Bobby R. Alford Department of
Otolaryngology-Head and Neck Surgery
Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature.
Juvenile Nasopharyngeal Angiofibroma
Etai Funk, M.D.
October 21, 2004
In 1841, Liston described the first surgically treated case of JNA and Chelius in 1847 noted its fibrous nature and the coincidence with puberty. Verneuil in 1878 proposed that these masses may arise from the embryonic fibrocartilage. In 1906, Chauveau coined the term “juvenile nasopharyngeal fibroma.” Freeberg, in 1940, noted the vascular nature of these masses and used the term “angiofibroma.” He implanted radon seeds into the tumor with secondary surgical diathermy as the primary mode of treatment; however, as the potential long term sequelae of XRT in the adolescent became evident, surgical options were once again explored. In 1948, Martin published the first series of JNA, and in 1973 Grigis proposed that these lesions may arise from paraganglionic tissue at the terminal branches of the internal maxillary artery.
The heavy male predominance has drawn intrigue into our hypothesis of an imbalance in the pituitary androgen-estrogen axis. There have been some cases of females reported; however, these are very, very few. The majority of patients present between 14-25 years of age with most of them around 15 years. The JNA accounts for 0.05% of head and neck tumors, and it is the most common benign nasopharyngeal tumor. Its incidence is about 1:5000 and 1:60,000 and it is more common in Asia and the Middle East.
This anatomy illustration is taken from Janfaza’s book and you can see the sphenopalatine foramen here, and the pterygoid process of the sphenoid bone here. Here is the pterygopalatine fossa. This is where these masses will emerge from, to enter into the infratemporal fossa with pterygoid plates here. These are normal axial CT scans just for comparative purposes and you can see the pterygopalatine fossa here extending into the infratemporal fossa. Here are the pterygoid plates and the pterygoid fossa in between them.
As for the histopathology; this is a benign mass that is non-encapsulated. The fibrous stroma is composed of spindle cells in a dense collagen matrix with extensive vascularity. These vessels, it should be noted, lack smooth muscle cells, which may cause a propensity for hemorrhage.
I want to spend some time on the theories for pathogenesis of the JNA, specifically on hormonal influence, as there is quite a bit of contention concerning this. Again, the overwhelming male predominance and the usual onset around puberty has raised suspicion that there is an inbalance in the pituitary adrenogenital hormonal system contributing to the pathogenesis of this tumor. Martin in 1948 and Schiff in 1959 reported the use of sex hormones, specifically estrogen, which they noted reduced the size of the lesions in addition to the vascularity of the tumor. However, subsequent studies have not been able to confirm this. In 1979, Lee and Farhag in 1987 demonstrated that androgen receptors are present inside these lesions; however, they could not demonstrate any estrogen or progesterone receptors. However, Gatalica in 1998 looked at 14 patients and 14 specimens, compared them to controls of the middle turbinate, and did not note any estrogen or progesterone receptors, however, and noted less than 5% of androgen receptors in both JNA specimens and controls. A 1992 paper by Shikani demonstrated that androgens could not stimulate growth of the JNA in nude mice or in vitro. So whether or not the JNA is dependent on androgen stimulation is still debated, with some studies showing that receptors are present while others do not. The questionable efficacy of estrogen therapy as well as the psychologic and physical side effects, which include testicular atrophy and gynecomastia, have decreased the popularity of this treatment, and it is currently no longer recommended. There have been, taking into account the possible androgen affect, studies on flutamide, which is an androgen receptor antagonist, on these lesions preoperatively. Gates reported five patients who were treated with flutamide and demonstrated a 44% reduction in tumor size; however, follow-up study by Labra from Mexico could not confirm these results and did not demonstrate any statistically significant decrease in tumor volume after flutamide treatment. Three of the theories include the desmoplastic response of the nasopharyngeal periosteum to an ectopic nidus of vascular tissue, the derivation from embryologic chondrocartilage during the development of the cranial bones, and lastly it was thought that the JNA may originate from non-chromaffin paraganglionic cells of the terminal end of the internal maxillary artery. None of these theories have been proven substantially; however, these growth factors have been found in JNA, which were proven by Schiff and Nagai to increase the size and the vascularity of these tumors.
It is important to note the location and where these tumors extend. They originate in the nasopharynx, specifically near the superior margin of the sphenopalatine foramen and they occur at the junction of three bones: the palatine bone, the horizontal ala of the vomer, and the root of the pterygoid process of the sphenoid.
There are five directions where this tumor can extend: anteriorly to the nasal cavity and the sinuses; posteriorly to the pterygoid fossa; laterally to the pterygopalatine fossa and infratemporal fossa; superiorly into the sphenoid, which can then erode through the posterior wall to the cavernous sinus or to the pituitary optochiasm; or it can enter the orbit, out through the inferior orbital fissure, and can enter back in through the superior orbital fissure to enter the cavernous sinus. Two general patterns of intracranial extension into the middle cranial fossa are via the destruction of the skull base at the attachment of the pterygoid process lateral to the internal carotid and through the posterior wall of the sphenoid to the cavernous sinus or the pituitaries. The medial extension can extend to the nasopharynx or the contralateral side. It is important to note that these tumors remain extradural and rarely enter intradurally, and they may form some adhesions to the dura. Twenty to 36% will present with intracranial masses. JNAs do not invade the skull base by cellular infiltration as malignant lesions do, but rather they lead to local bone resorption through relentless expansion. This is a chart from a study from Sennes of 33 patients which looked at extensions of the lesions. You can see that 100% of the lesions estended to the nasal cavity and nasopharynx. About 82% extended to the pterygopalatine fossa and the sphenoid sinus. In addition, the maxillary sinus had about 70% and the infratemporal fossa had about 57%.
More than 80% of patients will present with these two findings: nasal obstruction and epistaxis, the most common findings. Patients may also present with facial deformity including cheek swelling, ptosis, blindness, cranial nerve palsies. On exam, you will note a pale, bluish, smooth mass, which will be seen inside the nasopharynx. The differential diagnosis includes rhabdomyosarcoma, inflammatory polyps, hemangioma, teratoma, fibrous dysplasia, and lymphoepithelioma. Biopsy is almost always contraindicated in these cases; however, some reports state that if the clinical presentation is extremely unusual, if the patient is in the wrong age group, or the radiographs do not appear typical for a JNA, there is concern for a different diagnosis, then biopsy under controlled conditions, perhaps after arteriography, is reasonable.
A little on the radiology aspect of JNAs. Dr. Sessions and Dr. Alford in 1975 described the radiologic findings seen on plain film with JNA. The sphenoid hole is demonstrated on Water’s view or the submental view. This hole represents the eroded space through which the tumor invades. Bowing of the posterior wall of the maxillary sinus or the Holman-Miller sign was also described as one of the most consistently typical features of JNA on plain films. On these two CTs, you can see the mass here in front of the nasopharynx. You can see slight bowing of the maxillary sinus there, and this is post-resection. Here you can see invasion of the sphenoid sinus and the cavernous sinus, and here you can see widening of the pterygopalatine fossa with invasion into infratemporal fossa. Today we rely on CT and MRI. MRI allows us to better delineate surrounding soft tissues and offers other additional information about possible intracranial extension and cavernous sinus involvement. You can see on this MRI, widening of the pterygopalatine fossa, invasion of the infratemporal fossa, and the classic Holman-Miller sign. Arteriography is both helpful from a diagnostic and a therapeutic standpoint when we use embolization.
The blood supply to the JNA in almost 90-95% of the time will be the ipsilateral internal maxillary artery. However, the ascending pharyngeal has been noted to supply and, in addition, the contralateral side must also be arteriogrammed to make sure there is nothing coming from the external or internal carotid from that side. Surgery is usually scheduled within 12-48 hours after embolization. It is important, if you are planning on performing an infratemporal approach, to avoid compromising the blood supply to the temporalis muscle. Blood loss has ranged in all reports anywhere from 500-3000cc and the stage of the tumor, usually with higher stage tumors, will have more blood loss. Economou in 1988 described in a UCLA experience that, after embolization, he had decrease in blood transfusions in patients from 64% to 36%. Siniluoto in 1993 demonstrated a statistically significantly decrease in blood loss after embolization, and Li in 1998 demonstrated that intraoperative embolization decreases blood loss from an average of 1,136cc in non-embolized patients to 677cc in embolized patients, which was statistically significant. The only paper that demonstrated that there was no statistical significance in blood loss with embolized versus non-embolized patients was by Petruson from Sweden. Radkowski again was the one who demonstrated that the stage of the tumor coincides with the amount of blood loss. Embolization is usually preferred over ligation, as ligation is usually performed more proximal, which may lead to increased risk for a collateral circulation to form.
There are four staging systems that have been proposed on the JNA. The first was made here at Baylor, actually by Dr. Sessions and Dr. Alford. The IA is confined to the nose and the nasopharynx; IB extends into one or more sinuses; IIA demonstrates minimal extension into the pterygopalatine fossa, and IIB demonstrates full occupation of the pterygopalatine fossa with or without erosions of the orbital bones. On IIB, you will also note the Holman-Miller sign; IIC extends into the infratemporal fossa with or without cheek extension, and stage III is intracranial extension. Dr. Fisch performed another staging system, but his was mainly looking at the infratemporal fossa extension and the intracranial extension, which is not as clinically significant as Dr. Sessions’s and Alford’s. This is from Sessions’s paper, which showed some good pictures and radiographs, and you can see the IA stage confined here to the nasal cavity and nasopharynx and no extension into the sphenoid. Here you can see IB, minor extension in the sphenoid here. IIA you can see a small nubbin extending here into the pterygopalatine fossa, and notice that the posterior maxillary sinus is not bent in. And here on IIB you can see the pterygopalatine fossa is widened, and you have a positive Holman-Miller sign. Again, positive Holman-Miller sign extension into the infratemporal fossa makes this a stage IIC, and here you can see extension into the intracranial cavity and the orbit, making it a stage III. Chandler’s staging system was based on a system proposed for nasopharyngeal carcinoma by the American Joint Committee; however, it should be noted that JNA is a benign lesion with predictable growth pattern that differentiates it from malignant nasopharyngeal tumors. In addition, the inclusion of multiple sites into one staging system with variable resectability limits the clinical usefulness of the staging system. Radkowski in 1996 basically took Sessions’s staging and made one minor change, which was in stage IIC, which stated that extension posterior to the pterygoid plates in close proximity to the foramen lacerum made complete surgical excision more difficult and deserved a separate class with extension into the infratemporal fossa.
Our treatment is mainly based on surgery and radiotherapy. However, Goepfert actually reported five cases of angiofibroma successfully treated with chemotherapy for recurrent lesions if further surgery or radiation is not indicated. His was the only study looking at chemotherapy. Hormonal therapy has fallen out of favor, as I have mentioned. Sclerotherapy and cryotherapy have not been used much. This was a table taken from Dr. Fagan’s article, which looks at different extensions in terms of tumor location and which is the best approach for each one of these. It is a pretty good chart and looks at the endoscopic approach, which has become more popular; and is limited to the sinuses, the nasal cavity, and the nasopharynx. You can enter the pterygopalatine fossa by punching through the posterior wall of the maxillary sinus. Transpalatal approach is somewhat limited to tumors confined to the nasopharynx and the nasal cavity and the sphenoid sinus. The lateral rhinotomy is the workhorse of this lesion and with a partial maxillectomy can get you to the tumor in almost all locations aside from lateral infratemporal fossa and lateral cavernous sinus. Some prefer the midfacial degloving; however, at times, it is difficult to reach posteriorly through the midfacial degloving without a LeFort I osteotomy. Fisch recommended the infratemporal approach for lesions extensively into the infratemporal or the middle cranial fossa; however, as you can see, it is difficult to reach anterior lesions in the nasal cavity and the maxillary ethmoid sinuses by this approach.
Again, endoscopic resection is limited to small tumors, limited to the nasopharynx, nasal cavity, ethmoid, maxillary and sphenoid sinuses. Effective preoperative embolization is absolutely necessary with endoscopic resection, as control of hemorrhage can be difficult. Transpalatal technique, again it is a fairly limited procedure. At times, you may be able to reach the pterygopalatine fossa. In our case, we had to lift the palatine vessels up and extend our field actually here to the left where the lesion was. Complications of the transpalatal technique include palatal dehiscence, fistula, and VPI. The lateral rhinotomy, one of the big workhorses of this tumor, can pretty much access the tumor in almost all locations. You can see here the partial maxillectomy and here the tumor is being removed. Complications of this technique include persistent nasal crusting, facial paresthesias, lacrimal apparatus injury, and facial scarring. The midfacial degloving, is another excellent approach. However, some believe it is difficult to reach posteriorly with this approach, and you may have to perform a LeFort I osteotomy to gain better exposure. Here you can see a partial maxillectomy and removal through the antrum of this tumor. The infratemporal fossa approach described by Dr. Fisch is a type C approach, which offers excellent skull base exposure for extradural tumors. Basically a type B approach is first performed when the postauricular flap is raised anteriorly to the lateral orbital margin, which you can see here. Osteotomies are performed of the zygoma here and here. A temporalis flap is lifted up with the zygoma. You can see the TMJ and masseter here, and here you can see the pterygopalatine fossa with the V2 and the internal maxillary artery and here is V3, the middle meningeal artery, and the mandibular condyle. V3 is sectioned, the middle ear is obliterated in this approach. It avoids facial incisions and a craniotomy, and it also permits ligation of the IMA. However, there is a permanent conductive hearing loss with this type of approach, there is lower lip numbness, and, at times there is temporal depression. The intracranial approach is somewhat controversial. Proponents for this approach state that tumors with intracranial extension are more aggressive and have an increased risk for recurrence, and therefore need to be treated. However, Herman in a study in 1999 stressed three points. He stated that these tumors are extradural, and they can be approached extracranially as opposed to intracranially. He noted the high morbidity of intracranial approaches to these tumors, and he also noted that if you perform an extradural approach leaving a small bit intracranially these lesions actually may regress spontaneously.
I want to spend some time talking about radiation. As surgeons, you know, we believe radiation should be reserved for unresectable disease such as intracranial, cavernous sinus involvement, optic nerve involvement, or carotid artery involvement. Some believe it may only be reserved for recurrence. Usually, 30-35 Gy are used. Dr. Kuppersmith and Dr. Donovan actually described the advantages of intensity-modulated radiotherapy, which directs the radiation according to tumor depth, allowing one to treat with larger doses, about 45 Gy, more precisely and without disturbing surrounding normal tissue. There have been numerous studies that have shown excellent results with radiation. Cummings, in 1984 treated 55 patients with 30 Gy, and noted that he produced permanent tumor control in 80% of patients. However, two of his patients developed radiation-induced malignancy—one was a thyroid cancer and the other was a skin basal cell carcinoma. Drs. Reddy and Lee also reported 85% success rates with radiation in 15 and 27 patients, respectively, and Dr. McGahan and Dr. Parke actually looked here at Baylor at 15 patients who were treated with 30-35 Gy and demonstrated 100% success rates. So, with these high success rates, one can only wonder which modality is best for the patient with a JNA, radiation or surgery. So, Dr. Cummings in 1980 looked at the relative risks in terms of fatality of surgery versus radiotherapy, and he noted that the potential fatal complications with surgical resection were estimated to be about 1:100, which was found to be an order of magnitude similar to that of the risks of radiation.
Follow-up was discussed by Paris in one of his studies. He recommended CT and MRI at six months postop and annually for two years. Most of these tumors, if you note a recurrence, will usually recur within two years. If there is suspicion for recurrence, then he recommends further imaging and arteriography. It should be noted that with radiation these tumors may take two to three years to regress and may remain there for a while, whereas with surgery, these tumors are removed immediately. Therefore, with radiation, follow-up should be extended a little bit further. Recurrence has an astonishingly high rate. Some reports have noted a 55% recurrence, but the majority are somewhere around the 30% range. Usually, again, it occurs within one to two years and it increases once the tumor has progressed to the higher stages, which include the extension to the sphenoid, the infratemporal fossa, the cavernous sinus, and intracranial extension. Petruson from the Swedish study noted that patients at a younger age have an increased risk for recurrence and, in an interesting study Dr. McCombe noted that preoperative embolization may increase the risk for recurrence. He demonstrated this in a series of only six patients where five of six who were embolized actually had an increased risk for recurrence. He hypothesized that the embolization caused the tumors to shrink, making identification of the tumor extensions more difficult during surgery and resulting in a larger volume of residual tissue.
So, in summary, JNA is a benign nasopharyngeal tumor that occurs predominantly in male teenagers. Its presentation is usually nasal obstruction and epistaxis with a nasopharyngeal mass. There are many theories as to its pathogenesis, but none have definitely been proven. Thorough understanding of extension and staging is essential for treatment and follow-up decisions. The recommended imaging includes CT, MRI, angiography with embolization. Treatment is based on surgery and radiotherapy. Surgical approach is based on the surgeon’s experience, the stage of the tumor, the involved structures, and the resectability of the tumor. Close follow-up is mandatory, as recurrence rates can be high in this tumor.
Case Presentation
HV is a 9-year-old white male who presents with a one-month history of recurrent epistaxis. He denies any nasal obstruction, visual changes, or headaches. He has a past medical history of asthma and is taking dexamethasone, albuterol, advair, and singulair. The patient had an MRI at an outside facility which demonstrated a left nasopharyngeal mass.
On endoscopic exam in the clinic, he was noted to have a left pale blue mass in the L nasal cavity just posterior to the middle turbinate extending into the nasopharynx.
The patient had a CT scan done at TCH, which demonstrated this L nasal cavity mass with extension into the nasopharynx. There was no extension into the pterygopalatine fossa, infratemporal fossa, or sinuses. There was no bowing of the septum, pterygoid plates, or maxillary sinus wall.
Angiography with emoblization was performed at The Methodist Hospital and the patient was taken to the operating room that same day at TCH for endoscopic assisted transpalatal excision.
His postoperative course was uneventful and today he remains without recurrence and a well-healed palate.
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Bobby R. Alford Department of Otolaryngology-Head and Neck Surgery
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Last modified: Oct. 16, 2007