Phrenic Nerve Palsy As A Complication of Superior Vena Caval Stenting

Radiology Case Reports
10 May, 2019 ,

A 78-year-old woman, presented with phrenic nerve palsy as an unusual complication of superior vena caval stent placement. The case demonstrates that the technique is highly effective in providing relief of the acute and subacute results of obstruction, and that definitive tissue diagnosis and initiation of therapy need not be delayed.

Full content

A 78-year-old woman initially presented to the emergency department after 10 days of symmetrical facial and neck swelling. She had a tooth extracted 7 days into the initial 10 days of swelling, as she thought it may have been related to a dental abscess. This made no difference to the swelling. The tooth extraction examination did not have any findings suggestive of an abscess or infection. She did not have systemic signs or symptoms of infection, she was afebrile (36.2), without rigors, airway or respiratory function compromise, and had a normal white cell count and CRP. Her swelling was not responsive to an outpatient course of fexofenadine (Telfast, Sanofi-aventis, Macquarie Park, NSW, Australia), or a course of oral amoxicillin (APO-amoxycillin, Apotex PTY LTD, Macquarie Park, NSW, Australia)

She was admitted under the plastic surgery department and treated with amoxicillin, metronidazole, and gentamicin. A computed tomography (CT) of her facial bones showed a 6mm lucency within the maxilla posteromedial to the recent maxillary second right incisor (26) tooth extraction with the impression of a 2 mm direct communication with the underlying right maxillary antrum, as well as generalized right maxillary mucosal thickening. Generalized cellulitis within the soft tissues of the face, without focal abscess or collection was also seen on this scan. An orthopantomogram showed a tooth 16 periapical cyst which was thought to be potentially related to her symptoms, though was not removed due to the risk of oro-antral fistula. She was discharged after 3 days of IV antibiotics, on oral antibiotics. The facial swelling was unchanged at this point.

She represented after 6 days, with worsening facial, neck, and now bilateral upper limb, and upper thoracic swelling with associated dyspnoea, and reduced neck mobility. She also reported a new cough, and dysphagia without odynophagia, to liquids but not solids. On examination at this point, she had areas of distended superficial veins on the upper thoracic wall.

A right suprahilar mass with mediastinal invasion was seen on chest CT, most suggestive of primary small cell bronchogenic malignancy, or less likely, lymphoma. There was severe SVC narrowing and complete compression of the azygous arch with features of SVC syndrome. A small nonocclusive thrombus in the right subclavian vein was also seen. There was associated right hilar lymphadenopathy.

The patient proceeded to endobronchial ultrasound, and fine needle aspirate cytology from this procedure later revealed primary small cell lung carcinoma. Later on the same day, the patient was taken to the angiography suite with a view to placing an SVC stent across the obstruction. The stenosis was crossed with a 150 cm Bentson guidewire (Boston Scientific, Marlborough, MA) and a 5-French, 80 cm long, balloon dilatation catheter (Cook Medical, Bloomington, IN) via 10-French, 40 cm Introducer set (Cook Medical, Bloomington, IN) sheath in the right common femoral vein. Venography performed from both brachiocephalic veins confirmed the 84% stenosis of the upper to mid SVC.

Retrograde flow from the stenosis was evident with multiple collateral veins. A 100 cm long 10-French sheath (Optimed, Ettlingen, Baden-Wurttemburg, Germany) was advanced across the stenosis. A 20 × 60 mm sinus SL stent (Optimed, Ettlingen, Baden-Wurttemburg, Germany) was then deployed. Following deployment, the vein was conservatively venoplastied twice to an end diameter of 12 mm. Although the waist of the stenosis persisted, venography demonstrated markedly improved anterograde flow, therefore the procedure was terminated. A Heparin infusion (Heparin Sodium, Pfizer, West Ryde, Australia) at 500 units/h was commenced and the patient was sent to recovery.

During the postprocedure period, the patient became hypertensive (systolic > 200 mm Hg), and experienced dyspnoea, nausea and pain in her jaw, shoulder, and neck. She was also mildly dyspnoeic. A chest radiograph at this time showed an elevated right hemidiaphragm compared with a chest radiograph performed during the emergency admission the day prior.

The elevated right hemidiaphragm and associated clinical findings of dyspnoea and pain, were presumably related to a phrenic nerve palsy likely secondary to the plasty performed as part of the SVC filter placement. This provisional diagnosis was supported by a chest radiograph without diaphragmatic eventration less than 24 hours prior, and a new finding imaging finding which also coincided with the patient's clinical syndrome. The right phrenic nerve enters the thoracic inlet between the right subclavian artery and brachiocephalic vein, before marginating the lateral border of the SVC, making it highly vulnerable in anatomic position, to extrinsic compression from SVC venoplasty against the CT demonstrated tumour encasing it.

The radiograph performed in recovery did not show other clear causes for the sudden onset dyspnoea, and cardiac monitoring patterns were not suggestive of an acute coronary syndrome. Her hypertension and pain were treated with clonidine (APO-clonidine, Apotex PTY LTD, Macquarie Park, NSW, Australia) and fentanyl (Fentanyl, Teva Pharma, Macquarie Park, NSW, Australia), respectively. The patient was admitted to to a monitored bed in the HDU. She remained stable and was saturating at 97% on 4 L oxygen via nasal prongs.

Subsequent CT study of her brain and abdomen and an Fludeoxyglucose Positron Emission Tomography (FDG PET) scan, did not demonstrate any evidence of metastatic disease, and she was commenced on carboplatin and etoposide for the new diagnosis of SCLC. She remained well, hemodynamically stable and had ongoing clinical improvement of the facial, upper limb, and thoracic oedema and dyspnoea.

A repeat chest radiograph on day 1 postprocedure showed persistent elevation of the right hemidiaphragm, though this did not manifest as any obvious clinical finding. It also persisted on the FDG PET acquired a month later.

She unfortunately experienced heparin induced thrombotic thrombocytopenic syndrome secondary to the heparin she received as part of her management. This was incidentally found in her pathology investigations. On 3 day postdischarge follow-up, her clinical syndrome related to SVC syndrome had resolved to premorbid levels, and she remained well from a respiratory perspective.