Pediatric Respiratory Physiology

TOPIC OUTLINE
TOPIC
OUTLINE

I. Anatomy and physiology of the respiratory tract

II. Common respiratory problems in children
A. Infectious disorders
1. acute upper respiratory infections
2. Lower respiratory tract infections
B. Non-infectious disorders
foreign bodies
atelectasis
Asthma
 Course Content: (cont.)

C. Pulmonary tuberculosis
primary infection
progressive primary infection
Chronic pulmonary TB
multidrug resistant pulmonary
tuberculosis
miliary tuberculosis
 Good medical history and PE
very important!!!

Laboratory and other ancillary procedures

will confirm or define the character, severity,
extent and possible prognosis
Anatomy and physiology of the
Respiratory Tract
5 Stages of LUNG development
 STAGES OF LUNG DEVELOPMENT

Stage Human Features

lung buds originate as an

outgrowth from the ventral
Embryonic week 4 to 5 wall of the foregut where
lobar division occurs

conducting epithelial tubes

surrounded by thick
Pseudo
week 5 to 17 mesenchyme are formed,
glandular extensive airway branching
Terminal bronchioles
 Stage Human Features

Respiratory bronchioles are

produced, increasing number
of capillaries in close contact
Canalicular week 16 to 25 with cuboidal epithelium and
the beginning of alveolar
epithelium development
(Type I and II)

alveolar ducts and air sacs are

Saccular week 24 to 40 developed;
Surfactant synthesis

secondary septation occurs,

late fetal to 8 marked increase of the
Alveolar number and size of capillaries
years
and alveoli
 Extrauterine life not possible until 24-25
weeks of gestation

Sufficient pulmonary surfactant present

after 35 wks GA

Betamethasone can be given to pregnant

mothers at 24-34wks GA to accelerate
fetal surfactant production
 Postnatal Lung Development
Newborn
Airway branching complete
Alveolar formation is not complete

Age 1-10 years: number of alveoli increase

Age 10 to young adult: lung grows larger with
little alveolar growth
 PEDIATRIC UPPER AIRWAY

Tongue is large for the size of the oropharynx

Larynx is located high in the neck
 PEDIATRIC UPPER AIRWAY

Epiglottis is narrow, omega-shaped and

vertically positioned
Cartilaginous support is soft and compliant
 PEDIATRIC UPPER AIRWAY
Radius of the airway is small with the
narrowest portion at the cricoid ring where
its submucosa is non-fibrous
Fully developed
cricoid at 10-12

yrs
 ANATOMICAL differences in the
airway
ribs are oriented horizontally
rib cage is much softer
diaphragm is flatter and less domed;
moves less efficiently and contains fewer
fatigue-resistant muscle fibers (Type I)
Infants and young children rely on
diaphragm to breathe more than adults do
 MUSCLE FIBERS
Type I fibers
slow-twitch and high-oxidative in nature
Low contractility but are fatigue resistant

Type II fibers
fast-twitch and low-oxidative
have high contractility but are more prone to
fatigue.
 The proportion of type I fibers in the
diaphragm and intercostals of
premature infants is only around 10%.
This increases to around 25% in full-
term newborns and around 50% in
children >2 years.
Respiratory muscles of premature
babies and young infants are therefore
more susceptible to fatigue, resulting in
earlier decompensation.
 PHYSIOLOGICAL differences in
breathing between adults and children
Compliant chest wall creates a greater

negative inspiratory pressure ; sucks in

the floppy airway decreases airway
diameter increases the work of
breathing
 Chest wall compliance is a major
determinant of FRC.

The increased chest wall compliance in

infants allows greater chest wall retraction
because of less opposition to the lung
recoil, thereby decreasing FRC
Things to consider in evaluating
respiratory conditions:
Evidence of emergent respiratory failure
and of infection
Onset and natural course of the disease
Familial occurrence
effect of triggers or the environment
Pattern of illness
Response to treatment
DIAGNOSTICS
Pulse oximetry
ABG
PEFR
DIAGNOSTICS
PULSE OXIMETRY
- helps us to detect hypoxemia
Clinically, we can only detect hypoxemia
when the oxygen saturation is below 80%
Pulse oximetry is based on 2 physical
conditions:

1. Presence of pulsatile signal generated by

the arterial blood
2. Difference in the absorption spectra
between oxyhemoglobin and reduced
hemoglobin
Pulse oximetry
Accuracy is diminished when SaO2 falls to
80% or less
Adequate oxygenation: 94%
 PEAK EXPIRATORY FLOW RATE
(PEFR)
It is the max. Flow rate
during FVC maneuver in
the initial 0.1 sec.
Determines function of
caliber of the airways
Determines the strength
of expiratory muscles
 commonly used indicator
of airway obstruction in
asthma and other
obstructive lesions

a decrease in flow
is a reflection of increased
airway resistance
 THORACENTESIS
In pleural effusion
Main contraindication:
hemorrhagic diathesis
Most common
complications:
1. Pneumothorax
2. Hemothorax
Where do you insert
needle?
 PULMONARY
SIGNS & SYMPTOMS
 A child who appears in respiratory
distress might not have a respiratory
illness
abnormalities of central nervous system
(encephalitis)
neuromuscular disease such as Guillain-
Barre syndrome or myasthenia gravis and
those with an abnormal respiratory drive
metabolic acidosis (diabetic ketoacidosis)
 Respiratory Distress: S/S
diagnosed from
signs such as:
cyanosis
nasal flaring
grunting
tachypnea
wheezing
chest wall retractions
stridor
 Tachypnea
Less than 3 months: > 60 breaths per
minute
3 months - 12 months: > 50 breaths per
minute
1 year 4 years: > 40 breaths per minute
 valuable signs in localizing the site of
respiratory pathology

rate and depth of respiration

retractions
stridor
Wheezing
grunting
 AIRWAY : 3 anatomic parts

extrathoracic airway

intrathoracic-extrapulmonary airway

intrapulmonary airway
 AIRWAY : 3 anatomic parts
extrathoracic airway
from the nose to the thoracic inlet
Hallmark: Inspiratory stridor
retractions (chest wall, intercostal,
suprasternal)
 Intrathoracic-extrapulmonary airway
from the thoracic inlet to the main stem
bronchi
Hallmark: Expiratory wheezing
 Intrapulmonary airway
within the lung parenchyma
Rapid and shallow respirations (tachypnea)
Grunting
 GRUNT
is produced by expiration against a partially
closed glottis
is an attempt to maintain positive airway
pressure during expiration
most beneficial in alveolar diseases that
produce widespread loss of FRC, such as in
pulmonary edema, hyaline membrane
disease, and pneumonia
 Stridor
is a harsh, high-pitched respiratory sound
usually inspiratory but can be expiratory or
even biphasic
produced by turbulent airflow
a sign of upper airway obstruction
INTERPRETING THE CLINICAL SIGNS OF
RESPIRATORY DISEASE

EXTRA-THORACIC INTRATHORACIC- INTRA-PULMONARY

EXTRA
SIGN AIRWAY PULMONARY AIRWAY
AIRWAY
OBSTRUCTION OBSTRUCTION OBSTRUCTION

Tachypnea + + +++
Retractions ++++ ++ ++

Stridor ++++ ++

Wheezing ? +++ ++

Grunting ? ? +++
 DIAGNOSTIC PROCEDURES
CBC not very reliable
Cultures if (+) exudates
Chest radiographs
In infants and young children ( AP-Lateral
views)
Why? Lesions in the hilar areas maybe
obscured by the cardiac silhouette
ABG
RESPIRATORY DISORDERS
 Acute Upper Respiratory
Tract Infections in Children:
Most URTIs are caused by viruses & are
self-limited.

Acute rhinitis & pharyngitis (including

tonsillitis) are extremely common in
pediatric age groups.
 ACUTE RHINITIS
(Common colds)
is a viral illness
Rhinovirus (most common)
RSV
coronavirus
Inflammation of nasal mucosa
Occurs year-round
Highest incidence: rainy season
common in children under 5 years of age.
Frequency decreases with age
 ACUTE RHINITIS
(Common colds)
Pathogenesis varies according
to the virus involved
Rhinovirus : binds to ICAM-1 receptors on
respiratory epithelial cells
RSV, influenza virus, adenovirus: direct mucosal
invasion and disruption of the nasal epithelium
Corona virus: grows within the epithelium of the
respiratory tract
Results to release of cytokines producing the
general symptoms
 ACUTE RHINITIS
(Common colds)
Incubation period: 1-3 days
prominent symptoms:
Sore throat (50%)
1st sign to appear
noted 2-3 days prior to nasal congestion
Conjunctivitis (adenoviral)
Fatigue and severe myalgia (influenza)
Fever usually high in infants & children
Lasts 3-7 days
P.E. limited to the upper respiratory tract
 ACUTE RHINITIS
(Common colds)
Physical examination findings:
nasal turbinates are swollen and
erythematous
Clear to opaque white or yellow to
green secretion
Note: the color of secretion DOES NOT
differentiate viral from bacterial etiology
 A change in color or consistency of the
secretions is common during the course of
illness and is NOT indicative of sinusitis or
bacterial superinfection
A green or yellow nasal discharge should
not be construed as evidence of
secondary bacterial infection (neutrophils
cause yellow-green discoloration because
of their natural myeloperoxidase activity).
Epidemiology

Mode of transmission:
by aerosols
Small particle ( influenza virus)
Large particle
direct contact (Rhinoviruses and RSV)
40% to 90% recovery from hands.

Rhinoviruses remain viable on skin and also on

objects (fomites) for at least 2 hours.
 FORMS OF RHINITIS
allergic rhinitis nonallergic
(hay fever) rhinitis
(common cold)
pollen
dust mites RHINOVIRUSES
mold Adenoviruses
animal RSV
dander Coxsackies viruses
 Conditions that mimic common cold
CONDITION DIFFERENTIATING FEATURES
Prominent itching and sneezing
watery nasal discharge
Allergic rhinitis Family Hx atopy
Nasal smear: eosinophils
Unilateral, foul-smelling secretions
Foreign body Bloody nasal secretions

persistence of rhinorrhea without

Sinusitis improvement for > 10-14 days

Mucopurulent nasal discharge that

Streptococcosis excoriates the nares
Persistent rhinorrhea with onset in the 1st
Congenital syphilis 3 months of life
 Treatment (Symptomatic) :
fever antipyretics
( paracetamol)

nasal obstruction saline nasal

drops/solution

rhinorrhea antihistamines

decongestants if >2yrs old

How long? Risks?
 Complications:
Otitis media most common
Bacterial sinusitis
should be considered if rhinorrhea persists
without improvement for at least 10-14 days
or if signs of more-severe sinus involvement
such as fever, facial pain, or facial swelling
develop.
Exacerbation of asthma
 PREVENTION

Chemoprophylaxis or immunoprophylaxis is
generally not available for the common cold.

Vitamin C, Zinc and echinacea DO NOT prevent

the common cold.

Interrupting the chain involved in the spread of

virus by direct contact may prevent colds.
 PREVENTION

influenza vaccine
Good hygienic practices and proper waste
disposal
Boost ones immune system through
proper nutrition and adequate sleep
(MOST impt.)
 ACUTE PHARYNGITIS
Most common cause of sore throat
 Acute pharyngitis
Most common cause of sore throat
Inflammation of the pharynx and tonsils
often associated with the common cold
syndrome
Not common before 2-3 yr of age
peak incidence in the early school years,
and declines in late adolescence and
adulthood
 Pharyngitis: Etiology
A) Viral: Most common
Rhinovirus , RSV, adenovirus, coronavirus,
enterovirus and metapneumovirus
B) Bacterial:
Group A beta hemolytic streptococcus
(GABHS), Strep pneumoniae, Mycoplasma,
Corynebacterium, Neisseria
 Specific features with certain
viruses
Infectious mononucleosis (EB viruses)
Marked redness and swelling of the throat
Exudative tonsillitis
Lymph gland swelling
Rash
hepatosplenomegaly
 Specific features with certain
viruses
Herpes simplex virus
Mucosal or palatal ulcers, erosions or vesicles

Coxsackie virus (Herpangina)

Small vesicles on the soft palate, uvula and
tonsillar pillar
 Specific features with certain
viruses
Adenovirus (pharyngoconjunctival
fever)
Fever, conjunctivitis, sore throat, marked
pharyngeal edema, cervical lymph node
enlargement

Influenza virus
Fever, headache, myalgia, malaise, sore
throat, dry cough
 STREPTOCOCAL PHARYNGITIS
GABHS most
common bacterial
cause
s/s: fever, sore throat,
headache, vomiting,
abdominal pain
Pharynx and uvula
markedly erythematous,
petecchial hemorrhages
on the soft palate
 Diphtheria pharyngitis
sore throat, barking cough and
inspiratory stridor
Pseudomembrane around the pharynx
 Pathogenesis
Colonization of the pharynx by GABHS
can result in either asymptomatic carriage
or acute infection.

The M protein is the major virulence factor

of GABHS and facilitates resistance to
phagocytosis by polymorphonuclear
neutrophils
 DIAGNOSIS
based on PE
throat culture standard diagnostic
test
Rapid streptococcal antigen test
less sensitive but may provide
early identification
 Pharyngitis: Treatment
early antibiotic therapy hastens clinical
recovery by 12-24 hr and prevent local
suppurative complications and acute
rheumatic fever
Prevention of acute rheumatic fever is
successful if treatment started within 9
days of illness
 Pharyngitis: Treatment
BUT even with early treatment, it does not
decrease the likelihood of
poststreptococcal glomerulonephritis
Drug of Choice: Penicillin
if allergic to penicillin: erythromycin and
azithromycin
 Pharyngitis: Treatment
if resistant: cephalosporin
if multiple recurrences: clindamycin or
amoxicillin-
clavulanate
For carriers: clindamycin
 When to advice tonsillectomy?
For severe and recurrent pharyngitis
( > 7 episodes in the previous year
or >5 in each of the previous
2 years)
 Complications
include :
local suppurative complications such as
bacterial otitis media, sinusitis,
peritonsillar abscess, retropharyngeal
abscess
nonsuppurative illnesses, such as acute
rheumatic fever , RHD and acute
poststreptococcal glomerulonephritis
 ACUTE SINUSITIS
inflammation of the paranasal sinuses
Generally follows rhinitis
2nd only to otitis media as the most
common complication of common colds
Usually viral
If bacterial: Streptococcus pneumoniae
( 30%), non-typable Haemophilus
influenzae, Moraxella catarrhalis
 Both the ethmoidal and
maxillary sinuses are
present at birth, but only the
ethmoidal sinuses are
pneumatized
maxillary sinuses are not
pneumatized until 4 yr of age
sphenoidal sinuses are
present by 5 yr of age
frontal sinuses begin
development at age 7-8 yr
and are not completely
developed until adolescence.
PATHOGENESIS:
Obstruction of the sinus ostium due to
inflammatory changes in the nasal
epithelium blocks sinus drainage
and impairs ciliary activity and
phagocytosis
Provides a favorable milieu for
bacterial colonization sinusitis
 SINUSITIS
Can occur at any age
s/s: nasal congestion, purulent nasal
discharge, hyposmia, halitosis, postnasal
drip and cough
Suspected if the purulent nasal discharge
persists for more than 10-14days
 Diagnosis
What about transillumination? Is it
helpful?
Unreliable because of the small
sinuses and thick bones in the
anterior face of the maxilla
CT scan
Sinus aspirate culture (for ID)
 TREATMENT
50-60% of children with acute bacterial
sinusitis recover without antimicrobial therapy
For uncomplicated: Amoxicillin (40mg/kg/day)
for 10-14 days
For children who had antibiotics 3 months
prior and failed to respond to amoxicillin
within 72 hrs. or where drug resistance is
suspected: give Amox @ 80-90mg/kg/day or
co-amoxiclav
 Sinusitis - Complications
Eye complications:
peri-orbital/ orbital cellulitis

Intracranial complications:
Meningitis (most severe)
cavernous sinus thrombosis
brain abscess (most severe)
Subdural empyema
 PREVENTION
Because acute bacterial sinusitis can
complicate influenza infection, prevention
of influenza infection by yearly influenza
vaccine will prevent some cases of
complicating sinusitis
 OTITIS EXTERNA
Precipitating factors;
Trauma
Swimming
Impacted cerumen
Change from the normal acid to alkaline
pH of the external auditory canal
 OTITIS EXTERNA
Etiology: Staph aureus (most common)
Others: gram negative bacilli
(Pseudomonas aeruginosa,
Proteus vulgaris, E. coli)
s/s: ear pain aggravated by movement of
the tragus
hearing is normal
 TREATMENT
Cleansing and drying of External Auditory
Canal
If (+) infection: DO NOT irrigate
If (+) cellulitis and chondritis: Rx antibiotic
OXACILLIN or any penicillinase-resistant
penicillin
 OTITIS MEDIA
Inflammation of the mucoperiosteal lining of the
eustachian tube, tympanic cavity, mastoid
antrum and mastoid air cell system
 OTITIS MEDIA
Peak incidence: 1st 2 yrs
Three pathogens predominate in OM:
Streptococcus pneumoniae (most
common)
Haemophilus influenzae
Moraxella catarrhalis
Predisposing factors of developing otitis
media in children:

developmental alterations of the Eustachian

tube (short and more horizontal)
Diameter is smaller and mucosal wall is more
compliant
an immature immune system against bacteria
the usual lying-down position of infants favors
the pooling of fluids, such as formula.
 Pathogenesis:
Inflammation or obstruction of ET by
secretions can block the passageway,
disturb ventilation in the middle ear and
disrupt pressure equalization

Increase in negative pressure causes

nasopharyngeal reflux and allows fluid to
accumulate in the middle ear
 Symptoms of AOM are variable, especially
in infants and young children.
In young children, evidence of ear pain
may be manifested by irritability or a
change in sleeping or eating habits and
occasionally, holding or tugging at the ear
 Diagnosis: clinical and
confirmed by otoscopy
(TM)
Findings: opaque or an
erythematous and
bulging tympanic
membrane
air fluid level behind the
membrane and limited
mobility of the membrane
suggest EFFUSION
Pus may drain from the
ear
 Treatment
AGE GROUP EMPIRIC THERAPY
Neonates Ampicillin , 200mg/kg/24hrs
parenteral in 4-6 hrly doses

Amikacin, 15mg/kg/24hrs

1-15 years Trimethoprim-

sulfamethoxazole , 10-
20mg/kg/24hrs in 2 12 hourly
doses
 Otitis media
for persistent effusion- myringotomy
Tympanostomy tube in place

Chronic OM
 Infections causing Acute
Upper Airway Obstruction
(Croup, Epiglottitis, Laryngitis,
and Bacterial Tracheitis)
 Upper airway obstruction is an
EMERGENCY!
More common in pediatric age groups
Due to structural variations in the upper
airway anatomy of infants and young children
 With inflammation, the flow through the
narrowed airway INCREASES the
negative intraluminal pressure
enhances inward collapse of the
airway increased turbulence and
velocity of airflow and vibration of
the vocal cords and aryepiglottic
folds stridor
 TIMING of stridor
Inspiratory stridor and muffled voice
Supraglottic lesions
Inspiratory stridor and hoarseness
Glottic lesions
Expiratory stridor, brassy cough, does not
alter the voice Subglottic lesions
 Acute upper airway obstruction
Usually infectious
Predominant: acute
laryngotracheobronchitis
Other causes: epiglottits, bacterial
tracheitis, diphtheritic croup,
retropharyngeal abscess and peritonsillar
abscess
 CROUP
(Laryngotracheobronchitis)
Viral infection
the most common infectious cause of
upper airway obstruction in children
Peak incidence: 18-24 months
 CROUP
(Laryngotracheobronchitis)
Transmitted via aerosol droplets or
direct contact with contaminated
waste products
Caused by PIV 1 and 2
Parainfluenza virus 1 (PIV1) : most
frequent
 Swelling and inflammation of the larynx,
trachea and bronchi
Results in airway narrowing, especially
around the area of the cricoid cartilage
Decreases the ability of the vocal cord to
abduct
Increased mucus secrretion
 Croup: Signs/Symptoms
Low grade fever
coryza progressing to hoarseness
Dry, brassy, croupy or barking cough
Hoarse cry
Inspiratory stridor
Symptoms worsen at night and on lying down
Children prefer to be held upright or sit on bed
 Soft tissue neck radiograph
DIAGNOSIS
MAINLY A CLINICAL
DIAGNOSIS
RADIOGRAPH
NECK : STEEPLE
SIGN (subglottic
tracheal narrowing)
CROUP (Laryngotracheobronchitis)

Direct visualization via laryngoscopy:

swelling and hyperemia of the glottis and
subglottis
 ACUTE LTB
TREATMENT
MOIST OR HUMIDIFIED AIR
STEROIDS (controversial)
PREDNISOLONE PO 2mg/kg/day FOR 3 DAYS
NEBULIZED BUDESONIDE 2mg STAT
NEBULIZED ADRENALINE (EPINEPHRINE)
Causes vasoconstriction of the edematous
subglottic mucosa and relaxes the bronchial
muscle
Anticipate need to intubate
 ACUTE EPIGLOTTITIS
( Supraglottitis)
True medical emergency
Bacterial infection (Hemophilus influenzae
type B)
Affects supraglottis ( epiglottis, aryepiglottic
folds and false vocal cords)

Complete Airway
Obstruction
 Epiglottitis: Incidence

Peak incidence: 2-7 yrs

Pedia incidence falling due to HiB
vaccination
Can occur in adults, particularly elderly
 Epiglottitis
Supraglottic structures become
inflammed, edematous and ulcerative
leading to a narrowed airway.
During inspiration, the swollen epiglottis
tends to fall backwards and can
completely block the glottic opening
Usually DOES not involve subglottic
structures
 Epiglottitis: Signs/Symptoms

short history of high grade fever, sevre sore

throat and muffled voice
Rapid progression: 2-4 hrs ill looking ,
difficulty of swallowing, drooling, dysphonia,
respiratory distress
Severe hunger (tripod position)
 Epiglottitis: Signs/Symptoms

Tripod position:
Sits up, leans forward
chin up and mouth open :depicts
severe air hunger
Hyperextended neck
Inspiratory Stridor (late finding)
 ACUTE EPIGLOTTITIS
DIAGNOSIS:
CHERRY REDAPPEARANCE OF
EPIGLOTTIS ON LARYNGOSCOPY

THUMB SIGN ON LATERAL NECK

RADIOGRAPH
 Epiglottitis: Management
High concentration oxygen
Do not attempt to visualize airway
Antibiotics: IV ceftriaxone or cefotaxime
Rifampicin prophylaxis to close contacts
<48 months with no previous immunizations
<12 months with incomplete immunizations
immunocompromised patients
 Complications:
Pneumonia
Hypoxic Ischemic Encephalopathy
Septic arthritis
Meningitis
Pulmonary edema
 Croup and Epiglottitis
CROUP EPIGLOTTITIS
Age 18 months to 24 years Age 2 to 7 years

Slow onset Rapid onset

Patient may lie or sit upright Patient prefers to sit upright

Barking cough No barking cough, possible

inspiratory stridor

Lack of drooling Drooling, pain during

swallowing

Low-grade fever High fever

 BACTERIAL TRACHEITIS
Membranous LTB; pseudomembrane
CROUP
Bacterial infection of trachea associated
with viral URI
Potentially life threatening
Affects children 6 months to 8 yrs of age
 BACTERIAL TRACHEITIS
Most common pathogens: S. aureus,
H. influenzae type B
M catarrhalis
s/s: mild fever, cough, inspiratory stridor
(several days) then worsens
 BACTERIAL TRACHEITIS
Lateral neck X-ray: ragged tracheal
air column due to sloughing of the
pseudomembrane from the soft
tissues
Rx: cefuroxime for 10-14 days
If with profound toxicity : anti-staph
 DIPHTHERITIC LARYNGITIS
Serious and contagious infection due to
extension of the diphtheria infection from
the nasal cavity, tonsils and pharynx to the
larynx
Etiology: Corynebacterium diphtheriae
Spread via direct physical contact or
inhalation of infected droplets
 DIPHTHERITIC LARYNGITIS
Incubation period: 2-5 days
Fever, sore throat, fetor oris, membranous
pharyngitis, bull neck appearance
Diagnosis: confirmed by bacterial smear
and culture from the membrane
 DIPHTHERITIC LARYNGITIS
Treatment: Diphtheria antitoxin
Erythromycin or IM penicillin
given 14 days
Does not confer immunity
Diphtheria toxoid should be given during
convalescence
Complications: toxin-mediated
myocarditis, neuritis and pneumonia
 RETROPHARYNGEAL
ABSCESS
Deep neck space infection
Life threatening
Commonly affects children <6yrs old
Infection can extend from the base of the
skull into the mediastinum as far as T6
Usually polymicrobial
 RETROPHARYNGEAL
ABSCESS
s/s: fever, sore throat, dysphagia,
torticollis, neck pain
Diagnosis: soft tissue neck radiography
- widening of the prevertebral soft
tissue or gas in the
retropharyngeal space
 RETROPHARYNGEAL ABSCESS
Management:
Sniffing position
Oxygen
Drugs: ampicilin-sulbactam or
clindamycin
If airway is compromised: intraoral
surgical incision and drainage
 PERITONSILLAR ABSCESS
(QUINSY)
Collection of pus around the tonsils
Complication of tonsilltis
Causative agents: aerobes and anaerobes
Predominant: Strep pyogenes,
Staphylococci and Haemophilus
Affects children >10 yrs old
 PERITONSILLAR ABSCESS
(QUINSY)
s/s: about 2-8 days into the course of acute
tonsillitis child becomes more ill with
high fever, worsening unilateral sore
throat, referred otalgia, neck pain
with tender swollen lymph nodes
PE: bulging, hyperemic and edematous
tonsil pushing the uvula towards the
uninvolved side
 PERITONSILLAR ABSCESS
(QUINSY)
Rx: IV antibiotics
- penicillin most effective
- drug resistant cases: clindamycin
QUESTIONS?