a.

Practice Essentials
Sinusitis is characterized by inflammation of the lining of the paranasal sinuses.
Because the nasal mucosa is simultaneously involved and because sinusitis rarely
occurs without concurrent rhinitis, rhinosinusitis is now the preferred term for this
condition. Rhinosinusitis affects an estimated 35 million people per year in the
United States and accounts for close to 16 million office visits per year. [1] See the
image below.

Translate
Sinusitis ditandai oleh peradangan pada lapisan sinus paranasal. Karena mukosa
hidung terlibat secara simultan dan karena sinusitis jarang terjadi tanpa rinitis
bersamaan, rinosinusitis sekarang menjadi istilah yang lebih disukai untuk kondisi
ini. Rhinosinusitis mempengaruhi sekitar 35 juta orang per tahun di Amerika
Serikat dan menyumbang hampir 16 juta kunjungan kantor per tahun. [1] Lihat
gambar di bawah ini.
Anatomi
To properly diagnose and treat infectious disorders of the paranasal sinuses, the
clinician should have knowledge of the developmental milestones. The
development of the paranasal sinuses begins in the third week of gestation and
continues until early adulthood.
Development of paranasal sinuses
During the third week of embryonic development, proliferation and medial
migration of ectodermal cells form the notochord. After the heart tube and
pericardium have rotated from the cranial position to lie anteriorly, the notochord,
which is initially in the caudal region of the embryonic disc, rotates to lie posterior
to the primitive foregut. The paraxial layer of mesenchyme, which lies adjacent to
the notochord, differentiates into the somite ridges, intermediate cell mass, and
lateral plate mesoderm. From these mesodermal structures, the branchial arches
develop, the first of which gives rise to internal nasal structures.
The paranasal sinuses develop in conjunction with the palate from changes in the
lateral wall of the nasal cavity. At 40 weeks' gestation, 2 horizontal grooves
develop in the mesenchyme of the lateral wall of the nasal cavity. Proliferation of
maxilloturbinate mesenchyme between these grooves results in an outpouching of
tissue medially into the nasal lumen. This outpouching is the precursor of the
middle and inferior meatus as well as the inferior turbinate. Ethmoidoturbinate
folds develop superiorly to give rise to the middle and superior turbinates. Once
the turbinate structures are established, sinus development begins and continues
until early adult life.
The sinuses open into the nose via small openings called ostia. [5] The maxillary
and ethmoid sinuses form at 3-4 months' gestation. Thus, an infant is born with 3-
4 ethmoid cells and tiny teardrop-shaped maxillary sinuses. By the teenage years,
each maxillary sinus progressively enlarges to an adult capacity of 15 mL. In
healthy individuals, the ethmoid sinuses increase in number to 18-20, and each
drains by an individual ostium that is 1-2 mm in diameter.
The frontal sinus develops from an anterior ethmoid cell and moves to its
supraorbital position when the individual is aged 6-7 years. Frontal sinuses may
begin to develop at this age but usually do not appear radiologically until the
individual is aged approximately 12 years. The maxillary, anterior ethmoid, and
frontal sinuses drain into the middle meatus; the posterior ethmoid and sphenoid
sinuses drain into the superior meatus (see the image below).
 Sagittal section of the
lateral nasal wall demonstrating openings of paranasal sinuses. Conchae have
been cut to depict details of meatal structures.
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Structure and function of paranasal sinuses
The paranasal sinuses are air-filled bony cavities that extend from the skull base to
the alveolar process and laterally from the nasal cavity to the inferomedial aspect
of the orbit and the zygoma. The sinus cavities are lined with pseudostratified,
ciliated, columnar epithelium that is contiguous, via ostia, with the lining of the
nasal cavity. This epithelium contains a number of mucus-producing goblet cells.
These goblet cells in the epithelium and the submucosal seromucous glands
contribute to the airway surface liquid, [7] which is 5-100 μm thick and covers the
epithelium.
Anterior and posterior ethmoid sinuses are composed of multiple air cells
separated by thin bony partitions. Each cell is drained by an independent ostium
that measures only 1-2 mm in diameter. These small openings are readily clogged
by secretions or are occluded by swelling of the nasal mucosa. The sphenoid
sinuses sit immediately anterior to the pituitary fossa and just behind the posterior
ethmoid.
The arterial supply of the paranasal sinuses is from branches of the internal and
external carotid arteries, while the venous and lymphatic drainage path is through
the sinus ostia into the nasal cavity plexus. In addition, venous drainage occurs
through valveless vessels corresponding to the arterial supply.
All sinus ostia drain into the nares at locations beneath the middle and superior
turbinates. The posterior ethmoid and sphenoid sinuses drain into the superior
meatus below the superior turbinate. The ostia of the maxillary, anterior ethmoid,
and frontal sinuses share a common site of drainage within the middle meatus.
This region is called the ostiomeatal complex and can be visualized by coronal CT
scan. The common drainage pathway of the frontal, maxillary, and anterior
ethmoid sinuses within the middle meatus allows relatively localized mucosal
infection processes to promote infection in all these sinuses.
The successful maintenance of sinus drainage represents a complicated interaction
between ciliary action, mucus viscosity, size of sinus ostia, and orientation of
body structures. Ciliary beat at the rate of 8-15 Hz is continuously moved by the
cilia at a speed of 6 mm/min. The ciliary action can be affected due to local
factors, such as infection and local hypoxia that is associated with complete
occlusion of sinus ostia. The sinus mucosa has less secretory and vasomotor
function than the nasal cavity does. Cilia are concentrated near and beat toward
the natural sinus ostia. Blockage of the ostium results in stasis of mucous flow,
which can lead to development of disease.
The exact function of the paranasal sinuses is not well understood. The possible
roles of the sinuses may include reducing the weight of the skull; dampening
pressure; humidifying and warming inspired air; absorbing heat and insulating the
brain; aiding in sound resonance; providing mechanical rigidity; and increasing
the olfactory surface area.
Translate
Anatomi
Untuk mendiagnosis dan mengobati gangguan infeksi sinus paranasal dengan
benar, dokter harus memiliki pengetahuan tentang tonggak perkembangan.
Perkembangan sinus paranasal dimulai pada minggu ketiga kehamilan dan
berlanjut sampai dewasa awa
prognosis
Sinusitis does not cause any significant mortality by itself. However, complicated
sinusitis may lead to morbidity and, in rare cases, mortality.
Approximately 40% of acute sinusitis cases resolve spontaneously without
antibiotics. The spontaneous cure for viral sinusitis is 98%. Patients with acute
sinusitis, when treated with appropriate antibiotics, usually show prompt
improvement. The relapse rate after successful treatment is less than 5%.
In the absence of response within 48 hours or worsening of symptoms, reevaluate
the patient. Untreated or inadequately treated rhinosinusitis may lead to
complications such as meningitis, cavernous sinus thrombophlebitis, orbital
cellulitis or abscess, and brain abscess.
In patients with allergic rhinitis, aggressive treatment of nasal symptoms and signs
of mucosal edema, which can cause obstruction of the sinus outflow tracts, may
decrease secondary sinusitis. If the adenoids are chronically infected, removing
them eliminates a nidus of infection and can decrease sinus infection.
translate
Sinusitis tidak menyebabkan kematian yang signifikan dengan sendirinya.
Namun, sinusitis yang rumit dapat menyebabkan morbiditas dan, dalam kasus
yang jarang terjadi, kematian.

patofisiologi
The sinuses are normally sterile under physiologic conditions. Secretions
produced in the sinuses flow by ciliary action through the ostia and drain into the
nasal cavity. In the healthy individual, flow of sinus secretions is always
unidirectional (ie, toward the ostia), which prevents back contamination of the
sinuses. In most individuals, the maxillary sinus has a single ostium (2.5 mm in
diameter, 5 mm2 in cross-sectional area) serving as the only outflow tract for
drainage. This slender conduit sits high on the medial wall of the sinus cavity in a
nondependent position. Most likely, the edema of the mucosa at these 1- to 3-mm
openings becomes congested by some means (eg, allergy, viruses, chemical
irritation) that causes obstruction of the outflow tract stasis of secretions with
negative pressure, leading to infection by bacteria.
Retained mucus, when infected, leads to sinusitis. Another mechanism
hypothesizes that because the sinuses are continuous with the nasal cavity,
colonized bacteria in the nasopharynx may contaminate the otherwise sterile
sinuses. These bacteria are usually removed by mucociliary clearance; thus, if
mucociliary clearance is altered, bacteria may be inoculated and infection may
occur, leading to sinusitis
The pathophysiology of rhinosinusitis is related to 3 factors:
  Obstruction of sinus drainage pathways (sinus ostia)
 Ciliary impairment
 Altered mucus quantity and quality
Obstruction of sinus drainage
bstruction of the natural sinus ostia prevents normal mucus drainage. The
ostia can be blocked by mucosal swelling or local causes (eg, trauma, rhinitis), as
well as by certain inflammation-associated systemic disorders and immune
disorders. Systemic diseases that result in decreased mucociliary clearance,
including cystic fibrosis, respiratory allergies, and primary ciliary dyskinesia
(Kartagener syndrome), can be predisposing factors for acute sinusitis in rare
cases. Patients with immunodeficiencies (eg, agammaglobulinemia, combined
variable immunodeficiency, and immunodeficiency with reduced
immunoglobulin G [IgG]– and immunoglobulin A [IgA]–bearing cells) are also
at increased risk of developing acute sinusitis.
Mechanical obstruction because of nasal polyps, foreign bodies, deviated
septa, or tumors can also lead to ostial blockage. In particular, anatomical
variations that narrow the ostiomeatal complex, including septal deviation,
paradoxical middle turbinates, and Haller cells, make this area more sensitive to
obstruction from mucosal inflammation. Usually, the margins of the edematous
mucosa have a scalloped appearance, but in severe cases, mucus may completely
fill a sinus, making it difficult to distinguish an allergic process from infectious
sinusitis. Characteristically, all of the paranasal sinuses are affected and the
adjacent nasal turbinates are swollen. Air-fluid levels and bone erosion are not
features of uncomplicated allergic sinusitis; however, swollen mucosa in a poorly
draining sinus is more susceptible to secondary bacterial infection.
impaired ciliary function
Contrary to earlier models of sinus physiology, the drainage patterns of the
paranasal sinuses depend not on gravity but on the mucociliary transport
mechanism. The metachronous coordination of the ciliated columnar epithelial
cells propels the sinus contents toward the natural sinus ostia. Any disruption of
the ciliary function results in fluid accumulation within the sinus. Poor ciliary
function can result from the loss of ciliated epithelial cells; high airflow; viral,
bacterial, or environmental ciliotoxins; inflammatory mediators; contact between
2 mucosal surfaces; scars; and Kartagener syndrome.
Ciliary action can be affected by genetic factors, such as Kartagener syndrome.
Kartagener syndrome is associated with immobile cilia and hence the retention of
secretions and predisposition to sinus infection. Ciliary function is also reduced in the
presence of low pH, anoxia, cigarette smoke, chemical toxins, dehydration, and drugs
(eg, anticholinergic medications and antihistamines).

Exposure to bacterial toxins can also reduce ciliary function. Approximately 10%
of cases of acute sinusitis result from direct inoculation of the sinus with a large
amount of bacteria. Dental abscesses or procedures that result in communication
between the oral cavity and sinus can produce sinusitis by this mechanism.
Additionally, ciliary action can be affected after certain viral infections.
Several other factors can lead to impaired ciliary function. Cold air is said
to stun the ciliary epithelium, leading to impaired ciliary movement and retention
of secretions in the sinus cavities. On the contrary, inhaling dry air desiccates the
sinus mucous coat, leading to reduced secretions. Any mass lesion with the nasal
air passages and sinuses, such as polyps, foreign bodies, tumors, and mucosal
swelling from rhinitis, may block the ostia and predispose to retained secretions
and subsequent infection. Facial trauma or large inoculations from swimming can
produce sinusitis as well. Drinking alcohol can also cause nasal and sinus mucosa
to swell and cause impairment of mucous drainage.
Altered quality and quantity of mucus
Sinonasal secretions play an important role in the pathophysiology of
rhinosinusitis. The mucous blanket that lines the paranasal sinuses contains
mucoglycoproteins, immunoglobulins, and inflammatory cells. It consists of 2
layers: (1) an inner serous layer (ie, sol phase) in which cilia recover from their
active beat and (2) an outer, more viscous layer (ie, gel phase), which is
transported by the ciliary beat. Proper balance between the inner sol phase and
outer gel phase is of critical importance for normal mucociliary clearance.
If the composition of mucus is changed, so that the mucus produced is
more viscous (eg, as in cystic fibrosis), transport toward the ostia considerably
slows, and the gel layer becomes demonstrably thicker. This results in a
collection of thick mucus that is retained in the sinus for varying periods. In the
presence of a lack of secretions or a loss of humidity at the surface that cannot be
compensated for by mucous glands or goblet cells, the mucus becomes
increasingly viscous, and the sol phase may become extremely thin, thus allowing
the gel phase to have intense contact with the cilia and impede their action.
Overproduction of mucus can overwhelm the mucociliary clearance system,
resulting in retained secretions within the sinuses.

Translate
Sinus biasanya steril dalam kondisi fisiologis. Sekresi yang dihasilkan dalam
sinus mengalir melalui aksi silia melalui ostia dan mengalir ke rongga hidung.
Pada individu yang sehat, aliran sekresi sinus selalu searah (yaitu, menuju ostia),
yang mencegah kontaminasi kembali sinus. Pada kebanyakan individu, sinus
maksilaris memiliki ostium tunggal (diameter 2,5 mm, 5 mm2 di area
penampang) yang berfungsi sebagai satu-satunya saluran keluar untuk drainase.
Saluran ramping ini terletak tinggi di dinding medial rongga sinus dalam posisi
tidak tergantung. Kemungkinan besar, edema mukosa pada bukaan 1 - 3 mm ini
menjadi padat dengan beberapa cara (misalnya, alergi, virus, iritasi kimia) yang
menyebabkan penyumbatan pada saluran keluarnya aliran sekresi dengan tekanan
negatif, yang menyebabkan infeksi oleh bakteri.

Dipertahankan lendir , ketika terinfeksi , mengarah ke sinusitis

.Mekanisme lain hypothesizes sinus adalah, akibat praktik terus-menerus dengan
rongga hidung , dijajah bakteri dalam nasofaring dapat mengkontaminasi
sebaliknya sinus steril .Bakteri-bakteri ini biasanya dihapus oleh kliring
mucociliary; dengan demikian , jika kliring mucociliary diubah , bakteri mungkin
diinokulasi dan infeksi dapat terjadi , mengarah ke sinusitis

dari rhinosinusitis yang pathophysiology ini terkait dengan 3 faktor itu,

terhalangnya sinus di tengah pemukiman ( sinus ostia ) drainase ciliary kuantitas
dan kualitas gangguan diubah lender

obstruksi drainase sinus

obstruksi sinus ostia alami mencegah drainase lendir normal. Ostia dapat
tersumbat oleh pembengkakan mukosa atau penyebab lokal (misalnya, trauma,
rinitis), serta oleh gangguan sistemik terkait peradangan dan gangguan imun
tertentu. Penyakit sistemik yang mengakibatkan penurunan pembersihan
mukosiliar, termasuk fibrosis kistik, alergi pernapasan, dan diskinesia silia primer
(sindrom Kartagener), dapat menjadi faktor predisposisi untuk sinusitis akut pada
kasus yang jarang terjadi. Pasien dengan defisiensi imun (misalnya
agammaglobulinemia, defisiensi variabel imunodefisiensi gabungan, dan
defisiensi imunodefisiensi dengan penurunan imunoglobulin G [IgG] - dan sel
yang mengandung imunoglobulin A [IgA]) juga berisiko tinggi mengalami
sinusitis akut.
Obstruksi mekanik karena polip hidung, benda asing, septa menyimpang,
atau tumor juga dapat menyebabkan penyumbatan ostial. Secara khusus, variasi
anatomi yang mempersempit kompleks ostiomeatal, termasuk deviasi septum,
turbinat tengah paradoks, dan sel Haller, membuat area ini lebih sensitif terhadap
obstruksi dari peradangan mukosa. Biasanya, margin mukosa edematous memiliki
penampilan yang bergigi, tetapi dalam kasus yang parah, lendir dapat sepenuhnya
mengisi sinus, sehingga sulit untuk membedakan proses alergi dari sinusitis
infeksius. Secara karakteristik, semua sinus paranasal terpengaruh dan turbinat
hidung yang berdekatan membengkak. Tingkat cairan udara dan erosi tulang
bukan merupakan ciri dari sinusitis alergi yang tidak rumit; Namun, mukosa yang
bengkak pada sinus dengan drainase buruk lebih rentan terhadap infeksi bakteri
sekunder.

Gangguan fungsi silia

Berlawanan dengan model fisiologi sinus sebelumnya, pola drainase sinus

paranasal tidak tergantung pada gravitasi tetapi pada mekanisme transportasi
mukosiliar. Koordinasi metachronous dari sel epitel kolumnar bersilia mendorong
isi sinus menuju ostia sinus alami. Gangguan fungsi silia menyebabkan akumulasi
cairan di dalam sinus. Fungsi siliaris yang buruk dapat disebabkan oleh hilangnya
sel epitel bersilia; aliran udara yang tinggi; ciliotoxins virus, bakteri, atau
lingkungan; mediator inflamasi; kontak antara 2 permukaan mukosa; bekas luka;
dan sindrom Kartagener.

Tindakan siliaris dapat dipengaruhi oleh faktor genetik, seperti sindrom

Kartagener. Sindrom Kartagener dikaitkan dengan silia imobil dan karenanya
retensi sekresi dan kecenderungan infeksi sinus. Fungsi siliaris juga berkurang
dengan adanya pH rendah, anoksia, asap rokok, racun kimia, dehidrasi, dan obat-
obatan (misalnya, obat antikolinergik dan antihistamin).

Paparan racun bakteri juga bisa mengurangi fungsi silia. Sekitar 10%
kasus sinusitis akut terjadi akibat inokulasi langsung sinus dengan sejumlah besar
bakteri. Abses atau prosedur gigi yang menghasilkan komunikasi antara rongga
mulut dan sinus dapat menghasilkan sinusitis dengan mekanisme ini. Selain itu,
aksi silia dapat dipengaruhi setelah infeksi virus tertentu.

Beberapa faktor lain dapat menyebabkan gangguan fungsi silia. Udara

dingin dikatakan membuat pingsan epitel silia, yang menyebabkan gangguan
gerakan silia dan retensi sekresi di rongga sinus. Sebaliknya, menghirup udara
kering mengeringkan lapisan lendir sinus, yang menyebabkan berkurangnya
sekresi. Setiap lesi massa dengan saluran udara hidung dan sinus, seperti polip,
benda asing, tumor, dan pembengkakan mukosa akibat rinitis, dapat menghalangi
ostia dan cenderung menjadi sekresi yang tertahan dan infeksi berikutnya. Trauma
wajah atau inokulasi besar dari berenang dapat menghasilkan sinusitis juga.
Minum alkohol juga dapat menyebabkan mukosa hidung dan sinus membengkak
dan menyebabkan penurunan drainase mukosa.

Kualitas dan kuantitas lendir yang berubah

Sekresi sinonasal memainkan peran penting dalam patofisiologi

rinosinusitis. Selimut lendir yang melapisi sinus paranasal mengandung
mucoglikoprotein, imunoglobulin, dan sel-sel inflamasi. Ini terdiri dari 2 lapisan:
(1) lapisan serosa bagian dalam (yaitu, fase sol) di mana silia pulih dari denyut
aktifnya dan (2) lapisan luar, yang lebih kental (yaitu, fase gel), yang diangkut
oleh siliaris mengalahkan. Keseimbangan yang tepat antara fase sol dalam dan
fase gel luar sangat penting untuk pembersihan mukosiliar normal.
 Jika komposisi lendir berubah, sehingga lendir yang dihasilkan lebih
kental (misalnya, seperti pada cystic fibrosis), transportasi menuju ostia jauh lebih
lambat, dan lapisan gel menjadi lebih tebal. Ini menghasilkan kumpulan lendir
kental yang tertahan di sinus untuk berbagai periode. Di hadapan kurangnya
sekresi atau hilangnya kelembaban pada permukaan yang tidak dapat
dikompensasi oleh kelenjar lendir atau sel piala, lendir menjadi semakin kental,
dan fase sol mungkin menjadi sangat tipis, sehingga memungkinkan fase gel
untuk memiliki kontak intens dengan silia dan menghambat tindakan mereka.
Kelebihan produksi lendir dapat membanjiri sistem pembersihan mukosiliar,
menghasilkan sekresi yang tertahan di dalam sinus.