This document provides an overview of superior vena cava syndrome (SVCS) presented by Kedir Mohammed at Salale University College of Health Sciences. The presentation covers the anatomy and pathophysiology of SVCS, its typical etiologies such as lung cancer, signs and symptoms, diagnostic tests including CT scans and classification systems. Treatment options discussed include treating the underlying cause, chemotherapy, radiation therapy, endovascular procedures like stenting and thrombolytic therapy, as well as conservative approaches involving bed rest, oxygen, and diuretics to manage symptoms. The objective is for participants to understand what causes SVCS, how to diagnose it, and how it is typically managed or treated.

1. Salale University College of Health Sciences
Department of Adult Health Nursing
Presentation On : Superior Vena Cava Syndrome
Presented by : Kedir Mohammed ID : 182/15
Presented to: Taddala k.(Assistant Professor)
July 3/06/ 2023
Fiche

2. COURSE CONTENT
• Introduction
• Anatomy
• Pathophysiology
• Etiology
• Clinical features
• Classification
• Diagnosis
• Grading System
• Management
• PROGNOSIS
• Conclusion
• Reference

3. Objective
At the end of this presentation the studyparticipants will
be able to:
 Define Superior Vena Cava Syndrome.
 Review the anatomy and pathophysiology of superior
vena cava syndrome.
 Describe the causes of superior vena cava syndrome.
 Understand sign and symptoms of SVCS.
 Understand diagnostic methods of SVCS.
 Summarize the treatment options for superior vena cava
syndrome.

4. INTRODUCTION
• Superior Vena Cava Syndrome is defined as “The
symptoms resulting from compression or obstruction of
the SVC system at any level, from the left and right
brachiocephalic veins to the right atrium.”
• The venous obstruction may be due to the compression,
invasion, thrombosis, or fibrosis of the superior vena
cava.

5. INTRODUCTION
• It may behe partial or the complete obstruction of the
superior vena cava.
• SVCS has a distinct clinical presentation and can be life
threatening.
• It is a medical emergency and most often manifests in
patients with a malignant disease process,
approximately 70% of cases within the thorax.
• Fibrosing mediastinitis next most common cause.

6. Epidemiology
• An estimated 15,000 cases of SVC syndrome occur each
year in the United States, with studies pointing to
increasing frequency due to the concomitant rise in the
use of semipermanent intravascular catheters.
• The incidence of SVC syndrome reported in the literature
range from 1 in 650 to 1 in 3100 patients.

7. ANATOMY
• The SVC is a short large-diameter vein (about 7 cm long)
that carries deoxygenated blood from the upper half of
the body to the heart’s right atrium.
• The SVC is located in the anterior right superior
mediastinum, surrounded by the sternum, ribs, vertebral
bodies, and aorta.

8. Anatomy

10. PATHOPHYSIOLOGY
• The SVC due to the thin walls and inner low pressure,it is
easily obstructed by :
• I. External compression II. Invasion III. Constriction
IV. thrombosis
• Due to hypercoagulation, intimal damage, and/or stasis
may be involved.
• The obstruction causes distention of the axillary,
subclavian, and jugular veins.

12. PATHOPHYSIOLOGY
• The obstruction can increase edema in the luminal
diameter of the pharynx and larynx, which causes the
patient to develop stridor.
• Cerebral edema, which may result in headache and
confusion, could occur and lead to cerebral ischemia and
possible death.

13. (A) Obstruction of SVC involving the left and right brachiocephalic veins: collateral
veins formed.
(B) Obstruction of the SVC proximal to azygos entry point : blood flow is directed
to the azygos through the right superior intercostal vein.

16. (C) Obstruction of SVC at level of azygos and other chest wall
collateral veins (symptoms are usually more severe).
(D) Obstruction of SVC distal to azygos entry point( leading to
milder symptoms).

17. Etiology
It is most often caused by cancer or a tumor in the
mediastinum.
Other types of cancer that can lead to this condition
include:
• Malignant : Breast cancer, Lymphoma, Non–small cell
lung cancer, Small cell lung cancer
• Benign : Thyroid cancer, Cystic hygroma, primary germ
and Thymoma

18. Etiology
• SVC obstruction can also be caused by noncancerous
conditions that cause scarring. These conditions
include:
• Histoplasmosis (a type of fungal infection)
• Inflammation of a vein (thrombophlebitis)
• Lung infections (such as tuberculosis) Indwelling
catheters

19. Etiology
• Other causes of SVC obstruction include:
• Aortic aneurysm (a widening of the artery that
leaves the heart)
• Blood clots in the SVC
• Constrictive pericarditis (tightening of the thin lining
of the heart)
• Effects of radiation therapy for certain medical
conditions

20. Clinical Manifestations
Common symptoms of this syndrome are:
• Trouble breathing
• Coughing, Chest pain
• Swelling of the face, neck, upper body, and arms
• Headache
• Trouble swallowing
• Coughing up blood
Other signs of SVCS include:
• Swelling of neck or chest veins
• Hoarse voice
• Rapid breathing
• Pleural effusion

21. Clinical Manifestations
In rare cases, symptoms may include:
• Lips and skin look blue due to a lack of oxygen in the
blood This is called cyanosis.
• A group of symptoms called Horner's syndrome,
which is a small pupil, drooping eyelid, and no
sweating on 1 side of the face.
Symptoms often get worse when the person bends
forward or lies down.

23. Doty and Standford’s classification (anatomical)
Type I: Stenosis of up to 90% of the supra-azygos SVC
Type II: Stenosis of more than 90% of the supra azygos SVC
Type III: Complete occlusion of SVC with azygos reverse
blood flow.
Type IV: Complete occlusion of SVC with the involvement
of the major tributaries and azygos vein.

24. Yu’s classification (clinical)
• Grade 0: asymptomatic (imaging evidence of SVC
obstruction)
• Grade 1: mild (cyanosis, head and neck edema)
• Grade 2: moderate (grade 1 evidence + functional
impairment)
• Grade 3: severe (mild/moderate cerebral or laryngeal
edema, limited cardiac reserve)
• Grade 4: life-threatening (significant cerebral or laryngeal
edema, cardiac failure)
• Grade 5: fatal

25. Diagnosis Tests
• Patients with high clinical suspicion for SVC
syndrome should undergo imaging of the upper body
and vasculature.
 Chest radiograph
 Duplex ultrasound
 CT/MRI/MRV
 Venogram
 Radionuclide studies

26. Diagnostic Test
 Ultrasound : Ultrasound of the jugular, subclavian,
and innominate veins can help to identify a
thrombus within the vessel lumen.
 Radiographic imaging and MRI also play a critical role in
providing additional information as to the location,
severity, and etiology of the SVC obstruction.
 CT of the chest with the presence of collateral vessels is
associated with a diagnostic sensitivity of 96% and a
specificity of 92%.

27. Diagnostic Test
 Venography is widely accepted as the gold standard for
visualizing and diagnosing a venous obstruction.
• This modality should be used concomitantly with
endovascular intervention for patients with a severe
presentation of SVC syndrome.

28. Chest x-ray

29. CT Scan

30. MRI

31. MANAGEMENT
Goal : is to relieve symptoms and to attempt cure of the
primary malignant process.
• Treat symptoms (Salt restriction Diuretics, oxygen,
Elevate patient’s head)
• Treat underlying cause (Antibiotics for infection)
• Attempt cure of the primary malignant process
• Definitive treamtent-Chemotherapy, Radio therapy,
Invasive Therapy and Surgical

32. Management
• Blood thinners (anticoagulants)
• Treatment shouldn't start until the healthcare
provider finds the cause of the blockage.
• The treatment should be selected according to
the histologic disorder and stage of the primary
process.

34. Chemotherapy
• This is the treatment of choice for chemo-sensitive
tumors, such as lymphoma or small cell lung cancer
and germ Cell Tumors.
• Treating the cancer helps clear up the SVCS.

35. Radiation therapy
• If the blockage of the SVC is caused by a tumor that
doesn't respond or is slow to respond to
chemotherapy (such as non-small cell lung cancer,
Metastatic solid tumour), radiation therapy may be
given.
• It can quickly shrink tumors and ease symptoms.
• Effective modality for malignancy related SVCO.

36. Endovascular Therapies
• ET is emerging as the first-line therapy for the
treatment of SVC syndrome.
• Endovascular therapy offers an effective, minimally
invasive alternative with decreased mortality and
morbidity rates.
• The principal endovascular therapies in use today
include thrombolysis, PTA and stenting.

37. Endovascular Therapies
1. Thrombolytic therapy
• If the SVCS is caused by a blood clot.
• Thrombolytic agent suchas :
 Streptokinase, urokinase, or recombinant tissue-type
plasminogen activator) or
 Anticoagulants -to prevent embolization (eg, heparin
or oral anticoagulants).

38. Endovascular Therapies
• The tip of an infusion catheter is placed within the
thrombus, and the thrombolytic agent is infused at a slow
rate.
• 2. PTA (Percutaneous transluminal angioplasty)This
procedure opens coronary arteries that have been
narrowed or blocked due to the build-up of fatty deposits
known as plaque. This restores blood flow to the heart
muscle.
• is often successful in secondary intervention for recurrent
obstruction.

39. Endovascular Therapies
3. Stent placement - A stent is a small metal or plastic tube
that's put into the blocked part of the vein.
• Is used to open up the blocked vein. This can quickly
ease SVCS symptoms to allow blood to pass through and
also for recurrent obstruction after the use of
chemotherapy and radiation.

40. Conservative management
• Patients with clinical SVCS often gain significant
symptomatic improvement from conservative
treatment measures such as :
 Bed rest with the head elevated
 Supplemental Oxygen
 low sodium diet
Medicines to ease symptoms such as :
 Diuretics -can help you pass more urine to get rid of
extra fluid in your body.
 Steroids -can help reduce swelling and inflammation.

41. Treatment in BENIGN Case
• Substernal goiter=Resection
• Aneurism=cardiopulmonary bypass and resection.
• Thrombophlebitis=antibiotics+anticoagulants+fibrin
olytics(urokiase,streptokinase)
• Fibrosing mediastinitis=medial sternotomy& PTFE
graft.

42. Surgical Tx
• Surgical bypass of the SVC may be a useful way to palliate
symptoms in carefully selected patients with SVCS.
• For the most part, these are patients with advanced
intrathoracic disease amenable only to palliative therapy.
(ie, after failure of radiation therapy and chemotherapy).
• Patients with benign disease appear to be the best
candidates for bypass.

43. Surgical Tx

44. Surgical Tx

45. Differential Diagnosis
• Cardiac tamponade
• Mediastinitis
• Thoracic aortic aneurysm
• Tuberculosis

46. Prevention
• There aren’t any proven strategies to prevent
SVCS.

47. NURSING CONSIDERATIONS

48. SVC Syndrome and the stents

49. SVC Invasion by Lung Cancer

50. Lymphoma with SVC SD
• Chest x-ray showing tumor in the lung.

51. Fibrosing Mediastinitis

52. Outcomes
• The prognosis of patients with SVCS depends on the
cause.
• For patients with a benign cause of SVCS, the life
expectancy is not changed, but for malignant cases,
there is a significant drop in survival.
• Individuals who have features of cerebral and
laryngeal edema can develop life-threatening
symptoms and suddenly die.
• Patients with SVCS as a result of lung cancer usually
live less than 24 months. For those who do not
respond to radiation treatment, the survival is less
than a year.

53. CONCLUSION
• SVC syndrome is a disease with shifting etiologies and
expanding treatment options.
• Endovascular therapy is now considered appropriate first-
line treatment for SVC syndrome, regardless of benign or
malignant etiology.
• Thrombolysis, PTA, and stenting are often utilized in
combination approaches for effective and rapid relief of
symptoms.

54. Reference
• Parish JM, Marschke RF Jr, Dines DE, Lee RE. Etiologic
considerations in superior vena cava syndrome. Mayo Clin Proc
1981; 56:407-413.
• Perez CA, Presant CA, Van Amburg AL 3rd. Management of superior
vena cava syndrome. Semin Oncol 1978; 5:123-134.
• Perez-Soler R, McLaughlin P, Velasquez WS, et al. Clinical features
and results of management of superior vena cava syndrome
secondary to lymphoma. J Clin Oncol 1984; 2:260-266.
• Schraufnagel DE, Hill R, Leech JA, Pare JA. Superior vena caval
obstruction: Is it a medical emergency? Am J Med 1981; 70:1169-
1174.
• Urban T, Lebeau B, Chastang C, Lederc P, Botto MJ, Sauvaget J.
Superior vena cava syndrome in small-cell lung cancer. Arch Intern
Med 1993; 153:384-387.