest pain (22%), cough (19%) and dyspnea (15%); and those related to the peripheral foci of infection (24%) and shock (19%). Sources of infection included: skin and soft tissue (44%); infective endocarditis (27%); and infected peripheral deep venous thrombosis (17%). 35/41 (85%) were bacteremic with staphylococcus aureus. All patients had peripheral nodular lesions on chest CT scan. Treatment included intravenous antibiotics in all patients. Twenty six (63%) patients required pleural drainage and/or drainage of peripheral abscesses. Seven (17%) patients received systemic anticoagulants. Eight (20%) patients died due to various complications.

Conclusion: The epidemiology of septic pulmonary embolism has broadened over the past decade with an increase in identified extrapulmonary, non-cardiac sources. In the context of an extrapulmonary infection, clinical features of persistent fever, bacteremia and pulmonary complaints should raise suspicion for this syndrome, and typical findings on the chest CT scans confirm the diagnosis. Antibiotics, local drainage procedures and increasingly, anticoagulation are keys to successful outcomes.

No MeSH data available.


Related in: MedlinePlus