Peritonsillar abscess (PTA) was first described as early as the 14th century; however, it is only since the

advent of antibiotics in the 20th century that the condition has been described more extensively. A PTA
is a localized accumulation of pus in the peritonsillar tissues that forms as a result of suppurative
tonsillitis. An alternative explanation is that a PTA is an abscess formed in a group of salivary glands in
the supratonsillar fossa, known as Weber glands.

The nidus of accumulation is located between the capsule of the palatine tonsils and the constrictor
muscles of the pharynx. The anterior and posterior pillars, torus tubarius (superior), and pyriform sinus
(inferior) form the boundaries of this potential peritonsillar space. Because this area is composed of
loose connective tissue, severe infection may rapidly lead to formation of purulent material. Progressive
inflammation and suppuration may extend to directly involve the soft palate, the lateral wall of the
pharynx, and, occasionally, the base of the tongue.

PTA is usually a complication of an acute tonsillitis. Inflammatory edema may lead to significant difficulty
in swallowing. Dehydration frequently occurs secondary to the patient's avoidance of painful ingestion
of food and liquids. Expansion of the abscess may lead to extension of the inflammation into adjacent
fascial compartments of the head and neck, potentially resulting in airway obstruction.

The palatine tonsils are paired lymphoid organs found between the palatoglossal and palatopharyngeal
folds of the oropharynx. They are surrounded by a thin capsule that separates the tonsil from the
superior and middle constrictor muscles.

The anterior and posterior pillars form the front and back limits of the peritonsillar space. Superiorly,
this potential space is related to the torus tubarius, while inferiorly it is bounded by the pyriform sinus.
Composed solely of loose connective tissue, a severe infection may rapidly result in pus formation. The
inflammation and suppurative process may extend to involve the soft palate, the lateral wall of the
pharynx, and, occasionally, the base of the tongue.

The tonsillar fossa has a rich network of lymphatic vessels leading to the parapharyngeal space and the
upper cervical lymph nodes, which explains the pattern of adenopathy observed clinically. Ipsilateral
upper cervical lymphadenopathy is the result of the spread of infection to the regional lymphatics.
Occasionally, the severity of the suppurative process may lead to a cervical abscess, especially in very
fulminant or rapidly progressive cases.

The pathophysiology of PTA is unknown. The most widely accepted theory involves the progression of
an episode of exudative tonsillitis first into peritonsillitis and then into frank abscess formation.
Extension of the inflammatory process may occur in both treated and untreated populations. PTA also
has been documented to arise de novo without any prior history of recurrent or chronic tonsillitis. A PTA
also can be the presentation of an Epstein-Barr virus (ie, mononucleosis) infection.

Another theory proposes the origin of PTA in Weber glands. These minor salivary glands are found in the
peritonsillar space and are thought to help in clearing debris from the tonsils. Should obstruction as a
result of scarring from infection occur, tissue necrosis and abscess formation result, leading to PTA.

Any of the microorganisms that cause acute or chronic tonsillitis may be the cause of a PTA. Most
commonly, aerobic and anaerobic gram-positive organisms are identified by means of culture.
Cultures of affected patients reveal group A beta-hemolytic streptococci as most prevalent. Next most
commonly, staphylococci, pneumococci, and Haemophilus organisms are found. Finally, other
microorganisms that can be cultured include lactobacilli, filamentous forms such as Actinomyces
species, micrococci, Neisseria species, diphtheroids, Bacteroides species, and nonsporulating bacteria.
Some evidence indicates that anaerobic bacteria frequently cause these infections.[1]

The incidence of PTA in the United States is about 30 cases per 100,000 people per year, representing
about 45,000 new cases each year. No accurate data are available internationally.

Although tonsillitis is a disease of childhood, only one third of PTA cases are found in this age group. The
age of patients with the condition is variable, ranging from 1 to 76 years, with the highest incidence in
persons aged 15-35 years. No sexual or racial predilection has been established.

In a retrospective cohort study of 427 patients with PTA, Marom et al investigated how the
characteristics of PTA may have changed over time.[2]The results led the authors to conclude that PTA
currently tends to affect an older population than it once did, that its course in older individuals has
become longer and worse, and that smoking may be a predisposing factor in its development.

A study of 685 patients by Kordeluk et al looked at the relation between peritonsillar cellulitis and
abscess and outbreaks of acute tonsillitis.[3]The authors found peaks with seasonal variation for
presentations with acute tonsillitis but no association with PTA, which occurred at similar rates
throughout the calendar year.

Most patients treated with antibiotics and adequate drainage of their abscess cavity recover within a
few days. A small number present with another abscess later, requiring tonsillectomy. If patients
continue to report recurring or chronic sore throats after proper incision and drainage (I&D), a
tonsillectomy may be indicated.

In a nationwide retrospective cohort study from Taiwan, Wang et al found that the risk of PTA
recurrence rose with higher degrees of previous tonsillitis in patients of all ages, whereas such a rise was
associated with management by needle aspiration only in pediatric patients.[4]The risk of PTA
recurrence was highest in patients who were younger than 30 years and had experienced more than five
prior episodes of tonsillitis.

Patients with a peritonsillar abscess (PTA) typically present with a history of acute pharyngitis
accompanied by tonsillitis and worsening unilateral pharyngeal discomfort. Patients also may experience
malaise, fatigue, and headaches. They often present with a fever and asymmetric throat fullness.
Associated halitosis, odynophagia, dysphagia, and a "hot potato–sounding" voice occur.

Many patients present with ipsilateral referred otalgia with swallowing. Trismus (ie, a limitation in the
ability to open the oral cavity) of varying severity is present in all cases, reflecting lateral pharyngeal wall
and pterygoid musculature inflammation. Because of lymphadenopathy and cervical muscle
inflammation, patients often experience neck pain and even a limitation in neck mobility. Clinicians need
to be alerted to the diagnosis of a PTA in patients who have pharyngeal symptoms that persist despite
an adequate antibiotic regimen.
As the degree of inflammation and infection proceeds, symptoms include progression in the floor of the
mouth, the parapharyngeal space, and the prevertebral space. Extension in the floor of the mouth is
worrisome because of airway obstruction; the clinician must be aware of an eventual airway emergency.

The presentation may range from acute tonsillitis with unilateral pharyngeal asymmetry to dehydration
and sepsis. Most patients have severe pain. Examination of the oral cavity reveals marked erythema,
asymmetry of the soft palate, tonsillar exudation, and contralateral displacement of the uvula (see the
image below).

Indications for considering the diagnosis of a PTA include the following: Unilateral swelling of the
peritonsillar area, Unilateral swelling of the soft palate, with anterior displacement of the ipsilateral
tonsil, Nonresolution of acute tonsillitis, with persistent unilateral tonsillar enlargement.

In a retrospective study from the University of Ottawa, Kilty and Gaboury reported that in 50 adults with
PTA, clinical signs that had a significant association with the lesion included uvular deviation, trismus,
and inferior displacement of the superior pole of the tonsil on the affected side.[5]

A PTA ordinarily is unilateral and located at the superior pole of the affected tonsil, in the supratonsillar
fossa. At the level of the supratonsillar fold, the mucosa may appear pale and even show a small pimple.
Palpation of the soft palate often reveals an area of fluctuance. Flexible nasopharyngoscopy and
laryngoscopy are recommended in patients experiencing airway distress. The laryngoscopy is key to
ruling out epiglottitis and supraglottitis, as well as vocal cord pathology.

The degree of trismus depends on the extent of lateral pharyngeal space inflammation. If it is very
marked, one should be concerned about possible lateral pharyngeal space cellulitis. The finding of
tender ipsilateral cervical lymphadenopathy involving single or multiple nodes is not uncommon. The
affected lymph nodes may be quite firm. In presentations with significant nodal inflammation, the
patient may experience torticollis and limitation of neck mobility. A more detailed evaluation is essential
if suspicion of an accompanying cervical abscess exists.

Numerous clinical complications may occur if the diagnosis of a PTA is missed or delayed. The severity of
the complications depends on the rapidity of progression of the illness, as well as the characteristics of
the affected fascial spaces. Early management and intervention are important.

The fascial spaces of the neck are interconnected. Once inflammation exceeds the limits of the
peritonsillar space, involvement of the masticator space (with increasing degrees of trismus) occurs.
Extension may progress to the submandibular and sublingual spaces within the floor of the mouth
(Ludwig angina). At this point, emergency airway control through intubation or tracheotomy is indicated
to obviate obstruction from swelling of the base of the tongue. In severe cases, death may occur.

Other well-reported complications due to continued progression of the infection may lead to a
parapharyngeal abscess, descending necrotizing mediastinitis, Lemierre syndrome, and internal carotid
artery pseudoaneurysm.[6, 7, 8, 9]

Patients presenting with peritonsillar abscesses (PTAs) often are septic in appearance and may
demonstrate varying degrees of dehydration due to abstention from oral intake. Assessment of these
two entities should involve the collection of blood for a complete blood count, electrolyte level
measurement, and blood cultures.
In patients presenting with tonsillitis and bilateral cervical lymphadenopathy, a monospot test
(heterophile antibodies) should be considered. If the test results are positive, the patient requires
careful evaluation of hepatosplenomegaly. Liver function tests should be considered in patients with
hepatomegaly.

To facilitate the identification of infectious organisms, a throat swab and culture are to be considered.
The results may help the clinician select the most appropriate antibiotic once the organism is identified,
limiting the risk of antibiotic resistance.

Imaging may be particularly useful in cases where an attempt at incision and drainage (I&D) has failed or
where worsening edema in a treated peritonsillar cellulitis is noted. In certain cases, the abscess may be
within the tonsil itself or partially hidden (ie, inferior or posterior) by the tonsil.

Lateral soft tissue views of the nasopharynx and oropharynx may help the clinician rule out a
retropharyngeal abscess. In the anteroposterior view, the films reveal distortion of soft tissues but are
not useful in localizing an abscess.

In selected clinical settings and in very young patients, radiologic evaluation may be performed by
means of computed tomography (CT) of the oral cavity and neck using intravenous (IV) contrast
enhancement.

Common findings are the presence of a hypodense fluid collection in the apex of the affected tonsil,
with peripheral rim enhancement. Other findings may include an asymmetric enlargement of the tonsils
and surrounding fossa. Further delineation of cervical adenopathy is facilitated, as is the identification of
a possible intranodal fluid collection, which indicates a cervical abscess and helps in the planning of
surgical management.

Intraoral ultrasonography has been proposed as an imaging modality.[10]It is a simple, well-tolerated,

noninvasive technique that can help distinguish between cellulitis and the presence of an abscess.
Intraoral ultrasonography also allows the option of a more directed aspiration of the tonsillar fossa
before definitive surgical drainage is attempted. One study has shown that this approach is also clinically
useful in the evaluation of patients presenting in the emergency department.

Needle aspiration of the abscess site (see the image below) may be performed just before the drainage
procedure is attempted. It allows identification of the location of the abscess in the peritonsillar space.

The aspiration site is anesthetized by using lidocaine with epinephrine, and a large-bore (16- to 18-
gauge) needle is mounted on a 10-mL syringe. Infiltration is the method of choice for administering local
anesthesia for aspiration and incision of peritonsillar abscesses. The needle is passed through the
anesthetized mucosa, where aspiration of the site is performed. Aspiration of purulent material is
diagnostic, and the material may be sent for culture.

In cases of peritonsillar abscess (PTA), when incision and drainage (I&D) is performed, it leads to
immediate improvement of the patient's symptoms. Needle aspiration may be used as a diagnostic
modality and as a therapeutic one, because it allows the accurate localization of the abscess cavity. The
aspirated fluid may be sent for culture, and in some cases, I&D may not be necessary. If patients
continue to report recurring and/or chronic sore throats after proper I&D, a tonsillectomy may be
indicated.
Intraoral drainage has a high rate of success, with low morbidity and a low rate of recurrence. Normally,
unless the patient presents with recurrent tonsillitis or recurrent PTA, tonsillectomy is not indicated;
however, in situations where the abscess is located in an area difficult to access, a tonsillectomy may be
the only way to drain the abscess.

Patients with PTAs who are dehydrated require intravenous (IV) fluid administration until the
inflammation resolves and they are able to resume adequate oral fluid intake.

Antipyretics and analgesics are used to alleviate fever and discomfort. Oral and parenteral analgesics are
an integral part of the management and allow the patient to resume oral intake. Often, the pain relief
from I&D is so significant that the patient is able to resume oral intake with nonnarcotic analgesics.

Antibiotic therapy should begin after cultures are obtained from the abscess. High-dose IV penicillin
remains a good choice for empiric treatment of PTA. Alternatively, because of the polymicrobial nature
of cultured pus, agents that treat copathogens and resist beta-lactamases also have been recommended
as a first choice. Cephalexin or another cephalosporin (with or without metronidazole) is likely the best
initial option. Alternatives include the following:

Cefuroxime or cefpodoxime (with or without metronidazole)

Clindamycin

Trovafloxacin

Amoxicillin-clavulanate (if mononucleosis has been ruled out)

Oral antibiotics may be prescribed once the patient is able to tolerate oral intake; treatment should be
continued for 7-10 days.

The use of steroids has been controversial. In a study by Ozbek, the addition of a single dose of IV
dexamethasone to parenteral antibiotics significantly lessened the variables of hours hospitalized,
throat pain, fever, and trismus in comparison with treatment involving only parenteral antibiotics.[11]In
addition, the use of steroids in patients presenting with signs and symptoms of mononucleosis has not
led to the formation of a PTA.

Management of a patient with a suspected PTA should include a referral to an otolaryngologist or a

surgeon with experience in the management of this entity. Early referral should be considered if the
diagnosis is unclear and is indicated in patients who present with airway obstruction.

Discussing the pathophysiology and indications for surgery with the patient is essential. Informed
consent should be obtained from the patient or surrogate only after the potential complications have
been carefully described.

In cases in which airway access may be compromised, an emergency consultation with the
anesthesiologist is obtained, and the potential of airway obstruction is discussed. If necessary, the
anesthesiologist may perform an intubation using a flexible bronchoscope with the patient in the
semisupine position. A significant potential for airway obstruction exists if the patient's airway access is
limited by significant trismus or by edema of the oropharyngeal structures.
There continues to be controversy regarding the relative merits of needle aspiration and I&D as
definitive therapeutic modalities. With cooperative patients, procedures may be performed in an
examination chair. The supratonsillar fold is anesthetized by either mucosalization or injection of a local
anesthetic with epinephrine to reduce bleeding. If injection of a local anesthetic is performed, care
should be taken to superficially infiltrate the overlying mucosa and surrounding soft palate.

Needle aspiration can be carried out in children as young as 7 years, especially if conscious sedation is
used. Needle aspiration may be used both as a diagnostic and as a therapeutic modality because it
allows accurate localization of the abscess cavity. The fluid aspirated may be sent for culture, and in
some cases, needle aspiration may not have to be followed by I&D.

Intraoral I&D is performed by incising the mucosa overlying the abscess, usually located in the
supratonsillar fold. Once the abscess is localized, blunt dissection is carried out to break loculations. The
opening is left open to drain, and the patient is asked to gargle with a sodium chloride solution, allowing
the accumulated material to exit the abscess cavity. Successful aspiration or drainage leads to
immediate improvement of the patient's symptoms.

With very young or uncooperative patients or patients whose abscess is in an unusual location, the
procedure is best performed under general anesthesia.

Immediate tonsillectomy as part of the management of a PTA also has been a subject of controversy.
Many studies have shown the safety of a tonsillectomy in the setting of an acute abscess. Others have
shown that immediate or delayed tonsillectomy may not be necessary because of the high rate of
success and the low recurrence rate and morbidity associated with intraoral drainage. When the abscess
is located in an area that is difficult to access, a tonsillectomy may be the only way to drain it.

Smoking is often more common among patients with peritonsillar abscess and is often associated with
more complications.[12]

Because of the rapid alleviation of pain commonly achieved with surgical treatment, most patients may
be discharged immediately after the procedure if they are able to tolerate oral intake of fluids and
bleeding is not apparent. Some patients may require admission in the hospital setting for 24-48 hours or
until oral intake is properly reestablished and pain is well controlled.

IV hydration is important because most patients present with significant fluid deficits. Continued use of
antibiotics in the postoperative period is important as well. When the patient is able to take sufficient
fluids by mouth, antibiotics may be administered orally for 7-10 days. Because of the level of discomfort
from the ongoing inflammation, administration of oral analgesics is also helpful.

In patients treated with I&D, evaluating the patency of the opening is important. Premature closure
before the cavity has become obliterated is possible, leading to reaccumulation of pus. This may warrant
a second I&D procedure or a tonsillectomy.

Limiting the drainage incision to the mucosa of the soft palate and using blunt dissection within the
cavity are important for preventing serious bleeding. The terminal branches of the external carotid
artery lie on the posterior aspect of the tonsillar fossa and can be injured easily, particularly in children,
in whom they are relatively superficial.
Bleeding is a potential complication if branches of the external carotid artery are injured or if the
external carotid artery itself is injured. The bleeding may occur intraoperatively or in the early
postoperative period.

Intraoperative hemorrhage is an emergency and results from direct injury to the external carotid artery
or terminal branches thereof. Once the patient is stabilized hemodynamically, the tonsillar fossa is
reevaluated. The ipsilateral neck also should be prepared and draped in a sterile fashion to provide
access to the proximal external carotid artery. If the hemorrhage is controlled intraorally, the patient's
continued stabilization is pursued.[13]

If the bleeding appears to be too brisk, and it is not controlled by careful intraoral source identification,
an ipsilateral cervicotomy is performed, as follows.

The sternocleidomastoid is retracted laterally, and the carotid sheath contents are identified. The
internal jugular vein, the vagus nerve, and the carotid arteries (common, external, and internal) are
identified. A vascular loop is applied around the external carotid artery to assess temporization of
bleeding. The external carotid artery is dissected superiorly, with careful attention to preserving the
external laryngeal, the ansa hypoglossi, and the hypoglossal nerves. Ligation of the external carotid
artery may prove necessary.

The general approach to postoperative hemorrhage similarly is directed to the identification of the
source of bleeding. The patient is brought to the operating room, and the same procedure as described
above is followed.

Patients are seen routinely in follow-up in the office setting. Elements to consider at that time are
reduction of the amount of pain, defervescence, and ability to comfortably resume oral intake.

During the examination, it is important to inspect the drainage site carefully and to rule out
reaccumulation of pus. Assessment should include checking for improvement in tonsillar appearance,
inflammation, and the resolution of cervical lymphadenopathy. In general, unless the patient presents
with a history of recurring tonsillitis or recurrent PTA, tonsillectomy is not indicated.

1. Repanos C, Mukherjee P, Alwahab Y. Role of microbiological studies in management of

peritonsillar abscess. J Laryngol Otol. 2009 Aug. 123 (8):877-9. [Medline].
2. Marom T, Cinamon U, Itskoviz D, Roth Y. Changing trends of peritonsillar abscess. Am J
Otolaryngol. 2010 May-Jun. 31 (3):162-7. [Medline].
3. Kordeluk S, Novack L, Puterman M, Kraus M, Joshua BZ. Relation between peritonsillar infection
and acute tonsillitis: myth or reality?. Otolaryngol Head Neck Surg. 2011 Dec. 145 (6):940-5.
[Medline].
4. Wang YP, Wang MC, Lin HC, Chou P. The impact of prior tonsillitis and treatment modality on
the recurrence of peritonsillar abscess: a nationwide cohort study. PLoS One. 2014. 9
(10):e109887. [Medline]. [Full Text].
5. Kilty SJ, Gaboury I. Clinical predictors of peritonsillar abscess in adults. J Otolaryngol Head Neck
Surg. 2008 Apr. 37 (2):165-8. [Medline].
6. Thapar A, Tassone P, Bhat N, Pfleiderer A. Parapharyngeal abscess: a life-threatening
complication of quinsy. Clin Anat. 2008 Jan. 21 (1):23-6. [Medline].
 7. da Silva PS, Waisberg DR. Internal carotid artery pseudoaneurysm with life-threatening epistaxis
as a complication of deep neck space infection. Pediatr Emerg Care. 2011 May. 27 (5):422-4.
[Medline].
8. Roccia F, Pecorari GC, Oliaro A, Passet E, Rossi P, Nadalin J, et al. Ten years of descending
necrotizing mediastinitis: management of 23 cases. J Oral Maxillofac Surg. 2007 Sep. 65
(9):1716-24. [Medline].
9. Ehrenfried Berthelsen R, Hein L. [Lemierre's syndrome following peritonsillar abscess]. Ugeskr
Laeger. 2012 May 28. 174 (22):1534-5. [Medline].
10. Ramirez-Schrempp D, Dorfman DH, Baker WE, Liteplo AS. Ultrasound soft-tissue applications in
the pediatric emergency department: to drain or not to drain?. Pediatr Emerg Care. 2009 Jan. 25
(1):44-8. [Medline].
11. Ozbek C, Aygenc E, Tuna EU, Selcuk A, Ozdem C. Use of steroids in the treatment of peritonsillar
abscess. J Laryngol Otol. 2004 Jun. 118 (6):439-42. [Medline].
12. Marom T, Cinamon U, Itskoviz D, Roth Y. Changing trends of peritonsillar abscess. Am J
Otolaryngol. 2010 May-Jun. 31 (3):162-7. [Medline].
13. Heidemann CH, Wallén M, Aakesson M, Skov P, Kjeldsen AD, Godballe C. Post-tonsillectomy
hemorrhage: assessment of risk factors with special attention to introduction of coblation
technique. Eur Arch Otorhinolaryngol. 2009 Jul. 266 (7):1011-5. [Medline].

The tonsils begin developing early in the third month of fetal life. They arise from the endoderm lining,
the second pharyngeal pouch, and the mesoderm of the second pharyngeal membrane and adjacent
regions of the first and second arches. The epithelium of the second pouch proliferates to form solid
endodermal buds, growing into the underlying mesoderm; these buds give rise to tonsillar stroma.
Central cells of the buds later die and slough, converting the solid buds into hollow tonsillar crypts,
which are infiltrated by lymphoid tissue.

Both right and left tonsils form part of the circumpharyngeal lymphoid ring. The size of the tonsil varies
according to the age, individuality, and pathologic status. At the fifth or sixth year of life, the tonsils
rapidly increase in size, reaching their maximum size at puberty. At puberty, the tonsils measure 20-25
mm in vertical and 10-15 mm in transverse diameters.

Peritonsillar abscesses (PTAs) are common infections of the head and neck region, accounting for
approximately 30% of soft tissue head and neck abscesses. With an incidence of about 1 in 10,000, PTA
(see the image below) is the most common deep space infection of the head and neck that presents to
the emergency department.

A study by Johnson using the 2012 Nationwide Emergency Department Sample, the 2012 National
(Nationwide) Inpatient Sample, and the 2013 Nationwide Readmissions Database estimated the number
of emergency department visits in the United States for peritonsillar abscess to be 62,787, with the
estimated number of inpatient admissions and readmissions for the condition being 15,095 and 267,
respectively. Eighty percent of the emergency department patients were discharged home after
receiving nonoperative therapy, while 50% of the patients admitted to the hospital were treated
surgically.[1]
Symptoms of PTA usually begin 3-5 days before evaluation and may include the following:

Fever

Malaise

Headache

Neck pain

Throat pain (more severe on the affected side; occasionally referred to the ipsilateral ear)

Dysphagia

Change in voice

Otalgia

Odynophagia

Physical findings may include the following:

Mild-to-moderate distress

Fever

Tachycardia

Dehydration

Drooling, salivation, or trouble handling oral secretions

Trismus

“Hot potato” or muffled voice

Rancid or fetid breath

Cervical lymphadenitis in the anterior chain

Asymmetric tonsillar hypertrophy

Localized fluctuance

Inferior and medial displacement of the tonsil

Contralateral deviation of the uvula

Erythema of the tonsil

Exudates on the tonsil

No definitive studies are required to diagnose PTA. The following laboratory tests may be considered

Basic studies, such as complete blood count, electrolytes, and C-reactive protein (if the patient has
significant comorbidities)

Monospot test/heterophile antibody test (to rule out infectious mononucleosis if the etiology is unclear)

Culture of fluid from needle aspiration (to guide antibiotic selection or changes)

Blood cultures (if the clinical presentation is severe)

The following imaging studies may be considered:

Lateral soft tissue neck radiography (to help rule out other causes)

Intraoral ultrasonography

Computed tomography (CT) of the head and neck with intravenous (IV) contrast (if incision and drainage
fails, if the patient cannot open his or her mouth, or if the patient is young and uncooperative)

Diagnostic Considerations, These include the following:

Peritonsillar cellulitis

Tonsillitis

Parapharyngeal abscess

Tracheitis

Ludwig angina

Dental infection

Cervical adenitis

Neoplasms (leukemia, lymphoma)

Foreign body aspiration

Aneurysm of internal carotid artery

Laboratory Studies

No definitive studies are required to diagnose peritonsillar abscess. Physicians may consider basic
laboratory tests (ie, CBC, electrolytes, C-reactive protein) if the patient has significant comorbidities.

Monospot test/heterophile antibody test can be performed to rule out infectious mononucleosis if the
etiology is unclear. Infectious mononucleosis can coexist in 1.5-6% of patients with peritonsillar
abscesses.[15]
Culture of the fluid from needle aspiration may be performed to guide antibiotic selection or changes. A
recent literature review recommends obtaining aspirate culture in those at risk of infection with
resistant organisms (ie, those with recurrent or persistent infection, diabetes, or
immunocompromise).[15]