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Chest Wall Masses – Differential Diagnosis

This mainly boils down to neoplasm vs infection.

 

I.  NEOPLASTIC

  • Classified based on tissue of origin (bone or soft tissue) and further classified as benign vs malignant.
  •  More commonly are either metastases, or local invasion of an underlying adjacent tumor (vs primary chest wall tumor).
  • Primary chest wall tumors are rare and account for only  5% of all thoracic neoplasms.  Approximately 60% of primary chest wall tumors are malignant.  Of malignant tumors, chondrosarcoma and lymphoma are the most common in adults. 

Below is a few of the most common tumors:
A. Benign – includes Osteochondroma, Fibrous dysplasia, and Chondroma.
B.  Malignant - below are the most common malignant tumors.
1.  Chondrosarcoma – most common malignant chest wall tumor, located on anterior chest wall. Presents with slowly growing, painful mass with hard,fixed chest wall lesion.  10% have lung mets at presentation.
2. Askin tumor – part of the Ewing sarcoma/PNET spectrum of neuroendocrine tumors.  Usually arises in the pelvis, humerus, and femur, but can arise in chest wall in ~10% of cases.  Can cause bony destruction with lytic and blastic lesions and associated pleural effusions.   Can be confused with osteomyelitis radiographically.
3. Osteosarcoma – more commonly involves long bones, but can affect chest wall, often with lung mets.
4. Plasmacytoma – isolated form of multiple myeloma – can affect ribs.
5. Lymphoma

 

 

II.  INFECTIOUS

  • Chest wall infections are uncommon but potentially life-threatening due to their negative impact on respiratory mechanics, and potential for spread to the pleural space and mediastinum.
  • Risk factors include immunocompromised states, diabetes, and previous trauma or surgery (most commonly – chest tube insertion).  Also, IV drug abuse increases risk of septic arthritis of sternoclavicular, sternochondral, and manubriosternal joints. 
  • Outcome depends on early diagnosis, the degree of immunosuppression, the causative organism, and the extent of infection.
  • Plain radiographs are often unreliable; CT and MRI are better at delineating bone destruction and soft tissue involvement.

Microbiology:

  • Bacterial – Staph aureus, Strep, Pseudomonas.  Soft tissue infections/abscesses are often polymicrobial.   Less common pathogens include Actinomyces and Nocardia.
  • Fungal – Aspergillus, others are much more rare

 

Types of Infections:
1. Bone/Joint Infections

  • Sternoclavicular arthritis – uncommon (represents only ~2% of pyogenic arthritis), but often leads to abscess formation and spreads quickly beyond the joint.  Occurs in IV drug users, chronic dialysis, immunosuppressed patients.  Usually due to Staph aureus(general population) or Pseudomonas aeruginosa (IV drug users).   TB can cause it as well.
  • Sternal osteitis  - usually associated with sternotomy
  • Rib osteitis – pyogenic, TB, or fungal

2. Primary Soft Tissue Infections

  • Fairly rare, occur via direct inoculation (i.e. puncture, chest tube insertion), contiguously from other site, or hematogenous.   Can be necrotizing or non-necrotizing.  Necrotizing infections occur more commonly in abdomen, perineum (i.e. Fournier’s gangrene) and lower extremities but can occur on the chest wall.  Occurs in immunocompromised and diabetic patients.  Most commonly, due to polymicrobial infections including both aerobic and anaerobic bacteria; only small percentage caused by single organism such as Strep or Clostridium perfringens.  Therapy, as for other necrotizing infections, includes early surgical debridement, antibiotics, and hemodynamic resuscitation and support.

3. Atypical pathogens

  • Tuberculosis – chest wall infection accounts for ~10% of extra-pulmonary TB.  Can cause abscesses involving the ribs, costochondral junctions, costovertebral joints, vertebrae, and have strong predilection for the margins of the sternum.
  • Actinomycosis – gram-positive anaerobe that is part of the oral flora.  Thoracic actinomycosis results from aspiration in patient with poor oral hygiene – infection starts in lung parenchyma and progresses through the pleura to the chest wall.  Can rarely occur just in the chest wall without pulmonary involvement.  Difficult to culture; diagnosis can be made based on “sulfur granules” on histoplatholgy – grainy microcolonies of the organism.  Tx = long-term PCN. 
  • Nocardiosis – aerobic gram positive rod, partially acid-fast, usually affect immunocompromised patients (but 1/3 in immunocompetent).  Most common manifestation is pulmonary disease, mimics tuberculosis; can also cause cutaneous and disseminated disease. 
  • Fungal organisms - Aspergillus – generally in immunocompromised patients, via extension from a pulmonary lesion, through the bone and soft tissues.   Rarely occurs via hematogenous route.   Other fungal infections  - Hisoplasmosis, Blastomycosis, Cryptococcosis, Cocciodioidomycosis, are all rare causes of chest wall infections.

 

(Chanu Rhee MD, 4/8/11)