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In the first century AD, Celsus described tonsillectomy performed with sharp tools and followed by rinses with vinegar and other medicinals. Since that time, physicians have been documenting management of tonsillitis. Tonsillitis gained additional attention as a medical concern in the late 19th century. The consideration of quinsy in the differential diagnoses of George Washington's death and the discussion of tonsillitis in Kean's Domestic Medical Lectures, a home medical companion book published in the late 19th century, reflect the rise of tonsillitis as a medical concern.[1, 2] Understanding the disease process and management of this common malady remain important today. This article summarizes the current management of tonsillitis and highlights recent advances in the pathophysiology and immunology of this condition and its variations: acute tonsillitis (shown below), recurrent tonsillitis, and chronic tonsillitis and peritonsillar abscess (PTA).

Acute bacterial tonsillitis is shown. The tonsils are enlarged and inflamed with exudates. The uvula is midline.

Tonsillitis is inflammation of the pharyngeal tonsils. The inflammation usually extends to the adenoid and the lingual tonsils; therefore, the term pharyngitis may be used interchangeably. Pharyngotonsillitis and adenotonsillitis are considered equivalent for the purposes of this article. Lingual tonsillitis refers to isolated inflammation of the lymphoid tissue at the tongue base. A "carrier state" is defined by a positive pharyngeal culture of group A beta hemolytic Streptococcus pyogenes (GABHS), without evidence of an antistreptococcal immunologic response.

Viral or bacterial infections and immunologic factors lead to tonsillitis and its complications.


United States

Tonsillitis is a common illness. Nearly all children in the United States experience at least one episode of tonsillitis. Pharyngitis accompanies many upper respiratory tract infections. Between 2.5% and 10.9% of children may be defined as carriers. The mean prevalence of carrier status of school children for group A Streptococcus, a cause of tonsillitis, was 15.9% in one study.[3, 4] Children accounted for approximately one third of 45,000 peritonsillar abscess episodes estimated by Herzon et al to occur in the United States in 1995.[5]

Recurrent tonsillitis was reported in 11.7% of Norwegian children in one study and estimated in another study to affect 12.1% of Turkish children.[6] A family history of atopy and of tonsillectomy may predict the occurrence of tonsillitis in their children.

Because of improvements in medical and surgical treatments, complications associated with tonsillitis, including death, are rare.[7] Historically, scarlet fever was a major killer at the beginning of the 20th century, and rheumatic fever was a major cause of cardiac disease and mortality. Although the incidence of rheumatic fever has declined significantly, cases that occurred in the 1980s and early 1990s support concern over a resurgence of this condition.

Tonsillitis most often occurs in children; however, the condition rarely occurs in children younger than 2 years. Tonsillitis caused by Streptococcus species typically occurs in children aged 5-15 years, while viral tonsillitis is more common in younger children. Peritonsillar abscess (PTA) usually occurs in teens or young adults but may present earlier.

The patient's history determines the type of tonsillitis (ie, acute, recurrent, chronic) that is present.

Acute tonsillitis o Individuals with acute tonsillitis present with fever, sore throat, foul breath, dysphagia (difficulty swallowing), odynophagia (painful swallowing), and tender cervical lymph nodes.

Airway obstruction may manifest as mouth breathing, snoring, nocturnal breathing pauses, or sleep apnea. o Lethargy and malaise are common. o Symptoms usually resolve in 3-4 days but may last up to 2 weeks despite adequate therapy. Recurrent tonsillitis is diagnosed when an individual has 7 episodes in 1 year, 5 infections in 2 consecutive years, or 3 infections each year for 3 years consecutively. Individuals with chronic tonsillitis may present with chronic sore throat, halitosis, tonsillitis, and persistent tender cervical nodes. Children are most susceptible to infection by those in the carrier state. Individuals with peritonsillar abscess (PTA) present with severe throat pain, fever, drooling, foul breath, trismus (difficulty opening the mouth), and altered voice quality (the "hot potato" voice).

Physical examination should begin by determining the degree of distress regarding airway and swallowing function. Examination of the pharynx may be facilitated by opening the mouth without tongue protrusion, followed by gentle central depression of the tongue. Full assessment of oral mucosa, dentition, and salivary ducts may then be performed by gently "walking" a tongue depressor about the lateral oral cavity. Flexible fiberoptic nasopharyngoscopy may be useful in selected cases, particularly with severe trismus. The images below depict the oral examination.

Examination of the tonsils and pharynx. Oral mucosal examination. Physical examination in acute tonsillitis reveals fever and enlarged inflamed tonsils that may have exudates as seen in the image below.

Acute bacterial tonsillitis is shown. The tonsils are enlarged and inflamed with exudates. The uvula is midline. Group A beta-hemolytic Streptococcus pyogenes and Epstein-Barr virus (EBV) can cause tonsillitis that may be associated with the presence of palatal petechiae. Group A beta-hemolytic Streptococcus (GABHS) pharyngitis usually occurs in children aged 5-15 years. Open-mouth breathing and voice change (ie, a thicker or deeper voice) result from obstructive tonsillar enlargement.

The voice change with acute tonsillitis is usually not as severe as that associated with peritonsillar abscess (PTA). In peritonsillar abscess (PTA), the pharyngeal edema and trismus cause a hot potato voice.

Tender cervical lymph nodes and neck stiffness are observed in acute tonsillitis. Examine skin and mucosa for signs of dehydration. Consider infectious mononucleosis (MN) due to EBV in an adolescent or younger child with acute tonsillitis, particularly when tender cervical, axillary, and/or inguinal nodes; splenomegaly; severe lethargy and malaise; and low-grade fever accompany acute tonsillitis.

A gray membrane may cover tonsils that are inflamed from an EBV infection as seen in the image below. This membrane can be removed without bleeding.

Tonsillitis caused by Epstein-Barr infection (infectious mononucleosis). The enlarged inflamed tonsils are covered with gray-white patches. Palatal mucosal erosions and mucosal petechiae of the hard palate may be observed.

An individual with herpes simplex virus (HSV) pharyngitis presents with red, swollen tonsils that may have aphthous ulcers on their surfaces. Herpetic gingival stomatitis, herpes labialis, and hypopharyngeal and epiglottic lesions may be observed. Physical examination of a peritonsillar abscess (PTA) almost always reveals unilateral bulging above and lateral to one of the tonsils. Trismus is always present in varying severity. The abscess rarely is located adjacent to the inferior pole of the tonsil.

Inferior pole peritonsillar abscess (PTA) is a difficult diagnosis to make, and radiologic imaging with a contrast-enhanced CT scan is helpful. Tender cervical adenopathy and torticollis (neck turned in the cock-robin position) may be present. Ipsilateral otalgia may be observed.


Most episodes of acute pharyngitis and acute tonsillitis are caused by viruses such as the following: o HSV o EBV o Cytomegalovirus o Other herpes viruses o Adenovirus o Measles virus One study showing that EBV may cause tonsillitis in the absence of systemic mononucleosis found EBV to be responsible for 19% of exudative tonsillitis in children. Bacteria cause 15-30% of pharyngotonsillitis cases. Anaerobic bacteria play an important role in tonsillar disease. o GABHS causes most bacterial tonsillitis. o S pyogenes adheres to adhesin receptors that are located on the tonsillar epithelium. o Immunoglobulin coating of pathogens may be important in the initial induction of bacterial tonsillitis. Organisms such as Mycoplasma pneumoniae, Corynebacterium diphtheriae, and Chlamydia pneumoniae rarely cause acute pharyngitis. Arcanobacterium haemolyticum is an important cause of pharyngitis in Scandinavia and the United Kingdom but is not recognized as such in the United States. A rash similar to that of scarlet fever accompanies A haemolyticum pharyngitis. Neisseria gonorrhea may cause pharyngitis in sexually active persons. A polymicrobial flora consisting of both aerobic and anaerobic bacteria is observed in core tonsillar cultures from cases of recurrent pharyngitis. o Children with recurrent GABHS tonsillitis have different bacterial populations than do children who have not had as many infections. Other competing bacteria are reduced, offering less interference to GABHS infection. o Streptococcus pneumoniae, Staphylococcus aureus, and Haemophilus influenzae are the most common bacteria isolated in recurrent tonsillitis.

Bacteroides fragilis is the most common anaerobic bacterium isolated in recurrent tonsillitis. o The microbiology of recurrent tonsillitis in children and adults is different: adults show more bacterial isolates, with a higher recovery rate of Prevotella species, Porphyromonas species, and B fragilis organisms , while children show more GABHS. Also, adults more often have bacteria that produce beta-lactamase. A polymicrobial bacterial population is observed in most cases of chronic tonsillitis, with alpha- and beta-hemolytic streptococcal species, S aureus, H influenzae, and Bacteroides species identified. o One study, based on bacteriology of the tonsillar surface and core in 30 children undergoing tonsillectomy, suggests that antibiotics prescribed 6 months before surgery do not alter the tonsillar bacteriology at the time of tonsillectomy.[8] o A relationship between tonsillar size and chronic bacterial tonsillitis is believed to exist. This relationship is based on both the aerobic bacterial load and the absolute number of B and T lymphocytes. o H influenzae is the bacterium most often isolated in hypertrophic tonsils and adenoids. o With regard to penicillin resistance or beta-lactamase production, the microbiology of tonsils removed from patients with recurrent GABHS pharyngitis is not significantly different from the microbiology of tonsils removed from patients with tonsillar hypertrophy. Local immunological mechanisms are important in chronic tonsillitis. o The distribution of dendritic cells and antigen-presenting cells is altered during disease, with fewer dendritic cells on the surface epithelium and more in the crypts and extrafollicular areas. o Study of immunologic markers may permit differentiation between recurrent and chronic tonsillitis. Such markers in 1 study indicated that children more often experience recurrent tonsillitis, while adults requiring tonsillectomy more often experience chronic tonsillitis.[9] A polymicrobial flora is isolated from peritonsillar abscesses. Predominant organisms are the anaerobes Prevotella, Porphyromonas, Fusobacterium, and Peptostreptococcus species; major aerobic organisms are GABHS, S aureus, and H influenzae. Radiation exposure may relate to the development of chronic tonsillitis. A high prevalence of chronic tonsillitis was noted following the Chernobyl nuclear reactor accident in the former Soviet Union. Overcrowded conditions and malnourishment promote tonsillitis.


Lymphomas of the Head and Neck Malignant Nasopharyngeal Tumors Malignant Tumors of the Tonsil

Laboratory Studies

Tonsillitis and peritonsillar abscess (PTA) are clinical diagnoses. Testing is indicated when GABHS infection is suspected. o Throat cultures are the criterion standard for detecting GABHS. GABHS is the principal organism for which antibiotic therapy (sensitivity 90-95%) is definitely indicated. Growing concerns over bacterial resistance make monitoring acute tonsillitis with throat swabs for culture and sensitivity an important endeavor. Relying only on clinical criteria, such as the presence of exudate, erythema, fever, and lymphadenopathy, is not an accurate method for distinguishing GABHS from viral tonsillitis. o Beta-lactamase resistance of streptococcal species may now be observed in up to a third of community-based streptococcal infections. This resistance is probably due to the presence of copathogens that are beta-lactamaseproducing organisms, such as H influenzae and Moraxella catarrhalis. These organisms are able to degrade the beta-lactam ring of penicillin and make an otherwise sensitive GABHS act resistant to beta-lactam antibiotics. In one study, erythromycin did not inhibit nearly half of S pyogenes isolates. The limited precision of many throat swabs may reduce the usefulness of these samples. o A rapid antigen detection test (RADT), also known as the rapid streptococcal test, detects the presence of GABHS cell wall carbohydrate from swabbed material and is considered less sensitive than throat cultures; however, the test has specificity of greater than or equal to 95% and produces a result in significantly less time than that required for throat cultures. A negative RADT requires that a throat culture be obtained before excluding GABHS infection. o A culture or RADT is not indicated in most cases following antibiotic therapy for acute GABHS pharyngitis. Routine testing of asymptomatic household contacts is similarly not usually warranted. A Monospot serum test, CBC count, and serum electrolyte level test may be indicated. Serum may be examined for antistreptococcal antibodies, including antistreptolysin-O antibodies and antideoxyribonuclease (anti-DNAse) B antibodies. Titers are useful for documenting prior infection in persons diagnosed with acute rheumatic fever, glomerulonephritis, or other complications of GABHS pharyngitis. Laboratory evaluation in chronic tonsillitis relies upon documentation of results of pharyngeal swabs or cultures taken during prior episodes of tonsillitis. The usefulness and cost of throat swabs for pharyngitis are debated.

maging Studies

Routine radiologic imaging is not useful in cases of acute tonsillitis. For patients in whom acute tonsillitis is suspected to have spread to deep neck structures (ie, beyond the fascial planes of the oropharynx), radiologic imaging using plain films of the lateral neck or CT scans with contrast is warranted. In cases of peritonsillar abscess (PTA), CT scanning with contrast is indicated in general for the following situations:[10] o Unusual presentations (eg, an inferior pole abscess) o For patients at high risk for drainage procedures (eg, patients with coagulopathy or anesthetic risk)

CT scanning may be used to guide needle aspiration in the following situations: o Draining peritonsillar abscesses (PTAs) after an unsuccessful surgical attempt o Draining abscesses that are located in unusual locations and are anticipated to be difficult to reach with standard surgical approaches

Medical Care
Treatment of acute tonsillitis is largely supportive and focuses on maintaining adequate hydration and caloric intake and controlling pain and fever. Inability to maintain adequate oral caloric and fluid intake may require IV hydration, antibiotics, and pain control. IV corticosteroids may be administered to reduce pharyngeal edema.

Corticosteroids may shorten the duration of fever and pharyngitis in cases of infectious mononucleosis (MN). In severe cases of MN, corticosteroids or gammaglobulin may be helpful. Symptoms of MN may last for several months. Corticosteroids are also indicated for patients with airway obstruction, hemolytic anemia, and cardiac and neurologic disease. Inform patients of complications from steroid use. Antibiotics are reserved for secondary bacterial pharyngitis. Because of the risk of a generalized papular rash, avoid ampicillin and related compounds when MN is suspected. Similar reactions from oral penicillin-based antibiotics (eg, cephalexin) have been reported. Therefore, initiate therapy with another antistreptococcal antibiotic such as erythromycin. Administer antibiotics if conditions support bacterial etiology, such as the presence of tonsillar exudates, presence of a fever, leukocytosis, contacts who are ill, or contact with a person who has a documented GABHS infection. In many cases, bacterial and viral pharyngitis are clinically indistinguishable. Waiting 1-2 days for throat culture results has not been shown to diminish the usefulness of antibiotic therapy in preventing rheumatic fever. GABHS infection obligates antibiotic coverage. Bisno et al stated, in a practice guideline for the diagnosis and management of group A beta-hemolytic Streptococcus pyogenes (GABHS), the desired outcomes of therapy for GABHS pharyngitis are (1) prevention of acute rheumatic fever, (2) prevention of suppurative complications, (3) abatement of clinical symptoms and signs, (4) reduction in transmission of GABHS to close contacts, and (5) minimization of potential adverse effects of inappropriate antimicrobial therapy.

Administering oral penicillin for 10 days is the best treatment of acute GABHS pharyngitis. Intramuscular penicillin (ie, benzathine penicillin G) is required for persons who may not be compliant with a 10-day course of oral therapy. Penicillin is optimal for most patients (barring allergic reactions) because of its proven safety, efficacy, narrow spectrum, and low cost. Other antibiotics proven effective for GABHS pharyngitis are the penicillin congeners, many cephalosporins, macrolides, and clindamycin. Clindamycin may be of particular value because its tissue penetration is considered equivalent for both oral and IV administration. Clindamycin is effective even for organisms that are not rapidly dividing (Eagle effect), which explains its great efficacy for GABHS infection. Vancomycin and rifampin have also been useful. Reduced-frequency dosing is

recommended to improve compliance with medication regimens. A consensus on the efficacy of such dosing has not yet been formulated. Airway obstruction may require management by placing a nasal airway device, using intravenous corticosteroids, and administering humidified oxygen. Observe the patient in a monitored setting until the airway obstruction is clearly resolving. Most acute pharyngitis is self-limited with clinical improvement observed in 3-4 days. Recent clinical practice guidelines state that avoiding antibiotic therapy for this time period is safe and that a delay of up to 9 days from symptom onset to antimicrobial treatment should still prevent the major complication of GABHS (ie, acute rheumatic fever). Recurrent tonsillitis may be managed with the same antibiotics as acute GABHS pharyngitis. If the infection recurs shortly after a course of an oral penicillin agent, then consider IM benzathine penicillin G. Clindamycin and amoxicillin/clavulanate have been shown to be effective in eradicating GABHS from the pharynx in persons experiencing repeated bouts of tonsillitis. A 3- to 6-week course of an antibiotic against betalactamaseproducing organisms (eg, amoxicillin/clavulanate) may allow tonsillectomy to be avoided. Carrier state should be treated when the family has a history of rheumatic fever, a history of glomerulonephritis in the carrier, a "ping pong" spread of infection between household contacts of the carrier, familial anxiety regarding the implications of GABHS carriage, infectious outbreak within a closed community such as a school, an outbreak of acute rheumatic fever, or when tonsillectomy may be under consideration to treat the chronic carriage of GABHS. Peritonsillar cellulitis may respond to oral antibiotics. Antibiotics, either orally or intravenously, are required to treat PTA medically, although most peritonsillar abscesses (PTAs) are refractory to antibiotic therapy alone. Penicillin, its congeners (eg, amoxicillin/clavulanic acid, cephalosporins), and clindamycin are appropriate antibiotics. Aetius of Amida, a sixth century Byzantine physician, managed spontaneously draining abscesses with gargles of honey, milk and herbs, or rose extract. In rare cases of spontaneous peritonsillar abscess (PTA) rupture, mouthwashes are still recommended for hygienic reasons. A 10-day course of an oral antibiotic is prescribed.

urgical Care

Recurrent tonsillitis o Tonsillectomy is indicated for individuals who have experienced more than 6 episodes of streptococcal pharyngitis (confirmed by positive culture) in 1 year, 3 or more infections of tonsils and/or adenoids per year despite adequate medical therapy, or chronic or recurrent tonsillitis associated with the streptococcal carrier state that has not responded to beta-lactamaseresistant antibiotics. o Time missed from school or work and severity of illness (eg, whether hospitalization was required) are important considerations in recommending tonsillectomy. o Because adenoid tissue has similar bacteriology to the pharyngeal tonsils and minimal additional morbidity occurs with adenoidectomy if tonsillectomy is

already being performed, most surgeons perform adenoidectomy if adenoids are present and inflamed at the time of tonsillectomy. However, this point remains controversial. o Recurrent tonsillitis after tonsillectomy is extremely rare. Tonsillectomy reduces the bacterial load of GABHS and may also allow an increase in alphaStreptococcus, which can be protective against GABHS infection. Recurrent tonsillitis is usually due to regrowth of tonsillar tissue, which is treated by excision. Chronic tonsillitis o Tonsillectomy with or without adenoidectomy is the treatment of chronic tonsillitis. The details of the technique are reviewed in the article on Tonsillectomy. o In cases of chronic tonsillitis, specific technical considerations for tonsillectomy include awareness of a higher intraoperative and perioperative bleeding risk and awareness that dissection may be more difficult because of fibrosis and scarring of the tonsillar capsule. Such considerations may affect instrument selection and discharge decisions. Lingual tonsillitis o Surgery is rarely required for acute lingual tonsillitis. o Surgery is indicated for frequent and disabling episodes of this uncommon malady. Tonsillitis in cases of MN: Tonsillar hypertrophy that persists after resolution of MN and causes obstructive airway symptoms may require tonsillectomy. Peritonsillar abscess o Treatment of peritonsillar abscesses (PTAs) includes aspiration and incision and drainage (I&D). o Aetius recommended incision if an abscess did not spontaneously drain. o When peritonsillar abscess (PTA) is suspected, aspiration with a needle may be attempted to confirm the diagnosis and to remove some of the purulence. The area of the peritonsillar abscess (PTA) is first anesthetized by infiltration with local anesthetic or by spray or sponge application of topical anesthesia (eg, Americaine, benzocaine). Sedation may be helpful; administer sedation only in a facility that is appropriately staffed and equipped. An 18-gauge needle on a 1 mL tuberculin syringe is placed into the pointing area, taking care not to penetrate the pharyngeal mucosa more than 1 inch in order to prevent injury to the vessels and nerves of the parapharyngeal space. If attempt at aspiration from 3 different peritonsillar sites does not locate the abscess, treat the patient with oral or IV antibiotics. If symptoms persist after 24-48 hours of therapy, CT scanning with contrast may be performed. o Once purulence is detected, complete aspiration may be attempted. In the author's experience, limited aspiration is best, provided that sufficient material is available for Gram stain and cultures with antibiotic sensitivities. Not all patients need microbiologic evaluation. For those who are immunosuppressed or who have

developed a peritonsillar abscess (PTA) after several days of appropriate antibiotic therapy, send aspirated material for Gram stain, culture, and sensitivity tests. After needle aspiration, incision and drainage may be performed using a knife. The handle of a knife with an attached No 15 blade is taped 1 inch from the tip to prevent deep penetration through the mucosa. A gentle curvilinear incision, not more than half an inch deep, is fashioned along the perimeter of the tonsillar capsule and through the point from which pus was evacuated. A widely tipped blunt clamp (eg, Kelly clamp) is used to widely open the loculated pockets of purulence. A sponge-covered finger to break loculations is ideal. Rinsing with half-strength hydrogen peroxide solution aids hemostasis. When the patient is dehydrated and uncomfortable, this well-intentioned procedure is not greeted with enthusiasm from the patient. Sedation, hydration, analgesia, and anesthesia (at the least, topical or local) are important. Using the nondominant hand, the physician grasps the tongue with a sponge and observes the posterior oropharynx. In patients with severe trismus, a tongue blade may be used to depress the midportion of the tongue. Magnifying and illuminating loupes, such as the LumiView, are the best sources of light. A headlight or mirror is also effective. Arranging the instruments in order of use on a tray adjacent to the physician's dominant hand facilitates rapid accomplishment of this procedure. In experienced hands, this procedure should take fewer than 3 minutes from aspiration to rinsing with peroxide. Some adults and most children require deeper levels of sedation or general anesthesia for safe and adequate aspiration or drainage. An institution with a carefully designed policy for incision and drainage of peritonsillar abscess (PTA) with conscious sedation, including appropriate indications, staff, and criteria, may offer sedation to children. After the procedure, the patient is observed in accordance with sedation and anesthetic protocols. Hospitalization for adults and for older children is rarely required. The patient is discharged with a prescription for an oral antibiotic (10-d course of therapy), a prescription for an oral narcotic for pain control (taking care to avoid antiplatelet agents), and instructions to maintain hydration and control fever. Antibiotic therapy may be altered after cultures return. A follow-up office visit or telephone call is made in 2-4 weeks after the procedure to confirm symptomatic resolution. Tonsillectomy is indicated for peritonsillar abscess (PTA) associated with chronic or recurrent tonsillitis or for exposure of the abscess in unusual cases. Newer techniques and technologies offer improved recovery and reduced complications from surgery.[12] Acute tonsillectomy is generally regarded as a safe and effective treatment of peritonsillar abscess (PTA). Some physicians advocate immediate tonsillectomy for younger patients with peritonsillar abscess (PTA). Removing hot tonsils (ie, those that are acutely infected) carries the expectation of higher

intraoperative blood loss and a higher risk of immediate and delayed posttonsillectomy hemorrhage. The term quinsy tonsillectomy refers to tonsillectomy performed to treat peritonsillar abscess (PTA). Bilateral tonsillectomy is usually performed in these cases, and the abscessed tonsil is usually easier to remove during surgery than the inflamed contralateral tonsil. The abscessed tonsil is easier to remove because the abscess partially dissects the tonsil from the pharyngeal musculature. During surgery, if the abscess cannot be located in the usual superior lateral region of the tonsillar fossa, then careful exploration with needle aspiration may locate the collection, allowing for wide exposure and drainage. Tonsillectomy may be required for exposure in such cases. A CT scan with contrast may be indicated. Fleshy or pale, granular tonsillar tissue may indicate a neoplasm. Immunohistopathologic examination is indicated in such cases.

Consultations with infectious-disease, hematologic, and pediatric subspecialists are valuable in selected cases.


Hydration is important, and the oral route is usually adequate. Intravenous fluids may be required for severe dehydration. Hyperalimentation is rarely necessary.


Adequate rest for adults and children with tonsillitis accelerates recovery. In order to reduce risk of splenic rupture in persons diagnosed with systemic mononucleosis (MN), patients must be cautioned against activities that may cause abdominal injury.

Medication Summary
Medications used to manage tonsillitis include antibiotics, anti-inflammatory agents (eg, corticosteroids), antipyretics and analgesics (eg, acetaminophen, ibuprofen), and immunologic agents (eg, gammaglobulin).

urther Inpatient Care

Discharge of patient from the hospital occurs after the patient and caregivers can demonstrate compliance with oral pain medication and antibiotics.

Home intravenous therapy under the supervision of qualified home health providers or the independent oral intake ability of patients ensures hydration.

Further Outpatient Care

To confirm clinical improvement, follow-up care by telephone contact or physical examination may be useful in 2-4 weeks after the acute episode. Follow-up throat swabs and cultures are usually not necessary, unless family or personal history of rheumatic fever exists, significant recurrent tonsillitis is evident, or family members continue to reinfect each other.

Inpatient & Outpatient Medications

Order pain control, hydration, and antibiotics as discussed above for specific types of tonsillitis and associated complications.


Consider transfer of patient care when tonsillitis or its complications cannot be managed safely and expediently. o Ensure airway protection for transfer. o Ensure that appropriately trained personnel accompany the patient during transfer. Children younger than 3 years may require transfer because of the special care needed during tonsillitis or its complications. Patients with syndromic diagnoses (eg, trisomy 21) and patients with hematologic problems may benefit from transfer to facilities that have the availability of subspecialist care.


Consider transfer of patient care when tonsillitis or its complications cannot be managed safely and expediently. o Ensure airway protection for transfer. o Ensure that appropriately trained personnel accompany the patient during transfer. Children younger than 3 years may require transfer because of the special care needed during tonsillitis or its complications. Patients with syndromic diagnoses (eg, trisomy 21) and patients with hematologic problems may benefit from transfer to facilities that have the availability of subspecialist care.


Acute tonsillitis: Untreated or incompletely treated tonsillitis can lead to potentially lifethreatening complications.

Acute oropharyngeal infections can spread distally to the deep neck spaces and then into the mediastinum. Such complications may require thoracotomy and cervical exposure for drainage. Spread beyond the pharynx is suspected in persons with symptoms of tonsillitis who also have high or spiking fevers, lethargy, torticollis, trismus, or shortness of breath. Radiologic imaging using plain films of the lateral neck or CT scans with contrast is warranted for patients in whom deep neck spread of acute tonsillitis (beyond the fascial planes of the oropharynx) is suspected. o The most common complication is adjacent spread just beyond the tonsillar capsule. Peritonsillar cellulitis develops when inflammation spreads beyond the lymphoid tissue of the tonsil to involve the oropharyngeal mucosa. Peritonsillar abscess (PTA), historically referred to as quinsy, is caused by purulence trapped between the tonsillar capsule and the lateral pharyngeal wall; the superior constrictor muscle primarily comprises the lateral pharyngal wall in this area. o Rarely, acute pharyngotonsillitis may lead to thrombophlebitis of the internal jugular vein (Lemierre syndrome). The usual cause of this condition is Fusobacterium necrophorum. A patient who appears toxic following tonsillitis presents with spiking fevers and unilateral neck fullness and tenderness. CT scanning with contrast is necessary to help make the diagnosis. A prolonged course of IV antibiotics and treatment of the source of infection (eg, an abscess) are required. Anticoagulation is controversial. Ligation or excision of the internal jugular vein is required after multiple septic emboli become evident. Peritonsillar abscess o Peritonsillar abscess (PTA) may spread to the deep neck tissues; most often, peritonsillar abscess (PTA) spreads into the retropharyngeal space or into the parapharyngeal space. Spread may result in necrotizing fasciitis. o Treatment includes IV antibiotics, surgical debridement, and, in cases of associated toxic shock syndrome, possibly IV immunoglobulins. Distal abscess spread can be life threatening. Complications specific to GABHS pharyngitis are scarlet fever, rheumatic fever, septic arthritis, and glomerulonephritis. o Scarlet fever manifests as a generalized, nonpruritic, macular erythematous rash that is worse on the extremities and spares the face. The classic strawberry tongue is bright red and tender because of papillary desquamation. The rash lasts up to 1 week and is accompanied by fever and arthralgias. o Individuals at risk for this rash are those who do not have antitoxin antibodies to the exotoxin produced by GABHS. o Acute poststreptococcal glomerulonephritis (AGN) occurs in 10-15% of pharyngitis cases that are caused by the type-12 serotype. AGN follows GABHS by 1-2 weeks. Urinalysis to detect excreted protein may allow detection of subclinical renal injury for persons with recurrent tonsillitis. o Rheumatic fever follows acute pharyngitis by 2-4 weeks and was observed in up to 3% of streptococcal pharyngitides in the mid-20th century. Today, far fewer persons experience this complication, largely because of appropriate antibiotic therapy. Cardiac valvular vegetations affect the mitral and tricuspid valves, leading to murmurs, persistent relapsing fevers, and valvular stenosis or

incompetence. A throat swab does not identify the causative organism because a positive result may reflect colonization rather than pathogenicity. Elevated or rising titers of antistreptolysin (ASO) antibodies, anti-DNAse beta, or antihyaluronidase are required to make the diagnosis. Septic arthritis results in a painful hot joint that contains fluid with bacteria. Arthrocentesis is diagnostic and partially therapeutic. Treatment with IV antibiotics for 6 weeks is required to prevent long-term joint complications.