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CASE REPORT

CHRONIC TONSILLITIS

OVERVIEW

A. ANATOMY OF THE TONSILS Waldeyers 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 Rosenmller)

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 56 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. 2. 3. 4.

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. Subclinical infections of tonsils without an acute attack. Mostly affects children and young adults. Rarely occurs after 50 years. 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 bodys 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. Vincents 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-lactamaseresistant 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 Sex Age Address Date

: B.R (child) : Male :7 y.o. : Kemiri, Purworejo : 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 drugs 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). Patients mother also complained her child always snoring but didnt 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 T : 20 times/minute : 38 C : icteric sclera -/-, anemic conjunctiva -/-, lnn normal : symmetrical retraction: -. Vesicular +/+, murmur -/: flat, peristaltic + , no liver and spleen enlargement, tenderness : warm limb, swelling -

Head and neck Thorax Abdomen Extremity

Local status of ear, nose, and throat Physical examination of the ear: Inspection : Auricula AD AS AD : Hyperemic (-), swelling (-), discharge (-), Laceration (-) : Hyperemic (-), swelling (-), discharge (-), Laceration (-) : cerumen (-), swelling (-), pruritic (-), narrow lumen (-), discharge (-)

Auditory canal

AS

: cerumen (-), swelling (-), pruritic (-), narrow lumen (-), discharge (-) : AD (-), AS (-) : AD (-), AS (-)

Palpation : Tragus pain Auricle pain Otoscopy AD AS : tympanic membrane intact, cone of light (+), hyperemic (-), Effusion (-), Bulging : tympanic membrane intact, cone of light (+), hyperemic (-), Effusion (-), Bulging (-), retraction (-) (-), 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 Teeth and gum Tounge Palatum mole Uvula Tonsil dextra Tonsil sinistra : labioschisis (-), inflammation (-), mass (-) : caries dentis (-) : inflammation (-) : swelling (-), hyperemic (-) : low : hyperemic (+), swelling (+) T3, widen crypts, detritus (+) : 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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