SPN
isolated rounded opacity <30 mm on CXR
outlined by normal lung tissue (not in hilar lN)often found incidentally
malignant causes of SPN
primary lung CA (adenoCA)
carcinoid tumor
Metastatic dz (melanoma, colon, breast, kidney, testicular)
benign causes of SPN
Granuloma (infectious process)
benign tumor (hamaratoma, bronchiole adenoma )
SPN lesion characteristics indicative of malignancy
- increasing size - rapidly increasing likely CA
- SPN composition - solid/subsolid
- border characteristics - rougher edges = more likely (corona radiate most)
SPN risk of malignancy pt characteristics (7)
- increasing age
- smoking
- prior malignancy
- occupation
- female sex
- upper lobe lesion
- family history
risk factors for SPN infection
- immunocompromised
- history of TB or other mycosis
- residence or extensive travel in areas of endemic mycosis
work up of SPN
- non-contrast CT (thin cuts)
2. PET/CT scan
CT SPN imaging
looking for:
benign patterns of calcification
estimation of VDT
malignant patterns
SPN CT
benign patterns
diffuse homogenous calcification
central calficiation
lamellate calcification
popcorn calficiation
estimation of VDT - benign
fast ( <30) suggests infection
slow (>480 days)
malignant patterns of SPN CT
peripheral halo
cavitary lesions
Lymphadenopathy
solid nodules SPN
dense and homogenous
<8mm = too small for bx, less likely to be malignant
subsolid nodules SOB
less attenuation on imaging
normal parenchymal structures can be seen through them
part solid or ground glass (no solid components)
difficult to bx
PET/CT SPN
greater than 8 mm
assesses metabolic activity of nodule (most glucose uptake) via SUV
high SUV indicates high FDG, suggestive of malignancy
can exclude cancer
management of SPN
growing nodule should always be surgically removed ( > 2mm increase)
when is SPN growth considered stable?
solid: stable after 24 months no growth
subsolid: 5 yrs no change
what can we use to determine SPN management?
Fleischer guidelines
SPN biopsy
sampling to obtain tissue diagnosis
BAL, brushing, directed
indications for resection of SPN
- growing legion
- high probability of malignancy
- metabolically active on PET scan
- prior sampling nodule has proven malignant
bronchogenic lung carcinoma
second most common type of CA diagnosed but number one killer of persons (more than colorectal + breast + prostate CA)
lung CA screening
should benefit but hard to screen
annual low dose CT screen for HR individuals
high risk lung cancer defined:
who gets the screening
men or women ages 55-79 yrs with 30 pk year history
quit in last 15 yrs
risk factors for bronchogenic lung cancer
- smoking (90%)
- prior h.o. radiation tx (HL or brest)
- environmental exposure (second hand smoke, radon)
- Other lung dx, 5. HIV, 6. family history, 7. alcohol and diet
epidemiology of bronchogenic lung cancer
men > women, lower rates of survival
women: adenoma, high likelihood of local dz, younger age
AA = Caucasian women
AA > men (13% lower)
classifications of lung CA
- adenocarcinoma (MC, rising)
- Squamous cell carcinoma
- Large cell carcinoma
- Small cell carcinoma
adenosinecarcinoma
mucus gland of bronchi, peripheral nodule
predilicition for occurring at pre-existing scars, wounds or inflammation
MC found in non-smokers
bronchoalveolar cancer
subtype of adenocarcinoma
arises form type II pneumocystis
profuse, watery sputum
spreads alveolarly, present as an infiltrate or as single/multiple nodules
squamous cell cancer
CENTRAL portion
cavitary lesion in lumen of central bronchus
keratin pearls
presents as hemoptysis, exfoliates
most likely to produce hypercalcemia
large cell lung cancer
occurs peripherally
lg sheets of atypical cells, focal necrosis (no keratin pearls)
SOME = neuroendocrine component (LCNEC)
small cell carcinoma
begins centrally, infiltrates mucosa
spreads rapidly to hilar and mediastinal lymph node
exclusively in smokers
small blue CA cells, sparse cytoplasm
MC presentation of SCLC
large mediastinal mass with bulky hilar LAD
hemoptysis and post obstructive PNA uncommon, narrowing and late obstruction of bronchus
neuroendocrine activity
small cell carcinoma spread
prone to early hematogenous spread and very aggressive clinical course
sensitive initially to CXR but not durable
presentation of lung CA
insidious process
majority of patients will have advanced dz at diagnosis
symptoms of bronchogenic CA (9)
related to primary lesion, spread, distant metastasis, paraneoplastic syndromes
- new cough/chronic change
- dry/scantily productive thin mucoid secretions
- post obstructive PNA with thick sputum
- dyspnea
- change in voice
- hemoptysis
- chest pain
- atelectasis, PNA, malignant pleural effusion
- anorexia/weight loss
dyspnea of bronchogenic CA
wheezing and stridor
pleural or pericardial effusions (volume loss due to atelectasis)
volume loss and atelectasis/lobe collapse
chest pain in bronchogenic CA
dull, intermittent pain on side of tumor
severe or persistent pain = chest wall or mediastinal invasion
SVC syndrome
obstruction of superior vena cava causes
- superficial venous engorgement of chest
- facial edema and plethora
- signs of increased ICP, HA, tinnitus, bursting sensation
pancoast’s tumor
peripheral tumor (mc NCLC)
invade early and cause local destruction
invasion of nerves of brachial plexus and cervical sympathetic nerves (stellate ganglion) compression of vascular structures
pancoast’s tumor syndrome
horner’s syndrome
severe and unremitting pain (upper back and shoulder w/radiation into axilla down inner aspect of arm to hand)
muscle atrophy
compression causing edema
metastatic dz
mc sites
brain, bones, liver, adrenals, pericardium and spinal cord
pericardial lesions
heart is unable to expand to produce good CO
resulting in tamponade (JVD, HoTN, muffled heart sounds)
adrenal lesions
destruction of normal adrenal tissue and adrenal insufficiency
HoTN (fluid recesitation decrease), poor stress tolerance, non-specific (weak, tired)
symptoms of hepatic metastasis
increased transaminases/LFT’s
associated with weight loss
symptoms of brain metastasis
headache
n/v
seizures
AMS
symptoms of spinal cord metastasis
paralysis or peripheral weakness
sensory loss of extremity
n. invasion = intense pain
symptoms of bone metastasis
vertebrae most commonly involved
ribs and pelvis
primary symptoms: severe pain
pathologic fracture may occur
paraneoplastic syndromes
organ dysfunction related to immune mediated or secretory effects
occurs in 10-20%, may precede, accompany, or follow diagnosis
does not indicate metastasis
types of paraneoplastics syndrome
SCLC –> SIADH (free water reabsorption)
squamous cell –> hypercalcemia (PTHrP)
trousseau syndrome (adenocarcinoma)
neurological effects (LEMS, SCLC)
cushion’s syndrome (increased ACTH) SCLC
hematologic changes (anemia, thrombocytopenia)
digital clubbing
work up of lung mass
- CT w/contrast, entire area
- CBC, electrolytes, LFTs, LDH, albumin
- Pulm consult
- additional testing/tissue diagnosis
tissue diagnosis mechanisms
- fiberoptic bronchoscopy
- CT guided needle bx
- FNAB
- Sputum cytology
- thoracentesis
- VATS thoracotomy
fiberoptic broncoscapy
direct forceps biopsy, brushing
high sensitivity for central, endobronchial lesions
US may assist
CT guided needle biopsy
evaluation by IR, they skin to get tissue (PTX risk)
good for peripheral tissue
FNAB
supra-clavicular or cervical lymph nodes
diagnostic
thoracentesis
malignant pleural effusions, sensitivity 50-60%
may perform twice
additional testing for suspected lung CA
MRI of brian (CNS symptoms or focal findings)
pulmonary function testing
evaluation of cardiovascular status
PET/CT (look for dz not visible on CT + distant metastasis)
which part of node is hardest to visualize on PET/CT?
brain
v. difficult bc high uptake of glucose
surgical tx options for lung CA
NSCLC
- Pneumonectomy
- Lobectomy
- segmentectomy/wedge resection
- sleeve resection
pneumonectomy
removal of ENTIRE lung
MC tumor close to the center of chest
lobectomy
removal of an entire lobe containing tumor
procedure of choice
segmentectomy
part of love removed
suboptimal may be used if pt doesn’t have enough lung fxn to withstand lobectomy
sleeve resection
tx of CA in lg airways
resected with clear margins and distal lung reconnected to proximal airway
preserves lung function
FEV1 and surgery determinations
use PFTs to determine likelihood a patient will come off vent
good PFTs = radical surgery
chemo for lung CA
4-6 cycles, given over 1-3 days every 3 weeks
given MC to pts with NCLC, less successful SCLC
radiation for lung CA
radiation delivered to tumor, must pass thru other tissues to reach target
successful bc CA cells can’‘t recover from DNA result
differnt types of XT tx
A. conventional external beam: dose fractionation, overtime amount increases
B. stereotactic body radiation: fewer tx of beams, go at tumor from multiple angles
NSCLC surgery
stage I/II
tx with curative intent
surgical resection (lobectomy)
non-surgical candidates get radiation
NSCLC surgery
stage III
diverse options, curative intent, mediastinal involvement distinguish
none: surgical resection, adjuvant chemo +/- XT
involvement: definitive chemo-radiation, becomes modality of choice
NSCLC surgery
IV
tx is palliative intent (prolong survival)
combo platinum based chemo, targeted therapy if possible or after CTX
surgical removal of mets
driver mutations
tumor growth and progression depend heavily on it
blocking signals allows us to have attack o CA with few effects
EGFR, ALK
EGFR
driver mutation over expresses EGFR
MC in women, never smoker, adenoma, asians
EGFR targeted therapy
Tyrosine kinase inhibitors
first line or second line following initial chemotherapy
ALK
direct mutation promoting growth and spread
light or never smokers, young its with adnoCA and predicts sensitivity to ALK TKI
other forms of target therapy
molecules that block tumor angiogenesis via decreasing BEGF
decreases blood supply
good option for ALL cancers, not just driver mutations
immunotherapy
stimulates immune system to recognize and destroy CA cells
PDI ligand is targeted by drugs and destroyed using the body’s T cell/CD8 cells
PD-1 inhibitors
Pembrolizumab/Keytruda
nivolumab/Opdivo
Atezolizumab/Tecentriq
NSCLC prognosis
HIGHLY lethal
TMN stage of cancer at time of diagnosis is most imp. prognostic indicator
SCLC stages
limited (ipsilateral hemithorax, regional nodes) 5 yr <17%
extensive disease (distant mets, pericardial/pleural, contralateral supraclavicular or hilarious LAD) 2 yr < 5%
limited SCLC tx
prom tx
limited = NO lymph node = surgical resection/lobectomy + chemotherapy
limited SCLC + lymph involvement
candidates for chemoradiation
any response prophylactic cranial radiation
extensive stage SCLC tx
MC presentation
systemic chemotherapy, palliative intent
if responsive: thoracic XT, prophylactic WBRT
palliative care for lung CA
external radiation
pain control
chemotherapy
hospice control
external radiation in palliative care
control dyspnea and hemoptysis
pain from bony mets
obstruction from superior vena cava syndrome
symptomatic brain mets
chemotherapy palliative care
surgical procedures or chemotherapy to control dz
enough to prolong life but no toxicity
Neuroendocrine tumors
produce and secrete neuropeptides and neuroamines in a variety of places (GI, lungs)
typically slow growing vascular indolent malignant tumors
atypical are aggressive and necrotic
1-2% secrete ACTH causing Cushings
Neuroendocrine tumors epidemiology
women, caucasians >
before age 60
MC lung tumor in children
ass. with smoking
CT of Neuroendocrine tumors
well circumscribed centrally located males
25% are peripheral SPN
bronchial carcinoid tumors symptoms
hemoptysis (vascular tumor)
cough
focal wheezing
recurrent PNA
bc tumor grows centrally, obstructing ariway
carcinoid syndrome
caused by tumor chemical release, rare in lung NETs (vasoactive instead)
flushing, diarrhea, bronchospasm, wheezing, severe hyper-/hypotension
octreotide = tx
bronchial carcinoid tumors metastasis and diagnosis
mc site of metastasis is liver
diagnosed using CT, can do PET-CT
serotonin levels unhelpful bc not high enough [ ]
tx of bronchial carcinoid tumors
surgical excision
adjunct CTX for atypical
methods of metastatic spread
hematogenous (via blood)
lymphatic (via lymph)
direct extension
common site bc lungs recieve 100% of blood
common primaries in lung metastasis (BReAST)
Brest Renal Anal/Colon Skin (multiple melanoma) Testes/ovaries
metastasis on imaging
multiple sharply demarcated solid nodules/masses
Bilateral
lower lung fields
CXR/CT
Lots Little Lower
tx of metastasis
find and tx PRIMARY CA appropriately (routine screening)
address complications, resection of nodule
mesothelioma
primary tumor arising from pleura (also peritoneum, pericardium, testes)
begin as a small nodule in lower lung that grows to a sheet encasing pulmonary structures
mesothelioma epidemiology
men>women , 50-70 y/o
HIGHly associated with asbestos exposure
asbestos exposure
20-40 yrs prior to mesothelioma exposure
via insulation, shipyard work, building construction and demolition
mesothelioma diagnosis
typical pulmonary signs
CXR: nodular, irregular unilateral pleural thickening and effusion
Contrast CT to show extent, thoracentesis for effusion
VATS biopsy to confirm
mesothelioma course
progressive hardening to pericardium and diaphragm/abdomen
progressive pain and dypsena due to decreased lung expansion
staging mesothelioma
thorascopy +/- MRI
stage i: completely resected, disease free
ii: margins not clear, pleural LAD
iii: local extension, mediastinum and chest cavity
iv: distant mets
