ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Peritonsillar cellulitis and abscess

Peritonsillar cellulitis and abscess
Literature review current through: Jan 2024.
This topic last updated: Oct 08, 2023.

INTRODUCTION — The clinical features, evaluation, and management of peritonsillar cellulitis (also called peritonsillitis) and abscess will be discussed here. Cervical lymphadenitis, retropharyngeal cellulitis and abscess, and other deep neck space infections are discussed separately. (See "Cervical lymphadenitis in children: Etiology and clinical manifestations" and "Retropharyngeal infections in children" and "Deep neck space infections in adults".)

BACKGROUND — Suppurative infections of the neck are uncommon. However, they are potentially very serious. Suppurative cervical lymphadenitis is the most common superficial neck infection. Peritonsillar abscess (PTA, quinsy) is the most common deep neck infection [1,2]. Other deep neck infections include retropharyngeal abscess and parapharyngeal space abscess (also known as pharyngomaxillary or lateral pharyngeal space abscess). Pharyngeal space infection most often arises via contiguous spread of infection from a peritonsillar or retropharyngeal abscess.

DEFINITION — Two terms are used to describe infection of the peritonsillar region:

Peritonsillar cellulitis – Peritonsillar cellulitis is an inflammatory reaction of the tissue between the capsule of the palatine tonsil and the pharyngeal muscles that is caused by infection, but not associated with a discrete collection of pus. An alternate term for cellulitis is phlegmon.

Peritonsillar abscess – Peritonsillar abscess is a collection of pus located between the capsule of the palatine tonsil and the pharyngeal muscles.

In many patients, diagnosing the type of peritonsillar infection present requires needle aspiration or incision and drainage to determine if pus is present.

ANATOMY AND PATHOGENESIS — The peritonsillar space consists of loose areolar tissue overlying the tonsil and is surrounded by the superior pharyngeal constrictor muscle and the anterior and posterior tonsillar pillars. The palatine tonsils are located between the palatoglossal and palatopharyngeal arches (figure 1) [3]. They are surrounded by a capsule that provides a path for blood vessels and nerves.

Peritonsillar abscess (PTA) usually occurs in the superior pole of the tonsil, manifested by a defined collection of pus between the tonsillar capsule, the superior constrictor, and the palatopharyngeus muscle. PTA also may occur in the midpoint or inferior pole of the tonsil, or may be dispersed with multiple loculations in the peritonsillar space [4].

Peritonsillar infection generally is preceded by tonsillitis or pharyngitis and progresses from pharyngitis to cellulitis (phlegmon) to abscess [4]. PTA also may occur without preceding infection; such cases are thought to be caused by obstruction of the Weber glands (a group of salivary glands in the soft palate just superior to the tonsil and connected to the surface of the tonsil by a duct) [5,6]. Smoking appears to be a risk factor [7,8].

Peritonsillar infection may compromise the upper airway or spread to the surrounding structures, including the masseter and pterygoid muscles and the carotid sheath (figure 2) [3,4]. (See 'Complications' below.)

EPIDEMIOLOGY — Peritonsillar abscess (PTA) is the most common deep neck infection in children and adolescents, accounting for at least 50 percent of cases [1,2]. It occurs most frequently in adolescents and young adults but can also occur in younger children [9].

The estimated annual incidence of PTA is 30 per 100,000 persons 5 to 59 years of age [10]. In a population-based review, the overall incidence of suspected PTA, based upon clinical suspicion in children <18 years was 14 per 100,000; the incidence in adolescents was 40 per 100,000 [11]. The incidence of confirmed PTA by the presence of pus with drainage procedures was 3 per 100,000 for all ages.

MICROBIOLOGY — Peritonsillar abscesses are often polymicrobial. The predominant bacterial species are Streptococcus pyogenes (group A streptococcus [GAS]), Streptococcus anginosus, Staphylococcus aureus (including methicillin-resistant S. aureus [MRSA]), and respiratory anaerobes (including Fusobacteria, Prevotella, and Veillonella species) [12-16]. Haemophilus species are found occasionally. If appropriate microbiologic techniques are used, aerobes and anaerobes are commonly recovered simultaneously.

EVALUATION

Assess airway — The initial step in the evaluation of the patient with potential deep neck space infection is rapid assessment of the degree of upper airway obstruction. Anxious, ill-appearing patients with drooling and tripoding (leaning forward with the head in a sniffing position) must be monitored continuously in a setting where emergency artificial airway can be established if necessary. (See "Emergency evaluation of acute upper airway obstruction in children", section on 'Emergency airway assessment and management' and "Epiglottitis (supraglottitis): Clinical features and diagnosis", section on 'Clinical presentation'.)

Typical presentation — The typical clinical presentation of peritonsillar abscess (PTA) is a severe sore throat (usually unilateral), fever, and a "hot potato" or muffled voice. Pooling of saliva or drooling may be present. Trismus, related to irritation and reflex spasm of the internal pterygoid muscle, occurs in nearly two-thirds of patients; it helps to distinguish PTA from severe pharyngitis or tonsillitis [1,17]. Patients often have neck swelling and pain and may have ipsilateral ear pain [3]. Fatigue, irritability, and decreased oral intake may occur as a result of discomfort.

Historical features are important in guiding management. Important aspects of the history include frequency and severity of recurrent episodes of infectious pharyngitis, previous episodes of PTA, and snoring or other symptoms of obstructive sleep apnea. (See "Tonsillectomy and/or adenoidectomy in children: Indications and contraindications" and "Evaluation of suspected obstructive sleep apnea in children".)

Examination — The presence of trismus may limit the ability to perform an adequate examination. If drooling is present, suggesting the possibility of epiglottitis, care must be taken not to be aggressive during the examination of the oral cavity. If there is doubt about whether the patient has a PTA, epiglottitis, or other deep neck space infection, imaging or examination in the operating room may be necessary. Examination in the operating room permits controlled placement of an artificial airway [4]. (See 'Imaging' below and "Retropharyngeal infections in children" and "Epiglottitis (supraglottitis): Clinical features and diagnosis", section on 'Diagnosis'.)

Examination findings consistent with PTA include an extremely swollen and/or fluctuant tonsil with deviation of the uvula to the opposite side (picture 1) [4,18]. Alternatively, there may be fullness or bulging of the posterior soft palate near the tonsil with palpable fluctuance (picture 2). Findings in children with peritonsillar cellulitis may include an erythematous pharynx and enlarged tonsils with exudate; uvular deviation and trismus are usually absent [17]. Cervical and submandibular lymphadenopathy may be present in children with PTA or cellulitis.

Bilateral PTA is rare. Clinical diagnosis may be difficult because the classic asymmetric findings are absent [19-22]. Symptoms, such as odynophagia and trismus, may suggest the diagnosis, but are not always present. The uvula may be displaced anteriorly [23]. Bilateral PTA may be complicated by upper airway obstruction and snoring [19]. (See 'Complications' below.)

By comparison, children older than three years of age with simple streptococcal pharyngitis often have enlarged tonsils with exudate with associated tonsillar and/or palatal petechiae (picture 3). (See "Group A streptococcal tonsillopharyngitis in children and adolescents: Clinical features and diagnosis", section on 'Clinical features'.)

Laboratory evaluation — Laboratory evaluation is not necessary to make a diagnosis of PTA but may help gauge the level of illness and direct therapy.

The laboratory evaluation of a child with peritonsillar infection, therefore, might include [18]:

A complete blood count with differential: the white blood cell count (WBC) is usually elevated with a predominance of polymorphonuclear (PMN) leukocytes, although this is a nonspecific finding.

Serum electrolytes if the patient's oral intake has been decreased. (See "Clinical assessment of hypovolemia (dehydration) in children".)

A routine microbiologic test (culture or rapid antigen detection) for group A streptococcus.

Gram stain, culture (aerobic and anaerobic), and susceptibility testing of abscess fluid if a drainage procedure is performed. Although these results do not necessarily affect management of uncomplicated patients [10], they may help guide antimicrobial therapy in immunocompromised patients or those with complications or extension of infection. (See 'Drainage' below.)

Imaging — Imaging is not necessary to make the clinical diagnosis of PTA but may be helpful to differentiate PTA from peritonsillar cellulitis. For patients with clinical features of deep neck space infections (eg, retro- or parapharyngeal abscess) or epiglottitis, imaging may help differentiate these serious conditions from PTA (algorithm 1):

Distinguishing cellulitis from abscess – For patients with a clinical diagnosis of PTA, we suggest ultrasonography (US) by an experienced clinician, if available, to confirm the presence of an abscess prior to drainage [24-27]. For example, in a meta-analysis of 17 studies (812 patients, mostly adults), US was able to distinguish peritonsillar abscess from peritonsillar cellulitis with a pooled sensitivity of 86 percent (95% CI 78-91 percent), and specificity of 76 percent (95% CI 67-82 percent) with a positive likelihood ratio of 3.5 and a negative likelihood ratio of 0.19 [27]. Subgroup analysis suggested improved diagnostic characteristics for intraoral US and for radiologist-performed US. However, most patients underwent submandibular US, and the six individual studies that evaluated point-of-care US did not consistently identify the level of experience and training for the operators.

Performance of intraoral US may be hampered by trismus, pain, or gagging. Submandibular or transcervical US avoids these limitations and is uniquely suited for patients with an inadequate oropharyngeal examination [28]. US of the region by either approach appears to be more sensitive and specific than clinical examination [29,30]. PTA appears as an echo-free cavity with an irregular border, and peritonsillar cellulitis appears as a homogeneous or striated area with no distinct fluid collection [24,26,31].

In patients without airway compromise or other complications, response to a trial of antimicrobial therapy is an option if US is not definitive or not available. (See 'Approach' below.)

Because of the radiation exposure, we do not recommend computed tomography (CT) solely to distinguish PTA from cellulitis. However, contrast CT may demonstrate PTA in some patients undergoing evaluation for deep neck infections. On CT with contrast, PTA appears as a hypodense mass with ring enhancement [32]. Findings consistent with peritonsillar cellulitis include soft tissue swelling, loss of the fat planes, and lack of ring enhancement.

Deep space neck infection – CT with IV contrast is the preferred imaging modality for identifying deep space neck infections such as retro- or parapharyngeal abscess (image 1) and should be obtained instead of US in patients with suggestive clinical findings of these conditions (eg, neck stiffness, torticollis, bulging of the pharyngeal wall, soft palate, or floor of the oropharynx; cervical crepitus; trismus; and/or respiratory obstruction). (See "Deep neck space infections in adults", section on 'Clinical suspicion and urgent imaging' and "Retropharyngeal infections in children", section on 'Evaluation and diagnosis'.)

When performed, careful monitoring during transportation and CT scanning is imperative; mild airway distress can be exacerbated by sedation and positioning. CT should be omitted in children with moderate to severe respiratory distress, particularly when sedation is necessary; such children generally undergo evaluation in the operating room, where an artificial airway can be established as needed.

Lateral neck radiographs can also indicate retropharyngeal abscess (image 2) but are not definitive studies to establish the diagnosis. They are most useful when normal. (See "Deep neck space infections in adults", section on 'Clinical suspicion and urgent imaging' and "Retropharyngeal infections in children", section on 'Imaging'.)

Magnetic resonance imaging or angiography (MRI or MRA) may better delineate soft tissue involvement and vascular complications in patients with deep neck infections relative to CT but take longer. In addition, these studies have the disadvantage of requiring a patient with potentially compromised swallowing function and/or airway patency to lie supine. Sedation and, in young children or patients with airway compromise, anesthesia with endotracheal intubation may be necessary to obtain high quality images. For these reasons, MRI or MRA are seldom used. (See "Deep neck space infections in adults", section on 'Clinical suspicion and urgent imaging'.)

Epiglottitis – Patients with epiglottitis typically present with signs of upper airway obstruction and respiratory distress which typically differentiates it from PTA. Epiglottitis is less common in patients who have received vaccination against Haemophilus influenzae type b. Direct visualization of an inflamed epiglottis is the preferred method of diagnosis. However, a lateral neck plain radiograph, obtained in the presence of personnel with airway expertise and equipment to secure the airway immediately available, may be helpful in selected patients (image 3). (See 'Differential diagnosis' below and "Epiglottitis (supraglottitis): Clinical features and diagnosis", section on 'Imaging'.)

DIAGNOSIS — The diagnosis of PTA can usually be made clinically without laboratory data or imaging of any kind in the patient with medial displacement of the tonsil and deviation of the uvula (picture 1). Diagnosis is confirmed by collection of pus at the time of drainage [3,33]. Alternatively, if there is diagnostic uncertainty, an abscess may be confirmed by intraoral or submandibular ultrasonography prior to aspiration (algorithm 1). (See 'Imaging' above.)

Clinical features and imaging cannot always distinguish PTA from cellulitis [11,34]. A 24-hour trial of antimicrobial therapy (with or without antecedent imaging) may be helpful in this regard [34,35]. Failure to respond to a trial of appropriate antibiotic therapy suggests PTA, whereas response to therapy suggests cellulitis. Response is defined by improvement in at least one clinical parameter: sore throat, fever, trismus, or tonsillar bulge. (See 'Imaging' above and 'Needle aspiration' below and 'Suspected PTA' below.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of peritonsillar abscess (PTA) includes other causes of sore throat, upper airway obstruction, and pharyngeal swelling. Clinical features may be helpful in differentiating PTA from these conditions, but in some cases (particularly in young children) imaging and/or examination in the operating room may be necessary to make a definitive diagnosis (algorithm 1).

Major considerations in the differential diagnosis of PTA include [18]:

Epiglottitis – The classic teaching is that epiglottitis is more rapidly progressive than PTA and occurs in younger children. However, with widespread immunization of infants against Haemophilus influenzae type b, epiglottitis is more commonly seen in older children and adults; in these patients the presentation of epiglottitis may be subtle. Thus, epiglottitis is a diagnostic consideration in any patient with fever, sore throat, drooling, difficulty swallowing, and respiratory distress. (See "Epiglottitis (supraglottitis): Clinical features and diagnosis", section on 'Clinical presentation'.)

Oropharyngeal examination should be avoided in patients with marked respiratory distress. These patients should first have the airway secured. A rapid overview provides the approach to diagnosis and management (table 1). (See "Epiglottitis (supraglottitis): Management", section on 'Approach to airway management'.)

Retropharyngeal abscess or cellulitis – Retropharyngeal abscess or cellulitis typically occurs most commonly in younger children between two and four years of age and is associated with minimal peritonsillar findings.

Findings common to both PTA and retropharyngeal abscess include difficulty swallowing, drooling, “hot potato” or muffled voice, and trismus, although trismus is present in only about 20 percent of patients with retropharyngeal abscess. (See "Retropharyngeal infections in children", section on 'Clinical manifestations'.)

Unlike PTA, children with retropharyngeal abscess frequently have neck stiffness, pain on movement, especially neck extension (as opposed to increased pain with flexion as observed in meningitis), neck swelling or mass, neck tenderness, and if there is mediastinal extension of the abscess, chest pain. (See "Retropharyngeal infections in children", section on 'Clinical manifestations'.)

Abscess of the parapharyngeal space – In patients with abscess of the parapharyngeal space, examination may reveal bulging behind the posterior tonsillar pillar rather than superior to the tonsil [33]. Alternatively, there may be medial displacement of the lateral pharyngeal wall. The soft palate and tonsils typically appear normal.

Severe tonsillopharyngitis – Severe tonsillopharyngitis presents with bilateral equal tonsillar swelling with viral enanthem or exudate. Common causes include Epstein-Barr virus, herpes simplex virus, coxsackievirus (herpangina), adenovirus, diphtheria, group A streptococcus, or gonorrhea. Rarely, bilateral PTA can complicate severe tonsillopharyngitis. Severe trismus is less common. The presence of palpable fluctuance or ultrasonography can help distinguish bilateral PTA from tonsillopharyngitis.

MANAGEMENT

Approach — Prompt surgical intervention is indicated in patients who present with impending airway compromise, complications, enlarging masses, or significant comorbidities (eg, immunodeficiency) [4]. (See 'Drainage' below.)

Drainage, antimicrobial therapy, and supportive care are the cornerstones of management for peritonsillar abscess (PTA); peritonsillar cellulitis responds to antimicrobial therapy and supportive care alone [1,5,10,34,36-41]. Supportive care includes provision of adequate hydration and analgesia and monitoring for complications.

Hospitalization may be necessary, particularly in younger children [4]. Older patients with uncomplicated PTA who are well hydrated may be managed as outpatients if they are able to tolerate a drainage procedure and to take oral medications after the procedure [4,11].

There is no consensus regarding the optimal initial management for the remainder of patients with suspected PTA who do not require urgent surgical intervention [10,42]. In one observational study of over 210 adults and children presenting with PTA to the emergency department, medical therapy (antibiotics and corticosteroids) alone without surgical drainage had similar treatment success compared with medical therapy plus surgical drainage, with less pain, opioid use, and time off from work or school, especially for patients without trismus [43]. The approach depends upon a number of clinical factors, including the age and cooperativeness of the patient and the degree of certainty of the diagnosis (abscess versus cellulitis). Consultation with an otolaryngologist can help determine appropriate management for the individual patient.

Probable peritonsillar abscess (PTA) — We suggest needle aspiration or incision and drainage for patients with examination findings consistent with PTA (fever, trismus, voice change, peritonsillar swelling, and/or uvular deviation) who do not have indications for tonsillectomy. Needle aspiration is preferred to incision and drainage if the patient can cooperate [44]. The use of ultrasonography (US) prior to needle aspiration has been associated with improved success of aspiration compared with the landmark technique (use of anatomic landmarks as has been the tradition in otolaryngology). As an example, in a trial of 28 patients undergoing evaluation for PTA in an emergency department (18 ultimately diagnosed with PTA), aspiration facilitated by intraoral US was successful in 100 percent of patients with PTA (8 of 8) compared with 50 percent undergoing aspiration using the landmark technique (5 of 10 with PTA) [30]. Thus, when readily available by an experienced practitioner, US is suggested in patients undergoing needle aspiration in the emergency department. (See 'Needle aspiration' below and 'Incision and drainage' below.)

Probable cellulitis — We suggest a trial of antibiotics for patients with examination findings consistent with peritonsillar cellulitis who do not have indications for tonsillectomy or urgent surgical intervention. Intraoral or submandibular/transcervical ultrasonography can increase the diagnostic certainty of cellulitis. Such patients may respond to a 24 hour trial of appropriate parenteral antimicrobial therapy [4]. (See 'Imaging' above and 'Antibiotic therapy' below.)

Suspected PTA — When clinical findings do not clearly differentiate PTA from cellulitis, ultrasonography, needle aspiration, or response to antimicrobial therapy can be used to help differentiate the two conditions. (See 'Diagnosis' above.)

We suggest that patients with suspected PTA, indeterminate ultrasonographic findings, if performed, and no airway symptoms be admitted to the hospital for 24 hours of hydration, antibiotics, and analgesia without computed tomography (CT) of the neck (provided that CT is not necessary to exclude other conditions or complications). (See 'Imaging' above.)

Surgical intervention (tonsillectomy or incision and drainage) is reserved for those who do not respond to 24 hours of medical therapy [34]. This strategy was evaluated in a retrospective series of 102 children (8 months to 19 years) [35]. Approximately 50 percent of patients responded to medical therapy, and 50 percent underwent tonsillectomy, 80 percent of whom had abscesses at the time of surgery. Children younger than six years were more likely to respond to medical therapy.

Antibiotic therapy — Antibiotic therapy is indicated for all patients with peritonsillar infection [44]. In certain cooperative patients with less pain and ability to self-hydrate, antimicrobial therapy alone may be sufficient to treat a true abscess of the peritonsillar space [43]. Accordingly, an initial 24-hour trial of appropriate parenteral antimicrobials is justifiable in patients with presumed peritonsillar cellulitis who show no evidence of airway compromise, septicemia, severe trismus, or other complications [4,34]. Patients most likely to respond to a trial of antibiotics are those with probable cellulitis.

Children with PTA most likely to respond to antibiotics are those less than seven years of age, with small abscesses and fewer episodes of previous tonsillitis [45].

Parenteral — Empiric parenteral regimens are as follows [18]:

Patients who have a nontoxic appearance:

Ampicillin-sulbactam intravenously (IV) (50 mg/kg per dose [maximum single dose 3 g] every six hours in children; 3 g every six hours in adults)

or

Clindamycin IV (13 mg/kg per dose [maximum single dose 900 mg] every eight hours in children; 600 mg every six to eight hours in adults)

Patients who present with moderate or severe disease (eg, toxic appearance, temperature >39°C, drooling, and/or respiratory distress) or who do not respond to initial treatment with ampicillin-sulbactam or clindamycin:

Add one of the following to the chosen empiric regimen above:

-IV vancomycin (in children and adolescents, 15 mg/kg per dose every six hours, maximum single dose 2 g; in adults, 15 to 20 mg/kg per dose every 8 to 12 hours); adjust dose based upon therapeutic monitoring if using for longer than two to three days

or

-IV linezolid (in children and adolescents, 10 mg/kg per dose every eight hours, maximum single dose 600 mg; in adults, 600 mg every 12 hours)

Ampicillin-sulbactam does not provide antibacterial activity against methicillin-resistant S. aureus (MRSA) and, depending upon local susceptibility patterns, clindamycin may not be active against methicillin-susceptible S. aureus, MRSA, or group A streptococcus [46]. Vancomycin or linezolid provides optimal coverage for potentially resistant Gram-positive cocci.

Empiric therapy should include coverage for group A streptococcus, Staphylococcus aureus and respiratory anaerobes. Empiric therapy can be amended as necessary based upon culture results if drainage is performed or based upon clinical response to treatment. When tailoring therapy based upon culture results, it is important to bear in mind that PTAs are frequently polymicrobial, and not all microbes are consistently cultured.

If drainage is not performed, we decide about coverage for MRSA based upon the patient’s severity of illness, the prevalence of MRSA in the community, whether the patient is likely to be colonized with MRSA, and results of a swab of the nose and axilla.

Oral — Parenteral treatment is maintained until the patient is afebrile and clinically improved. Oral antibiotic therapy should then be continued to complete a 14-day course. Courses shorter than 10 days may be associated with recurrence [47].

Appropriate oral regimens for continuation of therapy in areas where S. aureus remains susceptible to methicillin include:

Amoxicillin-clavulanate

Children – 45 mg/kg per dose (maximum single dose 875 mg) every 12 hours

Adults – 875 mg every 12 hours in adults

or

Clindamycin (for patients who have responded to parenteral clindamycin)

Children – 10 mg/kg per dose (maximum single dose 600 mg) every eight hours

Adults – 300 to 450 mg every six hours

When vancomycin has been added to the parenteral regimen, oral therapy can be based upon susceptibility testing of the isolates, if available.

If empiric therapy was employed for presumed MRSA infection, oral regimens can include:

Clindamycin as above

or

Linezolid

Children

-<12 years old – 30 mg/kg per day in three doses

-≥12 years – 20 mg/kg per day in two doses

Adults – 600 mg twice per day

For all patients, the maximum daily dose for linezolid is 1200 mg

Drainage — PTA often requires surgical drainage through needle aspiration, incision and drainage, or tonsillectomy, procedures that are typically performed by an otolaryngologist [5]. Drainage with any of these procedures, in combination with antimicrobial therapy and hydration, results in resolution in more than 90 percent of cases [5,42]. Given that the procedures are comparable in efficacy, the choice of procedure depends upon other factors, such as the skill and experience of the health care provider, age and ability of the patient to cooperate, cost, and whether the patient has indications for tonsillectomy (eg, recurrent acute throat infection). Each procedure has advantages in certain situations [2,4].

An older, cooperative child, teenager, or adult without trismus or a previous history of pharyngitis may be able to undergo a needle aspiration or simple incision and drainage procedure as an outpatient with topical anesthesia or procedural sedation [5,48-51]. However, for a young, uncooperative child, the procedure must be performed in the operating suite. Special care must be taken with the administration of procedural sedation because the risk of airway complication is increased.

In the absence of a previous history of recurrent pharyngitis, needle aspiration or incision and drainage may be sufficient. In contrast, if there have been previous episodes of pharyngitis or PTA (either of which predict the possible recurrence of the PTA), then a quinsy tonsillectomy may be performed. (See 'Tonsillectomy' below.)

Needle aspiration — Needle aspiration of PTA (picture 4) may be performed in the outpatient setting with topical anesthesia by an experienced clinician (usually an otolaryngologist) [5,39,44,52]. Ultrasound may be helpful to confirm the clinical suspicion of an abscess and guide the procedure [25,30,31].

Patients generally tolerate needle aspiration better than incision and drainage because it is less invasive and less painful [10,38]. Needle aspiration is the procedure of choice for children whose general condition is too poor to tolerate a general anesthetic and those with a bleeding diathesis who wish to avoid blood transfusion [4].

In randomized trials comparing needle aspiration to incision and drainage, the procedures had similar initial success rates of >90 percent [38,42,52-54]. In one meta-analysis, needle aspiration had a 94 percent success rate for acute resolution (range 85 to 100 percent) [10]. A separate meta-analysis of 10 trials (612 patients, primarily adults) found that early recurrent abscess was more likely with needle aspiration than incision and drainage (RR 3.7). However, there was moderate heterogeneity in this pooled estimate and the evidence for recurrence was considered to be of very low quality [55]. Furthermore, the recurrence rate varied greatly by each procedure (5 to 80 percent in patients undergoing needle aspiration and 0 to 20 percent in patients undergoing incision and drainage) which differs markedly from the 10 to 15 percent recurrence rate typically described [10,42,47,52]. This wide variation suggests that there were likely significant differences in the competence of the physicians performing the procedures or the determination of recurrence that may have confounded the results [55].

Complications of needle aspiration may include hemorrhage and aspiration of pus and blood into the airway [56]. Carotid artery injury has not been reported as a complication of needle aspiration of PTA [5]; however, catastrophic hemorrhage may result from aspiration of a pseudoaneurysm mimicking PTA or necrosis of the carotid artery [57,58]. (See 'Differential diagnosis' above and 'Complications' below.)

The patient must be observed after the needle aspiration to make sure he or she can tolerate oral antimicrobial therapy, pain medications, and liquids. If the patient is not admitted to the hospital, he or she should be seen for follow-up in 24 to 36 hours [3]. (See 'Discharge instructions' below.)

Incision and drainage — Incision and drainage of PTA is usually performed by an otolaryngologist (picture 5) [5]. In older children, it may be performed in the outpatient setting with topical anesthesia or procedural sedation; general anesthesia is usually required for young children [5,33,47-49,52].

Incision and drainage is more painful than needle aspiration and causes more bleeding [5,33]. A second procedure may be required for complete resolution. Complications may include aspiration of the abscess contents.

Patients must be observed after the procedure to make sure they can tolerate oral antimicrobial therapy, pain medications, and liquids. Patients who are not admitted to the hospital should be seen for follow-up in 24 to 36 hours [3]. (See 'Discharge instructions' below.)

Tonsillectomy — Possible indications for tonsillectomy in patients with PTA include [2-5]:

Significant upper airway obstruction or other complications.

Previous episodes of severe recurrent pharyngitis or PTA (each of which predicts the possible recurrence of PTA).

Other indications for tonsillectomy (eg, chronic symptoms or signs of upper airway obstruction, such as snoring). (See "Tonsillectomy in adults: Indications" and "Tonsillectomy and/or adenoidectomy in children: Indications and contraindications".)

Failure of the abscess to resolve with other drainage techniques.

If tonsillectomy is required, it may be performed immediately (quinsy tonsillectomy or "tonsillectomy a chaud") or after resolution of the acute infection (interval tonsillectomy) [2,52,59-61]. Quinsy tonsillectomy avoids the need for repeat hospitalization and anesthesia, and minimizes loss to follow-up, but may be associated with increased risk of bleeding. Interval tonsillectomy may be more difficult technically if there is fibrosis following the acute infection.

Tonsillectomy is the most expensive of the drainage procedures, requires general anesthesia and hospitalization, and may delay drainage [5,33]. In five series involving 1027 patients, the overall incidence of bleeding after quinsy tonsillectomy in children and adults was 1 percent (range 0 to 7 percent) [4]. In the only series confined to children, none of the 55 patients had postoperative or delayed bleeding [62]. Additional complications and adverse effects of tonsillectomy are discussed separately. (See "Tonsillectomy in adults: Techniques and perioperative issues", section on 'Complications' and "Tonsillectomy and/or adenoidectomy in children: Indications and contraindications".)

Glucocorticoids — Evidence regarding the benefits of glucocorticoids in the management of PTA is inconsistent [11,63,64]. In one trial of 62 patients, glucocorticoids appeared to hasten symptomatic improvement in adolescent (>16 years) and adult patients treated with needle aspiration and intravenous antimicrobial therapy [63]. In another small trial of 41 adult patients undergoing needle aspiration for PTA, intravenous dexamethasone was associated with less pain at 24 hours than placebo but no other benefits [64]. In a retrospective case series of 249 episodes of PTA in children <18 years, glucocorticoids were used in 37 percent but without clear benefit or adverse outcomes [11]. Given the small number of patients in the trials and different results of these studies, additional information is necessary before the routine use of glucocorticoids can be recommended in the management of PTA [5].

Discharge instructions — Patients who are discharged from the emergency department or hospital after treatment for peritonsillar infection should be instructed that prompt reevaluation is necessary for:

Dyspnea

Worsening throat pain, neck pain, or trismus

Enlarging mass

Fever

Neck stiffness

Bleeding

Patients who are treated as outpatients should be seen for follow-up in 24 to 36 hours. Those who have been admitted to the hospital should have follow-up within several days of discharge.

Response to treatment — Successful treatment is defined by symptomatic improvement in sore throat, fever, and/or tonsillar swelling within 24 hours of intervention.

Treatment failure is defined by lack of symptomatic improvement or worsening despite 24 hours of antimicrobial therapy (with or without surgical drainage). Treatment failure may occur in patients who have developed complications, are infected with unusual organisms, or have underlying problems (eg, congenital cyst or tract). Reevaluation of such patients may include repeat imaging (CT with contrast to look for extension of infection) or surgical intervention. Broadening antimicrobial therapy also may be indicated.

COMPLICATIONS — Early diagnosis and prompt, appropriate management of peritonsillar infection is critical to avoiding complications. Complications of peritonsillar abscess (PTA) occur rarely but are potentially fatal. Infection can spread from the peritonsillar space to other deep neck spaces, to adjacent structures, and to the bloodstream.

Complications of PTA may include [3,4,65]:

Airway obstruction

Aspiration pneumonia if the abscess ruptures into the airway

Septicemia

Internal jugular vein thrombosis

Jugular vein suppurative thrombophlebitis (Lemierre syndrome) [66,67]

Carotid artery rupture

Pseudoaneurysm of the carotid artery (suggested by recurrent bleeding from the ear, nose, or throat, prolonged course, tachycardia, anemia, or 10th or 12th cranial nerve palsies) [68]

Mediastinitis

Necrotizing fasciitis [69,70]

Sequelae of group A streptococcus infection (when that organism is isolated) (see "Complications of streptococcal tonsillopharyngitis")

PROGNOSIS — With early and appropriate treatment, most peritonsillar infections resolve without sequelae. Recurrence is estimated to occur in 10 to 15 percent [10,42,47,52]. The risk of recurrence is increased in patients with a history of recurrent tonsillitis before development of the abscess (40 versus 9.6 percent) [71].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Peritonsillar cellulitis and abscess".)

SUMMARY AND RECOMMENDATIONS

Definition – Two terms are used to describe infection of the peritonsillar region (see 'Definition' above):

Peritonsillar cellulitis – Peritonsillar cellulitis is an inflammatory reaction of the tissue between the capsule of the palatine tonsil and the pharyngeal muscles that is caused by infection, but not associated with a discrete collection of pus. An alternate term for cellulitis is phlegmon.

Peritonsillar abscess – Peritonsillar abscess (PTA) is a collection of pus located between the capsule of the palatine tonsil and the pharyngeal muscles.

Clinical presentation – The typical clinical presentation of PTA consists of a severe sore throat, fever, a "hot potato" or muffled voice, drooling, and trismus. (See 'Typical presentation' above.)

Physical findings – Examination findings consistent with PTA include an enlarged and fluctuant tonsil with deviation of the uvula to the opposite side (picture 1). Alternatively, there may be fullness or bulging of the posterior soft palate near the tonsil with palpable fluctuance. (See 'Examination' above.)

Diagnosis – The diagnosis of PTA can be made clinically without laboratory or imaging studies in the patient with medial displacement of the tonsil and deviation of the uvula (picture 1). However, clinical features cannot always distinguish PTA from peritonsillar cellulitis. For patients with a clinical diagnosis of PTA, we suggest ultrasonography (US) by an experienced clinician, whenever available, to confirm the presence of an abscess and, if present, to help guide drainage (algorithm 1). (See 'Diagnosis' above.)

For patients with clinical features of deep neck space infections (eg, retro- or parapharyngeal abscess) or epiglottitis, imaging may help differentiate these serious conditions from PTA (algorithm 1).

Management – Antibiotic therapy is indicated for all patients with suspected peritonsillar infection. Empiric therapy should include coverage for group A streptococcus, S. aureus, and respiratory anaerobes. Therapy should be continued for 14 days. The choice of antibiotic and route of treatment depends upon the patient’s degree of illness and local patterns of antibiotic resistance. (See 'Antibiotic therapy' above.)

The need for surgical intervention and type of procedure varies by clinical findings:

Potential airway compromise or comorbidities – Prompt surgical intervention is indicated in patients with impending airway compromise, complications, enlarging masses, or significant comorbidities. (See 'Approach' above.)

Probable PTA – For cooperative patients with examination findings consistent with PTA and no indications for tonsillectomy, we suggest needle aspiration or incision and drainage in addition to antibiotic therapy (Grade 2C). (See 'Probable peritonsillar abscess (PTA)' above and 'Drainage' above.)

Peritonsillar cellulitis – For patients with examination findings consistent with cellulitis who do not have indications for tonsillectomy or urgent surgical intervention, we suggest a trial of antibiotics (Grade 2C). (See 'Probable cellulitis' above and 'Antibiotic therapy' above.)

Suspected PTA – For patients with suspected PTA, indeterminate findings on ultrasound, if performed, and no airway symptoms, we suggest hospital admission for 24 hours of hydration, antibiotics, and analgesia without computed tomography (CT) of the neck (provided that CT is not necessary to exclude other conditions or complications) (Grade 2C). Surgical intervention (tonsillectomy or incision and drainage) is reserved for those who do not respond to 24 hours of medical therapy. (See 'Suspected PTA' above.)

Treatment failure or clinical indications for tonsillectomy – For patients who fail to improve after other drainage techniques, develop complications, or have other indications for tonsillectomy (eg, previous episodes of PTA or recurrent severe pharyngitis, chronic upper airway obstruction), we suggest tonsillectomy (Grade 2C). (See 'Tonsillectomy' above.)

  1. Ungkanont K, Yellon RF, Weissman JL, et al. Head and neck space infections in infants and children. Otolaryngol Head Neck Surg 1995; 112:375.
  2. Schraff S, McGinn JD, Derkay CS. Peritonsillar abscess in children: a 10-year review of diagnosis and management. Int J Pediatr Otorhinolaryngol 2001; 57:213.
  3. Galioto NJ. Peritonsillar abscess. Am Fam Physician 2008; 77:199.
  4. Goldstein NA, Hammerschlag MR. Peritonsillar, retropharyngeal, and parapharyngeal abscesses. In: Textbook of Pediatric Infection Diseases, 8th ed, Cherry JD, Demmler-Harrison GJ, Kaplan SL, Steinbach WJ, Hotez PJ (Eds), Elsevier, Philadelphia, PA 2019. p.119.
  5. Herzon FS, Martin AD. Medical and surgical treatment of peritonsillar, retropharyngeal, and parapharyngeal abscesses. Curr Infect Dis Rep 2006; 8:196.
  6. Passy V. Pathogenesis of peritonsillar abscess. Laryngoscope 1994; 104:185.
  7. Lehnerdt G, Senska K, Fischer M, Jahnke K. [Smoking promotes the formation of peritonsillar abscesses]. Laryngorhinootologie 2005; 84:676.
  8. Dilkes MG, Dilkes JE, Ghufoor K. Smoking and quinsy. Lancet 1992; 339:1552.
  9. Friedman NR, Mitchell RB, Pereira KD, et al. Peritonsillar abscess in early childhood. Presentation and management. Arch Otolaryngol Head Neck Surg 1997; 123:630.
  10. Herzon FS. Harris P. Mosher Award thesis. Peritonsillar abscess: incidence, current management practices, and a proposal for treatment guidelines. Laryngoscope 1995; 105:1.
  11. Millar KR, Johnson DW, Drummond D, Kellner JD. Suspected peritonsillar abscess in children. Pediatr Emerg Care 2007; 23:431.
  12. Yellon RF, Falcone T, Roberson DW. Head and neck space infections. In: Bluestone and Stool's Pediatric Otolaryngology, 5th ed, Bluestone CD, Simons JP, Healy GB (Eds), People's Medical Publishing House, Shelton, CT 2014. p.1769.
  13. Klug TE. Peritonsillar abscess: clinical aspects of microbiology, risk factors, and the association with parapharyngeal abscess. Dan Med J 2017; 64.
  14. Inman JC, Rowe M, Ghostine M, Fleck T. Pediatric neck abscesses: changing organisms and empiric therapies. Laryngoscope 2008; 118:2111.
  15. Ehlers Klug T, Rusan M, Fuursted K, Ovesen T. Fusobacterium necrophorum: most prevalent pathogen in peritonsillar abscess in Denmark. Clin Infect Dis 2009; 49:1467.
  16. Plum AW, Mortelliti AJ, Walsh RE. Microbial Flora and Antibiotic Resistance in Peritonsillar Abscesses in Upstate New York. Ann Otol Rhinol Laryngol 2015; 124:875.
  17. Szuhay G, Tewfik TL. Peritonsillar abscess or cellulitis? A clinical comparative paediatric study. J Otolaryngol 1998; 27:206.
  18. Tebruegge M, Curtis N. Infections of the upper and middle airways. In: Principles and Practice of Pediatric Infectious Diseases, 5th ed, Long SS, Prober CG, Fischer M (Eds), Elsevier, New York, NY 2018. p.208.
  19. Simons JP, Branstetter BF 4th, Mandell DL. Bilateral peritonsillar abscesses: case report and literature review. Am J Otolaryngol 2006; 27:443.
  20. Safdar A, Hughes JP, Walsh RM, Walsh M. Bilateral peritonsillar abscess revisited. Ear Nose Throat J 2005; 84:791.
  21. Mobley SR. Bilateral peritonsillar abscess: case report and presentation of its clinical appearance. Ear Nose Throat J 2001; 80:381.
  22. Fasano CJ, Chudnofsky C, Vanderbeek P. Bilateral peritonsillar abscesses: not your usual sore throat. J Emerg Med 2005; 29:45.
  23. Fiechtl JF, Stack LB. Images in clinical medicine. Bilateral peritonsillar abscesses. N Engl J Med 2008; 358:e27.
  24. Froehlich MH, Huang Z, Reilly BK. Utilization of ultrasound for diagnostic evaluation and management of peritonsillar abscesses. Curr Opin Otolaryngol Head Neck Surg 2017; 25:163.
  25. Blaivas M, Theodoro D, Duggal S. Ultrasound-guided drainage of peritonsillar abscess by the emergency physician. Am J Emerg Med 2003; 21:155.
  26. Bandarkar AN, Adeyiga AO, Fordham MT, et al. Tonsil ultrasound: technical approach and spectrum of pediatric peritonsillar infections. Pediatr Radiol 2016; 46:1059.
  27. Kim DJ, Burton JE, Hammad A, et al. Test characteristics of ultrasound for the diagnosis of peritonsillar abscess: A systematic review and meta-analysis. Acad Emerg Med 2023; 30:859.
  28. Zhao X, Delaney M, Breslin K, et al. Impact of Transcervical Ultrasound for the Diagnosis of Pediatric Peritonsillar Abscesses on Emergency Department Performance Measures. J Ultrasound Med 2020; 39:715.
  29. Scott PM, Loftus WK, Kew J, et al. Diagnosis of peritonsillar infections: a prospective study of ultrasound, computerized tomography and clinical diagnosis. J Laryngol Otol 1999; 113:229.
  30. Costantino TG, Satz WA, Dehnkamp W, Goett H. Randomized trial comparing intraoral ultrasound to landmark-based needle aspiration in patients with suspected peritonsillar abscess. Acad Emerg Med 2012; 19:626.
  31. Lyon M, Blaivas M. Intraoral ultrasound in the diagnosis and treatment of suspected peritonsillar abscess in the emergency department. Acad Emerg Med 2005; 12:85.
  32. Patel KS, Ahmad S, O'Leary G, Michel M. The role of computed tomography in the management of peritonsillar abscess. Otolaryngol Head Neck Surg 1992; 107:727.
  33. Herzon FS, Nicklaus P. Pediatric peritonsillar abscess: management guidelines. Curr Probl Pediatr 1996; 26:270.
  34. Brodsky L, Sobie SR, Korwin D, Stanievich JF. A clinical prospective study of peritonsillar abscess in children. Laryngoscope 1988; 98:780.
  35. Blotter JW, Yin L, Glynn M, Wiet GJ. Otolaryngology consultation for peritonsillar abscess in the pediatric population. Laryngoscope 2000; 110:1698.
  36. Ophir D, Bawnik J, Poria Y, et al. Peritonsillar abscess. A prospective evaluation of outpatient management by needle aspiration. Arch Otolaryngol Head Neck Surg 1988; 114:661.
  37. Savolainen S, Jousimies-Somer HR, Mäkitie AA, Ylikoski JS. Peritonsillar abscess. Clinical and microbiologic aspects and treatment regimens. Arch Otolaryngol Head Neck Surg 1993; 119:521.
  38. Stringer SP, Schaefer SD, Close LG. A randomized trial for outpatient management of peritonsillar abscess. Arch Otolaryngol Head Neck Surg 1988; 114:296.
  39. Weinberg E, Brodsky L, Stanievich J, Volk M. Needle aspiration of peritonsillar abscess in children. Arch Otolaryngol Head Neck Surg 1993; 119:169.
  40. Johnson RF, Stewart MG. The contemporary approach to diagnosis and management of peritonsillar abscess. Curr Opin Otolaryngol Head Neck Surg 2005; 13:157.
  41. Hall SF. Peritonsillar abscess: the treatment options. J Otolaryngol 1990; 19:226.
  42. Johnson RF, Stewart MG, Wright CC. An evidence-based review of the treatment of peritonsillar abscess. Otolaryngol Head Neck Surg 2003; 128:332.
  43. Battaglia A, Burchette R, Hussman J, et al. Comparison of Medical Therapy Alone to Medical Therapy with Surgical Treatment of Peritonsillar Abscess. Otolaryngol Head Neck Surg 2018; 158:280.
  44. Long B, Gottlieb M. Managing Peritonsillar Abscess. Ann Emerg Med 2023; 82:101.
  45. Kim DK, Lee JW, Na YS, et al. Clinical factor for successful nonsurgical treatment of pediatric peritonsillar abscess. Laryngoscope 2015; 125:2608.
  46. Pesola AK, Sihvonen R, Lindholm L, Pätäri-Sampo A. Clindamycin resistant emm33 Streptococcus pyogenes emerged among invasive infections in Helsinki metropolitan area, Finland, 2012 to 2013. Euro Surveill 2015; 20.
  47. Apostolopoulos NJ, Nikolopoulos TP, Bairamis TN. Peritonsillar abscess in children. Is incision and drainage an effective management? Int J Pediatr Otorhinolaryngol 1995; 31:129.
  48. Bauer PW, Lieu JE, Suskind DL, Lusk RP. The safety of conscious sedation in peritonsillar abscess drainage. Arch Otolaryngol Head Neck Surg 2001; 127:1477.
  49. Suskind DL, Park J, Piccirillo JF, et al. Conscious sedation: a new approach for peritonsillar abscess drainage in the pediatric population. Arch Otolaryngol Head Neck Surg 1999; 125:1197.
  50. Luhmann JD, Kennedy RM, McAllister JD, Jaffe DM. Sedation for peritonsillar abscess drainage in the pediatric emergency department. Pediatr Emerg Care 2002; 18:1.
  51. Lamkin RH, Portt J. An outpatient medical treatment protocol for peritonsillar abscess. Ear Nose Throat J 2006; 85:658, 660.
  52. Powell J, Wilson JA. An evidence-based review of peritonsillar abscess. Clin Otolaryngol 2012; 37:136.
  53. Maharaj D, Rajah V, Hemsley S. Management of peritonsillar abscess. J Laryngol Otol 1991; 105:743.
  54. Spires JR, Owens JJ, Woodson GE, Miller RH. Treatment of peritonsillar abscess. A prospective study of aspiration vs incision and drainage. Arch Otolaryngol Head Neck Surg 1987; 113:984.
  55. Chang BA, Thamboo A, Burton MJ, et al. Needle aspiration versus incision and drainage for the treatment of peritonsillar abscess. Cochrane Database Syst Rev 2016; 12:CD006287.
  56. Steyer TE. Peritonsillar abscess: diagnosis and treatment. Am Fam Physician 2002; 65:93.
  57. Thomas JA, Ware TM, Counselman FL. Internal carotid artery pseudoaneurysm masquerading as a peritonsillar abscess. J Emerg Med 2002; 22:257.
  58. Blum DJ, McCaffrey TV. Septic necrosis of the internal carotid artery: a complication of peritonsillar abscess. Otolaryngol Head Neck Surg 1983; 91:114.
  59. Lockhart R, Parker GS, Tami TA. Role of quinsy tonsillectomy in the management of peritonsillar abscess. Ann Otol Rhinol Laryngol 1991; 100:569.
  60. Chowdhury CR, Bricknell MC. The management of quinsy--a prospective study. J Laryngol Otol 1992; 106:986.
  61. Fagan JJ, Wormald PJ. Quinsy tonsillectomy or interval tonsillectomy--a prospective randomised trial. S Afr Med J 1994; 84:689.
  62. Richardson KA, Birck H. Peritonsillar abscess in the pediatric population. Otolaryngol Head Neck Surg 1981; 89:907.
  63. Ozbek C, Aygenc E, Tuna EU, et al. Use of steroids in the treatment of peritonsillar abscess. J Laryngol Otol 2004; 118:439.
  64. Chau JK, Seikaly HR, Harris JR, et al. Corticosteroids in peritonsillar abscess treatment: a blinded placebo-controlled clinical trial. Laryngoscope 2014; 124:97.
  65. Goldenberg D, Golz A, Joachims HZ. Retropharyngeal abscess: a clinical review. J Laryngol Otol 1997; 111:546.
  66. Ramirez S, Hild TG, Rudolph CN, et al. Increased diagnosis of Lemierre syndrome and other Fusobacterium necrophorum infections at a Children's Hospital. Pediatrics 2003; 112:e380.
  67. Goldenberg NA, Knapp-Clevenger R, Hays T, Manco-Johnson MJ. Lemierre's and Lemierre's-like syndromes in children: survival and thromboembolic outcomes. Pediatrics 2005; 116:e543.
  68. Stevens HE. Vascular complication of neck space infection: case report and literature review. J Otolaryngol 1990; 19:206.
  69. Greinwald JH Jr, Wilson JF, Haggerty PG. Peritonsillar abscess: an unlikely cause of necrotizing fasciitis. Ann Otol Rhinol Laryngol 1995; 104:133.
  70. Wenig BL, Shikowitz MJ, Abramson AL. Necrotizing fasciitis as a lethal complication of peritonsillar abscess. Laryngoscope 1984; 94:1576.
  71. Kronenberg J, Wolf M, Leventon G. Peritonsillar abscess: recurrence rate and the indication for tonsillectomy. Am J Otolaryngol 1987; 8:82.
Topic 6079 Version 44.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟