CASE REPORT
CHRONIC TONSILLITIS
OVERVIEW
A. ANATOMY OF THE TONSILS
Waldeyer’s Ring - circle of lymphoid tissue consisting of:
1. palatine (fauceal) tonsils
2. pharyngeal tonsils (adenoids)
3. lingual tonsils and
4. Tubal tonsils of Gerlach (near fossa of Rosenmüller)
Anatomy of The Palatine Tonsils
Palatine tonsils are two in number. Each tonsil is an ovoid mass of lymphoid tissue
situated in the lateral wall of oropharynx, created by the palatoglossus muscle anteriorly and the
palatopharyngeus and superior constrictor muscle posteriorly and laterally. Actual size of the
tonsil is bigger than the one that appears from its surface as parts of tonsil extend upwards into
the soft palate, downwards into the base of tongue and anteriorly into palatoglossal arch. A tonsil
presents two surfaces-a medial and a lateral, and two poles- an upper and a lower.
Medial surface of the tonsil is covered by non
keratinizing stratified squamous epithelium
which dips into the substance of tonsil in the
form of crypts. Openings of 12-15 crypts can be
seen on the medial surface of the tonsil. One of
the crypts, situated near the upper part of tonsil is
very large and deep and is called crypta magna or
intratonsillar cleft From the main crypts arise the
secondary crypts, within the substance of tonsil.
Crypts may be filled with cheesy material
consisting of epithelial cells, bacteria and food debris which can be expressed by pressure over
the anterior pillar.
Lateral surface of the tonsil presents a well -defined fibrous capsule. Between the
capsule and the bed of tonsil is the loose areolar tissue which makes it easy to dissect the tonsil
in the plane during tonsillectomy. It is also the site for collection of pus in peritonsillar abscess.
Some fibres of palatoglossus and palatopharyngeus muscles are attached to the capsule of the
tonsil.
Blood Supply
The tonsil is supplied by five arteries:
1. Tonsillar branch of facial artery. This is the main artery.
2. Ascending pharyngeal artery from external carotid.
3. Ascending palatine, a branch of facial artery.
4. Dorsal linguae branches of lingual artery.
5. Descending palatine branch of maxillary artery.
Venous Drainage
Veins from the tonsils drain into paratonsilar vein which joins the common facial vein
and pharyngeal venous plexus.
Lymphatic Drainage
Lymphatics from the tonsil pierce the superior constrictor and drain into upper deep
cervical nodes particularly the jugulodigastric (tonsillar) node situated below the angle of
mandible.
Nerve Supply
Lesser palatine branches of sphenopalatine ganglion (CN V) and glossopharyngeal
nerve provide sensory nerve supply.
Function of the Tonsils
Both tonsils and adenoid are part of the Waldeyer ring, which is a ring of lymphoid
tissue in the pharyngx. Lymphoid tissue in this ring provides defense against pathogens. The
waldeyer ring is involved in the production of immunogloblins and the development of both B-
cell and T-cell lymphocytes.
B. TONSILLITIS
Definition of Tonsillitis
Tonsillitis is inflammation of the pharyngeal tonsils. The inflammation usually extends
to the adenoid and lingual tonsils. Lingual tonsillitis refers to isolated inflammation of the
lymphoid tissue at the tounge base.
Etiology
The oropharynx and Waldeyer tonsillar ring are normally colonized by many different
species of aerobic and anaerobic bacteria, including Staphylococcus, nonhemolytic streptococci,
Lactobacillus, Bacteroides, and Actinomyces. These organisms, as well as many other
pathogenic bacteria, viruses, fungi, and parasites, can cause infections of tonsillar and adenoid
tissue.
Viral Infections
Viruses such as adenovirus, rhinovirus, reovirus, respiratory syncytial virus (RSV), and
the influenza and parainfluenza viruses have all been shown to be possible pathogens. Most of
these infections are self-limited and require only symptomatic treatment.
The Epstein-Barr virus (EBV) causes acute pharyngitis as a part of infectious
mononucleosis syndrome. It is common in children and young adults, is transmitted by oral
contact, and manifests as fever, generalized malaise, lymphadenopathy, hepatosplenomegaly,
and pharyngitis. Upon examination, petechiae may be present at the junction of the soft and hard
palates. The tonsils are severely enlarged, sometimes to the point of compromising the airway,
and classically are covered with an extensive grayish-white exudate.
Tonsillar infections with the coxsackie virus result in herpangina, which presents as
ulcerative vesicles over the tonsils, posterior pharynx, and palate. The disease commonly occurs
in children under the age of 16. Patients present with generalized symptoms of headache, high
fever, anorexia, and odynophagia.
Fungal Infections
Oropharyngeal candidiasis (ie, thrush) often presents in immunocompromised patients
or in patients who have undergone prolonged treatment with antibiotics. On exam, there are
white cottage-cheese-like plaques over the pharyngeal mucosa, which bleed if removed with a
tongue depressor. Treatment consists of topical nystatin or clotrimazole (eg, Mycelex) troches.
Bacterial Infections
Group A beta-hemolytic Streptococcus is the most common and important pathogen
causing acute bacterial pharyngotonsillitis. This infection most commonly presents in children
aged 5–6 and is characterized by fever, dry sore throat, cervical adenopathy, dysphagia, and
odynophagia. The tonsils and pharyngeal mucosa are erythematous and may be covered with
purulent exudate; the tongue may also become red ("strawberry tongue").
Classification
1. Acute Tonsillitis
Primarily, the tonsil consists of (a) surface epithelium which is continuous with the
oropharyngeal lining; (b) crypts which are tube-like invaginations from the surface epithelium;
and (c) the lymphoid tissue.
Acute infections of tonsil may involve these components and are thus classified as:
1. Acute catarrhal or superficial tonsillitis. Here tonsillitis is a part of generalised pharyngitis
and is mostly seen in viral infections.
2. Acute follicular tonsillitis. Infection spreads into the crypts which become filled with
purulent material, presenting at the openings of crypts as yellowish spots
3. Acute parenchymatous tonsillitis. Here tonsil substance is affected. Tonsil is uniformly
enlarged and red.
4. Acute membranous tonsillitis. It is a stage ahead of acute follicular tonsillitis when exudation
from the crypts coalesces to form a membrane on the surface of tonsil.
Etiology
Haemolytic streptococcus is the most commonly infecting organism. Other causes of infect ion
may be staphylococci, pneumococci or H. influenzae. These bacteria may primarily infect the
tonsil or may be secondary to a viral infection.
2. Chronic Tonsillitis
Etiology
1. It may be a complication ot acute tonsillitis. Pathologically, microabscesses walled off by
fibrous tissue have been seen in the lymphoid follicles of the tonsils.
2. Subclinical infections of tonsils without an acute attack.
3. Mostly affects children and young adults. Rarely occurs after 50 years.
4. Chronic infection in sinuses or teeth may be a predisposing factor.
Types
1. Chronic follicular tonsillitis. Here tonsillar crypts are full of infected cheesy material which
shows on the surface as yellowish spots.
2. Chronic parenchymatous tonsillitis. There is hyperplasia of lymphoid tissue Tonsils are very
much enlarged and may interfere with speech, deglutition and respiration. Attacks of sleep
apnoea may occur. Longstanding cases develop features of cor pulmonale.
3. Chronic fibroid tonsillitis. Tonsils are small but infected,with history of repeated sore
throats.
PATHOPHYSIOLOGY
Immunology
The tonsils and adenoids are unique insofar as they involved in both local immunity and
in immune surveillance for the development of the body’s immunologic defense system. Chronic
bacterial infection (and other ongoing antigenic stimulators) in the tonsils and adenoids may
results in the production of local antibody, a shift of B and T cells ratios and according to some
researchers, an increase in the serum immunoglobulin levels, which return into normal after
tonsillectomy and adenoidectomy. In contrast to proper lymph nodes, the tonsils and adenoids
have no afferent lymphatics; therefore, their specialized epithelium plays an important role in
antigen presentation and processing. This is followed by both T cell and B cell responses,
including immunoglobulin production, expansion of memory clones and hyperplasia.
Pathogenesis of Adenotonsillar Disease
The pathogenesis of infectious and inflammatory disease in the tonsils and adenoids
most likely has its basis in their anatomic location and their inherent function as organs of
immunity, processing infectious material and other antigens, and then becoming, paradoxically a
focus of infection or inflammation. However, no single theory of pathogenesis has been
accepted. Viral infection with secondary bacterial invasion may be one mechanism of the
initiation of chronic disease, but the effects if the environment, host factors, the widespread use
of antibiotics, ecological considerations, and diet all may play role.
Recent work reveals that inflammation and loss of integrity of the crypt epithelium result
in chronic cryptitis and crypt obstruction, leading to stasis of crypt debris and persistence of
antigen. Bacteria even infrequently found in normal tonsil crypts may multiply and eventually
establish chronic infection.
DIAGNOSIS
Symptoms include:
red and/or swollen tonsils
white or yellow patches on the tonsils
tender of jaw and throat, stiff, and/or swollen neck
sore throat – last longer than 48 hours and may be severe
painful or difficult swallowing
cough
headache
sore eyes
body aches
otalgia
fever
chills
nasal congestions
Voice changes, loss of voice
Physical Examination:
Signs of infection (redness, discharge, swollen lymph glands)
Abscess (a shift in 1 tonsil toward the center and a shift of the uvula away from the
infected side)
Airway compromise (muffled speech, drooling, and inability to swallow)
Tests:
Blood count
Mononucleosis test
Sometimes, when the body reacts to an infection, antibodies are made that have nothing
to do with the germ. These are called heterophile antibodies. This test looks for such
antibodies. It is used to diagnosis infectious mononucleosis, a disease caused by the Epstein-
Barr virus (EBV). About 1 week after the onset of the disease, many patients develop
heterophile antibodies. Antibodies reach peak levels in 2 - 5 weeks and may persist for up to
1 year. However, a small number of persons with mononucleosis may never develop such
antibodies. A positive test means heterophile antibodies are present. These are usually a sign
of infectious mononucleosis.
Rapid strep test
The test requires a throat swab. The swab is tested to identify group A streptococcus.
Indications: pharingitis. An abnormal result means Group A streptococcus is present, and
confirms strep throat.
Throat swab culture
DIFFERENTIAL DIAGNOSIS
Acute Tonsillitis
Differential Diagnosis: must be made from the many conditions causing an acute pharyngitis.
The most important are:
1. Scarlet fever
2. Diphteriae-especially from the attenuated form seen in inoculated persons
3. Vincent’s infection
4. Agranulocytosis
5. Glandular fever (infectious mononucleosis)
Chronic tonsilitis
Differential Diagnosis: mainly from physiological enlargement, especially in childhood. Sinusitis
must be excluded
THERAPY
Acute Tonsillitis
Treatment:
1. patient is put to bed and encourage to take plenty of fluids
2. analgetics (aspirin or paracetamol) are given according to the age of the patient to relieve
local pain and bring down the fever
3. antimicrobial therapy. Most of the infections are due to streptococcus, and penicillin is the
drug of choice. Patient allergic to penicillin can be treated with erythromycin. Antibiotics
should be continued for 7- 10 days.
Chronic tonsillitis
Treatment:
1. Conservative treatment consist of attention to general health, diet, treatment of co-existent
infection of teeth, nose, and sinuses.
2. Tonsillectomy by indications.
Indications of tonsillectomy:
a. Absolute indications:
Enlarged tonsils that cause upper airway obstruction, severe dysphagia, sleep disorders, or
cardiopulmonary complications
Peritonsillar abcess that is unresponsive to medical management and drainage documented
by surgeon, unless surgery is performed during acute stage
Tonsillitis resulting in febrile convulsions
Tonsils requiring biopsy to define tissue pathology
b. Relative indications:
Three or more tonsils infections per year despite adequate medical therapy
Persistent foul taste or breath due to chronic tonsillis that is not responsive that is not
responsive to medical history
Chronic or recurrent tonsillitis in a streptococcal carrier not responding to beta-lactamase-
resistant antibiotics
Unilateral tonsil hypertrophy that is presumed to be neoplastic
COMPLICATION
Acute Tonsillitis
1. Chronic tonsillitis
2. Peritonsillar abcess
3. Parapharyngeal abcess
4. Servical abcess
5. Acute otitis media
6. Rheumatic fever
7. Acute glomerulonephritis (rare)
8. Subacute bacterial endocarditis
Chronic Tonsilitis
1. Peritonsillar abcess
2. Parapharyngeal abcess
3. Intratonsillar abcess
4. Tonsilloliths
5. Tonsillar cyst
6. Focus of infection in rheumatic fever, acute glomerulonephritis, eye and skin disorders.
CASE REPORT
PATIENT IDENTITY
Name : B.R (child)Sex : MaleAge :7 y.o. Address : Kemiri, Purworejo Date : March, 24th 2012
ANAMNESIS
Chief complain :Sore throat
Present Illness history :
Patient keep on complaining sore throat for a year. Having pain on swallowing , cough, coryza, and fever . He had check up to General Practitioner, was diagnosed with “amandel”. Had been prescribed antibiotic, medicine for flu and cough but his mother forgot the drug’s name. The symptoms relieve but have been recurrent (almost every month). A month ago, sore throat is getting worse. Patient felt pain on swallowing (eat). Patient’s mother also complained her child always snoring but didn’t effect his sleeping time, and have less interest on studies.
Current complains:
Snoring (+), nasal congestion (-), runny nose (-), sneezing (-), difficulty swallowing (-),
decreased appetite (-).
Ear Complains: hearing loss (-), ringing sensation in ear/ ears (-), ear pain (-), ear itching (-), sensation of fullness in the ear (-).
Past Illness History :
similar disease history (+)
allergy history (-)
asthma history (-)
Family Illness History :
similar disease history (-)
allergy history (-)
active smoker (+) father
Resume of Anamnesis
Sore throat (+)
History of cough and cold (+)
Recurrent (+)
Snoring (+)
Fever (+)
Physical Examination
General status : compos mentis, good nutritional status
Weight : 30 kg, Height : 135 cm
Vital signs :
BP : 110 / 80 mmHg
Pulse : 88 times/minute
RR : 20 times/minute
T : 38 ºC
Head and neck : icteric sclera -/-, anemic conjunctiva -/-, lnn normal
Thorax : symmetrical retraction: -. Vesicular +/+, murmur -/-
Abdomen : flat, peristaltic + , no liver and spleen enlargement, tenderness –
Extremity : warm limb, swelling -
Local status of ear, nose, and throat
Physical examination of the ear:
Inspection:
Auricula
AD : Hyperemic (-), swelling (-), discharge (-), Laceration (-)
AS : Hyperemic (-), swelling (-), discharge (-), Laceration (-)
Auditory canal
AD : cerumen (-), swelling (-), pruritic (-), narrow lumen (-), discharge (-)
AS : cerumen (-), swelling (-), pruritic (-), narrow lumen (-), discharge (-)
Palpation :
Tragus pain : AD (-), AS (-)
Auricle pain : AD (-), AS (-)
Otoscopy
AD : tympanic membrane intact, cone of light (+), hyperemic (-), Effusion (-),
Bulging (-), retraction (-)
AS : tympanic membrane intact, cone of light (+), hyperemic (-), Effusion (-),
Bulging (-), retraction (-)
Nose and paranasal sinuses
Inspection
Septum deviation (-), edema conchae (-), post nasal drip (-)
Palpation
Pain on palpation (-), crepitation (-)
Anterior rhinoscopy
Hyperemic mucosa (-/-), discharge (-/-), concha hypertrophy (-/-), septum deviation (-/-),
inferior nasal cavity and opening is normal
Posterior Rhinoscopy (-)
Oral cavity and oropharynx
Inspection
Lip : labioschisis (-), inflammation (-), mass (-)
Teeth and gum : caries dentis (-)
Tounge : inflammation (-)
Palatum mole : swelling (-), hyperemic (-)
Uvula : low
Tonsil dextra : hyperemic (+), swelling (+) T3, widen crypts, detritus (+)
Tonsil sinistra : hyperemic (+), swelling (+) T3, widen crypts, detritus (+)
Pharynx : hyperemic (-), granule (-)
Resume of physical examination
Tonsil dextra : hyperemic (+), swelling (+) T3, widen crypts, detritus (+)
Tonsil sinistra : hyperemic (+), swelling (+) T3, widen crypts, detritus (+)
Pharynx : hyperemic (-), granule (-)
DIAGNOSIS
Chronic tonsillitis
PLAN
Tonsillectomy
DISCUSSION
In this patient, chronic tonsillitis is diagnosed based on anamnesis and physical
examination. From the anamnesis we found that the patient has experienced snoring (+), sleep
apnea (-), recurrent fever(-), recurrent cough and flu (-) for four times in a year. From the
physical examination, the patient has hyperemic, swelling of left and right tonsils (T3), detritus
(+), and widened crypts (+).
Symptoms of tonsillitis are red and/or swollen tonsils, white or yellow patches on the
tonsils, tender of jaw and throat, stiff, and/or swollen neck, sore throat – last longer than 48 hours
and may be severe, painful or difficult swallowing, cough, headache, sore eyes, body aches,
otalgia, fever, chills, nasal congestions, and voice changes, loss of voice. From physical
examination, we can found some signs of infection (redness, swollen lymph glands), and airway
compromise (difficulty to swallow). This patient has swelling of left and right tonsils (T3),
detritus (+), widened crypts (+). All of that signs indicate signs of chronic tonsillitis.
Tonsillectomy is suggested since the patient has absolute and relative indications for
tonsillectomy. The patient has tonsil hypertrophy without sleep apnea which is one of absolute
indication of tonsillectomy. Patient also suffers from tonsillitis for few times in a year; a relative
indication.
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