Pemicu 2 Blok Respirasi

Oleh : Dhiya Lathifa Rasyid (405140236)

Learning Objective
1. 3M Anatomi Histologi fisiologi Hidung luar, dalam, sinus paranasal
2. 3M Sistem Imun Hidung
3. 3M kelainan di hidung luar
4. 3M kelainan di hidung dalam dan salurannya
5. 3M kelainan di sinus paranasalis
3M Anatomi Histologi fisiologi Hidung luar, dalam,
sinus paranasal
Anatomi
Histologi

A. Nasal Cavity
1. Respiratory Region
The respiratory region is lined by respiratory (pseudostratified ciliated
columnar) epithelium.
The subepithelial
• connective tissue is richly vascularized and possesses seromucous glands.
2. Olfactory Region
• The epithelium of the olfactory region is thick, pseudostratified ciliated
columnar epithelium composed of three cell types: basal cell,
sustentacular cells, and olfactory cells. The lamina propria is richly
vascularized and possesses
• Bowman’s glands, which produce a watery mucus
Respiratory Epithelium
- Most of the nasal cavities and the respiratory system’s conducting portion is lined with mucosa
• Having ciliated pseudostratified columnar epithelium,
• This epithelium has five major cell types, all of which contact an unusually thick basement
membrane:
• Ciliated columnar cells are the most abundant, each with 250-300 cilia on its apical
surface
• Goblet cells are also numerous and predominate in some areas with basal nuclei and
apical domains filled with granules of mucin glycoproteins.
• Brush cells are a much less numerous, columnar cell type, in which a small apical surface
bears sparse, blunt microvilli Brush cells are chemosensory receptors
resemblinggustatory cells, with similar signal transduction components and synaptic
contact with afferentnerve endings on their basal surfaces.
• Small granule cells (or Kulchitsky cells) are difficult to distinguish in routine preparations,
butpossess numerous dense core granules 100 to 300 nm in diameter. Like
enteroendocrine cells ofthe gut, they are part of the diffuse neuroendocrine system Like
brushcells, they represent only about 3% of the cells in respiratory epithelium.
• Basal cells are mitotically active stem and progenitor cells that give rise to the other
epithelial celltypes.
• The olfactory chemoreceptors for the sense of smell are located in
the olfactory epithelium,
• a specialized region of the mucous membrane covering the superior
conchae at the roof of the nasal cavity.
• In adult humans, it is about 10 cm2 in area and up to 100 Ām in
thickness. This thick,pseudostratified columnar epithelium has three
major cell types
• Olfactory neurons are bipolar neurons present throughout this epithelium. Their nuclei form
anirregular row near the middle of this thick epithelium. The apical (luminal) pole of
eacholfactory cell is its dendrite end and has a knoblike swelling with about a dozen basal
bodies.From the basal bodies emerge long cilia with nonmotile axonemes but considerable
surface areasfor membrane chemoreceptors. These receptors respond to odoriferous substances
by generatingan action potential along the axons extending from the basal ends of these neurons.
The axonsleave the epithelium and unite in the lamina propria as very small nerves that then pass
to thebrain through foramina in the cribriform plate of the ethmoid bone There theyform the
olfactory nerve, cranial nerve I, and eventually synapse with other neurons in theolfactory bulb.
• Supporting cells are columnar, with broad, cylindrical apexes containing the nuclei and
narrowerbases. On their free surface are microvilli submerged in a fluid layer. Well-developed
junctionalcomplexes bind the supporting cells to the olfactory cells. The supportive role of these
cells isnot well understood, but they express abundant ion channels that help maintain
amicroenvironment conducive to olfactory function and survival.
• Basal cells are small, spherical or cone-shaped cells near the basal lamina. These are the stem
cellsfor the other two types, replacing the olfactory neurons every 2 to 3 months and support
cells lessfrequently.
• Paranasal Sinuses are bilateral cavities in the frontal, maxillary,
ethmoid, and sphenoid bones ofthe They are lined with a thinner
respiratory epithelium with fewer goblet cells.The lamina propria
contains only a few small glands and is continuous with the
underlyingperiosteum. The paranasal sinuses communicate with the
nasal cavities through small openings;mucus produced there is moved
into the nasal passages by the activity of the ciliated epithelial cells.
Fisiologi

The nose acts as an air conditioning unit and performs three functions:
- humidification
- heat transfer
- filtration.
- The nose protects the lower airway by removing particles down to approximately 30 mm, including most pollens from the inspired
air.
- The shape and roughness of smaller particles may cause them to be deposited in the nose.
Inspired air travels through 1801 and velocity drops
markedly just after the nasal valve.
- Turbulence increases
deposition of particles.
- Particles in motion will tend to
carry on in the same direction: the larger the mass the
greater the tendency.
- Resistance to change in velocity is
greater in irregular particles because of the larger surface
area and the number of facets.
- Vibrissae will only stop the
largest particles.
Nasal secretions
- Nasal secretions are composed of two elements, mucus and water
- Glycoproteins are produced by the mucus glands and the water and
ions are produced mainly from the serous glands
- There are also two secretory cell types in the mixed nasal glands,
mucus and serous cells
- Glycoproteins found in mucus are produced in two cell types, the
goblet cells within the epithelium and the glandular mucus cells
- Glandular mucus and goblet cells contain large electron-lucent
secretory granules, containing acidic glycoproteins
- Serous cells contain discrete electron dense granules. They contain
neutral glycoproteins, enzymes such as lysozymes and lactoferrin as
well as immunoglobulins of the IgA2 subclass
Composition of mucus
- water and ions from transudation;
- glycoproteins: sialomucins, fucomucins, sulphomucins;
- enzymes: lysozymes, lactoferrin;
- circulatory proteins: complement, a2-macroglobulin,
- C reactive; protein;
- immunoglobulins: IgA, IgE, IgG, IgM, IgD;
- cells: surface epithelium, basophils, eosinophils,
- leukocytes.
LO 2 : 3M Sistem Imun Hidung

Nonspecific immunity
• Lactoferrin, lysozymes, complement, antiproteases andother
macromolecules interact with a number of bacteria,particularly those
without capsules, to give an innate nonspecific immunity. Polymorph
leukocytes and macrophagesphagocytose and destroy foreign
material. Many organisms and viruses are resistant and so
specificreactions are required.
Acquired immunity
IgG (except IgG4 subgroup) activates complement resultingin cell lysis
and phagocytosis. Viruses and mycobacteria initiate cell-mediated
immunity. IgA is divided into two subgroups: IgA1 and IgA2. IgA1 is
more frequentin the serum and is a monomer, IgA2 is more common in
nasal secretions and is a dimer. IgA accounts for up to
Allergy: basic mechanisms and tests

• Atopy refers to a predisposition to develop exaggerated

immunoglobulin E (IgE)-antibody responses against common inhaled
aeroallergens
• Atopy is defined clinically as a positive skin prick test and/or elevated
serum allergen-specific IgE concentration to one or more common
inhaled allergens, such as grass pollen, cat hair or house dust mite
(HDM).
AETIOLOGY
• Allergic diseases result from a complex interaction between genetic
and environmental influences
INFLUENCE OF TREATMENT
Antihistamines
Topical corticosteroids
Allergen injection immunotherapy
LO 3 : 3M kelainan di hidung luar
• The plethora of techniques for septal perforation repair described over the years attest to the fact
that there is still a challenging technical problem for the nasal surgeon, although reliable surgical
techniques with good outcomes have been published in the last 15 years. The variety of repairs
may be classified as:
free grafts:
– simple or composite autografts;
– allografts;
pedicled flaps:
– local nasal mucosal;
– buccal mucosal;
– composite septal cartilage and mucosa;
– composite skin/cartilage;
rotation/advancement of mucoperichondrial or
mucoperiosteal flaps.
Nasal fractures
A five-point grading system has been developed for the extent of lateral deviation
of the nasal pyramid:
• grade 0: bones perfectly straight;
• grade 1: bones deviated less than half of the width of
• the bridge of the nose;
• grade 2: bones deviated half to one full width of the
• bridge of the nose;
• grade 3: bones deviated greater than one full width of
• the bridge of the nose;
• grade 4: bones almost touching the cheek.
 details of how the injury was sustained;
• nasal obstruction;
• change in appearance;
• epistaxis;
• hyposmia;
• watery rhinorrhoea;
• visual disturbance;
• diplopia;
• epiphora;
• altered bite;
• loose teeth;
• trismus.
Treatment
• large number of patients will have a preexisting nasal deformity
caused by a previous incident. Manipulation of the nose will, at best,
only return it to its most recent appearance. Patients that fall into this
category are probably better advised to consider a formal rhinoplasty
• when everything has settled down some months later
LO 4 : 3M kelainan di hidung dalam dan salurannya
Allergic rhinitis
• Rhinitis is defined clinically by a combination of two or
• more nasal symptoms: running, blocking, itching and
• sneezing. Allergic rhinitis occurs when these symptoms
• are the result of IgE-mediated inflammation following
• exposure to allergen.
• Genetics and family history There is undoubtedly a genetic
component in allergic rhinitis, as in other allergic disease.6 The best
established
• risk factor for allergic rhinitis is a family history of allergy,especially of
allergic rhinitis.
• Seasonal allergic rhinitis increases the risk of asthma significantly on
the basis of analysis of all individuals and
• of discordant twin pairs.
• The genetics of rhinitis has not been studied as much as that of
asthma and atopy
• Rhinitis is more common in developed countries and increases in
Many possible factors have been suggested, such as lifestyle
changes,increased exposure to allergen, pollution and irritants,dietary
modifications responsible for diminution of protective nutrients,
decrease in infections, leading to a reduction in Th1-type immune
response (the hygiene hypothesis) and stress.
• Although not a severe disorder, allergic rhinitis significantly alters
patients’ social life, affects learning performanceat school and work
productivity.
• Other conditions associated with allergic rhinitis are asthma, sinusitis,
otitis media, sleep disorders, lower respiratory tract infection and
dental occlusion
• Rhinitis and asthma are linked by epidemiological, pathophysiological
characteristics and by a common therapeutic approach
• patients with persistent allergic rhinitis should be evaluated for
asthma
• AETIOLOGY:
• This is complex, involving cells, mediators, cytokines, chemokines,
neuropetides and adhesion molecules which cooperate in a complex
network to produce the specific symptoms of allergic rhinitis and the
nonspecific hyperreactivity.The reaction can be considered in four
phases
1. sensitization;
2. subsequent reaction to allergen – early phase;
3. late phase reaction;
4. systemic activation
• Most allergic rhinitis patients can be diagnosed by acombination of
history, examination and SPT or radioallergoabsorbent tests (RAST) for
specific IgE.
• Occasionally,other tests may be necessary History taking should be
thorough and may be aided by the use of a questionnaire. Presenting
symptoms,symptoms of co-morbidities and general medical
history,past history and family history, occupational and
environmental exposure, dietary history and drug use
Treatment
• Management of allergic rhinitis includes allergen avoidance,
pharmacotherapy, education and possibly immunotherapy.
• Surgery is rarely needed. Treatment strategies should involve both the
upper and lower airway where the latter is also affected.
• Pharmacotherapy
ANTIHISTAMINES
• These rapidly relieve running, itching and sneezing, but have little or
no effect on blockage although there are
• recent exceptions (desloratadine, levocetirizine) First-generation
antihistamines, such as chlorphenarimine and diphenhydramine,
should be avoided because of sedation, psychomotor retardation and
learning impairment which probably occur because the drugs cross
the blood–brain barrier and interact with central histamine receptors.
TOPICAL GLUCOCORTICOSTEROIDS
• These are the most effective treatment for rhinitis,especially if started
prior to allergen exposure. Regular treatment is necessary. Side
effects are minor and include epistaxis and nasal irritation in 5–10
percent of patients.
• Nasal steroids reduce inflammation and consequent hyperreactivity,
reduce nasal symptoms, eye symptoms and improve the sense of
smell. Their onset of action is slow with some improvement after 6–
12 hours and maximum effects occurring only after several days
SODIUM CROMOGLICATE
• This spray is weakly effective against all rhinitis symptoms, but needs
to be used three to four times daily
• and this limits compliance. Its safety means that it is useful for small
children (less than four years) for whom a
• topical corticosteroid is not available
DECONGESTANTS
• Used topically, these reduce nasal obstruction, but increase
rhinorrhoea. Regular use for more than a few days can result in
rhinitis medicamentosa
• Systemic decongestants are relatively ineffective and have side effects
such as hyperactivity and insomnia in children and hypertension in
adults
IPRATROPIUM BROMIDE
• This atropine-like nasal spray is useful against watery
• rhinorrhoea and may, if regularly used, be curative.104
• Occasionally it is helpful in patients with allergic
• rhinitis who do not respond to topical corticosteroids alone.
• Side effects can include worsening ofglaucoma or prostatism and dry
mouth and eyes.
SYSTEMIC CORTICOSTEROIDS
• These can be used to unblock the nose at the start of treatment or
provided for very severe symptoms during the hayfever season.
• Regular use is associated with significant systemic side effects and
therefore only occasional intermittent use for a few days at a time is
sensible.
• They should be combined with topical corticosteroid and the usual
precautions apply
ANTILEUKOTRIENES
• Leukotriene receptor antagonists have recently been licensed for use
in rhinitis. They are effective against
• congestion and mucus production, with efficacy similar to that of
loratadine
Nasal douching
• In rhinosinusitis, nasal douching improves quality of life and
endoscopic appearances
• Immunotherapy
• Immunotherapy results in a blunting of seasonal increases in allergen-
specific IgE, an increase in ‘blocking’ IgG antibodies and inhibition of
recruitment and activation of inflammatory cells to mucosal surfaces
including mast cells and basophils.
Nonallerg
These nonallergic aetiologic entities can broadly be classified as:
• idiopathic rhinitis (also referred to as vasomotor rhinitis, or nonallergic
noninfectious perennial rhinitis (NANIPER));
• nonallergic occupational rhinitis;
• hormonal rhinitis;
• drug-induced rhinitis; and
• other forms (nonallergic rhinitis with eosinophilia syndrome (NARES),
rhinitis due to physical and ic perennial rhinitis chemical factors, food-
induced rhinitis, emotioninduced rhinitis, atrophic rhinitis).
TYPES OF NONALLERGIC RHINITIS
Idiopathic rhinitis
• Idiopathic rhinitis is characterized primarily by symptoms of nasal blockage,
rhinorrhoea and sneezing, although the prevalence of sneezing,
conjunctival symptoms and pruritis is lower than that in allergic rhinitis.
• Although the subjects have traditionally been classified as either ‘runners’
(those with predominantly rhinorrhoea) or ‘blockers’ (those with
predominantly nasal congestion and blockage), many patients suffer from
more than one
• type of these symptoms, therefore making it difficult to subdivide the
patients into these groups.
• Among patients with chronic symptoms, the percentage with a
nonallergic aetiology increases progressively with age and reaches
>60 percent beyond the age of 50 years
Nonallergic occupational rhinitis
• Occupational rhinitis, as the term implies, may be defined as rhinitis
caused by exposure to airborne agents present in the work place.
These agents elicit predominantly sneezing, nasal discharge and/or
blockage and may act via
• both immunologic (IgE-mediated) and nonimmunologic mechanisms.
Drug-induced rhinitis
• Several commonly employed medications, such as aspirin, other
nonsteroidal antiinflammatory drugs (NSAIDs), beta-blockers,
angiotensin-converting enzyme (ACE) inhibitors, methyldopa, oral
contraceptives, psychotropic agents and nasal topical decongestants
(oxymetazoline,naphazoline, xylometazoline) may induce symptoms
of rhinitis
• on individual hypersensitivity to certain drugs, in particular aspirin,
which commonly exacerbates rhinitis and asthma
• persistent overuse of the topical nasal vasoconstrictors also leads to
nasal decongestion
• by a mechanism involving a rebound effect following withdrawal of
these drugs, excessive use of these agents may also lead to nasal
hyperreactivity and hypertrophy of the nasal mucosa, a condition
known as ‘rhinitis medicamentosa’
Hormonal rhinitis
• Hormonal rhinitis is often associated with pregnancy in particular,
although puberty is also known to induce the symptoms of rhinitis
Other forms of rhinitis
NARES
• The term NARES was originally introduced by Mullarkey and
colleagues, who characterized the condition on the basis of a
presence of greater than 20 percent eosinophils
• in nasal smears of symptomatic patients with perennial sneezing
attacks, a profuse watery rhinorrhoea, nasal pruritis, incomplete nasal
obstruction and occasional loss of smell
• In addition to these symptoms, a marked feature of the disease is the
lack of evidence of allergy, as indicated by negative skin prick tests
and/or absence of serum IgE antibodies to specific allergens
RHINITIS DUE TO PHYSICAL AND CHEMICAL FACTORS
• Nasal symptoms similar to those of rhinitis can be induced by physical
and chemical factors in individuals with sensitized nasal mucous
membranes
• Cold, dry air has been shown to lead to a condition known as skier’s
nose, in which rhinorrhoea features prominently.
• Exposure to chemicals, particularly air pollutants derived from
cigarette smoke and liquid petroleum fuels, have also been shown to
directly exacerbate symptoms of rhinitis in nonallergic individuals
FOOD-INDUCED RHINITIS

• Few studies have documented that certain foods and alcoholic beverages
can induce nonallergic rhinitis, although the underlying mechanisms are
largely unknown.
• Hot and spicy foods, in particular, which contain capsaicin lead to a watery
rhinorrhoea termed ‘gustatoryrhinitis’, probably as a result of the capsaicin
stimulating
• the sensory nerves to release neuropeptides and tachykinins
• In contrast, alcoholic beverages are thought to induce symptoms as a result
of vasodilation
EMOTIONALLY INDUCED RHINITIS
• Although not studied extensively, emotional factors such as stress and
sexual arousal have been documented to
• affect the nose, likely as a result of autonomic stimulation.
ATROPHIC RHINITIS
• Primary atrophic rhinitis is a condition that occurs predominantly in
women and is characterized by progressive atrophy of the nasal
mucosa and underlying bone of the turbinates
• This leads to the formation of thick crusts, which leave a constant foul
smell (ozaena)in the nose
• it has been suggested that this may be a result of infection with
Klebsiella ozaenae and other bacteria
DIAGNOSIS AS A STEP-WISE APPROACH
In daily clinical practice, the diagnosis of nonallergicrhinitis and its subgroups is
mainly based on a thoroughcase history, check possible stimuli, severity and
duration of disease;
• check drug use (systemic and topic), exposure at
• work place, hormonal status (pregnancy,hypothyroidism, acromegaly) and
involvement of other organs (asthma, hormonal status);
• exclude other nasal disease (rigid nasal endoscopy);
• exclude allergy: skin prick test, serum IgE-antibodies to the most frequent
inhalant allergens, and ultimately nasal provocation testing in selected cases;
• exclude chronic rhinosinusitis (computed tomography (CT) scan);
• perform nasal cytology (eosinophilia), and if shown to be positive then perform
oral aspirin challenge
• Intranasal anticholinergics (ipratropium bromide) may be useful in
patients with nasal secretion as the predominant symptom, whereas
nasal decongestants should be avoided or limited to ten days.
• Topical steroids and antihistamines are the two main classes of drugs
employed
Epistaxis
• Epistaxis is defined as bleeding from the nose. This prosaic definition
belies the difficulties associated with one of otolaryngology’s most
common and most difficult to treat emergencies
• epistaxis has been classified on the basis of presumed aetiology and
publications include long lists of factors thought to cause the
condition
• The terms anterior and posterior epistaxis are frequently used, but
their definitions are imprecise and inconsistent.
• Pearson attempted to standardize the term posterior epistaxis as a
bleeding point which could not be located
• Anterior epistaxis: Bleeding from a source anterior to the plane of
the piriform aperture. This includes bleeding from the anterior
septum and rare bleeds from the vestibular skin and mucocutaneous
junction.
• Posterior epistaxis: Bleeding from a vessel situated posterior to the
piriform aperture. This allows further subdivision into lateral wall,
septal and nasal floor bleeding.
• Aetiology
CHRONOBIOLOGY
• The frequency of admission is greatest in the autumn and winter
months. This seasonal variation correlates with fluctuations in
enviromental temperature and humidity
NONSTEROIDAL ANTIINFLAMMATORY DRUGS
• Adult pattern epistaxis is associated with the use of nonsteroidal
antiinflammatory drugs (NSAID). Patients are more likely than
controls to consume NSAIDs
ALCOHOL
• Similar aetiological associations to those of NSAIDs have been found
with alcohol. Epistaxis patients are more likely to consume alcohol
than matched control patients and are more likely to have consumed
alcohol within 24 hours of hospital admission than other emergency
admissions
HYPERTENSION
SEPTAL ABNORMALITIES
• Management Effective management of adult epistaxis follows an
incremental sequence of interventions
LO 5 : 3M kelainan di sinus paranasalis

Rhinosinusitis
• The term ‘sinusitis’ refers to a group of disorders characterized by
inflammation
• Because the inflammation nearly always also involves the nose, it is
now generally accepted that ‘rhinosinusitis’ is the preferred term to
describe this inflammation of the nose and paranasal
• Acute bacterial rhinosinusitis has been defined as sudden in onset
and with a duration of less than four weeks
• Inflammation in the nose and sinuses from a variety of causes can
result in sinus ostia obstruction and predispose to the development
of an infection. Many factors have been described as playing a role in
the development of ABRS
• The pathophysiology of ABRS has been postulated.Typically, acute
rhinosinusitis develops in conjunction with an acute viral upper
respiratory tract infection. This may occur more commonly in
predisposed individuals, as mentioned previously. The infection
results in mucosal swelling with occlusion or obstruction of the sinus
ostia. A reduction in oxygen tension occurs which can reduce
mucociliary transport and transudation of fluid into the sinuses
• The inflammation also results in changes in the mucous that become
more viscous and alterations in cilia beat frequency often occurs.
These changes in the nasal–sinus environment lead to mucostasis and
bacterial colonization.
• Antimicrobial resistance appears to be increasing for the common
pathogens in rhinosinusitis, particularly for H. influenzae and S.
pneumoniae. This increasing resistance appears to be largely related
to the use of antibiotics. In parts of the world, particularly the Far
East, resistance rates of 50 percent are not uncommon for both
macrolides and the beta-lactams. Resistance mechanisms
1. antibiotic deactivating enzymes;
2. alterations in the target site of the antibiotic;
3. changes in the influx/efflux process
Diagnosis
• It has become increasingly clear that the diagnosis of ABRS is best
made on clinical grounds and criteria
• In areas where prevalence rates are lower, then clinical criteria
including symptoms and physical findings are preferred
• The diagnosis for research should usually include more objective
information.
FUNGAL RHINOSINUSITIS
• Allergic fungal rhinosinusitis (AFRS), in the strictest sense, is defined
as an immunocompetent patient with an allergy to fungus
• The fungi which are the cause of the hypersensitivity reside in the
mucin and provide continued stimulation
Medical management of chronic
rhinosinusitis
The European Position Paper on Rhinosinusitis and Nasal Polyps
Rhinosinusitis (including nasal polyps) is defined as inflammation of the
nose and the paranasal sinuses characterized by two or more of the
following symptoms:
• blockage/congestion;
• discharge: anterior/posterior (discoloured);
• facial pain/pressure;
• reduction or loss of smell;
plus either: endoscopic signs of:
– polyps;
– mucopurulent discharge from middle meatus;
– or oedema/mucosal obstruction primarily inmiddle meatus;
and/or:
computed tomography (CT) changes:
mucosal changes within ostiomeatal complex and/or sinuses.
Medical therapy
allergen and/or irritant avoidance;
• douching;
• corticosteroids;
• decongestants;
• antibiotics;
• antifungals;
• antileukotrienes;
• aspirin;
• immunotherapy;
• other therapies.
Complication of rhinosinusitis
• Acute complications of rhinosinusitis can be divided into those that
are due to local progression of the disease, and systemic, presumed
haematogenous spread.
• LOCAL
- Local progression is via areas where the surrounding bone is thin,
such as the lamina papyracea, or where there is a
- direct anatomical connection by way of a nerve or blood
• vessel, such as the infraorbital canal, or the diploeic veins of the
frontal and sphenoid bones
• The absence of valves in the veins between the orbit and the sinuses
facilitates retrograde venous spread of infection
• Frontal
A subperiosteal abscess may result from an acute episode of frontal
rhinosinusitis if the local progression of the disease is through the
outer table of the skull
• Ethmoid
The most important and frequent acute complication of ethmoid
rhinosinusitis is orbital cellulitis, which can vary in degree and severity
1. Preseptal cellulitis. Inflammation does not
• extend beyond the orbital septum (the site at
• which the medial orbital periosteal reflection
• attaches to the medial eyelid at the tarsal plate).
2. Postseptal cellulitis or orbital cellulitis without abscess. Inflammation
extends into the tissues of the orbit.
3. Subperiosteal abscess. There is abscess formation
• deep to the periosteum of the orbital bones,
• usually the lamina papyracea.
4. Orbital abscess. There is abscess formation within
• the orbit which has breached the periosteum.
5. Cavernous sinus thrombosis/abscess. The
• inflammatory process has extended through the
• optic foramen into the cavernous sinus which
• thromboses and possibly progresses to abscess
• formation.
• Maxillary
Isolated maxillary rhinosinusitis rarely gives rise to acute local complications.
Patients with acute swelling of the cheek are almost invariably suffering from
a complication of primary dental disease rather than sinus infection,
although there might be an associated maxillary rhinosinusitis secondary to
the dental disease.
• Sphenoid
Acute local complications of sphenoid rhinosinusitis are rare, as indeed is
sphenoid rhinosinusitis itself, but can result in cavernous sinus thrombosis by
direct spread
Additionally, intracranial complications can occur as a result of a base of
skull fracture through the sphenoid sinus
DISTANT
• Brain abscess
this would most commonly occur as a complication of local spread, but
haematogenous spread may occur and has been described secondary
to maxillary rhinosinusitis associated with dental disease.
• Septicaemia As in any infective condition, progression to septicaemia
and its sequelae may occur. Toxic shock syndrome This has been
described on at least one occasion; in any patient with systemic septic
condition
Chronic complications of rhinosinusitis will usually be the result of
chronic rhinosinusitis and are invariably local. As with acute
complications, the nature of the complication depends on the
particular sinus or group of sinuses involved.
• Mucocoeles are chronic, slowly expanding lesions in any of the
sinuses that may result in bony erosion and subsequent extension
beyond the sinus. If the mucocoele becomes secondarily infected and
the contents purulent, it is described as a pyocoele
• In the maxillary sinus due to the proximity of the dental roots, which
may even protrude into the maxillary antrum, the teeth may be
affected by maxillary rhinosinusitis. It is unusual for chronic
rhinosinusitis to cause orbital cellulitis or intracranial complications
unless there is an acute exacerbation.
• Nasal polyposis