Necrotizing Pneumonia: Diagnosis and Treatment Options

Brian D. Skidmore, BS¹ and Veronica A. Arteaga, MD²

¹College of Medicine and ²Department of Medical Imaging

Banner-University Medical Center

University of Arizona

Tucson, AZ USA

Abstract

We present the case of a patient who was initially diagnosed with community-acquired pneumonia that was later discovered to have necrotizing changes. The case illustrates the challenges in diagnosing necrotizing pneumonia and the preferred treatment methods.

Case Presentation

History of Present Illness

The patient is a 51-year old woman who presents with right upper lobe pneumonia and a failed outpatient regimen of levofloxacin. She returned one week after being seen in the emergency department with worsening dyspnea, productive cough, and fever in addition to new symptoms of right chest pain and post-tussive emesis. The chest pain is stabbing in quality and constantly present. She denied any calf pain/swelling, previous history of deep venous thrombosis, or long trips or travels.

Physical Exam

Upon admission, blood pressure was 103/56 with a pulse of 114 and respiratory rate of 18. Her temperature was 38.1 °C (100.5 °F) but spiked at 39.5 °C (103.1 °F) and her SpO₂ was 94.0% on room air. Her breathing was unlabored and her lungs were clear to auscultation bilaterally except for crackles in the right upper lung field. The remainder of the exam was unremarkable.

Laboratory and Imaging

A chest radiograph was initially obtained and showed a right upper lobe consolidation consistent with community-acquired pneumonia (Figure 1).

Figure 1. Chest radiograph showing right upper lobe consolidation with possible volume loss.

One week later, a contrast-enhanced chest CT was performed and revealed a heterogeneously enhancing right upper lobe consolidation with cavitation and foci of air diagnostic of necrotizing pneumonia (Figure 2).

Figure 2. Contrast-enhanced chest CT showing right upper lobe pneumonic consolidation with peripheral enhancement, central necrosis, and small foci of air.

Laboratory studies revealed a markedly elevated C-reactive protein of 16.61 mg/dL and a white blood cell count of 18,000 cells/ μL. In addition, the red blood cell count, hemoglobin, and hematocrit were all reduced with values of 3,390,000 cells/ μL, 10.0 g/dL, and 31.0% respectively.

Hospital Course

A chest CT was ordered and the patient was diagnosed with necrotizing pneumonia. She was given IV vancomycin and piperacillin-tazobactam as empiric therapy. Tylenol was administered for fever management and steroids were deferred because her CURB-65 score for pneumonia severity was 0.

Attention was then given to identifying the infectious agent. Blood and respiratory cultures were obtained and a TB test was ordered. The cultures showed no growth and the TB test was negative. A bronchoalveolar lavage showed a highly neutrophilic cell count, however no pathogen was ever identified.

Given improvement with empiric therapy, during her hospital course she was discharged on oral amoxicillin and clavulanate until follow up with pulmonary in outpatient 6 weeks later. Imaging at that time showed post inflammatory changes and no evidence of infection.

Discussion

Necrotizing pneumonia is a rare complication of bacterial lung infections affecting 4% of all patients with community-acquired pneumonia (1). The infection can be patchy, segmental, or involve the entire lung. While the pathogenesis of necrotizing pneumonia is not clearly defined, most studies indicate that it is either an inflammatory response to toxins produced by the pathogen or it is the result of associated vasculitis and venous thrombosis. Patients typically present with common symptoms of pneumonia such as fever, cough, shortness of breath, and chest pain but can also rapidly develop hemoptysis, septic shock, and respiratory failure as the necrosis progresses (2). Because necrotizing pneumonia is associated with increased morbidity and mortality, it is important to distinguish it from non-necrotizing cases (3).

The diagnosis of necrotizing pneumonia may be difficult to make because of its similar presentation to non-necrotizing pneumonias and the limitations of standard chest radiographs. Chest radiographs may show an area of consolidation but are limited in identifying the extent of parenchymal disease (Figure 1) (2). Therefore, contrast-enhanced chest CT is an optimal exam for diagnosing necrotizing pneumonia. Disease may first appear as an in-homogeneously enhancing consolidation with focal areas of low attenuation (Figure 2).  Foci of air may subsequently develop in these areas of hypo-enhancing necrotic tissue indicating cavitation (4).

Laboratory studies may also be helpful in diagnosing necrotizing pneumonia. When compared to pneumonias without a necrotizing component, patients with necrotizing pneumonia show more elevated white blood cell counts and inflammatory markers (1). In one study, patients with necrotizing pneumonia had an average WBC count of 14,970/μL, an average ESR of 70 mm/h, and an average CRP of 18.8 mg/dL. Average values for patients with non-necrotizing pneumonia were significantly lower at 10,130/μL, 48 mm/h, and 11.4 mg/dL respectively (p<0.001) (3). These changes are also evident in the presented case with elevated WBC and CRP values of 18,000/μL and 16.61 mg/dL.

Necrotizing pneumonia is initially treated with intravenously administered broad-spectrum antibiotics that should target pathogens that commonly cause necrotizing changes. The most common microbes are Staphylococcus aureus, Streptococcus pneumoniae, and Klebsiella pneumoniae, however several other bacteria species may also cause necrosis (Table 1) (2).

Transition to oral antibiotics may be considered for patients that show improvement (1). A more focused treatment plan should be initiated once a specific pathogen is identified, however this is only accomplished in approximately 26% of cases (3).

Surgical resection may also be considered for patients who show no progress on antibiotic therapy and continue to decline. However the optimal timing and indications for surgery are not clearly defined. The extent of the resection should always be as conservative as possible and commonly involves debridement or segmentectomy of the damaged tissue. In cases where the parenchyma is extensively affected, lobectomy or pneumonectomy may be required (2).

References

1. Nicolaou EV, Bartlett AH. Necrotizing pneumonia. Pediatr Ann. 2017;1;46(2):e65-e68. [CrossRef] [PubMed]
2. Tsai YF, Ku YH. Necrotizing pneumonia: a rare complication of pneumonia requiring special consideration. Curr Opin Pulm Med. 2012;18(3):246-52. [CrossRef] [PubMed]
3. Seo H, Cha SI, Shin KM, et al. Clinical relevance of necrotizing change in patients with community-acquired pneumonia. Respirology. 2017;22(3):551-8. [CrossRef] [PubMed]
4. Walker CM, Abbott GF, Greene RE, Shepard JO, Vummidi D, Digumarthy SR. Imaging Pulmonary Infection: Classic Signs and Patterns. AJR Am J Roentgenol. 2014;202(3) 479-92. [CrossRef] [PubMed]

Cite as: Skidmore BD, Arteaga VA. Necrotizing pneumonia: diagnosis and treatment options. Southwest J Pulm Crit Care. 2017;15(6):274-7. doi: https://doi.org/10.13175/swjpcc137-17 PDF

Staphylococcus aureus Sternal Osteomyelitis: a Rare Cause of Chest Pain

Manjinder Kaur DO

Courtney Walker DO

Emily S. Nia MD

Jeffrey R. Lisse MD

Department of Medicine

Banner University Medical Center

Tucson, AZ USA

Abstract

Chest pain is a common presenting symptom with a broad differential. Life-threatening cardiac and pulmonary etiologies of chest pain should be evaluated first. However, it is critical to perform a thorough assessment for other sources of chest pain in order to limit morbidity and mortality from less common causes. We present a rare case of a previously healthy 45 year old man who presented with focal, substernal, reproducible chest pain and Staphylococcus aureus bacteremia who was later found to have primary Staphylococcus aureus sternal osteomyelitis.

Case Report

A 45 year old previously healthy man presented to the emergency department with sudden onset substernal chest pain of two days duration. The pain was described as constant, achy, worsened with movement, and improved with lying still.  Palpation of the manubrium reproduced pain and was associated with an appreciable “bump”. The patient denied recent trauma or surgery and reported no fevers, weight loss, night sweats, cough, or history of intravenous drug use. He had multiple tattoos covering his thorax and abdomen obtained while incarcerated twenty years prior to admission. On examination, the patient was uncomfortable due to severe sternal pain. He was diaphoretic, tachycardic, tachypneic, and afebrile. His manubrium was tender to palpation and the overlying skin was warm and mildly swollen without apparent erythema, induration, or drainage. Laboratory results were remarkable for leukocytosis of 18,4000/uL with 92% neutrophils, serial troponins less than 0.01 ng/mL, ESR 15 mm/hr, c-reactive protein (CRP) 13.40 mg/dL, nonreactive HIV antibodies, and positive hepatitis C virus (HCV) antibody with detectable but unquantifiable HCV RNA. Electrocardiogram showed normal sinus rhythm without ischemia. Bibasilar atelectasis was appreciated on chest x-ray and chest CT with contrast revealed no bone or chest wall lesions. Sternum MR with contrast (Figure 1) showed enhancing edema in the subcutaneous soft tissues overlying the sternomanubrial joint with extension into the pectoralis major musculature symmetrically without abscess or bony involvement.

Figure 1. Sagittal and axial T2 fat sat images (A and B) demonstrate inflammatory changes involving the soft tissues overlying the sternum including the pectoralis muscles bilaterally. Sagittal and axial T1 post contrast images (C and D) demonstrate avid enhancement involving the soft tissues overlying the sternum consistent with phlegmonous change without a rim enhancing loculated fluid collection to suggest an abscess formation. No underlying osseous involvement is present. A tissue marker corresponds to the patient’s site of pain. 

On day two of admission, blood culture results were reported positive for Staphylococcus aureus oxacillin susceptible (MSSA). Positive blood cultures persisted despite appropriate antibiotics. A transesophageal echocardiogram (TEE) was performed and showed no vegetations. Although chest imaging was negative for osteomyelitis, the persistent bacteremia and focal sternomanubrial pain was clinically suggestive of primary sternal osteomyelitis. The patient was discharged to home and completed a six week course of intravenous cefazolin for presumed MSSA sternal osteomyelitis.  

Repeat MR sternum performed eight weeks after initial presentation showed osteomyelitis across the sternomanubrial joint with improved soft tissue edema
(Figure 2).

Figure 2. Sagittal and axial T2 fat sat images (A and B) demonstrate interval improvement in inflammatory changes involving the soft tissues overlying the sternum with persistent edema present at the sternomanubrial joint (red arrow). Sagittal T1 image (C) demonstrates focal hypointense bone marrow about the sternomanubrial joint (red arrow). Sagittal and axial T1 post contrast images (D and E) demonstrate enhancement of the sternomanubrial joint (red arrow). Overall findings are consistent with osteomyelitis of the sternomanubrial joint.

Given that the patient had completed six weeks of parenteral antibiotic therapy, his sternal chest pain had resolved, and CRP had normalized, additional antibiotics were not prescribed and the patient was asked to follow up with his primary care provider as needed. There was no incidence of further complication and the patient was diagnosed with primary MSSA sternal osteomyelitis.

Discussion       

Primary osteomyelitis of the sternum in immunocompetent patients is extremely rare, accounting for 0.3% of all cases of osteomyelitis reported in the literature (1). Common risk factors for primary sternal osteomyelitis are trauma, pneumonia, diabetes, immunodeficiency, or history of IV drug use (2,3). Our patient had none of these risk factors. Risks for secondary sternal osteomyelitis are due to complications from sternal incision post-thoracic surgery(1-3). Staphylococcus aureus is the most common organism of both primary and secondary sternal osteomyelitis (2).

Early diagnosis of acute osteomyelitis is critical in order to prevent necrosis of bone, as well as other local and systemic complications, from delayed antibiotic therapy. Multiple imaging modalities are available to confirm the presumed clinical diagnosis of osteomyelitis. MRI is 82% to 100% sensitive and 75% to 96% specific and is considered the gold standard in diagnosis of acute osteomyelitis (4). However, as evidenced by our case, imaging findings may lag behind clinical presentation. Clinicians need to consider primary osteomyelitis in the differential diagnosis of a young patient who presents with focal sternal chest pain, swelling, and bacteremia. A strong index of suspicion for acute osteomyelitis is needed in order to promptly initiate antibiotic therapy to reduce morbidity and mortality associated with untreated osteomyelitis (1,2).

References

1. de Nadai TR, Daniel RF, de Nadai MN, da Rocha JJ, Féres O. Hyperbaric oxygen therapy for primary sternal osteomyelitis: a case report. J Med Case Rep. 2013;7:167. [CrossRef] [PubMed]
2. Gill EA Jr, Stevens DL. Primary sternal osteomyelitis. West J Med. 1989;151(2):199-203. [PubMed]
3. Vacek TP, Rehman S, Yu S, Moza A, Assaly R. Another cause of chest pain: Staphylococcus aureus sternal osteomyelitis in an otherwise healthy adult. Int Med Case Rep J. 2014;7:133-7. [CrossRef] [PubMed]
4. Pineda C, Espinosa R, Pena A. Radiographic imaging in osteomyelitis: the role of plain radiography, computed tomography, ultrasonography, magnetic resonance imaging, and scintigraphy. Semin Plast Surg. 2009;23(2):80-9. [CrossRef] [PubMed] 

Cite as: Kaur M, Walker C, Nia ES, Lisse JR. Staphylococcus aureus sternal osteomyelitis: a rare cause of chest pain. Southwest J Pulm Crit Care. 2015;11(4):167-70. doi: http://dx.doi.org/10.13175/swjpcc131-15 PDF