CT signs of pressure induced expansion of paranasal sinus structures

Several articles have been written about hyper infl ated sinus structures. Never before, however, a complete overview of all possible pressure induced variations of sinus anatomy have been published. The aim of this study was to make an inventory of the most common CT signs of hyper infl ated paranasal sinus structures. During a period of 2 years all CT-scans of the paranasal sinuses made in an ENT-department were studied and the most typical shapes of hyper infl ated sinus structures were recorded.


Methodology
The investigation consisted of a careful prospective evaluation of all the CT-scans made during a 2 year period in a university outpatient ENT clinic (2002)(2003) with the aim to describe all possible signs of bony deformities of the paranasal sinuses that eventually could be attributed to high intranasal pressures. Because the ethmoid is the only bone in the human body that can produce paper thin bony lamellae and as a consequence the bone that most often will show deformities induced by increased pressures, the authors propose a classi ication that deals with deformities of the paranasal sinuses anterior to the ethmoid, the etmoid and posterior to the ethmoid.

Results
The abnormalities of bony paranasal sinus structures on the CT-scans that could be attributed to increased pressures, observed by the author, can be divided in 3 subgroups: abnormalities of  The interior of the cell is free of disease. After removal of the cell the mucosa of the frontal sinus becomes normal. C+D: Two CT-scans at the same level with a 2 year difference in a patient with a frontal cell in the frontal sinus. Note that the cell has increased in size (D).

Figure 3: (A-E) A+B+C:
Coronal CT-scans. Two frontal cells, right one (1) fi lling the frontal sinus for 30 % and the left one (2) for more than 50 % (A). Interior of the cells shows no pathology. The frontal sinus on both sides are opaque. In A there are also two agger nasi cells on both sides. Also in B there is a second cell fi lling on the right side the infundibulum of the frontal sinus, showing some bossing of the orbital rim. C shows a clear-cut hyperinfl ated anterior frontal complex and supra-orbital recess. On the left side the ostiomeatal complex shows signs of mucosal swelling. Note the presence of a concha media bullosa on the right side. There exists a septal deviation towards the left side (resulting in a paradoxical bending of the inferior turbinate) close to the fl oor. D. Parasagital CT-scans of the same patient (left side) showing fl attening of the skull base due to hyperpneumatisation of the frontal recess and frontal sinus by hyperinfl ated cells (aspect of a "bunch of grapes"). Compare this confi guration of these cells and fl attening of the skull base with a normal case (E).

Discussion
In the literature many signs of hyper in lated paranasal sinus structures have been described. However, most of these described hyper in lated structures concern the bony framework: [1][2][3][4][5][6][7][8][9][10][11][12][13]. Only a few of the anomalies of the ethmoid have been described such as: presence of the frontal cells in the frontal sinus [16,18], infra-orbital cells in the maxillary sinus [19], and pneumatisation of the uncinate process [20]. Several signs of hyper pneumatisation of the ethmoid bone are described for the irst time in this article, such as "ballooning" and "cobble stone" appearance of the lamina orbitalis, ethmoidal emphysema (nearly empty ethmoid) and "egg shaped" ethmoid.
The pneumatisation of the facial bones is a continuous process that doesn't stop after puberty. The life ongoing pneumatisation of the maxilla has been described already a very long time. Especially the dentition and the loss of dentition seem to be involved in the development of this sinus. Sometimes this pneumatisation can derail and result in EMSP [14] or a pneumosinus dilatans. Mostly, however, the signs of hyper pneumatisation are more discrete such as overdeveloped frontal or sphenoidal sinus, supra-orbital hyper pneumatisation of the frontal bone resulting in a rounding of the supra-orbital recess.
All the facial bones have in common that they are solid bony structures making up the frame-work of the face. The ethmoidal bone, on the contrary, is a unique bone. It is the only bone in the human body that forms very thin bony lamellae, thin bony cellular structures and thin bony conchae (media and superior). So it is not surprising that these thin delicate bony structures will be deformed more often than the thick bones of the facial skeleton. It is remarkable, however, that some of the deformations of the bony lamellae ("ballooning", "cobble stone" and "egg-shaped" aspect of the lamina orbitalis) have never been described before.
Another unique feature of the ethmoidal bone is that it can invade other facial bones (extramural cells). More in particular its cellular structures can invade the space that has been created by the pneumatisation of the thick facial bones such as: frontal cells invading the frontal sinus and infra-orbital cells invading the maxillary sinus. The invasion of these facial bones by these very thin ethmoidal cells seems to be an in time dynamic process (Figures 2C-2D). From CT-scan studies it is obvious that the ethmoid has a tendency to expand outside its borders. This expansion can be limited whenever a lot of resistance is encountered (orbital content stops the hyperextension of the lamina orbitalis resulting in "ballooning" and "cobble stone" aspect) or the extension can be more important when there is enough space available (frontal cells in the frontal sinus, infra-orbital cells in the maxillary sinus). Sometimes the expansion is towards the open space into the nasal cavity, blocking the ostiomeatal complex at the level of the middle meatus. When these hyperin lated structures are becoming too voluminous they will obstruct the narrow spaces of the ostiomeatal complex and interfere with proper ventilation and drainage of the involved sinuses, resulting in in lammation of the trapped mucosa. Frontal cells will induce chronic frontal sinusitis (Figure 2), hyper in lated ethmoid and uncinate process will close the infundibulum ethmoidale and obstruct the drainage of the maxillary sinus ( Figure 12) or of the ostiomeatal complex at the level of the middle meatus resulting in a chronic sinusitis characterized on CTscan by a "black halo" con iguration (Figures 5,8).
One of the driving forces of the pneumatisation of the facial bones and the hyperin lation of the ethmoidal structures must be pressure. From table 1 [21] one can see that the maximum pressure generated by forced breathing are not very high (between 31 daPa and 75 daPa). The pressures, however, generated by nose blowing, are much higher (from 523 daPa to 950 daPa). The maximum positive pressure measured in this study reached even a level of 2420 daPa. One can imagine that such extreme high pressures can induce hyper pneumatisation of the facial bones and result into deformation and hyperin lation of the thin bony structures of the ethmoid. The amount of expansion will depend on one hand by the static and dynamic pressures generated during nose blowing manoeuvre and on the other hand by the yield or give way of the bony structures of the paranasal sinuses and the surrounding tissue. The static pressure will expand all sinuses in a similar way, the dynamic pressure will be directed mainly towards the anterior ethmoid complex via the hiatus semilunaris and the infundibulum ethmoidale towards the frontal and supra-orbital recess, maxillary and frontal sinus.
From the results of the pressure measurements, it is obvious that patients with chronic sinusitis generate higher pressures than normal test subjects. Patients with chronic sinusitis not only blow their noses harder than normal test subjects, but they  blow their noses also more frequently. So it might be possible that in a subgroup of patients with chronic sinusitis (excluding systemic diseases such as ASA, PCD and cystic ibrosis) bony deformities reach a size that will start to interfere with the drainage of the ostiomeatal complex [22] and sinuses.
Stammberger [20] described the "bottle neck" phenomenon where touching mucosae are responsible for an impaired mucociliary clearance, leading to chronic sinusitis. During a common cold, however, every patient experiences a severe blocked nose and examination of the nasal cavities shows presence of a swollen mucosa, blocking completely the middle meatus. Nevertheless a common cold seldom induces polyps. To generate chronic rhino sinusitis eventually with nasal polyps, the touching of the mucosae must be permanent and this is only possible when there exists an underlying bony deformity that closes off the narrow spaces of the ostiomeatal complex permenantly [22].
In recent literature a lot has been written on the role of fungae [23] and Staphylococcus aureus superantigens [24] in the pathogenesis of chronic rhino sinusitis. Recently, however, Bhattacharyya [25] was able to show no signi icant difference whatsoever in the positive culture rates of aerobic, anaerobic bacteriae and fungae between sides in patients with unilateral sinusitis. So this author concludes that there exists some doubt on the exact etiologic role of bacteria in chronic rhino sinusitis, suggesting other factors or other agents in the pathogenesis. Experimental studies show that to produce a bacterial bio ilm in rabbits [26] one not only has to inoculate the maxillary sinus but one also has to block the maxillary ostium to be able to induce an experimentally induced chronic maxillary sinusitis in these animals. So impairment of the drainage is imperative in the production of a bacterial bio ilm resulting in chronic sinusitis. The same goes for fungae. The fungal spores that are inhaled need at least one and a halve hour to germinate. This is only possible when the mucociliary transport is impaired.
All these data suggest that impaired mucociliary clearance of the ostiomeatal complex is still a very important factor in the etiology of chronic sinusitis [22]. Hyper in lated ethmoidal structures can impair mucociliary clearance and one can assume that high pressures generated during nose blowing are the most probable cause of hyper in lated bony structures blocking this clearance. During a common cold the frequency of nose blowing increases dramatically and one can imagine that the high pressures generated during forcefull nose blowing can be trapped in the sinuses because of a ball valve mechanism. Gwaltney et al. [17] showed that nose blowing can also blow pathological secretions in the sinuses (a kind of inoculation). So nose blowing does not only result in blocking the mucociliary drainage by expanding bony structures resulting in permanent obstruction of the narrow spaces of the ostiomeatal complex, but it can also inoculate the normally sterile paranasal sinuses of an adult. Both conditions i.e. blockage and inoculation that are necessary for an experimental induced rhino sinusitis can be generated by the nose blowing manoeuvre in patients. To avoid the generation of these extremely high pressures during nose blowing patients should be instructed to blow their noses one side at a time, without blocking both nostrils and building there extremely high pressures ( Figure 14). Nose blowing is only useful when it is productive. When a nasal cavity is completely blocked by swollen mucosa nose blowing will only increase the mucosal swelling.
All the above described hyper in lated structures do also exist in healthy persons with no signs whatsoever of sinusitis. Chaiyasate et al. [27] studied twins without any sinus disease and in 40 % of the cases "cobblestone" aspect and in 38 % "ballooning" of the lamina orbitalis. In their study the two previous decscribed anomalies seemed to be rather acquired than from genetic origin.
It is very dif icult to quantify these abnormalities. One can state that these oversized anomalies become pathological when the mucosa of the narrow spaces around these hyper in lated structures become in lamed. 19 More studies are needed to evaluate the prevalence of these bony anomalies in normal test subjects and patients. Also the natural history of chronic sinusitis, from its early stage with discrete signs of sinusitis on the CT-scan but no or minimal complaints and normal endoscopy towards full blown chronic sinusitis, with obvious complaints and clear-cut signs of mucosal in lammation on CT-scan and endoscopy is poorly documented. Mostly the ENT surgeon sees these patients in a later stage, when medical therapy has failed and surgery is needed. The fact, however, remains that FESS alone can restore mucociliary clearance and ventilation of the paranasal sinuses and can induce healing in a major part of these patients, demonstrating that a simple obstruction of the ostiomeatal complex is still an important etiologic factor in the pathophysiology of chronic rhino sinusitis.

Conclusion
CT scans of patients with chronic sinusitis show many signs of hyper in lated paranasal sinus structures. It is possible that frequent and forced noseblowing could enhance these anomalies and as such may play a role in the pathophysiology of chronic rhino sinusitis.