Disorders of the Upper

Respiratory Tract
Introduction: URTI
• URTI involve infections of the nose, sinuses, pharynx, larynx and the
trachea
• Usually caused by a variety of viruses and bacteria
• Most common virus is rhinovirus, other viruses include Influenza virus,
Parainfluenza virus, adenovirus, enterovirus and respiratory syncytial virus
• Bacteria may cause ~15% of acute pharyngitis, most common being S.
pyogenes
• Usually associated with cough but no proof of pneumonia.
• URTI usually among the top three diagnoses in out-patient settings and
account for a large number of missed day of schools in children
Risk Factors for URTI
• Seasonal, common during the cold season
• Close contact with/ among children (day-care, schools)
• Inflammation/ obstruction in medical disorders e.g Asthma, allergic
rhinitis are prone to developing URTI
• Smoking: alters mucosal resistance to URTI
• Immunocompromise that affect cellular humoral immunity
• Anatomical anomalies e.g cleft palate, nasal polyposis
Pathophysiology
• URTI usually involves direct invasion of the upper airway mucosa
by the organism
• Usually acquired by inhalation of infected droplets
• Barriers that prevent organisms from attaching to the mucosa
include:
• Hair-lining that traps pathogens
• Mucus which also traps organism
• Angle between the pharynx and the nose that prevents particles from
falling into the airways
• Ciliated cells in the lower airways that transport the pathogens back to the
pharynx
Infectious disorders of the Upper
Respiratory Tract
• Common cold (Rhinitis)
• Pharyngitis
• Epiglottitis
• Acute Laryngotracheobronchitis
Common cold (Rhinitis)
• Incidence rates highest in children under 5years of age
• Pathogens include rhinovirus, adenovirus, parainfluenza virus, respiratory
syncytial virus , enterovirus, coronavirus
• After deposition in the anterior nasal mucosa, replication and infection
begin upon muco-ciliary transport to the posterior nasopharynx and
adenoids
• About 10-12hrs after inoculation, symptoms may begin
• Nasal mucosa infection and host inflammatory response cause vaso- dilation
and increased vascular permeability
• There is resulting nasal obstruction and rhinorrhoea
• Cholinergic stimulation causes mucus production and sneezing
Rhinitis
• Symptoms include cough, sore-throat, runny nose, nasal congestion, low grade fever,
facial pressure, sneezing, malaise
• Onset of symptoms usually begins 1-3 days after exposure and lasts 7-10 days and
can persist up to 3 weeks
• Diagnosis is clinical and testing usually not necessary
• Goal of treatment is to achieve symptom relief: Steam inhalation, frequent warm
fluids, bed-rest
• Avoid cough preparation/syrup in children: suppresses cough
• Evidence based data does not support the use of antibiotics for common cold
• Usually benign and self-limiting
• May have secondary bacterial infection
• Complications are usually rare ( otitis media, sinusitis, bronchiolitis may follow)
Pharyngitis
• Inflammation of the pharynx, including the lymphoid tissues of
the posterior pharynx and lateral pharyngeal bands.
• Etiologic agents include viruses, bacteria, fungi
• Most cases are due to viral infections: Adenovirus, Influenza virus,
Coxsakievirus, Herpes simplex virus, Epstein-Barr virus,
Cytomegalovirus etc
• Group A beta-hemolytic streptococcus or Streptococcus pyogenes is
the most important bacterial agent associated with acute pharyngitis
and tonsillitis (20-30%% in children)
Pharyngitis
• Viral pathogens invade the mucosal cells of the nasopharynx and oral cavity,
resulting in oedema and hyperaemia of the mucous membranes and tonsils
• Also, bacteria attach to and invade the mucosal cells
• Peaks in children 4-7 years of age
• Clinical manifestations:
• Red, sore or ‘scratchy’ throat, difficulty/ pain in swallowing, foul breath
• Inflammatory exudate or membranes may cover tonsils/tonsillar pillars
• Depending on pathogen, fever and systemic manifestations such as malaise,
myalgia, headache may be present, especially in viral causes
• Submandibular/anterior cervical lymphadenopathy may be present in bacterial
pharyngitis
Pharyngitis
• Erythema, swelling or exudates of the pharynx or tonsils with high
grade fever is usually seen in bacterial pharyngitis
• A peritonsillar abscess may manifest as unilateral palatal/ tonsillar
pillar swelling with downward/medial displacement of the tonsils
• Uvular may tilt to the opposite side
• Bulging of the posterior pharyngeal wall may signal a
retropharyngeal abscess
• Less comon findings include palatal petechae and a scarlatiniform
rash
Pharyngitis
• Goal in Diagnosis of pharyngitis is to identify cases that are due to group
A Beta haemolytic streptococcus as well as the more unusual and
potentially serious infections.
• The various forms cannot be distinguished on clinical grounds
• Routine throat swap for culture and sensitivity should be done
• For confirming viral nasopharyngeal infection, viral cultures remain standard
• Rapid tests for viruses include various antigen, immunoflorescence and
PCR assays
• Serologic studies may confirm viral, mycoplasmal or chlamydial pathogens
Pharyngitis
• Symtomatic treatment is recommended for viral pharyngitis except for
herpes simplex infection (Acyclovir)
• Specific antiviral agents will depend on the causative organisms
• Mycoplasma and Chlamydial infections: Macrolides
• Typically resolves in 1-2weeks but immunocompromised may have a
severe course
• Complications from Group A streptococcal pharyngitis : Acute Rheumatic
Fever, Acute glomerulonephritis, peritonsillar abscess, retropharyngeal
abscess
• Mortality from group A streptococcal infection is rare but serious
morbidity/ death may result from its complications
Pharyngitis
• Oral penicillin or Amoxycillin for 10days is recommended for Group
A streptococcal pharyngitis—
• First generation Cephalosporin –in non-Penicillin allergy
• Macrolides ( Erythromycin/ Azthromycin/ Clarithromycin) should be
considered in penicillin allergy
• Deep tissue infections of adjacent structures such as peritonsillar
abscess warrant hospitalization and surgical intervention
Epiglotittis
• Infection/inflammation of the superior portion of the larynx and supra-glottic area: a medical
emergency
• Most common causative pathogen: Haemophilus influenza type b
• Affects children age 2-7years, peak incidence at 3years
• May be preceded by a viral URT infection
• Upon infection, rapid progressive erythema and swelling of the epiglottis ensue.
• Bacteraemia is usually present
• Manifestations include acute onset of fever, sore-throat, hoarseness, drooling, dysphagia,
globus sensation of a lump in the throat.
• Usually toxic- looking, in tripod or sniffing posture (sitting upright, supported by hands and
head forward
• There is rapid progression within a few hours to severe respiratory distress and prostration
• Clinical course can be fulminant and fatal hence immediate admission is indicated
Epiglottitis
• Avoid instrumentation until ready for intubation: insertion of tongue depressors or other instruments may
provoke airway spasm and precipitate respiratory compromise
• “Cherry red” epiglottis is seen on direct visualization
• Note: direct visualization of the upper airway for confirmation of diagnosis should be performed only
when emergency endotracheal intubation can be performed safely
• During the procedure, swab sample can be taken for m/c/s
• Intubation should be performed to ensure patency of airway
• Lateral soft tissue Xray of neck: shows ‘thumbprint’ sign (manifestation of an oedematous / enlarged tonsil)
• Supplemental Oxygen should be administered if SP02 is less than 92%
• Administer intravenous Antibiotics after collection of culture specimen: Ceftriaxone or other 3 rd generation
Cephalosporins
• Avoid sedatives
• Keep nil per os
• Administer IV fluids for maintenance and deficits
Epiglottitis
• May cause mortality due to sudden airway obstruction
• With proper airway management, prognosis is favourable
 Laryngotracheobrochitis/Croup
• Inflammation of larynx, trachea and bronchi.
• Typically caused by Parainfluenza virus type1, 2or 3 in80% of cases
• Other viruses include Influenza virus, RSV, adenovirus , measles virus etc
• Bacterial laryngitis are far less common than viral laryngitis
• Occurs in children 6 months to 6 years, peak incidence is in the 2ndyear of life
• Infection causes inflammation of the larynx, trachea and bronchi.
• Obstruction is caused by the swelling and inflammatory exudates develop and become pronounced
in the subglottic region: producing stridor
• High pitched stridor is heard at rest and when agitated
• Nasopharyngitis often precedes laryngitis/ tracheitis by several days
• Hoarseness or loss of voice is a key manifestation of laryngeal involvement
• Characteristic cough is brassy or barky accompanied by inspiratory stridor
• Fever is usually low grade or absent
LTB
• Diagnosis is clinical
• IV or oral glucocorticoids reduce symptoms : reduce oedema by suppressing local
inflammation (Dexamethasone 0.15-0.6mg/kg/dose)
• Inhaled racemic epinephrine temporarily dilate the airways by relaxing bronchial
smooth muscles and causing vasoconstriction that may reduce mucosal
inflammation– consider in moderate-severe cases
• Correct dehydration
• Moist air inhalation
• Administer Humidified oxygen to hypoxeamic patients
• Avoid sedatives
• Intubation is reserved for severe cases not responding to treatment
LTB
• Lateral neck Xray reveals the Steeple/pencil-tip sign: sub-glottic
narrowing (not pathognomonic)
• Differential diagnosis: Epiglottitis, foreign body aspiration,
anaphylaxis
• Complications are rare but include secondary bacterial infection,
dehydration, pneumothorax
Upper Respiratory Tract: Allergic
Conditions
• Allergic rhinitis/ hay-fever
• Acute, non –infective inflammatory disease of the nasal airways due to acquired reactivity to an
exogenous antigen (allergen)
• An example of a type 1, IgE-dependent, mast cell-mediated immune reaction whereby the release of
mast cell or basophil mediators create responses to sensitizing agents
• There is mast cell release of inflammatory mediators, followed by a chronic inflammatory response, in
which eosinophils play a predominant role which leads to hyper responsiveness of the nasal mucosa to
subsequent stimulation
• Common, though benign, impacts the quality of life and contributes to a large health expenditure
• Sensitization to outdoor allergens occur in children older than 4-6years while children older than
2yearsare are affected with sensitization to indoor allergens
• Irritants include dust mite, pollen, animal dander, cock-roaches, molds
• Clinical triad: recurrent sneezing, nasal discharge and nasal obstruction, feathers
• In children, sneezing predominates over obstruction
• Recurrent /prolonged cold, constant nose/palate itch/ rubbing , throat clearing , watery eyes, snoring
Allergic Rhinitis
associated allergic conjunctivitis, asthma
• Symptoms usually worse at night
• History may reveal a household pet, distinct seasonal variation,
family allergy, infantile eczema, exposure to cigarette smoke
• Pale nasal turbinates are present with or without clear nasal discharge
• Polyps rarely observed
• Allergic shiners (dark puffy, eyelids)
• Allergic salute(nose rubbing)
• Erythema of palpebral conjunctival, chemosis, watery eye discharge
Allergic rhinitis
• Cobblestoning (polygonal cells bulge out from mucosa surfaceto a
varying degree) in posterior pharynx/laterally behind the tonsils is
a sign of follicular hypertrophy of lymphoid tissue due to chronic
nasal congestion and postnasal drainage
Allergic rhinitis
• Antihistamines are effective treatment agents but do not
completely control symptom of nasal congestion
• Leucotriene-receptor antagonists are as effective as antihistamines
• Intranasal steroids are superior to antihistamines in efficacy
• Immunotherapy is effective for refractory allergic rhinitis and can
be administered, sublingual, subcutaneous
• Complications: sinusitis, recurrent/chronic otitis media
• Differential diagnosis: common cold, adenoid hyperplasia, foreign
body
Allergic rhinitis
• Prognosis: rarely outgrown in childhood
• Management: avoidance of allergens/ environmental control,
• Remove trigger factors medications, allergen-specific immunotherapy
• Surgical intervention (turbinectomy for symptom relief)
Upper Respiratory Tract :
Obstructive conditions
• Upper airway obstruction varies from narrowing to partial and
complete occlusion of the upper airway structures, potentially
leading to a compromise in ventilation
• Serious and potentially life threatening conditions, thus require
prompt assessment and management
• It is important to take a good history and perform efficient and
comprehensive exam to determine the aetiology / level of
obstruction and urgency of subsequent management
• A vital clinical sign is noisy breathing: stertor or stridor
Upper respiratory tract: obstructive
conditions

• Stertor is noisy breathing which occurs at the level of nasal/oral

cavities/ naso-oropharynx.
• Stridor: noisy breathing that occurs at the level of the larynx or
below.
Etiology: URT obstructive conditons
• It helps to classify the causes of upper airway obstruction by the type of noisy
breathing
• STERTOR: Snoring, low –pitched noise arising from the level of nasal/oral
cavities/naso-oropharynx
• Congenital causes of stertor include:
• Craniofacial syndromes that cause midfacial hypoplasia e.g Apert and Crouzon), Pierre Robin
Sequence and other causes of micro/retrognathia, choanal atresia, lymphovascular
malformations of tongue and neck, glossoptosis, macroglossia
• Acquired (acute): Urticaria, nasal turbinate hypertrophy, tonsillitis,
parapharyngeal/retropharyngeal/ peritonsillar abscess, croup, foreign body aspiration
• Acquired (Chronic ) cause: Adenotonsillar hypertrophy, bilateral vocal cord palsy,
subglottic haemangioma, subglottic stenosis (post intubation),
Stridor
• High pitched sound associated with obstruction at the level of the
larynx, trachea
• Congenital causes: laryngomalacia, vocal cord paralysis, laryngeal
web, subglottic stenosis/hemangioma
• Acquired causes: Epiglottitis, ALTB, burn, caustic injury to the upper
airway
• External compression of trachea (extraluminal): vascular ring/aortic
abnormalities
• Intraluminal causes: Foreign body Aspiration
Upper respiratory tract: obstruction
• Foreign body aspiration in children is an emergency that is more
frequently encountered than in adults.
• Aspirated substances may be organic or inorganic (e.g peanuts,
buttons, and beads)
Evaluation of Upper Airway
Obstruction
• On general examination, note facial feature for any syndromic features, posture
(tripod) and respiratory effort
• Children in respiratory distress may show increased work of breathing via the use
of accessory muscles
• If respiratory failure is reached, there is shallow breathing, bradycardia, and altered
mental status hence monitor mental status
• Any noisy breathing and quality of the breathing, including dysphonia, should be
noted.
• It is important to assess for septal deviation, hypertrophy of the nasal turbinates, or
nasal polyposis during nasal examination
• A bedside test to assess choanal patency can be performed by watching for mist on
cold metal spatula when patient exhales (‘nasal misting test’)
Evaluation of Upper airway
obstruction
• The oral cavity should also be thoroughly examined for presence of
micrognathia, protruding/large tongue, floor of mouth or tongue
edema, swelling/tumor or palatal fullness with uvular deviation(as in
the case of a peri-tonsillar abscess).
• Basic vital signs, i.e.,temperature, pulse, respiratory rate, blood
pressure, and O2 saturation, should occur initially as part of the ABCs
of assessment.
• Oxygen saturations are an essential first step in assessing a patient
with airway obstruction, as it can act as a marker for the severity of
their obstruction.
Evaluation of Upper airway
obstruction
• The oral cavity should also be thoroughly examined for presence of
micrognathia, protruding/large tongue, floor of mouth or tongue
edema, swelling/tumor or palatal fullness with uvular deviation(as in
the case of a peri-tonsillar abscess).
• Basic vital signs, i.e. temperature, pulse, respiratory rate, blood
pressure, and O2 saturation, should occur initially as part of the ABCs
of assessment.
• Oxygen saturations are an essential first step in assessing a patient
with airway obstruction, as it can act as a marker for the severity of
their obstruction.
Evaluation of Upper airway
obstruction
• Further evaluation includes flexible nasendoscopy/ laryngoscopy to assess the pharynx
and larynx dynamically.
• This can help diagnose turbinate inflammation, septal deviation, adenoidal
hypertrophy, Waldeyer’s ring hypertrophy, or laryngeal/hypopharyngeal pathology.
• Particularly useful when assessing the dynamic function of the larynx such as
assessing vocal cord movement and relatively common conditions affecting the larynx,
such as laryngomalacia in children.
• If a child with a possible inhaled foreign body is stable, inspiratory, and expiratory, chest
radiographs can aid in diagnosis. For example, if there is a foreign body partially
obstructing the left main bronchus, there may be hyperlucency of the left lung due to
hyperinflation secondary to the ball-valve effect of the foreign body.
• Ultrasound or MRI are the imaging modalities of choice in children, as they do not
involve radiation.
Evaluation of Upper airway
obstruction
• CT is used in situations that are time-sensitive or in cases that may
need surgical intervention, such as a retropharyngeal abscess or a
possible inhaled foreign body.
Upper airway obstruction:
Management
• Steam/ moist air inhalation may relief nasal congestion
• Antibiotics should be administered as indicated in infective cases
(e.g tonsillitis, epiglottitis)
• Tracheostomy may be necessary in upper airway obstruction cases
where intubation is anticipated to be very difficult or impossible
• In the case of suspected inhaled foreign body in children, a direct
laryngoscopy / bronchoscopy should be performed to remove the
foreign body.
• Occasionally, as in the case of children with adenotonsillar
hypertrophy, surgery can be the primary treatment
Upper Airway Obstruction:
Mangement
• The initial step in airway obstruction management is ‘ABC,’ i.e.,
Airway, Breathing, Circulation
• An oxygen saturation monitor should be placed, and supplemental
oxygen administered as indicated
• If patient is stable, there may be time to perform imaging studies,
initiate antibiotic treatment, etc.
• In the unstable patient in the acute setting, it is crucial to efficiently
assess the patient while also taking a quick history/collateral history.
Upper airway obstruction
Prognosis/ complication
• untreated upper airway obstruction causing respiratory distress can
lead to respiratory failure, and ultimately cardiorespiratory arrest.
• Smaller size foreign body can enter the lungs causing atelectasis,
pneumonia, or pneumothorax.
Disorders of Ears, Nose and Throat
Ear infections (otitis)
• Broadly divided into two groups:
• Otitis externa: infections of the outer ear
• Otitis media: infection of the middle ear
• Can also be divided into acute or chronic
Otitis Externa (OE)
• Otitis externa is an inflammation or infection of the external auditory
canal (EAC), the auricle, or both.
• Mostly caused by bacterial pathogen: Pseudomonas , Staphylococcus
spp, anaerobes, gram –negatives
• Fungal : Aspergillus, Candida
• Eczematous conditions
Risk Factors : OE
• Previous episodes
• Swimming
• Use of earplugs, probing of the EAC
• Hot, humid weather
• Use of hearing aid
• Coexistent eczema, rhinitis, asthma
• Immunosuppression/compromise
Pathophysiology: OE
• OE is a superficial infection of the skin in the EAC, auricles.
• Subtypes exist: Acute diffuse OE, Aute localised, Chronic OE, Eczematous OE, necrotizing OE,
Otomycosis
• Processes involved include obstruction of EAC- results in water retention, absence of
cerumen - may occur as a result of repeated water exposure or overcleaning the ear, trauma
and alteration of the pH of the canal
• Moisture trapped in the EAC may cause maceration of the skin and provide a medium for
growth of organisms
• Obstruction by excessive cerumen, debris can also contribute to above
• Trauma allows invasion of bacteria into the damaged skin
• Once infection is established, inflammatory response occurs with skin oedema
• Exudate and pus may appear in the EAC
• If severe, infection may spread to face, neck- cellitis
Examination: OE
• The auricle should be examined for tenderness, swelling, deformity, and erythema; face- for paresis, the neck for masses.
• The key physical finding of OE is pain upon palpation of the tragus (tragal tenderness) or application of traction to the pinna (the
hallmark of OE).
• Eczema, furunculosis, cellulitis of the pinna may be present.
• OTOSCOPY:
• For optimal viewing in a child, pull the auricle posteriorly. Remove any debris or cerumen to allow an adequate examination.
Proceed with the examination as follows:
• First, examine the EAC for masses, skin changes, otorrhea, foreign body
• Next, examine all parts of the tympanic membrane (eg, pars tensa and pars flaccida)
• Next, assess the motion of the tympanic membrane by means of pneumatic otoscopy
• Finally, attempt a thorough examination of the middle ear contents through the tympanic membrane, though this examination may
be limited by the opacity of the membrane itself.
• Examination reveals erythema, edema, and narrowing of the external auditory canal (EAC), and a purulent or serous discharge may
be noted
• There may be conductive deafness
• No cranial nerve involvement (ie, of CNs VII and IX-XII)
• The tympanic membrane may be difficult to visualize and may be mildly inflamed, but it should be normally mobile on insufflation.
OE: Clinical features
• Otalgia - Ranges from mild to severe, typically progressing over 1-2 days
• Hearing loss (conduction type)
• Ear fullness or pressure
• Erythema, edema, and narrowing of the EAC
• Tinnitus
• Fever (occasionally)
• Itching (especially in fungal OE or chronic OE)
• Severe deep pain - Immunocompromised patients may have necrotizing (malignant) OE
• Discharge - Initially, clear; quickly becomes purulent and foul-smelling
• Cellulitis of the face or neck or lymphadenopathy of the ipsilateral neck (occasionally)
• Bilateral symptoms (rare)
• History of exposure to or activities in water (eg, swimming)
• History of preceding ear trauma (usually) (eg, forceful ear cleaning, use of cotton swabs, or water in the ear
canal)
OE : Management
• Gram staining and culture of any discharge from the auditory canal may be helpful
• Analgesic (Acetaminophen, NSAID) for pain
• Topical acidifying and drying agents (given to alter the pH and to inhibit the growth of
microorganisms) may be used in mild or resolving cases and are useful in fungal infections.
• Topical antibiotic preparations (antibacterial/antifungal drops) which control microorganism
growth; some also combine steroid in the preparation
• In severe cases, oral or intravenous (IV) antibiotic therapy and narcotic analgesics may be
required. [
• Removal of debris from the ear canal improves the effectiveness of the topical medication.
• Removal of foreign body, if present
• Irrigation with a mix of peroxide and warm water may be useful for removing debris from the
canal, but only if the tympanic membrane is intact.
• Antipruritic/antihistamine
OE: Complications
• Complications of OE are rare and may include the following:
• Necrotizing OE (the most significant complication)
• Mastoiditis
• Chondritis of the auricle (from spread of acute OE to the pinna,
particularly in patients with newly pierced ears)
• Bony erosion of the base of the skull (skull base osteomyelitis [15] )
• Central nervous system (CNS) infection
• Cellulitis or lymphadenitis
Prevention/prognosis
• Eliminate any self-inflicted trauma to the ear canal, such as may occur
with the use of cotton swabs or the insertion of objects (eg, bobby
pins) into the EAC
• Avoid frequent washing of the ears with soap; this leaves an alkaline
residue that neutralizes the acidic pH of the EAC
• Avoid swimming in polluted waters
• Ensure that the ear canals are emptied of water after swimming or
bathing
• Prognosis :Usually resolves fully in 7-10 days
 Otitis Media
• Inflammation/ infection of the middle ear cleft and mastoid cavity
• Most frequent complaint in infant below 3 years old
• Commonly seen between 6-2 4months, declines after age 5
• Recurrent acute otitis media is common, affecting 10-20% of
children by age of one year
• Acute form lasts less than 2weeks
• Chronic form lasts 2 weeks or more
Otitis Media: Etiology
• Etiology can be viral, bacterial co-infection
• Common bacterial organisms include Streptococcus pneumoniae(25-
50%), Haemophilus influenza and Moraxella catarrhalis
• Viral pathogens include RSV, coronaviruses, influenza viruses,
adenoviruses
• Though viral pathogens are important in the pathogenesis, majority
of cases will develop subsequent to bacterial colonization, and hence
AOM should be considered a predominantly bacterial infection.
OM: Risk factors
• Preceding URTI
• Male gender
• Lack of breastfeeding
• Adenoid hypertrophy
• Allergy
• Day-care attendance,
• Smoke exposure
• Pacifier-use
• Immuno-defiency /compromise
• Parental history of recurrent childhood otitis mddia
• Anatomic abnormalities e.g cleft palate
• Ciliary dysfunction
OM: Pathophysiology
• OM begins as an inflammatory process following a viral URTI involving the
mucosa of the nose, mouth nasopharynx, middle ear mucosa and Eustachian
tubes.
• The edema caused by the inflammatory process obstructs the narrowest part
of the Eustachian tube and leads to decrease in ventilation
• There is more reduced (negative)pressure in the middle ear with increased
accumulation of mucosal secretions (this allows for viral/bacterial colonisation
in the middle ear)
• Growth of micro-organisms lead to suppuration and ultimately, frank pus in
the middle ear space and the tympanic membrane may be bulging from the
accumulation
• Rupture of Tympanic membrane leads to otorrhoea
OM: Clinical features
• Ear discharge, Earache (older children), irritability (infants),poor feeding ear-tugging.
• Fever may be high/low present. If high, may be associated with systemic infection
• Otoscopy classically shows a bulging hyperaemic tympanic membrane (), fluid in the
middle ear sapace
• If recurrent AOM occurs along with recurrent infections in other body systems an
underlying immune deficiency should be considered.
• Culture and sensitivity of ear discharge may yield offending organism
• Tympanometry / acoustic reflectometry may also be used to evaluate for middle
ear effussion
OM: Management

• In suppurativeform, fluid from the middle ear can extend to the adjacent
anatomical locations resulting in complications(perforation, mastoiditis,labyrimthitis,
petrositis, meningitis, brain abscess, hearing loss etc
• High- dose Amoxycillin (90mg/kg/day) for 10days is the choice antibiotic
• Amoxycillin- Clavulanate can be given to patients whose symptoms fail to improve
• For Penicillin allergy, Macrolides (Clarithromycin, Azithromyicn),cephalosporins can
beadministered
• Analgesics such as NSAID for pain control.
• Complicatons : hearing loss, TM perforation, mastoiditis, petrositis, meningitis,
subdural empyema, brain abscess, lateral sinus thrombosis
Mastoiditis
• Mastoiditis occurs when infection spreads from the middle ear space to the
mastoid portion of the temporal bone, which lies just behind the ear and
contains air-filled spaces.
• Mastoiditis can range in severity from inflammation of the mastoid
periosteum to bony destruction of the mastoid air cells (coalescent
mastoiditis) with abscess development.
• Mastoiditis can occur in any age group, but more than 60% of the patients
are younger than 2 years. Many children do not have a prior history of
recurrent AOM
• The most common pathogens are S pneumoniae, H influenzae and S
pyogenes.
• Rarely, gram-negative bacilli and anaerobes are isolated
Mastoiditis: Clinical findings
• Post-auricular pain, fever, and an outwardly displaced pinna.
• On examination, the mastoid area often appears indurated and red and
with disease progression may become swollen and fluctuant.
• The earliest finding is severe tenderness on mastoid palpation.
• AOM is almost always present.
• Late findings include a pinna that is pushed forward by post-auricular
swelling and an ear canal that is narrowed due to pressure on the
postero-superior wall from the mastoid abscess.
• In infants younger than 1 year, the swelling occurs superior to the ear
and pushes the pinna downward rather than outward
Mastoiditis: Investigation
• Early mastoiditis may be radiographically indistinguishable from AOM,
with both showing opacification but no destruction of the mastoid air
cells.
• CT Scan best determines the extent of disease
• With progression of mastoiditis, coalescence of the mastoid air cells is
seen.
Mstoiditis: Management
• Intravenous antibiotic treatment alone may be successful if there is no evidence of
coalescence or abscess on CT. However, if there is no improvement within 24–48
hours, surgical intervention should be undertaken. Minimal surgical management
starts with tympanostomy tube insertion, during which cultures are taken.
• If a subperiosteal abscess is present, incision and drainage is also performed, with or
without a cortical mastoidectomy.
• Intracranial extension requires complete mastoidectomy with decompression of the
involved area.
• Antibiotic therapy (intravenous and topical ear drops) is instituted along with surgical
management and relies on culture directed antibiotic therapy for 2–3 weeks.
• An antibiotic regimen should be chosen which is able to cross the blood-brain barrier.
After significant clinical improvement is achieved with parenteral therapy, oral
antibiotics
Mastoiditis:
• Complications include Meningitis, facial palsy, sigmoid sinus
thrombosis, epidural abscess, cavernous sinus thrombosis, and
thrombophlebitis
• Prognosis for full recovery is good.
Rhinosinusitis
• Nasal and sinus mucosa are involved in similar and concurrent inflammatory processes
• Can be acute or chronic
• Acute bacterial rhinosinusitis (ABRS) is a bacterial infection of the paranasal sinuses which lasts less than 30
days and in which the symptoms resolve completely.
• Recurrent rhinosinusitis occurs when episodes of ABRS clear with antibiotic therapy but recur with each or
most upper respiratory infections.
• Chronic rhinosinusitis (CRS) is diagnosed when the child has not cleared the infection in the expected time
but has not developed acute complications.
• Almost always preceded by a viral upper respiratory infection (cold).
• Other predisposing conditions include allergies and trauma.
• Diagnosis of ABRS is made when a child with a cold does not improve by 10–14 days or worsens after 5–7
days.
• The maxillary and ethmoid sinuses are most commonly involved. (These sinuses are present at birth).
• The sphenoid sinuses typically form by the age of 5 years, and the frontal sinuses by age 7–8 years. Frontal
sinusitis is unusual before age 10 years.
Rhinosinusitis: Pathogenesis
• Inflammation of sino-nasal mucosa and obstruction of sinus drainage
underlie the development of rhinosinusitis.
• A combination of anatomic, mucosal, microbial, and immune
pathogenic factors are believed to be involved.
• Viral upper respiratory infections may cause sinus mucosal injury and
swelling, resulting in osteo-meatal obstruction, loss of ciliary activity,
and mucus hypersecretion.
• The bacterial pathogens that commonly cause acute rhinosinusitis are
S pneumoniae, H influenzae (non typeable), M catarrhalis, and β-
hemolytic streptococci.
Rhinosinusitis
• Onset of symptoms in the acute bacterial form may be gradual or
sudden
• Upper respiratory infection symptoms are present 10 or more days
beyond onset, or symptoms worsen within 10 days after an initial
period of improvement
• Commonly include nasal drainage, nasal congestion, facial pressure or
pain, postnasal drainage, hyposmia or anosmia, fever, cough, fatigue,
maxillary dental pain, and ear pressure or fullness.
• Radiographic findings of ABRS, include sinus opacification, fluid, and
mucosal thickening
Rhinosinusitis
• Patients who are toxic, or who have evidence of invasive infection or CNS complications,
should be hospitalized
• Antibiotics are indicated:
• Amoxycillin/ Amoxycillin-Clavulanic acid,
• Cephalosporins
• Macrolides in Penicillin-allergy
• Antibiotic therapy in the chronic rhinosinusitis is similar to that used for ABRS, but the
duration is longer, typically 3–4 weeks.
• Nasal saline irrigations and intranasal steroid sprays have been shown to be helpful in the
reduction of symptoms of CRS
• The mainstay of treatment for pediatric CRS is medical management, with appropriate
antibiotic therapy and treatment of comorbid conditions such as allergic rhinitis and asthma.
• Only a small percentage of children will warrant surgical management
Adenoidal hypertrophy
• The lymphoid tissue in the pharynx consist of the Waldeyer ring :
The Adenoid mass of lymphoid tissue is situated on the posterior
vall of nasopharynx and occupies much of the cavity in young
children; the palatine tonsils at the lateral walls and the lingual
tonsils
• At about 6-7 years atrophy of the lymphoid tissue commences and
is usually complete by 15years
• The adenoid lymphoid tissues may undergo hypertrophy as a result
of repeated upper respiratory tract infection, especially in young
children (1-4 years)
Adenoidal hypertrophy
• Nasal obstruction results in mouth breathing (dry, partially open)
• Recurrent pharyngeal/ chest infections
• Snoring, disturbed sleep (episodic sleep apnea)
• Diagnosis of enlarged adenoids can be confirmed by lateral soft
tissue Xray of the neck (reduced post-nasal space)
• Adenoidectomy is curative
• Complications: failure to thrive, obstructive sleep, apnea
Retropharyngeal abscess
• Retropharyngeal lymph nodes, which drain the adenoids, nasopharynx, and
paranasal sinuses, can become infected
• Commonly due to β-hemolytic streptococci and S aureus.
• If the pyogenic adenitis remains untreated, a retropharyngeal abscess forms.
• This occurs most commonly during the first 2 years of life.
• After 2years of age, the most common cause of retropharyngeal abscess is
superinfection of a penetrating injury of the posterior wall of the oropharynx.
• The diagnosis of retropharyngeal abscess should be strongly suspected in a
child with fever, respiratory symptoms, and neck hyperextension
Retropharyngeal Abscess:Features
• Dysphagia, drooling, dyspnoea, and gurgling respirations are also
present.
• Prominent swelling on one side of the posterior pharyngeal wall is
characteristic.
• Swelling usually stops at the midline because a medial raphe divides
the prevertebral space.
• On lateral neck x-ray, the retropharyngeal tissues are wider than the
C4 vertebral body.
• CT scan with contrast is more helpful.
Retropharyngeal abscess
• Immediate hospitalization and intravenous antimicrobial therapy with
a semisynthetic penicillin or clindamycin is required
• Immediate surgical drainage is required when a definite abscess is
seen radiographically or when the airway is compromised.
• In the child with adenitis, fever will decrease and oral intake will
increase within 24hours.
• A child with retropharyngeal abscess will not improve and may
continue to deteriorate.
• Incision and drainage of the abscess under anesthesia is indicated
Peritonsillar Abscess
• Tonsillar infection occasionally penetrates the tonsillar capsule, spreading to the
surrounding tissues, causing peritonsillar cellulitis.
• Necrosis may occur and a peritonsillar abscess forms.
• The most common pathogen is β-hemolytic streptococcus, but others include
group D streptococcus, S pneumoniae, and anaerobes.
• The patient complains of a severe sore throat even before the physical findings
become marked.
• A high fever is usually present, and the process is almost always unilateral.
• The tonsil bulges medially, and the anterior tonsillar pillar is prominent.
• The soft palate and uvula on the involved side are edematous and displaced
toward the uninvolved side.
Peri-tonsillar Abscess
• As the infection progresses, trismus, ear pain, dysphagia, and drooling may occur.
• The most serious complication of untreated peritonsillar abscess is a lateral
pharyngeal abscess
• In some children, it is possible to aspirate the peritonsillar space to diagnose and
treat an abscess.
• Intravenous antimicrobial therapy is indicated, because aggressive treatment of
cellulitis can usually prevent suppuration.
• Therapy with a penicillin or clindamycin is appropriate.
• Failure to respond to therapy during the first 12–24 hours indicates a high
probability of abscess formation.
• Incision and drainage or for aspiration under anesthesia should be done.
Evaluation of a Child with Stridor
• A symptom, not a diagnosis hence cause must be diagnosed
• Stridor is a high-pitched, monophonic sound produced due to turbulent air-flow through a
partially obstructed upper airway at the level of the larynx or trachea (compared to the
polyphonic sound heard in the lower airway in wheezing)
• A common presentation in the paediatric population that necessitates prompt evaluation and
intevention
• It can be variable in character (musical, harsh, breathy)
• Depending on its timing in the respiratory cycle, may be inspiratory, expiratory or biphasic
(helps to determine the anatomic location of airway obstruction)
• Inspiratory stridor suggests laryngeal obstruction
• Expiratory stridor suggests tracheobronchial obstruction
• Biphasic: at the level of larynx
• Treatment for stridor must be tailored to the underlying condition
Stridor: Pathophysiology

• Gases produce pressure in all directions, however when moving in a linear

direction, it produces pressure in a forwad veccctor and decreses the
lateral pressure
• When air passes through a narrowed flexible airway in a child, the lateral
pressure can drop precipitously (Bernoulli Principle) and cause the tube to
close
• Above process obstructs airflow and produces stridor
• A decrease in radius of airway o the upper airway also lead to increased
airway resistance and increase effort of breathing
• Due to the smaller diameter of the paediatric airway compared to that of adults,
minor changes can lead to a marked reduction in overall airway calibre/ patency
 Stridor: Etiology
• Acute Stridor Chronic Stridor
• LTB Laryngotracheomalacia
• Foreign body aspiration Subglottic Stenosis
• Epiglottitis Vocal cord dysfynction
• Retropharyngeal abscess Laryngeal web/ cysts
• Peritonsillar abscess Vacular rings, slings
• Allergic reaction, anaphylaxis
Stridor: Clinical Features- History
• Noisy breathing –loud, raspy (most common)
• May be acute or chronic depending on underlying condition
• Age of onset(congenital/ acquired), duration, progression and severity should be noted
• Precipitating events
• Positioning
• Quality and nature of crying, aphonia
• Associated symptom: cough, fever, drooling, cyanosis, respiratory distress, cessation of
breathing, snoring etc
• Allergies, infection
• Prenatal history: type of delivery, endotracheal intubation/duration, congenital
anomalies
• Previous surgery that may have caused damage to the reurent laryngeal nerve
Stridor: Examination

• If stridor is of acute onset, severity of stridor and respiratory

compromise should be assessed
• The following should be noted: pulse rate, respiratory rate,
cyanosis, use of accessory muscles of respiration, nasal flaring, level
of consciousness and responsiveness
Stridor: Management steps:
Emergency Medical care
• Vital signs are crucial in identifying patients with impending respiratory collapse.
• Continuous pulse oximetry and close observation is paramount in a patient presenting with acute stridor.
• Arterial blood gas : moderate – severe cases
• Observe respiratory effort by assessing for: retractions (intercostal, supraclavicular, and substernal),
nasal flaring, drooling, cyanosis, agitation.
• Resuscitate: ABC
• Administer supplemental oxygen as indicated
• Obtain samples as indicated
• Commence antibiotics for infections (Epiglottitis)
• Steroids as indicated (LTB)
• Heimlich manoeuver (may be done if complete obstruction is suspected (unable to speak, breathe) -
has improved mortality rate but can dislodge the foreign body further into lower airways if the
obstruction is partial
• Thumb/ back hits (in infants)
Stridor: Management
• Lab evaluation may be formed as indicated by clinical situation e.g CBC/ Blood culture in infective
condition such as epiglottitis
• Laryngoscopy/Bronchoscopy for direct evaluation of airway (avoid in epiglottitis except you can
intubate): laryngomalacia, true vocal cord paresis, laryngeal web/cyst
• Laryngeal / subglottic foreign bodies need urgent intervention : may be removed by rigid
bronchoscope
• Antero-posterior and lateral radiographs of neck and chest help to define the size of the
epiglottis, retropharyngeal profile and anatomy of trachea
• Barium esophagography: vascular compression, TEF
• CT/MRI: delineate lesions in the upper airway and vascular anomalies
• Occasionally, Tracheostomy may be instated to protect the airway to bypass laryngeal/ tracheal
abnormalities e.g retropharyngeal abscess
• Surgery: Severe laryngomalacia, laryngeal stenosis/large cysts, pappilloma/ haemangioma, foreign
body