563275
other2014
CPJXXX10.1177/0009922814563275Clinical PediatricsSawyer and Potisek
Resident Round
Chest Pain in an Adolescent Male With a Leg Abscess
Clinical Pediatrics 2015, Vol. 54(6) 604–606 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0009922814563275 cpj.sagepub.com
Carolyn M. Sawyer, MD1 and Nicholas M. Potisek, MD2
Case Report
Hospital Course
A previously healthy 17-year-old African American male presented to the emergency department with acute onset of chest pain and shortness of breath that awoke him from sleep. He denied fevers, cough, palpitations, abdominal pain, vomiting, diarrhea, or rash and was maintaining adequate oral intake with normal urine output. Two weeks prior to presentation, he fell and scraped his right leg on asphalt while playing basketball. He subsequently developed purulent abscesses overlying his right shin. He was evaluated for these wounds the day prior to presentation and was started on cephalexin and trimethoprim/sulfamethoxazole. Physical examination revealed vital signs appropriate for age and normal oxygen saturation on room air. He generally appeared uncomfortable, though he exhibited no respiratory distress, had clear lung fields bilaterally, and had a regular cardiovascular examination without murmurs. He also had multiple small (1-cm diameter) purulent abscesses with surrounding erythema overlying his anterior right leg. In the emergency department, he received a dose of ketorolac and hydromorphone for pain control. Initial workup was notable for elevated inflammatory markers with a normal electrocardiogram, chest radiograph, complete metabolic panel, and complete blood count. Further workup with chest computed tomography to evaluate for pulmonary embolism demonstrated multiple nodular lesions in the periphery of the bilateral lung fields concerning for septic pulmonary embolism (SPE) or bronchopneumonia (see Figure 1). Empiric therapy with intravenous (IV) vancomycin and clindamycin was started after wound and blood cultures were collected. He was placed on a morphine patient-controlled analgesia infusion for pain relief and was admitted for further evaluation and management.
The patient was admitted to the hospital for IV antibiotic therapy. A transthoracic echocardiogram showed no vegetations as the source of his SPE. Magnetic resonance imaging (MRI) of the right lower extremity demonstrated cellulitis and superficial abscesses without evidence of septic joint, deep abscesses, or osteomyelitis, and a deep vein thrombosis (DVT) was unlikely as no blood flow abnormalities were detected on MRI. Initial wound and blood cultures grew methicillinresistant Staphylococcus aureus (MRSA) with no growth on subsequent blood cultures. Testing for human immunodeficiency virus was negative. No further evaluation for immunodeficiency was done as the patient had no history of recurrent bacterial or viral infections. Shortly after admission the patient became febrile, and his hospital course was complicated by the development of a large right pleural effusion with associated hypoxia requiring the placement of a chest tube. After clinical improvement, chest tube removal, resolution of fever, and downtrend of inflammatory markers, he was discharged home on monotherapy with IV clindamycin. The patient had short-term follow-up with a pediatric infectious disease specialist and completed a 5-week course of intravenous antibiotics with normalization of inflammatory markers and return to baseline state of health.
Discussion Septic pulmonary embolism is an uncommon diagnosis in the pediatric population and occurs in the setting of bacteremia when emboli containing microorganisms from an area of infection travel into the venous system to 1
Duke University Medical Center, Durham, NC, USA Wake Forest School of Medicine, Winston-Salem, NC, USA
2
Final Diagnosis Septic pulmonary embolism secondary to a soft tissue infection.
Corresponding Author: Carolyn M. Sawyer, Department of Pediatrics, Duke University Medical Center, Box 3352, Durham, NC 27710, USA. Email: [email protected]
Downloaded from cpj.sagepub.com at Stockholm University Library on November 15, 2015
605
Sawyer and Potisek
Figure 1. Axial views of computed tomography scan of chest with contrast demonstrate septic emboli throughout both lung fields with lower lobe predominance.
the pulmonary vasculature causing infarction and even abscesses within the lungs. SPE typically presents with fever, respiratory symptoms, and lung infiltrates visualized on imaging of the chest.1 Patients with SPE have been found to present with a variety of respiratory symptoms, which may include dyspnea, pleuritic chest pain, cough, and hemoptysis. Radiographs are often abnormal with the most common finding of diffuse bilateral nodular lesions; however, this finding is nonspecific and often warrants further evaluation based on the clinical presentation.2,3 CT may reveal further findings suggestive of SPE in addition to bilateral nodular densities, such as pulmonary cavities or a “feeding vessel” sign, which is an identified blood vessel on imaging that leads directly into a nodule suggesting hematogenous spread.2,3 Septic pulmonary embolism has been associated with right-sided endocarditis, indwelling catheters, intravascular disease, purulent skin or soft tissue infections, IV drug use, and deep tissue infections in adult patients.2,4,5 In the pediatric population, SPE is often associated with Lemierre’s syndrome, or septic thrombophlebitis of the internal jugular vein. Lemierre’s syndrome typically affects adolescents or young adults with precedent pharyngitis, subsequent infiltration into the internal jugular vein leading to thrombophlebitis and then hematogenous spread to the lungs and other organs.6 The gramnegative, anaerobic rod Fusobacterium necrophorum is the primary causative organism found in this syndrome. There have also been several cases of SPE in pediatric patients associated with deep tissue infections such as osteomyelitis, septic arthritis, pyomyositis, and cellulitis.3,7-9 With deep tissue infections, SPE often is associated with underlying DVT and is suspected to be from local vascular congestion and inflammation
resulting in thrombophlebitis and hematogenous spread, similar to the pathogenesis in Lemierre’s syndrome.7,8 It remains unclear how SPE occurs in the setting of more superficial skin and soft tissue infections. When SPE occurs in the setting of a deep tissue infection, community-acquired MRSA (CA MRSA) should be suspected and empiric antibiotics selected with this organism in mind.3,4,7,10 Some studies have shown CA MRSA carrying the Panton–Valentine leukocidin genes have a higher propensity to infect the lungs which may explain why we are seeing more pulmonary infections in the setting of CA MRSA infections.7,10 If there is strong clinical suspicion for SPE secondary to a deep tissue infection, a blood culture should be obtained prior to initiation of antibiotic therapy. Additionally, a wound culture should be obtained if possible in the setting of an identified abscess or a septic arthritis. Further evaluation of SPE should include consideration of a transthoracic echocardiogram to exclude right-sided endocarditis. In the setting of a deep tissue infection, MRI of the infected area should be considered to evaluate for underlying osteomyelitis. If concern for a DVT arises, lower extremity venous Doppler should be performed, and if a DVT is detected a hypercoagulability workup should be considered. Physicians treating patients with SPE should be mindful of potential complications including pulmonary effusions, empyemas, pneumatocoeles, and pneumothorax that may cause clinical deterioration.3 There are limited data about the appropriate duration of antibiotic therapy for patients with SPE, but prolonged courses of antibiotics are used for most intravascular infections. In published reports, patients with SPE from an underlying deep tissue infection received
Downloaded from cpj.sagepub.com at Stockholm University Library on November 15, 2015
606
Clinical Pediatrics 54(6)
antibiotics for 4 to 8 weeks depending on the type of underlying infection.2,4,7,8 The majority of these patients were treated with only IV antibiotic therapy, or a combination of IV and oral antibiotics.2,4,7 If a DVT is identified, a specialist in pediatric hematology oncology should be consulted regarding initiation of anticoagulation therapy, expected duration of treatment, and outpatient follow-up of DVT resolution. In our patient, we suspect the source of the SPE was the multiple small abscesses found on his right leg, especially in the setting of a positive wound culture and blood culture with MRSA. We had low suspicion for a DVT contributing to this clinical picture as MRI findings did not demonstrate any bone or muscle involvement from the superficial cellulitis and abscesses, though a lower extremity venous Doppler was considered.
Conclusion Skin and soft tissue infections are commonly encountered by pediatricians in a variety of settings and are often managed with either antibiotic therapy or incision and drainage. SPE is a rare diagnosis in the pediatric population and is often the result of a primary deep tissue infection, but may occur in more superficial skin and soft tissue infections. Pediatricians should be aware of SPE when encountering a patient with an underlying tissue infection and respiratory symptoms to promptly guide their initial evaluation and management of this condition. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
References 1. Rossi SE, Goodman PC, Franquet T. Nonthrombotic pulmonary emboli. AJR Am J Roentgenol. 2000;174:14991508. doi:10.2214/ajr.174.6.1741499. 2. Cook RJ, Ashton RW, Aughenbaugh GL, Ryu JH. Septic pulmonary embolism: presenting features and clinical course of 14 patients. Chest. 2005;128:162-166. doi:10.1378/chest.128.1.162. 3. Wong KS, Lin TY, Huang YC, Hsia SH, Yang PH, Chu SM. Clinical and radiographic spectrum of septic pulmonary embolism. Arch Dis Child. 2002;87:312-315. doi:10.1136/adc.87.4.312. 4. Lin MY, Rezai K, Schwartz DN. Septic pulmonary emboli and bacteremia associated with deep tissue infections caused by community-acquired methicillin-resistant staphylococcus aureus. J Clin Microbiol. 2008;46:15531555. doi:10.1128/JCM.02379-07. 5. Ye R, Zhao L, Wang C, Wu X, Yan H. Clinical characteristics of septic pulmonary embolism in adults: a systematic review. Respir Med. 2014;108:1-8. doi:10.1016/ j.rmed.2013.10.012. 6. Bliss SJ, Flanders SA, Saint S. A pain in the neck. N Engl J Med. 2004;350:1037-1042. doi:10.1056/NEJMcps032253 7. Gonzalez BE, Teruya J, Mahoney DH, et al. Venous thrombosis associated with staphylococcal osteomyelitis in children. Pediatrics. 2006;117:1673-1679. doi:10.1542/ peds.2005-2009. 8. Schaub RL, Rodkey ML. Deep vein thrombosis and septic pulmonary emboli with MRSA osteomyelitis in a pediatric patient. Pediatr Emerg Care. 2012;28:911-912. doi:10.1097/PEC.0b013e318267ea4e. 9. Gorenstein A, Gross E, Houri S, Gewirts G, Katz S. The pivotal role of deep vein thrombophlebitis in the development of acute disseminated staphylococcal disease in children. Pediatrics. 2000;106:E87. doi:10.1542/ peds.106.6.e87. 10. Gonzalez BE, Hulten KG, Dishop MK, et al. Pulmonary manifestations in children with invasive communityacquired Staphylococcus aureus infection. Clin Infect Dis. 2005;41:583-590. doi:10.1086/432475.
Downloaded from cpj.sagepub.com at Stockholm University Library on November 15, 2015
other2014
CPJXXX10.1177/0009922814563275Clinical PediatricsSawyer and Potisek
Resident Round
Chest Pain in an Adolescent Male With a Leg Abscess
Clinical Pediatrics 2015, Vol. 54(6) 604–606 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0009922814563275 cpj.sagepub.com
Carolyn M. Sawyer, MD1 and Nicholas M. Potisek, MD2
Case Report
Hospital Course
A previously healthy 17-year-old African American male presented to the emergency department with acute onset of chest pain and shortness of breath that awoke him from sleep. He denied fevers, cough, palpitations, abdominal pain, vomiting, diarrhea, or rash and was maintaining adequate oral intake with normal urine output. Two weeks prior to presentation, he fell and scraped his right leg on asphalt while playing basketball. He subsequently developed purulent abscesses overlying his right shin. He was evaluated for these wounds the day prior to presentation and was started on cephalexin and trimethoprim/sulfamethoxazole. Physical examination revealed vital signs appropriate for age and normal oxygen saturation on room air. He generally appeared uncomfortable, though he exhibited no respiratory distress, had clear lung fields bilaterally, and had a regular cardiovascular examination without murmurs. He also had multiple small (1-cm diameter) purulent abscesses with surrounding erythema overlying his anterior right leg. In the emergency department, he received a dose of ketorolac and hydromorphone for pain control. Initial workup was notable for elevated inflammatory markers with a normal electrocardiogram, chest radiograph, complete metabolic panel, and complete blood count. Further workup with chest computed tomography to evaluate for pulmonary embolism demonstrated multiple nodular lesions in the periphery of the bilateral lung fields concerning for septic pulmonary embolism (SPE) or bronchopneumonia (see Figure 1). Empiric therapy with intravenous (IV) vancomycin and clindamycin was started after wound and blood cultures were collected. He was placed on a morphine patient-controlled analgesia infusion for pain relief and was admitted for further evaluation and management.
The patient was admitted to the hospital for IV antibiotic therapy. A transthoracic echocardiogram showed no vegetations as the source of his SPE. Magnetic resonance imaging (MRI) of the right lower extremity demonstrated cellulitis and superficial abscesses without evidence of septic joint, deep abscesses, or osteomyelitis, and a deep vein thrombosis (DVT) was unlikely as no blood flow abnormalities were detected on MRI. Initial wound and blood cultures grew methicillinresistant Staphylococcus aureus (MRSA) with no growth on subsequent blood cultures. Testing for human immunodeficiency virus was negative. No further evaluation for immunodeficiency was done as the patient had no history of recurrent bacterial or viral infections. Shortly after admission the patient became febrile, and his hospital course was complicated by the development of a large right pleural effusion with associated hypoxia requiring the placement of a chest tube. After clinical improvement, chest tube removal, resolution of fever, and downtrend of inflammatory markers, he was discharged home on monotherapy with IV clindamycin. The patient had short-term follow-up with a pediatric infectious disease specialist and completed a 5-week course of intravenous antibiotics with normalization of inflammatory markers and return to baseline state of health.
Discussion Septic pulmonary embolism is an uncommon diagnosis in the pediatric population and occurs in the setting of bacteremia when emboli containing microorganisms from an area of infection travel into the venous system to 1
Duke University Medical Center, Durham, NC, USA Wake Forest School of Medicine, Winston-Salem, NC, USA
2
Final Diagnosis Septic pulmonary embolism secondary to a soft tissue infection.
Corresponding Author: Carolyn M. Sawyer, Department of Pediatrics, Duke University Medical Center, Box 3352, Durham, NC 27710, USA. Email: [email protected]
Downloaded from cpj.sagepub.com at Stockholm University Library on November 15, 2015
605
Sawyer and Potisek
Figure 1. Axial views of computed tomography scan of chest with contrast demonstrate septic emboli throughout both lung fields with lower lobe predominance.
the pulmonary vasculature causing infarction and even abscesses within the lungs. SPE typically presents with fever, respiratory symptoms, and lung infiltrates visualized on imaging of the chest.1 Patients with SPE have been found to present with a variety of respiratory symptoms, which may include dyspnea, pleuritic chest pain, cough, and hemoptysis. Radiographs are often abnormal with the most common finding of diffuse bilateral nodular lesions; however, this finding is nonspecific and often warrants further evaluation based on the clinical presentation.2,3 CT may reveal further findings suggestive of SPE in addition to bilateral nodular densities, such as pulmonary cavities or a “feeding vessel” sign, which is an identified blood vessel on imaging that leads directly into a nodule suggesting hematogenous spread.2,3 Septic pulmonary embolism has been associated with right-sided endocarditis, indwelling catheters, intravascular disease, purulent skin or soft tissue infections, IV drug use, and deep tissue infections in adult patients.2,4,5 In the pediatric population, SPE is often associated with Lemierre’s syndrome, or septic thrombophlebitis of the internal jugular vein. Lemierre’s syndrome typically affects adolescents or young adults with precedent pharyngitis, subsequent infiltration into the internal jugular vein leading to thrombophlebitis and then hematogenous spread to the lungs and other organs.6 The gramnegative, anaerobic rod Fusobacterium necrophorum is the primary causative organism found in this syndrome. There have also been several cases of SPE in pediatric patients associated with deep tissue infections such as osteomyelitis, septic arthritis, pyomyositis, and cellulitis.3,7-9 With deep tissue infections, SPE often is associated with underlying DVT and is suspected to be from local vascular congestion and inflammation
resulting in thrombophlebitis and hematogenous spread, similar to the pathogenesis in Lemierre’s syndrome.7,8 It remains unclear how SPE occurs in the setting of more superficial skin and soft tissue infections. When SPE occurs in the setting of a deep tissue infection, community-acquired MRSA (CA MRSA) should be suspected and empiric antibiotics selected with this organism in mind.3,4,7,10 Some studies have shown CA MRSA carrying the Panton–Valentine leukocidin genes have a higher propensity to infect the lungs which may explain why we are seeing more pulmonary infections in the setting of CA MRSA infections.7,10 If there is strong clinical suspicion for SPE secondary to a deep tissue infection, a blood culture should be obtained prior to initiation of antibiotic therapy. Additionally, a wound culture should be obtained if possible in the setting of an identified abscess or a septic arthritis. Further evaluation of SPE should include consideration of a transthoracic echocardiogram to exclude right-sided endocarditis. In the setting of a deep tissue infection, MRI of the infected area should be considered to evaluate for underlying osteomyelitis. If concern for a DVT arises, lower extremity venous Doppler should be performed, and if a DVT is detected a hypercoagulability workup should be considered. Physicians treating patients with SPE should be mindful of potential complications including pulmonary effusions, empyemas, pneumatocoeles, and pneumothorax that may cause clinical deterioration.3 There are limited data about the appropriate duration of antibiotic therapy for patients with SPE, but prolonged courses of antibiotics are used for most intravascular infections. In published reports, patients with SPE from an underlying deep tissue infection received
Downloaded from cpj.sagepub.com at Stockholm University Library on November 15, 2015
606
Clinical Pediatrics 54(6)
antibiotics for 4 to 8 weeks depending on the type of underlying infection.2,4,7,8 The majority of these patients were treated with only IV antibiotic therapy, or a combination of IV and oral antibiotics.2,4,7 If a DVT is identified, a specialist in pediatric hematology oncology should be consulted regarding initiation of anticoagulation therapy, expected duration of treatment, and outpatient follow-up of DVT resolution. In our patient, we suspect the source of the SPE was the multiple small abscesses found on his right leg, especially in the setting of a positive wound culture and blood culture with MRSA. We had low suspicion for a DVT contributing to this clinical picture as MRI findings did not demonstrate any bone or muscle involvement from the superficial cellulitis and abscesses, though a lower extremity venous Doppler was considered.
Conclusion Skin and soft tissue infections are commonly encountered by pediatricians in a variety of settings and are often managed with either antibiotic therapy or incision and drainage. SPE is a rare diagnosis in the pediatric population and is often the result of a primary deep tissue infection, but may occur in more superficial skin and soft tissue infections. Pediatricians should be aware of SPE when encountering a patient with an underlying tissue infection and respiratory symptoms to promptly guide their initial evaluation and management of this condition. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
References 1. Rossi SE, Goodman PC, Franquet T. Nonthrombotic pulmonary emboli. AJR Am J Roentgenol. 2000;174:14991508. doi:10.2214/ajr.174.6.1741499. 2. Cook RJ, Ashton RW, Aughenbaugh GL, Ryu JH. Septic pulmonary embolism: presenting features and clinical course of 14 patients. Chest. 2005;128:162-166. doi:10.1378/chest.128.1.162. 3. Wong KS, Lin TY, Huang YC, Hsia SH, Yang PH, Chu SM. Clinical and radiographic spectrum of septic pulmonary embolism. Arch Dis Child. 2002;87:312-315. doi:10.1136/adc.87.4.312. 4. Lin MY, Rezai K, Schwartz DN. Septic pulmonary emboli and bacteremia associated with deep tissue infections caused by community-acquired methicillin-resistant staphylococcus aureus. J Clin Microbiol. 2008;46:15531555. doi:10.1128/JCM.02379-07. 5. Ye R, Zhao L, Wang C, Wu X, Yan H. Clinical characteristics of septic pulmonary embolism in adults: a systematic review. Respir Med. 2014;108:1-8. doi:10.1016/ j.rmed.2013.10.012. 6. Bliss SJ, Flanders SA, Saint S. A pain in the neck. N Engl J Med. 2004;350:1037-1042. doi:10.1056/NEJMcps032253 7. Gonzalez BE, Teruya J, Mahoney DH, et al. Venous thrombosis associated with staphylococcal osteomyelitis in children. Pediatrics. 2006;117:1673-1679. doi:10.1542/ peds.2005-2009. 8. Schaub RL, Rodkey ML. Deep vein thrombosis and septic pulmonary emboli with MRSA osteomyelitis in a pediatric patient. Pediatr Emerg Care. 2012;28:911-912. doi:10.1097/PEC.0b013e318267ea4e. 9. Gorenstein A, Gross E, Houri S, Gewirts G, Katz S. The pivotal role of deep vein thrombophlebitis in the development of acute disseminated staphylococcal disease in children. Pediatrics. 2000;106:E87. doi:10.1542/ peds.106.6.e87. 10. Gonzalez BE, Hulten KG, Dishop MK, et al. Pulmonary manifestations in children with invasive communityacquired Staphylococcus aureus infection. Clin Infect Dis. 2005;41:583-590. doi:10.1086/432475.
Downloaded from cpj.sagepub.com at Stockholm University Library on November 15, 2015
