Pediatric Annals

Special Issue Article 

Necrotizing Pneumonia

Elitsa V. Nicolaou, MD; Allison H. Bartlett, MD, MS

Abstract

Necrotizing pneumonia refers to the development of necrosis, liquefication, and cavitation of the lung parenchyma from an infectious pathogen. Nearly 4% of all community-acquired pneumonias are necrotizing, although studies retrospectively evaluating the incidence have found it to be increasing during the past 20 years. Common presenting symptoms include fever, tachypnea, and cough, and most of those afflicted also develop complications such as parapneumonic effusions, empyemas, or bronchopleural fistulae. When compared to age-matched controls with parapneumonic effusions or severe pneumonias without a necrotizing component, those with necrotizing pneumonia have been shown to have more elevated white blood cell counts and inflammatory markers that take longer to normalize, a longer duration of symptoms despite initiation of therapy, and a longer hospital stay. Despite the high incidence of complications during the acute phase of illness, the overall prognosis of necrotizing pneumonia has been shown to be promising, with nearly all children surviving the illness. [Pediatr Ann. 2017;46(2):e65–e68.]

Abstract

Necrotizing pneumonia refers to the development of necrosis, liquefication, and cavitation of the lung parenchyma from an infectious pathogen. Nearly 4% of all community-acquired pneumonias are necrotizing, although studies retrospectively evaluating the incidence have found it to be increasing during the past 20 years. Common presenting symptoms include fever, tachypnea, and cough, and most of those afflicted also develop complications such as parapneumonic effusions, empyemas, or bronchopleural fistulae. When compared to age-matched controls with parapneumonic effusions or severe pneumonias without a necrotizing component, those with necrotizing pneumonia have been shown to have more elevated white blood cell counts and inflammatory markers that take longer to normalize, a longer duration of symptoms despite initiation of therapy, and a longer hospital stay. Despite the high incidence of complications during the acute phase of illness, the overall prognosis of necrotizing pneumonia has been shown to be promising, with nearly all children surviving the illness. [Pediatr Ann. 2017;46(2):e65–e68.]

This article discusses necrotizing pneumonia in children, including its presentation, diagnosis, and treatment.

Illustrative Case

A 28-day-old, full-term infant presented to a referring hospital with a 3-day history of cough. The cough was described as intermittent and worse in the mornings. It became productive of green mucous on the morning of presentation, prompting the mother to bring the infant to the hospital emergency department (ED). The patient had no fever, emesis, rash, difficulty breathing, or cyanosis. Oral intake of formula, urine output, and stool output were normal. Birth history was unremarkable. In the ED, the patient was afebrile with a pulse of 136 beats per minute, respiratory rate of 28 breaths per minute (bpm), and oxygen saturation of 95% on room air. The child was noted to be awake, alert, and active on physical examination without any respiratory distress or focal findings on auscultation of the lungs. The white blood cell count was 16,000/mcL (28% neutrophils, 11% band forms, 41% lymphocytes, and 20% monocytes), hemoglobin was 13.5 g/dL, hematocrit was 40%, and platelets were 483,000/mcL. Serum chemistries were normal except for a potassium of 5.8 mmol/L. Chest radiograph revealed a left lower lobe infiltrate, and the patient was transferred to our institution with concern for pneumonia.

Upon arrival at our institution, the patient's vital signs were unchanged except for a respiratory rate of 48 bpm. Her weight (2,845 g) was unchanged from her birth weight. Examination revealed an infant resting comfortably with an intermittent wet cough, and no increased work of breathing. Lung examination was normal. Chest radiograph revealed a lucency in the right lung field suspicious for possible congenital pulmonary airway malformation (CPAM) and possible pneumonia with air cavitation. A contrast-enhanced chest computed tomography (CT) scan was obtained to further characterize the lung pathology and demonstrated multiple bilateral cystic and nodular lesions, many with central cavitation and air fluid levels, concerning for necrotizing pneumonia and possible underlying CPAM (Figure 1 and Figure 2).


            Axial view in lung window from the patient's contrast-enhanced chest computed tomography scan showing right lung base opacities with multiple cavitary lesions, as well as left-sided opacities with cavitary lesions, suggestive of necrotizing pneumonia.

Figure 1.

Axial view in lung window from the patient's contrast-enhanced chest computed tomography scan showing right lung base opacities with multiple cavitary lesions, as well as left-sided opacities with cavitary lesions, suggestive of necrotizing pneumonia.


            Axial view in mediastinal window from the patient's contrast-enhanced chest computed tomography scan, showing right lung base opacities with cavitary lesions bilaterally.

Figure 2.

Axial view in mediastinal window from the patient's contrast-enhanced chest computed tomography scan, showing right lung base opacities with cavitary lesions bilaterally.

The Pediatric Infectious Diseases, Pediatric Pulmonology, and Pediatric Surgery teams were consulted. Despite the lack of fever, concern for an infectious etiology, possibly superimposed upon a congenital malformation, remained high. Although the bilateral nature of parenchymal involvement argued against an underlying congenital malformation, a superinfection would need to be treated prior to additional surgical intervention. Ultrasound of the head and abdomen were also performed, the results of which were normal and not revealing of further cystic lesions to suggest a congenital malformation.

Given the broad differential list of pathogens (routine bacterial, fungal, mycobacterial, viral) and the clinical stability of the patient, the subspecialty teams that were consulted thought it best to wait to initiate antimicrobial therapy until a pathogen had been identified. Noninvasive testing for cytomegalovirus (urine and serum polymerase chain reaction testing), aspergillus (serum galactomannan), and syphilis (rapid plasma reagin) was sent, as well as blood cultures and a respiratory viral panel, all which returned negative; testing for acid-fast bacilli (AFB) from gastric lavage also returned negative.

Given the unusual presentation of an extensive area of pulmonary involvement in the absence of fever and tachypnea, there was concern for an underlying immunodeficiency. Quantitative immunoglobulins, lymphocyte subsets, neutrophil oxidative burst, and HIV testing were all normal.

The consensus among the Pediatric Surgery, Interventional Radiology, and Pediatric Pulmonology teams was that bronchoscopy would be the safest method to obtain specimens for diagnostic purposes. Bronchoscopy was performed on hospital day 3, and proved challenging due to the small size of the patient's airway and hypoxia requiring bag-mask ventilation during the procedure. After the bronchoscopy, the patient required supplemental oxygen via high-flow nasal cannula; this was successfully weaned off within 12 hours. Antibiotic therapy, with ceftriaxone and vancomycin, was started after the procedure.

Bronchoalveolar lavage (BAL) fluid was sent for aerobic and anaerobic culture, AFB smear and culture, fungal smear and culture, aspergillus antigen, and Pneumocystis jirovecii assay. Quantitative culture grew 68,000 colony-forming units (CFU) per milliliter of methicillin-resistant Staphylococcus aureus (MRSA), along with 1,000 CFU per milliliter of normal flora; all other studies were negative. The MRSA was also resistant to clindamycin, so the patient was treated with vancomycin monotherapy. Throughout the entirety of her hospitalization she remained afebrile. She completed a 21-day course of vancomycin and was doing well when seen at a follow-up outpatient visit. Repeat chest CT 2 months after her presentation showed a pneumatocele and linear scarring at the prior site of pneumonia, not concerning for a CPAM.

The patient was diagnosed with necrotizing pneumonia secondary to MRSA. Interestingly, however, her clinical stability, lack of fever, and unremarkable respiratory status throughout her hospital course is surprising given the extent of her MRSA pneumonia on imaging.

Necrotizing Pneumonia

Necrotizing pneumonia refers to the development of necrosis, liquefication, and cavitation of the lung parenchyma from an infectious pathogen. Approximately 3.7% of all community-acquired pneumonias are necrotizing, although studies retrospectively evaluating the incidence have found it to be increasing during the past 20 years.1–3 The median age of affected children is 4 years, and most are immunocompetent.1–3

Necrotizing pneumonia secondary to MRSA has been infrequently reported in infants younger than age 1 month. A case report of a previously healthy, full-term infant with community-acquired MRSA necrotizing pneumonia presenting at 23 days of postnatal life reported a tortuous course involving total pneumonectomy and use of high-frequency oscillatory ventilation.4 This is a stark contrast to our patient. MRSA necrotizing pneumonia has also been reported in an extremely premature infant born at 25 weeks of gestation who became septic and required mechanical ventilation at 19 days of postnatal life.5 This infant had been in the neonatal intensive care unit since birth and presented with lethargy, hypoxia, and a distended abdomen. In addition to the MRSA necrotizing pneumonia, he was found to have MRSA bacteremia and a perforated abdominal viscus. Interestingly, the MRSA isolate from this patient was found to be identical to strains that primarily cause community-associated skin and soft tissue infections.5

Common presenting symptoms of necrotizing pneumonia include fever (96%), tachypnea (90%), and cough (84%), and more than 85% of those afflicted also develop complications such as parapneumonic effusions, empyemas, or bronchopleural fistulae.1–3 When compared to age-matched controls with parapneumonic effusions or severe pneumonias without a necrotizing component, those with necrotizing pneumonia have been shown to have more elevated white blood cell counts and inflammatory markers that take longer to normalize, a longer duration of symptoms despite initiation of therapy, including time to defervesence, and a longer hospital stay.2

Blood and pleural fluid culture is also often obtained in patients with necrotizing pneumonia, although pleural fluid culture has been shown to be higher yield. A causative organism is identified less than half the time (as low as 11% in some studies), which may be due to the frequent initiation of outpatient antibiotics at the onset of illness prior to the development of a more severe disease course.1–3Streptococcus pneumoniae is the most common pathogen identified, followed by S. aureus, Mycoplasma pneumoniae, and Klebsiella species.1–3,6 Other organisms, including cytomegalovirus, have been shown to cause a severe and diffuse necrotizing pneumonia in infants.7 MRSA pneumonia more commonly affects children at approximately age 4 years, and often is associated with a preceding viral infection.8 In contrast, the most common bacteria causing invasive infections in infants younger than age 1 month are Group B Streptococcus, Escherichia coli, and other gram-negative enteric agents.5

Most patients afflicted with necrotizing pneumonia tend to be immunocompetent, and it is not fully understood why the same pathogen may lead to a more extensive disease process in one healthy host versus another, although variations in host inflammatory response, antibiotic resistance, and timely initiation of effective antibiotics all likely play a role.6

A typical treatment course for necrotizing pneumonia includes empiric intravenous antimicrobial therapy with possible transition to oral antibiotics for a median duration of 28 days.1,2 Empiric therapy of suspected invasive infections in neonates often consists of ampicillin, with a goal of providing Group B Streptococcus coverage, combined with gentamicin or cefotaxime for gram-negative coverage.9

When a pathogen is identified as the cause of necrotizing pneumonia, therapy can be tailored; interestingly, outcomes of those with and without a pathogen identified do not seem to differ.1 Standard empiric antimicrobial coverage for our patient would not have treated her infection. Given local resistance trends (89% of S. aureus isolates are sensitive to clindamycin), we use clindamycin as empiric S. aureus coverage in a well-appearing child, which would allow for eventual transition to oral antibiotics. If we had started vancomycin in the absence of culture data, and the patient had improved, we could be committing the patient to a 4-week intravenous course of antibiotics.

As more than 85% of patients with necrotizing pneumonia also have involvement of the pleural cavity, various surgical interventions including chest tube placement, thoracentesis, video-assisted thoracoscopic surgery, and pneumonectomy may also be performed, with the former being the most common.1–3 These may be done for diagnostic or therapeutic reasons, and in the case of our patient, bronchoscopy proved essential in making a diagnosis.

Despite the high incidence of complications during the acute phase of illness, the overall prognosis of necrotizing pneumonia has been shown to be promising, with nearly all children surviving the illness.1–3 Furthermore, signs and symptoms as well as radiographic evidence of disease has been shown to resolve by 6 months after initial presentation, with one retrospective study reporting complete clinical resolution of all patients by 2 months after presentation.1,3

Conclusion

The diagnosis of necrotizing pneumonia may be a challenging one to make, but timely recognition remains critical given the high incidence of complications during the acute phase of illness.

The infant in this illustrative case presented with surprisingly few symptoms and strikingly abnormal imaging. Rather than having an infection with a typical pathogen expected for her age, she was diagnosed with MRSA based on a culture of bronchoalveolar lavage fluid. Although MRSA infections are on the rise and neonates can be colonized during or soon after birth with S. aureus, the majority do not develop infectious sequelae, and even fewer develop invasive disease.1–3,8,10 This case highlights the importance of a thoughtful, multidisciplinary approach and the benefit of obtaining a culture in a diagnostically challenging patient who remained well-appearing despite invasive disease.

References

  1. Krenke K, Sanocki M, Urbankowska E, et al. , Necrotizing pneumonia and its complications in children. Adv Exp Med Biol. 2015;857:9–17. doi:10.1007/5584_2014_99 [CrossRef]
  2. Hacimustafaoglu M, Celebi S, Sarimehmet H, et al. , Necrotizing pneumonia in children. Acta Paediatr. 2004;93(9):1172–1177. doi:10.1111/j.1651-2227.2004.tb02744.x [CrossRef]
  3. Sawicki G, Lu F, Valim C, et al. , Necrotising pneumonia is an increasingly detected complication of pneumonia in children. Eur Respir J. 2008;31:1285–1291. doi:10.1183/09031936.00099807 [CrossRef]
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  8. McAdams R, Mazuchowski E, Ellis M, et al. , Perinatal/neonatal case presentation: necrotizing Staphylococcal pneumonia in a neonate. J Perinatol. 2005;25:677–679. doi:10.1038/sj.jp.7211364 [CrossRef]
  9. Bradley J, Byington C, Shah S, et al. , The management of community-acquired pneumonia in infants and children older than 3 months of age: clinical practice guidelines by the Pediatric Infectious Disease Society and the Infectious Diseases Society of America. Clin Inf Dis. 2011;53(7):25–76. doi:10.1093/cid/cir531 [CrossRef]
  10. Gerber J, Coffin S, Smathers S, Zaoutis T. Trends in the incidence of methicillin-resistant Staphylococcus aureus infections in children's hospitals in the United States. Clin Infect Dis. 2009;49(1):65–71. doi:10.1086/599348 [CrossRef]
Authors

Elitsa V. Nicolaou, MD, is a Pediatric Resident, Comer Children's Hospital, Pritzker School of Medicine, The University of Chicago. Allison H. Bartlett, MD, MS, is an Assistant Professor of Pediatrics, Section of Infectious Diseases, Comer Children's Hospital, Pritzker School of Medicine, The University of Chicago.

Address correspondence to Elitsa V. Nicolaou, MD, The University of Chicago, 5721 S. Maryland Avenue, Room K155, MC8016, Chicago, IL 60637; email: elitsa.nicolaou@uchospitals.edu.

Disclosure: The authors have no relevant financial relationships to disclose.

10.3928/19382359-20170120-02

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