TONSILLITIS
SWETHA.
S
22100136
• Medial surface is covered by stratified squamous epithelium continuous with that
of the mouth. This surface has 12 to 15 crypts. The largest of these is called the
intratonsillar cleft. Crypts may be filled with cheesymaterial consisting of
epithelial cells, bacteria and fooddebris which can be expressed by pressure over
the an-terior pillar.Lateral surface is covered by a sheet of fascia which forms the
hemicapsule of the tonsil. The capsule is an extension of the pharyngobasilar
fascia. It is only loosely attached to the muscular wall of the pharynx, formed
here by the superior constrictor and by the styloglossus, but anteroinferiorly the
capsule is f irmly adherent to the side of the tongue (suspensory ligament of
tonsil) just in front of the insertion of the palatoglossus and the palatopharyngeus
muscle. This firm attachment keeps the tonsil in place during swallowing. The bed
of the tonsil is formed from within outwards by: a. Pharyngobasilar fascia b.
Superior constrictor and palatopharyngeus muscles c. Buccopharyngeal fascia d.
In the lower part, the styloglossus e. Glossopharyngeal nerve.
• Anterior border is related to the palatoglossal arch with its
muscle. 4. Posterior border is related to the palatopharyngeal
arch with its muscle. 5. Upper pole is related to the soft palate,
and the lower pole, to the tongue
• A tri-angular fold of mucous membrane extends from
anteriorpillar to the anteroinferior part of tonsil and encloses
aspace called anterior tonsillar space. The tonsil is
separatedfrom the tongue by a sulcus called tonsillolingual
sulcuswhich may be the seat of carcinoma.
• BLOOD SUPPLYThe tonsil is supplied by five arteries (Figure
51.3).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 DRAINAGEVeins from the tonsils drain
into paratonsillar vein whichjoins the common facial vein and
pharyngeal venousplexus.
• LYMPHATIC DRAINAGELymphatics from the tonsil pierce the
superior constrictorand drain into upper deep cervical nodes
particularly thejugulodigastric (tonsillar) node situated below
the angleof mandible.NERVE SUPPLYLesser palatine branches
of sphenopalatine ganglion (CN V)and glossopharyngeal nerve
provide sensory nerve supply.
• Local Immunity. Tonsils and adenoids are lined bysquamous epithelium, surface area of which is further in-
creased by several crypts of tonsils and folds of adenoid.This epithelium is specialized and contains M-cells,
an-tigen processing cells and micropores. Through themantigenic material is brought into contact with
subepi-thelially situated lymphoid follicles. Follicles have a ger-minal centre rich in B-cells and a mantel
zone rich inlarge lymphocytes. B-cells when stimulated change toplasma cells and produce antibodies.
Bacteria and virusesare also phagocytosed by the macrophages and destroyed.
• Surveillance Mechanism. It identifies the in-truder and alerts the body for wider response. If thedose of
antigen is high, B-cells of the germinal centreproliferate and undergo hyperplasia and also enter theblood
stream. Complex immune system comes intoplay with antigen processing cells, memory cells, den-dritic
cells, macrophages, T-helper and T-suppressorcells. Antibodies produced by the plasma cells preparethe
antigen to be phagocytosed by neutrophils andother phagocytes. The antibodies also get attached
tomacrophages and give them enhanced ability to catchthe antigens.Tonsils are most active from 4 to 10
years of age. In-volution begins after puberty resulting in decrease of B-cell production and relative
increase in ratio of T to Bcells.There has been a common notion that removal oftonsils and adenoids will
impair the integrity of immunesystem and make the patient susceptible to poliovirus orincrease the
incidence of Hodgkin disease in them. Thishas not been substantiated by clinical and epidemiologi-cal
observations. Removal of tonsil and adenoid has alsonot affected general immune surveillance function.
Ton-sil and adenoid, however, should only be removed onspecific indications.
ACUTE TONSILLITIS
• the tonsil consists of
• (i) surface epitheliumwhich is continuous with the oropharyngeal lining,(ii) crypts
which are tube-like invaginations from the sur-face epithelium and (iii) the
lymphoid tissue
• Acute in-fections of tonsil may involve these components and arethus classified
as:1. Acute catarrhal or superficial tonsillitis. Here tonsil-litis is a part of
generalized pharyngitis and is mostlyseen in viral infections.2. Acute follicular
tonsillitis. Infection spreads into thecrypts which become filled with purulent
material,presenting at the openings of crypts as yellowish spots(Figure 51.4).3.
Acute parenchymatous tonsillitis. Here tonsilsubstance is affected. Tonsil is
uniformly enlarged andred.4. Acute membranous tonsillitis. It is a stage ahead
ofacute follicular tonsillitis when exudation from thecrypts coalesces to form a
membrane on the surface oftonsil.
AETIOLOGY
• AETIOLOGYAcute tonsillitis often affects school-going children,
butalso affects adults.
• Haemolytic streptococcus is the most commonly infect-ing
organism. Other causes of infection may be staphylo-cocci,
pneumococci or H. influenzae.
• Viral: adenovirus, rhinovirus, ebv whivh may secondarily affect
the tonsil
CLINICAL FEATURES
• SYMPTOMS:
• Sore throat.2. Difficulty in swallowing. The child may refuse to eatanything due to local pain.3.
Fever. It may vary from 38 to 40 °C and may be associ-ated with chills and rigors. Sometimes, a
child presentswith an unexplained fever and it is only on examina-tion that an acute tonsillitis is
discovered.4. Earache. It is either referred pain from the tonsil orthe result of acute otitis media
which may occur as acomplication.5. Constitutional symptoms. They are usually moremarked
than seen in simple pharyngitis and may in-clude headache, general body aches, malaise and
con-stipation. There may be abdominal pain due to mes-enteric lymphadenitis simulating a
clinical picture ofacute appendicitis.SIGNS1. Often the breath is foetid and tongue is coasted.2.
There is hyperaemia of pillars, soft palate and uvula.3. Tonsils are red and swollen with
yellowish spots ofpurulent material presenting at the opening of crypts(acute follicular
tonsillitis) or there may be a whitishmembrane on the medial surface of tonsil which canbe
easily wiped away with a swab (acute membranoustonsillitis, Figure 51.5). The tonsils may be
enlargedand congested so much so that they almost meet inthe midline along with some
oedema of the uvula andsoft palate (acute parenchymatous tonsillitis). The jugulodigastric
lymph nodes are enlarged and ten-der
TREATMENT
• TREATMENT1. Patient is put to bed and encouraged to take
plenty offluids.2. Analgesics (aspirin or paracetamol) are given
accordingto the age of the patient to relieve local pain and
bringdown the fever.3. Antimicrobial therapy. Most of the
infections are due toStreptococcus and penicillin is the drug of
choice. Pa-tients allergic to penicillin can be treated with
erythro-mycin. Antibiotics should be continued for 7–10 days.
COMPLICATIONS
• COMPLICATIONS1. Chronic tonsillitis with recurrent acute attacks.
Thisis due to incomplete resolution of acute infection.Chronic
infection may persist in lymphoid follicles ofthe tonsil in the form of
microabscesses.2. Peritonsillar abscess.3. Parapharyngeal abscess.4.
Cervical abscess due to suppuration of jugulodigastriclymph nodes.5.
Acute otitis media. Recurrent attacks of acute otitis me-dia may
coincide with recurrent tonsillitis.6. Rheumatic fever. Often seen in
association with tonsil-litis due to Group A beta-haemolytic
Streptococci.7. Acute glomerulonephritis. Rare these days.8.
Subacute bacterial endocarditis. Acute tonsillitis in a pa-tient with
valvular heart disease may be complicatedby endocarditis. It is
usually due to Streptococcus viri-dans infection.
• DIFFERENTIAL DIAGNOSIS OF MEMBRANEOVER THE TONSIL1. Membranous tonsillitis. It
occurs due to pyogenic or-ganisms. An exudative membrane forms over the
medialsurface of the tonsils, along with the features of acutetonsillitis.2. Diphtheria.
Unlike acute tonsillitis which is abruptin onset, diphtheria is slower in onset with less
local dis-comfort, the membrane in diphtheria extends beyond thetonsils, on to the soft
palate and is dirty grey in colour.It is adherent and its removal leaves a bleeding
surface.Urine may show albumin. Smear and culture of throatswab will reveal
Corynebacterium diphtheriae.3. Vincent angina. It is insidious in onset with less fe-ver
and less discomfort in throat. Membrane, which usu-ally forms over one tonsil, can be
easily removed reveal-ing an irregular ulcer on the tonsil. Throat swab will showboth the
organisms typical of disease, namely fusiformbacilli and spirochaetes.4. Infectious
mononucleosis. This often affects youngadults. Both tonsils are very much enlarged,
congestedand covered with membrane. Local discomfort is marked.Lymph nodes are
enlarged in the posterior triangle ofneck along with splenomegaly. Attention to disease
isattracted because of failure of the antibiotic treatment.Blood smear may show more
than 50% lymphocytes,of which about 10% are atypical. White cell cou
• Paul–Bunnell test (mono test) will show high titre of het-erophil antibody.5. Agranulocytosis.
It presents with ulcerative necrot-ic lesions not only on the tonsils but elsewhere in
theoropharynx. Patient is severely ill. In acute fulminantform, total leucocytic count is
decreased to <2000/cumm or even as low as 50/cu mm and polymorph neutro-phils may be
reduced to 5% or less. In chronic or recur-rent form, total count is reduced to 2000/cu mm
with lessmarked granulocytopenia.6. Leukaemia. In children, 75% of leukaemias areacute
lymphoblastic and 25% acute myelogenous orchronic, while in adults 20% of acute
leukaemias are lym-phocytic and 80% nonlymphocytic.Peripheral blood shows TLC
>100,000/cu mm. It maybe normal or less than normal. Anaemia is always presentand may
be progressive. Blasts cells are seen on examina-tion of the bone marrow.7. Aphthous
ulcers. They may involve any part of oralcavity or oropharynx. Sometimes, it is solitary and
mayinvolve the tonsil and pillars. It may be small or quitelarge and alarming. It is very
painful.8. Malignancy tonsil (see p. 305)9. Traumatic ulcer. Any injury to oropharynx healsby
formation of a membrane. Trauma to the tonsil areamay occur accidently when hit with a
toothbrush, a pen-cil held in mouth or fingering in the throat. Membraneappears within 24
h.10. Candidal infection of tonsil
• Diagnosis of ulceromembranous lesion of throat thusrequires:1.
History.2. Physical examination.3. Total and differential counts
(for agranulocytosis, leu-kaemia, neutropenia, infectious
mononucleosis).4. Blood smear (for atypical cells).5. Throat
swab and culture (for pyogenic bacteria,Vincent angina,
diphtheria and Candida infection).6. Bone marrow aspiration or
needle biopsy.7. Other tests. Paul–Bunnell or mono spot test
and biopsyof the lesion
FAUCIAL DIPHTHERIA
• Aetiology) It is an acute specific infection caused by the Gram-pos-itive bacillus, C. diphtheriae. It
spreads by droplet infec-tion.
• In the oropharynx, a greyish white membrane formsover the tonsils and spreads to the soft palate and
pos-terior pharyngeal wall. It is quite tenacious and causesbleeding when removed. Cervical lymph
nodes, partic-ularly the jugulodigastric, become enlarged and tender,sometimes presenting a “bull-
neck” appearance. Patientis ill and toxaemic but fever seldom rises above 38
°C.COMPLICATIONSExotoxin produced by C. diphtheriae is toxic to the heartand nerves. It causes
myocarditis, cardiac arrhythmias andacute circulatory failure.Neurological complications usually
appear a few weeksafter infection and include paralysis of soft palate, dia-phragm and ocular
muscles.In the larynx, diphtheritic membrane may cause air-way obstruction.TREATMENTTreatment of
diphtheria is started on clinical suspicionwithout waiting for the culture report. Aim is to neutral-ize the
free exotoxin still circulating in the blood and tokill the organisms producing this exotoxin. Dose of
anti-toxin is based on the site involved and the duration andseverity of disease. It is 20,000–40,000
units for diphthe-ria in less than 48 h, or when the membrane is confinedto the tonsils only; and
80,000–120,000 units, if diseasehas lasted longer than 48 h, or the membrane is moreextensive.
Antitoxin is given by i.v. infusion in saline inabout 60 min. Antibiotics used are benzyl penicillin 600 mg
6 hourlyfor 7 days. Erythromycin is used in penicillin-sensitive in-dividuals (500 mg 6 hourly orally).
CHRONIC TONSILLITIS
• Persistent inflammation of tonsils is usually due to repeated
episodes of acute tonsillitis
• AETIOLOGY1. It may be a complication of acute tonsillitis.
Pathologi-cally, microabscesses walled off by fibrous tissue
havebeen 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 oc-curs after
50 years.4. Chronic infection in sinuses or teeth may be a
predis-posing factor.
• TYPES1. Chronic Follicular Tonsillitis. Here tonsillarcrypts are
full of infected cheesy material which showson the surface as
yellowish spots.2. Chronic Parenchymatous Tonsillitis. There
ishyperplasia of lymphoid tissue. Tonsils are very much en-
larged and may interfere with speech, deglutition and res-
piration (Figure 51.6). Attacks of sleep apnoea may occur.Long-
standing cases develop features of cor pulmonale.3. Chronic
Fibroid Tonsillitis. Tonsils are small butinfected, with history of
repeated sore throats.
• CLINICAL FEATURES1. Recurrent attacks of sore throat or acute tonsillitis.2.
Chronic irritation in throat with cough.3. Bad taste in mouth and foul breath
(halitosis) due topus in crypts.4. Thick speech, difficulty in swallowing and
chokingspells at night (when tonsils are large and
obstructive).EXAMINATION1. Tonsils may show varying degree of
enlargement.Sometimes they meet in the midline (chronic paren-chymatous
type).2. There may be yellowish beads of pus on the medialsurface of tonsil
(chronic follicular type).3. Tonsils are small but pressure on the anterior
pillar ex-presses frank pus or cheesy material (chronic fibroid type).4.
Flushing of anterior pillars compared to the rest of thepharyngeal mucosa is
an important sign of chronictonsillar infection.5. Enlargement of
jugulodigastric lymph nodes is a reli-able sign of chronic tonsillitis. During
acute attacks,the nodes enlarge further and become tender.
• TREATMENT1. Conservative treatment consists of attention to gen-eral health,
diet, treatment of coexistent infection ofteeth, nose and sinuses.2. Tonsillectomy
is indicated when tonsils interfere withspeech, deglutition and respiration or
cause recurrentattacks (see Chapter 94).COMPLICATIONS1. Peritonsillar abscess
(see p. 299, Figure 52.4).2. Parapharyngeal abscess.3. Intratonsillar
abscesIntratonsillar abscess. It is accumulation of pus withinthe substance of
tonsil. It usually follows blocking ofthe crypt opening in acute follicular tonsillitis.
There ismarked local pain and dysphagia. s.4. TonsillolithsTonsilloliths (calculus
of the tonsil). It is seen in chronictonsillitis when its crypt is blocked with
retention of de-bris. Inorganic salts of calcium and magnesium are
thendeposited leading to formation of a stoneThey areeasily diagnosed by
palpation or gritty feeling on prob-ing. Treatment is simple removal of the stone
or tonsillec-tomy,5. Tonsillar cyst.6. Focus of infection in rheumatic fever, acute
glomerulo-nephritis, eye and skin disorders.
• DISEASES OF LINGUAL TONSILS1. Acute lingual tonsillitis. Acute infection of a
lingualtonsil gives rise to unilateral dysphagia and feeling oflump in the throat.
On examination with a laryngealmirror, lingual tonsil may appear enlarged and
con-gested, sometimes studded with follicles like the onesseen in acute
follicular tonsillitis. Cervical lymphnodes may be enlarged. Treatment is by
antibiotics.2. Hypertrophy of lingual tonsils. Mostly, it is a com-pensatory
hypertrophy of lymphoid tissue in responseto repeated infections in
tonsillectomized patients.Usual complaints are discomfort on swallowing, feel-
ing of lump in the throat, dry cough and thick voice.3. Abscess of lingual tonsil.
It is a rare condition butcan follow acute lingual tonsillitis. Symptoms are se-
vere unilateral dysphagia, pain in the tongue, exces-sive salivation and some
degree of trismus. Protrusionof the tongue is painful. Jugulodigastric nodes will
beenlarged and tender. It is a potentially dangerous con-dition as laryngeal
oedema can easily follow.d
