A. Types of Masses

1. Small Cell Lung CA (SCLC, Oat Cell Ca)
2. Squamous Cell CA
3. Adenocarcinoma
4. Large Cell CA
5. Carcinoid
6. Mesothelioma
7. Bronchogenic and Other Cysts
8. Abscess
9. Metastatic Cancer
10. Hemangioma

B. Symptoms

1. Asymptomatic (vast majority)
2. Pain
3. Hemoptysis
4. Dyspnea
5. Cough
6. Sputum production
7. Superior vena cava (SVC) syndrome (see below)
8. Pancoast Syndrome [5]
   1. Pain in ipsilateral shoulder
   2. Horner's Syndrome (ptosis, miosis, anhidrosis)
   3. Weakness and atrophy of hand muscles
   4. Less common: SVC syndrome, phrenic or recurrent laryngeal nerve effects

C. Solitary Pulmonary Nodule [2]

1. Found on ~0.15% of chest radiographs (CXR)
   1. Usually defined as <3cm opacity without atelectasis or hilar adenopathy
   2. Lesions >3cm are typically called true pulmonary masses and are often malignant
   3. Computed tomographic (CT) scans are standard of care for evaluation
   4. Stability for >2 years or nonmalignant calcification or uncalcified --> no further testing [2]
2. Etiology
   1. Bronchogenic Ca (35-50%): Non-small cell Ca masses are more common than small cell
   2. Metastatic Cancer (breast, colon, renal)
   3. Carcinoid Tumor (~10%)
   4. Granulomatous: Tuberculosis, Histoplasma, Coccidiomycosis, Cryptococcus, Aspergillus
   5. Other: Bronchial Cyst, AV Fistula, Fibromatosis, Rheumatoid Nodule, Hematoma, Sarcoid
   6. Rounded Atelectasis, Hamartoma
   7. Larger apical masses may present with Pancoast Syndrome ("Pancoast Tumors")
3. Factors Favoring Malignancy
   1. Older age of patient
   2. Smoker
   3. Margins Not Sharp
   4. Uncalcified, or Calcification NOT laminated, homogeneous or popcorn
   5. Change in size on chest radiograph over 2 years
   6. Size >2-3cm
4. Detection and Radiologic Evaluation
   1. Chest radiography (CXR) is most common initial test but is not sensitive for small lesions
   2. Use of low dose computerized tomography (CT) for lung cancer screening may increase the rates of detection and reduce the size of masses detected (<1 cm) [3]
   3. Nodules <2cm require thin section CT study
   4. >2cm is often a bronchogenic CA; staging with chest and abdominal CT required
   5. Positron emission tomography (PET) with fluorodeoxyglucose (FDG) may be useful in noninvasively differentiating malignant from nonmalignant lesions (see below) [6]
   6. FDG-PET should be reserved only for selected patients; CT is preferred initial test [9]
5. CXR Results of Benign Lesions
   1. Calcification usually means benign (<1% malignancies appear calcified on CXR)
   2. Benign Calcifications: laminated (granuloma), popcorn (hamartoma), homogeneous
   3. No change in size over 2 years
   4. CT scan gives better assessment of size and calcification
6. PET Scanning [6,9]
   1. Optimal sensitivity and specificity of PET±FDG ~91% for detecting malignant lesions
   2. In current practice, sensitivity ~97% and specificity for malignant lesions ~78%
   3. Detection of lesions 1-3cm versus >3cm was similar
   4. PET+FDG may be suitable for noninvasively ruling out malignant pulmonary lesions but should be reserved for selected patients
   5. Recommended for patients with intermediate (or high) pretest probability and discordant CT findings, particularly those at elevated surgical risk [9]
7. Evaluation [2]
   1. Sputum cytology and bronchoscopy used for evaluation of central lesions
   2. Transthoracic needle biopsy when lesion is located in lung periphery
   3. Sputum Cytology: diagnostic 20% of malignancies (endobronchial tumors often exfoliate)
   4. Fiberoptic Bronchoscopy: Diagnostic yields 50-75%; drops off for lesions <2cm
   5. Transthoracic Aspiration: Diagnostic <2cm ~60%, >2cm ~85%
   6. Tissue is generally required for definitive diagnosis
   7. For poor surgical candidates and low cancer risk, serial high resolution CT recommended
8. Tissue Biopsy [11]
   1. Mediastinoscopy is standard for staging and pathological confirmation
   2. Minimal endoscopic staging with needle aspiration is used
   3. Traditional transbronchial needle aspiration (TBNA)
   4. Endobronchial ultrasound-guided FNA (EBUS-FNA)
   5. Transesophageal endoscopic US-FNA (TEUS-FNA)
   6. EBUS-FNA more sensitive than TBNA (70% versus 36%) for malignant node detection
   7. Combination of TEUS-FNA and EBUS-FNA had 93% sensitivity and 97% negative predictive; superior to other methods
   8. Combined TEUS-FNA and EBUS-FNA may allow near-complete minimally invasive mediastinal staging in patients with suspect Lung Ca
9. Large masses centrally located can be treated with interventional bronchoscopy [7]

D. Pulmonary Cystic Disease [4]

1. Metabolic - cystic fibrosis
2. Lymphangioleiomyomatosis [8]
   1. Immature smooth muscle proliferation around vascular and lymphatic structures
   2. Occurs mainly females of 20-40 years, 3 per 100,000
   3. Initially, cystic lung disease, progressing to diffuse honeycombing
   4. Accompanied by abdominal tujmors (angiomyolipomas), meningiomas, other mass lesions
   5. Express progesterone receptors and are hormonally sensitive
   6. Probably related to hormonally induced smooth muscle proliferation
   7. Hormonal manipulation used: oopherectomy, tamoxifen, progesterone may be effective
   8. Lung transplantation may be used in end-stage patients [6]
3. Inflammatory
4. Traumatic
5. Developmental
   1. Bronchopulmonary sequestration - cystic masses with no normal communication to lung
   2. Bronchogenic cysts - from abnormal budding of respiratory tract
6. Parasitic - echinococcal cysts are most common (hydatid disease)

E. Fibromatosis [5]

1. Differentiated fibroblastic tumor (also called desmoid tumor)
2. Biologic behavior intermediate between benign fibroma and malignant fibroscarcoma
3. Local invasion is possible, but does not have metastatic potential
4. Main categories: superficial and deep
5. Superficial
   1. Palmar (Dupuytren's Disease or Contracture)
   2. Plantar (Ledderhose's Disease)
   3. Penile (Peyronie's Disease)
6. Deep
   1. Extra-abdominal
   2. Abdominal
   3. Intra-abdominal
7. Clonal tumors with trisomy 8, trisomy 20, or both commonly found
8. Treatment
   1. Surgical resection
   2. Radiation for recurrent disease
   3. Some concern that radiation can convert tumor to malignant many years after use
   4. Observation - especially for lesions on arms and legs

F. Superior Vena Cava (SVC) Syndrome [10]

1. Occurs in ~15,000 patients per year in USA
2. Syndrome occurs due to obstruction of SVC
3. Symptoms and Signs
   1. Increased venous pressure in upper body
   2. Edema of head (~80%), neck, arms (~45%)
   3. Often with cyanosis, plethora, distended subcutaneous vessels (50-65%)
   4. Dyspnea is present in ~55% of cases
   5. Laryngeal edema (~20%) may manifest as cough, hoarseness, dyspnea, stridor
   6. Dysphagia can occur due to pharyngeal edema
   7. Cerebral edema may lead to headache, confusion, coma (may be fatal)
   8. Decreased venous return may result in hemodynamic compromise, including syncope ~10%
4. Symptoms develop over ~2 weeks in ~35% of the patients
5. Pathophysiology
   1. Generally gradual obstruction of the SVC
   2. Increase in cervical enous pressure from normal of 2-8 mmHg to 20-40 mmHg
   3. Leads to engorgement of azygos ven and inferior vena cava
   4. Collateral vessels dilate and grow usually requiring several weeks
6. Causes
   1. Malignancy in ~65% of cases
   2. Of malignant causes, non-small cell (50%) and small cell (25%) lung cancers most common
   3. Lymphoma and metastatic lesions each ~10% of malignant causes
   4. Nonmalignant conditions in ~35% of cases - thrombosis most commonly, aortic aneurysm
7. Imgaging with CT with contrast of chest is usually first step
8. For treatment of malignancy, rdiation, systemic chemotherapy, surgery, stents are used

References

1. Libby DM, Henschke CI, Yankelevitz DF. 1995. Am J Med. 99(5):491
2. Ost D, Fein AM, Feinsilver SH. 2003. NEJM. 348(25):2535
3. Henschke CI, McCauley DI, Yankelevitz DF, et al. 1999. Lancet. 354(9173):99
4. Kornfeld H and Mark EJ. 1999. NEJM. 341(13):974 (Case Record)
5. Delaney TF and Nielsen GP. 2000. NEJM. 342(24):1814 (Case Record)
6. Gould MK, Maclean CC, Kuschner WG, et al. 2001. JAMA. 285(7):914
7. Szeijo LM and Sterman DH. 2001. NEJM. 344(10):740
8. Moss J, DeCastro R, Patronas NJ, Taveira-DaSilva A. 2001. JAMA. 286(15):1879
9. Gould MK, Sanders GD, Barnett PG, et al. 2003. Ann Intern Med. 138(9):724
10. Wilson LD, Detterbeck FC, Yahalom J. 2007. NEJM. 356(18):1862
11. Wallace MB, Pascual JM, Raimondo M, et al. 2008. JAMA. 299(5):540