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: Vincents

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

Pastias 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 bullneckappearance

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

Vincents 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

Vincents 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 Sabourauds 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

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

Other Bugs

Diptheria: concern for toxicity and airway compromise; treat immediately if

suspecting, dont 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
Vincents 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

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, Ludwigs 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,
ballooningof 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 dont 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 Ludwigs 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 webers 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

Dont 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, cant 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, Ludwigs
angina, mediastinitis, myocarditis, carotid artery erosion, jugular vein
thrombophlebitis, septic embolization, postanginal septicemia (Lemierres
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,
Ludwigs 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 Ludwigs 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 Ludwigs 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: horners

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

Lemierres 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

LUDWIGS 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, woodyconsistency 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,

Wegeners syndrome, Kartageners 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: Waters view (maxillary sinusitis), Caldwell

(ethmoid and frontal), Lateral (sphenoid), submentovertex (sphenoid and
ethmoid)

What views should be done: Waters view alone; add other views if
Waters 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
1
2
3
4

0.1
0.5
1.1
2.6
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