Introduction
The sphenopalatine artery is the main blood supply to the posterior nose, and its ligation is the currently favoured intervention to control intractable posterior epistaxis.Reference Agreda, Urpegui, Ignacio Alfonso and Valles1
This paper presents the previously unreported complication of septal perforation and bilateral middle turbinate partial necrosis following bilateral endoscopic ligation of the sphenopalatine artery.
Case report
A 45-year-old man presented with recurrent epistaxis with no detectable cause. There was no associated history of, or physical findings for, hypertension, anticoagulant therapy or drug abuse. Routine laboratory tests, including bleeding profile, were normal. The patient had been a heavy smoker for 25 years, but gave no history of alcohol consumption, cardiovascular or general vascular diseases, or other chronic medical diseases (e.g. diabetes or syphilis).
The patient was hospitalised for severe posterior epistaxis. He was treated with a posterior nasal pack, but epistaxis recurred after pack removal.
Therefore, it was decided to perform sphenopalatine artery ligation under general anaesthesia. No mechanical damage from the posterior nasal pack was detected at the time of endoscopic arterial ligation. Because no bleeding side could be identified, bilateral ligation was performed using two medium-size titanium clips. The area was then inspected and no significant bleeding, necrotic tissue or other abnormality was detected. Light nasal packs were placed overnight and removed on the first post-operative day without complication. The patient was then discharged home.
The patient was lost to follow up. However, he re-presented four months later with nasal obstruction, persistent nasal crusting and bleeding on crust separation. He had received no other intervention since his sphenopalatine artery ligation procedure. Examination showed black nasal crusting bilaterally over the septum and turbinates.
Computed tomography showed bilateral soft tissue shadows indicating mucosal oedema and nasal crusting, together with bony septal perforation.
Under general anaesthesia, endoscopic examination, crust removal and nasal toilet were performed. Necrosis of the lower middle turbinate (Figure 1) and perforation of the lower bony septum (Figure 2) were encountered, and necrotic parts of the middle turbinate were excised. The post-operative period was uneventful, with no further complaints.
Endoscopic view showing necrosis of the inferior part of the middle turbinate.
Endoscopic view showing the nasal septal perforation.
There was no clinical evidence of inflammatory or autoimmune disease, on either history or examination. The patient showed a normal complete blood count, negative Venereal Disease Research Laboratory test, negative Treponema pallidum immobilisation test, and negative antinuclear antigen and anti-double-stranded DNA tests. The erythrocyte sedimentation rate was 8 mm in the first hour and 23 mm in the second hour, and the C-reactive protein level was 0.31 mg/dl. One year after the excision of necrotic tissue, an endoscopic examination of the nasal cavity revealed apparently normal nasal mucosa, with no masses or visible pathology (Figure 3). These laboratory and endoscopic findings indicated that the patient did not suffer from any additional inflammatory or autoimmune disease.
Endoscopic view of the left nasal cavity, showing nasal septal perforation and apparently healthy nasal mucosa, 12 months after removal of necrotic tissue.
Discussion
Sphenopalatine artery ligation is becoming increasingly popular for treatment of posterior epistaxis, replacing the traditional transantral surgical ligation of the internal maxillary artery. This is because the former procedure targets the vessel as it enters the nasal cavity, thus minimising the potential for persistent bleeding from collateral circulation, a risk considered one of the drawbacks of transantral ligation.Reference Orlandi2
Sphenopalatine artery ligation is considered reliable, with only a short hospital stay required, and few complications; the latter include nasal crusting, nasal and palatal paraesthesia, acute sinusitis, septal perforation and xerophthalmia.Reference Snyderman, Goldman, Carrau, Ferguson and Grandis3 Necrosis of the inferior turbinate has also been reported in a patient who had previously been treated with multiple nasal packs.Reference Moorthy, Anand, Prior and Scott4
In the case we describe, the patient's bilateral middle turbinate partial necrosis and septal perforation point to ligation of the main arterial trunk before it branches into the septal and posterolateral nasal arteries. The sphenopalatine artery is known to leave the pterygopalatine fossa already branched in 80 per cent of cases.Reference Agreda, Urpegui, Ignacio Alfonso and Valles1 Middle turbinate partial necrosis is mostly due to occlusion of the middle turbinate branch of the posterolateral nasal artery; in our patient, this may have been the only branch supplying the inferior part of the middle turbinate.
• A case is presented of bilateral lower middle turbinate necrosis and posterior septal perforation following bilateral sphenopalatine artery ligation for epistaxis
• Sphenopalatine artery ligation risks ischaemic necrosis if collateral blood supply is absent
• Staging of bilateral artery ligation may need to be considered
Patients presenting with intractable epistaxis almost always show diffuse, bilateral mucosal anomalies on catheter angiography, with no clearly identifiable source of bleeding.Reference Mahadevia, Murphy, Obray and Gailloud5 Thus, bilateral sphenopalatine artery ligation is often needed in these cases.
Our patient's septal perforation may have been due to bilateral interruption of the blood supply to the posterior septum, with resulting ischaemic necrosis.
Conclusion
Following sphenopalatine artery occlusion, ischaemic necrosis is a potential risk in anatomical areas that may be supplied only by this artery. More research is needed to evaluate the possibility of staging bilateral sphenopalatine artery ligation, in order to avoid sudden bilateral interruption of the blood supply to the posterior nasal septum.
