Thoracic vascular disease in oncologic patients

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Radiología. 2011;53(4):335---348
www.elsevier.es/rx
UPDATE IN RADIOLOGY
Thoracic vascular disease in oncologic patients夽
D. Varona Porres∗ , J. Andreu Soriano, E. Pallisa Núñez,
O. Persiva Morenza, A. Roque Pérez
Departamento de Radiodiagnóstico, Hospital Vall d Hebron, Barcelona, Spain
Received 28 October 2010; accepted 31 January 2011
KEYWORDS
Thoracic diseases;
Vascular diseases;
Clinical oncology;
Multidetector CT
PALABRAS CLAVE
Enfermedades
torácicas;
Enfermedades
vasculares;
Oncología clínica;
TC multicorte
夽
∗
Abstract Patients with oncologic disease require frequent imaging tests (predominantly computed tomography) for follow-up. These patients may have thoracic vascular disease that can
influence the diagnosis, treatment, and prognosis of their cancer. Primary vascular tumors
can involve the thoracic vessels, like the pulmonary arteries (pulmonary artery sarcoma), and
the neoplastic disease can extend locally (lung tumor) or remotely to the thoracic vessels
(pulmonary tumor embolism and pulmonary tumor thrombotic microangiopathy). Oncologic
treatment results in multiple complications that involve the thoracic vessels and can even
compromise the patient’s life in certain cases. CT, and especially multislice CT, makes it possible
to evaluate neoplastic disease and associated thoracic vascular disease in oncologic patients.
© 2010 SERAM. Published by Elsevier España, S.L. All rights reserved.
Patología vascular torácica en pacientes oncológicos
Resumen La patología oncológica requiere frecuentes controles mediante pruebas de imagen, de forma predominante con tomografía computarizada (TC). En estos pacientes podemos
encontrar patología vascular torácica que puede influir en el diagnóstico, el tratamiento y el
pronóstico de su enfermedad neoplásica. Los tumores primarios vasculares pueden afectar a
los vasos torácicos, como las arterias pulmonares (sarcoma de arteria pulmonar), y la enfermedad neoplásica se puede extender localmente (neoplasia pulmonar) o a distancia hacia los
vasos torácicos (embolia pulmonar tumoral y microangiopatía trombótica tumoral pulmonar).
El tratamiento oncológico es la causa de múltiples complicaciones sobre los vasos torácicos que
en determinados casos llegan a comprometer la vida del paciente. La TC, especialmente con
técnica multicorte, permite la evaluación de la enfermedad neoplásica y la patología vascular
torácica asociada en el paciente oncológico.
© 2010 SERAM. Publicado por Elsevier España, S.L. Todos los derechos reservados.
Please cite this article as: Varona Porres D, et al. Patología vascular torácica en pacientes oncológicos. Radiología. 2011;53:335---48.
Corresponding author.
E-mail address: [email protected] (D. Varona Porres).
2173-5107/$ – see front matter © 2010 SERAM. Published by Elsevier España, S.L. All rights reserved.
336
Introduction
At present, oncological radiology represents much of the
activity of the departments of radiodiagnosis. It is thus
important to have an extensive knowledge of oncologic
pathology as well as of the possible complications that may
arise from the treatment, which can often be aggressive and
potentially toxic.
Oncologic disease can involve the thoracic vessels, either
in the form of primary tumor or secondary to thoracic neoplasms, especially lung tumor. In addition, the treatment of
oncology patients is associated with vascular complications
involving the thoracic region that compromise the management and even the lives of these patients.
Neoplastic disease
Primary neoplasms
Primary pulmonary artery (PA) sarcomas (Fig. 1) are often
misdiagnosed as pulmonary thromboembolic disease.
They originate from mesenchymal cells of the intima
of the PA1 and may appear as polypoid intraluminal
or sessile masses. In approximately half of the cases,
the tumors remain intraluminal; in the other half, they
spread transmurally into the adjacent lung, bronchial
wall, or lymph nodes.2 Pulmonary nodules may also be
seen.2
The most common symptoms are dyspnea (72%), chest
pain (45%), cough (42%) and hemoptysis (24%).3 A chronic
clinical course without acute dyspnea suggests PA sarcoma.
The age of presentation is 13---81 years (mean 49.3 years)
with no gender prevalence.3
D. Varona Porres et al.
Chest radiography most often demonstrates a unilateral
hilar mass in an arterial distribution projecting into the lung.
If there is parenchymal spread, the lesion can mimic lung
cancer.
Computed tomography (CT) findings demonstrate a heterogeneous mass distending the PA with extraluminal
extension, pulmonary condensation or subpleural nodules,
pleural effusion or cardiomegaly. It may be misdiagnosed
as pulmonary embolism. In 86% of cases, CT demonstrates a
filling defect occupying the entire lumen of the main or proximal PA with distension of some portion of the PA involved.3
Extraluminal extension is an additional specific finding. The
presence of a filling defect occupying the entire lumen of
the main or proximal arteries may be the initial finding on
CT.
Unlike pulmonary embolism, PET/CT scan may show FDG
uptake.1
The prognosis is poor (five-year survival rate is 6%)4 and
the mean survival time after onset of symptoms is approximately 12 months.3
Secondary neoplasms
Extrinsic compression or local invasion of the thoracic
vessels
Superior vena cava syndrome (SVCS) is the result of the
obstruction of the superior vena cava (SVC) or its major
tributaries by intraluminal occlusion, extrinsic compression
and/or invasion by malignant or benign disease.5 The most
common causes are malignancies5 ; however, thrombosis
related to catheters or pacemakers has increased in recent
years. There might be direct extension of the tumor or adjacent lymph nodes or extrinsic compression. Vascular invasion
may lead to thrombophlebitis and complete occlusion.5
Figure 1 (A) 68-Year-old man presents with a 3-month history of dyspnea with exertion that has progressed to dyspnea at rest over
the last 15 days and chest pain from the onset of the symptoms, with palpitations, orthopnea and paroxysmal nocturnal dyspnea.
Multidetector CT (MDCT) showed a filling defect involving the entire right main pulmonary artery, extending to the ipsilateral lobar
branches and to the main branch of the pulmonary arteries, with increased maximum diameter and lobulated right pulmonary
artery (arrows). (B) PET-CT demonstrated a linear hypermetabolic area along the trajectory of the pulmonary artery suggestive of
malignancy (SUV max 12 g/ml). The patient was diagnosed with primary pulmonary artery sarcoma.
Figure 2 49-Year-old man with non-small cell lung cancer
(NSCLC) and a 10-day history of chest pain and dysphagia, with
jugular vein engorgement and eyelid swelling. MDCT showed a
right paratracheal mediastinal mass invading the superior vena
cava (SVC) (*) and that induced the formation of collateral
vessels, particularly at the expense of the azygos-hemiazygos
system (arrows).
Lung neoplasm is the most common cause of SVCS (80%),
being the non-small cell lung carcinoma (NSCLC) the most
common (50%) (Fig. 2), followed by small cell carcinoma
(SCLC) (25%) and non-Hodgkin lymphoma (NHL) (10%).6 Overall, 2---4% of lung neoplasms result in SVCS at some point in
the disease,7 being more frequent in SCLC (approximately
10% at diagnosis).7,8 SVCS appears in less than 2% of patients
with NSCLC, but the higher incidence of this type of tumor
results in more frequent SVCS than in SCLC.7
SVCS appears in 2---4% of NHL, being the most common subtypes the diffuse large cell and lymphoblastic
lymphoma.9 Diffuse large B cell lymphoma with sclerosis
is the subtype that most frequently causes SVCS.10 Most
NHLs result in SVCS secondary to extrinsic compression by
lymph nodes, but intravascular proliferation can also occur
(angiotropic lymphoma).11
There are other malignancies associated with SVCS,
including mediastinal lymph node metastases.12
The severity depends on the development of the collateral vascular system.5 In most cases, the symptoms develop
gradually but sometimes this condition is asymptomatic.
Dyspnea is the most common symptom. At physical examination, other symptoms include facial rubor and erythema,
face, neck and chest edema, and dilated cutaneous veins
over the abdomen, chest and upper extremities.5
The five main collateral pathways are the:
1.
2.
3.
4.
5.
Azygos-hemiazygos system.
Paravertebral.
Internal mammary.
Lateral thoracic and thoracoepigastric veins.
Anterior jugular venous system.
Some authors describe the veins around the scapula, on
the back and shoulder as the most common whereas others
mention the azygos vein.5
Chest radiography shows abnormal findings in 84% of
cases,13 being the most common signs the widening of the
mediastinum (64%) and pleural effusion (26%).
337
CT is essential in the evaluation of SVCS allowing us to see
the level and extent of the obstruction and to identify the
collateral pathways and the underlying cause. The presence
of collateral vessels is a strong indicator of SVCS.5,14 Multidetector CT with MIP and 3D reconstructions is useful in the
detection of local stenosis and to evaluate the relationship
of the great vessels and the extent of collateral vessels5,15
(Fig. 2).
The treatment depends on the type and extent of the
tumor, being the average life expectancy about 6 months.16
Chemotherapy provides good results in about 60% of SCLC
and lymphomas.5 Radiotherapy gives a complete response in
15---60% of cases, even though with side effects.5 Endovascular stenting is a more effective and less invasive technique,
providing good mid-term results.5
Extrinsic compression or invasion from a pulmonary neoplasm can affect the pulmonary veins (PV) (Fig. 3). It has
also been described the extension through the PV into the
left autrium from a pulmonary neoplasm, most commonly a
bronchogenic carcinoma, and to a lesser degree pulmonary
sarcomas or metastases of carcinoma.17,18 This can result in
cardiac arrest caused by obstruction of the mitral valve or
pulmonary tumor embolism.17,19
Extension into the great vessels of the mediastinum is
considered stage T4 in NSCLC staging; therefore, surgical
treatment is not the first choice. Great vessels include
the aorta, SVC, inferior vena cava, main PA (pulmonary
trunk), intrapericardial portions of the right and left PA and
intrapericardial portions of the left and right superior and
inferior PV. Invasion of more distal branches does not qualify
for T4.20
Extrinsic compression or invasion from lung neoplasms
also can affect the PA (Fig. 4). However, PA invasion by a
lung neoplasm detectable on CT is rare,21,22 but microscopic
vascular invasion is common.23 It can be misdiagnosed with a
primary PA tumor or pulmonary thromboembolism. The prognostic significance is unclear although vascular invasion has
Figure 3 73-Year-old former smoker. MDCT revealed a pulmonary mass in the left lower lobe (*) invading the pulmonary
veins and a thrombus in the left upper pulmonary vein and
amputation at the left lower pulmonary vein (arrows). The
patient underwent left pneumonectomy combined with left
atrium resection. Histopathological analysis revealed a poorly
differentiated squamous cell carcinoma with invasion of the left
atrial wall.
338
Figure 4 74-Year-old smoker with a 2-month history of dyspnea and cough. MDCT showed a pulmonary mass in the middle
lobe invading the right pulmonary artery (arrow). Fiberbronchoscopy and biopsy were performed and the patient was
diagnosed with endobronchial SCLC and died one month after
diagnosis.
been described as a poor prognostic factor. A retrospective
study found no correlation between macroscopic arterial
invasion and histologic type and grade and lymph node staging for bronchogenic carcinoma.24 Lung carcinomas with
polypoid growth in the main PA seem to belong to a more
aggressive subtype called adenosquamous carcinoma.22
Although invasion of the main trunk or intrapericardial portions of the PA by a NSCLC qualify for T4 and, therefore surgical treatment is not indicated, the management of these
patients is controversial. Recent articles have reported a
more favourable outcome for patients undergoing extended
surgery with postoperative pathological N0 disease.21
Lung tumors with infiltration of the thoracic aorta are
even less common than advanced tumors infiltrating the
espine, the carina or the apex of the lung (Fig. 5).25 There
might be hemoptysis secondary to direct invasion of the
aortic wall by lung cancer, resulting in an aortobronchopulmonary fistula.26 Direct invasion by an infectious process,
an aortic aneurysm or dissection that breaks open and
bleeds into the lung or erodes into a bronchus may also
result in acute and massive hemoptysis.26 Symptoms include
back pain, cough, dyspnea and hemoptysis. Hemoptysis is
the most common symptom (about 95%) and is frequently
massive, but can also be minor and intermittent.26 Minor
hemoptysis may precede a fatal hemorrhage with cases
described anywhere from 2 days to 1 year.27
Cases of periaortic lymphoma, dissection of the ascending aorta caused by neoplastic disease and invasion of the
aortic wall by a squamous cell carcinoma mimicking an intramural hematoma have also been described.28---30
Chest radiographic findings include pulmonary condensation, widening of the mediastinum and pleural effusion
(hemothorax).26,27
Infiltration of the thoracic aorta by a malignant pulmonary neoplasm has poor prognosis; however, tumor
resection including the involved aorta provides long-term
survival with N0 disease.31
Distant spread
Pulmonary tumor embolism (PTE) is rarely diagnosed
before death, probably because the clinical and radiological findings are unspecific. Autopsy findings revealed
that 2---26% of patients with a known malignancy develop
PTE.32,33 Breast, lung and gastric cancer are the most
common neoplasms associated with PTE, but cases of
Figure 5 71-Year-old smoker and heavy drinker presented to our hospital with hemoptysis. He reported having a several-day
history of hemoptysis and had four more episodes on the day of admission to the emergency department. At admission, he had
a new episode of hemoptysis of fresh blood. He also reported anorexia and weight loss over the last year. The sputum cytology
revealed atypical cells suspicious for malignancy. MDCT showed a lung mass and air bubbles within the lesion, probably caused
by necrosis, in close contact with the descending thoracic aorta that showed irregularities in the left lateral wall indicative of
infiltration (arrow). 72 h after admission, the patient had an episode of life-threatening hemoptysis that needed arteriography with
embolization. Radiation therapy or surgery was not performed and the patient had a new episode of massive hemoptysis with
respiratory failure and cardiopulmonary arrest. Patient died 18 days after admission.
339
Figure 6 (A) 57-Year-old man with a left renal tumor waiting for surgery. Preoperative chest radiograph showed an increase in size
and density of the right pulmonary hilum (arrows). (B) MDCT with multiplanar reconstruction showed a central filling defect with
increase in size of the right pulmonary artery and of the lower segmental branches (white arrows). Lower image shows a renal mass
(*) with thrombosis of the left renal vein (black arrow). These findings are compatible with hyperhephrona with renal vein invasion
and pulmonary tumor embolism. The patient underwent chemotherapy for 2 months before surgery, which reduced significantly the
lesions in the right pulmonary artery and lower segmental branches on follow-up CT scan. Subsequently, the patient underwent left
radical nephrectomy.
neoplasms in liver, prostate, pancreas, bone, indifferentiated carcinoma, ovary, renal bladder, cervix, colorectal,
kidney, mesothelioma, Wilms tumor, esophagus, parotid,
melanoma, myxoma, thyroid, choriocarcinoma, vulvar carcinoma and neurogenic sarcoma have also been reported.34
Mortality rates are very high, but early diagnosis and
proper treatment (primary tumor resection) can provide
a cure in selected cases (hypernephroma, myxoma and
choriocarcinoma).32
Most cases have been previously diagnosed with malignancy; however, in some cases PTE is the first manifestation.
Right atrial myxoma and hypernophrona tend to embolize to
the central and segmental PA33 (Fig. 6).
In many instances, distant metastases appear before the
onset of respiratory symptoms. Dyspnea is the most common presenting symptom and is severe, usually acute or
subacute and invariably progressive. Other symptoms are
pleuritic chest pain, cough, weight loss, fatigue, syncope
and hemoptysis.32
In most cases, there is also pulmonary hypertension and
right atrial overload. The presence of cor pulmonale is a poor
prognostic sign often leading to death within 4---12 weeks.32
340
Figure 7 (A) 38-Year-old man with a 2-month history of irritating dry cough. He had dyspnea that progressed to dyspnea with minimal exertion over the past 8 days, so he sought emergency care. MDCT scan demonstrated lymph adenopathies at the supra-aortic
trunk level as well as left para-aortic (arrow), right hilar, mesenteric and retroperitoneal adenopathies. (B) MDCT also showed an
Chest radiographic findings are normal in most cases. Cardiomegaly and prominent PA are rare (less than 50%). There
might be local or diffuse interstitial opacities. The absence
of pulmonary opacities with dyspnea and hypoxemia suggests pulmonary vascular disease.32
IV contrast enhanced CT scan reveals filling defects in
the main branches of the PA, obstructions and dilations
of subsegmental branches, subpleural lines and wedgeshaped opacities secondary to pulmonary infarction, and
signs of pulmonary venous hypertension. The presence of
lymphadenopathy or lymphangitic carcinomatosis may suggest PTE.33
Ventilation-perfusion lung scintigraphy produces a typical pattern of multiple small, peripheral and subsegmental
perfusion defects, with normal ventilation.32
The four main types of PTE are32 :
1. Large proximal tumor embolism resulting in acute pulmonary hypertension syndrome secondary to occlusion
of the main PA or main lobar branches.
2. Microscopic tumor embolism involving small arteries and
arterioles, with progressive dyspnea and subacute pulmonary hypertension.
3. Microvascular pulmonary invasion that may be part of the
generalized lymphatic involvement, which can explain
the presence of diffuse interstitial opacities.
4. Combination of the three previous mechanisms.
Pathologic findings include tumor emboli mixed with
malignant cells with or without obliterative arteritis,32 and
may coexist with lymphangitic carcinomatosis.33
Differential diagnosis includes pulmonary thromboembolism or pulmonary embolism secondary to other
causes (septic, fat, amniotic fluid, foreign bodies and
parasites).32
Biopsy may be indicated in those cases where the definite
diagnosis is needed for treatment.32
Pulmonary tumor thrombotic microangiopathy (PTTM) is
a rare form of tumor embolism (Fig. 7). It is seen at autopsy
in 0.9---3.3% of patients with extrathoracic malignancies.35
High-resolution chest CT reveals centrilobular nodules
and branching linear opacities with tree-in-bud appearance.
This pattern is caused not only by small airway diseases, but
also by vascular abnormalities.35
There are two pathogenic mechanisms36 :
1. Filling of centrilobular arteries with tumor cells.
2. Thrombotic microangiopathy: extensive fibrocellular
intimal hyperplasia in small PA and arterioles (carcinomatous endarteritis) induced by tumor microemboli.
341
Histologic findings reveal arterial occlusion caused by tumor
cell, peripheral arterial dilation and extensive fibrocellular intimal hyperplasia.36 PTTM must be included in the
differential diagnosis of dyspnea of unknown origin, particularly in case of prior diagnosis of mucin secretory
adenocarcinoma.37 A pulmonary biopsy establishes the diagnosis, but antemortem diagnosis is uncommon.37
Vascular disease related to oncology
treatment
Surgery
Thromboembolic events may occur in as much as 26% of
patients after pulmonary resection.38 Vascular stumps are
more vulnerable to thrombus formation. A case of postbilobectomy stump thrombosis for lung cancer has been
described38 ; however, most cases reported in the literature
refer to pneumonectomies.39,40
Postpneumonectomy PA stump thrombosis most commonly appears during the first days after surgery (Fig. 8). In
12.4% of a series of patients, stump thrombosis was observed
at postpneumonectomy CT (in 82% of patients the thrombus
was present on the initial CT scan and on subsequent CT
examinations).39 There might be reduction in thrombus size
and those that remain stable have concave shape.39 Almost
none of the patients develop propagation of the thrombus
outside of the stump, suggesting a benign natural history
of this condition.39,40 Stump thrombi appear with equal frequency on either side. There seems to be a relationship
between stump length and the development of thrombosis, probably a consequence of a change in flow dynamics.
It seems, therefore, prudent to leave the PA stump as short
as possible.39,40
Pulmonary embolism secondary to deep venous thrombosis and tumor recurrence should be considered in the
differential diagnosis.
Radiation therapy
Radiation-induced cardiovascular complications often
develop late after therapy.41 Vascular complications include
early stenosis of the coronary artery or calcifications of the
ascending aorta.
Radiation-induced vasculopathy is time and dose
dependent.42 Venous capillaries and sinusoids are the most
sensitive to ionizing radiation, being endothelial cells the
most vulnerable.42 Radiation-induced vasculopathy usually
occurs after about 10 years and is limited to the radiation
field.41,42 When thrombosis and rupture occur, the damage
increase in diameter of the main trunk of the pulmonary arteries (right image) and cardiomegaly at the expense of the right heart
cavities (left image). (C) MDCT (lung window) showed multiple centrilobular opacities with bilateral and diffuse distribution with no
clear lobar preference. (D) During hospitalization, the patient had chest pain and dyspnea with cardiopulmonary arrest and death.
Post-mortem examination revealed disseminated metastatic disease of a signet-ring cell carcinoma with pancreatic immunophenotype and massive bilateral pulmonary tumor embolism. Histopathological analysis (hemotoxylin---eosin staining) revealed intimal
hyperplasia related to fibroblast growth with reduced arterial size and pulmonary thrombi occluding the arterial lumen (*). These
finding were compatible with pulmonary tumor thrombotic microangiopathy.
342
as a sequela of a scarred intima or media after aortitis41 and
are indistinguishable from atherosclerosis.
Chemotherapy
Figure 8 58-Year-old man with lung cancer treated with
pneumonectomy and subsequent chemo- and radiation therapy.
Initial MDCT (right image) did not show pulmonary artery abnormalities, but a 2-year follow-up MDCT scan showed a concave
filling defect in the stump of the left pulmonary artery postpneumonectomy (arrow).
becomes clinically significant. Stenoses and occlusions are
the most common lesions.
Coronary stenosis occurs after radiation therapy mainly
given for Hodgkin disease and it involves the proximal
portions.1
Calcifications of the ascending aorta (Fig. 9) are secondary to radiation-induced aortitis and appear thin and
well-defined.41,43 They are due to deposition of calcium salts
Central venous catheter-related complications
Central venous catheters (CVC) are commonly used in
cancer patients allowing delivery of medication. Incidence of complications is 15%.44 They can be immediate
(6.2---11.7%) or long-term (6.6% reported in a retrospective study).45 Immediate complications include arterial
puncture and hematoma (the most common), misplacement or pneumothorax---hemothorax.45 Most common late
complications include infection, venous thrombosis and pulmonary embolism, mechanical (pinch off syndrome, rupture
or migration) and extravasation.
CVC thrombosis occurs in 41% of patients despite preventive measures, increasing the risk of infection.46 Thrombosis
and infection are the most common late complications. Only
one-third is symptomatic,46 and it can result in SVCS associated with collateral vessel formation. Complications related
to CVC thrombosis include postphlebitic syndrome (15---30%)
and pulmonary embolism (11%; only half are symptomatic).46
Risk factors include type of malignancy, type of CVC and
locations of insertion site and catheter tip.45,46 Placement of
the catheter tip high in the SVC and insertion from the left
subclavian vein result in a higher incidence of thrombosis.46
Treatment includes medical treatment or catheter removal.
Figure 9 85-Year-old man with hypertension and ischemic cardiomyopathy (unstable angor) that was asymptomatic for years.
He was diagnosed with NSCLC that was treated with radical radiation therapy during 1.5 months (70 Gy). MDCT, comparing the
initial study performed with IV contrast administration (right upper image) with the post radiation therapy study without contrast
administration (left upper image) performed one year later, revealed calcifications that appeared more pronounced in the aortic
button on the post radiation therapy study (*). Lower images show a significant improvement in the lung mass on the post-radiation
therapy scan (arrow). Later, the mass progressed and, given the cardiovascular comorbidity of the patient, it was decided to provide
symptomatic treatment.
343
Figure 10 (A) Gastric cancer in a 41-year-old man undergoing chemotherapy. MDCT showed a central venous catheter (CVC) in
the superior vena cava (SVC) properly positioned (white arrow) and a migrated catheter located in the pulmonary arteries (black
arrow). (B) MDCT oblique MIP reconstruction showed the CVC properly positioned in the SVC (white arrow) and the migrated catheter
in the right main pulmonary entering the lower lobar branch, bending on itself and becoming apparent in the contralateral main
pulmonary artery (black arrows). Removal of the catheter was unsuccessful; the old reservoir was retrieved confirming that the
catheter was fractured 2---3 cm from it and a new CVC was placed.
Removal is indicated in case of infection, misplacement of
the distal end of the catheter or irreversible obstruction.
Extravasation is a severe complication that occurs in
0.1---6.5% of cases.45 Its causes include rupture and migration
of the catheter or perforation of the SVC wall.45 Extravasation of chemotherapy agents results in significant adjacent
tissue damage and tissue necrosis can occur in severe cases,
requiring surgery.45
Fracture of a CVC is a rare complication (0.2---1%).47 Fracture may happen at the moment of insertion or anytime
after.47 The pinch-off syndrome involves the compression of
the catheter in the subclavian vein between the clavicle and
first rib, causing the catheter to fracture and migrate.48 Clinical presentation of this complication may be subtle and only
a minority of patients present with symptoms (chest pain,
palpitations or arrhythmias).47 Migration of the fragmented
catheter may result in PA thromboembolism and pseudoaneurysm, the removal of the catheter is thus indicated49,50
(Fig. 10).
Pulmonary embolism
The association between thromboembolic disease and cancer is well established in the literature. Along with cancer
itself, chemotherapy also contributes to the activation of
coagulation.51,52 Patients with malignant neoplasms and
thrombosis have a lower survival rate. Moreover, patients
with cancer have a four- to eightfold higher risk of dying
after an acute thrombotic event.53
In oncology patients, pulmonary thromboembolism
occurs in three settings: synchronous diagnosis of thromboembolism and tumor, incidental diagnosis during cancer
follow-up, or diagnosis in symptomatic patients.
Cancer diagnosed at the same time as an episode of
venous thromboembolism is associated with advanced disease stage and poorer prognosis51 (Fig. 11).
Incidental pulmonary embolism is seen in 1.5% of routine CT and in 1.8---4% of oncology patients in retrospective
studies.52,54 Retrospective studies reported that in 67---75% of
cases the emboli were not detected at the initial CT. For this
reason, careful evaluation of the PA during CT follow-up is
important in these patients.52,54 Prevalence increases in hospitalized patients, in advanced stages of the disease and in
patients undergoing chemotherapy.53,55 The most common
malignancies associated with thrombosis are those of the
breast, colon, and lung, reflecting the prevalence of these
malignancies in the general population. When data were
adjusted for disease prevalence, the cancers most strongly
associated with thrombotic complications are those of the
Figure 11 NSCLC in a 66-year-old woman with pleural fluid cytology positive for adenocarcinoma. Initial MDCT showed a pulmonary
mass in the left upper lobe (*) and pleural effusion with nodular thickening compatible with primary lung neoplasm with metastatic
pleural involvement. Filling defects were seen in the upper lobar and segmental branches of the right pulmonary artery (arrows),
compatible with pulmonary thromboembolism associated with the malignancy.
344
Figure 12 (A) 63-Year-old woman with mesothelioma undergoing chemotherapy. MDCT, comparing the initial study (left) and the
two-month follow-up (right), demonstrated a filling defect corresponding to a pedunculated thrombus in the left lateral wall of
the thoracic descending aorta (arrow). (B) Sagittal MDCT multiplanar reconstruction clearly demonstrated the mobile pedunculated
thrombus at the origin of the thoracic descending aorta (arrow). (C) MDCT, comparing the initial study (right) and the two-month
follow-up (left), shows a scar in the spleen corresponding to splenic infarction (black arrow in upper left image), and a triangularshaped hypodense lesion in the right kidney, corresponding to a renal infarction (white arrow in lower left image). Radiological
findings were compatible with a mobile thrombus in the thoracic descending aorta that caused the splenic and renal infarction
secondary to visceral embolism.
345
Figure 13 (A) 79-Year-old woman with renal cancer treated with nephrectomy and presenting subsequent metastasis. Chemotherapy included sorafenib. Follow-up MDCT scans (initial, at three, five and eight months) demonstrated an aortic dissection in the
thoracic descending aorta that worsened gradually. (B) MDCT with oblique multiplanar reconstruction demonstrated localized
dissection of the thoracic descending aorta (arrow) and as a result, sorafenib therapy was discontinued.
pancreas, ovary, and brain.53 Locations are usually lobar and
segmental and with a right-sided predominance.54
Symptomatic pulmonary embolism has a prevalence
of 11.8% on CT-angiography52 and a retrospective study
reported that pulmonary embolism is usually central and
with lower density thrombi.56
Thoracic aortic mobile mural thrombus
TAMT is a rare condition that involves an aortic thrombus in
a normal aorta and is a potential source of cerebral, visceral
and peripheral embolism (Fig. 12).
The most common location is the descending thoracic
aorta (28%) or the distal aortic arch (16%) with a preferente
for the aortic isthmus,56,57 being the ascending thoracic
aorta a less common location (5%).56
The ethiopathogenesis of TAMT is different from that
of embolism associated with atherosclerotic disease. Possible causes include malignant neoplasms, hematologic
diseases, therapy with exogenous steroids and estrogens,
and primary endothelial dysfunction. Generalized hypercoagulability (cancer patients or patients in chemotherapy)
and endothelial vasculopathy have been proposed as the
most important factors in TAMT formation, with hypercoagulability seen in 40% of cases.57
It can be an incidental finding, but most TAMT are
detected during evaluation for distal emboli to the viscera
346
or extremities. In autopsy series, the incidence was 0.45%.57
Incidence of TAMT with embolism ranges between 0.8% and
9%.58 Embolization to the lower extremities is the most
common (60%), followed by mesenteric embolism (18%).
Embolization to the lower extremities originates in the
abdominal aorta in 80% of cases and in the descending
thoracic aorta in 20% of cases. Mesenteric emboli originate
in the abdominal aorta in 56% of cases and in the thoracic
aorta in 44% of cases. There can also be emboli to the renal
arteries (6%), upper extremities (6%), cerebral arteries (2%)
and coronary arteries (1%).57
Transesophageal echography used to determine the origin of thombi allows visualization of pedunculated thrombi
floating in the aortic lumen. However, part of the aortic
arch and the abdominal aorta usually cannot be visualized
with transesophageal echocardiography.57 Magnetic resonance and multidetector CT can be useful in the diagnosis of
TAMT as well as to determine the location and extent of the
mural thrombus. Identification of the base of implantation
can be useful to determine the optimal surgical approach
and technique.57
Its management is not clear and there are several
therapeutic approaches. Medical treatment is the first alternative, particularly in symptomatic patients. Surgery may
be performed when heparin therapy fails. Stenting can be a
valid alternative to surgery.57
A new embolization event may occur in 14.7% of cases and
the average recurrence is about 8 months in a different location from the initial event.57 This fact supports the need of
long-term anticoagulant therapy after surgery or endovascular treatment, and of clinical follow-up with imaging studies.
This condition should be included in the differential
diagnosis of embolic events, particularly in young patients
without a history of heart disease or recurrent peripheral
embolism without a known cause.57
Aortic dissection
An aortic dissection is a serious condition associated with
hypertension. Some drugs such as bevacizumab have been
associated with hypertension and worsening of preexisting hypertension, and can therefore result in aortic
dissection59,60 (Fig. 13). This drug acts as an antiangiogenic
and it is used in combination with cytotoxic chemotherapy. Hypertension is the most common toxicity associated
with bevacizumab (up to 32%).59 Other antiangiogenic agents
such as sunitinib and sorafenib can induce hypertension.
If the medical treatment cannot control the hypertension,
the antiangiogenic therapy should be discontinued.59 Bevacizumab is used for the treatment of colon, lung and kidney
cancer, usually in the elderly, in whom the incidence of
hypertension is higher.59
Conclusions
Thoracic vascular disease of oncology patients can influence the treatment, management and prognosis of these
patients. Multidetector CT represents an excellent tool in
the diagnosis and follow-up of these patients. Due to the
fast development and the emergence of new cancer therapies, further complications may arise in the near future,
especially related to thoracic vascular disease.
Authorship
Responsible for the integrity of the study: DVP.
Conception of the study: DVP and JAS.
Design of the study: DVP.
Acquisition of data: DVP, JAS, OPM, ARP and EPN.
Analysis and interpretation of data: DVP, JAS, OPM, ARP and
EPN.
Statistical analysis: not applicable.
Bibliographic search: DVP and JAS.
Drafting of the work: DVP.
Critical review with intellectually relevant contributions:
DVP, JAS, OPM, ARP and EPN.
Approval of the final version: DVP, JAS, OPM, ARP and EPN.
Conflict of interest
The authors declare no conflict of interest.
References
1. Chong S, Kim TS, Kim BT, Cho EY, Kim J. Pulmonary artery sarcoma mimicking pulmonary thromboembolism: integrated FDG
PET/CT. AJR Am J Roentgenol. 2007;188:1691---3.
2. Bressler EL, Nelson JM. Primary pulmonary artery sarcoma:
diagnosis with CT, MR imaging, and transthoracic needle biopsy.
AJR Am J Roentgenol. 1992;159:702---4.
3. Yi CA, Lee KS, Choe YH, Han D, Kwon OJ, Kim S. Computed
tomography in pulmonary artery sarcoma: distinguisihing features from pulmonary embolic disease. J Comput Assist Tomogr.
2004;28:34---9.
4. Simpson Jr WL, Mendelson DS. Pulmonary artery and aortic sarcomas: cross-sectional imaging. J Thoracic Imaging.
2000;15:290---4.
5. Eren S, Karaman A, Okur A. The superior vena cava syndrome
caused by malignant disease. Imaging with multi-detector row
CT. Eur J Radiol. 2006;59:93---103.
6. Rice TW, Rodríguez RM, Light RW. The superior vena cava syndrome: clinical characteristics and evolving etiology. Medicine
(Baltimore). 2006;85:37---42.
7. Rowell NP, Gleeson FV. Steroids, radiotherapy, chemotherapy
and stents for superior vena caval obstruction in carcinoma of
the bronchus: a systematic review. Clin Oncol (R Coll Radiol).
2002;14:338---51.
8. Urban T, Lebeau B, Chastang C, Leclerc P, Botto MJ, Sauvaget
J. Superior vena cava syndrome in small-cell lung cancer. Arch
Intern Med. 1993;153:384---7.
9. Perez-Soler R, McLaughin P, Velasquez WS, Hagemeister FB,
Zornoza J, Manning JT, et al. Clinical features and results of
management of superior vena cava syndrome secondary to lymphoma. J Clin Oncol. 1984;2:260---6.
10. Lazzarino M, Orlandi E, Paulli M, Boveri E, Morra E, Brusamolino
E, et al. Primary mediastinal B-cell lymphoma with sclerosis:
an aggressive tumor with distinctive clinical and pathologic
features. J Clin Oncol. 1993;11:2306---13.
11. Savarese DM, Zavarin M, Smyczynski MS, Rohrer MJ, Hutzler MJ.
Superior vena cava syndrome secondary to an angiotropic large
cell lymphoma. Cancer. 2000;89:2515---20.
12. Chen JC, Bongard F, Klein SR. A contemporary perspective on
superior vena cava syndrome. Am J Surg. 1990;160:207---11.
13. Parish JM, Marschke Jr RF, Dines DE, Lee RE. Etiologic considerations in superior vena cava syndrome. Mayo Clin Proc.
1981;56:407---13.
14. Kim HJ, Kim HS, Chung SH. CT diagnosis of superior vena
cava syndrome: importance of collateral vessels. AJR Am J
Roentgenol. 1993;161:539---42.
15. Sheth S, Ebert MD, Fishman EK. Superior vena cava
obstruction evaluation with MDCT. AJR Am J Roentgenol.
2010;194:W336---46.
16. Yellin A, Rosen A, Reichert N, Lieberman Y. Superior vena
cava syndrome. The myth-the facts. Am Rev Respir Dis.
1990;141:1114---8.
17. Schiller HM, Madge GE. Neoplasms within the pulmonary veins.
Chest. 1970;58:535---8.
18. Remy-Jardin M, Remy J. Spiral CT angiography of the pulmonary
circulation. Radiology. 1999;212:615---36.
19. Lin MT, Ku SC, Wu MZ, Yu CJ. Intracardiac extension of lung
cancer via the pulmonary vein. Thorax. 2008;63:1122.
20. International Association for the Study of Lung Cancer (IASLC).
Staging manual in thoracic oncology. International Association
for the Study of Lung Cancer. Orange Park: Editorial Rx Press;
2009.
21. Okamoto Y, Tsuchiya K, Nakajima M, Yano K, Kobayashi T. Primary lung cancer with growth into the lumen of the pulmonary
artery. Ann Thorac Cardiovasc Surg. 2009;15:186---8.
22. Yamaguchi T, Suzuki K, Asamura H, Hondo H, Niki T, Yamada
T, et al. Lung carcinoma with polypoid growth in the main
pulmonary artery: report of two cases. Jpn J Clin Oncol.
2000;30:358---61.
23. Roberts TE, Hasleton PS, Musgrove C, Swindel R, Lawson RA.
Vascular invasion in non-small cell lung carcinoma. J Clin
Pathol. 1992;45:591---3.
24. Kolin A, Koutoulakis T. Invasion of pulmonary arteries by
bronchial carcinomas. Hum Pathol. 1987;18:1165---71.
25. Klepetko W. Surgical intervention for T4 lung cancer with infiltration of the thoracic aorta: are we back to the archetype of
surgical thinking? J Thorac Cardiovasc Surg. 2005;129:804---8.
26. Tsui P, Lee JH, MacLennan G, Capdeville M. Hemoptysis as an
unusual presenting symptom of invasion of a descending thoracic aortic aneurysmal dissection by lung cancer. Tex Heart
Inst J. 2002;29:136---9.
27. Coblentz CL, Sallee DS, Chiles C. Aortobronchopulmonary fistula complicating aortic aneurysm: diagnosis in four cases. AJR
Am J Roentgenol. 1988;150:535---8.
28. Lotto AA, Kendall SW, Hartley R, Walker P. A case of a periaortic
lymphoma presenting with the features of descending thoracic
aorta dissection. Br J Radiol. 2007;80:e30---2.
29. Ugurlu BS, Hazan E, Badak O, Yörüglu K, Oto O. Dissection of
ascending aorta due to metastatic carcinoma. Ann Thorac Surg.
2001;72:614---5.
30. Draznin J, Spencer KT. Squamous cell carcinoma masquerading as a thoracic intramural hematoma. Echocardiography.
2001;18:175---7.
31. Ohta M, Hirabayasi H, Shiono H, Minami M, Maeda H, Takano
H, et al. Surgical resection for lung cancer with infiltration of
thoracic aorta. J Thorac Cardiovasc Surg. 2005;129:804---8.
32. Chan CK, Hutcheon MA, Hyland RH, Smith GJ, Patterson BJ,
Matthay RA. Pulmonary tumor embolism: a critical review of
clinical, imaging, and hemodynamic features. J Thorac Imaging. 1987;2:4---14.
33. Frazier AA, Galvin JR, Franks TJ, Franks TJ, Rosado-DeChristenson ML. From the archives of the AFIP: pulmonary
vasculature: hypertension and infarction. Radiographics.
2000;20:491---524.
34. Roberts KE, Hamele-Bena D, Saqi A, Stein CA, Cole RP. Pulmonary tumor embolism: a review of the literature. Am J Med.
2003;115:228---332.
35. Franquet T, Giménez A, Prats R, Rodríguez-Arias JM, Rodríguez
C. Thrombotic microangiopathy of pulmonary tumors: a vascular cause of tree-in-bud pattern on CT. AJR Am J Roentgenol.
2002;179:897---9.
347
36. Bosmans S, Weynand B, Coche E. Pulmonary metastatic
microangiopathy of colon cancer presenting as a ‘‘tree in bud’’
pattern. Br J Radiol. 2008;81:e11---2.
37. Seppala N, Cala A, Klebe S. Unusual presentation of pulmonary
tumor thrombotic microangiopathy with no detectable primary
tumor. J Postgrad Med. 2009;55:38---40.
38. Wechsler RJ, Salazar AM, Gessner AJ, Spirn PW, Shah RM,
Steiner RM. CT in situ vascular stump thrombosis after
pulmonary resection for cancer. AJR Am J Roentgenol.
2001;176:1423---5.
39. Kwek BH, Wittram C. Postpneumonectomy pulmonary artery
stump thrombosis: CT features and imaging follow-up. Radiology. 2005;237:338---41.
40. Kim SY, Seo JB, Chae EJ, Do KH, Lee JS, Song JW, et al.
Filling defect in a pulmonary arterial stump on CT after pneumonectomy: radiologic and clinical significance. AJR Am J
Roentgenol. 2005;185:985---8.
41. Mesurolle B, Qanadli SD, Merad M, Mignon F, Baldeyrou P, Tardivon A, et al. Unusual radiologic findings in the thorax after
radiation theraphy. Radiographics. 2000;20:67---81.
42. Fajardo LF, Berthrong M. Vascular lesions following radiation.
Pathol Annu. 1988;23:297---330.
43. Coblentz C, Martin L, Tuttle R. Calcified ascending aorta after
radiation. AJR Am J Roentgenol. 1986;147:477---8.
44. McGee DC, Gould MK. Preventing complications of central
venous catheterization. N Engl J Med. 2003;348:1123---33.
45. Gallieni M, Pittiruti M, Biffi R. Vascular access in oncology
patients. CA Cancer J Clin. 2008;58:323---46.
46. Kuter DJ. Thrombotic complications of central venous
catheters in cancer patients. The Oncologist. 2004;9:207---16.
47. Sattari M, Kazory A, Phillips RA. Fracture and cardiac migration
of an implanted venous catheter. Interact Cardiovasc Thorac
Surg. 2003;2:532---3.
48. Hinke DH, Zandt-Stastny DA, Goodman LR, Quebbeman EJ,
Krzywda EA, Andris DA. Pinch-off syndrome: a complication
of implantable subclavian venous access devices. Radiology.
1990;177:353---6.
49. Kim OK, Kim SH, Kim JB, Jeon WS, Jo SH, Lee JH, et al. Transluminal removal of a fractured and embolized indwelling central
venous catheter in the pulmonary artery. Korean J Intern Med.
2006;21:187---90.
50. Oz K, Demirhan R, Onan B, Sancakli I. Pulmonary artery pseudoaneurysm after a vascular access port catheter implantation.
Ann Thorac Surg. 2009;87:295---7.
51. Numico G, Garrone O, Dongiovanni V, Silvestris N, Colantonio I,
Di Constanzo G, et al. Prospective evaluation of major vascular
events in patients with nonsmall cell lung carcinoma treated
with cisplatin and gemcitabine. Cancer. 2005;103:994---9.
52. Hui GC, Legasto A, Wittram C. The prevalence of symptomatic
and coincidental pulmonary embolism on computed tomography. J Comput Assist Tomogr. 2008;32:783---7.
53. Cronin CG, Lohan DG, Keane M, Roche C, Murphy JM.
Prevalence and significance of asymptomatic venous thromboembolic disease found on oncologic staging CT. AJR Am J
Roentgenol. 2007;189:162---70.
54. Gladish GW, Choe DH, Marom EM, Sabloff BS, Broemeling LD,
Munden RF. Incidental pulmonary emboli in oncology patients:
prevalence, CT evaluation, and natural history. Radiology.
2006;240:246---55.
55. Tallón Guerola P, Arenas Jiménez J, De la Hoz Rosa J, Massutí
Sureda B, García Marco JM. Diagnóstico casual de tromboembolismo pulmonar: descripción de las características clínicas y
radiológicas y su evolución. Radiologia. 2008;50:239---43.
56. Hasenberg U, Paul T, Feuersenger A, Goyen M, Kröger K. Cancer patients and characteristics of pulmonary embolism. Eur J
Radiol. 2009;69:478---82.
57. Piffaretti G, Tozzi M, Mariscalco G, Bacuzzi A, Lomazzi C,
Rivolta N, et al. Mobile thrombus of the thoracic aorta:
348
management and treatment review. Vasc Endovascular Surg.
2008;42:405---11.
58. Choukroun EM, Labrousse LM, Madonna FP, Deville C.
Mobile thrombus of the thoracic aorta: diagnosis
and treatment in 9 cases. Ann Vasc Surg. 2002;16:
714---22.
59. Aragon-Ching JB, Ning YM, Dahut WL. Acute aortic dissection
in a hypertensive patient with prostate cancer undergoing chemotherapy containing bevacizumab. Acta Oncol.
2008;47:1600---1.
60. Sica DA. Angiogenesis inhibitors and hypertension: an emerging
issue. J Clin Oncol. 2006;24:1329---31.

Thoracic vascular disease in oncologic patients

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