Transcript UPPER respiratory lecture 2011 ped (2)

Upper respiratory
tract infection in
pediatrics (URTI)
RTI ( respiratory tract
infection) IMPORTANCE
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Nearly 50% of all paediatric consultations in
industrialized countries are caused by respiratory tract
infections (RTIs). Acute RTIs are among the leading
causes of childhood mortality, especially in developing
countries.
Their annual incidence per child decreases with age:
6.1 in children less than 1 year
5.7 in children aged 1-2
4.7 in children aged 3-4
3.5 in children aged 5-9
2.7 in children aged 10-14
2.4 in children aged 15-19.
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Upper respiratory tract infection (URTI)
represents the most common acute illness .
Rates are highest in children younger than 5
years. Children who attend school or daycare
are a large reservoir for URIs, and they
transfer infection to those who care for them.
Acute pharyngitis accounts for 1% of all
ambulatory visits.
The incidence of viral and bacterial
pharyngitis peaks in children aged 4-7 years.
Rhinopharyngitis
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Nasopharyngitis (rhinopharyngitis or the
common cold) = Inflammation of the
nares, pharynx, hypopharynx, uvula, and
tonsils
Occur year round, but mostly during fall
and winter. Epidemics is most common
during cold months, with a peak
incidence in late winter to early spring.
Humidity may also affect the prevalence
of colds, because most viral URI agents
thrive in the low humidity characteristic
of winter months
Etiology of
rhinopharyngitis
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Rhinoviruses: These cause approximately 30-50%
RSV
Coronaviruses: Enteroviruses, including
coxsackieviruses, echoviruses, and others: These
are also leading causes of the common cold.
Other viruses: Adenoviruses, orthomyxoviruses
(including influenza A and B viruses),
paramyxoviruses , EBV, account for many URIs.
Varicella, rubella, and rubeola
Bacteria ( very rare): streptococci , staph, diphteria,
B pertussis, Haemophilus, Pneumococcus,
Neisseria, Treponema
Risk factors for URIs
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Contact: Close contact with small children settings, such as
school or daycare, increases the risk of URI.
Travel: , exposure to large numbers of individuals in closed
settings. Increased exposure to respiratory pathogens
Environmental factors such as passive smoking and
exposure to pollutants
Immunocompromise that affects cellular or humoral
immunity: Splenectomy, HIV infection, corticosteroids,
immunosuppressive treatment , familial predisposition
with immunological defects or anatomical and/or
physiological features
Malnutrition
Atopic status
Lack of breast-feeding
Cilia dyskinesia syndrome and cystic fibrosis
Anatomic changes due to facial dysmorphisms
Upper airway trauma, and nasal polyposis
Anemia, rickets, malnutrition
Carrier state
Pathophysiology URI
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Direct invasion of the mucosa lining the upper
airway
Person-to-person spread of viruses by hand with
pathogens to the nose or mouth or inhaling
respiratory droplets from an infected person who is
coughing or sneezing.
Barriers, including physical, mechanical, humoral,
and cellular immune defenses.
Hair lining the nose filters
Mucus coats
Ciliated cells lower in the respiratory tract trap and
transport pathogens up to the pharynx, where they
are then swallowed into the stomach
Adenoids and tonsils contain immune cells that
respond to pathogens.
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local swelling, erythema, edema, secretions, and
fever, result from the inflammatory response of
the immune system to invading pathogens and
from toxins
initial nasopharyngeal infection may spread to
adjacent structures, resulting in sinusitis, otitis
media, epiglottitis, laryngitis, tracheobronchitis,
and pneumonia
Humoral immunity (immunoglobulin A) and
cellular immunity
Normal nasopharyngeal flora, including various
staphylococcal and streptococcal species, help
defend against potential pathogens
Suboptimal humoral and phagocytic immune
function have URI increased risk and have severe
or prolonged course of disease.
SYMPTOMS OF RF
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Nasal obstruction
Congestion of nasal breathing
Sneezing
Rhinorrhea : secretions often evolve from clear
to opaque white to green to yellow within 2-3
days of symptom onset
Cough
Anorrhexia
Fever
5-10 days
– Foul breath: This occurs as resident flora process
the products of the inflammatory process.
– Hyposmia: Also termed anosmia, it is secondary to
nasal inflammation.
– Headache
– Sinus symptoms: These may include congestion
or pressure and are common with viral URIs.
– Photophobia or conjunctivitis: adenovirus .
– Influenza : pain behind the eyes, pain with eye
movement, or conjunctivitis.
– Itchy, watery eyes are common in patients with
allergic conditions.
– Fever: This is usually slight or absent, but
temperatures can reach 39.5°C in infants and
young children. If present, fever typically lasts
for only a few days.
– Gastrointestinal symptoms: Symptoms such as
nausea, vomiting, and diarrhea may occur in
persons with influenza, especially in children.
Nausea and abdominal pain may be present in
individuals with strep throat and viral syndromes.
LABORATORY
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CBC, ES, CRP, to find bacterian infection, Leucocytosis
with neutrophilia suggest bacterian, low level of WBC,
lymphocytes raised – in viral infections
Because viruses cause most URIs, the diagnostic role of
laboratory investigations and radiologic studies is
limited. Viral culture, rapid antigen detection, or
polymerase chain reaction (PCR) assay of influenza virus
on a nasopharyngeal swab could be done if specific
antiviral therapy is recommended. Similar tests are also
available for adenovirus, respiratory syncytial virus, and
parainfluenza virus.
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The use of reverse-transcriptase PCR for the
diagnosis of enterovirus and rhinovirus
infections is not currently available for daily
clinical care.
Serologic tests for mononucleosis
Influenza serologies only have epidemiologic
value and should not be used for clinical care.
A pharyngeal swab for rapid antigen
detection of GABHS (Group A Beta-Hemolytic
Streptococci ) is 90% sensitive and 95%
specific
NOSE AND THROAT cultures
COMPLICATIONS
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Sinusitis is a complication in only approximately
2% of persons with viral URIs
Otitis
Epiglottitis occurs at a rate of 6-14 cases per
100,000 children
Croup, or laryngotracheobronchitis usually
occurs in children aged 6 months to 6 years
with peak incidence in the second year of life
Pneumonia
Digestive complications: anorrhexia, vomiting,
diarrhea, dehidration,
Seizures may appear when fever is more than
38,5 ̊ C
Imaging Studies for URTI
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A lateral neck radiograph should be taken in a patient with
stridor to assess the airways if epiglottitis is clinically suspected
Chest radiography should be reserved for patients with acute
tracheobronchitis , those with abnormal vital signs or signs of
consolidation on chest examination, or those with persistent
symptoms for longer than 3 weeks.
Plain radiography has been largely replaced by computed
tomography (CT) in the evaluation of sinusitis, particularly in
preparation for corrective surgery. Complete opacification and
air-fluid level are the most specific findings for acute sinusitis.
However, a large proportion of patients with the common cold
have radiologic abnormalities on CT. Imaging is recommended
for patients who do not respond to treatment with antibiotics and
decongestants, but is not advised for the diagnosis of
uncomplicated sinusitis. Mastoiditis and other intracranial
complications of URIs should be evaluated by CT or magnetic
resonance imaging.
PREVENTION AND
TREATMENT
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Prevention : VACCINES, IMMUNOSTIMULANTS,
VITAMINS
– Parent education on risk factor modification, in particular avoiding
smoking indoors
– General hygiene methods for children attending day care centres
– Breast feeding
Management
– Rest
– Lot of fluid intake.
– Nasal wash with hypertonic salt water or 0.9% saline
– Decongestants to unblock the opening of sinuses and reduce
symptoms of nasal congestion in children above 3 years
– Paracetamol 30-40 mg/kg/day for fever and pain reliever
– Antibiotics to treat the bacterial infection very rare ( fever, ES high,
CRP+leucocytosis, children with immune handicaps)
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ADENOIDITIS
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Adenoids begin forming in 3rd month of
fetal development
Covered by pseudostratified ciliated epithelium
Fully formed by 7 month
Palatine tonsils begin development in 3rd month of fetal
development
Acute adenoiditis
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! Symptoms include:
– Purulent rhinorrhea
– Nasal obstruction
– Fever
Frequent complication: otitis media
Recurrent Acute Adenoiditis
! 4 or more episodes of acute adenoiditis in a
6 month period
! Similar presentation as recurrent acute
rhinosinusitis
! In older children nasal endoscopy can help
Chronic adenoiditis
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! Symptoms include:
– Persistent rhinorrhea
– Postnasal drip
– Malodorous breath
– Associated otitis media >3 months
– Think of reflux
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Obstructive Adenoid Hyperplasia
! Signs and Symptoms
– Obligate mouth breathing
– Hyponasal voice
– Snoring and other signs of sleep
disturbance
Obstructive Tonsillar Hyperplasia
! Snoring and other symptoms of sleep
disturbance
! Muffled voice
! Dysphagia
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Surgery to Remove the Adenoids
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Adenoids are lymph nodes located high in the back of
the throat. They can become enlarged from repeated
ear infections and can affect the Eustachian tubes that
connect the middle ears and the back of the nose. An
adenoidectomy (removal of the adenoids) may help
children with recurring ear infections have fewer of
them. Adenoidectomy is typically done when recurring
ear infections continue despite antibiotic treatment.
ACUTE PHARYNGITIS
(TONSILITIS)
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viral pharyngitis
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Adenovirus, which may also cause laryngitis and conjunctivitis
Influenza viruses
Coxsackievirus
HSV
EBV (infectious mononucleosis)
Cytomegalovirus
causes of bacterial pharyngitis
– Group A streptococci (approximately 15% of all cases of
pharyngitis)
– Group C and G streptococci
– N gonorrhoeae
– Arcanobacterium (Corynebacterium) hemolyticum
– Corynebacterium diphtheriae
– Atypical bacteria (eg, M pneumoniae, C pneumoniae):
Anaerobic bacteria
Immunology and Function
TONSILS AND ADENOIDS
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! Part of secondary immune system
! Exposed to ingested or inspired antigens
passed through the epithelial layer
! Immunologic structure is divided into 4
compartments: reticular crypt
epithelium, extra follicular area,
mantle zone of the lymphoid
follicle, and the germinal center of the
lymphoid follicle
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Membrane cells and antigen presenting cells
are involved in transport of antigen from the
surface to the lymphoid follicle
! Antigen is presented to T-helper cells
! T-helper cells induce B cells in germinal
center to produce antibody
! Secretory IgA is primary antibody produced
! Involved in local immunity
Acute Tonsillitis
Signs and symptoms:
 – Fever
 – Sore throat
 – Tender cervical lymphadenopathy
 – Dysphagia
 – Erythematous tonsils with exudates
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Pharyngeal erythema: Marked erythema
:adenoviral infection. In contrast, rhinoviral
and coronaviral infections do not have
severe erythema.
Exudates: half the patients with adenovirus
infections. Exudative pharyngitis and
tonsillitis may be seen with mononucleosis
caused by EBV Yellow or green secretions do
not differentiate a bacterial pharyngitis from
a viral one.
Foul breath: This may be noted because
resident florae process the products of the
inflammatory process.
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Conjunctivitis -adenovirus.
Scleral icterus - infectious mononucleosis.
Rhinorrhea - viral cause.
Tonsillopharyngeal/palatal petechiae - GAS infections and
infectious mononucleosis.
A tonsillopharyngeal exudate - streptococcal infectious
mononucleosis and occasionally in M pneumoniae, C
pneumoniae, A haemolyticus, adenovirus, and herpesvirus
infections.
exudate does not differentiate viral and
bacterial causes.
Oropharyngeal vesicular lesions are seen in coxsackievirus and
herpesvirus
Lymphadenopathy
Cardiovascular: Murmurs
Pulmonary: Pharyngitis and lower respiratory tract infections
with M pneumoniae or C pneumoniae,
Abdomen: Hepatosplenomegaly - mononucleosis infection
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Tonsillar hypertrophy: Peritonsillar abscess may
manifest as unilateral palatal and tonsillar pillar
swelling, with downward and medial tonsil
displacement; the uvula may tilt to the opposite
side. Bulging of the posterior pharyngeal wall
may signal a retropharyngeal abscess.
Tender anterior cervical adenopathy: This may be
present with streptococcal infection or with viral
infections. In persons with diphtheria,
submandibular and anterior cervical edema may
be present along with adenopathy.
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Erythema: This may be especially
prominent in persons with group A
streptococcal pharyngitis. Palatal petechiae
may be seen.
Exudates of the pharynx: These are
common with bacterial pharyngitis,
manifesting as white or yellow patches. A
whitish coating may appear on the tongue,
causing the normal bumps to appear more
prominent. Yellow or green coloration does
not differentiate bacterial pharyngitis from
a viral nasopharyngitis.
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A whitish adherent membrane forming
on the nasal septum, along with a
mucopurulent blood-tinged discharge,
should prompt a consideration of
diphtheria. Pharyngeal and tonsillar
diphtheria may manifest as an adherent
blue-white or gray-green membrane over
the tonsils or soft palate; if bleeding has
occurred, the membrane may appear
blackish.
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Fever: Compared with other URIs, group A
streptococcal infections are more likely cause fever,
with temperatures around 38.3°C fever is not
reliable to differentiate viral or bacterial etiologies.
Group A beta-hemolytic streptococci: The classic
clinical picture includes a fever, tonsillopharyngeal
erythema and exudate; swollen, tender anterior
cervical adenopathy; headache; emesis in children;
palatal petechiae; midwinter to early spring season;
and absent cough or rhinorrhea.
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Conjunctivitis: This symptom may be seen
with adenoviral pharyngoconjunctival fever
and is present in one half to one third of all
adenoviral URIs. Watery, injected conjunctiva
may also be seen with allergic conditions.
Cough: This is more suggestive of a viral than
a bacterial etiology.
Diarrhea: If associated with a URI, it suggests
a viral etiology.
Fever: EBV infections and influenza cause
fever.
Bacterial pharyngitis
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This may be difficult to distinguish from viral
pharyngitis. Assessment for group A streptococci
warrants special attention. Physical findings that
suggest a high risk for group A streptococcal
disease are erythema, swelling, or exudates of
the tonsils or pharynx; temperature of 38.3°C or
higher; tender anterior cervical nodes (>1 cm);
and an absence of conjunctivitis, cough, or
rhinorrhea, which are suggestive of viral illness.
•Mucosal ulcers, erosions, vesicles: The presence of palatal
vesicles or shallow ulcers is characteristic of primary infection with
HSV.
• Ulcerative stomatitis may also occur in coxsackievirus or other
enteroviral infection. Mucosal erosions may also be seen in
primary HIV infection. Small vesicles on the soft palate, uvula, and
anterior tonsillar pillars suggest infection by coxsackievirus, known
as herpangina.
Tonsillar hypertrophy
Foul breath: Halitosis may be noted because resident florae
process the products of the inflammatory process.
Anterior cervical lymphadenopathy: This is seen with viral and
bacterial infections.
Approximately half of EBV mononucleosis cases involve
generalized adenopathy or splenomegaly. An enlarged liver may
also be palpable. Primary HIV infection may also include
lymphadenopathy.
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A rash may be seen with group A
streptococcal infections, particularly in
patients younger than 18 years.
This scarlet fever rash appears as tiny
papules over the chest and abdomen,
creating roughness like sunburned
appearance.
The rash spreads, causing erythema in the
groin and armpits. The face may be flushed,
with pallor around the lips. Approximately 25 days later, the rash begins to resolve.
Peeling is often noted on the tips of toes
and fingers
COMPLICATIONS
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In the neighbourhood:
Adenitis
Retropharyngeal abscess
Peritonsilar abcess
Otitis
Sinusitis ( epiglotitis)
At distance:
acute glomerulonephritis, acute rheumatic fever,
and rheumatic heart disease
toxic shock syndrome for GAS ( group A
Streptococcus )
Recurrent Acute Tonsillitis
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! Same signs and symptoms as acute
! Occurring in 4-7 separate episodes
per year
! 5 episodes per year for 2 years
! 3 episodes per year for 3 years
Medical Management
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! Penicillin is first line treatment
! Recurrent or unresponsive infections require
treatment with beta-lactamase resistant
antibiotics
such as
Erytromycin, Claritromycin
Clindamycin
Augmentin: 30-40 mg/kg in 2 doses. Syrup,
tablets
Cephalosporins ( Ist and II gen)
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Tonsillectomy
! Current clinical indicators :
– 3 or more infections per year despite adequate
medical therapy
– Hypertrophy causing dental malocclusion or
adversely affecting orofacial growth
documented by orthodontist
– Hypertrophy causing upper airway obstruction,
severe dysphagia, sleep disorder,
cardiopulmonary complications
Peritonsillar abscess
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! Abscess formation outside tonsillar capsule
! Signs and symptoms:
– Fever
– Sore throat
– Dysphagia/odynophagia
– Drooling
– Trismus
– Unilateral swelling of soft palate/pharynx
with uvula
deviation
Peritonsillar abscess
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Peritonsillar abscess unresponsive to medical
management and drainage documented by
surgeon,
unless surgery performed during acute stage
– Persistent foul taste or breath due to chronic
tonsillitis
not responsive to medical therapy
– Chronic or recurrent tonsillitis associated with
streptococcal carrier state and not responding to
betalactamase
resistant antibiotics
– Unilateral tonsil hypertrophy presumed
neoplastic
Chronic Tonsillitis
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! Chronic sore throat
! Malodorous breath
! Presence of tonsilliths
! Peritonsillar erythema
! Persistent tender cervical
lymphadenopathy
! Lasting at least 3 months
OTITIS MEDIA
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The eustachian tubes equalize the pressure between the
middle ear cavity and the outside atmosphere and allow
fluid and mucus to drain out of the middle ear cavity.
Inflammation of the middle ear causes the tubes to
close causing the fluid to become trapped. Bacteria from
the back of the nose travel through the eustachian tube
directly into the middle ear cavity and multiply in the
fluid. The inflammation can occur as a result of an
infection extending up the eustachian tube. This tube
may become blocked by a bacterial or viral infection or
by enlarged adenoids. Fluid produced by the
inflammation cannot drain off through the tube and
instead collects in the middle ear.
The Eustachian tube is a
canal that connects the
middle ear to the throat.
It is lined with mucus,
just like the nose and
throat; it helps clear
fluid out of the middle
ear and into the nasal
passages. Cold, flu, and
allergies can irritate the
Eustachian tube and
cause the lining of this
passageway to become
swollen.
Ear Infection
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diagnose an ear
infection by
looking at the
outer ear and the
eardrum with a
device called an
otoscope. A
healthy eardrum
(shown here)
appears
transparent and
pinkish-gray. An
infected eardrum
looks red and
swollen.
If the Eustachian tube
becomes blocked, fluid
builds up in the middle
ear. This creates an
environment for bacteria
and viruses, which can
cause infection; fluid is
detected in the middle
ear with a pneumatic
otoscope. This device
blows a small amount of
air at the eardrum,
making the eardrum
vibrate. If fluid is
present, the eardrum will
not move as much as it
should.
Ruptured Eardrum
When too much fluid
builds up in the middle
ear, it can put pressure
on the eardrum until it
ruptures (shown here).
Signs of a ruptured
eardrum include yellow,
brown, or white fluid
draining from the ear.
Pain may disappear
suddenly because the
pressure of the fluid on
the eardrum is gone.
Although a ruptured
eardrum sounds
frightening, it usually
heals itself in a couple of
weeks.
SIGNS AND SYMPTOMS
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Ear Infection Symptom
Sudden, piercing pain in the ear which may be worse when lying
down, making it difficult to sleep.
Trouble hearing.
A fever of up to 40 ̊ C .
Tugging or pulling at one or both ears.
Fluid drainage from ears.
Loss of balance.
Nausea, vomiting, or diarrhea.
Congestion.
Ear Infection Symptoms: Babies
It can be difficult to identify an ear infection in babies or
children :crankiness, trouble sleeping, and loss of
appetite. Babies may push their bottles away because
pressure in the middle ear makes it painful to swallow.
Laboratory
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WBC, ES, Fg, CRP, high if bacterian
Local exam with otoscope
Cultures of otic discharge
Imagery when progresses through
otomastoiditis
COMPLCATIONS
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CRONIC OTITIS
OTOMASTOIDITIS
DEAFNESS
CEREBRAL VENOUS TROMBOSIS
CEREBRAL ABCESS
MENINGITIS
DIARRHEEA, DEHIDRATION
SEIZURES
PREVENTION OF OTITIS
MEDIA
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• Encouraging breast-feeding
• Feeding child upright if bottle fed
• Avoiding exposure to passive smoke
• Teaching adults and children careful hand
washing technique
• Limiting exposure to viral upper respiratory
infections
• Ensure immunizations are up-to-date;
including influenza and 7 valent conjugated
polysaccharide vaccine (PCV7)
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One solution is for your doctor to
insert small tubes through the
eardrum. Ear tubes let fluid drain out
of the middle ear and prevent fluid
from building back up. This can
decrease pressure and pain, while
restoring hearing. The tubes are
usually left in for 8 to 18 months until
they fall out on their own.
Treatment of otitis media
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Desinfection of nasopharynx
Analgesics (oral and topical pain killing
therapy)
Paracetamol, ibuprophene, NO aspirin
Children with low risk be treated with a
wait-and-see approach.
Low-dose amoxicillin (40 mg/kg/day)
may be used if low risk (greater than two
years, no day care, and no antibiotics for
the past three months)
Failure to respond to initial treatment drug (resistant
or persistent acute otitis media)
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amoxicillin/clavulanate potassium,
• cefuroxime axetil,
• • cefpodoxime proxetil.
• Trimethoprim sulfamethoxasone: Bactrim, biseptol 6-8 mg/kg in 2
daily doses
• Clarithromycin 15-20 mg/kg
• Erythromycin ethylsuccinate and sulfisoxazole acetyl: 30-40mg/kg
• Azithromycin
a single dose of ceftriaxone 50 mg/kg could be equivalent
to a 10-day course of oral antibiotics for new cases of acute
otitis media
ceftriaxone sodium: prescribe one dose for new onset otitis media
and a three-day course for a truly resistant pattern of otitis media
or if oral treatment cannot be given, 5 days
Acute inflamation of larynx
Laryngotracheobronchitis
(croup)
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is a viral infection of the upper respiratory tract that
causes varying degrees of airway obstruction
prodrome of several days of fever and symptoms of
mild upper respiratory infection
the infection extends to the proximal trachea,
diffuse inflammation with exudate and edema of
the subglottic area causes narrowing of the airway.
5 cases per 100 children per year during the second
year of life
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Typically, between 6 pm and 6 am, the child develops stridor
(mainly inspiratory), hoarseness, and barking cough.
Worsening symptoms on the second night of the illness.
The child is fatigued.
Physical
The physical examination may range from totally unremarkable
on presentation to severe respiratory distress.
Restless (common); prefers sitting upright in a parent's lap
Appears nontoxic
Normal voice or laryngitis
Mild fever
Tachycardia
Tachypnea
Varying stridor, predominantly inspiratory
Absence of drooling
Retractions of the accessory chest muscles
No change in stridor with positioning
ETIOLOGY
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parainfluenza type 1, although parainfluenza type 2 and type
3 also may cause disease. Paramyxovirus
Influenza virus type A
Respiratory syncytial virus (RSV)
Adenovirus
Rhinoviruses
Enterovirus
Coxsackievirus
Enteric cytopathogenic human orphan virus (ECHO virus)
Reovirus
Measles virus
DIFFERENTIAL DG
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Diphtheria
Foreign Bodies IN Trachea
Epiglottitis
Foreign Body Ingestion
Subglottic stenosis
Retropharyngeal abscess
Subglottic hemangioma
Laboratory
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A pulse oximetry measurement
CBC count Leukopenia in early stage of illness, leukocytosis in
later stage of patients with severe disease
Anteroposterior (AP) soft tissue neck radiograph may show
subglottic narrowing
Rapid antigen tests
Direct laryngoscopy
Fiberoptic laryngoscopy
Bronchoscopy
Treatment
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Make the child as comfortable as possible.
Avoid agitating the child Humidified air or mist
therapy may be used, but both have unproven
efficacy.
Provide oxygen (humidified) L -epinephrine
(1:1000) is as effective as racemic epinephrine.
Dexamethasone has been shown to reduce
symptoms in patients with moderate-to-severe
croup. (0.6 mg/kg IM, not to exceed 10 mg)
Nebulized budesonide (2 mg) has been shown
in several studies to be equivalent to oral
dexamethasone. Inhaled Decadron is also used
when budesonide is unavailable.
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Racemic epinephrine: 0.25-0.5 mL of 2.25%
solution (equivalent to 1% epinephrine) via
nebulizer (diluted in 3 mL of isotonic sodium
chloride solution or sterile water); may be
repeated 3 times
Antiinflamatory: paracetamol, ibuprophen
Antibiotherapy: amoxicillin, augmentin,
cephalosporin, macrolides
Epiglottitis
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Epiglottitis, also termed supraglottitis, is an inflammation
of the epiglottis and/or the supraglottic tissues
surrounding the epiglottis, including the aryepiglottic
folds, arytenoid soft tissue, and, occasionally, the uvula.
This condition is more often found in children aged 15 years who present with a sudden onset of
symptoms:
Sore throat
Drooling, odynophagia or dysphagia, difficulty or pain
during swallowing, globus sensation of a lump in the
throat
Muffled dysphonia or loss of voice
Dry cough or no cough, dyspnea
Fever, fatigue or malaise
Etiology
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H influenza type B (HiB)
and Streptococcus pneumonia, S
aureus, Varicella can cause a primar
or secondary infection often with
group A beta-hemolytic
streptococci,C albicans, especially in
immunocompromised
patients.Several viruses, including
herpes species and parainfluenza
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The clinical triad of drooling,
dysphagia, and distress is the classic
presentation. Fever with associated
respiratory distress or air hunger
occurs in most patients.
the patient appears acutely ill, anxious, and
usually assumes a characteristic tripod position
child may have stridorous respirations, but as
the disease progresses, airway sounds may
diminish. Additional signs of upper airway
obstruction are also evident including
suprasternal, subcostal, and intercostal
retractions.
Pathophysiology
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Bacterial infection of the epiglottis leads to acute onset of
inflammatory edema, beginning on the lingual surface of
the epiglottis where the submucosa is loosely attached.
Swelling significantly reduces the airway aperture.
Edema rapidly progresses to involve the aryepiglottic folds,
the arytenoids, and the entire supraglottic larynx. The
tightly bound epithelium on the vocal cords halts edema
spread at this level. Aspiration of oropharyngeal
secretions or mucus plugging can cause respiratory
arrest.
Mortality rates as high as 10% can occur in children whose
airways are not protected by endotracheal incubation. With
endotracheal intubation, mortality is less than 1%.
Differential Diagnoses
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Bacterial tracheitis
Pediatrics, Pertussis
Foreign Bodies, Trachea
Pharyngitis
Mononucleosis
Pneumonia
Anaphylaxis
Peritonsillar Abscess
Croup or Laryngotracheobronchitis
Retropharyngeal Abscess
Foreign Body Ingestion
Toxicity, Caustic Ingestions
Laboratory
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CBC, ESR, Fg, CRP, Oximetry (periferal O2
concentratin in
Blood cultures and culture of the epiglottis )
In cases of HiB epiglottitis, blood cultures
Lateral neck radiographs may show an
enlarged epiglottis. Chest radiography may
also reveal a pneumonia
CT scan of the neck
Treatment EMERGENCY:
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Immediate transport to the nearest appropriate facility
Position of comfort.
Oxygen
Orotracheal intubation or needle cricothyroidotomy
may be necessary in emergent situations
Percutaneous transtracheal ventilation
Also termed needle cricothyroidotomy or translaryngeal ventilation,
percutaneous transtracheal ventilation is a temporizing method used to
treat cases of severe epiglottitis when the patient cannot be intubated
proceeding to a formal tracheostomy.
Percutaneous transtracheal ventilation involves inserting a needle
through the cricothyroid membrane, which lies inferior to the thyroid
cartilage and superior to the cricoid cartilage. The cricothyroid artery
typically courses through the superior portion of the membrane.
Antibiotics
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Empiric antimicrobial therapy must cover all likely
pathogens in the context of the clinical setting for
7-10 days
Ceftriaxone (Rocephin) 75-100 mg/kg/d IV q1224h
Ampicillin 100-200 mg/kg/d IV divided q6h
Clindamycin 25-40 mg/kg/d IV divided q6-8h
Ampicillin and sulbactam (Unasyn)
3 months to 12 years: 100-200 mg ampicillin/kg/d
(150-300 mg Unasyn) IV divided q6h
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SINUSITIS
Chronic maxillary sinusitis , frontal sinusitis.
Etiology and risk factors:
viral upper respiratory tract infections (URTIs) or nasal
allergies and the host response to these insults,allergic
rhinitis, anatomical abnormalities,gastroesophageal
reflux (GER), immune deficiency, and disorders of
ciliary function
Approximately 5-13% of URTIs are complicated
by bacterial sinusitis
Children are susceptible to serious sequelae
from a complication of sinusitis such as orbital
cellulites (in about 9.3% of the cases) and
intracranial complications (in 3.7-11% of
patients).
ETIOLOGY
– Streptococcus pneumoniae - 20-30%
– Haemophilus influenzae - 15-20%
– Moraxella catarrhalis - 15-20% Streptococcus
pyogenes (beta-hemolytic) - 5%
– Chronic sinusitis more commonly a polymicrobial
infection
– Commonly cultured bacteria
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Alpha-hemolytic streptococci
Staphylococcus aureus
Coagulase-negative staphylococci
Nontypeable H influenzae – More common than acute
sinusitis
Moraxella catarrhalis
Anaerobic bacteria, including Peptostreptococcus,
Prevotella, Bacteroides, andFusobacterium species
Pseudomonads - More common after multiple courses of
antibiotics; consider immunodeficiency
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Several anatomical abnormalities of the lateral nasal wall can
predispose to sinusitis.
Immune deficiencies are more common in the general
population than cystic fibrosis or ciliary disorders. In order of
decreasing prevalence, the most common types are common
variable, immunoglobulin G (IgG) subclass, and selective
antibody.
Impaired nasal function increases postnasal drip and irritant
burden on the lower airways, which can exacerbate asthma
symptoms.
Gastroesophageal reflux disease ( GER may lead to
inflammation of the eustachian tube orifices or sinus ostia
secondary to mucosal irritation. )
SIGNS AND SYMPTOMS
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Signs and symptoms of severe infection :
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Nasal congestion
Infrequent fever
Otitis media (50-60% of patients)
Irritability
Headache
Purulent rhinorrhea
High fever (ie, >39°C)
Periorbital edema
Uncomplicated sinusitis spontaneously resolves in
40% of patients.
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Acute sinusitis :signs and symptoms normally clear within
30 days; URTI symptoms persisting longer than 7-10 days
suggest acute sinusitis
Chronic sinusitis is defined as low-grade persistence of signs
and/or symptoms lasting longer than 90 days without
improvement.
The patient may have 6 or more recurrent episodes per year.
The patient may have a history of acute exacerbations without
ever being completely well between episodes.
Night time cough is more prevalent.
Anterior rhinoscopy
Difficult in young children.
Examine the middle turbinate and middle meatus for evidence
of purulence or sinus discharge with a vasoconstrictive agent,
such as oxymetazoline and lidocaine.
Polyps may suggest cystic fibrosis.
Laboratory and Imagery
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CBC, ES, Fg, IgE,
CT scanning is the criterion standard for evaluation of both mucosal
inflammation and anatomical abnormalities in the paranasal sinuses.
Plain radiography/sinus series
Rigid or flexible nasal endoscopy
Indications for maxillary sinus puncture in children include the following:
 Severe toxic illness
 Acute illness unresponsive to antibiotics within 72 hours
 Immunocompromised patients
 Suppurative complications
 Workup for fever of unknown origin
 Nasal and maxillary cultures.
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Complications
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Preseptal cellulitis - Eyelid edema, erythema, normal globe
movement
Orbital cellulitis - Proptosis, chemosis
Periorbital abscess - Proptosis with globe displaced
inferolaterally, decreased extraocular muscle movement
Orbital abscess - Severe proptosis, impaired visual acuity,
fixed globe, toxic patient
Cavernous sinus thrombosis - High fever, bilateral symptoms
Intracranial involvement usually occurs subsequent to direct
spread from sphenoid or frontal sinus disease.
Subdural and frontal lobe abscesses are most common.
Meningitis may occur.
TREATMENT
Nasal decongestants and mucolytics orally or nebulization are effective
 Antibiotherapy: uncomplicated cases of acute sinusitis are responsive to
amoxicillin; for children allergic to penicillin, a second- or third-generation
cephalosporin can be used ; a macrolide or clindamycin can be used.
Amoxicillin: 80 mg/kg/d PO divided bid; consider in children in
large day care settings
 Amoxicillin-clavulanate (Augmentin)
<3 months: 125 mg/5mL PO susp based on amoxicillin; 30 mg/kg/d divided
bid for 7-10 d
>3 months: If using 200 mg/5 mL or 400 mg/5 mL susp, 45 mg/kg/d PO
divided q12h; if using 125 mg/5 mL or 250 mg/5 mL suspension, 40
mg/kg/d PO divided q8h for 7-10 d, or high dose 80-90 mg/kg/d PO divided
bid
Cefuroxime 20-30 mg/kg/d PO divided bid
Azithromycin (Zithromax) 10 mg/kg PO first d, 5 mg/kg/d PO next 4 d
Vancomycin:10 mg/kg IV q6 h
Clindamycin: 8-20 mg/kg/d PO divided tid/qid 20-40 mg IV divided q6-8h
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Allergic rhinitis: Measures include allergen
avoidance, optimal environment, nasal steroids, a
second-generation antihistamine, and possible
immunotherapy.
Gastroesophageal reflux: Conservative measures
include elevating the head of the bed, not feeding
immediately before bedtime, and thickening feeds.
Medical therapy includes H-2 blockers, prokinetic
agents, and hydrogen ion pump inhibitors.
Consider surgery as a last resort in the pediatric
population