Rhinitis is defined as inflammation of the nasal membranes

[1]
and is
characterized by a symptom complex that consists of any combination of the
following: sneezing, nasal congestion, nasal itching, and rhinorrhea

Allergic rhinitis involves inflammation of the mucous membranes of the nose, eyes, eustachian
tubes, middle ear, sinuses, and pharynx. The nose invariably is involved, and the other organs are
affected in certain individuals. Inflammation of the mucous membranes is characterized by a
complex interaction of inflammatory mediators but ultimately is triggered by an immunoglobulin
E (IgE)mediated response to an extrinsic protein.
[10]

The tendency to develop allergic, or IgE-mediated, reactions to extrinsic allergens (proteins
capable of causing an allergic reaction) has a genetic component. In susceptible individuals,
exposure to certain foreign proteins leads to allergic sensitization, which is characterized by the
production of specific IgE directed against these proteins. This specific IgE coats the surface of
mast cells, which are present in the nasal mucosa. When the specific protein (eg, a specific pollen
grain) is inhaled into the nose, it can bind to the IgE on the mast cells, leading to immediate and
delayed release of a number of mediators.
[10, 11, 12]

The mediators that are immediately released include histamine, tryptase, chymase, kinins, and
heparin.
[11, 12]
The mast cells quickly synthesize other mediators, including leukotrienes and
prostaglandin D2.
[13, 14, 15]
These mediators, via various interactions, ultimately lead to the
symptoms of rhinorrhea (ie, nasal congestion, sneezing, itching, redness, tearing, swelling, ear
pressure, postnasal drip). Mucous glands are stimulated, leading to increased secretions. Vascular
permeability is increased, leading to plasma exudation. Vasodilation occurs, leading to congestion
and pressure. Sensory nerves are stimulated, leading to sneezing and itching. All of these events
can occur in minutes; hence, this reaction is called the early, or immediate, phase of the reaction.
Over 4-8 hours, these mediators, through a complex interplay of events, lead to the recruitment of
other inflammatory cells to the mucosa, such as neutrophils, eosinophils, lymphocytes, and
macrophages.
[16]
This results in continued inflammation, termed the late-phase response. The
symptoms of the late-phase response are similar to those of the early phase, but less sneezing and
itching and more congestion and mucus production tend to occur.
[16]
The late phase may persist for
hours or days.
Systemic effects, including fatigue, sleepiness, and malaise, can occur from the inflammatory
response. These symptoms often contribute to impaired quality of life.
Symptoms that can be associated with allergic rhinitis include sneezing,
itching (of nose, eyes, ears, palate), rhinorrhea, postnasal drip, congestion,
anosmia, headache, earache, tearing, red eyes, eye swelling, fatigue,
drowsiness, and malaise.
[2]
Determine which organ systems are affected and the specific symptoms.
Some patients have exclusive involvement of the nose, while others have
involvement of multiple organs. Some patients primarily have sneezing,
itching, tearing, and watery rhinorrhea (the classic hayfever presentation),
while others may only complain of congestion. Significant complaints of
congestion, particularly if unilateral, might suggest the possibility of
structural obstruction, such as a polyp, foreign body, or deviated septum.



Otitis media (OM) is the second most common disease of childhood, after upper respiratory
infection (URI). OM is also the most common cause for childhood visits to a physician's office.
Annually, an estimated 16 million office visits are attributed to OM; this does not include visits to
the emergency department.
OM is any inflammation of the middle ear without reference to etiology or pathogenesis. OM can
be classified into many variants on the basis of etiology, duration, symptomatology, and physical
findings.
Acute OM (AOM) implies rapid onset of disease associated with one or more of the following
symptoms:
Otalgia
Fever
Otorrhea
Recent onset of anorexia
Irritability
Vomiting
Diarrhea
These symptoms are accompanied by abnormal otoscopic findings of the tympanic membrane
(TM), which may include the following:
Opacity
Bulging
Erythema
Middle ear effusion (MEE)
Decreased mobility with pneumatic otoscopy
AOM is a recurrent disease. More than one third of children experience 6 or more episodes of
AOM by age 7 years.
OM with effusion (OME), formerly termed serous OM or secretory OM, is MEE of any duration
that lacks the associated signs and symptoms of infection (eg, fever, otalgia, irritability). OME
usually follows an episode of AOM.
Chronic suppurative OM is a chronic inflammation of the middle ear that persists at least 6 weeks
and is associated with otorrhea through a perforated TM, an indwelling tympanostomy tube (TT;
see image below), or a surgical myringotomy.
The most important factor in middle ear disease is eustachian tube (ET) dysfunction. In ET
dysfunction (ETD), the mucosa at the pharyngeal end of the ET is part of the mucociliary system
of the middle ear. Interference with this mucosa by edema, tumor, or negative intratympanic
pressure facilitates direct extension of infectious processes from the nasopharynx to the middle
ear, causing OM. Esophageal contents regurgitated into the nasopharynx and middle ear through
the ET can create a direct mechanical disturbance of the middle ear mucosa and cause middle ear
inflammation.
In children, developmental alterations of the ET, an immature immune system, and frequent
infections of the upper respiratory mucosa all play major roles in AOM development. Studies have
demonstrated how viral infection of the upper respiratory epithelium leads to increased ETD and
increased bacterial colonization and adherence in the nasopharynx.
[1]
Certain viral infections cause
abnormal host immune and inflammatory responses in the ET mucosa and subsequent microbial
invasion of the middle ear. The host immune and inflammatory response to bacterial invasion of
the middle ear produces fluid in the middle ear and the signs and symptoms of AOM.
Although interactions between the common pathogenic bacteria in AOM and certain viruses are
not fully understood, strong evidence indicates that these interactions often lead to more severe
disease, lowered response to antimicrobial therapy, and OME development following AOM.
Suspect acute otitis media (AOM), with or without effusion, in children with a history of
the following symptoms:
o Head and neck
Otalgia: Young children may exhibit signs of otalgia by pulling on the
affected ear or ears or pulling on the hair. Otalgia apparently occurs
more often when the child is lying down (eg, during the night, during
nap time), which may be due to increased ETD when the child is in a
recumbent position.
Otorrhea: Discharge may come from the middle ear through a recently
perforated TM, through a preexisting TT, or through another
perforation. For trauma patients, excluding a basilar skull fracture with
associated cerebrospinal fluid (CSF) otorrhea is important.
Headache
Concurrent or recent URI symptoms (eg, cough, rhinorrhea, sinus
congestion)
o General
Two thirds of children with AOM have a history of fever, although
fevers greater than 40C are uncommon and may represent bacteremia
or other complications.
Irritability may be the sole early symptom in a young infant or toddler.
A history of lethargy, although nonspecific, is a sensitive marker for
sick children and should not be dismissed.
o GI tract: Symptoms include anorexia, nausea, vomiting, and diarrhea.
OME often follows an episode of AOM. Consider OME in patients with recent AOM in
whom the history includes any of the following symptoms:
o Hearing loss: Most young children cannot provide an accurate history. Parents,
caregivers, or teachers may suspect a hearing loss or describe the child as
inattentive.
o Tinnitus: This is possible, although it is an unusual complaint from a child.
o Vertigo: Although true vertigo (ie, room-spinning dizziness) is a rare complaint
in uncomplicated AOM or OME, parents may report some unsteadiness or
clumsiness in a young child with AOM.
o Otalgia: Intermittent otalgia tends to worsen at night.
OM treatment widely varies based on the duration of symptoms, past therapeutic failures,
and severity of current symptoms.
Exposure to environmental risk factors is another important aspect of the history and
includes the following:
o Passive exposure (ie, secondhand) to tobacco smoke
o Group daycare attendance
o Seasonality: AOM prevalence is much higher in winter and early spring than in
summer and early fall.
o Supine bottle feeding (ie, bottle propping)

Chronic suppurative otitis media (CSOM) is a perforated tympanic membrane with persistent
drainage from the middle ear (ie, lasting >6-12 wk).
[1, 2]
Chronic suppuration can occur with or
without cholesteatoma, and the clinical history of both conditions can be very similar. The
treatment plan for cholesteatoma always includes tympanomastoid surgery with medical treatment
as an adjunct.
CSOM differs from chronic serous otitis media in that chronic serous otitis media may be defined
as a middle ear effusion without perforation that is reported to persist for more than 1-3 months.
The chronically draining ear in CSOM can be difficult to treat.
[3]
McKenzie and Brothwell
demonstrated evidence of chronic suppurative otitis in a skull found in Norfolk, United Kingdom,
which is thought to be from the Anglo-Saxon period.
[4]
Radiologic changes in the mastoid caused
by previous infection have been seen in a number of specimens, including 417 temporal bones
from South Dakota Indian burials and 15 prehistoric Iranian temporal bones.
[5, 6]

CSOM is initiated by an episode of acute infection. The pathophysiology of
CSOM begins with irritation and subsequent inflammation of the middle ear
mucosa. The inflammatory response creates mucosal edema. Ongoing
inflammation eventually leads to mucosal ulceration and consequent
breakdown of the epithelial lining. The host's attempt at resolving the
infection or inflammatory insult manifests as granulation tissue, which can
develop into polyps within the middle ear space. The cycle of inflammation,
ulceration, infection, and granulation tissue formation may continue,
eventually destroying the surrounding bony margins and ultimately leading
to the various complications of CSOM
Patients with chronic suppurative otitis media (CSOM) present with a draining ear of some
duration and a premorbid history of recurrent acute otitis media, traumatic perforation, or the
placement of ventilation tubes. Typically, they deny pain or discomfort. A common presenting
symptom is hearing loss in the affected ear. Reports of fever, vertigo, and pain should raise
concern about intratemporal or intracranial complications. A history of persistent CSOM after
appropriate medical treatment should alert the physician to consider cholesteatoma.
The external auditory canal may or may not be edematous and is not typically tender. The
discharge varies from fetid, purulent, and cheeselike to clear and serous. Granulation tissue is
often seen in the medial canal or middle ear space. The middle ear mucosa visualized through the
perforation may be edematous or even polypoid, pale, or erythematous.
A 512-Hz tuning fork examination is a critical part of the evaluation to establish if hearing loss is
present and whether it is conductive or sensorineural.

In the United States, acute otitis media (AOM) is the most common affliction necessitating
medical therapy for children younger than 5 years. The total annual cost to society for this disease
and for otitis media with effusion (OME) runs into the billions of dollars. Yet, despite research
into prevention and therapy, the costs of this disease continue to rise while the incidence remains
unabated.
AOM is defined by convention as the first 3 weeks of a process in which the middle ear shows the
signs and symptoms of acute inflammation. OME is defined as the presence of fluid in the middle
ear with accompanying conductive hearing loss and without concomitant symptoms or signs of
acuity. OME is classified as subacute when it persists from 3 weeks to 3 months after the onset of
AOM and is classified as chronic thereafter.
The emergence of antimicrobial-resistant bacteria requires reevaluation of traditional management.
Nevertheless, there is still a consensus that antibiotics are the initial therapy of choice for AOM.
Surgical management of AOM can conveniently be divided into 3 related procedures:
tympanocentesis, myringotomy, and myringotomy with insertion of a ventilating tube.
patofis
Obstruction of the eustachian tube appears to be the most important antecedent event associated
with AOM. The vast majority of AOM episodes are triggered by an upper respiratory tract
infection (URTI) involving the nasopharynx.
Viral and bacterial infection,
Immunologic factors
Immunologic activity may play a significant role in the frequency of AOM and its outcome.
Although most research has focused on the immunologic aspects of OME, certain relations
between AOM and the patients immune status have been demonstrated, as follows:
Production of antibodies may promote clearance of a middle ear effusion after an acute
attack
Previous exposure or immunization may have a preventative role by suppressing
colonization of the nasopharynx by pathogens
The formation of antibodies during an attack may prevent or modify future attacks;
unfortunately, antibodies to both Streptococcus pneumoniae and Haemophilus influenzae
are of the polysaccharide type and the ability to product them develops late unless
conjugated to proteins
Minor or transient immunologic defects may give rise to recurrent otitis media
Much attention has been focused on the immunoglobulins and the patients ability to form them.
Immunoglobulin G2 (IgG2) and immunoglobulin G4 (IgG4) are responsible for immunity against
polysaccharide antigens; deficiencies in the formation of these antibodies invariably lead to otitis
media. Many patients with Down syndrome show decreased function of immunoglobulin A (IgA),
IgG2, or IgG4, which partially explains their increased risk for chronic rhinitis and otitis media.
The immunologic aspects of AOM are not confined to the middle ear. The nasopharynx plays an
important role in the pathogenesis of AOM, and immunologic modifications in this lymphoid
tissue provide some protection from pathogens by preventing their adherence to mucosal surfaces.
The presence of nasopharyngeal IgA antibodies to pneumolysin toxin released by pneumococcal
autolysis appears to protect against invasion by healthy pneumococci.
On the other hand, not all immunoglobulins in the nasopharynx are protective. Bernstein describes
the effects of immunoglobulin E (IgE) hypersensitivity or hyperimmune effects on the eustachian
tube mucosa.
[4]
The allergic response in the nasopharyngeal end of the eustachian tube promotes
stasis and the subsequent formation of a middle ear effusion.
In the neonate, irritability or feeding difficulties may be the only indication of a septic focus. Older
children begin to demonstrate a consistent presence of fever (with or without a coexistent upper
respiratory tract infection [URTI]) and otalgia or ear tugging. These latter symptoms are not
entirely exclusive to AOM; teething pain or pharyngitis (particularly coxsackievirus infection) can
mimic these symptoms.
In older children and adults, hearing loss becomes a constant feature of AOM and otitis media
with effusion (OME), with reports of ear stuffiness noted even before the detection of middle ear
fluid. Otalgia without hearing loss or fever is observed in adults with external otitis, dental
abscess, or pain referred from the temporomandibular joint. Orthodontic appliances often elicit
referred pain as the dental occlusion is altered.
Rinoskopi Anterior adalah pemeriksaan rongga hidung dari
depan dengan memakai spekulum hidung. Tangan kiri memegang
speculum dengan ibu jari (di atas/depan) dan jari telunjuk
(dibawah/belakang) pada engsel speculum. Jari tengah diletakan
dekat hidung, sebelah kanan untuk fiksasi. Jari manis dan kelingking
membuka dan menutup spekulum. Speculum dimasukkan tertutup ke
dalam vestibulum nasi setelah masuk baru dibuka. Tangan kanan
bebas : dapat membantu memegang alat-alat pinset dan kait dsb,
menahan kepala dari belakang/tengkuk atau mengatur sikap kepala.
Melebarkan nares anterior dengan meregangkan ala nasi. Melihat
jelas dengan menyisihkan rambut hidung. Hal-hal yang harus
diperhatikan pada rinoskopi anterior :
Mukosa. Dalam keadaaan normal berwarna merah muda,
pada radang berwarna merah, pada alergi pucat atau kebiruan
(livid)
Septum. Normalnya terletak ditengah dan lurus,
perhatikan apakah terdapat deviasi, krista, spina, perforasi,
hematoma, abses, dll.
Konka. Perhatikan apakah konka normal (eutrofi),
hipertrofi, hipotrofi atau atrofi
Sekret. Bila ditemukan sekret perhatikan jumlah, sfat dan
lokalisasinya
Massa.

otoskopi
Tangan kiri, jari tengah dan jari kelingking memegang bagian atas
daun telinga dan menariknya ke superoposterior. Tangan kanan
memasukkan corong telinga ke dalam kanalis auditorius eksterna.
Corong kemudian dipegang dengan tangan kiri, ibu jari dan jari
telunjuk mengamati telinga luar dan sekitarnya. Memeriksa kanalis
auditorius eksterna dan membrana timpani.

Tinitus adalah salah satu bentuk gangguan pendengaran berupa
sensasi suara tanpa adanyarangsangan dari luar, dapat berupa sinyal
mekanoakustik maupun listrik. Keluhan suara yang didengar sangat
bervariasi, dapat berupa bunyi mendenging, menderu, mendesis,
mengaum, atau berbagai macam bunyi lainnya. Suara yang didengar
dapat bersifat stabil atau berpulsasi. Keluhan tinitus dapat dirasakan
unilateral dan bilateral.Serangan tinitus dapat bersifat periodik
ataupun menetap. Kita sebut periodik jika serangan yang datang
hilang timbul.