Tonsillitis and Peritonsillar Abscess Clinical Presentation

Updated: Feb 18, 2022
  • Author: Udayan K Shah, MD, FACS, FAAP; Chief Editor: Arlen D Meyers, MD, MBA  more...
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The patient's history determines the type of tonsillitis (ie, acute, recurrent, chronic) that is present.

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, sleep-disordered breathing, nocturnal breathing pauses, or sleep apnea. Lethargy and malaise are common. Symptoms usually resolve in 3-4 days but may last up to 2 weeks despite adequate therapy.

Recurrent streptococcal tonsillitis is diagnosed when an individual has 7 culture-proven 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

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. Examination of the tonsils and pharynx.
Oral mucosal examination. Oral mucosal examination.

Acute tonsillitis

Physical examination in acute tonsillitis reveals fever and enlarged inflamed tonsils that may have exudates (see the image below).

Acute bacterial tonsillitis is shown. The tonsils 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 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 due to EBV in an adolescent or younger child with acute tonsillitis, particularly when it is accompanied by tender cervical, axillary, and/or inguinal nodes; splenomegaly; severe lethargy and malaise; and low-grade fever. A gray membrane may cover tonsils that are inflamed from an EBV infection (see the image below). This membrane can be removed without bleeding. Palatal mucosal erosions and mucosal petechiae of the hard palate may also be observed.

Tonsillitis caused by Epstein-Barr infection (infe Tonsillitis caused by Epstein-Barr infection (infectious mononucleosis). The enlarged inflamed tonsils are covered with gray-white patches.

HSV pharyngitis

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.

Peritonsillar abscess

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 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.



Be vigilant for signs of impending complications from tonsillitis (eg, mental status changes, severe trismus, high fevers). When necessary, perform further tests or other diagnostic evaluations (eg, CBC counts, CT scanning) in patients with signs of impending complications from tonsillitis.

Treatment of suspected streptococcal pharyngitis with appropriate antibiotics may lead to complications, such as acute rheumatic fever and glomerulonephritis.

Acute tonsillitis

Untreated or incompletely treated tonsillitis can lead to potentially life-threatening 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.

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 pharyngeal wall in this area. Most often, PTA spreads into the retropharyngeal space or into the parapharyngeal space. Spread may result in necrotizing fasciitis. Treatment includes IV antibiotics, surgical debridement, and, in cases of associated toxic shock syndrome, possibly IV immunoglobulins. Distal abscess spread can be life threatening.

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.

GABHS pharyngitis

Complications specific to group A beta-hemolytic Streptococcus pyogenes (GABHS) pharyngitis are scarlet fever, rheumatic fever, septic arthritis, and glomerulonephritis.

Scarlet fever

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. Individuals at risk for this rash are those who do not have antitoxin antibodies to the exotoxin produced by GABHS.

Acute poststreptococcal glomerulonephritis

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.

Rheumatic fever

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

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.