Download The sore throat

Contents
Syllabus: Department Textbook
Teaching: Daily teaching over 6 weeks in 3 sessions (2 weeks each)
A. Ear Session
B. Nose Session
C. Throat Session
Each day:
A. 9-10 am (academic hour),
B. 10-11 am diagnostic approach,
C. 11 am to 12 pm clinical tour (according to schedule)
Ear Diagnostic Approach "flowchart"
a. Acute otitis media
b. Facial weakness
c. SNHL
d. Vertigo
Nose Diagnostic Approach "flowchart"
a. Nasal obstruction
b. Epistaxis
c. Headache
Throat Diagnostic Approach "flowchart"
a. Sore throat
b. Neck mass
c. Stridor
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Acute Otitis Media Flowchart
>12 months,
Immune-competent
Analgesia,
No antibiotics for
1st 24-48 hours
Yes
No
Analgesia, Antibiotics:
Amoxicillin 45 mg/kg/d/ 5days
Amoxicillin-clavulanic acid 45 mg/kg/d/ 5days
Ceftriaxone 50 mg/kg monotherapy (FDA)
No
Symptoms
Resolved
Yes
Symptoms improved
by 48 hours
Yes
Check for OME if HL or
persistent irritability
> 2-3 months
No
Alternative diagnosis
None
Double the dose of
antibiotic for 5 days
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Facial weakness and Bells palsy flowchart
Gradual onset > few days or
feeling unwell
Yes
Unlikely to be Bell,s
 Neurology
No
Is there any other
Neurological deficit?
Yes
 Neurology
Neuro-imaging
Yes
 Neurology
Neuro-imaging
No
Spared forehead muscles?
No
Head & facial trauma?
Yes
 Neurosurgery
 ENT surgery
 Plastic surgery
Imaging
No
Signs of OM, Parotitis,
Mastoiditis or Ear surgery?
Yes
 ENT surgery
No
Blisters on ear or face?
Yes
Acyclovir for HSV or HZV
No
Treat as Bell's Palsy
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Sensori-Neural Hearing Loss
History & assessment
Elderly: Presbyacusis
Young / Middle age
PTA
Symmetric
High frequency:
Presbyacusis
Systemic cause:
Infective
Metabolic
Endocrine
Haematologic
Trauma
Asymmetric
Low frequency:
Meniere's disease
MRI: Rule
out
acoustic
neuroma
ECoG
Caloric test,
Blood
Any
Frequency
Aetiology of SNHL
Developmental and hereditary
 Nonsyndromic hereditary hearing loss
 Waardenburg’s syndrome
 Alport’s syndrome
 Usher’s syndrome
 Inner ear anomalies
Infectious disorders
 Labrynthitis
 Otitis media
 Viral infections
 Bacterial-syphilis
Drug induced
Renal
Trauma
Irradiation
Neurological
|Page4
Vertigo: Differential diagnosis
Vertigo does imply some form of illusion of movement, mostly spinning. All other
symptoms are grouped under dizziness.
After taking a history and doing an examination the clinician needs to decide the
following:
Illusion of
movement
Other
(Dizziness)
Spinning
(Vertigo)
Central
Peripheral
Unilateral
Bilateral
Brainstem
Cerebellar
Three typical forms of peripheral vestibular dysfunction can be identified, based on
their characteristic symptoms and signs:
1. Acute or subacute unilateral vestibular failure: rotational vertigo, oscillopsia, and
a tendency to fall toward the affected ear usually acute vestibular neuritis.
2. Bilateral peripheral vestibular failure (bilateral vestibulopathy): instability of gait
and posture, and oscillopsia induced by head movement.
3. Paroxysmal peripheral vestibular stimulation or inhibition: attacks of vertigo and
oscillopsia, e.g. in BPPV, Meniere’s disease, and vestibular paroxysmia.
The patient who is having a first attack of acute spontaneous vertigo may have acute
vestibular neuritis or a cerebellar infarction are commonly misdiagnosed in the casualty
department as having ‘labyrinthitis’ or ‘middle-ear infection’.
Acute vestibular neuritis will cause a unidirectional nystagmus pattern that improves
with fixation, produces a positive head impulse test and mostly the patient will be able to
stand alone, in contrast to cerebellar infarction in which they tend to fall when walking.
Brainstem ischaemia symptoms such as diplopia, reduced vision, dysarthria, and
dysphagia will be present in less than 50% of patients with cerebellar infarction.
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It is estimated that approximately 90% of individuals over 65 years of age have
visited their physician at least once with vertigo as their primary complaint.
History
A diagnosis can be made on:
1. History alone in 70% of patients.
2. Physical examination in 10% of patients.
3. Special tests in 20% of patients.
The key history points are:
1. Is it vertigo?
2. What is the time course?
3. What are the precipitating/exacerbating factors?
4. Are there accompanying symptoms?
Vertigo can be an illusion that the external world is moving relative to an individual or
the individual relative to space. Rotational vertigo or other illusionary sensations of
motion indicate vertigo (vestibular symptoms), whereas a sensation of light-headedness,
giddiness, drowsiness, or impending fainting implies dizziness of non-vestibular origin.
Non-spinning dizziness when standing or walking usually indicates a neurological gait
problem rather than vestibular vertigo.
Vertigo onset is usually sudden and comes in spells varying from seconds or minutes to
hours. Some peripheral vertigo is brought on by a change in position and most patients
will improve by lying still. Tinnitus, hearing loss, and aural fullness frequently
accompany peripheral disease.
Unlike peripheral vertigo, central causes of dizziness produce a more variable picture.
Patients may describe it as spinning, tilting, forced to one side, light-headedness,
clumsiness or blacking out. If loss of consciousness is documented, a peripheral aetiology
for dizziness is rarely – if ever – the reason.
The following symptoms also point to a central cause, i.e. dysarthria, dysphagia,
diplopia, hemiparesis, severe localised cephalgia, seizures or memory loss.
Some specific questions in the history can point to diagnosis:
• Do you become dizzy just rolling over in bed?
o Benign paroxysmal positional vertigo (BPPV)
• Are you light sensitive during your dizzy spell?
o Vestibular migraine
• Does one ear feel full before or during an attack?
o Meniere’s disease
• Does a loud sound make you dizzy or make your world jiggle?
o Superior semi-circular canal dehiscence
• Did your first attack of severe vertigo last hours, with nausea and vomiting?
o Vestibular neuritis
• Are you light-headed when you get up from a bed or chair for a few seconds?
o Blood pressure/cardiovascular disease (CVS)
• Do you pass out completely with your dizziness?
o CVS
|Page6
Difference between peripheral and central vertigo
Peripheral
Definite
Usually paroxysmal
Usually severe
Seconds to hours
Frequently
Present
Uni-directional, increased by
loss of fixation
Hallucinations of movement
Onset
Intensity
Duration
Induced by head position
Nystagmus
Nystagmus pattern
Autonomous nervous system
symptoms
Tinnitus
Hearing loss
Disturbance of consciousness
Other neurological signs
Definite
Central
Less definite
Seldom paroxysmal
Less severe
Weeks to months
Seldom
Present or absent
Direction changing, no
change with fixation, other
forms of nystagmus
Less definite or absent
Frequently present
Frequently present
Absent
Usually absent
Seldom present
Seldom present
More frequently present
Frequently present
Differential diagnosis of vertigo
Peripheral
Common
 BPPV
• Vestibular neuritis
• Meniere’s disease
• Bilateral vestibulopathy
• Vestibular schwannoma/acoustic
neuroma
Rare
 Superior semi-circular canal dehiscence
(SSCD)
• Vestibular paroxysmia (vascular loop
compression)
• Perilymph fistula
• Labyrinthitis
• Auto-immune inner-ear diseases
Other problems (physiological/
pathological stimulation)
 Motion disease
• Caloric stimulation
• Water exposure
• Wind exposure
• Rotational stimulation
• Flying
• Driving
• Pressure changes
• Changes in specific gravity
• Alcohol-induced vertigo
Central
Common
• Phobic postural vertigo
• Vestibular migraine
• Pathological forms of nystagmus, e.g.
• Down-beat nystagmus
• Up-beat nystagmus
• Gaze nystagmus
Rare
 Central positioning vertigo
• Dizziness syndromes of unclear
aetiology/familial
• Episodic ataxia type II
• Arnold-Chiari malformation
• Psychogenic dizziness
CNS disease (causes)
• Multiple sclerosis
• Vascular disease
• Tumours
• Epilepsy
• Infections
• Medications
|Page7
Is it vertigo?
• Yes
• Rotatory
o Vestibular neuritis
o BPPV
o Meniere’s disease
o Vestibular migraine
• Sensation of boat
o Bilateral vestibulopathy
• No
o Dizziness
Duration
• Seconds to minutes
o BPPV
o Vestibular paroxysmia
• Minutes to hours
o Meniere’s disease
o Vestibular migraine
• Hours to days
o Vestibular neuritis
• Varies
o Fistula
o SSCD
Precipitating/exacerbating factors
• Present in rest
o Vestibular neuritis
• Worse when walking
o Bilateral vestibulopathy
• Precipitated by turning the head to the left and right
o Vestibular paroxysmia
• Turning in bed to one side
o BPPV
• Coughing/pressing/sounds
o Fistula
o SSCD
• Social or environmental condition
o Phobic postural vertigo
Accompanying symptoms
• Inner ear
o Tinnitus, hearing loss, aural fullness
• Central nervous system
o Diplopia, dysphagia, sensory disturbances, dysarthria, paralysis of arms or
legs
• Headache
o Vestibular migraine
|Page8
The sore throat
Presentation of a patient with pharyngitis
Viral
A viral pharyngitis usually presents with mild symptoms, most patients complaining of a
sore throat, dysphagia, fever and erythema of the pharyngeal mucosa with enlarged
tonsils. There is normally not an exudate present, as would be seen with certain bacterial
pharyngitis.
Coxsackie virus causes small vesicles to form with erythematous bases that can ulcerate
and spread over the anterior tonsillar pillars, palate and pharyngeal wall.
Herpes simplex virus is normally associated with a ‘cold sore’. It affects older children
and young adults, and may cause exudative or non-exudative pharyngitis.
Epstein-Barr virus (EBV) infection is important for two characteristic clinical traits.
Firstly, it can lead to very rapid enlargement of tonsils (sudden onset of snoring in patient
with large dirty-gray tonsils). Petechiae at the junction of the hard and soft palate may be
present. The airway obstruction may be life-threatening and should be managed promptly.
Secondly, it can lead to the formation of a maculopapular rash in a large percentage of
patients who are given penicillin (as high as 95%), even if no previous incidents of
reactions against penicillin are documented.
Influenza is readily transmitted and therefore of epidemiological importance.
The sore throat associated with influenza may be distinguished from streptococcal
pharyngitis by several features:
 The presence of influenza cases in the community (epidemic)
 Association with cough
 Myalgias.
Bacterial
Group A β-haemolytic Streptococcus (GABHS) is the most common cause of acute
bacterial pharyngitis. Acute rheumatic fever and glomerulonephritis are part of the
autoimmune-mediated group of complications due to GABHS infection and can occur
after a latent period of 2 - 3 weeks. Acute rheumatic fever presents with various
manifestations that may include carditis, chorea, arthritis, subcutaneous nodules and
erythema marginatum.
GABHS infection has a peak incidence at about 5 - 6 years of age but can occur in
children younger than 3 and in adults older than 50. Acute symptoms include: dry throat,
malaise, fever, odynophagia, dysphagia, otalgia, headache, body aches and pains and
cervical lymphadenopathy. Examination of the mouth and pharynx may reveal a dry
tongue and enlarged tonsils with yellowish white spots on the tonsils. A membrane or
purulent exudates may be present over tonsils or pharynx.
When symptoms that include coughing, diarrhoea, conjunctivitis and coryza are
present, a viral aetiology is more likely.
With other non-infective causes of pharyngitis (reflux, postnasal drip, cancer, fungal
infections, cigarette smoke), the aetiology is normally identifiable and can be treated or
avoided.
|Page9
Approach (Algorithm) to a patient with a sore throat.
The decision to treat with antimicrobials remains a difficult one despite the available
special investigations, and most decisions are still made on clinical findings.
This unfortunately leads to massive overtreatment of patients with antibiotics.
1. Listen to the patient – if the symptoms initially improved and then worsened, it may
indicate an initial viral infection that became complicated by a secondary bacterial
infection, which normally happens after 7 - 8 days.
2. GABHS remains the most prominent pathogen requiring treatment in patients of all
ages, so the decision is whether or not the pharyngitis is attributable to group A
streptococci.
3. Other pathogens that may require specific treatment are:
 EBV mononucleosis (splenic enlargement and airway obstruction)
 non-group A streptococci (confirmed by culture)
 influenza virus (high-risk patient with severe symptoms)
 primary HIV infection
 N. gonorrhoeae.
Diagnosis of acute GABHS tonsillitis
Most cases are diagnosed clinically, and the Centor criteria are based on clinical
evaluation of symptoms and signs. It is widely used and accepted. The four criteria are:
1.
2.
3.
4.
Tonsillar exudates
Tender anterior cervical adenopathy (JDLN)
Fever by history
Absence of coughing.
 The presence of 3 - 4 of the criteria has a positive predictive value for GABHS of
40 - 60%.
 The absence of 3 - 4 of the criteria has negative predictive value of 80%.
A rapid antigen test (RADT) for GABHS has been developed which has helped the
decision whether or not to treat patients with antibiotics.




Unfortunately even one prior dose of antibiotics may result in a negative test.
It is highly specific but not as sensitive as a throat culture, which remains the gold
standard, although results are delayed.
Proper collection (vigorous swabbing of tonsils and posterior pharyngeal wall)
and transport of the sample are keys to making a correct diagnosis.
If the RADT is negative it should be followed by a throat swab for culture if
streptococcal tonsillitis is strongly suspected. This, however, might lead to overtreating because it is difficult to reliably differentiate between acute and chronic
infection from a throat culture.
Reasons to treat GABHS:
 To prevent post-streptococcal sequelae − acute rheumatic fever is a significant
problem in developing countries
 To prevent suppurative complications − peritonsillar abscess, sinusitis and
| P a g e 10


retropharyngeal abscess
To reduce symptoms − there is a modest (approximately one day) reduction in
symptoms with early antibiotic treatment and for patients with more severe
symptoms it might be two and a half days (severe symptoms ≥3 Centor criteria)
To prevent transmission − while this is important in paediatrics, due to extensive
exposures, it is considered far less important in adults.
Management of a sore throat
Symptomatic management
The primary decision in these patients is whether to give antibiotics and to treat the
specific underlying aetiology, e.g. reflux. If no antibiotics are given treatment is
symptomatic. Basic principles remain:
 Rest
 Adequate fluid intake
 Antipyretics
 Pain management.
Systemic treatment options include antimicrobial agents, pain medication and possibly
anti-inflammatory agents. The use of glucocorticoids remains controversial and the
benefit may be limited to infectious mononucleosis
The local or topical treatment options include:




Lozenges
Sprays
Oral rinses (gargles)
Alternative medicines.
Clinical and epidemiological findings and diagnosis of pharyngitis due to group
A β-haemolytic streptococci (GABHS)
Features suggestive of GABHS as aetiological agent
A. The four criteria:
1. Patchy discrete exudate
2. Tender, enlarged anterior cervical nodes
3. Fever
4. No cough
B. General constitutional S:
1. Headache, Nausea, vomiting, and abdominal pain
C. Incidence:
1. Patient aged 5 - 15 years
2. Presentation in winter or early spring
3. History of exposure
D. Local Symptoms:
1. Sudden onset
2. Sore throat
3. Inflammation of pharynx and tonsils
.
| P a g e 11
Clinical manifestations of specific organisms in acute pharyngitis
Viruses
Rhinovirus
Coronavirus
Adenovirus
Influenza virus
Para-influenza virus
Coxsackie virus
Herpes simplex virus
Epstein-Barr virus
Cytomegalovirus
Human immunodeficiency virus
Common cold
Common cold
Pharyngoconjunctival fever
Influenza
Cold, croup
Herpangina, hand–foot–mouth disease
Gingivostomatitis (primary infection)
Infectious mononucleosis
Mononucleosis-like syndrome
Acute (primary) infection syndrome
Bacteria
Group A streptococci
Group C and group G streptococci
Mixed anaerobes
Fusobacterium necrophorum
Arcanobacterium haemolyticum
Neisseria gonorrhoeae
Treponema pallidum
Francisella tularensis
Corynebacterium diphtheria
Yersinia enterocolitica
Yersinia pestis
Mycoplasma pneumonia
Chlamydophila pneumonia
chlamydophila psittaci
Pharyngitis, scarlet fever
Pharyngitis
Vincent’s angina (ANUG)
Lemierre’s syndrome (septic thrombophlebitis of the internal jugular vein)
Pharyngitis, scarlatiniform rash
Pharyngitis
Secondary syphilis
Pharyngeal tularemia
Diphtheria
Pharyngitis, enterocolitis
Plague
Bronchitis, pneumonia
Bronchitis, pneumonia
psittacosis
| P a g e 12
Sore Throat
If the patient is acutely ill?
PPA, Retropharyngeal a,
Epiglottitis, EBV
Tonsillar hypertrophy,
Diphtheria, Lemierre's
No
Yes
Unilaterally enlarged tonsil
Yes
Peritonsillar abscess
No
Mucosal lesion
Yes
Systemic disease?
Yes
No
Steven Jonson S
Behcet S
FB
No
FB Observed?
Yes
Herpes
stomatitis
Infectious pharyngitis
NO
Inflammation in pharynx
Yes
Not suggestive of GAS Pharyngitis
Possible GAS Pharyngitis
Irritative
pharyngitis
Referred pain
Psychogenic
If Negative
Symptomatic ttt
No
Throat Culture
If Positive
If Negative
RADT
If Positive
Antimicrobial therapy
| P a g e 13
Evaluation of adenotonsillar hypertrophy
Not severe, without
episodes of apnea
Resolves
Witnessed apnea or snoring
with severe obstruction
Worsens
Adenotonsillar
hypertrophy on exam
Adenotonsillar
hypertrophy on exam
Adenotonsillectomy
Sleep Study
Not Severe OSAS
Observe
Severe OSAS
CPAP or
Surgery
| P a g e 14
Management of post-tonsillectomy bleeding
Immediate
Active
Delayed
Stops
spontaneously
Clot in fossa
Control in OR
Screen for Clotting defect
Overnight observation in Hosp
If No Further bleeding
discharge
Screen for Clotting defect
No Active
bleeding
Active
bleeding
Control in OR
Screen for Clotting defect
Recurrent bleeding
Consider angiogram
Un-controllable
bleeding
ECA Ligation
If patient stable: angiogram
| P a g e 15
Hoarseness
Onset
Acute
Viral & bacterial laryngitis (self-limited)
Epiglottitis (high fevers, sore throat,
drooling) Surgery
FB ingestion
Chronic
Voice abuse,
Smoke exposure,
GE, LP reflux,
Neoplasm
Any patient with a significant history of smoking
and drinking alcoholic beverages
Who has unremitting and worsening hoarseness
Accompanied by throat pain
Should be considered to have laryngeal cancer
until it is proven otherwise
Constant: (Anatomic
deficit)
Benign VC (nodules,
polyps) Malignant (SCC
Course
the improved Monday-morning
voice of someone whose weekday
job requires frequent voice use.
larynx). Traumatic VC injury.
Behavioral (functional
aphonia): rarely
Postnasal drip
Timing
Worst in the morning:
GE or LP reflux
Benign or malignant
lesions: rough or harsh
voice can result
VC paresis or abductor
spasmodic dysphonia:
breathy or weak voice
as the vocal cords fail to
meet at midline
Intermittent or fluctuating:
Periodic voice abuse, eg. by
Voice Quality
Progressively worsens
throughout the day:
Voice abuse, Myasthenia gravis
A laryngitis: whisper
because of the pain &
discomfort
Adductor spasmodic
dysphonia: tense,
high-pitched voice
with frequent breaks
| P a g e 16
FLOW DIAGRAM FOR EPISTAXIS MANAGEMENT
Active bleeding
History
Clinical examination:
Anterior rhinoscopy
Rigid/flexible nasendoscopy
Assess for hypovolaemic shock
Identify site of
bleeding:
Anterior
Posterior
Anteroposterior
Suction and VC:
5% cocaine solution
Adrenaline
Phenylephrine
Stop the bleeding
Pinch nostrils
Assess: hypovolaemic
shock
Resuscitat
e
Nasal packing
Posterior packing
Balloon packing
Tamponade with
BIPP/Vaseline
Anterior packing
BIPP
Vaseline gauze
Merocel
Surgicel
Remove packing
Unsuccessful
Repacking
Nasal Cautery:
Electrocautery.
Chemical cautery:
"Trichloracetic acid,
Silver nitrate"
Remove packing
Idiopathic causes: Ointment
Successful
Re-bleeding
Bleeding disorder: Refer to
haematologist
Identify cause
Surgical intervention
Arterial ligation
Submucosal
resection
Endoscopic cautery
Re-bleeding
Advice
No further bleeding
Infective, Trauma, Druginduced, Neoplasm: Manage
accordingly/ Refer to ENT surg
No further treatment
Embolization
| P a g e 17
Neck Masses – Diagnostic approach
Etiology of a neck mass is most closely linked to age:
Pediatrics ~ 80 - 90% benign
Adult ~ 80% neoplastic (except thyroid masses) 80% of those are malignant
(except thyroid and parotid masses)
Location is a key factor in developing differential diagnosis:
Any new lateral neck mass in an adult > 40 years old is likely to be malignant
Many upper aerodigestive tract cancers present with the chief concern of a
painless neck mass
Location helps guide differential dx:
•Lateral neck most common site for metastatic disease from UADT
- upper neck anterior/deep to SCM
• Midline neck masses likely related to thyroid, elevates with swallowing
Neck Masses – Differential Dx
Inflammatory/infectious
- Lymphadenopathy/lymphadenitis LN > 1.5 cm
bacterial, viral, fungal, parasitic can become neck abscess
- Infectious granulomatous disease
TB, atypical mycobacteria, cat scratch
- Non - infectious granulomatous disease
sarcoidosis, Kawasaki, Castleman, Kikuchi, Kimura
- Sialadenitis/sialolithiasis
Congenital
- Branchial cleft cysts very rare in adults > 40
- Laryngocele
Traumatic
Vascular
Neoplastic
- Metastatic disease usually from lesion of mucosa of upper
aerodigestive tract , skin
- Primary neoplasms
• Lymphoma
• Thyroid
• Salivary gland
• Neurogenic
• Paraganglioma
• Lipoma
• Sarcoma
• Other
| P a g e 18
LN Levels of the Neck
Level I: A: submebntal, B: submandibular
Level II:
Upper
deep
cervical
Level III:
Middle
deep
cervical
Level
Level VI:
Anterior
triangle
Level V:
Posterior
triangle
Level IV:
Lower
deep
cervical
Silent areas in head and neck
Thyroid gland
Nasopharynx
Base of the tongue
Valleculae
Ventricle and
saccule of the larynx
Maxillary sinus
Valleculae
Pyriform fossa, and
postcricoid area
| P a g e 19
New Neck Mass
Young adult (16-40) Y
Pediatric <15 Y
Older Adult > 40 Y
Infectious Symptoms
Order Imaging
Order Imaging
No
Yes
Antibiotic
trial
Cystic?
Vascular origin
(paraganglioma,
Hemangioma)
Yes
No
Resolution?
No
Yes
Yes
No
Do imaging
characteristics fit with
congenital origin
(TGDC, Branchial cyst,
etc)
Yes
No
FNA
| P a g e 20