Pathogenesis of Peritonsillar Abscess ‘Victor Passy, MD ‘The pathogenesis of peritonsillar abscess is de- scribed in textbooks asbeing adirect communication snd progression of acute exudative tonsillitis. Little judy has been done on the true etiology and patho- ‘genesis of peritonsillar abscess. This paper focuses ‘on the pathogenesis of peritonsillar abscess. A group of salivary glands (Weber's glands) proven to be lo- ‘cated in the supratonsillar space have been shown to be implicated in the pathogenesis of peritonsillar abscess. A review of peritonsillar abscess has been ‘undertaken, and evidence has been presented to sup- port the premise that the true cause for peritonsillar abscess is not necessarily an extension of an acuto exudative tonsillitis, but an abscess formation of We- ber’ salivary glands in the supratonsillar fossa. INTRODUCTION In the second and third centuries 0, Celsust described two types of tonsil disease, one in which there was swelling without ulceration and the other in which there was swelling and obstruction to breath- ing. He recommended draining the tonsils if pus did not drain spontaneously. This report by Celsus theo- retically may be the first documented account of and treatment for peritonsillar abscess. Since that time, many instruments and modifica- tions of instruments for excising the tonsils have been proposed.2-4 A review of the literature indicates that peritonsillar abscess, as we know it today, was first described in the early 1700s, and was only vaguely mentioned prior to the beginning of this century. Before the advent of antibiotics in the late 1930s and early 1940s, some type of surgical intervention was required for most peritonsillar abscess infections. ‘Usually, total tonsillectomy was done after the infec- tion subsided (interval tonsillectomy), After 1947, im- ‘mediate surgical excision for these cases was popular (Chaud tonsillectomy) For the past 8 years, the treat- ment for peritonsillar abscess by needle aspiration and use of parenteral antibiotics rather than immedi- ate incision and drainage has grown in popularity. From the Department of Otalaryngology—Head and Neck Surgery, ‘Univer of Califone, vie. ‘itr Note: This Mamuerit was aceptd for publiaton Janay 12,1988, ‘Send Reprint Reguetsta Vitor Puy MD, University of Califa, Irvin, Dparenent of DtlnrynglogyHetd and Neck Surgery 101 Cy Drive South, Orange, CA 82068, Laryngoscope 104: February 1884 ‘Some surgeons do not advocate tonsillectomy in pa- tients without previous tonsillar infections because the recurrence rate, previously thought to be very high, is now interpreted as very low. This recent change in thinking may imply that the pathogenesis of peritonsillar abscess (quinsy) is not as clear-cut as described in modern textbooks. ‘The textbook definition of peritonsillar abscessis “The involvement of an episode of acute exudative tonsillitis inappropriately treated or not treated at all ‘that progresses to abscess formation’ Itis important that we evaluate and question with logic the definition proposed by our textbooks for peritonsillar abscess. Parkinson (1951) in his book, Tonsils and Allied Problems,” described the anatomy of the tonsillar fossa and its surroundings, an anatomical study ‘which has been overlooked by today's anatomists. The ‘mucous membrane of the oral cavity is studded with selivary glands. Parkinson mentions a group of sali- vary glands described by Weber in 1927 as Weber's glands,® which are located in the supratonsillar space, just above the tonsil in the soft palate. These glands consist of approximately 20 to 25 mucous salivary glandular structures sending a common duct from the gland posterior to the midportion of the tonsil, pene- trating the capsule of the tonsil and sending its ductal system to the surface ofthe tonsil (Fig. 1). The salivary secretions are thought to assist digestion of food par- tially caught in the tonsil crypts.” Many clinical findings of peritonsillar abscess come to mind. Of the many types of peritonsillar abscesses encountered, the initial swelling is almost always situated in the soft palate ust above the tonsil, causing the tonsil to bulge forward medially. Only in rare instances of peritonsillar abscess are the tonsils actively infected with exudation either unilaterally or bilaterally. The classic onset of peritonsillar abscess symptoms begins only 3 or 5 days before the evalua- tion and diagnosis. The clinician should reexamine current concepts and ask the following questions: 1. Where is the source of the abscess. 2. What: time clement does the abscess form. 3. Why is the abscess almost always in the supratonsillar space bulging into the soft palate. 4. Why are the tonsils almost never involved in exudation? ‘The clinical signs, symptoms, and pathogenesis, of abscesses known today do not fall into line. Passy: Peritonsiiar Abscess 185seating on the fone and Allog Problems. Macmillan, New York, 1851.) ‘A review of Parkinson's anatomical description of the tonsillar fossa and his deseription of the group of selivary glands in the supratonsillar space, called ‘Weber's glands, should stimulate one to question this as the possible etiology and site of origin of peritonsil lar abscess and not, as the current literature de- seribes, as secondary to a progression of acute exuda- tive tonsillitis. The functional significance of Weber's glands is described as simply to secrete salivary juices, onto the surface ofthe tonsillar crypts, thus helping to digest trapped remnants of food and debris for diges- tion and evacuation.” If it is true that this group of salivary glands is the probable etiological cause and predisposing factor in peritonsillar abscess, this could explain why peritonsillar abscess is always in the supratonsillar space. This etiology would explain why the tonsils are not exudative at the onset of peritonsil- lar abscesses, why the symptomatology of sore throat, begins only 8 to 5 days from the onset of diagnosis, and why tonsillectomy prevents recurrence of periton- sillar abscesses. ‘This paper describes a new theory for the patho- genesis of peritonsillar abscess. DISCUSSION In the superior pole of the tonsillar fossa, small Laryngoscope 104: February 1994 186 ‘masses of fat-like tissue rest on the tonsillar capsule within this supratonsillar space.” Weber®® first de- scribed these mucous salivary glands in 1927. Baum! ‘and Keleman** confirm that these glands are mucous in type and are similar to the sublingual salivary glands. Some state that the ducts of these glands open into the tonsillar crypts, but others believe the ducts empty into the superior tonsillar pole.70.1 Tn the supratonsillar space, these glands are normally clus- tered in groups of 20 or 80 glandular strutures (We- ber’s glands) ‘The precise role of bacterial virulence is not clear in the development of peritonsillar infections. Cul- tures have grown aerobic and anaerobic bacterial populations as well as mixed flora involving both gram-negative and gram-positive organisms. Over half of the cases of quinsy have a history of previous tonsillar infections.22 Peritonsillar cellulitis and abscess formation are fairly common occurrences in the young adult, but are rare in young children and in older people. This im- plies a peculiar susceptibility to infection from im- mune deficiency, malnutrition, diabetes, leukemia, or other systemic diseases. Freed and Forest reported 27% of their series of 84 peritonsillar abscesses were regarded as having significant dental caries and al- lergies, and postulated these maladies as being con- tributory factors in the etiology of chronic tonsillitis, which probably plays a role in the development of peritonsillar abscess. In the development of peritonsillar abscess, tis- sue necrosis and pus formation result in abscess between the tonsillar capsule and the lateral pharyn- geal wall and the supratonsillar space. In one series, only 10% of abscesses were localized outside of this, area.Sa4 As infectious fibrosis increases, the normal plane of cleavage existing between the tonsil and its under- lying aponeurosis is obliterated. This scarring can cause ductal obstruction to Weber's salivary mucous gland secretions, resulting in a glandular distension. If not treated appropriately, one episode or repeated attacks of peritonsillar cellulitis, or chronic infections, of Weber's glands and its ductal system, can result in abscess formation. This disease may be associated with an attack of acute exudative follicular tonsillitis; however, in most; cases the tonsil is not exudative? (Table ). The abscess formation primarily involves the supratonsillar space of the soft palate located immediately above the supe- rior pole of the tonsil. This supratonsillar space ini tially becomes inflamed and cellulitis begins, which results in pus formation into the supratonsillar space and surrounding muscles, especially the internal ptyergoids, producing spasm of the muscle with re- sulting trismus. Ifuntreated, the abscess will rupture into the superior tonsillar crypt or may point and drain along the bulging of the soft palate, discharging Passy: Perltonsilar AbscessTABLE ‘Summary o 100 Consecutive Peilonsila Abscess Cases. ‘ge Group 4-76 years ‘Average age group 2.4 years Greatest age group 20-40 years (65%) Location of abscess ‘Supratonslar fossa 90% ‘Abscess elsewhere 1% Bilateral abscess 1% Presenting symptoms ‘Sore throat 100% yao 97% Fever 97% “Tiemus 100% Daye rom symptom to abscoss 2-8 dye (avg. = 3.8 doy) ton ‘No exudation tonsit 96% Exudation tons om No provious toniitis 7% Previous tonsitis 23% History of recurcont pharyngitis 100% Recurronce of abscess ‘After tonsilactomy om No tonsllectomy 8% its contents into the throat or mouth. ‘Teed! points out that peritonsillar abscesses are rare in infants and children. Berman"® cites a patient 9 weeks old who developed peritonsillar abscess, youngest in the literature reviewed. Beeden and Evans!” state that the mean age for this disease is between 20 and 30 years, affecting males and females equally. The swelling of the abscess has been de- scribed mainly as occurring in the supratonsillar space in the soft palate, although rare instances are reported where the swelling and abscess occurred in ‘and around the tonsil.18 Cultures from the drainage of the abscess show any types of bacteria, no one dominant type being found in any abscess.1°-2° Sever- al authors report rare cases in which bilateral tonsil- lar abscesses have been identified.2*-2" Ifthis disease is not treated by tonsillectomy, the recurrence rate has been reported to range from 7% by Holt and ‘Tinsley®® to 63% by Nielsen and Greisen.? Some studies report recurrence of abscesses even after ton- sillectomy.50.31 ‘The most serious complications of the peritonsil- lax abscess occurred prior to the 1980s, before the advent of antibiotics, when spreading parapharyn- ‘geal infections would track along the carotid sheath to form excessive infective planes.?? Fatal neurologic sequelae resulted if the neck was not handled ade- quately under these circumstances. °°-36 In addition to hemorrhage and infections of the parapharyngeal spaces, other complications of peri- tonsillitis and peritonsillar abscess are endocarditis, polyarthritis, cervical abscess, and general sepsis. ‘When treated early with appropriate antibiotics and drainage, these complications can completely resolve. Laryngoscope 104: February 1994 TABLEN, ‘Ago of Palionts With Peritonsilar Abscess. "Youngest palon was 4 your O. Odes pallont was 78 years ol Since the advent of antibiotics in the 1990s, these complications have been somewhat rare and fatalities have been few. ‘Symptoms of peritonsillar abscess are sore ‘throat, severe pain on swallowing, trismus, drooling, salivation, fever, headaches, a rise in pulse rate, and general malaise. Patients express anxiety and extreme distress when the airway is compro- mised.17262022 ‘The prominence of one or both tonsils, or any peritonsillar swelling must be included in the differ- ential diagnosis, infectious mononucleosis, foreign bodies, tumors such as lymphomas, Hodgkin’ disease, certain leukemias, extensive cervical adenitis, aneu- rysm of the internal carotid artery and dental infec- tions. These must be excluded either by blood counts, biopsies, and diagnostic measurements to rule out any of these possible critical diagnoses. TREATMENT If the abscess has already formed, incision and drainage is the treatment of choice, accompanied by intramuscular or intravenous penicillin, which should bring about a rapid improvement, in the patient's condition, ‘The incision is made over the point of maximum bulging and fluctuance, which is usually in the region just above the superior pole of the tonsil in the soft palate.9.90 The pain from incision soon disappears. ‘The pus should be suctioned out to avoid aspiration, which could resultin pneumonitis. Occasionally, ifthe incision is not made deep enough, it must be reopened and enlarged. Since quinsy has'a tendency to recur, one should consider tonsillectomy in 3 to 4 weeks after the disappearance of swelling and inflammation, fno pus is found, a diagnosis of peritonsillar cellulitis is considered, and the patient should continue to receive penicillin or similar antibiotic medication.°7.98 ‘At the present time, there is controversy as to whether a tonsillectomy should be done during the acute phase of a peritonsillar abscess (Chaud tonsil- lectomy)90-82.9-44 versus waiting 3 or 4 weeks for the Passy: Peritonsillar Abscess 187inflammation to subside followed by tonsillectomy (interval tonsillectomy).**48 The time interval for performing a tonsillectomy is still a matter of debate, with good arguments on both sides. In Gray's series, 57 of 84 patients with peritonsillar cellulitis had no tonsillectomy done, and 72% of these patients had no farther episodes of tonsillitis or abscess. Nineteen percent of these 84 patients had suffered two or more previous attacks of tonsillitis.47 However, most clini- cians appear to favor interval tonsillectomy when there have been two or more previous episodes of tonsillitis. Most recently, Herzon, et al. have sug- gested that simple perimucosal needle aspiration is the simplest and most cost-effective method for man- aging peritonsillar abscess, and have shown good 5-year follow-ups.#®-8 Schechter and his colleagues treated patients in this manner and found that only 39% of their patients had previous tonsillar disease and only 24% of the patients had any further problems with their tonsils.6 These current findings may stim- ulate the hypothesis to support the pathogenesis of Weber's gland in peritonsillar abscess. REVIEW OF RECORDS ‘The charts of 100 sequentially treated peritonsil- lar abscesses were reviewed at our university hospital in an attempt to evaluate and identify the patho- genesis of peritonsillar abscess. In our review, the following parameters were evaluated: J the age group involved, 2. area where the abscesses were identified, 3. the presenting symptoms, 4. the days from the ‘onset ofthe symptoms to the abscess formation, 5. the determination as to whether exudation was found on Laryngoscope 104: February 1994 188 the tonsil, 6. whether the patient had a previous tonsillectomy (either before or after the onset of the abscess), 7. when a tonsillectomy was done, and 8. the recurrence rate of peritonsillar abscesses. This chart review provided answers to the questions in our pre- sumption of the pathogenesis of peritonsillar abscess (Table D, The charts of 100 sequential peritonsillar ab- scesses were reviewed. The age range was from 4 to 76 years (Table II), Over 65% of the patients were 20 to 40 years of age; only 6% were under the age of 10 years. ‘Only 4% of the patients were found to have any form of exudation on the tonsils. Ninety-nine percent of the patients demonstrated a supratonsillar swelling as the primary site of disease. One patient developed swelling localized in the inferior pole of the tonsil which, upon further evaluation, was noted to be a lateral pharyngeal wall abscess. Right and left sides were affected equally. Eleven of the 100 patients were diagnosed as having peritonsillar cellulitis, since no pus could be extracted from the supratonsillar space of the soft palate; all were treated successfully with antibiotics. Eight patients who did not have subse- quent tonsillectomy developed recurrent abscesses on. the same side within a period of 11 months. Patients who had subsequent tonsillectomy had no recurrence of the disease. One patient developed bilateral peri- tonsillar abscesses at the same time and was treated rigorously because of airway impingement. A time interval of2 to 8 days elapsed (mean time for abscess production of 3.9 days) from the initial signs and symptoms of the disease to the development of the abscess. All 100 patients experienced trismus. Seven- Passy: Peritonsillar Abscessty-seven percent of the patients had no history of previous tonsillitis, but recurrent pharyngitis was seen in all cases (Table 1). HISTOLOGICAL FINDINGS ‘Toidentify and validate the existence ofthe group of salivary glands called Weber's glands described by Parkinson,’ histological sections of the soft palate in ‘the supratonsillar space thought to contain these glands were examined, This study was made difficult, because the parameters of the study required no previous tonsillectomy. Identification and confirmation of the existence of ‘Weber's mucous salivary glands in the supratonsillar space were confirmed by histological sections of this area (Fig. 2), Structurally, they are compounded or branching tubular-type structures arranged in small lobules. The lobules are bound together loosely in lobes or bound together to form the body of the gland. ‘The tubular gland is composed of irregular cuboidal cells arranged in a circular manner around a central opening of the duct or tubule. The whole gland had a soft consistency due to the amount of connective tis- sue that held several elements together. This glandu- lar mass is found above the tonsillar capsule in the Laryngoscope 104: February 1994 superior pole outside the tonsillar capsule, ‘Tofurther support the pathogenesis and develop- ment of peritonsillar abscess as being the inflamma- tory result of salivary glands in the supratonsillar space known as Weber's glands, a patient in whom a documented peritonsillar abscess had resolved was Drought to the operating room and an extended tonsil- lectomy, which included the supratonsillar space, was performed. This specimen was sent to the pathologist forhistological sectioning, The histologic examination showed destruction and inflammatory changes of th surrounding salivary gland congregate known as We- ber’s glands (Fig. 3). These histological findings port the theory of fibrosis from abscess formation within Weber’ salivary gland. COMMENTS AND DISCUSSION Many articles are found in the literature that expound on the bacteriology, age group, treatment, and recurrence rate of peritonsillar abscesses. No articles are identified relating to the true patho- genesis of peritonsillar abscess. Most authors accept tthe position that peritonsillar abscess is secondary to an acute exudative tonsillitis. This paper questions that assumption. The bacteriology from pus extracted from peritonsillar abscesses show mixed flora with a predominance of hemolytic streptococcus as described by Littman, et al.20 Other authors describe multiple other bacteria as the inciting cause?202429 Most authors agree that most incidences of disease occur between the ages of 20 and $0.111616.52 Ifit is agreed that this disease is caused by acute exudative ton- sillitis, the pathogenesis of the disease should be ‘questioned because the usual incidence of acute exu- dative tonsillitis is in the age group from 5 to 15 years of age, much younger than the age group for periton- sillar abscess. ‘The swelling with this disease is almost always in the supratonsillar space. Ifperitonsillar abscess is secondary to acute exudative tonsillitis, why is this space always involved with a characteristic swelling, pushing the tonsil to the midline and down? Other fonsillar areas or spaces would be expected to be involved. If the infected tonsils are the inciting cause and progression of this disease, it would be expected that the tonsils would be exudative at the time of the peritonsillar swelling, but they have been found not to be exudative (Table D: The signs of abscess formation begin approximately 8.9 days before the abscess is formed and the symptoms begin. Tt would appear that, if this was secondary to acute exudative ton- sillitis, the symptoms would have begun a week or longer before the onset of the formation ofthe abscess. ‘The recurrence rete of those patients who have had tonsillectomy is almost nil, although it has been re- ported.18 The recurrence rate of patients who have not had tonsillectomy is reported from 79 to 63% with an average of over 20%,2820.0137 Passy: Peritonsillar Abscess 189‘The answers to these questions can be found by reviewing the anatomy and theory that Weber's sali- vary glands in the supratonsillar space, resting in the superior pole of the capsule of the tonsil, can easily develop infections leading to cellulitis ‘or abscess which ean spread in the supratonsillar space and form a peritonsillar abscess. ‘The nature of Weber's glands may have practical importance. Because of their small size, they probably do not contribute greatly to the oral salivary function other than to clean the debris on the tonsillar erypts 2s proposed in this study. They may, however, have a real surgical and pathological importance. Parkinson (1951) stated, “These salivary masses found in the supratonsillar region appear to be most important because they are involved in the production of periton- sillar abscess also known as quins} This potential finding is of educational signifi- cance. If this hypothesis is accepted, treatment for peritonsillar abscesses will take a different form in the future. There is not enough evidence to de- finitively prove the pathogenesis of peritonsillar ab- sees, and further studies are necessary. The question that should be asked is, “Is this fact or fallacy?” It is hoped, however, that this study will create a better understanding of this serious oropharyngeal infection and stimulate further research, BIBLIOGRAPHY Medicine ofA. Coreliue Cele in Eight Book, ‘Grd ed) London 1688, Mackansi M: Disease ofthe Throat and Nose, 183, 1860. Hil 28: What ie Wrong with Se Tonsil Operatic? Arn Otal hinol Laryngol, pais, 1096, Holding, AB: The Nod or Improved Techlquein Tnslectony. Tamenoascore, 45:84, 156. Bateman, Gl and Kotick, ds Primary Qunsy Tnaletomy. ‘An Biel Laryngo, 6:816-331 1088. Engleh, GM. Oroeryngology. Harper & Row, New Yor, 1976. Parkinson, Ril: The Bnet onal and Tonal Poss fn Tone and Aled Problems: Macmillan Co, New York, 1981 3. Weber, Im Blandiuoh Der Bibrosapachen Anaiomie des “Menachen (Va 1) 1927 9, Von, Mallendort, Ws Handbuch Der Mikroshopachen Anatomie vie Menchen, VL 1,258,102. 20, Baum, His Miucous anisole PalatainRalaton athe Upper Plot th Tels. nn Oto Rhinol Larynge, 881,108, 22, Keleman, Gs The Pastine Tonalin the Sixth Decade. Ann Gol "Rhino Laryngol, 62:43, 1943. rive Trans. 22, Malel, RL: Peritonsillar Abecest: Tonsil Antibiotic Levels fn Patients With Treated by Acute Abscess Surgery. Lameno- lctomy as the reat Results With Special Autontion to Pharyngitis. J Laryngol V: Bilateral Encapsulated Pertonsllar Abscess in a Child. Arch Otolaryngol, 22:90, 1996. 16, Berman, HL: Quinay in a Young Iniant, Arch Otolaryngol, 193176, 1584. 17. Beeden,A.G. and vans, N.G.: Quinsy Tonsillectomy—A Fur ‘thar Report. J Laryngol Ota, 84:448—448, 1870. 18, Stage, sand Bonding, P: Pertonsller Abscess With Pe ‘pharyngoel Involvement Ineidence and Treetment, Clix Oto. Teynge, 123-8, 1987, 18, Hagggstror, A, Engqula, 8. ond Hollander, H.: Bacteriology in ‘Peritonalitis. Acta Otolaryngol (Stock), 109:18-166, 1987, 20, Littman, RLS, Ausmay, SA, Shu, ANG ARetrospective Study of Laryngoscope 104: February 1994 190 24, Kanetada, K. and Mogi, G: Bilateral Pertonsillar Abscess “Auris Nasue Laryns, 8:36-89, 961. 2, Brook, and Shoh, Bilateral Pertonslla Abscess: An Unusu- ‘al Presentation, South Med J, T:514-616, 1981, 126, Dalton, RE, Abed, E. and Slemanis, A: Blaterl Pritonillar ‘Abscessos and Quinay Tonslleciomy. J Nat! Med Assoc, ‘Tra07-812, 1988, 27, Kristensen, 8, Juul, A. and Nileen, R: Quingy: A Bilateral ‘Prosenttion J Laryngol Otol, 99:161-402, 198 28, Holt, GR. and Tinsley, PP: Prltonsllar Absceasesin Children. ‘Laswcoscore, 91:1226-1230, 1081 Laryngol Otel, 96:801-807, 80, Randall,C.-and JfTis, AR! Quinsy olowing Tonsillectomy (5 ‘Case Reporte J Laryngol Otol, $8:967—960, 198 51, Stage, HR end Schousboe M Periton ‘Christchurch 1081-1984, NZ Red J, 00:5 42, Robainn MES and Rabinsan 13 Slings ofthe Sot Plate: ‘ADiegroste Trap. NZ Med J, 97:775~777, 1084, axle. JH. and Smith, HW: Tonsliectomy-Treatment ‘of Pertonalllar Abscesa.Tvane Am Aead Ophthalmal Oto: Toryngol, 7417-429, 1973. 84, Salinger. and Pearlman, 8.J: Haomorchage From Pharyngea! ‘ind Poritenaillar Abecesses. Arch Otolaryngol, 18:379-884, 13a, 85, Sipila P, Palva, Ay Sort M, fal: Atlantoaxil Subluxation ~ “An Unusual Complication After Local Anesthesia or Tunsllc- tom. Arch Otolaryngol, 10781-18219, 36, Wills, Pi. end Vernon, B: Complicatins of Space Infections of and Neck, Larecoscore, 01:129-1198, 2981. 87, Lime, 1A. and Auti, J; Immediate Unilateral Tosilectomy Tor Severe Pertonillar Infections In Children Int J Pediatr Otorhinolaryngol, 6:187-198, 1988. 38, Chrstonsen, PH. and Schnated-Mdeen, U: Unilateral Immedl- ‘ste Tonsillectomy asthe Treatment of Peritonilar Abscess: Results With Special Attention to Pharyngitis. J Laryngol rol, 87:1105-1108, 1983, 80, Valka, P:Immedlateonsileetomy in the Prasence of Quinsy. J rolaryngol, 12:259-260, 1083, 40, Leek dif: Sat Tonallleetomy for Peritonlllar Abs “ed, 63:699-700, 1980 41, Harmia, LA, dla, E, Ruopp, Pet al: Abscess Tonillestom: ‘Acta Otolaryngol Suppl (Stock) 360:67-89, 1979, 42. Temples, JW. Bolinger LD, Wood, RP, ef al: Immediate Tonsll- Tectomy forthe Treatment ofPoritonsllarAbsrese.Am J Surg, 134:506-98,1977 49, MeCurdy,A.:PeritondllarAbscass A Comparison of Treatment ‘by Immediate Tonalllectomy and interval Tonsillectomy. Arch rolaryngel, 08:414—435, 2 44, Brandlow, EC: Immediate Tonsillectomy for Pritosillar Ab- ‘eats, Frans Am Acad Ophthalmol Otolaryngol, 7732-416, i7s, 45, Isaac, JH Je and Cassis, No: Quinsy: Peritonilar Abscess "Revisited, J Fla Med Assoc, 68:09-102, 108 46, Loo, Kd, Tranlr, LH, Smith, H.W, eal: Tonilectomy: Treat ‘ont of Perltonilar Abe ‘Am Acod Ophthaimol Otolaryngol 7:8417-8428, 1079, 47, Gray, LP: Untazaral Tonsilloctomy Indications and Results. J gol Otol, 97-1111-119, 1988, 48, Horzon, FS. and Aldridgo, Lil: Poritonillar Abscess: Neodlo ‘Aspiration, Otolaryngo Head Neck Surg, 89:910-011, 1981, 49, Herzan, PS: Permusoesl Noodle Drainage of Peritonsillar Ab- ‘seestos, A 6-Year Experience, Arch Otolaryngol, 110:104-106, nation 5. Minn set, 50. Lexow, H.: Puncture of a Peritonsillar Abscess. Tideskr Nor ‘aesforen, 106-819-1820, 1986. 51, Schechter, Gl, ly, MDE, Roper, A.L,et al: Changing Face of ‘Treatment of Peritonsilar Abscess. Larwcosoove, 82:657— 659, 1982, assy: Peritonsillar Abscess,