Chapter 26: Acute oncology
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Superior vena cava obstruction
Definition
Anatomy and physiology
The SVC is a thin‐walled vessel approximately 4–6 cm in length and 1.5–2 cm wide in adults. It extends from the confluence of the brachiocephalic veins and terminates in the superior right atrium and is confined by the chest wall and surrounding structures (Watson et al. [304], Wilson et al. [308]). A mediastinal mass, for example, impinging on the SVC can easily obstruct the blood flow; after a short period (1–2 weeks) this results in high venous pressure and upstream vessel engorgement. This in turn promotes collateral vein dilatation to reduce the pressure (McCurdy and Shanholtz [173]).
Related theory
SVCO was first described in 1757 due to obstruction from syphilitic aortitis (McCurdy and Shanholtz [173]). Lung cancer is the most common malignant cause (90%), although lymphoma, metastatic mediastinal tumours and indwelling catheters (including pacemaker leads) can also cause superior vena cava syndrome (Beeson [15], Cohen et al. [43], McCurdy and Shanholtz [173]). Patients with SVC syndrome usually have advanced disease, and less than 10% survive more than 30 months after treatment (Beeson [15]).
Procedure guideline 26.1
Carotid artery rupture (CAR)
Diagnosis
Understanding the regional anatomy will enable the cancer nurse to appreciate the clinical manifestations of SVC syndrome (Cohen et al. [43]). SVC syndrome presents with symptoms related to engorgement of the upper extremities, upper thorax and head as the venous drainage is obstructed. The extent of the obstruction and therefore degree of SVC compromise will determine the clinical presentation (Higdon and Higdon [108]).
Symptoms can be as mild as slight facial and upper extremity oedema or as extreme as intracranial swelling, seizures, haemodynamic instability and tracheal obstruction (Higdon and Higdon [108]). The patient may report that their symptoms are worse in the morning and when lying flat or bending forward. Along with these symptoms there may also be venous hypertension, headaches, visual changes, dizziness, cough, engorged conjunctivae, periorbital oedema, non‐pulsatile dilated neck veins and dilated collateral veins in the chest and arms.
Baseline observations are the start of diagnosis and must include respiratory rate and oxygen saturations. If the patient is breathless then cannulation and bloods, from the opposite side to the SVCO or CVAD if present (venous lactate, full blood count [FBC], urea and electrolytes [U&Es]), will help determine the level of physiological distress of the patient (Manzi et al. [163]). Although SVC syndrome is a clinical diagnosis, plain radiography, computed tomography (CT) and venography are used for confirmation of the cause (Higdon and Higdon [108]). CT scan may differentiate between extrinsic compression and intravascular thrombosis, but on occasion a venogram may be necessary, particularly if an intravascular stent is being considered (Walji et al. [301]).
Management
Management of SVCO includes symptomatic relief and treatment of the complications and underlying clinical condition (McCurdy and Shanholtz [173]).
In a patient who presents in advanced acute SVCO the following actions are recommended:
- Sit the patient upright and give 60% oxygen via a facemask.
- Maintain calmness. This will help to reduce anxiety and thus improve the efficacy of breathing in the patient. Low‐dose subcutaneous midazolam may be required.
- Ensure that blood pressure is not monitored on the right arm as this may increase pressure on the SVCO. The use of a manual cuff may be required if the electronic monitor upper limit cannot be reset.
- Give any medication as soon as it is prescribed, explaining to the patient the rationale for its use. Clear communication will help reduce the patient and their family's anxiety.
- Dexamethasone 16 mg PO/IV.
- Furosemide 40 mg PO/IV.
- If the SVCO is due to a thrombus along the outside of the CVAD, initial management is removal of the device. It is recommended that the patient has an ultrasound to ascertain the size and location of the thrombosis and then is commenced on anticoagulant therapy (see Figure 26.3). If the catheter is to be removed, this should be done 72 hours after commencing anticoagulants (Pittiruti [232]). If a patient has a thrombosis but the catheter lumen is still patent, it can be used for IV therapy. The exception to this would be if the thrombosis were occluding the tip of the catheter. This can be distressing for the patient if they are needle phobic or have remaining cycles of chemotherapy. Working with the clinician is essential to ensure that the rationale is simply explained to the patient.
- Recommended treatments include chemotherapy and radiation to reduce the tumour that is causing the obstruction (Beeson [15], McCurdy and Shanholtz [173]). However, treatment with intravenous stents is becoming increasingly common (Beeson [15]). In cases of compression, dilation and stenting of the SVC may be performed; in some cases a bypass of the SVC may be indicated (Cohen et al. [43]). Percutaneous stent placement in cases of SVC syndrome in malignancy is a simple, safe and effective technique to rapidly relieve SVC syndrome. Alleviation of severe compressive symptoms using tracheal and SVC stents in a patient with advanced lung carcinoma has been reported (McCurdy and Shanholtz [173]).
