4. • A 77-year-old man comes to the ED complaining of
the acute onset of dyspnea and presyncope that
occurred 2 hours ago while retrieving his luggage
after a 6-h plane flight.
• He didn’t notice any chest pain or hemoptysis.
• His medical history is remarkable for long-standing,
poorly controlled hypertension; diastolic heart
failure; and an ischemic stroke 6 weeks ago with a
residual mild right-sided hemiparesis.
5. • His medications include:
Aspirin, 325 mg daily;
Lisinopril, 40 mg daily; and
Verapamil, 360 mg daily.
• On physical examination, he appears anxious. He has
a BP of 122/83 mm Hg, heart rate of 113/min,
temperature of 36.6C, respiratory rate of 26/min,
and oxygen saturation of 86% on room air.
6. • Laboratory studies reveal the following:
D-dimer level of 9.57 g/mL (52.40 nmol/L),
Brain natriuretic peptide level of 968.2 pg/mL
(968.2 ng/L), and
Cardiac troponin T level of 0.06 ng/mL (0.06
g/L).
8. • An echocardiogram is performed, which reveals left ventricular
hypertrophy with normal systolic function. The right ventricle is
moderately enlarged, and there is severe basal RV systolic
dysfunction. Paradoxical septal motion and a D-shaped
intraventricular septum are noted in both systole and diastole.
The inferior vena cava expiratory diameter is dilated. Moderate
tricuspid regurgitation is noted with an estimated right
ventricle systolic pressure of 65 mm Hg. There are no other
valvular abnormalities. At the main pulmonary artery
bifurcation, there is an area of increased echogenicity
protruding into both main pulmonary arteries that could
represent a clot.
9. • The patient receives supplemental oxygen and
IV unfractionated heparin (UFH), and is
admitted for close monitoring.
• Two hours after admission, his BP drops to
86/52 mm Hg.
• He is given fluid without any response and
vasopressor support is initiated. In addition
to continuing the fluids and vasopressors,
• Your next best step is to:
10. A. Switch to a low-molecular-weight heparin
(LMWH).
B. Insert an inferior vena cava filter.
C. Perform catheter embolectomy.
D. Administer systemic thrombolytic therapy.
large bilateral central clot on
CT angiography
11. According to ACCP antithrombotic
guidelines published (2008)
• Recommend thrombolytic therapy for all
patients with hemodynamic compromise
unless there are major contraindications
owing to bleeding risk (Grade 1B).
12. Major contraindications include
• A history of intracranial hemorrhage
• Known intracranial aneurysm or arteriovenous
malformation
• Significant head trauma
• Active internal bleeding
• Known bleeding diathesis
• Intracranial or intraspinal surgery within 3
months
• A cerebrovascular accident within 2 months.
14. • This patient has a major and several relative
contraindications, so systemic thrombolysis
would not be the best option (choice D is
incorrect).
• The ACCP guidelines also recommend that, in
patients with massive PE who cannot receive
thrombolysis because of contraindications or
time, interventional catheterization techniques
are used if appropriate expertise is available
(Grade 2B). Catheter-directed therapy provides a
less extreme advanced treatment option than
surgical embolectomy.
15. • Many experts agree that patients that meet
the following criteria should be considered for
catheter embolectomy:
(1) acute PE with hemodynamic instability;
(2) subtotal or total filling defect in the left
and/or right main pulmonary artery; and
(3) the presence of a major contraindication to
systemic thrombolysis, including ischemic
stroke. and thus is an ideal candidate (choice
C is correct).
16. Summary
• This patient has massive pulmonary embolism
(PE) (confirmed acute PE with shock and
obvious right ventricular dysfunction) in the
setting of several contraindications to systemic
thrombolysis
17. So the next best step is to:
A. Switch to a low-molecular-weight heparin
(LMWH).
B. Insert an inferior vena cava filter.
C. Perform catheter embolectomy.
D. Administer systemic thrombolytic therapy.
19. The ACCP’s recommendation
classification system:
1 = “recommendation”
2 = “suggestion”
A = based on strong evidence from
randomized trials
B = moderate evidence that may include
randomized trials or observational studies
C = weak evidence, mostly consensus opinion
20. Which patients with acute pulmonary embolism
should I treat with systemic thrombolytics?
The ACCP suggests using systemic thrombolytics to
treat patients with acute PE who are hypotensive
(they propose a cutoff of systolic blood pressure
less than 90 mm Hg). (Grade 2C).
21. Which patients with acute pulmonary embolism
should I treat with systemic thrombolytics?
ACCP recommends against treating most patients
with acute PE without hypotension with systemic
thrombolytics (Grade 1C).
22. Which patients with acute pulmonary embolism
should I treat with systemic thrombolytics?
*However, patients deemed to be at high risk for
becoming hypotensive according to clinical course
are suggested to receive systemic thrombolytics, if
they have a low bleeding risk (Grade 2C).
*“Looking sick,” dyspneic and hypoxic, right
ventricular
dysfunction
on
echocardiogram,
elevated troponins, elevated neck veins, severe
tachycardia have all been proposed as risk factors.
23. How should I treat acute pulmonary embolism
with systemic thrombolytics?
*A short infusion time of 2 hours for systemic
thrombolytics is suggested, rather than a longer
infusion (Grade 2C). Tissue plasminogen activator
(tPA) has a short infusion time and has been
recommended as the best agent for this reason.
*Infuse
systemic thrombolytics through
a
peripheral vein, rather than a pulmonary artery
catheter (Grade 2C).
24. How should I treat acute pulmonary embolism
with systemic thrombolytics?
Randomized trials show that thrombolytics
improve pulmonary artery pressures, oxygenation,
and cardiac performance on echocardiography
within 24 hours in people with acute pulmomary
embolism. However, this comes at a significantly
higher risk of bleeding compared to other
therapies.
25. How should I treat acute pulmonary embolism
with systemic thrombolytics?
ACCP’s recommendations to provide thrombolytics to
people with massive PE (with hypotension) or who are
high risk for soon becoming that way. In large part,
this is based on the observed mortality seen in series
of patients with acute pulmonary embolism:
~5% of people with pulmonary embolus who receive
treatment die (from that or another PE) within 7 days.
~2% mortality in patients without hypotension;
~30% mortality when there is shock necessitating
inotropes;
~70% mortality if cardiopulmonary arrest occurs.
26. Catheter-Based Thrombus Removal for the
Initial Treatment of
Patients With PE
In patients with acute PE associated with
hypotension and who have (i) contraindications to
thrombolysis, (ii) failed thrombolysis, or (iii) shock
that is likely to cause death before systemic
thrombolysis can take effect (eg, within hours), if
appropriate expertise and resources are available,
we suggest catheter-assisted thrombus removal
over no such intervention (Grade 2C).
27. What shall I do with the heparin infusion during
administration of thrombolytic therapy for acute
PE?
*There is no ACCP recommendation for this
question, stating it is “acceptable … to continue or
suspend the unfractionated heparin infusion during
administration of thrombolytics.”
*In the U.S., regulatory bodies advise stopping
unfractionated heparin during t-PA infusion and
restarting it when aPTT is <= 80 sec after t-PA is
complete.
*In many other countries, heparin infusion is
continued during t-PA.
30. Saddle PE :that lodges at the bifurcation of the
main pulmonary artery
31. Multidetector-CT
Findings
• Partial or complete filling defects in lumen of
pulmonary arteries
– Most reliable sign is filling defect forming acute
angle with vessel wall with defect outlined by
contrast material
– “Tram-track sign”
• Parallel lines of contrast surrounding thrombus in vessel
that travels in transverse plane
– “Rim sign”
• Contrast surrounding thrombus in vessel that travels
orthogonal to transverse plane
• RV strain indicated by straightening or
leftward bowing of interventricular septum
Macdonald S; Mayo J. Semin. Ultrasound CT. 2003;24(4):271-231.
32. Large saddle thrombus with extensive clot burden. Arrows
demonstrating tram-track sign (A), rim sign (B), complete
filling defect (C), and a fully non-contrasted vessel (D)
33. Embolic burden scoring system. Schematic of the pulmonary
arterial tree with scores for nonocclusive emboli according to
vessel. Emboli in a segmental pulmonary artery are given a score of
1. Emboli in more proximal pulmonary arteries are given a score
based on the total number of segmental pulmonary arteries
supplied.
37. Multidetector-CT
Findings
• Partial or complete filling defects in lumen of
pulmonary arteries
– Most reliable sign is filling defect forming acute
angle with vessel wall with defect outlined by
contrast material
– “Tram-track sign”
• Parallel lines of contrast surrounding thrombus in vessel
that travels in transverse plane
– “Rim sign”
• Contrast surrounding thrombus in vessel that travels
orthogonal to transverse plane
• RV strain indicated by straightening or
leftward bowing of interventricular septum
Macdonald S; Mayo J. Semin. Ultrasound CT. 2003;24(4):271-231.
38. Large saddle thrombus with extensive clot burden. Arrows
demonstrating tram-track sign (A), rim sign (B), complete
filling defect (C), and a fully non-contrasted vessel (D)
39. Acute pulmonary embolism and deep venous thrombosis (DVT) in a 48-year-old woman. (a) Contrast
material–enhanced pulmonary CT arteriogram (1.25-mm collimation) obtained at the level of the basal
subsegmental pulmonary artery shows multifocal low-attenuation emboli (arrows) in segmental and subsegmental
arteries in the right lower lobe. (b) Contrast-enhanced indirect CT venogram (5-mm collimation) obtained at the level
of the pelvic inlet 3 minutes after injection shows large low-attenuation thrombi filling the left common iliac vein
(arrow).
40. Acute pulmonary embolism in a 41-yearoldwoman. Coronal gadolinium-enhanced threedimensional pulmonary MR angiogram shows a large embolus (arrows) in the proximal
right interlobar artery.
41. Embolic burden scoring system. Schematic of the pulmonary
arterial tree with scores for nonocclusive emboli according to
vessel. Emboli in a segmental pulmonary artery are given a score
of 1. Emboli in more proximal pulmonary arteries are given a
score based on the total number of segmental pulmonary arteries
supplied.
42. Helical CT Findings in Chronic PTE
Cardiac abnormalities
Right ventricular enlargement
Right atrial enlargement
Thrombi in the right atrium or ventricle*
Vascular abnormalities
Eccentric, flattened defect at an obtuse angle with
the vessel wall*
Irregular or nodular arterial wall
Abrupt narrowing of the vessel diameter
Abrupt cutoff of distal lobar or segmental artery
Recanalization of thrombosed vessel
Webs or bands (less frequent)
Parenchymal abnormalities
Bronchial artery dilatation
Bronchiectasis
Areas of decreased attenuation in the lung (mosaic
perfusion pattern)
43.
44. Septic Pulmonary Embolism
Septic pulmonary embolism in a 28-year-old intravenous drug abuser with human
immunodeficiency viral infection. Repeated blood cultures disclosed a positive culture for
Nocardia. (a) Radiograph shows multiple cavitary nodules throughout both lungs. (b) CT scan
(10-mm collimation) obtained at the level of the azygos arch demonstrates the feeding vessel
sign (vessel leading directly to the nodule) in several nodules
56. • History of exposure to asbestos more than 45
years ago.
• He had long-standing bilateral pleural plaques,
upper lobe nodules, and interstitial disease in
a UIP pattern, the latter two of which are
attributable to the RA
• The patient began to notice streaky
hemoptysis mixed with yellowish sputum
about 5 months ago, but it cleared
spontaneously after a few weeks, only to recur
3 weeks ago.
57. • A 72-year-old man is seen for evaluation of
hemoptysis.
• He had a 14-year history of rheumatoid
arthritis (RA) previously treated with
hydroxychloroquine, methotrexate, gold,
penicillamine, and etanercept.
• Currently, he is taking adalimumab and an
NSAID.
• He had a 40 pack-year smoking history but
quit 10 years ago and
58. • He denied any fever, sweats, chills, or weight
loss and stated that his chronic respiratory
symptoms were stable.
• His only complaint was severe neck pain
attributable to severe, unstable cervical spine
disease with planned fusion surgery.
• Physical examination revealed bibasilar late
inspiratory crackles halfway up both lung
fields.
• There was nothing to suggest pulmonary
hypertension.
59. • His spirometry revealed an FEV1 of 2.49 L
(78% of predicted) and an FVC of 2.98 L (71%
predicted), with an FEV1/FVC of 0.84.
• A representative image from his CT scan is
shown in Figure
60. • Bronchoscopy revealed some old blood in the
left upper lobe but no active bleeding or
endobronchial lesions were seen.
• Results of cytologic studies and initial smears
for infectious organisms were negative.
61. Which is the best-recommended therapy at the
present time?
A. Bronchial artery embolization.
B. Itraconazole.
C. Surgical resection.
D. Oral corticosteroids
62. • The CT scan reveals a left upper lobe cavity
with a mass inside, highly suggestive of a
fungus ball.
• Preferred therapy in a patient with reasonably
preserved lung function, as in this patient, is
surgical resection (choice C is correct).
63. • For patients who are considered poor
operative candidates, a number of alternative,
to surgery exist.
• These include bronchial artery embolization if
an area of active bleeding can be found in a
patient with massive hemoptysis. This is really
a temporizing measure because bleeding
tends to recur due to the development of
massive collaterals (choice A is incorrect).
64. • Inhaled, intracavitary, and endobronchial
instillations of antifungal agents have been
tried in small numbers of patients without
consistent success.
• The most promising results have been with
the use of oral itraconazole, perhaps related
to its high tissue penetration.
• However, it works slowly and would not be
recommended in patients with significant
hemoptysis who were otherwise good surgical
candidates (choice C is incorrect).
65. • There are some older reports on the use of
radiation therapy or corticosteroids to control
hemoptysis, but neither affects long-term
outcomes, and steroids carry the risk of
dissemination or fungus ball enlargement
(choice D incorrect)
66. • A fungus ball, or mycetoma, is the saprophytic
colonization of a preexisting parenchymal cavity.
This cavity may be due to previous infection (eg,
TB), bronchiectasis, bullous emphysema,
sarcoidosis, and rheumatoid arthritis, among
others.
• The fungus ball is made up of fungal hyphae
matted together with mucus, fibrin, and tissue
debris that together cause local inflammation.
The fungus ball may move around within the
cavity, making diagnosis easier, but rarely invades
the surrounding parenchyma of the lung.
67. • The most common fungus causing a mycetoma is
Aspergillus, hence, the use of the term aspergilloma,
but other fungal species, including Zygomycetes and
Fusarium, have also been reported as a cause.
• The majority of patients with a mycetoma are
asymptomatic, but somewhere between 50% and 74%
of affected individuals will develop hemoptysis that can
be life threatening.
• Cough, fever, weight loss, and dyspnea have all been
reported, but many of these may be related to the
underlying pulmonary condition.
• The majority of patients will have sputum or
bronchoalveolar lavage fluid cultures that are positive
for Aspergillus species, most commonly A niger.
68. • CT scanning usually shows an intracavitary
mass, as in this patient, often with an air
crescent sign.
• Treatment of choice, as discussed previously,
is surgical resection once hemoptysis starts
but before it becomes too severe.
• Surgical mortality ranges from 7% to 23% and
is usually attributable to the underlying
condition and poor pulmonary function.
69. • Poor prognostic factors includes:
1. The severity of the underlying lung disease.
2. Increasing size or number of lesions seen
on chest radiographs.
3. Immunosuppression(including
corticosteroids)
4. Recurrent large volume hemoptysis
5. Underlying HIV infection.
70. Surgical resection revealed
classic fungus ball (fig-1)
containing numerous fungal organisms on staining (Fig 2), some of which were invading the
surrounding lung tissue, somewhat suggestive of necrotizing aspergillosis
71. • An aortic erosion from the Aspergillus cavity
was also found and repaired.
72. So........
The best-recommended therapy at the present
time?
A. Bronchial artery embolization.
B. Itraconazole.
C. Surgical resection.
D. Oral corticosteroids
74. Pulmonary Aspergillosis
Pulmonary aspergillosis can be subdivided into
five categories:
(a) saprophytic aspergillosis (aspergilloma),
(b) hypersensitivity reaction (allergic bronchopulmonary
aspergillosis),
(c) semi-invasive (chronic necrotizing) aspergillosis,
(d) airway-invasive aspergillosis (acute
tracheobronchitis, bronchiolitis, bronchopneumonia,
obstructing bronchopulmonary aspergillosis), and
(e) Angioinvasive aspergillosis.
75. Saprophytic Aspergillosis (Aspergilloma)
*Saprophytic aspergillosis (aspergilloma) is characterized
by Aspergillus infection without tissue invasion.It typically
leads to conglomeration of intertwined fungal hyphae
admixed with mucus and cellular debris within a preexistent
pulmonary cavity or ectatic bronchus.
* The most common underlying causes are tuberculosis and
sarcoidosis. Other conditions that occasionally may be
associated with aspergilloma include bronchogenic cyst,
pulmonary sequestration,and pneumatoceles secondary to
Pneumocystis carinii pneumonia in patients with acquired
immunodeficiency syndrome (AIDS) (3–5). Although
aspergillomas are usually single, they may also be present
bilaterally.
76. Saprophytic Aspergillosis (Aspergilloma)
*Although patients may remain asymptomatic, the most
common clinical manifestation of saprophytic aspergillosis is
hemoptysis. Surgical resection is indicated for patients with
severe lifethreatening hemoptysis, and selective bronchial
artery embolization can be performed in those with poor lung
function.
79. Hypersensitivity Reaction (Allergic
Bronchopulmonary Aspergillosis)
*Allergic bronchopulmonary aspergillosis is seen most
commonly in patients with long-standing bronchial asthma.
*Acute clinical symptoms include recurrent wheezing, malaise
ith low-grade fever, cough, sputum production, and chest pain.
Patients with chronic allergic bronchopulmonary aspergillosis
may also have a history of recurrent pneumonia.
81. Semi-invasive (Chronic Necrotizing)
Aspergillosis
*Factors associated with the development of this form of
aspergillosis include chronic debilitating illness, diabetes
mellitus, malnutrition, alcoholism, advanced age, prolonged
corticosteroid therapy, and chronic obstructive pulmonary
disease.
* Clinical symptoms are often insidious and include chronic
cough, sputum production, fever, and constitutional
symptoms. In patients with chronic obstructive pulmonary
disease, semiinvasive aspergillosis may manifest with a
variety of nonspecific clinical symptoms such as cough,
sputum production, and fever lasting more than 6 months.
Hemoptysis has been reported in 15% of affected patients
84. Airway-invasive Aspergillosis
*It occurs most commonly in immunocompromised
neutropenic patients and in patients with AIDS
* Clinical manifestations include acute tracheobronchitis,
bronchiolitis, and bronchopneumonia.
86. Airway-invasive Aspergillosis
Obstructing bronchopulmonary aspergillosis is a noninvasive
form of aspergillosis characterized by the massive
intraluminal overgrowth of Aspergillus species, usually A
fumigatus, in patients with AIDS .Affected patients exhibit
cough,fever, and new onset of asthma. Patients may cough
up fungal casts of the bronchi and present with severe
hypoxemia.
87. Angio-invasive Aspergillosis
*Angioinvasive aspergillosis occurs almost exclusively in
immunocompromised patients with severe neutropenia.
*Increase risk of invasive asprigellosis is due to the
development of new intensive chemotherapy regimens for
solid tumors, difficult-to-treat lymphoma, myeloma,and
resistant leukemia as well as an increase in the number of
solid organ transplantations and increased use of
immunosuppressive regimens for other autoimmune
diseases. Despite having a normal neutrophil count,
affected patients have functional neutropenia because the
function of the neutrophils is inhibited by the use of highdose steroids.
94. • The most likely etiology of the lesion is:
A. Thymoma.
B. Bronchogenic cyst.
C. Schwannoma.
D. Lymphoma.
95. • The very large mass is identified to be in the
posterior mediastinum.
• The posterior mediastinum is bounded
anteriorly by the pericardium, posteriorly by
the vertebral bodies, and laterally by the
mediastinal pleura.
• Contained with this compartment is the
thoracic descending aorta, the greater and
lesser azygos veins, splanchnic nerves, the
esophagus, thoracic duct, and lymphatic
tissue.
96. • Schwannomas, neurofibromas,
and
malignant tumors of the nerve sheath
originate from the peripheral nerves
while ganglioneuromas, ganglioneuroblastomas, and neuroblastomas develop
in the sympathetic ganglia. Together,
they account for 30% to 50% of posterior
mediastinal masses (choice C is correct).
97. • Schwannomas and neurofibromas
affect men and women equally,
appearing in the third to fourth
decades of life. These tumors are
spherical and sharply demarcated.
• Surgical resection is the treatment
of choice in patients who are
symptomatic.
98. • Neurogenic tumors are the most common
cause of posterior mediastinal masses. They
account for 20% of all adult mediastinal
masses and 35% of pediatric mediastinal
masses.
• 90% of all neurogenic tumors occur in the
posterior mediastinum. The vast majority of
neurogenic tumors, 70% to 80%, are benign
and slow growing.
99. • Nearly one-half of all tumors are
asymptomatic and found incidentally.
• In those that are symptomatic, regional
compressive
symptoms
or
neurologic
impairment occurs.
• The tumors arise from the peripheral nerves,
sympathetic ganglia, and on rare occasions,
the parasympathetic ganglia
100. • Thymomas are the most common tumors of
the anterior mediastinum, comprising 20% of
anterior mediastinal neoplasms in adults
(choice A is incorrect).
• Bronchogenic
cysts
are
congenital
abnormalities that develop as the result of
anomalous budding of the laryngotracheal
groove. Bronchogenic cysts are well defi ned,
round masses often arising adjacent to the
carina within the middle mediastinum (choice
B is incorrect).
101. • Mediastinal lymphoma is typically an
extension of widespread regional or systemic
disease.
• Primary mediastinal lymphoma, accounting
for 10% mediastinal lymphomas, may occur in
any of the three compartments but typically
arises in the anterior mediastinum (choice D is
incorrect)
103. Symptoms associated with mediastinal masses
No symptoms (discovery by chance)
Paraneoplastic
Local
retrosternal pain
cough
signs of malignancy
dyspnea (compression, phrenic palsy)
109. Lymphoma
23% of tumors in anterior mediastinum in adults
Young adults
Policyclic nodular aspect
Non-surgical treatment (chemotherapy /chemo-radiation)
122. Diagnosis / treatment myasthenia gravis
ACHE inhibitor
Acetylcholinesterase
Antibody
ACH
Degradation
ACH Receptor
123. Thymic tumors and myasthenia gravis
40% of patients with thymoma have myasthenia gravis
20% of patients with myasthenia gravis have thymoma
No difference in MG remission after thymectomy (+ thymoma)
No influence on survival after thymectomy for thymoma (+ MG)
Wright CD, Thorac Cardiovasc Surg 2005
124. Thymic tumors
Classification according Masaoka
Stage I /II
I
Encapsulated without infiltration (macroscopic /
microscopic)
II
Microscopic invasion
Capsule (A)
Mediastinal fat (B)
127. Thymic tumors
Histological WHO (Müller-Hermelink)
classification
A (medullary)
AB (mixed)
A: « atrophic », the thymic cells of adult life
B: « bioactive » biologically active organ of the fetus / infant
C: « carcinoma »
128. Thymic tumors
Histological WHO (Müller-Hermelink)
classification
B1 (organoid)
B2 (cortical)
A: « atrophic », the thymic cells of adult life
B: « bioactive » biologically active organ of the fetus / infant
C: « carcinoma »
B3 (WDTC)
129. Thymic tumors
Histological WHO (Müller-Hermelink)
classification
C (thymic carcinoma)
A: « atrophic », the thymic cells of adult life
B: « bioactive » biologically active organ of the fetus / infant
C: « carcinoma »
137. Thymic tumors
Management
40y old female: VATS resection of thymoma
Resection by minimally invasive approach (VATS)
Risk of incomplete resection / pleural dissemination
138. Thymic tumors
Management
7 years later recurrence (thymic carcinoma)
Resection by minimally invasive approach (VATS)
Risk of incomplete resection / pleural dissemination
139. Thymic tumors
Management
Minimally invasive resection B2 thymoma
Pleural dissemination 2 years later
Resection by minimally invasive approach (VATS)
Risk of incomplete resection / pleural dissemination
140. Thymic tumors
Management
Small (< 5 cm) encapsulated
lesion
Thymectomy
Stage p I
no RT
Stage p II, III
RT
Port J, Chest Surg Clin N Am 2001
141. Resection of thymic tumors
Results (n=71)1
Mortality during follow up
27%
Tumor-related mortality
14%
Recurrence local
14%
local and distant
1Mean
4%
follow up 8.3 years; complete follow up 97%
Lardinois D, Ann Thorac Surg 2000
142. Results after resection of thymic tumors
Predictors for survival
Age
Gender
ns
ns
Myasthenia gravis
ns
Masaoka classification
p < 0.05
Histology
p < 0.05
143. Results after resection of thymic tumors
Predictors for disease-free survival
Age
Gender
ns
ns
Myasthenia gravis
ns
Masaoka classification
p < 0.0001
Histology
p < 0.004
144. Thymic tumors
Management
Tumors > 5 cm
Tumors with invasive pattern
1. Biopsy (true-cut)
2. Induction chemotherapy
3. Resection
Port J, Chest Surg Clin N Am 2001
145. Stage III thymic tumors
Before CHT
Partial response after chemotherapy
After CHT
146. Stage III thymic tumors
Clamshell incision
Resection after induction chemotherapy
Replacement of
VCS
4y follow up
147. Stage III thymic tumors
Induction therapy
Cisplatin-based combination CHT
Response rates
Resectability rates
79 - 100%
36 - 69%
Machiarini P, Cancer 1991
Rea F, J Thorac Cardiovasc Surg 1993
Loehrer PJ, J Clin Oncol 1997
Shin DM, Ann Intern 1998
Berutti A, Br J Cancer 1999
Kim ES, Proc Am Soc Clinic Oncol 2001
151. Mediastinal germ cell tumors (MGCT)
15% of tumors in anterior mediasinum in adults
Average age 30 years (1-73)
Teratoma
men = women
Malignant MGCT
men 95%
176. Regional lymph node classification for lung cancer staging
adapted from the American Thoracic Society mapping scheme
Supraclavicular nodes
1. Low cervical, supraclavicular and sternal notch nodes
From the lower margin of the cricoid to the clavicles and
the
upper
border
of
the
manubrium.
The midline of the trachea serves as border between 1R
and 1L.
Superior Mediastinal Nodes 2-4
2R.Upper Paratracheal
•
2R nodes extend to the left lateral border of the trachea.
From upper border of manubrium to the intersection of
caudal margin of innominate (left brachiocephalic) vein
with the trachea.
2L.Upper Paratracheal
From the upper border of manubrium to the superior
border
of
aortic
arch.
2L nodes are located to the left of the left lateral border
of the trachea.
177. Regional lymph node classification for lung cancer staging
adapted from the American Thoracic Society mapping scheme
3A. Pre-vascular
These nodes are not adjacent to the trachea like the
nodes in station 2, but they are anterior to the
vessels.
3P.Pre-vertebral
Nodes not adjacent to the trachea like the nodes in
station 2, but behind the esophagus, which is
prevertebral.
•
4R. Lower Paratracheal
From the intersection of the caudal margin of
innominate (left brachiocephalic) vein with the
trachea to the lower border of the azygos vein.
4R nodes extend from the right to the left lateral
border of the trachea.
4L. Lower Paratracheal
From the upper margin of the aortic arch to the upper
rim of the left main pulmonary artery.
178. Regional lymph node classification for lung cancer staging
adapted from the American Thoracic Society mapping scheme
Aortic Nodes 5-6
5. Subaortic
These nodes are located in the AP window lateral to
the ligamentum arteriosum.
These nodes are not located between the aorta and
the pulmonary trunk but lateral to these vessels.
•
6. Para-aortic
These are ascending aorta or phrenic nodes lying
anterior and lateral to the ascending aorta and the
aortic arch.
Inferior Mediastinal Nodes 7-9
7.Subcarinal Nodes below carina.
8. Paraesophageal
9. Pulmonary Ligament
Nodes lying within the pulmonary ligaments.
179. Regional lymph node classification for lung cancer staging
adapted from the American Thoracic Society mapping scheme
Hilar, Lobar and (sub)segmental Nodes 1014
These are all N1-nodes.
10. Hilar nodes
These include nodes adjacent to the main stem
bronchus and hilar vessels.
On the right they extend from the lower rim of
the azygos vein to the interlobar region.
On the left from the upper rim of the pulmonary
artery to the interlobar region.
180. 1. Supraclavicular zone nodes
1. Supraclavicular zone nodes
These include low cervical,
supraclavicular and sternal
notch nodes.
Upper border: lower margin of
cricoid.
Lower border: clavicles and upper
border
of
manubrium.
The midline of the trachea serves
as border between 1R and 1L.
181. 2R. Right Upper Paratracheal
2R nodes extend to the left lateral
border
of
the
trachea.
Upper border: upper border of
manubrium.
Lower border: intersection of caudal
margin
of
innominate
(left
brachiocephalic) vein with the
trachea.
2L.
Left
Upper
Paratracheal
Upper border: upper border of
manubrium.
Lower border: superior border of
aortic arch.
On the left a station 2 node in front of
the trachea, i.e. a 2R-node.
There is also a small prevascular node,
i.e. a station 3A node
182. 3. Prevascular and Prevertabral nodes
Station 3 nodes are not adjacent to
the trachea like station 2 nodes.
They are either:
3A anterior to the vessels or
3B behind the esophagus, which lies
prevertebrally.
Station 3 nodes are not accessible
with mediastinoscopy.
3P nodes can be accessible with
endoscopic ultrasound (EUS).
3A and 3P nodes
183. On the left a 3A node in the
prevascular space.
Notice also lower paratracheal nodes
on the right, i.e. 4R nodes.
184. 4R.
Right
Lower
Paratracheal
Upper border: intersection of caudal
margin
of
innominate
(left
brachiocephalic) vein with the
trachea.
Lower border:lower border of azygos
vein.
4R nodes extend to the left lateral
border of the trachea.
185. On the left we
paratracheal nodes.
see
4R
In addition there is an aortic
node lateral to the aortic arch,
i.e. station 6 node.
186. 4L. Left Lower Paratracheal
4L nodes are lower paratracheal nodes that
are located to the left of the left tracheal
border, between a horizontal line drawn
tangentially to the upper margin of the
aortic arch and a line extending across the
left main bronchus at the level of the upper
margin of the left upper lobe bronchus.
These include paratracheal nodes that are
located medially to the ligamentum
arteriosum.
Station 5 (AP-window) nodes are located
laterally to the ligamentum arteriosum.
187. On the left an image just above the level of the
pulmonary trunk demonstrating lower paratracheal
nodes on the left and on the right.
In addition there are also station 3 and 5 nodes
188. On the left an image at the level of the lower trachea just above the
carina.
To
the
left
of
the
trachea
4L
nodes.
Notice that these 4L nodes are between the pulmonary trunk and
the aorta, but are not located in the AP-window, because they lie
medially to the ligamentum arteriosum.
The node lateral to the pulmonary trunk is a station 5 node.
189. 5. Subaortic nodes
Subaortic or aorto-pulmonary window nodes are lateral to the ligamentum
arteriosum or the aorta or left pulmonary artery and proximal to the first branch
of the left pulmonary artery and lie within the mediastinal pleural envelope.
6. Para-aortic nodes
Para-aortic (ascending aorta or phrenic) nodes are located anteriorly and
laterally to the ascending aorta and the aortic arch from the upper margin to the
lower margin of the aortic arch.
190. 7. Subcarinal nodes
These nodes are located caudally to the carina of the trachea, but are not
associated with the lower lobe bronchi or arteries within the lung.
On the right they extend caudally to the lower border of the bronchus
intermedius.
On the left they extend caudally to the upper border of the lower lobe bronchus.
On the left a station 7 subcarinal node to the right of the esophagus.
191. 8 Paraesophageal nodes
These nodes are below the carinal nodes and extend caudally to
the diaphragm.
On
the
left
an
image
below
the
carina.
To the right of the esophagus a station 8 node.
192. On the left a PET image demonstrating FDG uptake in a station 8
node.
On the corresponding CT image the node is not enlarged (blue
arrow).
The probability that this is a lymph node metastasis is extremely
high since the specificity of PET in unenlarged nodes is higher than
in enlarged nodes.
193. 9. Pulmonary ligament nodes
Pulmonary ligament nodes are lying within the pulmonary
ligament, including those in the posterior wall and lower part of the
inferior pulmonary vein.
The pulmonary ligament is the inferior extension of the mediastinal
pleural reflections that surround the hila.
194. 10 Hilar nodes
Hilar nodes are proximal lobar nodes, distal to the mediastinal
pleural reflection and nodes adjacent to the intermediate bronchus
on the right.
Nodes in station 10 - 14 are all N1-nodes, since they are not located
in the mediastinum.
195. 10 Hilar nodes
Hilar nodes are proximal lobar nodes, distal to the mediastinal
pleural reflection and nodes adjacent to the intermediate bronchus
on the right.
Nodes in station 10 - 14 are all N1-nodes, since they are not located
in the mediastinum.
196. Axial CT of Lymph Nodes
•
Scroll through the images on the left.
1-Sternal notch nodes are just seen at this level and
above this level
2-Upper Paratracheal: below clavicles and on the right
above the intersection of caudal margin of
innominate (left brachiocephalic) vein with the
trachea and on the left above the aortic arch.
3-Pre-vascular and Retrotracheal : anterior to the
vessels (3A) or prevertebral (3P)
4-Lower Paratracheal : below upper margin of aortic
arch down to level of main bronchus
5-Subaortic (A-P window): nodes lateral to
ligamentum arteriosum or lateral to aorta or left
pulmonary artery
6-Para-aortic: nodes lying anterior and lateral to the
ascending aorta and the aortic arch beneath the
upper margin of the aortic arch
7-Subcarinal
8-Paraesophageal (below carina)
9-Pulmonary Ligament: nodes lying within the
pulmonary ligament.
10--14: nodes are all N1 nodes
197. •
•
Conventional mediastinoscopy
The following nodal stations can be biopsied by cervical
mediastinoscopy: the left and right upper paratracheal nodes (station
2L and 2R), left and right lower paratracheal nodes (station 4L and 4R)
and
the
subcarinal
nodes
(station
7).
Station 1 nodes are located above the suprasternal notch and are not
routinely accessed by cervical mediastinoscopy.
198. Extended mediastinoscopy
Left upper lobe tumors may metastasize to the subaortic lymph nodes (station 5) and
paraaortic nodes (station 6). These nodes can not be biopsied through routine
cervical mediastinoscopy. Extended mediastinoscopy is an alternative for the
anterior-second interspace mediastinotomy which is more commonly used for
exploration of mediastinal nodal stations.
This procedure is far less easy and therefore less routinely performed than
conventional mediastinoscopy.
199. EUS-FNA
Endoscopic Ultrasound with Fine Needle Aspiration can be performed
of all the mediastinal nodes that that can be assessed from the
oesophagus. In addition the left adrenal gland and the left liver lobe
can be visualized.EUS particularly provides access to nodes in the lower
mediastinum (station 7,8 and 9)
