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��ࡱ�>��	EH����D�������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������y�	��+5bjbj��	.B�{�{�,+�������������8Th$0���������������$2 ��"B�����������---�����-��---�������=Q�������r-m�0-&#*&#-&#-@��-�������-���������������������������������������������������������������������������&#���������� �:	HHALLER CELL: A DOUBLE- EDGED SWORD IN SILENT SINUS SYNDROME
Jiaying Liu1 , Jason SY Hwang 1 
1 Department of Otolaryngology. Changi General Hospital. Singapore

Corresponding author
Dr Jiaying Liu
Address:  85 Thomson Green. Singapore 574952. 
Email: 	 HYPERLINK "mailto:liu.jiaying@sgh.com.sg" liu.jiaying@sgh.com.sg
Tel: (65)81211670
Fax: None

Abstract
Objective
This paper contrasts two cases of Silent sinus syndrome to demonstrate how the presence of an infra-orbital ethmoid (Haller) cell can significantly alter the ease of surgical resection and limit the amount of bony distortion.
Method
Case reports of two patients with Silent sinus syndrome but with differing anatomy
Results
An infra-orbital ethmoid (Haller) cell contributes to the evolution of Silent sinus syndrome by causing maxillary sinus ostial narrowing. However, its presence is helpful in conferring a margin of safety from the lamina papyracea during uncinectomy, allowing surgery to proceed with ease. Haller cells also limit the extent of bony distortion of the inferior orbital floor, resulting in less marked enopthalmos and less change in facial appearance.
Conclusion
Haller cell can be both a hinderance and a help in the pathophysiology and surgical management of Silent sinus syndrome.

Key Words
Silent sinus syndrome; Chronic maxillary atelectasis; Sinusitis; Haller cell; Enopthalmos; Hypoglobus; Ostial occlusion


Introduction
Silent sinus syndrome is a condition characterized by unilateral enopthalmos, asymptomatic maxillary sinus disease, and inferior displacement of the orbital floor. This occurs in the absence of orbital trauma or congenital facial deformity, with no history of chronic rhinosinusitis or acute rhinosinusitis in the preceding 6 months1,2. 
Surgery in Silent sinus syndrome is traditionally challenging as the uncinate process is almost adherent to the lamina papyracea. This paper contrasts two cases of Silent sinus syndrome to show how the presence of an infra-orbital ethmoid (Haller) cell can significantly alter the ease of surgical resection and limit the amount of bony distortion. This is followed by a review of the pathophysiology of silent sinus syndrome, in which Haller cells have been implicated in its evolution.  
Case One
A 39 year-old lady presented to us with left enopthalmos for 3 years and left maxillary pain for 2 years. There was no visual disturbance or ocular dysmotility. Although the patient previously had a history of recurrent sinusitis, she now experienced minimal nasal complaints except for left sided nasal obstruction. On examination, she had a deepened upper lid sulcus and malar depression. Her nasal septum was deviated to the left and the left middle turbinate was lateralized. Computed tomography (CT) scan showed features characteristic of silent sinus syndrome with the left uncinate process apposed to the inferomedial orbital floor, causing occlusion of the infundibulum (Figure 1). The left maxillary sinus was completely opacified with inferior retraction of the inferior orbital wall. 
She underwent septoplasty, left uncinectomy and middle meatal antrosotomy to reestablish physiological ventilation of the maxillary sinus. Maxillary antrostomy was performed with great care because the uncinate process was closely adherent to the lamina papyracea, carrying a high risk of orbit injury. The orbital floor was not repaired as reinflation of the sinus is sufficient to stop the progression of orbit displacement. Post operatively, there was some improvement in enopthalmos. However, nasoendoscopy still showed some residual bowing of the inferior orbital floor. 
Case Two
A 17 year old boy with a history of epilepsy was referred to us for maxillary sinusitis detected incidentally on CT Brain during an admission for breakthrough seizures. He experienced no nasal symptoms, enopthalmos, or facial asymmetry. Nasal examination was unremarkable except for an edematous left middle meatus. CT of the paranasal sinuses showed a hypoplastic left maxillary sinus which was opacified, with a low maxillary sinus roof. Diagnosis of Silent sinus syndrome was made. Unlike the patient in Case One, this patient�s uncinate process was separated from the lamina papyracea by a Haller cell. (Figure 2)
He underwent left uncinectomy and middle meatal antrostomy. The Haller cell appears to be a double edged sword in this case. While it predisposes to silent sinus syndrome by further narrowing the maxillary sinus natural ostium, it also prevents close apposition of the uncinate process to the orbit. This confers a margin of safety during uncinectomy, allowing the surgery to proceed with relative ease. Presence of the Haller cell also limits the amount of bowing in the inferior orbital floor, hence reducing bony distortion within the maxillary sinus. This translates into less enopthalmos, with little or no perceptible change in facial appearance in this patient as compared to the patient in Case One. 
Discussion
Silent sinus syndrome is a rare condition of spontaneous unilateral enopthalmos and chronic maxillary atelectasis. Till today, much of its pathophysiology remains unclear. However, a few theories have been proposed to explain its evolution.  
Bolger first noted lateralization of the uncinate process in all subjects in his case series. He proposed that this caused a one way outflow pneumatic valve mechanism within the osteomeatal unit, leading to progressive negative pressure within the maxillary sinus and resultant maxillary atelectasis. 
The current leading theory is an amalgamation of evidence gathered from different studies. It begins with maxillary ostial occlusion which causes sinus hypoventilation. Several mechanisms of ostial occlusion have been postulated 2. These include:
1.	Occlusion by inspissated mucus.
2.	Lateralized or hypermobile medial infundibular wall, or lateralized middle turbinate.
3.	Mucocele or nasal polyp occluding the antrum or ostium.
4.	Inflammed mucosa with or without rhinosinusitis.
5.	Hypoplastic maxillary sinus and antrum leading to decreased ostial diameter resulting in more frequent occlusion.
6.	Presence of infraorbital ethmoid (Haller) cells which narrow the maxillary ostium. 
Presence of mucosal inflammation and sinus hypoventilation give rise to a transient increase in sinus pressure. As the gases trapped within the maxillary sinus are absorbed by sinus mucosa, negative intra-sinus pressure develops. The in-vivo pressure within an atelectatic sinus has been measured by Davidson to be -23 mmHg4. Meanwhile, Wolfman8 found that osteoclastic activation in sinus bone begins after 2 weeks of continuous pressure of 2mmHg or more. This explains how persistently elevated pressures cause bone demineralization leading to centripetal bowing of maxillary sinus walls and ultimately chronic maxillary atelectasis. 
Chronic maxillary atelectasis and silent sinus syndrome have often been reported as the same clinical entity. Although both conditions are characterized by decreased maxillary sinus volume, chronic maxillary atelectasis is often associated with complaints of facial pain, congestion or postnasal drip. Silent sinus syndrome stands apart from chronic maxillary atelectasis by the presence of enopthalmos without the typical symptoms of chronic sinusitis. 
In fact, Silent sinus syndrome is thought to fit within the staging classification of Chronic maxillary atelectasis 5,7 (Table 1). Stage I and II describe anatomic changes with possible symptoms of sinusitis. Stage III identifies clinical deformity as a result of the anatomic changes of the first two stages. Stage III Chronic maxillary atelectasis therefore corresponds to the asymptomatic spontaneous enopthalmos seen in silent sinus syndrome 9. 
Facial pressure and pain is more common early in the course of Chronic maxillary atelectasis because of the development of negative pressure within the maxillary sinus. Once the maxillary sinus opacifies completely and wall atelectasis occurs, the intra-sinus pressure has reached an equilibrium. Hence facial symptoms are less marked in Silent sinus syndrome (stage III of Chronic maxillary atelectasis). This theory is supported by the work of Kass in which he found that an advancing stage of enopthalmos and bony deformity is negatively correlated to disease symptoms 10. Advanced enopthalmos also had smaller atmospheric-to-maxillary differentials ie; less negative pressure within the sinus10.  
Since Silent sinus syndrome lies on the tail end of the spectrum for Chronic maxillary atelectasis, detection of the disease process at Stage I or II when the patient is symptomatic, allows for early surgical intervention before clinical deformity sets in. 
From a surgical perspective, the significance of recognizing Silent sinus syndrome lies in avoiding orbital injury during uncinectomy. An unsuspecting surgeon, unaware of the close proximity of the uncinate to the orbit, could easily penetrate the low orbital floor, especially if a sickle knife is used for the uncinectomy, instead of a back biting instrument. Anatomic variation in the form of Haller cells aid the sinus surgeon because they confer a margin of safety during uncinectomy, hence reducing the risk of orbital injury. Haller cells also limit the degree of bowing in the inferior orbital floor hence reducing severity of enopthalmos and changes in facial appearance.
Summary
�	Recognition of uncinate process lateralization is integral to preventing orbital complications during surgery for silent sinus syndrome. Presence of infraorbital ethmoid (Haller) cells can be both a hinderance and a help. Although it causes narrowing of the maxillary ostium, it lowers the risk of orbital injury during uncinectomy. 
�	Haller cells limit the degree of bowing in the inferior orbital floor hence reducing severity of enopthalmos and changes in facial appearance.
�	Silent sinus syndrome occurs as end-stage Chronic maxillary atelectasis. Patients with early Chronic maxillary atelectasis, if detected early, can benefit from timely surgery before the onset of clinical deformity. 
 
References

1. Soparkar  CN, Patrinely JR, Cuaycong MJ, et al. The silent sinus syndrome. A cause of spontaneous enopthalmos. Opthalmology 1994; 101: 772-778.
2. Vander Meer JB, Harris G, Toohill RJ, et al. The silent sinus syndrome: A case series and literature review. Laryngoscope 2001; 111: 975-978.
3. Antonelli PJ, Duvall AJ III, and Teitelbaum SL. Maxillary sinus atelectasis. Ann Otol Rhinol Laryngol 1992; 101: 977-981.
4. Davidson JK, Sparkar CN, Williams JB, et al. Negative sinus pressure and normal predisease imaging in silent sinus syndrome. Arch Opthalmol 1999; 117: 1653-1654.
5. Brandt MG, Wright ED. The silent sinus syndrome is a form of chronic maxillary atelectasis: A systematic review of all reported cases. Am J Rhinol 2008; 22: 68-73.
6. Wise SW, Wojno TH, DelGaudio JM. Silent sinus syndrome: Lack of orbital findings in early presentation. Am J Rhinol 2007; 21, 489 � 494.
7. Kass ES, Salman S, Montgomery WW. Manometric study of complete ostial occlusion in chronic maxillary atelectasis. Laryngoscope 1996; 106: 1255-1258.
8. Wolfman DE, Chole RA. Osteoclast stimulation by positive middle-ear pressure. Arch Otolaryngol 1986; 112: 1037-1042
9. Ende K, Mal L, Kass ES. Progression of late-stage chronic maxillary atelectasis. Ann Otol Rhinol Laryngol 2002; 111: 759-762.
10. Kass ES, Salman S, Rubin PAD, et al. Chronic maxillary atelectasis. Ann Otol Rhinol Laryngol 1997; 106: 109-116.









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