INTRODUCTION

Tonsillopharyngitis is acute infection of the pharynx, palatine tonsils, or both.

Symptoms may include sore throat, dysphagia, cervical lymphadenopathy, and fever. Diagnosis
is clinical, supplemented by culture or rapid antigen test. Treatment depends on symptoms and,
in the case of group A β-hemolytic streptococcus, involves antibiotics.

Etiology

The tonsils participate in systemic immune surveillance. In addition, local tonsillar defenses
include a lining of antigen-processing squamous epithelium that involves B- and T-cell
responses.

Tonsillopharyngitis of all varieties constitutes about 15% of all office visits to primary care
physicians.

Etiology

Tonsillopharyngitis is usually viral, most often caused by the common cold viruses (adenovirus,
rhinovirus, influenza, coronavirus, respiratory syncytial virus), but occasionally by Epstein-Barr
virus, herpes simplex virus, cytomegalovirus, or HIV.

In about 30% of patients, the cause is bacterial. Group A β-hemolytic streptococcus (GABHS) is
most common (see Gram-Positive Cocci: Streptococcal and Enterococcal Infections), but
Staphylococcus aureus, Streptococcus pneumoniae, Mycoplasma pneumoniae, and Chlamydia
pneumoniae are sometimes involved. Rare causes include pertussis, Fusobacterium, diphtheria,
syphilis, and gonorrhea.

GABHS occurs most commonly between ages 5 and 15 and is uncommon before age 3.

Symptoms and Signs

Pain with swallowing is the hallmark and is often referred to the ears. Very young children who
are not able to complain of sore throat often refuse to eat. High fever, malaise, headache, and GI
upset are common, as are halitosis and a muffled voice. A scarlatiniform or nonspecific rash may
also be present. The tonsils are swollen and red and often have purulent exudates. Tender
cervical lymphadenopathy may be present. Fever, adenopathy, palatal petechiae, and exudates
are somewhat more common with GABHS than with viral tonsillopharyngitis, but there is much
overlap. GABHS usually resolves within 7 days. Untreated GABHS may lead to local
suppurative complications (eg, peritonsillar abscess or cellulitis) and sometimes to rheumatic
fever or glomerulonephritis.
Diagnosis

• Clinical evaluation
• GABHS ruled out by rapid antigen test, culture, or both

Pharyngitis itself is easily recognized clinically. However, its cause is not. Rhinorrhea and cough
usually indicate a viral cause. Infectious mononucleosis is suggested by posterior cervical or
generalized adenopathy, hepatosplenomegaly, fatigue, and malaise for > 1 wk; a full neck with
petechiae of the soft palate; and thick tonsillar exudates. A dirty gray, thick, tough membrane
that bleeds if peeled away indicates diphtheria (rare in the US).

Because GABHS requires antibiotics, it must be diagnosed early. Criteria for testing are
controversial. Many authorities recommend testing with a rapid antigen test or culture for all
children. Rapid antigen tests are specific but not sensitive and may need to be followed by a
culture, which is about 90% specific and 90% sensitive. In adults, many authorities recommend
using the following 4 criteria:

• History of fever
• Tonsillar exudates
• Absence of cough
• Tender anterior cervical lymphadenopathy

Patients who meet 1 or no criteria are unlikely to have GABHS and should not be tested. Patients
who meet 2 criteria can be tested. Patients who meet 3 or 4 criteria can be tested or treated
empirically for GABHS.

Treatment

• Symptomatic treatment
• Antibiotics for GABHS
• Tonsillectomy considered for recurrent GABHS

Supportive treatments include analgesia, hydration, and rest. Penicillin V is usually considered
the drug of choice for GABHS tonsillopharyngitis; dose is 250 mg po bid for 10 days for patients
< 27 kg and 500 mg for those> 27 kg (see also Gram-Positive Cocci: Pharyngitis). Amoxicillin
Some Trade Names
AMOXIL
TRIMOX
Click for Drug Monograph
is effective and more palatable if a liquid preparation is required. If compliance is a concern, a
single dose of benzathine penicillin 1.2 million units IM (600,000 units for children ≤ 27 kg) is
effective. Other oral drugs include macrolides for patients allergic to penicillin, a 1st-generation
cephalosporin, and clindamycin Some Trade Names
CLEOCIN
Click for Drug Monograph
.
Treatment may be started immediately or delayed until culture results are known. If treatment is
started presumptively, it should be stopped if cultures are negative. Follow-up throat cultures are
not done routinely. They are useful in patients with multiple GABHS recurrences or if
pharyngitis spreads to close contacts at home or school.

Tonsillectomy: Tonsillectomy should be considered if GABHS tonsillitis recurs repeatedly (> 6

episodes/yr, > 4 episodes/yr for 2 yr, > 3 episodes/yr for 3 yr) or if acute infection is severe and
persistent despite antibiotics. Other criteria for tonsillectomy include obstructive sleep disorder,
recurrent peritonsillar abscess, and suspicion of cancer.

Numerous effective surgical techniques are used to perform tonsillectomy, including

electrocautery, microdebrider, radiofrequency coblation, and sharp dissection. Significant
intraoperative or postoperative bleeding occurs in < 2% of patients, usually within 24 h of
surgery or after 7 days, when the eschar detaches. Patients with bleeding should go to the
hospital. If bleeding continues on arrival, patients generally are examined in the operating room,
and hemostasis is obtained. Any clot present in the tonsillar fossa is removed, and patients are
observed for 24 h. Postoperative IV rehydration is necessary in ≤ 3% of patients, possibly in
fewer patients with use of optimal preoperative hydration, perioperative antibiotics, analgesics,
and corticosteroids. Postoperative airway obstruction occurs most frequently in children < 2 yr
who have preexisting severe obstructive sleep disorders and in patients who are morbidly obese
or have neurologic disorders, craniofacial anomalies, or significant preoperative obstructive sleep
apnea. Complications are generally more common and serious among adults.

INTRODUCTION- I

Acute tonsillopharyngitis is an inflammatory process of the

oropharynx. It can become a particularly horrible throat infection

involving Mycoplasma pneumoniae and Chlamydia pneumoniae

organisms that often occur in children. It can also come to pass in

patients who are given antibiotics for simpler infectins and founder

to take the prescribed regimen (dose and time).

Viruses

The adenoviruses are the most common cause of tonsillopharyngitis,

especially types 1, 2, 3, and 5, which are the types that infect small children

most frequently. Other respiratory viruses are less common causes of

tonsillitis; the parainfluenza viruses probably are the most frequently isolated
in this group. Herpes simplex virus also is recognized as an occasional cause

of tonsillopharyngitis, as is Epstein-Barr virus. The most frequent causes of

the common cold, the rhinoviruses and coronaviruses, involve the tonsils.

Bacteria. Group A Streptococcus is the most important and frequent cause

of tonsillopharyngitis. It is frequently associated with acute rheumatic fever

and acute glomerulonephritis. Appropriate treatment of streptococcal

pharyngotonsillitis prevents the occurrence of rheumatic fever.

Epidemiology

Prevalence. The average incidence of all acute URIs is five to seven per

child per year. It is estimated that children have one streptococcal infection

every 4 to 5 years. Group A streptococci is isolated in 30-36.8% of children

with pharyngitis.

Age Occurrence. Pharyngitis is infrequent in the first 2 years of life, when

all URIs are most frequent. Most cases of pharyngitis occur in school-age

children, when the incidence of all infections is still high but less than in the

first 2 years.

Etiology

Viruses are isolated in about 50% of children less than 2 years old but

infrequently after that.

Group A streptococcus is isolated most frequently in school-age children,

while M pneumoniae is most often in teenagers.

Contact

All respiratory agents are spread by close contact or large droplets, with the

exception of influenza, which also is spread by small droplets and the

airborne route.

A history of a household, school, or outside contact with another patient who

has tonsillopharyngitis due to a known agent, especially the group A

Streptococcus, increases the likelihood that the index infection has the same

etiology.

ANATOMY AND PHYSIOLOGY- III

The upper respiratory tract primarily refers to the parts of the respiratory

system lying outside of the thorax or above the sternal angle. Another

definition commomly used in medicine is the airway above the glottis or

vocal cords. Some specify that the glottis (vocal cords) is the defining line

between the upper and lower respiratory tracts; yet even others make the

line at the cricoid cartilage..

Upper respiratory tract infections are amongst the most common infections

in the world.

Picture:::::::::

NOSE: Physically a nose is an organ on the face. Anatomically, a nose is a

protuberance in vertebrates that houses the nostrils, or nares, which admit

and expel air for respiration in conjunction with the mouth. Behind the nose

is the olfactory mucosa and the sinuses. Behind the nasal cavity, air next

passes through the pharynx, shared with the digestive system, and then into

the rest of the respiratory system. In humans, the nose is located centrally

on the face; on most other mammals, it is on the upper tip of the snout.

NASAL CAVITY: A large fluid filled space above and behind the nose in the

middle of the face.

PHARYNX: The part of the neck and throat situated immediately posterior

to (behind) the mouth and nasal cavity, and cranial, or superior, to the

esophagus, larynx, and trachea.

NASOPHARYNX: The uppermost part of the pharynx. It extends from the

base of the skull to the upper surface of the soft palate; it differs from the

oral and laryngeal parts of the pharynx in that its cavity always remains

patent (open).

OROPHARYNX: Reaches from the Uvula to the level of the hyoid bone. It

opens anteriorly, through the isthmus faucium, into the mouth, while in its

lateral wall, between the two palatine arches, is the palatine tonsil.

LARYNX: Commonly called the voice box, is an organ in the neck of

mammals involved in protecting the trachea and sound production. It

manipulates pitch and volume. The larynx houses the vocal folds, which are

an essential component of phonation. The vocal folds are situated just below

where the tract of the pharynx splits into the trachea and the esophagus

VITAL INFORMATION- IV

Name: Ms. J.D.A.

Age: 8

Address: Roxas City, Capiz

Civil status: Single

Religion: Roman Catholic

Occupation: Student

Date & time admitted: 08/04/10

Ward: Blessed Sr. Roselie Rendu Ward Room 115

Chief complaint: Fever

Impression / admitting diagnosis: ATP w/ Exudative t/c Pneumonia t/c Dengue

Fever

Final diagnosis: ATP w/ Exudative t/c Pneumonia t/c Dengue Fever

CLINICAL ASSESSMENT- VI
A)NURSING HISTORY

2 days prior to admission, the patient experienced fever accompanied

with pain in the throat, fatigue, and signs of weakness pt. Family thought

it was dengue and consulted the attending physician and was advised to

be admitted.

B) PAST HEALTH PROBLEM/STATUS

a) Flu

b) Fever

c) Sore throat

d) Cough

e) No allergies noted

f) No records of past hospitalization

C) FAMILY HISTORY OF ILLNESS

Family has history of

a) Heart disease,

b) Diabetes,

c) HTN

CLINICAL EXAMINATION- VII

A. General

Ms. J.D.A. An 8 year old girl strong and with good sensory and motor

response to the people around her she lies with a pillow on her head

and with an IVF at the left metacarpal vein.

a. Upon admission

• Temperature: 38.2˚C

• Blood Pressure 110/80

•
Cardiac rate: 90 bpm

Respiratory rate: 23 breaths per minute

b. During care

Temperature: 36.5˚C

• Blood Pressure 100/70

Cardiac rate: 83 bpm

Respiratory rate: 20 breaths per minute

Head, Eyes, Ear, Nose, Hair, Mouth, Throat

• Head – skull is normocephalic.

Hair – long length hair, quantity is normal, evenly distributed,

black color and there is presence no flakes.

• Eyes – the conjunctive is pinkish, eye lashes are black, eyebrows

are also black and it is evenly distributed, pupil size is 3mm and

corneas are clear and no lesions noted upon inspection.

• Ears - there is presence of ear wax in the ear canal, its upper

portion is in line with the outer part of the eye and he has a good

hearing acuity.

• Nose – the mucosa is pinkish in color and the nasal septum is at

the midline.

Mouth – lips are symmetrical, pale, dry and without lesions. Oral

mucosa is pink and the frenulum under the tongue is at the

center.

Throat – no inflammations noted but slight pain noted upon

inspection.

Neck

Its color is similar to other body parts. No lumps or goiter

noted upon inspection. No palpable lymph nodes noted upon

palpation but pain of 5 out of 10 was noted noted.

eart

Cadiac rate is 83 beats per minute during my care. No S3 and S4

heart sound noted upon auscultation.

Abdomen

• It is symmetrical and the umbilicus is at the center. No lesions

noted upon inspection.

Back

• Symmetrical to the head, straight and there are no lesions but

sores are noted upon inspection. He has a skin color similar to

other body parts.

Upper and lower extremities

• They are symmetrical to their opposites. Finger nail are non-

cyanotic and no clubbing noted upon inspection. Skin color is

similar to other body parts.

Skin

•
Color of the skin is light brown, its moisture is dry, warm to touch

and she has a good skin tugor.

General Appraisal:

a.

Hygiene: has a good personal hygiene.

b.

Sleep: has normal sleep pattern.

c.

Language: speaks in the dialect but is noted to be shy in

communicating with strangers

d. Hearing: has a good hearing acuity to moderate voice.

e.

Memory: can remember well as evidence by

remembering the medication name that she takes.

LABORATORY & DIAGNOSTIC DATA- VIII

X-RAY

L lower lung field and retrocardiac area are hazy

The CP angles and diaphragm are intact

• The trachea is at the midline

• The osseous and soft tissue structures are unreadable

Impression: L basal pneumonia

HEMATOLOGY 08/05/10

HEMATOCRIT 0.37

HEMOGLOBIN 123 gm/L

RED CELL COUNT 4.31x10^12/L

WHITE CELL

COUNT4.9x10^9/L

PLATELET 312X10^9/L

HEMATOLOGY 08/04/10

HEMATOCRIT 0.35

HEMOGLOBIN 116 gm/L

RED CELL COUNT 4.08x10^12/L

WHITE CELL

COUNT7.6x10^9/L

PLATELET 278X10^9/L

PATHOPHYSIOLOGY- IX

Viral Bacterial Fungal

Miscellaneous

Influenza Streptoccus Candida Toxoplasma

(parasite)

Para-influenza (Group A beta

Chlamydia

Herpes simplex hemolytic)

Measles Diphtheria

Chickenpox Gonococcus

Cytomegalo-virus

Rhinovirus
MILD INFECTIONS:

Discomfort in throat

Malaise

Low grade fever

Congested pharynx but no lymphadenopathy

MODERATE TO SEVERE INFECTIONS

Pain in throat

Dysphagia

Headache

DISCHARGE PLANNING- XII

A. Medication

Difflam gargle TID until total relief.

B. Exercise

Be sure to get enough rest and sleep on a daily basis.

C. Treatment

Don’t start smoking even if at the legal age already

Avoid stress, fatigue, sudden change in temperature and excessive

alcohol intake when already in legal age, all of them lowers resistance

to pneumonia.

D. Hygiene

Take a bath daily

Promote frequent oral hygiene

E. Diet

Drink plenty of water (at least 8 glasses everyday), especially during

warm weather.
Eat a healthy, balanced diet and take in a sufficient amount of non-

alcoholic fluids each day.

PHARYNGITIS (TONSILLOPHARYNGITIS)
PRINCIPLES OF DISEASE
 Pathophysiology
 Inflammatory syndrom of the oropharnx primarily caused by infection
 Transmission usually through respiratory secretions, but fomite, food
transmission also possible
 Infection localizes in lymphatic tissue: tonsils, cervical ln.s
 Rare significant complications of airway obstruction, decreased oral intake
and dehydration
 Chronic pharyngitis: inflammation and infection of the tonsillar crypts
rather than the tonsils themselves
 Beta-lactamase production is extremely common in bacteria responsible
for chronic pahryngitis
 Microbiology
 Viral most common cause: 80 - 90%; rhinovirus, adenovirus, coronavirus,
CMV, parainfluenza, rubella, influenza, HSV, coxsachie, EBV
 Bacterial (children): group A Beta-hemolytic Streptococcus (GAS)
(Streptococcus pyogenes)
 Bacterial (adults): Beta-hemolytic strep (all groups), H.flu, Mycoplasma,
Chlamydia
 Other causes: Actinomyces, Francissella tularenssi, Yersinia
enterocolitica, Group B, C, G Streptococci
 Cultures: often mixed aerobes (staph aureus, Hflu, moraxella) and
anaerobes (bactroides, anaerobic gram + cocci, fusobaclterium)
CLINICAL FEATURES
 Hx:pharyngeal pain and odynophagia
 PE: pharyngeal erythema, pharyngeal or tonsillar exudate, tonsillar enlargement,
tender
cervical lymphadenopathy
 Strawberry tongue: petecheiae or hemorrhagic lesions suggesting scarlet fever
 Gingival lesions with ulcerating tonsillitis and pseudomembranous exudate: Vincent’s
angina
 Bull neck: diptheria
 Vesicles: HSV, coxxachie
 Rash: sand-papery with scarlet fever, erythematous maculopapular with EBV
 Clinical differentiation of etiology is virtually impossible; some clues
 Viral: associated rhinitis, cough, myalgia, headache, stomatitis,
conjunctivitis, exanhem, odynophagia, low-grade fever, white exudate;
cervical lymphadenopathy less common
 Bacterial: rhinitis, conjuctivitis, exanthem, lymphadenopathy less common;
exudate, high fever, cervical lymphadenompathy, abscence of cough
more common
VIRAL PATHOGENS
 Systemic viral infections: measles, CMV, rubella, HIV (mono-like illness)
 Influenza: fever, headache, myalgias; 50% with pharyngeal pain but minority with
exudate and cervical lymphadenopathy
 Adenovirus: 30% associated with conjunctivitis
 Mononucleosis: pharyngitis is common presentation, tonsillar exudate or membrane
(creamy or cheesy whit), generalized lymphadenopathy in 90%, splenomegaly in 50%,
periorbital edema and rash less common. Macular rash after amoxicillin is common
(90% of those with mono given amoxil)
 HSV pharyngitis: young adults, painful superficial vesicles on erythematous base,
ulcers
may be present on lips/pharyng/tongue/gingiva/buccal mucosa, pharyngeal erythema
and exudate + fever + ln.s for 1-2 weeks, can be primary or secondary, bacterial
superinfection a complication
BACTERIAL PATHOGENS
 Group A Beta-Hemolytic Streptococcus
 primarily 5 - 15, winter and spring, incubation 12hr - 4 days
 < 15% of pharyngitis in > 15yo, rare < 3 yo, epidemics occur
 fever > 38.3, tonsillar exudates, palatal and uvular petechiae, uvular
edema and erythema, tender anterior cervical ln.s, absence of
cough/rhinitis.
 Rash: associated with diffuse erythematous fine sandpaper rash, first in
flexor areas then generalized, concentrated in axilla, inguinal, popliteal
fossa; characteristically FADES on pressure; lasts 7 days then
desquamates (scarlet fever); not sensitive or specific; due to pyrogenic
toxin; occurs in minority
 Pastia’s lines: petechiae in folds of the joints
 Strawberry tongue can occur with scarlet fever
 Toxic shock syndrome: sepsis and cardiovascular collapse, < 1%,
pyrogenic exotoxin A, high mortality
 Diptheria
 uncommon b/c of vaccinations, potentially lethal, consider in immigrants
 sore throat, fever, dysphagia, gray or white exudate that coalesce to form
a pseudomembrane which is a gray-green layer over the tonsils,
pharyngeal mucosa, and occassionally the uvula and may extend to
involve the larynx (hoarseness, cough, stridor)
 severe inflammation and edema can produce dysphonia and a “bullneck”
appearance
 laryngeal, nasal, and cutaneous involvement possible (sharply
demarcated ulcer with membranous base)
 must ask for special culture medium
 Corynebacterium diptheriae produces a systemic toxin ----> myocarditis,
arrythmias, polyneuritis, vascular collapse, organ necrosis, death
 Arcanobacterium hemolyticum
 previously called Corynebacterium hemolyticum, 10 - 30 year old
 similar to GAS pharyngitis, most have rash scarlatiniform/urticarial/or
erythema multiforme (may be only complaint)
 usually nontoxic and afebrile; can produce membrane similar to diptheria;
associated with chronic pharyngitis
 Vincent’s angina
 anaerobic pharyngitis and acute necrotizing ulcerative gingivitis (ANUG)
 also called Trench Mouth
 etiology: Borellia vincenti
 superficial ulceration and necrosis that often results in the formation of a
pseudomembrane and gingival lesions
 food deposits in gingival crevice, gingivitis, frank ulceration and bleeding,
pseudomembranous necrotic exudate in gingival margins, spread to
tonsils and pharynx
 foul-smelling breath, odynophadia, submandibular lymphadenopathy,
exudate often present, poor oral hygiene common
 Gonococcal pharyngitis
 STD, may be independent of genital infection, can be asymptomatic
carrier, latent period common, important cause of gonococcemia
 Syphillitic pharyngitis
 primary or tertiary syphillus, painless mucosal lesions
 Tuberculosis pharyngitis
 hoarseness, dysphagia, pharyngeal ulcers in patient with advanced
disease
 Candidal pharyngtitis
 dysphagia, odynophagia, adherent white plaques with focal bleeding
points, immunocompromised
 Mycoplasma pneumoniae
 mild pharyngitis, epidemics occur, up to 10% of all adult pharyngitis, may
have LRTI as well
 Chlamydia pneumoniae
 epidemics, severe, selling and pain of deep cervical lymph nodes, +/-
LRTI, hallmarks are recurrence and persistence
 Chlamydia trachomatis
 STD, urogenital and partner testing required, mild symptoms or
asymptomatic
DIFFERENTIAL DIAGNOSIS
 Deep space infections, Tumors, Foreign bodies
 Pemphigus, Steven Johnson syndrome, Drug reaction
 Allergic reaction, Angioedema
 Chemical and thermal burns
 Esophagitis, GERD
 Epiglotitis, thyroiditis
DIAGNOSTIC STRATEGIES
 Mononucleosis
 Monospot: 95% sensitive in adults, 90% sensitive in > 5yo, 75% sensitive
in 2 - 4yo, 30% sensitive in 0 - 2yo; commonly negative in first week of
illness; specificity can be a concern as test may remain positive for up to
a year following the illness; POOR in young and early in dz
 EBV IgM antibodies can be measured
 EBV nuclear antigens develp w/i 3-6weeks and can be useful if initial
testing is negative
 Peripheral blood smear reveals atypical mononuclear cells in 75% with
peak incidence in 2nd to 3rd week of illness
 Group A Beta-Hemolytic Strep
 Important to diagnose and treat w/ abx to prevent rheumatic fever
 Antibiotic do NOT prevent post - strep glomerulonephritis
 Difficult to dx or r/o accurately with clinical assessment
 Serology: Anti-Streptolysin O (ASO) titers acute and convelescent are only
reliable way to diagnose; looks for grp A only; very specific but sensitivity
is variable (60 - 90%)
 Throat swab cultures 90 - 95% sensitive for detection of Streptococcus
pyogenes but specificity (50%) may be poor as asymptomatic carriage is
common; lab only looks for GAS, must ask for diptheria etc
 Rapid diagnostic tests: latex agglutination, ELISA, optical immunoassay,
chemiluminescent DNA probes; looks for streptococcal antigen in the
throat swab (only grp A); sensitivities range from 30 - 100% and
specificities range from 70 - 100% in trials but lower in practice; use is
controversial considering significant false +ve and false -ves
 Clinical scoring system
fever
> 38.3
cervical
lymphadenopathy
tonsillar
exudate
absence
of cough
 Other testing
 Diptheria: requires specific culturet, toxigenicity testing must also be
performed
 A. hemolyticum: suspect if rash present, including EM
 Vincent’s angina: clinical suspicion and a gram stain
 Gonococcus: requires a Thayer-Martin agar
 TB: requires acid-fast staining
 Syphilus: dark-field microscopy, direct immunofluorescence, serology
 Candida: yeast on KOH prep of throat swab or Sabouraud’s agar
 Mycoplasma: serology or culture
 Chlamydia: serology or antigen detection tests
 HSV: culture of vesicles
MANAGEMENT
 Group A Beta-hemolytic Strep
 Clinical judgement unreliable, poor diagnostic tests, vastly overtreated
 Benefit of antibiotics: shorten course of illness by < 1 day (2or3 vs 3or4),
decreases transmission, prevention of complications, decrease incidence
of rheumatic fever (or is a change in strain pattern, because rheumatic
fever rarely seen today compared to 50 years ago, is it really the antibiotic
use?)
 Disadvantage of antibiotics: increased bacterial resistance, increased
recurrence, decreased immune response, patient expectation of abx
 Rheumatic Fever: treatment w/i 9 days will prevent RF, incidence
dramatically decreased after antibiotic use, peak incidence in 5 - 15yo
where Grp A Beta - hemolytic strep common, currently occurs in 0.3% of
GAS pharyngitis and may increase to 3% with epidemics
 Tonsillectomy: > 5 episodes per year
 Antibiotics does NOT prevent post-strep glomerulonephritis
 Four ED strategies
throat
culture all and only treat positives: costly, poor
specificity of positive culture b/c of carriage rate, delay in
waiting for cultures, problems with f/u from ED,
treat
all, culture all, stop if culture negative: ineffective and
costly
perform
rapid strep test and treat those who are positive:
false +ve lead to over treatment, negative test requires
follow up cultures,
treat
all who have reasonable clinical probabililty of GAS:
leads to over-treatment but avoids problems with testing
COMBINATION:
high clinical probability should be treated
without testing, low clinical probability should be treated if
testing is positive (culture or rapid strep testing)
 Group A Beta-hemolytic Strep antibiotic regimen
Penicillin
V 250 mg po qid X 10days
Penicillin
V 250 mg po qid X 2/7 then 500 mg bid X 8/7
Benzathine
Penicillin 1.2 million units im X 1 dose
Frequent
dosing necessary, im dose has more reactions
Erythromycin
500 mg bid X 10/7 for pen allergic
Penicillin
failure due to noncompliance, re-infection, or Beta
- lactamase production; penicillin resistance growing,
erythromycin resistance uncommon
Alternatives:
cephalosporins, macrolads, clindamycin (not
shown to prevent RF although probably do)
Amoxicillin,
ampicillin, and penicillinase - resistant
penicillins offer no advantage over uncomplicated GAS
infections
 Other Bugs
 Diptheria: concern for toxicity and airway compromise; treat immediately if
suspecting, don’t wait for tests; equine ANTITOXIN is indicated based on
clinical grounds, dose varies, consultation required; antibiotics eradicate
the bug but not the toxin, use erythromycin or rifampin; Td booster for
immunized contacts and erythromycin + full vaccination course for
unimmunized contacts
 A. hemolyticum: erythromycin d of c b/c of penicillin resistance
 Vincent’s angina: penicillin or clindamyucin and aoral oxidizing agent
(hydrogen peroxide)
 Gonoccocus: ceftriazone 125 mg im or cipro/cifixime single dose;
concomitant treatment with azithromycin or doxy to cover chlamydia
 TB: multiple drug regimen
 Syphillus: benzthine penicillin 2.4 million units or doxycycline X 14 days
 Candida: nystatin swish and swallow, versus oral
GAS CLINICAL SCORING SYSTEM
(i) fever > 38.3 (ii) cervical ln.s (iii) tonsillar
exudate (iv) NO cough
0 - 1: no treatment or testing
2 - 3 : test, treat if positive
4: treat empirically
fluconazole/itraconazole/clotirmazole; chronic suppression with HIV
 Mycoplasma pneumonia: erythromycin, doxycycline, tetracycline
 Chlamydial: doxy or macrolide
 Recurrent tonsillitis: B-lactamase resistent antibiotics
 HSV: acyclovir X 1 week if primary infection
 Steroids? Mayshorten the duration of symptoms without increasing the
complication rates
 Symptomatic
 Tylenol, ibuprofen
 Warmed fluids, topical anesthetics (cepacol, etc)
 Mononucleosis
 Supportive, hydration, consider steroids
 Avoid sports or contact for 6-8 weeks (risk of splenic rupture)
 Acyclovir or famiciclovir if immunocompromized
DISPOSITION
 Complications may necessitate consultation and admission: Airway compromise,
Local
and distant spread of infection, Deep neck abscesses, Necrotizing fascitis, Sleep apnea,
Bacteremia/sepsis
 Complications of mono: airway obstruction, tonsillar and peritonsillar abscess, lingual
tonsillitis, necrotic epiglottitis, hepatic dysfunction, splenic rupture, neurologic
disorders,
pneumonitis, pericarditis, hematologic disorders
 GAS complications
 Suppurative: PTA, RPA, deep space abcessess, suppurative cervical
lymphadenitis, OM, sinusitis, mastoidtits, bacteremia, sepsis, OM,
meningitis,
 Nonsuppurative: RF, GN, pericarditis, myocarditis, erythema nodosum,
streptococcal toxic shock syndrome
Rheumatic
Fever: rare, 18 days after infection is average,
carditis and secondary valve disease, certain serotypes
more of a problem (with M-protein), prevented with abx w/i
9 days
Glomerulonephritis:
uncommon, 10 days after infection is
average, usually nephritic syndrome, uncommon
progression to CRF, serotype M-type 12, NOT prevented
by abx
ADULT EPIGLOTTIS
PRINICPLES OF DISEASE
 Potentially life-threatening condition from airway obstruction
 Increased incidence and recognition in adults; uncommon in peds after Hflu vaccine
 Localized cellulitis of upper airway
 Marked involvement of the supraglottic structuress: base of tongue, vallecular,
aryepiglottic folds, arytenoid soft tissues, lingual tonsils, epiglotis
 Inflammation does NOT extend to the infraglottic rections b/c the submucosa is so
densely adherent to the mucosa below the vocal cords
 Supraglossitis: reports of severe supraglottic involvement with normal epiglottis
 H. influenza type B is most common isolate
 Majority have NO organisms identified by blood or supraglottic cultures
 ? viral (adenoviral) role
CLINICAL FEATURES
 No age, seasonal prevelance
 Males, smokers more commonly affected
 Prodrome variable: hours - days
 Rapid progression is predictor of airway compromise
 Sore throat, odynophagia, dysphagia (pain severe), STRIDOR
 Dysphonia and muffled voice common; usually NOT hoarse
 Fever in 50% and late
 Tacchycardia out of proportion to fever
 Tenderness over anterior neck in hyoid region and on moving larynx are reliable
 Imminent airway obstruction: stridor, drooling, respiratory distress, sniffing position
 Pharyngeal examination does not r/o epiglottis b/c of concominant pharyngitis,
uvulitis,
tonsillitis, Ludwig’s angina, PTA, parotitis
DIAGNOSIS
 Differential diagnosis
 Misdiagnosis common: strep pharyngitis is most common misdiagnosis
 Monon, deep space infections, lingual tonsillitis, diptheria, pertussis,
croup, angioedema, allergy, FB, laryngospasm, tumor, toxic inhalant,
aspiration, laryngeal trauma
 Laryngoscopy
 Direct, indirect, or fiberoptic visualization if not in respiratory distress
 Swollen epiglottis and surrounding structures, epiglottis may be “cherry
red” but often is pale and edematous
 Respiratory distress, stridor, drooling, aphonia: indirect laryngoscopy
contraindicated and direct laryngoscopy only if prepared for airway
 Lateral soft tissue of neck
 Sensitivity 80 - 90% (does NOT rule out)
 Xrays: obliteration of vallecula, swellin of arytenoids and aryepiglottic
folds, edema of prevertebral and retropharyngeal soft tissues,
“ballooning”of the hypopharynx and mesopharynx, edematous thumb
shaped epiglottis (Epiglottis > 8mm or Aryepiglottic fold > 7mm)
 Direct laryngoscopy indicated if suspecting and Xrays normal
MANAGEMENT
 Expect sudden, unpredictable airway obstruction
 Minimize stimulation, have airway equipment by the bed, have cric tray at bedside,
notify
OR and consult ENT emergently if airway compromise present or expected
 Hands off and transfer to OR for definitive airway management if at all possible
 If airway obstructs in ED: try orotracheal, could try LMA, be set up and ready for TTV
or
cricothyrotomy
 Safety and efficacy of Orotracheal and laryngoscopic guided nasotracheal intubation
reported
 Blind nasotracheal intubation may lead to airway obstruction and is contraindicated
 Lateral neck Xray (portable) may be helpful but don’t waste time to OR
 Start antibiotics ASAP: cefuroxime, ceftriaxone, cefotaxime
 ? role for steroids and racemic epinephrine
 Disposition
 Mild cases: mild swelling on laryngoscopy without drooling, stridor, or
respiratory distress --------> ICU for treatment and monitoring without
intubation
 Moderate/Severe: to OR for intubation, to ICU
 So who needs intubation? Alert, stable, not tiring, no resp distress can be
monitored
 Complications
 Meningitis, RPA, pneumothorax, empyema, pneumonia, sepsis, ARDS,
pulmonary edema
DEEP SPACE INFECTIONS OF THE
LOWER FACE AND NECK
 Deep space infection of neck are dangerous and require rapid treatment
 Much less common because of dental hygeine and antibiotics
 Distorted airway anatomy = difficult airway
 Paralytics may cause muscular laxity and worsen the degree of airway obstruction
 Fiberoptic intubation useful
 BNI can cause abscess rupture, airway damage, further compromise
 Submandibular space: conglomerate of the sublingual and submaxillary spaces which
clinically function as a single space
 Sumandibular space is involved in Ludwig’s angina
 Five clinically relevant potential spaces in neck (figure 70-4)
 Peritonsillar space
 Parapharyngeal space: carotid, jugular vein, CN IX –> XII, sympathetics
 Retropharyngeal space: lies in the midline, medial to the parapharyngeal
space and extends from the base of the skull to the superior mediastinum
at the level of T2; superior constrictor muscle adheres to the prevertebral
fascia and forms a raphe in the medial aspect ot the retropharyngeal
space :. retropharyngeal abscesses tend to occur lateral to the midline
 Danger space: base of the skull to the diaphragm: abscesses will be
midline
 Prevertebral space: base of the skull to the coccyx: abcesses will be
midline
 Retropharyngeal, danger space, and prevertebral space infections have easy access
to
mediastinum, Danger space, Prevertebral space which all communicate
 Rapid spread of infection occurs easily through facial planes and spaces
PERITONSILLAR CELLULITIS (PTC)AND
PERITONSILLAR ABSCESS (PTA)
PRINCIPLES OF DISEASE
 PTC and PTA are a continuum of peritonsillitis
 PTA (quinsy) is the most common deep infection of the adult head and neck
 Result of acute tonsillitis: infection of weber’s glands or tonsillar crypts invades the
peritonsillar tissues leading to cellulitis that may progress to abscess formation
 Fibrous fascial septae divide the peritonsilar space into compartments and direct the
infection anteriorly and superiorly
 Risk factors: chronic tonsillitis, mono, smoking, CLL, tonsilloliths, dental infection
 All age groups, CAN occur with previous tonsillectomy, recurrence in up to 50%
 Polymicrobial aerobes (GAS, strep milleri, Hflu, strep viridans) and anaerobes
(fusobacterium, bacteroides, peptostreptococcus, actinomyces)
CLINICAL FEATURES
 Odynophagia, dysphagia, drooling, trismus, referred otalgia, muffled “hot potato”
voice,
rancid breath, systemic symptoms of fever, dehydration, malaaise
 Recurrent tonsillitis hx common
 PE: trismus, inflammed and erythematous oral mucosa in peritonsillar area, purulent
tonsillar exudates that may cover the tonsil, tender cervical lymph nodes
 PTC versus PTA can be difficult
 TRISMUS and UVULAR DEVIATION are the best predictors of abscess
versus cellulitis
DIAGNOSIS
 Clinical diagnosis for PTC
 Aspiration of pus for PTA
 Mono common (20%) and monospot testing may be relevant
 Xrays of limited utility
 Contrast CT, intraoral ultrasound, transcutaneous ultrasound useful when patients
unable to co-operate with needle aspiration
 PTA needle aspiration
 Adv: diagnostic and therapeutic, easy and safe in ED, minimal pain
compared to surgical incision and drainage
 Disadv: difficult if uncooperative or children, may miss abscess and lead
to misdiagnosis of PTC, greater recurrence of PTA c/p to I&D, carotid
artery puncture theoretical (NO case reports in literature)
 Differential diagnosis
 Hypertrophic tonsillitis, mono, diptheria, deep space infections of neck,
cervica adenitis, congenital or traumatic internal carotid artery aneuryms,
foreign bodies, neoplasms
MANAGEMENT
 No suspicious findings for abscess = suspect Peritonsillar Cellulitis
 Don’t attempt ED aspiration
 IV antibiotics and f/u with HPTP
 Suspected Peritonsillar Abcess
 Needle aspiration in ED (except in peds)
 Start IV abx
 F/U with HPTP
 Arrange ENT follow up
 Controversies
 Aspiration equivalent to I&D in three small studies
 Indications for tonsillectomy: two PTAs, septic, etc
 Do all need to see ENT? recurrent, large, can’t aspirate in ED
 Which antibiotic?
Ancef
+ flagyl
Ceftriaxone
+ flagyl
Pencillin
+ flagyl
Clindamycin
alone (general choice in peds)
 IV antibiotics and observation before surgical intervention an option
 Complications
 Airway obstruction is most important complication
 Other: abscess rupture with aspiration, pneumonia, empyema, pulmonary
abcess, prapharyngeal and retropharyngeal spread of infection, Ludwig’s
angina, mediastinitis, myocarditis, carotid artery erosion, jugular vein
thrombophlebitis, septic embolization, postanginal septicemia (Lemierre’s
syndrome) and cervicothoracic necrotizing fascitis
 Intracranial: meningitis, venous sinus thrombosis, cerebral abscess
 Systemic: dehydration, sepsis, toxic shock
 Dispostion
 Admission: dehydration, inability to tolerate po intake, toxic, underlying
diseases, severe pain, complications
 Discharge: generally iv abx through outpatient iv program
RETROPHARYNGEAL (RPA) AND
PREVERTEBRAL SPACE ABSCESSES
PRINCIPLES OF DISEASE
 Retropharyngeal swelling occurs from expansion of either the retropharyngeal space,
danger space, or the prevertebral space (figure 70-4) -----------> collectively described as
retropharyngeal abscesses (RPA)
 Previously a childhood disease, but increasing adult incidence
 Children < 4yo have prominent retropharyngeal lymph nodes that become infected,
lead
to retropharyngeal cellulitis and RPA formation
 Retropharyngeal nodes atrophy after 4 - 6 yo and thus decreasing incidence and
different pathology in adults
 Adults: cellulitis in retropharyngeal area and abscess may form; nasopharyngitis, OM,
parotitis, tonsillitis, PTA, dental infections and procedures, upper airway
instrumentation,
Ludwig’s angina, lateral pharyngeal space infection, endoscopy are all implicated as
causes
 Blunt and penetrating trauma also causes: FB, fish bones, cautic ingestion, vertebral
fracture
 Hematologic spread less common
 Diabetes and immunocompromised states may be important
 Polymicrobial aerobes and anaerobes is most common
 Vertebral osteomyelitis leading to RPA is most commonly staph
 Tuberculosis was a common cause, but not now
CLINICAL FEATURES
 Sore throat, odynophagia, dysphagia, drooling, muffled voice, neck stiffness, neck
pain,
fever
 Dysphonia described as a duck “quack” (cri du canard)
 May be toxic, airway obstruction and respiratory distress possible
 Sniffing position to protect airway can occur
 May have posterior neck or shoulder pain with swallowing
 Physical Examination
 Tender cervical ln.s, tender cervical musculature, neck swelling, torticollis,
high fever, trismus may be present
 Diffuse edema/erythema of posterior pharynx with retropharyngeal
cellulitis
 Palpation of abscess: unreliable, risk of rupture
 Visualization of abscess: midline lump with prevertebral or danger space
and unilateral if retropharyngeal space
 Tenderness on moving the larynx and trachea side to side (tracheal rock
sign)
DIAGNOSIS
 Lateral neck Xray
 Inspiratory film with widening of retropharyngeal space and forward
displacement of esophagus and trachea
 Diffuse swelling with cellulitis, more localized with abcess
 Xrays are unreliable to distinguish RP cellulitis versus RP abscess
 Other: loss of cervical lordosis, air-fluid level in abcess, FB, vertebral body
destruction (AIR in RP space is good predictor of abscess)
 Retropharyngeal space > 7mm at level of C2 is abnormal in kids and
adults
 Retropharyngeal space > 14mm adults and 21mm kids at level of C6
 Other
 CXR to evaluate mediastinal involvement
 CT or MR good for detection of complications
 CT with iv contrast is considered the “gold standard” for diagnosis but
studies show sensitivity 90 - 100% and specificity 60 - 70 % (low) for RPA
vs RPC
 U/S useful tod etect RPC from RPA
 Differential Dx
 Cold abscesses: tuberculosis; insidious onset, chronic, constitutional
symptoms, minimal fever, symptoms >> physical findings
 RP tumors, FB, hematoma, aneurysm, hemorrhage, lympadenopathy,
edema, retropharyngeal thyroid tissue, tendinitis of longus colli muscle
MANAGEMENT
 RPC: iv antibiotics, choices as per Ludwig’s angina, consider TB and fungal
 RPA: surgical incision and drainage, iv antibiotics (may try abx X 48hr before surgery)
 Cold abscesses: drained extraorally, unless in acute distres
 Vertebral body destruction: neck immobilization could be necessary with vertebra
osteomyelitis or atlantoaxial separation; external fixation possibly required
 Complications: abscess rupture and aspiration, pneumonia, empyema; extension to
mediastinum, pericarditis, pleuritis, empyema; vascular erosion; atraumatic atlantoaxial
separation due to damage of transverse ligament of atlas (wide predental space on Xray
or CT); acute transverse myelitis, epidural abcess; esophageal erosion, necrotizing
fascitis, ARDS, sepsis
 Disposition
 Admitted, consultation with ENT, surgical intervention
PARAPHARYNGEAL ABSCESS (PPA)
PRINICPLES OF DISEASE
 Parapharyngeal space (lateral pharyngeal space, pharyngomaxillary space) divided
into
two compartements by the styloid process
 Anterior compartment: muscle, lymph nodes, connective tissue
 Posterior compartment: carotid sheath (carotid artery, internal jugular vein,
vagus nerve, CNIX/X/XI/XII, cervical sympathetic chain)
 Etiology: dental infections, pharyngotonsillary infections are most common causes
 Other causes: spread from surrounding deep spaces, parotits, sinusitis, neck tumors,
infected branchial cleft cysts, mastoiditis, suppuration of local lymphadenitis, iatrogenic
introduction by anesthetic blocks/tonsillectomy/nasal intubation/dental work
 Polymicrobial
CLINICAL FEATURES
 Pain and swelling of the neck, odynophagia, dysphagia
 Classic: medial tonsillar displacement and posterolateral pharyngeal wall bulge
 Other findings: fever, trismus, edema, swelling at angle of jaw,
erythematous/tender/and
nonfluctuant mass at angle of mandible
 Diagnosis
 Clinically diagnosis
 Lateral neck Xray: upper prevertebral soft tissue swelling, otherwise not
helpful
 U/S, CT, MR useful
 Ddx: as per RPA
MANAGEMENT
 ENT consultation
 IV antibiotics as per Ludwig’s angina
 Surgical drainage
COMPLICATIONS
 AWO, rupture, aspiratoin, pneumonia, empyema, mediastinitis, necrotizing fascitis,
bacteremia, sepsis, pericarditis, osteomyelitis of mandible, parotid abcess, cavernous
sinus thrombosis, meningitis
 Unique complication of posterior pharyngeal infections
 Cervical sympathetic chain: horner’s
 Carotid artery erosion and aneurysms: oral, nasal, aural warning bleeding
is common; unexplained bleeding with H/N infections is serious and
warrants aggressive investigation, persistent peritonsillar swelling and
unilateral tender pulsatile masses may be clues
 CN IX —> XII palsies
 “Lemierre’s syndrome” (also called postanginal septicemia): IJ thrombophl
 Young, healthy patients, pharyngitis that improves then followed by severe
sepsis, confused with right sided endocarditis or aspiration pneumonia
 Pharyngeal infection spreads to the paraphyngeal space and causes
septic thrombophlebitis of the jugular vein
 Metastatic infectious spread to lungs cause bilateral nodular infiltrates,
pleural effusion, pneumothoraces
 Septic arthritis, osteomyelitis, meningitis, vesiculopustular rash are also
reported result of septic embolization
 Leukocytosis, incr bilirubin, incr LFTs, hematuria, renal failure, all reported
 Full septic picture with its complications reported
 Fusobacterium and Staph aureus are most common causes
 Antibiotics +/- jugular vein ligation and resection
LUDWIG’S ANGINA
PRINCIPLES OF DISEASE
 Progressive cellulitis of the connective tissues of the floor of the mouth and neck that
begins in the submandibular space
 Potentially fulminant, death within hours is possible
 Dental disease is the MCC: infected or recently extracted tooth in almost all cases
 Lower 2nd and 3rd molars are the MC teeth afftected
 Dentoalveolar abscesses may easily break through the relatively thin cortex of the
mandible below the mylohyoid ridge and infect the submandibular spaace
 Other causes: mandible fracture, FB or laceration to floor of the mouth, tongue
piercing,
traumatic intubation/bronch, oral Ca that gets infected, OM, submandibular
sialoadenitis,
PTA, furuncle, infected thyroglossal cyst, sepsis
 Polymicrobial: aerobes/anaerobes (staph, strep, bactroides, pseudomonas, klebsiella,
candida)
CLINICAL FEATURES
 Sublingual and submaxillary space infections leads to edema and soft tissue
displacement which may result in airway obstruction
 Symptoms: dysphagia, neck swelling, neck pain, dysphonia (“hot-potato”),
odynophagia,
dysarthria, drooling, tongue swelling, pain in floor of mouth, restricted neck movement,
sore throat, history of dental extractions/dental pain, foul taste in mouth; air release,
creptius, unilateral pharyngitis in any one with recent dental extraction is a clue
 PE: bilateral submandibular swelling and elevation or protrusion of the tongue,
elevation
of the floor of the mouth, posterior displacement of the tongue, “woody”consistency of
the
floor of the mouth, tense edema and brawny induration of the neck above the hyoid
(“bull
neck”), marked tenderness of neck, subQ emphysema of neck, trismus, fever, cervical
LN, percussion tenderness over teeth
DIAGNOSIS
 Five diagnostic criteria
 Cellulitis with little or no pus present in the submandibular space
 Bilateral cellulitis
 Gangrene present with serosanguinous, putrid fluid
 Connnective tissue, fascia, muscle involvement but glandular tissue
spared
 Cellulitis spread by continuity and not by lymphatic vessels
 Investigations
 Lab not very helpful
 Fluid for culture and gram stain
 Xrays: swelling of affected area, gas collections, panorex may
demonstrate periodontal abscess and other dz
 Ultrasound: cellulitis versus abscess
 Differential Dx
 Deep cervical node suppuration, PTA, other deep neck abscesses,
parotid abscess, submandibular gland abscess, oral cancer, angioedema,
submandibular hematoma, laryngeal diptheria
MANAGEMENT
 Airway
 Airway obstruction and asphyxiation is the MCC of death
 Airway may obstruct rapidly
 Continuous monitoring essential
 Stridor, tachypnea, dyspnea, inability to handle secretions are indicators
of impending airway obstruction
 Fiberoptic nasotracheal intubation is the preferred method of intubation
 Definitive therapy
 Antibiotics: high dose penicillin + flagyl or ptip-tazo or clinda
 Steroids: unknown role
 Surgery: incision and drainage if failure of antibiotics, crepitus and
purulent collections
 Dental extraction
 Complications
 Spread of infection: deep spaces of neck, empyema, mediastinitis,
mediastinal abscess, pericarditis, aspiration pneumonia, lung abscess
 IJ thrombosis, carotid artery erosion, bacteremia, sepsis, subphrenic
abscess, necrotizing fascitis, spontaneous pneumothorax
 Disposition
 Admission, iv abx, ENT consult, +/- ICU monitoring
SINUSITIS
PRINCIPLES OF DISEASE
 Definition: inflammation of one or more of paranasal sinuses; acute < 4/52, chronic>
3/12
 Common, viral URTIs complicated by sinusitis in 0.5 - 2.0%
 Viral sinusitis 200Xs more common than bacterial sinusitis
 Pranasal sinuses: frontal, maxillary, ethmoid, sphenoid based on which bone they are
in
 Maxillary sinus: triangular, base being the lateral nasal wall and apex extending into
the
zygoma
 Ethmoid: anterior and posterior, 2 - 8 anterior air cells and 1 - 8 posterior air celss
 Ethmoid: blood supply connects tot eh opthalmic vessels and cavernous sinus;
dangerous re spread tot eh orbit or CNS
 Frontal: variable pneumatization from aplastic to extensive; bony septum between
left
and right;
 Sphenoid: bony septum, optic nerve and carotied artery occupy the lateral walls of
the
sphenoid sinus
 Ethmoid and maxillary sinuses are present at birth
 Sphenoid sinuses start to develop at 2yrs and not well developed until 6 yrs - 12 yrs
 Frontal sinuses start to develop at 2 yrs, are small until 6 years, not full developed
until
teens
 Medial meatus: drainage for the maxillary, anterior ethmoid, frontal sinuses; located
b/w
the inferior and middle turbinates; this area is the ostiomeatal complex and is the focal
point of sinus disease
 Superior meatus: drainage for the posterior ethmoid
 Sphenoid sinus drains just above th superior turbinate
 Healthy sinus depends on patent ostia with free air exchange and mucus drainage so
that it does not accumulate mucus and remains sterile. URTI and allergic rhinits are the
MCC of ostial obstuction with resultant sinusitis
 Ciliary abnormalities are also important: URTI, genetic syndromes
 Compromised drainage leads to resorption of air, lowers oxygen tension, increased
metabolism, lowers the pH, bacterial introduction by coughing or blowing nose,
inflammation and bacterial overgrowth
 Allergic sinusitis: sneezing, itchy eyes, allergen exposure, prior episodes
 Viral sinusitis up to 200Xs more common than bacterial
 Bacterial pathogens: pneumococcus, Hflu (50% together), Moraxella catarrhalis
(10%)
are primary bacteria; anaerobes, streptococcal species, staph aureus more important in
chronic sinusitis (polymicrobial often associated with dental disease); pseudomonas
(HIV
and CF)
 Immunocompromised: aspergillus, candida, histoplasma, blastomyces, coccidioides,
cryptococcus, rhizopus, etc (especially with DKA)
 Mucormyocosis
 Invasive, aggresive fungal sinusitis in the Immunocompromised
 Fever, localized nsal pain, cloudy rhinorrhea, grey/friable/anesthetic
terbinates that do not bleed because of angioinvasion (may be necrotic
and black tissue)
 Risk Factors
 Medical conditions: resp infections, allergic rhinitis, CF, immunodeficiency,
Wegener’s syndrome, Kartagener’s syndrome
 Irritants: smoke, polution, chorine, cocaine
 Anatomy: deviated septum, adnoidal hypertrophy, immotile cilia, polpys,
tumors, foreign bodies, NG tubes
 Trauma: facial fractures, dental procedures, diving
CLINICAL FEATURES
 Symptoms
 Worsening symptoms after 5 days or persistent after 10 days
 Double sickening: cold who improves initially only to have worsening sinus
congestion and discomfort Nnasal congestion, nasal obstruction,
mucopurulent discharge, post-nasal drip that may lead to cough,
pressure/pain over the involved sinus, malaise, fever
 Pain over the affected sinus is the main symptom
 Sphenoid sinus: vague bitemporal h/a or various focal points anywhere in
head
 Maxillary sinusitis: pain over the zygoma, canine or bicuspids, or
periorbitally
 Ethmoid sinusitis: medial canthal pain and periorbital or temporal
headache
 Chronic Sinusitis: slow onset, prolonged duration, recurrence; symptoms
similar to acute but may also have cough, fetid breath, laryngitis,
bronchitis, worsening asthma
 Pediatric sinusitis symptoms: more nonspecific; persitant URTI X 10 - 14
days with persistent nasal discharge and continued unwell state (+/- fever,
irritabiliby, lethargy, cough, poor feeding) -----> consider foreign bodies,
asthma, tumors, polyps, CF
 Physical Examination
 Periorbital edema or other facial swelling
 Tenderness by palpation or percussion over the maxillary or frontal sinus
(no way to palpate the ethmoid or sphenoid sinuses)
 Maxillary teeth tenderness (10% related to dental infection)
 Malodorous breath in absence of other cause
 Anterior rhinoscopy (est performed after application of topical
decongestant)
Erythema
and edema
Mucopurulent
discharge in nose
Mucopurulent
discharge from middle meatus or sinus ostia
Anatomic
anomalies (polyps, deviated septum)
 Transillumination
 How: dark room, light against infraorbital rim and look in pt mouth to see
how much light is transmitted through maxilla (or can put light in mouth);
place at supraorbital rim and aim toward frontal sinus
 Only 55% of patients with findings on CT have findings on
transillumination and CT is nonspecific :. transillumination is not sensitive
 Interobserver reliability 60%
 Questionable role in adults
 No role in kids < 9 b/c thick bone and soft tissues, different rates of sinus
development b/w kids and b/w sides, lack of aeration of sinuses
RADIOLOGY
 Plain films
 What to look for: sinus opacification, air - fluid level (insensitive but more
specifice), mucous membrane thickness > 5 - 6mm (sensitive but
nonspecific)
 What views can be done: Water’s view (maxillary sinusitis), Caldwell
(ethmoid and frontal), Lateral (sphenoid), submentovertex (sphenoid and
ethmoid)
 What views should be done: Water’s view alone; add other views if
Water’s is inconclusive or specifically looking for non-maxillary sinusitis
 Overall 50% accurracy
 Xrays: false -ve in up to 40%, poor correlation with CT, sensitivities
reported range from 40 - 90% and specificity 75 - 100% but CT or MRI is
used as gold standard which is problematic
 Who should be Xrayed: if diagnosis uncertain but possible based on
clinical criteria (2-3 out of 5 above criteria)
 Be more aggressive with Xrays in looking for frontal sinusitis b/c of
important consequences of rupture into CNS
 Xrays in < 1yo not useful b/c of false opacification due to facial asymmetry
and redundant mucosa
 Axial or coronal CT
 Considered the radiological gold standard (A/F levels, sinus opacification,
sinus wall displacement, 4 mm or greater mucosal thickening)
 Need iv contrast to look for orbital or CNS complications
 CT is sensitive but lacks specificity thus CT findings need clinical
correlation (CT findings suggestive of sinusitis as incidental findings and
in 84% of early cold symptoms)
 Indications for CT: chronic sinusitis, suspected complication, failure of
medical treatment
DIAGNOSIS
 Clinical diagnosis: definitive diagnosis is difficult
 No single symptom or sign is diagnostic
 Antral aspiration is gold standard: difficult, uncomfortable, maxillary only, not useful
in ED
 Nasal and nasopharyngeal cultures correlate poorly with antrostomy cultures
 Culture and biopsy only for chronic and suspected fungal sinusitis
 Endoscopy of sinuses can be done
 Ultimately: clinical diagnosis; minimize testing as sensitivity and specificity are
lacking
 Differential dx
 Rhinits: increased response to deongestants, clear nasal discharge,
absence of pain, no ostial obstruction and thus no facial pain
 Tension headache, vascular headache, FB, dental disease, brain
abscess, epidural abscess, meningitis, subdural empyema
 Making the Diagnosis by History and Physical Examination: Williams 1992
 Looked at various findings on hx and physical exam
 Note that sinusitis gold standard was defined radiographically (sinus
opacification, air - fluid level, mucous membrane > 6 mm thick)
Symptom Sensitivity Specificity
- maxillary toothache 18 93
- nonresponse to decongestants 41 80
- hyposmia 56 64
- colored discharge 72 52
- myalgias 48 66
- cough 70 44
- preceeding URTI 50 61
- headache 68 30
- facial pain 52 43
- painful chewing 13 84
Signs
- purulent secretion 51 76
- sinus tenderness 48 65
- abnormal transillumination 73 54
- temp > 38 16 83
 CMAJ 1997: Likelihood of acute sinusitis as determined by number of signs and
symptoms....
Symptom/Sign LR +ve
Maxillary toothache 2.5
History of colored nasal secretion 1.5
Poor response to decongestant 2.1
Abnormal transillumination 1.6
Purulent nasal secretion visualized 2.1
Number of findings
0 0.1
1 0.5
2 1.1
3 2.6
4 6.4
 Management based this
0
- 1: ruled out based on clinical features, no Xray
2
- 3: diagnosis unclear, sinus Xray recommended
4
- 5: actue bacterial sinusitis ruled in, no Xray
MANAGEMENT
 MOST will resolve spontaneously (60%), viral and bacterial
 Antibiotics
 Antibiotics should be started if suspecting bacterial etiology
 Treatment approach similar to otitis media
 Amoxicillin X 10/7 is drug of choice (may be ineffective if B-lactamase
common): adequate coverage, best activity against penicillin intermediate
B-lactam resistant pneumococcus, few side-effects, low resistance
potential, no other antibiotic has been shown to be superior to amoxil in
RCTs
 Consider high dose amoxil for high risk children b/c of abx use w/i 3
months or day care (90 mg/kg/day tid instead of 40 mg/kg/day tid)
 Penicillin allergic: trimethoprim - sulfamethoxazole, azithromicyin,
cefuroxime
 Rx failure after 7days: amoxicillin-clavulanate, cefuroxime, clindamycin,
ciprofloxacin, clarithromycin, +/- flagyl
 Chronic: cover B-lactamase and anaerobes
 Complications: iv abx, admission, ENT consultation
 Decongestants /Adjuncts
 Reduces tissue edema, facilitates drainage, maintains patency of ostia
 NO good scientific evidence of effectiveness
 Topical and systemic should be used inconjunction
 Topical: phenylephrine 0.5%, oxymetazolin 0.05%; use for 3 - 5 days only
b/c extended use leads to rhinitis medicimentosa
 Oral: pseudoephrine, phenylpropanolamine (caution with TCA, MAO-I,
nonselective Beta-blockers)
 Antihistamines contraindicated unless allergic sinusitis (impedes sinus
drainage)
 Steroids for chronic and allergic sinusitis (controversial)
 Steam, humidifiers, nasal saline spray may help (indeterminate)
 Disposition
 Most discharged home with oral abx
 Immunocompromised, severe co-morbid illness, toxic, poor follow up,
inability to tolerate po meds ----> admission for iv abx and observation
 Failure of definitive therapy means chronic sinusitis and ENT referral
 Frontal and sphenoid sinusitis with A/F levels may require hospitalization
 Fungal sinusitis requires admission, ENT consultation, iv antifungals,
surgical debridement —> watch for mucormyocosis which is aggressive
and dangerous
 RTED for severe headache, neurologic symptoms, visual changes
 ENT referral: > 4 episodes of bacterial sinusitis per year, chronic sinusitis,
anatomic abnormalities, complications
COMPLICATIONS
 Facial cellulits, periorbitral cellulitis, periorbital abscess, optic neuritis, blindneess,
orbital
abscess
 Orbital complications: marked swelling, decreaed ocular motility, decreased visual
acuity
 Intracranial: meningitis, cavernous sinus thrombosis, epidural or subdural empyema,
brain abscess; suspect with neuro s/s,
MISCELLANEOUS
LINGULAR TONSILLITIS
 Rare cause of pharyngitis that usually occurs in patients who have had their palatine
tonsils removed
 Lingual tonsils are a collection oof nonencapsulated lymphoid tissue most commonly
located symmetrically on either side of the midline just below the inferior pole of the
palatine tonsil and anterior to the vallecula at the base of the tongue
 This lymphoid tissue may enlarge after puberty, repeated infections, tonsillectomy
 Sore throat that worsens with movement of tongue and phonation
 May have classic “hot potato” voice and complain of feeling a swelling in the throat
 Dysphagia, fever, resp distress, stridor may be present
 PE: normal appearing pharynx with mild hyperemia
 Laryngoscopy: edematous lingual tonsil covered with a purulent exudate
 Lateral neck Xray: normal epiglottis and aryepiglottic folds with a scalloped
appearance
of the anterior surface of the vallecula caused by the enlarged tonsils
 Mx
 Airway, abx, supportive
 AWO possible but rare
 Humidified oxygen, hydration, corticosteroids
 Nebulized epi for AWO may help
 Antibiotics as per pharyngitis
LARYNTITIS
 Hoarseness and aphonia
 Viral URTI
 Bacterial possible (strep, diptheria)
 TB, syphilis, leprosy, actinomyocosis, other fungal rare
 Consider epiglottitis
 Antibiotics only if suspecting bacterial
VIRAL RHINITIS
 > 100 viruses: rhinovirus, parinfluenza, RSV, etc
 Winter peak incidence
 Transmission via resp secretions
 Incubation 3 - 7 days
 Duration 3 - 7 days
 Antipyretics, nasal saline drops, humidified air, decongestants
ORAL ANGIOEDEMA: UVULITIS
 IgE mediated reaction characterized by edema of dermis especially in face/neck
 Non-pruritic, well-demarcated, localized, nonpitting edema of deep subcutaneous
tissue
that primarily involves the periobital, perioral, intraoral regions
 CLUE: angioedema is NOT itchy
 Note: facial findings can be lateralized (one side only)
 Heriditary angioedema (HAE)
 Autosomal dominant condition lacking C1 esterase inhibitor or functional
deficiency
 Cardinal s/s: edema of face, airway, or extremities, agdominal pain
associated with N/V/D
 Precipitated by trauma, stress
 Airway management is cornerstone of approach
 Acute management as per anaphylaxis although does not usually respond
well to epinephrine, antihistamines, or steroids
 FFP contains some C1 inhibitor; case reports of effectiveness
 C1 esterase concentrate replacement is probably the most important
treatment in a known HAE
 High dose epi may be effective
 Acquired Angioedema
 ACE-I, NSAIDS, sulpha drugs, others
 Idiopathic is common
 Angioedema occurs with ACE - Is in 0.2% and can be at any time
(including years after onset); more common in blacks
 Mechanism: ? inhibition of bradykinin metabolism
 Management as above: consider FFP, d/c offending agent
 Management
 Severe: treat as per anaphylaxis, intubate ASAP
 Moderate: treat as per anaphylaxis, watch airway closely
 Mild
Bendadryl
Steroid
X one dose
Monitor
4-6hrs for progression__

Definition

Pharyngitis is the swelling and inflammation of the pharynx. The pharynx is the back of the throat,
including the back of the tongue. Tonsillopharyngitis is the swelling of the pharynx and the tonsils. The
tonsils are soft tissue that make up part of the throat's immune defenses. Both pharyngitis and
tonsillopharyngitis are commonly called a sore throat. Sore throats can easily be treated. If you have a
sore throat for more than two days, contact your doctor.

Sore Throat Due to Inflammation

© 2009 Nucleus Medical Media, Inc.

Causes

Many things can cause pharyngitis and tonsillopharyngitis. Causes include:

o Infection with a virus, such as the viruses that cause influenza (the flu) and the common cold
o Infection with bacteria, such as the bacteria that cause strep throat
o Mucus from your sinuses that drains into your throat
o Smoking
o Breathing polluted air
o Drinking alcoholic beverages
o Hay fever or other allergies
 o Acid reflux from the stomach
o Allergies
o Food debris collecting in small pockets in the tonsils
o Infectious mononucleosis

Risk Factors

A risk factor is something that increases your chance of getting a disease or condition. Almost everyone
will get a sore throat. These risk factors increase your chance of getting a sore throat:

o Age: children and teens, and people aged 65 or older

o Exposure to someone with a sore throat or any other infection involving the throat, nose, or ears
o Situations that cause stress, such as traveling, working, or living in close contact with people
o Exposure to cigarette smoke, toxic fumes, industrial smoke, and other air pollutants
o Having other medical conditions that affect your immune system, such as AIDS or cancer
o Stress
o Hay fever or other allergies

Symptoms

Your symptoms depend on the cause of the condition. If you experience any of these symptoms, do not
assume it is due to pharyngitis or tonsillopharyngitis. These symptoms may be caused by other health
conditions. If you experience any one of them, see your doctor.

Symptoms include:

o Sore throat
o Pain or difficulty when swallowing
o Difficulty breathing
o Fever
o Enlarged lymph nodes in your neck

Diagnosis

The doctor will perform a physical exam, looking closely at your mouth, throat, nose, ears, and the lymph
nodes in your neck.

o This physical exam may include:

o Using a small instrument to look inside the nose, ears, and mouth
o Gently touching the lymph nodes (glands) in your neck to check for swelling
o Taking your temperature
o Examining your ears
o The doctor will ask questions about:
o Your family and medical history
o Recent exposure to someone with strep throat or any other infection of the throat, nose,
or ears
o Other tests include:
o Rapid strep test or throat culture—using a cotton swab to touch the back of the throat to
check for strep throat
 o Blood tests —to identify conditions that may be causing the sore throat
o Mono spot test (if mononucleosis is suspected)

Treatment

Treatment depends on the cause of the sore throat. Treatment options include:

Medications
o Antibiotics for strep throat
o Drugs to reduce sore throat pain; these drugs include:
o Ibuprofen (Motrin, Advil)
o Acetaminophen (Tylenol)
o Aspirin
o Note : Aspirin is not recommended for children or teens with a current or recent
viral infection. This is because of the risk of Reye's syndrome . Ask your doctor
which other medicines are safe for your child.
o Numbing throat spray for pain control
o Decongestants and antihistamines to relieve nasal congestion and runny nose
o Throat lozenges
o Corticosteroids (used in combination with antibiotics for severe cases)

Home Care
o Get plenty of rest.
o Drink plenty of water.
o Gargle with warm salt water several times a day.
o Drink warm liquids (tea or broth) or cool liquids.
o Avoid irritants that might affect your throat, such as smoke from cigarettes, cigars, or pipes, and
cold air.
o Avoid drinking alcohol.

If you have been diagnosed with pharyngitis, be sure to follow your doctor's instructions .

Prevention

Here are ways to reduce your chance of getting a sore throat:

o Wash your hands frequently, especially after blowing your nose or after caring for a child with a
sore throat.
o If someone in your home has a sore throat, keep his eating utensils and drinking glasses
separate from those of other family members. Wash these objects in hot, soapy water.
o If a toddler with a sore throat has been sucking on toys, wash the toys in soap and water.
o Immediately get rid of used tissues, and then wash your hands.
o If you have hay fever or another respiratory allergy, see your doctor. Avoid the substance that
causes your allergy.