Pulmonary

Last 50 Pulmonary Postings

(Click on title to be directed to posting, most recent listed first, CME offerings in Bold)

April 2017 Pulmonary Case of the Month
March 2017 Pulmonary Case of the Month
February 2017 Pulmonary Case of the Month
January 2017 Pulmonary Case of the Month
December 2016 Pulmonary Case of the Month
Inhaler Device Preferences in Older Adults with Chronic Lung Disease
November 2016 Pulmonary Case of the Month
Tobacco Company Campaign Contributions and Congressional Support
   of the Cigar Bill
October 2016 Pulmonary Case of the Month
September 2016 Pulmonary Case of the Month
August 2016 Pulmonary Case of the Month
July 2016 Pulmonary Case of the Month
June 2016 Pulmonary Case of the Month
May 2016 Pulmonary Case of the Month
April 2016 Pulmonary Case of the Month
Pulmonary Embolism and Pulmonary Hypertension in the Setting of
   Negative Computed Tomography
March 2016 Pulmonary Case of the Month
February 2016 Pulmonary Case of the Month
January 2016 Pulmonary Case of the Month
Interval Development of Multiple Sub-Segmental Pulmonary Embolism in
Mycoplasma Pneumoniae Bronchiolitis and Pneumonia
December 2015 Pulmonary Case of the Month
November 2015 Pulmonary Case of the Month
Why Chronic Constipation May be Harmful to Your Lungs
Traumatic Hemoptysis Complicating Pulmonary Amyloidosis
Staphylococcus aureus Sternal Osteomyelitis: a Rare Cause of Chest Pain
Safety and Complications of Bronchoscopy in an Adult Intensive Care Unit
October 2015 Pulmonary Case of the Month: I've Heard of Katy
   Perry
Pulmonary Hantavirus Syndrome: Case Report and Brief Review
September 2015 Pulmonary Case of the Month: Holy Smoke
August 2015 Pulmonary Case of the Month: Holy Sheep
Reducing Readmissions after a COPD Exacerbation: A Brief Review
July 2015 Pulmonary Case of the Month: A Crazy Case
June 2015 Pulmonary Case of the Month: Collapse of the Left Upper
   Lobe
Lung Herniation: An Unusual Cause of Chest Pain
Valley Fever (Coccidioidomycosis): Tutorial for Primary Care Professionals
Common Mistakes in Managing Pulmonary Coccidioidomycosis
May 2015 Pulmonary Case of the Month: Pneumonia with a Rash
April 2015 Pulmonary Case of the Month: Get Down
March 2015 Pulmonary Case of the Month: Sticks and Stones May
   Break My Bronchi
Systemic Lupus Erythematosus Presenting As Cryptogenic Organizing 
   Pneumonia: Case Report
February 2015 Pulmonary Case of the Month: Severe Asthma
January 2015 Pulmonary Case of the Month: More Red Wine, Every
   Time
December 2014 Pulmonary Case of the Month: Bronchiolitis in Adults
November 2014 Pulmonary Case of the Month: BAL Eosinophilia
How Does Genetics Influence Valley Fever? Research Underway Now To
   Answer This Question
October 2014 Pulmonary Case of the Month: A Big Clot
September 2014 Pulmonary Case of the Month: A Case for Biblical
   Scholars

 

For complete pulmonary listings click here.

The Southwest Journal of Pulmonary and Critical Care publishes articles broadly related to pulmonary medicine including thoracic surgery, transplantation, airways disease, pediatric pulmonology, anesthesiolgy, pharmacology, nursing  and more. Manuscripts may be either basic or clinical original investigations or review articles. Potential authors of review articles are encouraged to contact the editors before submission, however, unsolicited review articles will be considered.

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Tuesday
Dec012015

December 2015 Pulmonary Case of the Month

Zachary M. Berg, MD

Kashif Yaqub, MD 

Brian Wojek, MD

Khang Tran, MD

Karen L. Swanson, DO

 

Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ

 

History of Present Illness

The patient is a 70-year-old man with a history of a chronic dry cough for 5 years, who presented to the emergency department with worsening cough and shortness of breath.

Two weeks prior to symptom onset, was on trip in the United Kingdom, he developed gastroenteritis which spontaneously resolved.

Past Medical History, Social History, and Family History

  • Old healed TB scar with positive PPD at 17 years of age prior to joining Air Force.  No treatment given and patient was asymptomatic from a pulmonary point of view since then.
  • Squamous cell carcinoma of the skin on the scalp, status post excision complicated by osteomyelitis, status post surgical graft from hip with prolonged course of IV antibiotics in 2010.
  • Fractured left clavicle, status post repair 20 years ago.
  • Hay fever.
  • Hyperlipidemia.
  • Squamous cell carcinoma removed from left arm.
  • Varicose veins, lower extremity.
  • Married. Retired police officer. Does not smoke.
  • Family history is noncontributory

Physical Examination

  • General:  In moderate respiratory distress.  
  • Vitals: SpO2 on room air of 65%, 94% on high flow oxygen.  Blood pressure 124/84, afebrile  
  • Lungs:  Fine bibasilar crackles posteriorly.  
  • Heart: Regular rhythm without murmur.
  • The remainder of the physical examination was normal.

Laboratory Evaluation

  • CBC: unremarkable except white blood cell count 20.5 x 103 cells/ɥL, neutrophil predominant
  • BNP: 366 pg/mL
  • Mycobacterium Quantiferon: Positive
  • Mycoplasma IgM: Positive at 1.18 U/L

Radiography

Initial chest x-ray is shown in Figure 1.

Figure 1. Initial chest x-ray.

What is the best next step in the patient's evaluation? (Click on the correct answer to proceed to the second of five panels)

  1. Begin erythromycin or doxycycline for Mycoplasma pneumonia
  2. Begin heparin for presumptive pulmonary embolism
  3. Thoracic CT scan
  4. 1 and 3
  5. All of the above

Cite as: Berg ZM, Yaqub K, Wojek B, Tran K, Swanson KL. December 2015 pulmonary case of the month. Southwest J Pulm Crit Care. 2015;11(6):240-5. doi: http://dx.doi.org/10.13175/swjpcc146-15 PDF

Sunday
Nov012015

November 2015 Pulmonary Case of the Month

Kristal Choi, MD

Lewis J. Wesselius, MD

 

Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ

 

History of Present Illness

A 66 year-old woman was admitted to neurology with acute-onset dysarthria, right facial droop, and right-sided hemiparesis as a stroke alert. She also had a nonproductive cough and intermittent dyspnea for 4 months.

Past Medical History, Social History and Family History

  • She has a history of hypertension and hyperlipidemia. 
  • She smoked 1-2 packs/day for 15 years but quit 35 years ago. She drinks two glasses of wine per day.
  • There is a family history of bowel and breast cancer.

Physical Examination

  • Vital signs: T 36.8, HR 81, BP 129/75, RR 18, O2 sat 93% RA
  • General: No acute distress. Awake and alert.
  • Heart, abdomen, and lungs: No significant abnormalities
  • Neurological: Mild right-sided nasolabial fold flattening.  Evidence of ptosis o the right eyelid. Hemiparesis on the right, the arm greater than leg. Sensation intact. Dysmetria on the right upper and lower extremities.

Laboratory Evaluation

  • CBC: Hemoglobin 11.9 g/dL, white blood cells (WBC) 7,900 cells/mcL, platelets 290,000 cells/mcL
  • Basic metabolic panel: Na+ 139 mEq/L, K+ 4 mEq/L, Cl- 100 mEq/L , bicarbonate 22 mEq/L, creatinine 0.7 mg/dL

Radiography

A head CT angiogram (CTA) was performed (Figure 1).

Figure 1. Representative images from CTA of the head.

Which of the following should be done next? (Click on the correct answer to proceed to the second of six panels)

  1. Administer an intravenous injection of tissue plasminogen activator (TPA)
  2. Administer detachable coils (coiling or endovascular embolization) or stereotactic radiosurgery
  3. Begin an anti-convulsant and dexamethasone
  4. 1 and 3
  5. All of the above

Cite as: Choi K, Wesselius LW. November 2015 pulmonary case of the month. Southwest J Pulm Crit Care. 2015;11(5):200-8. doi: http://dx.doi.org/10.13175/swjpcc134-15 PDF

Thursday
Oct292015

Why Chronic Constipation May be Harmful to Your Lungs: A Case Report and Review of Lipoid Pneumonia and Mycobacterium fortuitum Leading to Acute Respiratory Failure and Septic Shock

Sandra Till, DO

Manoj Mathew, MD 

Da-Wei Liao, MD

Christina Ramirez, MD 

Banner University Medical Center

Phoenix, AZ

 

Case Report

A 43 year-old female with a past medical history of right-sided hemiparesis secondary to motor vehicle accident 17 years prior presented a two week history of cough, fever and right-sided pleuritic chest pain. Her baseline status included using a wheelchair, living alone at home and working as a teacher.

On admission she had a temperature of 39.6º C, was tachycardia and hypotensive requiring vasopressors. Labs were remarkable for a white count of 25,000 cells/mcL. Chest x-ray showed right-sided infiltrate and pleural effusion (Figure 1).

Figure 1. Chest x-ray on presentation.

Bronchoscopy and thoracentesis was performed upon admission. The pleural fluid wasexudative with a glucose of 78 and no suggestion of loculations on chest x-ray or ultrasound. The patient was started on therapy for community-acquired pneumonia.

On day 4 after admission, the patient had increasing sinus tachycardia, hypotension and was worsening despite being on antimicrobial therapy. A CT angiogram of the chest was performed (Figure 2).

Figure 2. Initial CT scan on day 4 of admission. Panel A: axial view showing pneumonia and right pleural effusion. Panel B: coronal view.

CT angiogram was negative for pulmonary embolism and a percutaneous chest tube was placed on day 4 for drainage of pleural effusion due to development of loculations. On day 7, the pleural fluid from initial thoracentesis grew acid-fast bacteria identified as Mycobacterium fortuitum.

Bronchoscopy was performed on day 8 and there was no endobronchial obstruction.

Bronchoscopic alveolar lavage cultures grew Mycobacterium fortuitum. She had no history of bronchiectasis, skin infection, or immunoglobulin deficiency. Treatment with amikacin and levofloxacin was initiated based on susceptibilities.

The pleural chest tube was removed on day 14 (Figure 3). At this time the patient was transferred to a skilled nursing facility.

Figure 3. CT scan on day 13 prior to chest tube removal. Panel A: axial view. Panel B: coronal view.

The patient continued antibiotic treatment for Mycobacterium fortuitum with amikacin and levofloxacin, however, serial sputum cultures remained positive. On day 25, in the skilled nursing facility, the patient developed respiratory failure due to increased right effusion and worsening pneumonia. She was transferred to our facility were she was intubated and a new right-sided chest tube was placed. After placement of chest tube and drainage the right lung did not expand. Decompensation was felt to be related to the inadequate evacuation of the empyema with plans to solely continue antimicrobial therapies by the outside facility.

Figure 4. CT scan on day 30 showing trapped lung. Panel A: axial view. Panel B: coronal view. 

Repeat pleural fluid cultures and BAL once again grew Mycobacterium fortuitum. She was taken for decortication and right middle and lower lobe resection by thoracic surgery. Due to extensive disease the patient required right thoracotomy, decortication, parietal pleurectomy, right middle lobectomy, and wedge resection of a right lower lobe lung abscess.

The lung pathology is shown below and was consistent with lipoid pneumonia (Figure 5).

Figure 5. Panels A & B: CD 163 stains showing lipid present within histiocytes. Panels C & D: histology demonstrating severe lipoid pneumonia. Panels E & F: Granulomatous inflammation with giant cells. Panel G: pleura. Panel H: abscess.

There were no mycobacteria cultured on the lung biopsy. There were areas of both acute and chronic fibrosis noted on pathology report along with areas of acute interstitial pneumonitis and granulomatous inflammation.

During post-operative phase the patient confirmed that she was drinking mineral oil chronically for treatment of constipation. Repeat sputum cultures 7 days post operatively were negative for Mycobacterium fortuitum. She continued to improve with treatment of Mycobacterium fortuitum and postoperative cultures remained negative. She was able to liberate from the ventilator and returned home at after a prolonged course of rehabilitation.

Lipoid Pneumonia and Associated Mycobacterial Infection

The association between acid-fast bacteria and lipoid pneumonia was first reported in 1925 and since case reports have been noted. In 1953, a case report and literature review documented six cases of “saprophytic” mycobacteria was noted in conjunction with lipoid pneumonia. It was observed at this time that the fatty environment of lipoid pneumonia might assist with the growth of mycobacterium (1). Since then, intermittent case reports have been published reporting lipoid pneumonia with atypical mycobacteria.

There are two main categories of lipoid pneumonia, endogenous and exogenous. The endogenous form is also known as cholesterol pneumonia or golden pneumonia. It is associated with lysis of lung tissue distal to obstruction due to malignancy, fat storage disease such as Neiman-Pick or Gaucher's, medications and therapies including chemotherapeutic agents, amiodarone and radiation therapy. Pulmonary alveolar proteinosis has also been reported in idiopathic cases with granulomatosis with polyangiitis and connective tissue diseases (2-4). In polarized light microscopy after staining with sulfuric and acetic acid, the sample reveals cholesterol crystals, which is diagnostic of endogenous lipoid pneumonia (3).

Exogenous lipoid pneumonia occurs when external substances enter the lungs due to inhalation or aspiration (3). Cases have been reported from mineral oil, paraffin use, oil based nasal drops, total parenteral nutrition, mineral oil nose drops, black fat tobacco smoking, milk, and liquid hydrocarbons used by flame blowers (2-6). The pulmonary reaction to each substance varies. For example, mineral oils are fairly inert and less likely to produce alveolar inflammation, where milk fats are hydrolyzed by lung lipases leading to a significant inflammatory response (2).

The clinical presentation and appearance of lipoid pneumonia is variable from consolidation to effusion to nodule. Nodules from lipids may have elevated standardized uptake value (SUV) on positron emission tomography (PET) scan. The BAL from lipoid pneumonia may demonstrate lipid laden foamy macrophages (2). Mineral oil granuloma (paraffinoma) also can present as a spiculated mass mimicking malignancy.

Mineral oil is notorious for causing lipoid pneumonia by aspiration for several reasons. First, it floats on the column of undigested material in the esophagus so it is first to be aspirated (5); secondly, it impairs phagocytosis at the alveolar level; and lastly, it inhibits the cough reflex and motor function of ciliated mucosa (7).

The impairment of phagocytosis associated with lipoid pneumonia is thought to be a contributing factor in why atypical mycobacterium strives in the lipid rich environment of lipoid pneumonia (5,6). Malnutrition is also thought to be a component of risk as it due to impairment in cell mediated immunity (6). Lipid acts as mechanical protection for the mycobacteria favoring tissue necrosis facilitating secondary infection. Also it is thought that lipids may activate the cell walls of the atypical mycobacteria leading to increased virulence of the mycolic acids within the wall of the bacteria (8).

Mycobacterium fortuitum rarely causes pulmonary disease unless associated with lipoid pneumonia. This is often related to gastroesophageal disease and chronic vomiting and aspiration of contents. It is typically associated with skin and soft tissue infections and is a rapid growing mycobacterium and most frequently found in water and soil (2,8,9)

This case demonstrates an atypical presentation of lipoid pneumonia and Mycobacterium fortuitum infection leading to septic shock and ventilator failure. Although the association of lipoid pneumonia and mycobacterial infections is well documented, the rapid and acute decline in this patient’s clinical status is unusual. This can be attributed to incomplete drainage of the initial empyema prior to transfer to the skilled nursing facility.

The etiology of the lipoid pneumonia was chronic aspiration of mineral oil producing an ideal environment for growth of Mycobacterium fortuitum. The absence of bronchiectasis, immunoglobin deficiency, skin infections should prompt further evaluation for abnormal lung architecture serving as a nidus for Mycobacterium fortuitum Infection. In our case, failure to improve is attributed to a persistent nidus for infection. We advocate resection of diseased lung segments of lipoid pneumonia to facilitate successful treatment of Mycobacterium fortuitum. In conclusion, if a patient has lipoid pneumonia with signs of clinical infection, the possibility of rapidly growing mycobacterium such as M. fortuitum should be considered.

References

  1. Gibson JB. Infection of the lungs by saprophytic mycobacteria in achalasia of the cardia, with report of a fatal case showing lipoid pneumonia due to milk. J Pathol Bacteriol. 1953;65(1):239-51. [CrossRef] [PubMed]
  2. Hasan A, Swamy T. Nocardia and Mycobacterium fortuitum infection in a case of lipoid pneumonia. Respiratory Medicine CME 2011: 75-78. [CrossRef]
  3. Betancourt SL, Martinez-Jimenez S, Rossi SE, Truong MT, Carrillo J, Erasmus JJ. Lipoid pneumonia: spectrum of clinical and radiologic manifestations. AJR Am J Roentgenol. 2010;194(1):103-9. [CrossRef] [PubMed]
  4. Harris K, Chalhoub M, Maroun R, Abi-Fadel F, Zhao F. Lipoid pneumonia: a challenging diagnosis. Heart Lung. 2011;40(6):580-4. [CrossRef] [PubMed]
  5. Hughes RL, Freilich RA, Bytell DE, Craig RM, Moran JM. Clinical conference in pulmonary disease. Aspiration and occult esophageal disorders. Chest. 1981;80(4):489-95. [CrossRef] [PubMed]
  6. Tranovich VL, Buesching WJ, Becker WJ. Pathologic quiz case. Chronic pneumonia after gastrectomy. Pathologic diagnosis: chronic aspiration lipoid pneumonia with Mycobacterium abscessus. Arch Pathol Lab Med. 2001;125(7):976-8. [PubMed]
  7. Jouannic I, Desrues B, Léna H, Quinquenel ML, Donnio PY, Delaval P. Exogenous lipoid pneumonia complicated by Mycobacterium fortuitum and Aspergillus fumigatus infections. Eur Respir J. 1996;9(1):172-4. [Pubmed]
  8. Couto SS, Artacho CA. Mycobacterium fortuitum pneumonia in a cat and the role of lipid in the pathogenesis of atypical mycobacterial infections. Vet Pathol. 2007;44(4):543-6. [CrossRef] [PubMed]
  9. Vadakekalam J, Ward MJ. Mycobacterium fortuitum lung abscess treated with ciprofloxacin. Thorax. 1991;46(10):737-8. [CrossRef] [PubMed] 

Cite as: Till S, Mathew M, Liao D-W, Ramirez C. Why chronic constipation may be harmful to your lungs: a case report and review of lipoid pneumonia and mycobacterium fortuitum leading to acute respiratory failure and septic shock. Southwest J Pulm Crit Care. 2015;11(4):193-9. doi: http://dx.doi.org/10.13175/swjpcc118-15 PDF 

Thursday
Oct152015

Traumatic Hemoptysis Complicating Pulmonary Amyloidosis

Erwan Oehler, MD1

Charlotte Courtois, MD2 

Florent Valour, MD1

 

1Department of Internal Medicine

2Department of Pulmonary Medicine

French Polynesia Hospital Center

98716 Pirae, Tahiti

French Polynesia

 

Case Presentation

We present a 74-year-old man admitted to hospital for a fall occurring at home. His past medical history included histologically-proven pulmonary amyloidosis followed for fifteen years (Figure 1A), without involvement of other organs.

Figure 1A. Frontal chest radiography shows bilateral confluent, somewhat nodular and dense-appearing opacities with a background of faint linear and reticular opacities.

At admission, he complained of left chest pain related to a rib fracture (Figure 1B, arrow).

Figure 1B. Detail radiograph of the left upper thorax shows a fracture (arrow) of a posterolateral rib, superimposed on the background of dense-appearing linear and nodular parenchymal disease.

The next day, he presented with moderate hemoptysis, prompting performance of thoracic CT (Figure 1C and D) which showed a cavity filled with material of soft tissue attenuation.

Figure 1C and D. Axial thoracic CT displayed in soft tissue windows shows extensive bilateral nodular hyperattenuating tissue consistent with alveolar septal / diffuse pulmonary parenchymal amyloidosis. A cystic lesion with internal, dependent soft tissue attenuation (arrow, D) is present, consistent with a hematoma.

This soft tissue-filled cavity was located at the same level as the rib fracture, surrounded by calcified tissue, and presumably reflected a pulmonary parenchymal hematoma resulting from traumatically induced laceration of the inelastic calcified lung tissue.

Discussion

Pulmonary amyloidosis is a rare disease resulting from the extracellular deposition of insoluble fibrillar proteins aggregating in a β–pleated sheet configuration (1). Amyloidosis is classified according to the chemistry of the amyloid protein as AA secondary amyloidosis (SAA protein) -often related to chronic inflammatory disease- AL amyloidosis (monoclonal immunoglobulin light chains of the lambda or kappa type)-secondary to B lymphoproliferative disorders-and hereditary or familial amyloidosis (transthyretin and gelsolin). Dialysis-associated amyloidosis (βR2R microglobulinemia) and “senile” amyloidosis SAA (wild-type transthyretin) are also recognized. Pulmonary amyloidosis may occur in three forms: tracheobronchial, nodular parenchymal and alveolar septal / diffuse parenchymal patterns (2). The two first forms (which include primitive pulmonary amyloidosis) are often remain localized to the respiratory system, whereas the alveolar septal / diffuse parenchymal form of amyloidosis, whose prognosis is more severe, often presents in a systemically. Parenchymal amyloid nodules grow slowly and generally remain asymptomatic but patients may also present with dyspnea, cough, hemoptysis or recurrent pneumonia (3).

References

  1. Chu H, Zhao L, Zhang Z, Gui T, Yi X, Sun X. Clinical characteristics of amyloidosis with isolated respiratory system involvement: A review of 13 cases. Ann Thorac Med. 2012 (4):243-9. [CrossRef] [Pubmed]
  2. Gilmore JD, Hawkins PN. Amyloidosis and the respiratory tract. Thorax. 1999;54:444-51. [CrossRef] [PubMed]
  3. Vieira IG, Marchiori E, Zanetti G, Cabral RF, Takayassu TC, Spilberg G, Batista RR. Pulmonary amyloidosis with calcified nodules and masses - a six-year computed tomography follow-up: a case report. Cases J. 2009;2:6540. [CrossRef] [PubMed]

Cite as: Oehler E, Courtois C, Valour F. Traumatic hemoptysis complicating pulmonary amyloidosis. Southwest J Pulm Crit Care. 2015;11(4):173-5. doi: http://dx.doi.org/10.13175/swjpcc133-15 PDF

Tuesday
Oct132015

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  

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