Sinusitis - Science topic

Phil Geis

The bright spots you’re seeing are likely contaminants, might be bacteria, fungal spores, or cellular debris.

In this case my suggestion is that:

1. do Gram staining or bacterial fluorescent stain to check if it’s bacterial or else?

2. Change to fresh sterile culture media to rule out contaminated supplies.

3. Assess cell viability just to ensure the issue isn’t due to the cell stress or death?

It shows sinus rhythm, supraventricular bigeminism and WPW pattern.

As you mentioned, invasive fungal sinusitis primarily affects individuals with compromised immune systems, such as those undergoing chemotherapy, organ transplant recipients, or individuals with uncontrolled diabetes, HIV/AIDS, or other conditions that weaken the immune system.

The severity of immunosuppression plays a critical role in determining the outcome of invasive fungal sinusitis. Patients with more profound immunocompromised states are at higher risk of developing severe and potentially life-threatening complications from the infection.

Other factors that can influence the prognosis of invasive fungal sinusitis include the type of fungus causing the infection, the extent of tissue involvement, the timing of diagnosis and initiation of appropriate treatment, and the overall health status of the patient.

Invasive fungal sinusitis is a serious condition that requires immediate and aggressive medical intervention. Successful management often involves a combination of antifungal medications, surgical debridement to remove infected tissue, and optimal management of the underlying immuno-compromising condition.

NT Fascicle 11 Chapter 1.pdf (arppress.org)

Thats is exactly what I am lookin for, did you find any solution?

Erik you are very right multiple visits pose more problems and a canal that is dry at the time of obturation, means it is free from microbes.The periapical infection will resolve in due course of time as the cause has been removed.

Dear Ahmed!!

The photomicrograph looks like an Aspergillus, however it is not enough. I recommend that you set up a microculture, PDA, Czapeck and water agar cultures, make detailed descriptions of growth with different light and temperature conditions, morphology and reproduction structures supporting international Keys, so you can possibly get to a gender, for the species I recommend doing DNA analysis. Good luck with the identification.

Thanks Sir Khaled Elsayed

Hi,

Here are my thoughts on the topic. The PWM techniques, differ only in terms of the high-frequency undesirable harmonics, which will be outside the bandwidth of your system, during transients as well as steady state operation. Whereas, their low frequency content, which depends on the reference wave for PWM generation, will be same in both cases. So, I agree with what you have said, the two should have similar performance in terms of dynamics.

This link might help you -

Julie Joseph

Thank you so much again!

I'm kind of relieved to hear that editors and reviewers can't make me redo the experiment again with the procedure they prefer.

I'll think about which way of transplant to choose. Actually, I'm a little afraid of holding mice for anesthetic procedure, so I feel more comfortable with tail vein injection.

Clinically, sinus headache and migraine are very similar, so it is no surprise to find excess sinus abnormalities on MRI in migraine.

I' m an Ear Nose Throst doctor, I suggest to ask Neuro surgeon or Neurologist

Robert

What question are you asking? Are you making comparisons between or within individuals? I assume you are simply comparing the groups correct?

Vitamin d3 is necessary for good immune system

Thanks Dr. Magdy for your valuable sharing.

I am of view a Sinus Capture beat negates the ECG Diagnosis of Fasicular VT - a micro re-entrant tachycardia.

nasal adhesions (synechiae) according to nayak etal 1998; type a  at middle turbinate attachment to lateral nasal wall, type b partial synechiae  at the caudal end /inferior border of middle turbinate to lateral wall, type c complete synechiae at caudal end, type d adhesion between inferior/ middle turbinate and septum. 

I hope this can help

I am not an arrhythmologist (I am a general cardiologist), but in my opinion, the EHRA score can be used for assessement AF related symptoms and to queality of life after ablation. therefore, maybe pre and post ablation EHRA score is useful for detection of effectiveness of the procedure. 

Dear Beatrice, thanks a lot for your precious comment. Please check this out. It's your turn. For figures please go directly to the website.

Most sincerely,

Prof. Mladina

Balkan Med J. 2015 Apr; 32(2): 137–146.

Published online 2015 Apr 1. doi:  10.5152/balkanmedj.2015.159957

PMCID: PMC4432693

Clinical Implications of Nasal Septal Deformities

Ranko Mladina,1 Neven Skitarelić,2 Gorazd Poje,1 and Marin Šubarić3

Author information ► Article notes ► Copyright and License information ►

 

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Abstract

The first attempts to systematize septal distortions have been given by Cottle who defined four groups of septal deformities: subluxation, large spurs, caudal deflection and tension septum. Fortunately, the variations of the septal deformities show a certain order, thus enabling more precise classification. Mladina was the first to make user-friendly classification of septal deformities in six basic types. He also described the seventh type, named “Passali deformity”, which presents individually, but is always a well-defined combination between some of the previous six types. Mladina types of septal deformities (SD) are divided in two main groups: so called “vertical” deformities (types 1, 2, 3 and 4), and “horizontal” ones (types 5 and 6). This classification was immediately well accepted by rhinologists worldwide and started to be cited from the very beginning. Since then it has been continuously cited increasingly more often, thus making Mladina classification a gold standard whenever clinical researches on nasal septum are concerned. More than forty clinical studies based on this classification have been performed to date. It is extremely important to make a strict distinction between the types of SD since all of them play some specific role in the nasal and general physiology in man.

Keywords: Classification, nasal septum, nose deformities

First of all, one should determine a difference between the term septal deviation and septal deformity, since “deviation” generally means a slight declination from the medio-sagittal plane, whereas deformity means the change of shape or change of form. The basic form of the septum should mostly be a straight plane that divides the nose into two cavities, but in reality it is not like that. Many authors have tried to delve deeper into the problem of variations in septal shape. Because of that, there were almost no data published on the matter of the relationship between particular septal deformities (SD) and the related health problems, be it local or general, until the early 1990s. The first attempts to systematize septal distortions were given as early as 1958 by Cottle (1) who defined four groups of “septal deviations”: subluxation, large spurs, caudal deflection and tension septum. Fortunately, the variations of the septal shapes (deformities) show a certain order, thus enabling more precise classification. In 1987, Mladina was the first to make user-friendly classification of (SD) in six basic types (2). He also described a seventh type, named Passali deformity, which presents individually, but is always a well-defined combination of some of the previous six types. Mladina types of SD are divided into two main groups: so-called vertical deformities (types 1, 2, 3 and 4), and horizontal ones (types 5 and 6). Vertical deformities have the longer axis in a vertical plane, i.e. they concern the unilateral crook(s) that can be imagined as a result of the force acting against the nasal septum in an antero-posterior direction. The horizontal deformities, however, have a longer axis in the horizontal plane, i.e. they are crooked as if the force against the septum has been acting from superior to inferior. This classification was immediately well accepted by rhinologists worldwide and was cited from the very beginning. The number of citations has been growing since then, and this has been the standard method at least 40 clinical researches in various countries all over the world (3–42).

Twelve years after Mladina published his classification and after it had been used for many clinical researches, in 1999, Guyuron published his suggestions, promoting six types which, at first sight, seemed to be more user friendly than Mladina’s (43). Guyuron suggested the following types: tilt, antero-posterior C, antero-posterior S, cephalo-caudal S, cephalo-caudal C, and wide spurs. This classification, as for that described by Mladina, includes six types of SD. Moreover, his antero-posterior C corresponds to Mladina type 3, the antero-posterior S looks exactly like Mladina’s type 4, the cephalo-caudal C is extremely rare and exists only as an exception after the really serious trauma to the nose (superior-inferior direction of force), and, finally, the cephalo-caudal S is extremely similar to Mladina’s well-known type 6. Finally, so-called “wide spurs” are the same as Mladina’s type 5. Therefore, overall, both classifications describe almost the same deformities but in “different languages”.

Four years later, in 2003, Buyukertan classified SD by separating the nasal septum into 10 segments with an intention to better localize the deformity (44).

After that, in 2007, the Baumanns published a new classification of septal “deviations” (45). According to their schematic drawings, not real endo-photographs, types 1 and 2 appear to be the same as Mladina’s type 5, their type 3 corresponds to Mladina’s type 6, types 4 and 5 are very similar to type 7, i.e. a combination of type 5 and type 2 in their type 4, and type 5 and type 3 in their type 5, whereas their type 6 very closely resembles Mladina’s type 3. However, the Baumanns’ classification does not include “S-shaped” or “reverse S-shaped” septums, i.e. Mladina’s type 4 or Guyuron’s “anterior-posterior S”.

Some studies on the incidence of SD in man, based on the Mladina classification and simple anterior rhinoscopy without the decongestion and endoscopy of the nose, showed the incidence of septal deformities to increase slowly from childhood to adulthood, finally becoming very high, reaching close to 90% of the population in the world (29–31).

Once it became obvious that SD in man are well defined and differ between themselves, it became very interesting to see how a particular type of septal deformity can influence the owner’s nose. We have been using the Mladina classification since 1987 and have realized the close relationship between some of them and the related sino-nasal pathology.

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CLINICAL IMPLICATIONS of SEPTAL DEFORMITIES

Type 1 means a mild unilateral vertical ridge in a valve area which slightly interferes with the function of the nasal valve; thus, in most cases, this has mild clinical importance (Figure 1a, b).

FIG. 1. a, b.

Right-sided septal deformity type 1 (a). Right-sided septal deformity type 1. Inferior turbinate can be followed almost the entire way to the choana. The anterior half of the middle turbinate can also be easily seen (b).

Clinically, some people, for reasons which are unclear, tolerate this type better than others. The exception could appear when this type is connected to subluxation or even luxation of the columellar septal edge. The subluxation or luxation could bother patients both aesthetically and functionally sense, while the septal deformity type 1 is, in most cases, irrelevant in terms of the patient’s subjective valuation of nasal breathing quality.

Exceptionally, it can act as a predilection factor for impaired nasal breathing in patients with unusually high columella and thin, flagging alar cartilages. In these cases, the entrance to the nose is already narrower than usual since a high columella enables a certain degree of nasal alae stretching. In cases where they are thin and lax, they will collapse during deep nasal breaths. The result will be the nestling of both alae to the anterior septum, which will be much stronger on the side of the deformity (Figure 2a, b).

FIG. 2. a, b.

Typical shape of the nostrils during normal nasal breathing (a). During the forced inspiration through the nose, the left, flagging ala adheres strongly to the septum, thus blocking any further nasal breathing through the left nose (b).

Type 2 means a unilateral vertical ridge, which is much more emphasized in this case, i.e. it stays in close contact with the anterior nasal valve and thus, from the physical point of view, remarkably narrows or even totally blocks the air passage on the related nasal side.

From the clinical point of view, the shape of this deformity produces a typical situation: the buds of the nasociliary and palatinal nerves (belonging to V1 and V2 branches of the trigeminal nerve), which have a dense network in the nasal cavity, do not have appropriate contact with the airstream of the inspired air. In fact, they cannot be adequately agitated by the airstream produced while passing through the nose. Because of that, the beginning of the afferent arm of the so-called naso-pulmonary reflex that connects the nose and the lung is blocked and the nuclea of the trigeminal nerve in the medulla oblongata cannot be reached and agitated. Furthermore, the closest “neighbors” to the trigeminal nuclea in the medulla oblongata are nuclea of the cervical plexus. In addition, the phrenic nerve is located within the cervical plexus. The phrenic nerve, furthermore, is responsible for the innervation of diaphragm muscles (efferent arm of the naso-pulmonary reflex). Because the phrenic nerve cannot be adequately agitated in these circumstances, no consequent contraction of the diaphragm muscles can be expected on the related thoracic side. Furthermore, a weak contraction of the diaphragm also results in more superficial pulmonary breathing on this side. In addition, septal deformity itself disables a direct contact between the airstream and nasal fontanel receptors, thus impeding normal regulation of the tracheobronchal vagal tone. The naso-pulmonary reflex is distorted or totally blocked (46–48). Therefore, the most important clinical feature connected to the type 2 septal deformity is impaired nasal and pulmonary breathing.

One should not forget the usual endoscopic finding of the most posterior parts of the nasal cavity in type 2: a strawberry-like hypertrophy of the mucosa of the inferior turbinate tail (Figure 3a–c).

FIG. 3. a–c.

Right nasal cavity. Choana is blocked by hypertrophic mucosa of the inferior turbinate tail (a). Left-sided type 2 septal deformity (b). The same situation is seen with the mucosa of the left inferior turbinate tail. Please note that the endo-photographs ...

Even more, there are data in the literature that suggest the strong influence of type 2, combined with the consequently hypertrophic mucosa of the tail of the inferior turbinate, to the middle ear pressure (23).

Type 3 means unilateral vertical deformity, i.e. unilateral convexity next to the anterior edge of the head of the middle turbinate (Figure 4). The nasal cavity is very narrow on this side and very wide on the opposite one.

FIG. 4.

Left-sided type 3 deformity. Although nasal decongestant and local superficial anesthesia have been applied, the deformity covers the view to the great part of the middle turbinate and remains in close contact with it.

From a clinical point of view, it must be stressed that type 3 is the most frequent septal deformity in the general population and very frequently found in all cases of chronic rhinosinusitis (CRS). The incidence of type 3 in CRS patients was 21.63% (41). In addition, the allotment of the type 3 within type 7 among adults suffering from CRS was found to be almost 90%. Since type 7 was found to be present in 29.92% of CRS patients, this suggests that type 3 is the most frequent SD in CRS patients.

Here, one should not forget the fact that pathohistological analysis of the mucosa taken from the most convex and most concave part of the nasal septum in type 3 SD has shown a multilayer squamous cell metaplasia (6,12) (Figure 5). The same has been shown in the mucosa covering the head of both middle turbinates. In such conditions, with no trace of cylindrical respiratory epithelium, one cannot expect to have a normal mucociliary clearance system, which is important and typical for the respiratory system. The metaplastic multilayer squamous cell epithelium allows only the stagnation and final block of the mucociliary transport system, thus widely opening the door for bacterial and viral invasion.

FIG. 5.

The right-sided type 3 SD. Histological picture of the piece of septal mucosa taken from the narrowest part of the nasal cavity, just opposite the head of the middle turbinate. The epithelium shows typical appearance of the squamous cell metaplasia.

In most of the cases with a bent (scoliotic) external nose (“C” or “reverse-C” shape of the external nose), the background is type 3 septal deformity. Therefore, an adequate correction of the scoliotic nasal pyramid always requires appropriate septal surgery.

Type 4 is a bilateral vertical deformity (Figure 6), consisting of previously mentioned types, i.e. type 2 on one side, and type 3 on the other (so called “S-shaped” septum, or “reverse S-shaped” septum). Clinically, it summarizes all clinical implications of both types.

FIG. 6. a, b.

“Z-shaped” type 4 SD. Right-sided type 2, staying very close to the head of the inferior turbinate despite the abundant decongestion and local superficial anesthesia (a). Left nasal cavity shows much deeper vertical deformity (white arrow), ...

Type 5 is a unilateral deformity, which is known in the literature as a “septal spur”. It causes a unilateral horizontal deformity, discretely ascending from anterior to posterior, appearing as a crest which juts out more laterally than deeper in the nose, resulting in most cases in the impaction of its tip to the region of the sphenopalatine foramen (Figure 7a, b).

FIG. 7. a, b.

Right-sided type 5. Right-sided, typically deep and in most cases hidden and (without the decongestion) invisible horizontal basal crest, getting in a very close contact to the lateral nasal wall as getting deeper in the nose (a). Coronal MSCT scan clearly ...

Clinically, it always means unilaterally impaired nasal breathing. The opposite side of the septum is almost flat. Sometimes, this deformity can provoke ipsilateral intermittent attacks of the headache, so called hemicranial pains (Sluder’s headache), since the tip of the deformity is in close contact with the sphenopalatine cable containing the sphenopalatine artery, vein and a nerve in this case.

More theoretically, this type could also influence the development of chronic otitis media since it mechanically disturbs the normal flow-direction of mucous drainage from the ostiomeatal complex to the nasopharynx, just directing it more superiorly, i.e. towards the Eustachian tube orifice, because mucous flow has to skip the dam, i.e. the tip of this deformity.

This deformity is also one of the most frequent in the general population. Its incidence is low in childhood and starts to grow by adolescence, achieving full frequency in adults when it finally reaches around 28% (3,29).

Fortunately, despite the fact that, in most cases of type 5, the native anterior rhinoscopy simply enables this deformity to remain undiscovered behind more anterior parts of the nasal cavity mucosa, endoscopy of the nose is not mandatory: it can also be seen and recognized on the coronal MSCT scans of the paranasal sinuses (Figure 7b).

This deformity seems to be inherited, since it is usually found in close relatives in a particular family (patient’s closest relatives). The side of the deformity and its intensity are not usually the same, but there is always a typical appearance of this type.

Type 6 is also a so-called horizontal deformity, consisting of two separate components: an anteriorly positioned basal septal crest on one side and more or less massive wing of the inter-maxillary bone on the opposite side. Between the intermaxillary bone wing and the septum there is a horizontal groove. The groove is a strict characteristic which determines type 6 (Figure 8a, b). It can be shallow and very deep; this does not matter at all. Its existence is crucial even when extremely shallow.

FIG. 8. a, b.

An anterior, basal crest can be seen (white arrow). In most cases, it touches the mucosa of the inferior turbinate. This photograph was taken after the decongestion and superficial local anesthesia; thus, much closer contact between the crest and inferior ...

Clinically, type 6 is found in more than 96% of all children suffering from cleft lip/palate, and in more than 76% of their parents (39). Additionally, in adult subjects carrying type 6 SD without a manifest cleft, one must palpate the hard palate (submucosal cleft?), take a precise look at the uvula (bifid or not?), and perform an obligatory analysis of the subject’s hearing abilities because submucosally hidden weakness of the palate could also mean a weakness of levator veli palatini and tensor veli palatini muscles. The weakness of these two muscles directly influences normal function of the Eustachian tube orifice, thus also influencing ventilation and drainage of the middle ear, which directly leads to the possible ipsilateral conductive hearing impairment.

Type 6 can be found in the vast majority of patients suffering from REKAS (Recurrent Epistaxis from Kiesselbach’s Area Syndrome) (49,50). Finally, there is another similarity: as in type 5, this type can also be easily recognized on coronal MSCT scans (Figure 9).

FIG. 9.

Coronal MSCT-scan of the paranasal sinuses. Septal deformity type 6 is clearly recognizable with a typical groove (yellow arrow) and basal crest (white arrow). Dotted blue line shows the asymmetry of the nasal floor, which is always found in this type ...

This deformity, like type 5, also seems to be inherited (38), since it can be found in all members of the family (patient’s closest relatives). Like in type 5, the side and intensity are not necessarily the same as in the index patient, but a typical appearance is always present. The deep anterior groove defines the side of the deformity, i.e. if the patient carries type 6 with the groove on his left side, the deformity should be recorded as “Type 6 L”. The anterior basal crest therefore is located on the opposite side.

Type 7 (“crumpled septum”) is very variable and presents a combination of previously mentioned types with all of their clinical implications (Figure 10). In fact, it always involves a combination of one of two horizontal deformities (type 5 and/or type 6) with one of those belonging to so-called vertical deformities (types 1,2,3 or 4).

FIG. 10. a, b.

Clinical appearance of type 7 (Passali deformity or “crumpled septum”). The right nasal cavity is almost completely blocked by the septal deformity (a). Left cavity, after decongestion and application of the superficial local anesthetic, ...

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DISCUSSION

General considerations

Septal deformities appear in six well-defined types, and also as a combination of some of them in many cases, which are called type 7 “crumpled septum”.

It is extremely important to make a strict distinction between the types of SD since all of them play a specific role in nasal and general physiology in man.

It is absolutely irrelevant whether one call some type of septal deformities by number or an abbreviated name, or distinguish them according to the shorter or longer verbal descriptions. However, to us it appears to be much easier to simply use numbers.

For a single septal spur (or crest), our classification has a simple sign: type 5. However, to assign some “crumpled septa” is not that easy. If verbally described, it will take at least one or, more probably, two lines of typewriting. On the contrary, to say, for example, “Type 7 (type 3 right+ type 5 left)” means that there is a “crumpled septum”, i.e. for a combination between right-sided type 3 and left-sided type 5. This will not be possible when using Guyuron’s classification since it does not offer type 7 at all.

As all of us are dealing with the problem of deformed nasal septa, deprived from any vanity, it is necessary to speak the same language regarding the types of SD; this will enable the general knowledge on this matter to certainly blossom. It is difficult to compare individual results until we speak different languages and thus do not understand each other.

In addition, the term “septal fractures” has been firmly accepted and used among rhinologists for years and decades despite the fact that it is purely used for dogmatic apprehension. Namely, it should be known that even in cases of obvious anterior vertical crooks of the nasal septum (types 1 and 2), no obvious “fracture” of the cartilage or any tissue gap was found, be it during the septal surgery or during the histological analysis. Regarding histology, the only issue that can normally be found in the region of the crook is local proliferation of the chondrocytes in the “heart” of the deflection (Figure 11a, b). The real disruption of the septal cartilage can be seen exceptionally as a result of serious nasal trauma. In these cases, the tissue discontinuity, i.e. the gap between two or more parts of the cartilage can be identified. Besides, in cases of serious trauma to the nose, the distortions of the pyramid can also be seen (Figure 12).

FIG. 11. a, b.

Histology of the septal cartilage (horizontal section!) through the right-sided vertical crook (type 2 septal deformity) of an adult patient. Despite an emphasized angulation, there are no signs of discontinuity of the cartilage (a). A close-up view of ...

FIG. 12.

The appearance of the cartilaginous external nose one year after the latero-lateral trauma against the nose. Please note that the bony frame of the pyramid is still straight (dotted line). The cartilaginous part inclines strongly to the right (red curved ...

Type 3, which is also a vertical deformity, but substantially deeper than types 1 and 2, i.e. it is positioned at the borderline between the perpendicular lamina of the ethmoid bone and quadrangular cartilaginous plate (cartilago quadrangularis), never shows any sign of fracture. The conjunction between the bone and cartilage always remains untouched, regardless of how acute the angle between them is.

Besides, insisting on trauma against the nose as an exclusive reason for the onset of type 3 does not seem to be well-founded. Sometimes it is easy to “see through the external nose”, i.e. in cases of rhinoscoliosis it is understandable that the septum follows the shape of the external nose, as the canvas would follow the distorted frame (Figure 13). However, in the vast majority of type 3 cases, there are no signs of the distorted external nose at all.

FIG. 13.

Rhinoscoliosis (“reverse-C” shaped pyramid). One can presume that such a distorted bony frame brings along left-sided type 3 septal deformity. The bony frame has been distorted (dotted line).

Reliability

Despite the fact that having a unique, user friendly classification makes reliable multicenter studies on the incidence of nasal SD and their clinical implications possible, all classifications published so far suffer from subjectivity when anterior, vertical deformities are concerned: whether some deformity will be assigned as type 1 or type 2 is a matter of the observer’s impression since there is no objective parameter which could allow the observer to distinguish between these two types.

However, regardless of that, the most prominent cognitions that we have today regarding the clinical implications of SD are evidence-based. Evidence-based medicine is the future. In terms of that, good classification must have a high degree of reliability. This is particularly important in our case since our classification concerns some important physiologic and pathophysiologic interactive mechanisms between the nose and the organism in general.

For instance, the relationship between type 2 and the quality of pulmonary breathing is well known and has been meticulously described under the section “Type 2”.

Type 3 has been found to be the dominant septal deformity in cases of CRS, i.e. the incidence of type 3 in CRS patients was 21.63% (41). In addition, the allotment of type 3 within type 7 among adult patients suffering from CRS was found to be almost 90% (41). Since type 7 was found to be present in 29.92% of CRS patients, this supports the fact that the type 3 is the most frequent SD in CRS patients. Histological changes of the middle turbinate and neighboring septal mucosa have been found on an everyday basis. The consequences of the lack of respiratory mucosa in the crucial nasal regions, responsible for good pulmonary breathing, have been precisely described in the section on Type 3. Even fontanel receptors have been shown to be blocked in cases of emphasized SD of type 3.

Type 4 summarizes all that which has been stated for types 2 and 3.

Type 5 has been proven to be an absolutely inherited deformity. In the vast majority of unilateral hemicranial headaches of Sluder’s type, type 5 could be found in the deepest parts of the nose. Type 5 has been named septal spur or septal crest for decades, but its heritability has never been mentioned. Owing to this classification, we now know that this deformity can be found in all of the closest relatives in a certain family. This is evidence-based knowledge. Besides, “spurs” have never been explained as a deformity that cannot be found in small children and the fact that it is very rare among children in elementary school, means that this type “comes to the surface” only during puberty and adolescence. Therefore, this fact is evidence-based (29,43).

Finally, now we know that this type is heritable, we know at the same time that it cannot be the consequence of any type of trauma against the nose.

This knowledge can be useful when the doctor is asked by the court to give an opinion on the consequences of some trauma to the nose. The opinion in such cases will always be the same: this septal deformity has nothing to do with the trauma against the nose.

Type 6 has nothing to do with childhood as well; it is only evident at puberty, step by step, becoming more and more evident in adolescence and reaches its final form only in mature individuals, but again always appears in the closest relatives. Unfortunately, except for the knowledge on this matter based on long-lasting clinical experience, there is no official, published evidence on the absolute heredity of this type at all. On the other hand, the close relationship between type 6 and cleft lip/palate syndrome, REKAS has been clinically proven, thus being an evidence-based matter; this gives some hope that the genetic background for this type of SD will be found in the near future (39,50). If so, perhaps it will be possible to change the constellation of those genes in the individuals carrying type 6 SD. This hypothetic removal of the “bad guys” from the organism presumably could dramatically change the incidence of this type of septal deformity in man, at the same time diminishing the possibilities of the onset of cleft lip/palate and REKAS (51).

It is extremely important to again stress that these two types (5 and 6) have nothing to do with trauma against the nose. This is crucial knowledge and should be kept in mind. Type 5 is a very posterior deformity that in many cases remains undiscovered during examination of the nose by simple anterior rhinoscopy. At least decongestion is needed to enable the doctor to see the deepest parts of the nasal cavity. Even then, a very deep septal spine can be overlooked because the mucosa of the turbinates and anterior parts of the septum itself just cover it.

In other words, only endoscopy of the nose is reliable in terms of proving the existence of type 5.

Type 6 is an extremely anterior deformity, “screaming from the nose”, and can be seen immediately after the nasal speculum opens the nostril. Therefore, a typical horizontal groove located between the septum and big, laterally protruding intermaxillary bone wing can by no means be overlooked. Neither can be the basal crest on the opposite side, located in the corresponding position of the groove. There are no data in the literature to prove that there are any signs of fracture, be it of the cartilage or the bone, in these two septal deformities. They belong to the developmental deformities determined by given factors, most probably by some gene sequences that are as yet unknown.

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Footnotes

 

Ethics Committee Approval: Ethics committee approval was received for this study.

Informed Consent: Written informed consent was obtained from patient who participated in this study.

Peer-review: Externally peer-reviewed.

Author contributions: Concept - R.M., N.S.; Design - N.S., G.P., M.Š.; Supervision - R.M., N.S.; Resource - G.P., M.Š.; Materials -R.M., N.S., G.P., M.Š.; Data Collection &/or Processing - R.M., N.S.; Analysis &/or Interpretation - R.M., N.S.; Literature Search - G.P., M.Š.; Writing - R.M., N.S.; Critical Reviews - R.M., N.S., G.P., M.Š.

Conflict of Interest: No conflict of interest was declared by the authors.

Editor-in-chief’s note: One of the authors of this article, Ranko Mladina is the member of the editorial advisory board ofBalkan Medical Journal. However, he did not take place at any stage on the editorial decision of the manuscript.

Financial Disclosure: The authors declared that this study has received no financial support.

 

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Articles from Balkan Medical Journal are provided here courtesy of Trakya University Faculty of Medicin

in normal sinus, the mucosa is not seen on CT, as well as in sinus endoscopy. In chronic cases the thickness varies with the time course and degree of local commitment.

Biomaterials such as phosphate tricalcium and bovine bone have proved to lead to high implant survival rates, comparable with implants placed in native bone avoiding the morbidity of harvesting a graft.

As already mentioned by Timo Weimar and Christian Zemlin, times have changed since the Initial phase of the MAZE III. Controls have become more strict, especially since the introduction of the event recorders and - not every MAZE IV is really performed completely, as described by J. Cox with the complete lesion set on the left and right side!

Dear Dr.

It is advised to continue warfarin for two months then depending on risk factors.

Best regards

Dr. Hyder O. Mirghani

What about cholchicine? It is recommended both in acute and chronic pericarditis and af suppression postoperatively.

https://my.americanheart.org/idc/groups/ahamah-public/@wcm/@sop/@scon/documents/downloadable/ucm_433742.pdf 

Dear DR Hazem ,thank you for your interesting question,   it is well known  that  Nitric oxide (NO) is present in very high concentrations in air derived from the para nasal airways. In contrast, only weak NO synthase activity was found in the epithelium of the nasal cavity (NO) . in humans  it  is produced by the axons   of  the   epithelial cells in the paranasal sinuses  ,  that(NO)  produced during T2R38 ACTIVATION AND THROUGH MULTIPLE CHEMICAL REACTIONS  LEADS TO INCREASE CILLIA BEATING . AS WILL (NO) IS  AHIGHLY REACTIVE RADICAL THAT CAN DIFFUSE INSIDE THE BACTERIA CELL AND DAMAGE BACTERIA DNA, MEMBRANE LIPIDS AND ENZYMES. IN VITRO(NO) WAS FOUND TO DIFFUSE TO SUERFACE LIQUIED  AND HAVE DIRECT BACTERICIDAL   EFFECT   AGANIST P. AERUGINOSA SO WE CAN CONCLUD THAT THE SINUS AIR PLY ROLE IN SINONASAL INNATE IMMUNITY  .

I think it is not the (angle) only, but also the points of contact between the septum and lateral nasal wall (at that site) have an effect.

I recently read the guidelines for treatment of acute bacterial sinusitis in Choosing wisely I found this a useful and sensible approach.

You may like to check this.

"Yes it can unfortunately!"

So do you have the reference for just one published case where the infection cannot be secondary to any leak of cranial fluids into the cranial air cavities?  If the infection was unilateral, an explanation needs to be provided for that fact.

E. jeanselmei may produce a wide spectrum of diseases including phaohyphomycosis (PHM), chromoblastomycosis (CBM), mycetoma and fungemia.

Histopathology is crucial to separate CBM from PHM and mycetoma. When causing CBM. E, jeanselmei  produces muriform cells (sclerotic bodies). If causing PHM, septated pigmented hyphae, toruloid hyphae, vesicular fungal elements, etc. E. jeanselmei produces peculiar eumycetoma grains.

Thanks much Dr. Vincent for your sharing. Are there any recent experience in your institute regarding steroid nasal irrigation & what is the protocol of use & outcome?

Dear Matti,

I suggest all participants to read our paper: Mladina R, Skitarelić N, Casale M. Two holes syndrome (THS) is present in more than half of the postnasal drip patients? Acta Otolaryngol 2010;130:1274-1277.

Type 2 and 3 are clear however type 1 isnot . I don't think bolger ey al clearly defined this type. I consider adult patients with maxillary sinus floor above nasal cavity floor as type 1 , I need a reference to support this

RS should be classified in to acute and chronic varieties and subclassified in to types, if the patient has anotomical defects like DNS etc.. or if patient has polyposis/PAR etc..

Which helps in planning the treatment.

Whilst there is general agreement that 90% of objective halitosis cases are related to conditions in the mouth, notably odorigenic biofilm on the posterior dorsal tongue and gingivitis/periodontitis, the epidemiology of the remaining 10% of cases which are related to extra-oral pathoses is unclear. There are widely divergent reports in the literature, some groups say upper respiratory tract pathology accounts for most cases of extra-oral halitosis, particularly xerostomia secondary to nasal obstruction and mouth breathing (in children) and chronic caseous tonsillitis/tonsillolithiasis (tonsil stones). Other groups state that the blood borne halitosis mechanism is the most important extra-oral cause of halitosis, related to pulmonary excretion of odorant volatiles during gas exchange in association with various systemic conditions.

The reasons for this lack of clarity are manifold, but likely relate to a lack of scientific consensus as to how to define, classify, diagnose, quantify and manage the halitosis symptom. Consequently there is variation in the methodology from one publication to the next. Chronic rhinosinusitis is commonly cited as a cause of halitosis in the literature, and even forms a minor diagnostic criterion in some schemes, but it is impossible to determine with any level of certainty what proportion of halitosis cases are attributable to CRS.

The mechanism of halitosis in rhinosinusitis is also unclear. I have proposed in a publication the possible mechanisms:

"Stasis and stagnation of secretions, the result of mucosal inflammation which obstructs drainage, will likely be associated with increased bacterial load. Consequently, increased volatile sulfur compound (VSC) release may occur, along with other volatiles. In purulent sinusitis, the presence of pus may contribute to the malodor, particularly if anaerobic bacteria predominate in the infection. The so called post nasal drip syndrome is postulated to be caused by sinusitis among other things, and it is said to be a cause of halitosis in addition. In post nasal drip, mucus drains onto the posterior dorsal tongue via the nasopharynx.[51] However, it has been argued that nasal mucus dripping down the back of the throat occurs in normal, healthy people, and furthermore there are no pathologic or biochemical tests for this condition.[52] Also, the relationship between post nasal drip and halitosis has not been formally investigated. Some have suggested that obstructive nasal pathology can cause mouth breathing, which results in oral malodor (intra-oral halitosis) secondary to xerostomia.[53][54] Xerostomia reduces the mechanical cleansing and antimicrobial action of saliva and results in a sharp increase in bacterial growth in the mouth. The higher the bacterial load, the more VSC are released during bacterial putrefaction. The nasal congestion which accompanies sinusitis is readily imagined as a cause of nasal obstruction. However, to contradict this possible mechanism, others report that mouth breathing is not associated with halitosis.[55] On the other hand, subjective halitosis (odor perceived only by the patient) could be explained by dysosmia, retronasal olfaction, or a foul taste caused by posterior nasal discharge."

To confirm if halitosis comes from the upper respiratory tract, smell the patients nose breath with their mouth closed, and then second smell their mouth breath with their nose occluded. Sinonasal origin of halitosis is said to be more strongly detectable on the nose breath but in practice this is not reliable.

To my knowledge there is no research available which investigated the efficacy of nasal irrigation as a method to treat halitosis. If there is a surgically correctable defect such as deviated nasal septum sometimes ENT surgery is reported to resolve halitosis.

If I find any evidence I will update - Nov 2013

Amoxicillin 40-50 mg/kg and or 80-90 mg/kg for 2-3weeks and 4-6 weeks respectively in child and adult.

Fungal sinusitis is not always due to aspergillosis and not treated with iatroconazole alone. The options for post operative care would depend on the invasivenesss of the fungus,it's sensitivity, the immune status of the patient (AFRS or otherwise), and the completeness of resection in the inaccessable area. Indeed, mucormycosis is different fron AFRS. Iatroconazole, voriconazole and ampotericin B are used . The options for post op care would vary from steroid therapy to ampotericin B as the need dictates. We cannot treat all "polyps" with fungal sinusitis as one.