Peritonsillar Abscess in Emergency Medicine

Background
Peritonsillar abscesses (PTAs) are common infections of the head and neck region and comprise approximately 30% of soft tissue head and neck abscesses.[1] Physicians must be aware of the typical clinical presentation and diagnostic strategies in order to quickly diagnose and appropriately treat these patients to prevent complications and further propagation of the infectious process. A peritonsillar abscess is shown in the image below.

Right peritonsillar abscess. The soft palate, which is erythematous and edematous, is displaced anteriorly. The patient has a "hot potatosounding" voice.

Pathophysiology
The 2 palatine tonsils are on the lateral walls of the oropharynx in the depression between the anterior and posterior tonsillar pillars. Each pillar is composed primarily of the glossopalatine and the pharyngopalatine muscles. During embryonic development, the tonsils arise from the second pharyngeal pouch as buds of endodermal cells.[2] The tonsils then grow irregularly and reach their ultimate size and shape at approximately age 6-7 years. Each tonsil is surrounded by a capsule, a specialized portion of the intrapharyngeal aponeurosis that covers the medial portion of the tonsils and provides a path for blood vessels and nerves.[2] It is within this potential space between the tonsil and capsule that peritonsillar abscesses form.[3] Note that the peritonsillar space is anatomically contiguous with several deeper spaces, and infections can potentially involve the parapharyngeal and retropharyngeal spaces.[4] Peritonsillar abscesses usually progress from tonsillitis to cellulitis and ultimately to abscess formation. Weber glands are thought to also play a key role in the etiology of the infection. These mucous salivary glands are located superior to the tonsil in the soft palate and clear the tonsillar area of debris. If these glands become inflamed, local cellulitis develops. As the infection progresses, inflammation worsens and results in tissue necrosis and pus formation, most commonly just above the superior pole of the tonsil where the glands are located.[3]

Epidemiology
Frequency
United States

In the United States, the incidence of peritonsillar abscess has been estimated at 30 cases per 100,000 persons per year, accounting for approximately 45,000 cases annually.It has also been estimated to result in at least $150 million a year in health care expenditures. [5] Most infections occur during November to December and April to May, which coincide with the highest incidence rates of streptococcal pharyngitis and exudative tonsillitis.[3] International A higher rate due to recurrence and antibiotic resistance is reported internationally.

Mortality/Morbidity
Mortality of peritonsillar abscess is unknown. Morbidity of peritonsillar abscess is due mostly to pain, cost of treatment, lost time from work and school, and complications.

Race
No racial predilection of peritonsillar abscess is noted.

Sex
The male-to-female ratio of peritonsillar abscess is equal.

Age
Peritonsillar abscess can occur in anyone aged 10-60 years according to one source, although peritonsillar abscess is most commonly seen in those aged 20-40 years.[6] The younger children who get peritonsillar abscess are often immunocompromised.

History
Symptoms of peritonsillar abscess usually begin 3-5 days prior to evaluation. Fever Malaise Headache Neck pain Throat pain markedly more severe on the affected side and occasionally referred to the ipsilateral ear Dysphagia Change in voice Otalgia Odynophagia

Physical
Physical findings of peritonsillar abscess include the following:

Mild/moderate distress Fever Tachycardia Dehydration Drooling, salivation, trouble handling oral secretions

Trismus resulting from pain from inflammation and spasm of masticator muscles Hot potato/muffled voice Rancid or fetor 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

Causes
Peritonsillar abscesses are usually polymicrobial. A recent prospective study carried out to elucidate significant pathogens involved in peritonsillar abscesses demonstrated that the most prominent aerobic pathogen was Streptococcus pyogenes. Other aerobic pathogens isolated included Staphylococcus aureus,Neisseria species, and Corynebacterium species. In the same study, the most common anaerobic species found was Fusobacterium necrophorum, an obligate, anaerobic, Gram-negative rod. Other Fusobacterium species andPrevotella species were also isolated. Though the study was carried out in Denmark, studies within the United States have demonstrated similar results.[3, 7, 2, 8]

Differential Diagnoses

Dental, Infections

Laboratory Studies
No definitive studies are required for the diagnosis of peritonsillar abscess, although one might consider obtaining CBC count and electrolyte evaluations if the patient had significant comorbidities. Monospot test/heterophile antibody test can be performed to rule out infectious mononucleosis if the etiology is unclear. Culture of fluid from needle aspiration may be performed. Blood cultures may be indicated if the clinical presentation is severe.

Imaging Studies
Lateral soft tissue neck radiographs may help rule out other causes. The anteroposterior (AP) view of the neck may demonstrate distortion of soft tissue. Intraoral ultrasonography (US) has a sensitivity of 95.2% and specificity of 78.5%. This method is cost-effective and fast, although it does require a cooperative patient. A recent study carried out at an academic level I emergency department included 43 patients who received intraoral US for suspected peritonsillar abscess. Thirty-five were diagnosed with an abscess on US, and these patients subsequently received needle aspiration using US guidance. There was one false positive, but no patients returned unexpectedly after drainage, and, on reexamination, there was no evidence of persistent or recurrent peritonsillar abscess or cellulitis. This study supports the

use of US for both the diagnosis and treatment of peritonsillar abscesses.[9] Prior studies of US use have shown similar successful results.

Head and neck CT scanning with intravenous (IV) contrast is useful if incision and drainage fails, if the patient cannot open his or her mouth, or if the patient is young (< 7 y) and uncooperative. A hypodense fluid collection with rim enhancement may be seen in the affected tonsil. Foreign bodies, such as fish or chicken bones, may also be found as an inciting factor.

Procedures
Three options are available for acute surgical management of peritonsillar abscess: needle aspiration, incision and drainage, and quinsy tonsillectomy (eg, simultaneous tonsillectomy with open abscess drainage). A systematic review by Johnson et al attempted to determine the best technique for acute surgical management. Forty-two articles were analyzed. Five level I clinical studies indicated that all 3 techniques were equally effective for initial management.
[10]

Needle aspiration
The main advantage of needle aspiration is ease of the procedure, decreased pain for the patient, and cost-effectiveness.[5, 10] The patient should be sitting upright. Lidocaine with epinephrine should be used to anesthetize the area. A 16- to 18-gauge needle with a 10-mL syringe should be used to aspirate from the area that is most fluctuant. A needle guard may be used to prevent accidental carotid artery puncture due to the tip of the needle migrating too far posteriorly. Only 0.5 cm of the needle needs to be exposed. If a needle guard is unavailable, a curved clamp can be used to expose a small portion of the needle before inserting it into the area for aspiration. Aspirate at the superior pole initially, as this is the most common place for abscess development. Aspiration of the middle one third and then the lower one third should then be attempted if pus is not returned from the superior pole. Also, see Drainage, Peritonsillar Abscess.

Pus is aspirated through a wide-bore needle from the right peritonsillar abscess. An additional incision will be made to drain any other pus pockets.

Abscess incision and drainage [11] The patient should be sitting upright with a pan available to spit out any blood or pus. A tongue depressor is used to retract the tongue. After local infiltration with lidocaine with epinephrine, a No. 11 blade scalpel is used to make a small incision 0.5 cm long and no more than 1 cm deep. Be certain that the incision is not extended laterally as the carotid artery lies in that vicinity. Use a small hemostat to probe the abscess and release the pus. To prevent the risk of aspiration, allow the patient to hold the Yankauer catheter tip and to suction the pus.

Tonsillectomy
No clear evidence indicates that routine elective tonsillectomy is indicated to prevent future peritonsillar abscesses. However, if the patient has had multiple recurrent episodes of peritonsillar abscessor has other clear indications such as sleepdisordered breathing, elective tonsillectomy should be considered.[5] Additionally, if general anesthesia is required because of the patient's age or lack of cooperation, tonsillectomy should be considered, as the complication rate is low and although the data do not support this, consideration for the most definitive procedure should be made.[5, 10]

Prehospital Care
Prehospital care for peritonsillar abscess includes transport with supplemental oxygen.

Emergency Department Care

ABCs, paying attention to the patient's airway, should be evaluated. If the patient's airway is compromised, he or she needs immediate endotracheal intubation. If this cannot be completed, a cricothyroidotomy or a tracheotomy may be required. Alternatively, if the resources are available, one study concluded that awake fiberoptic bronchoscopy was the method of choice for intubating patients with significant pharyngeal edema.[5] These patients are often dehydrated because of their avoidance of food and liquid and may need fluid resuscitation. Antipyretics should be administered for elevated temperature, and adequate analgesia should be provided for pain. Acute surgical management should be carried out as discussed above. Empiric antibiotics should be administered. Steroids are often used as adjunctive treatment. In the systematic review carried out by Johnson et al, no published studies on the use of steroids in peritonsillar abscess were found, but the authors did identify a randomized controlled trial that demonstrated a benefit

for steroids for severe, acute pharyngitis. It is likely that the use of steroids for PTA derived from this management strategy Patients can be managed in an outpatient setting unless they show signs of toxicity, sepsis, airway compromise, inability to swallow, or other complications.

Consultations
An otolaryngologist may be required if the patient's presentation is severe. An anesthesiologist or surgeon may be required for management of a difficult airway

Medication Summary
Antibiotics are the main component of therapy. Begin antibiotic therapy prior to needle aspiration and report of culture results. Though several studies have shown intravenous penicillin alone is clinically effective (provided the abscess is adequately drained), other studies have reported that greater than 50% of cultures grow beta-lactamase producing anaerobes, leading to the tendency to use broader-spectrum antibiotics such as clindamycin or a second- or third-generation oral cephalosporin. In those patients allergic to penicillin, clindamycin is a good choice. Analgesics and throat washes are recommended. As mentioned above, some physicians report using adjunctive steroids to decrease edema and pain.

Antibiotics
Class Summary
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
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Clindamycin (Cleocin)
Semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of parent compound lincomycin. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Widely distributes in the body without penetration of CNS. Protein bound and excreted by the liver and kidneys. Oral or parenteral antibiotic for anaerobic or susceptible streptococcal, pneumococcal, or staphylococcal species. Considered to have good absorption into bloodstream in both oral and parental forms.
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Penicillin G benzathine (Bicillin L-A)

DOC in combination with metronidazole. Effective in approximately 98% of patients. Interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.
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Metronidazole (Flagyl)
DOC in combination with penicillin. Effective in approximately 98% of treated patients. Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Appears to be absorbed into the cells of microorganisms that contain nitroreductase. Unstable intermediate compounds are formed that bind DNA and inhibit synthesis, causing cell death.
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Nafcillin (Unipen)
Initial therapy for suspected penicillin G-resistant streptococcal or staphylococcal infections. Use parenteral therapy initially in severe infections. Change to PO therapy as condition warrants. Because of thrombophlebitis, particularly in elderly persons, administer parenterally only for short term (1-2 d); change to PO route as clinically indicated.
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Erythromycin (E.E.S, Ery-Tab, Erythrocin)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal (including S aureus) and streptococcal infections. Indicated if patient is allergic to penicillin.

Further Inpatient Care

Observation, imaging studies, airway management, and intravenous hydration may be required. Other methods of operative management strategy may be indicated and should be performed by an otolaryngologist. Recurrence obviates the need for a second hospitalization for interval tonsillectomy after needle decompression or incision and drainage. To prevent recurrence, interval tonsillectomy may be considered 3-4 weeks after resolution of edema and symptoms.

Further Outpatient Care

If outpatient care is used, the patient can be discharged on an appropriate regimen of antibiotics and pain medications.

Relative indications for elective tonsillectomy can be identified in almost a third of all patients who present with paratonsillar abscess (eg, recurrent tonsillitis).

Complications
Complications of peritonsillar abscess may include the following:

Necrotizing soft tissue infection of the neck and chest wall[12] Recurrence Aspiration, which may lead to pneumonia or pneumonitis Cervical abscess Mediastinitis Meningitis Sepsis Cerebral abscess Jugular vein thrombosis Carotid artery rupture/necrosis Carotid artery injury (from I&D or needle aspiration)

Prognosis
Uncomplicated, treated peritonsillar abscess has a resolution rate of 94%. In the United States, the recurrence rate is 10%, although this rate jumps to 15% internationally.

Patient Education
For patient education resources, see the Ear, Nose, and Throat Center, as well asPeritonsillar Abscess, Tonsillitis, and Antibiotics.

ABSES PERITONSIL
Diposkan oleh Taufik Abidin oleh: Taufik Abidin

PENDAHULUAN Abses peritonsiler dapat terjadi pada umur 10-60 tahun, namun paling sering terjadi pada umur 20-40 tahun. Pada anak-anak jarang terjadi kecuali pada mereka yang menurun sistem immunnya, tapi infeksi bisa menyebabkan obstruksi jalan napas yang signifikan pada anak-anak. Infeksi ini memiliki proporsi yang sama antara laki-laki dan perempuan. Bukti menunjukkan bahwa tonsilitis kronik atau percobaan multipel penggunaan antibiotik oral untuk tonsilitis akut merupakan predisposisi pada orang untuk berkembangnya abses peritonsiler. Di Amerika insiden tersebut kadang-kadang berkisar 30 kasus per 100.000 orang per tahun, dipertimbangkan hampir 45.000 kasus setiap tahun4.

Abses leher dalam terbentuk dalam ruang potensial diantara fasia leher dalam sebagai akibat dari penjalaran infeksi dari berbagai sumber, seperti gigi, mulut, tenggorok, sinus paranasal, telinga tengah dan leher tergantung ruang mana yang terlibat. Gejala dan tanda klinik dapat berupa nyeri dan pembengkakan. Abses peritonsiler (Quinsy) merupakan salah satu dari Abses leher dalam dimana selain itu abses leher dalam dapat juga abses retrofaring, abses parafaring, abses submanidibula dan angina ludovici (Ludwig Angina) 3. Abses peritonsiler adalah penyakit infeksi yang paling sering terjadi pada bagian kepala dan leher. Gabungan dari bakteri aerobic dan anaerobic di daerah peritonsilar. Tempat yang bisa berpotensi terjadinya abses adalah adalah didaerah pillar tonsil anteroposterior, fossa piriform inferior, dan palatum superior4. Abses peritonsil terbentuk oleh karena penyebaran organisme bakteri penginfeksi tenggorokan kesalah satu ruangan aereolar yang longgar disekitar faring menyebabkan pembentukan abses, dimana infeksi telah menembus kapsul tonsil tetapi tetap dalam batas otot konstriktor faring5. Peritonsillar abscess (PTA) merupakan kumpulan/timbunan (accumulation) pus (nanah) yang terlokalisir/terbatas (localized) pada jaringan peritonsillar yang terbentuk sebagai hasil dari suppurative tonsillitis. ETIOLOGI Abses peritonsil terjadi sebagai akibat komplikasi tonsilitis akut atau infeksi yang bersumber dari kelenjar mucus Weber di kutub atas tonsil. Biasanya kuman penyebabnya sama dengan kuman penyebab tonsilitis. Biasanya unilateral dan lebih sering pada anak-anak yang lebih tua dan dewasa muda2. Abses peritonsiler disebabkan oleh organisme yang bersifat aerob maupun yang bersifat anaerob. Organisme aerob yang paling sering organisme menyebabkan anaerob abses yang peritonsiler berperan adalah Streptococcus pyogenes(Group A Beta-hemolitik streptoccus), Staphylococcus aureus, danHaemophilus influenzae. Sedangkan adalah Fusobacterium. Prevotella, aerobik dan anaerobik6. PATOLOGI Porphyromonas, Fusobacterium,dan Peptostreptococcus

spp. Untuk kebanyakan abses peritonsiler diduga disebabkan karena kombinasi antara organisme

Patofisiologi PTA belum diketahui sepenuhnya. Namun, teori yang paling banyak diterima adalah kemajuan (progression) episode tonsillitis eksudatif pertama menjadi peritonsillitis dan kemudian terjadi pembentukan abses yang sebenarnya (frank abscess formation). Daerah superior dan lateral fosa tonsilaris merupakan jaringan ikat longgar, oleh karena itu infiltrasi supurasi ke ruang potensial peritonsil tersering menempati daerah ini, sehingga tampak palatum mole membengkak. Abses peritonsil juga dapat terbentuk di bagian inferior, namun jarang. Pada stadium permulaan, (stadium infiltrat), selain pembengkakan tampak juga permukaan yang hiperemis. Bila proses berlanjut, daerah tersebut lebih lunak dan berwarna kekuningkuningan. Tonsil terdorong ke tengah, depan, dan bawah, uvula bengkak dan terdorong ke sisi kontra lateral. Bila proses terus berlanjut, peradangan jaringan di sekitarnya akan menyebabkan iritasi pada m.pterigoid interna, sehingga timbul trismus. Abses dapat pecah spontan, sehingga dapat terjadi aspirasi ke paru. Selain itu, PTA terbukti dapat timbul de novo tanpa ada riwayat tonsillitis kronis atau berulang (recurrent) sebelumnya. PTA dapat juga merupakan suatu gambaran (presentation) dari infeksi virus Epstein-Barr (yaitu: mononucleosis). GEJALA KLINIS DAN DIAGNOSIS Selain gejala dan tanda tonsilitis akut, terdapat juga odinofagia (nyeru menelan) yang hebat, biasanya pada sisi yang sama juga dan nyeri telinga (otalgia), muntah (regurgitasi), mulut berbau (foetor ex ore), banyak ludah (hipersalivasi), suara sengau (rinolalia), dan kadang-kadang sukar membuka mulut (trismus), serta pembengkakan kelenjar submandibula dengan nyeri tekan. Bila ada nyeri di leher (neck pain) dan atau terbatasnya gerakan leher (limitation in neck mobility), maka ini dikarenakan lymphadenopathy dan peradangan otot tengkuk (cervical muscle inflammation)1. Prosedur diagnosis dengan melakukan Aspirasi jarum (needle aspiration). Tempat aspiration dibius / dianestesi menggunakan lidocaine dengan epinephrine dan jarum besar (berukuran 1618) yang biasa menempel pada syringe berukuran 10cc. Aspirasi material yang bernanah (purulent) merupakan tanda khas, dan material dapat dikirim untuk dibiakkan.

Pada penderita PTA perlu dilakukan pemeriksaan7: 1. Hitung darah lengkap (complete blood count), pengukuran kadar elektrolit (electrolyte level measurement), dan kultur darah (blood cultures). 2. Tes Monospot (antibodi heterophile) perlu dilakukan pada pasien dengan tonsillitis dan bilateral cervical lymphadenopathy. Jika hasilnya positif, penderita memerlukan evaluasi/penilaian hepatosplenomegaly. Liver function tests perlu dilakukan pada penderita dengan hepatomegaly. 3. Throat culture atau throat swab and culture: diperlukan untuk identifikasi organisme yang infeksius. Hasilnya dapat digunakan untuk pemilihan antibiotik yang tepat dan efektif, untuk mencegah timbulnya resistensi antibiotik. 4. Plain radiographs: pandangan jaringan lunak lateral (Lateral soft tissue views) dari nasopharynx dan oropharynx dapat membantu dokter dalam menyingkirkan diagnosis abses retropharyngeal. 5. Computerized tomography (CT scan): biasanya tampak kumpulan cairan hypodense di apex tonsil yang terinfeksi (the affected tonsil), dengan peripheral rim enhancement. 6. Ultrasound, contohnya: intraoral ultrasonography. KOMPLIKASI Komplikasi yang mungkin terjadi ialah2: 1. Abses pecah spontan, mengakibatkan perdarahanm aspirasi paru, atau piema. 2. Penjalaran infeksi dan abses ke daerah parafaring, sehingga terjadi abses parafaring. Kemudian dapat terjadi penjalaran ke mediastinum menimbulkan mediastinitis.

3. Bila terjadi penjalaran ke daerah intracranial, dapat mengakibatkan thrombus sinus kavernosus, meningitis, dan abses otak. Sejumlah komplikasi klinis lainnya dapat terjadi jika diagnosis PTA diabaikan. Beratnya komplikasi tergantung dari kecepatan progression penyakit. Untuk itulah diperlukan penanganan dan intervensi sejak dini. DIAGNOSIS BANDING Infiltrat peritonsil, tumor, abses retrofaring, abses parafaring, aneurisma arteri karotis interna, infeksi mastoid, mononucleosis, infeksi kelenjar liur, infeksi gigi, dan adenitis tonsil2,8,9. TERAPI Pada stadium infiltrasi, diberikan antibiotika dosis tinggi dan obat simtomatik. Juga perlu kumur-kumur dengan air hangat dan kompres dingin pada leher. Antibiotik yang diberikan ialah penisilin 600.000-1.200.000 unit atau ampisilin/amoksisilin 3-4 x 250-500 mg atau sefalosporin 34 x 250-500 mg, metronidazol 3-4 x 250-500 mg2. Bila telah terbentuk abses, dilakukan pungsi pada daerah abses, kemudian diinsisi untuk mengeluarkan nanah. Tempat insisi ialah di daerah yang paling menonjol dan lunak, atau pada pertengahan garis yang menghubungkan dasar uvula dengan geraham atas terakhir. Intraoral incision dan drainase dilakukan dengan mengiris mukosa overlying abses, biasanya diletakkan di lipatan supratonsillar. Drainase atau aspirate yang sukses menyebabkan perbaikan segera gejalagejala pasien. Bila terdapat trismus, maka untuk mengatasi nyeri, diberikan analgesia lokal di ganglion sfenopalatum. Kemudian pasien dinjurkan untuk operasi tonsilektomi a chaud. Bila tonsilektomi dilakukan 3-4 hari setelah drainase abses disebut tonsilektomi a tiede, dan bila tonsilektomi 4-6 minggu sesudah drainase abses disebut tonsilektomi a froid. Pada umumnya tonsilektomi dilakukan sesudah infeksi tenang, yaitu 2-3 minggu sesudah drainase abses2. Tonsilektomi merupakan indikasi absolut pada orang yang menderita abses peritonsilaris berulang atau abses yang meluas pada ruang jaringan sekitarnya. Abses peritonsil mempunyai kecenderungan besar untuk kambuh. Sampai saat ini belum ada kesepakatan kapan tonsilektomi dilakukan pada abses peritonsil. Sebagian penulis menganjurkan tonsilektomi 68 minggu

kemudian mengingat kemungkinan terjadi perdarahan atau sepsis, sedangkan sebagian lagi menganjurkan tonsilektomi segera10.

Penggunaan steroids masih kontroversial. Penelitian terbaru yang dilakukan Ozbek mengungkapkan bahwa penambahan dosis tunggal intravenous dexamethasone pada antibiotik parenteral telah terbukti secara signifikan mengurangi waktu opname di rumah sakit (hours hospitalized), nyeri tenggorokan (throat pain), demam, dan trismus dibandingkan dengan kelompok yang hanya diberi antibiotik parenteral. PROGNOSIS Abses peritonsoler hampir selalu berulang bila tidak diikuti dengan tonsilektomi., maka difunda sampai 6 minggu berikutnya. Pada saat tersebut peradangan telah mereda, biasanya terdapat jeringan fibrosa dan granulasi pada saat oprasi. DAFTAR PUSTAKA 1. Adams, G.L. 1997. Penyakit-Penyakit Nasofaring Dan Orofaring. Dalam: Boies, Buku Ajar Penyakit THT, hal.333. EGC,Jakarta. 2. Fachruddin, darnila. 2006. Abses Leher Dalam. Dalam: Buku Ajar Ilmu Kesehatan, TelingaHidung-Tenggorokan, hal. 185. Balai Penerbit FKUI, Jakarta. 3. Soepardi,E.A, Iskandar, H.N, Abses Peritonsiler, Buku Ajar Ilmu Kesehatan Telinga, Hidung dan Tenggorokan, Jakarta: FKUl, 2000; 185-89. 4. Mehta, Ninfa. MD. Peritonsillar Abscess. Available from.www.emedicine.com. Accessed at Juli 2007. 5. Adrianto, Petrus. 1986. Penyakit Telinga, Hidung dan Tenggorokan, 296, 308-09. EGC, Jakarta.

6. Bailey, Byron J, MD. Tonsillitis, Tonsillectomy, and Adenoidectomy. In : Head and Neck Surgey-Otolaryngology 2nd Edition. Lippincott_Raven Publisher. Philadelphia. P :1224, 123334. 7. Anurogo, Dito. 2008. Tips Praktis Mengenali Abses Peritonsil.

Accessed: http://www.kabarindonesia.com/berita.php?pil=3&dn=20080125161248. 8. Preston, M. 2008. Peritonsillar Abscess (Quinsy).

accessed:http://www.patient.co.uk/showdoc/40000961/. 9. STEYER, T. E. 2002. Peritonsillar Abscess: Diagnosis and Treatment.

accessed:http://www.aafp.org/afp/20020101/93.html. 10. Hatmansjah. Tonsilektomi. Cermin Dunia Kedokteran Vol. 89, 1993. Fakultas Kedokteran Universitas Indonesia, hal : 19-21.