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SOURCE: Department of Otolaryngology, UTMB, Grand Rounds 
DATE: October 9, 1996 
RESIDENT: Ravi Pachigolla, M.D. 
FACULTY: Ronald Deskin, M.D. 
SERIES EDITOR: Francis B. Quinn, Jr., M.D. 

"This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion." 

I. History of Tonsil and Adenoid Surgery:

Celsus first authenticated removal of the tonsils in the first century. He used a primitive scalpel to remove parts of the tonsils. Paul of Aegina also gave original descriptions of tonsillectomy in 625. Caque of Rheims performed the first tonsillectomy in 1757 even though tonsillotomy remained the customary procedure of the day. 

Various forceps were designed for grasping and extirpating the tonsils. Philip Syng described an instrument that became the forerunner of the modern tonsillotome. Sluder designed a guillotine that was first used by P.S. Physick in 1827 for removal of elongated uvulae. Subsequent tonsillectomy was then performed with satisfactory results. Wilhelm Meyer performed the first adenoidectomy on October 26, 1867 on a 20 year old country woman who complained of reduced hearing and nasal stenosis. He found her rhinopharynx blocked by a soft, spongy tissue and decided to remove this tissue. He constructed a ring knife that he inserted through the nasal cavities and made several up and down movements with his knife so that free respiration was established. 

Samuel Crowe improved technique and brought scientific principles to tonsil and adenoid surgery. He described in detail preoperative considerations, precise techniques for performing surgery, anesthetic factors, and need for postoperative hospitalization. Adenotonsillectomy began to increase in the early part of this century as the then-popular "focus of infection" theory attributed various systemic disorders, most notably "rheumatism," to diseased tonsils and adenoids. Enthusiasts began to recommend adenotonsillectomy as a treatment for such diseases as anorexia, mental retardation, enuresis, and as a general measure to promote good health. Wholesale surgery was even performed on entire populations of school children in public school buildings. 

Within the first 3 weeks of embryonic life, the developing tissues that become the embryonic disk thicken. The proximal head fold is produced and surface invaginations create the primitive oral pit. The pharynx is formed as a tubelike diverticulum of entoderm. A buccopharyngeal membrane ruptures to produce continuity between the primitive oral cavity and the pharynx. The primitive face and neck develop with the five ectodermal grooves that are separated by the branchial arches. Through growth and lateral expansion of the pharynx, the second pharyngeal pouch is largely absorbed into the pharyngeal wall. However, dorsal remnants of the pouch persist to become the epithelium of the palatine tonsils and the supratonsillar fossa. The tonsillar pillars are formed from the second and third branchial arches through dorsal extension of mesenchyme into the developing soft palate. 

The development of the palatine tonsils can be seen in fetal studies during the 14th gestational week when mononuclear cells invade the mucosa of the tonsillar fossa. Mesenchymal condensations then differentiate into the tonsillar lymphoid tissue. By the 16th week, nodular structures begin to form with invagination of the surface epithelium to form the tonsillar crypts. Programmed cell death occurs allowing formation of the crypts. By the third trimester, organized lymph follicles are noted. Functional germinal centers may be lacking until birth and then are prevalent thereafter. 

The lingual tonsils develop in association with the posterior two-thirds of the tongue and crypts do not appear until after birth. This development coincides with the development of the palatine tonsils. During the fourth to sixth weeks of development, lymphatic tissue also forms within the posterior wall of the nasopharynx to become the pharyngeal tonsil. This tissue develops modified crypts that may cover ducts of adjacent mucous glands. 

The lingual (floor), pharyngeal (roof), and palatine tonsils (lateral walls) compose the bulk of the so-called Waldeyer's ring of lymphatic tissue that lines the walls of the nasopharynx and oropharynx. Smaller aggregates of lymphoid tissue in this area include: the tubal tonsils, lateral pharyngeal bands, pharyngeal granulations, and lymphoid tissue within the laryngeal ventricle. These lymphoid tissues are unique in that they contain only efferent and no afferent lymphatic circulation; thus lymph is not filtered through the tonsillar nodules. 

The lingual tonsil forms nonencapsulated nodular masses of lymphoid tissue within the base of the tongue. The sulcus terminalis, anterior to the circumvallate papillae, separates the lingual tonsil from the mucosa of the anterior portion of the tongue. Lymphocytes enter crypts of stratified squamous epithelium. The lingual tonsils are connected with adjacent mucous glands whose ducts open either within the tonsillar crypts or onto the free epithelial surfaces. The lymphoid follicles of the lingual tonsil vary in number from 30 to 100 and are somewhat irregular in size and form. The arterial blood supply of the lingual tonsils is provided by the lingual branches of the external carotids. The venous drainage occurs primarily through the lingual veins to the internal jugular vein. Lymphatic plexuses can be found around the tonsillar follicles, and they drain primarily to the superior deep cervical or jugular nodes. The sensory supply to the lingual tonsils and the base of the tongue is provided by the lingual branch of the glossopharyngeal nerve, although some small contribution may come from the superior laryngeal branch of the vagus nerve. 

The pharyngeal tonsil is formed by numerous variable folds of lymphoid tissue within the mucous membrane of the roof and posterior wall of the nasopharynx. These folds can also extend into the lateral recesses of Rosenmuller's fossa. In addition, Gerlach's tonsil is formed by small inclusions of lymphoid tissue within the lip of each eustachian tube orifice. The lymphoid tissue is covered by stratified squamous epithelium and form invaginations that resemble crypts but are not homologous to the true crypts of the palatine tonsils. Blood supply is provided by the ascending palatine branch of the facial artery, ascending pharyngeal artery, pharyngeal branch of the internal maxillary artery, and ascending cervical branch of the thyrocervical trunk. Venous drainage courses to the pharyngeal plexus, to the pterygoid plexus, and ultimately into the internal jugular and facial veins. Efferent lymphatic drainage flows from the retropharyngeal lymph nodes to the upper deep cervical lymph nodes, especially the posterior triangle nodes. Sensory innervation is derived from nasopharyngeal branches of the glossopharyngeal and vagus nerves. This tissue increases rapidly in size during the first 6 to 7 years of life and generally atrophies by adolescence. 

The two oval palatine tonsils can be found in the tonsillar fossa in between the anterior (palatoglossal) and posterior (palatopharyngeal) tonsillar pillars. At birth the palatine tonsils are approximately 5 mm in anteroposterior diameter and 3.5 mm in vertical diameter, and weigh about .75 gms. During childhood the tonsils descend within their fossa as their vertical diameter grows faster than their anteroposterior diameter. In contrast to other oronasal lymphoid tissues, the palatine tonsils are covered with a pharyngobasilar capsule fascia. The capsule is separated from the underlying musculature by loose connective tissue. The glossopharyngeal nerve and styloid process descend almost vertically on the lateral surface of this musculature. The internal carotid travels 2.5 cm posteriolaterally to the tonsils. One anatomic study revealed that the internal carotids were in direct contact with the tonsillar fossa in 2 out of 81 patients. Variable folds are formed by the mucosa overlying the tonsil between each tonsillar pillar. The plica triangularis is a variable fold that lies dorsal to the palatoglossal arch between the tongue and the inferior palatoglossus muscle. This position means that the anterior tonsillar fossa is a potential recess between the plica and the tonsil. 

A similar mucosal fold at the posterior inferior border of the tonsil may overlie the variable posterior tonsillar fossa. The plica semilunaris is a third fold of mucosa and drapes the apex of the tonsil. Blood supply to the palatine tonsils include the ascending pharyngeal and ascending palatine arteries which lie deep to the tonsillar fossa. Other vessels include the anterior tonsillar branches of the dorsal lingual artery, the inferior tonsillar branches of the facial artery, and the superior tonsillar branches of the descending palatine artery. Venous drainage occurs through a pericapsular plexus of veins into the lingual or pharyngeal veins and then into the internal jugular. Efferent lymphatics pass to the superior deep cervical and deep jugular nodes. Alternate lymphatic pathways exist to the submandibular and superficial cervical nodes. 

Sensory innervation derives from the lesser palatine nerves which transmits afferent fibers to the sphenopalatine ganglion. Additional innervation is provided by the lingual branch of the glossopharyngeal nerve which provides the pathway for referred otalgia. The inferior ganglion of CN IX has cell bodies of the tympanic nerve which provides general sensation to the medial surface of the TM and middle ear mucosa. Both of these cell bodies project to the thalamus and because of the common central projections, simultaneous pain may be felt in the oropharynx and ear. 

Immunology and Microbiology
The role of the pharyngeal lymphoid tissue in host immune defenses has yet to be defined, although lymphocyte production is an established function. B and T cells are present in equal numbers. During early life, tonsils may play an important role in providing host resistance to infection as a result of the inspired air stream passing thru the pharyngeal tissues. Pathogenic bacteria have been isolated from the tonsils without having caused disease implying that these organisms may somehow be made less virulent and act as antigens to provoke antibody formation. Most studies have failed to demonstrate significant alterations of immune globulin in patients with recurrent tonsillar infections or have not shown any objective changes in the incidence of systemic infections in post-tonsillectomy patients. Some evidence suggests that removal of the tonsils and adenoids does lead to low IgA production. 

Children who were previously immunized orally with live poliovirus vaccine dropped their titers 3 and 4 fold after tonsillectomy and adenoidectomy. The clinical significance of this is not completely known since poliovirus epidemics no longer occur. 

Organisms begin to populate the throat following the beginning of oral feedings. The normal adult flora contains both gram-positive and negative organisms, as well as anaerobic bacteria. Gram positive bacilli predominate and include lactobacilli, Actinomyces and others. Pathogenic bacteria have been found in the normal oral cavities of children up to 5 years of age without causing disease with their frequency decreasing as age increases. In pathogenic conditions of the tonsils and adenoids, B-lactamase resistant organisms begin to predominate and after removal of the offending tissues, the oral flora may return to near normal. Other organisms include saprophytic fungi, spirochetes (when teeth present), and viral flora. 

Non-neoplastic Diseases of the Tonsils and Adenoid
Acute tonsillitis is usually a self-limiting infection of one or both tonsils. The most prevalent bacterial organisms to be cultured are beta-hemolytic strep, although staph, pneumococci, Hemophilus, and anaerobes can be found. Viral pathogens account for between 50%-90% of acute tonsillitis depending on the symptom complex. Viral causes predominate in pre-school children. 
Acute tonsillitis usually affects adolescents and young adults. Predisposing factors include fatigue, temperature extremes, viral URI's (particularly Adenovirus), and metabolic and immune disorders. Acute tonsillitis is manifested by a dry throat, thirst, malaise, fever, throat fullness, odynophagia, dysphagia, otalgia, altered speech, headache, limb and back pain, swelling of regional nodes, and shivering. The symptoms typically last 4-6 days. Exam reveals enlarged injected tonsils that may be covered with exudate which may be follicular or coalescent (more common with bacterial pathogens although adenovirus may cause an exudative tonsillitis). Tender cervical adenopathy is common. Treatment includes sufficient oral intake, proper hygiene, lavages, analgesics, and antibiotics for 7 - 10 days (PCN, EEM, Tetra). This treatment reduces the duration of the episodes and prevents rheumatic fever and may help glomerulonephritis. Failure rates from PCN is about 10%-20% usually due to anaerobes that are penicillase producing. Viral tonsillitis responds to symptomatic treatment. 

Diphtheria may mimic acute bacterial tonsillitis. Here, the onset may be more gradual with less pronounced systemic complaints. Adenopathy may be less and hoarseness, stridor and croupy coughing frequently occur. A firm, leathery gray membrane is adherent to the tonsils and is pathognomonic. Exotoxin can be produced that is both neurotoxic and cardiotoxic. Finding Klebs- Loffler bacillus confirms the diagnosis. Antitoxin and high dose PCN should be given in the first 48 hours. People immunized may be carriers and should be treated with antibiotics. Antitoxin may cause severe allergic reactions. 

Vincent's angina is caused by simultaneous infection with a spirochete and a fusiform bacillus. Poor hygiene contributes to this condition. A gray necrotic pseudo membrane forms over the tonsils. Treatment is with high dose PCN. Infectious mononucleosis may resemble a severe attack of acute tonsillitis. Manifestations are similar but may also include posterior cervical adenopathy, palatal petechiae, liver damage, splenomegaly, rash, and a white irregular membrane may form over the tonsils. Treatment is symptomatic and may include artificial airways and high dose steroids. 

Other causes of tonsillar inflammation include agranulocytosis, leukoplakia, pemphigus, malignancies, fungi, syphillitic gumma and TB. Complications from acute tonsillitis include rheumatic fever and glomerulonephritis to a lesser extent. Endotoxin produced by the bacterium produce an erythematous rash, lymphadenopathy, sore throat, vomiting, headache, fever, tachycardia, a friable yellow membrane over the tonsils, and a strawberry tongue with enlarged papillae. Treatment is high dose PCN G with a usual good response. The ear complications, necrotizing otitis media, can be disastrous, with complete loss of the tympanic membrane and ossicles. 

Chronic tonsillitis results from recurrent acute or subclinical infections from inadequate antibiotic treatment for acute tonsillitis. Inflammatory debris collects in the crypts producing a constant sore throat, halitosis and dysphagia. Exam reveals cryptic, large tonsils that may be fibrotic. This usually affects adults. Blood flow may be reduced so antibiotics will not work and definitive therapy becomes necessary. Differential diagnoses include pharyngeal TB, scrofula, lupus, leprosy, actinomycosis, blastomycosis, leishmaniasis, and Crohn's. Diagnoses are based on cultures and biopsies. 

Peritonsillar abscess results from suppurative infection of the tonsils. The infections penetrates the capsule (usually at a superior location) and extends into the connective tissue space between the capsule and the posterior wall of the tonsillar fossa. Anaerobes predominate. Clinically, usually young adult patients present 7 -10 days with persistent sore throats that get worse despite treatment. Localization, fevers to 102-105, odynophagia, drooling, trismus, altered speech, and tender adenopathy are common. Uvula deviation occurs medially. Medical measures may abort an early peritonsillar abscess or cellulitis. However, once loculated pus forms, some form of incision and drainage procedure is necessary followed by antibiotics. Parapharyngeal abscess may result if pus penetrates the superior constrictor. Patients have toxemia, neck and throat pain, and tender swelling in the region of the mandible and possibly an intraoral bulge behind the vertical ramus. If the infection spreads anteriorly, a Ludwig's angina may occur. The infection may also infect the carotid sheath posteriorly. Treatment involves external drainage usually below the submaxillary gland. A retropharyngeal abscess may also develop as a complication of acute tonsillitis. This usually occurs in children due to suppuration of lymph nodes in this region. Treatment is surgical drainage. 

Intratonsillar abscess is a relatively uncommon occurrence and represents a localized accumulation of pus caused by crypt obstruction. Signs, symptoms, & treatment are similar to peritonsillar abscess. 

Tonsillar hypertrophy is caused by a variety of factors including diet, genetics, humoral changes, and infections. It occurs most commonly during puberty. One specific cause for tonsillar hypertrophy is Tangier disease, a yellow-orange hypertrophy of the tonsil from massive cholesterol storage within the tonsil and is a consequence of alpha-lipoprotein deficiency. Tonsillar hypertrophy is the most common cause of OSA in adolescents. Other conditions affecting the tonsils include hyperkeratosis, tonsilloliths and Eagle's syndrome. 

Adenoid hypertrophy is common in preadolescent children and its cause is multifactorial related to repeated infections or possibly generalized lymphoid hypertrophy. Symptoms include nasal obstruction, mouth breathing, snoring, mucoid anterior nasal discharge, hyponasal speech, epistaxis, OME, sinusitis and the characteristic adenoid facies (pinched nose, short protruding upper lip, open mouth, flat nasal arch). 

Acute adenoiditis usually follows with acute tonsillitis however it can also occur alone. Chronic adenoiditis is similar to chronic tonsillitis and usually progresses to hypertrophy. Tornwaldt's bursa is presumed to represent persistence of an embryonic communication between the anterior tip of the notochord and the roof of the pharynx. This communication usually persists in the fetus until the second month of development after which resolution occurs. However, adhesions may form to result in its persistent patency. Symptoms include a dull occipital HA with persistent PND and crusting in the nasopharynx. Treatment of the infected bursa requires appropriate antibiotics and surgical drainage. 

Lingual tonsillitis and abscess are similar to palatine tonsillitis and abscess. However foreign body sensations may predominate. Lingual hypertrophy sometimes results after adenotonsillectomy and can also be treated by lingual tonsillectomy. 

Surgical Indications For Adenotonsillectomy
Surgical indications for tonsillectomy include recurrent acute tonsillitis (5x/year, 4x/year x 2 years, 3x/year x 3 years), tonsillar hypertrophy with sleep disturbance described as loud snoring, frequent waking, enuresis, and respiratory pauses (>10 seconds). Sleep study not required if clinical Hx & PE agree unless central apnea suspected, hypertrophy causing dental malocclusion or adversely affecting orofacial growth documented by orthodontist, hypertrophy causing upper airway obstruction, severe dysphagia or cor pulmonale, recurrent peritonsillar abscess or peritonsillar abscess in patient with history of recurrent tonsillitis, chronic tonsillitis, unilateral tonsillar hypertrophy presumed neoplastic. An acute tonsillitis may be defined by one or more of the following: T>38.3, cervical node enlargement, tonsillar exudate, or positive culture for beta- hemolytic strep. Chronic tonsillitis may be defined as a sore throat lasting 6 mos. that does not respond to beta-lactamase resistant antibiotics and possibly manifested by enlarged cervical lymph nodes. 

Other more equivocal indications for Tonsillectomy include recurrent sore throats, otalgia, rhinitis, snoring, failure to thrive, enlarged tonsils, tuberculous adenitis, cervical lymphadenitis, systemic diseases secondary to beta-hemolytic strep infections, streptococcal carriers, valvular heart problems, diphtheria carriers, and dysphagia. 

Indications for adenoidectomy include purulent rhinorrhea (4 episodes per year), obstructive sleep apnea secondary to adenoid hyperplasia, adenoid facies, recurrent SOM after one set of tubes, and nasal obstruction of ostia resulting in sinusitis. Equivocal indications are similar to those for tonsillectomy. 
Contraindications to adenoidectomy include a submucous cleft palate which may lead to velopharyngeal insufficiency after surgery. If the adenoid obstruction is severe enough, then only superior half adenoidectomy is performed. Avoid surgery in patients with hemoglobin/hematocrits less than 10/30. Perform surgery at least 2 weeks after the last attack of acute tonsillitis and wait at least 6 weeks after polio vaccination. Avoid surgery in patients with uncontrolled systemic diseases (ie. leukemia). 

Preoperative Considerations
A careful history and physical examination should be performed with attention paid to any bleeding tendencies, other medical problems, allergies. Complete blood counts are usually done. Avoid aspirin and Ibuprofen for three weeks preoperatively. Special lab studies are done as relates to the medical history. Preoperatively, patients should fast for 8 hours. They may receive mild laxatives, sedatives, and drying agents as necessary. Anesthesia is general endotracheal although a few cooperative adults may undergo the procedures with local anesthetic and intravenous sedation. Avoid hyperextension of neck in Down's patients. Propofol induction may decrease post- operative vomiting compared to Halothane. Pre-incisional Bupivicaine and pre-op Dexamethasone may also reduce post-op pain and vomiting. 

Operative techniques
The patient should be positioned supine on the OR table and the surgeon should have on a headlamp. Although the surgery is not sterile, all instruments and drapes should be sterile. After insertion of the Crowe-Davis mouth gag or similar device, surgery is begun. Tonsillectomy is performed after adenoidectomy if both procedures are to be done. 

Despite the many techniques available for tonsillectomy, it is proper surgical technique that determines success or failure. The standard dissection and snare method involves first incising the mucosa with a sickle knife. Begin at the superior pole and dissect inferiorly with a Dean knife in the loose connective tissue layer. At the inferior pole, a wire loop snare is passed around the tonsil. The tonsil is then amputated by closing the snare loop. Bleeding can be controlled with cautery, simple figure of eight sutures placed at both poles, dilute epinephrine solutions or simple packing. Several studies have shown decreased postoperative pain, vomiting and increased oral intake compared to electrocautery. Average blood loss might be greater compared to electrocautery. 

The tonsil guillotine technique can be performed if the tonsil can be everted through the opening of the instrument. It is used in children in whom the tonsillar capsule is in loose contact with the constrictors posteriorly. The technique involves displacing the tonsil forward by digital manipulation over the alveolar eminence of the mandible. The tonsil is inserted through the fenestra of the instrument and the guillotine blade is closed to amputate the tonsil and its capsule. Lymphoid tissue may be left in the region of the plica triangularis and this must be removed. 

Tonsillectomy with Local Anesthesia puts the patient in a modified upright position for surgery. After topical anesthesia, local lidocaine with epinephrine is infiltrated into the anterior and posterior pillars and tonsillectomy is performed. Cryogenic tonsillectomy can be done by placing an operative probe with liquid nitrogen onto the tonsil. 2 applications, each lasting 3 to 4 minutes are necessary. Delayed necrosis of the tonsil occurs within hours and is complete within several days. Laser tonsillectomy can be performed with decreased postoperative pain compared to electrocautery. Electrocautery can be performed similar to the dissection and snare method. However, there might be a slightly increased risk for post-op pain and decreased oral intake compared to the dissection and snare method. 

Adenotome or adenoid curette may be used to perform adenoidectomy. The soft palate is retracted with a metal palatal retractor or small rubber catheters passed through the nose and brought out through the mouth. Using an adenoid curette of appropriate size, it is placed against the posterior edge of the vomer and using the thumb as the fulcrum, the blade is pushed along the vault of the nasopharynx and over the odontoid process. Remnants may be removed with small curettes or electrocautery. Avoid curettage of the eustachian tube orifices. A LaForce adenotome can be used in performing adenoid dissection. The basket engages the central adenoid mass and is pressed against the posterior pharyngeal wall and rotating it downward with closure of the blade. Curettes are then passed laterally to remove lateral adenoid tissues. 

Success of Adenotonsillectomy
Tonsillectomy has been shown to reduce the number of recurrent throat infections, improve obstructive symptoms, and cor pulmonale. Tonsillectomy has not been shown to improve otitis media. Adenoidectomy has been shown in conflicting reports to help otitis media and in others no benefit has been shown. However, it does improve dental occlusion, mouth breathing, obstructive symptoms, sinusitis (37% of cases) and improve the adenoid facies. 

Postoperative Care
The patient should be taken back to the recovery room and placed on the side in a modified Trendelenburg position. Gentle suctioning with a Yankauer may be done. Intake of oral fluids should be encouraged. Mild analgesics may be given. Soft diets should be maintained for 3 weeks at which time the pharynx usually heals and a regular diet can be begun. Patients are sent home with antibiotics. Observation with true sleep apnea patients in a monitored ICU setting is recommended to watch for post obstructive pulmonary edema and/or post obstructive respiratory depression secondary to rapid blood gas correction. Avoid heavy sedation or narcotics in these patients. Criteria for inpatient overnight admission include but are not limited to: 

Condition 1: Age less than three 
Condition 2: Abnormal coagulation values with or without an identified bleeding disorder in the patient or family 
Condition 3: Evidence of obstructive sleep disorder or apnea due to tonsil and/or adenoidal hypertrophy 
Condition 4: Systemic disorders that put the patient at increased preop cardiopulmonary, metabolic or general medical risk 
Condition 5: Child with craniofacial and/or other airway abnormalities 
Condition 6: When the procedure is being done for acute peritonsillar abscess 
Condition 7: When extended travel time, weather conditions, and home social conditions are not consistent with close observation, cooperativeness, and ability to return to the hospital quickly at the discretion of the attending physician. 


Immediate complications from adenoidectomy include hyperextension of neck so that when the adenoid curette is passed, excision of portions of the posterior pharyngeal wall, muscles and cartilage can occur. Immediate complications can also include bleeding that can be controlled in a variety of ways including suturing of the pillars with a mattress suture. Hemorrhage, the most common complication after adenotonsillectomy occurs approximately 1%-2%. It is caused by intercurrent infection or dietary indiscretions. It occurs several days after the surgery when premature separation occurs of the granulating membrane over the pharynx. Treatment varies and can include operative control and possible ligation of the external carotid. 

Postoperative pain tends to be less in the very young patient and is best managed with analgesics. Localized infections can be treated with topical therapies. Occasionally significant infections will occur, particularly in the dehydrated patient and they may require antibiotics. 

Operative trauma has included amputation of the anterior portion of a child's tongue, internal carotid thrombosis, tissue necrosis leading to rerouting of salivary ducts into the tonsillar fossa. Excessive scarring has produced nasopharyngeal stenosis that later required surgical repair using local mucosal flaps or skin grafts. This occurs in about 3 per 100,000 adenotonsillectomies. Infection of the deep cervical muscles has occurred causing atlantoaxial subluxation. Decalcification of the vertebrae and laxity of the anterior transverse ligament between the atlas and axis occur (Grisel's Syndrome). Persistent hypernasality occurs in about 1 out of 1500 patients even those without cleft palate. Surgery may be necessary to correct this in about 50% of patients. Speech therapy works the rest of the time. 

Neplastic Diseases of the Tonsils
Precancerous lesions occur less frequently compared to the oral cavity but may include leukoplakia, erythroplakia, lichen planus, and nicotine mucositis. These lesions occur most often on the palate. Between 70%-80% on tonsillar cancers are squamous cell, 12%-15% lymphoma, and others the rest. Benign tumors are extremely rare in the tonsil but may include lipomas. Melanomas have occasionally been metastatic to the tonsils also. 

The most significant etiologic factor associated with squamous cell carcinoma is use of tobacco, although the correlation is less than with the oral cavity. Alcohol potentiates the carcinogenic effects of tobacco. In some patients, there appears to be a relationship between papillomavirus and cancers of the tonsil. DNA changes associated with papillomavirus have been documented in some patients with tonsillar carcinoma. 

The anterior tonsillar pillar and the tonsil are the most common locations for tumors within the oropharynx. Rarely a primary tumor is limited to the posterior pillar. As lesions enlarge, they may spread to the retromolar trigone and extend laterally to the buccal mucosa. Once they involve the buccal mucosa, occult spread to the buccal fat pad may occur and appear as a subtle fullness in the cheek. Some anterior tonsillar pillar lesions extend to the soft and hard palate. Anterior tonsillar lesions may extend to the mandible and especially in elderly patients with edentulous mandibles, inferior alveolar nerve involvement may occur because it is more superficial and prone to involvement from overlying mucosal cancers. 

Lesions of the tonsillar and pillar areas drain to the upper cervical nodes. Cancers involving the anterior tonsillar pillar have less risk of forming clinically positive lymph nodes compared to lesions limited to the tonsillar fossa. The anterior tonsillar pillar drains into the upper internal jugular vein lymph nodes, as well as into the submaxillary gland lymph nodes. The risk of their involving the spinal accessory and posterior triangle lymph nodes is low. Contralateral spread infrequently occurs in early lesions, but the risk of occult metastases in clinically negative necks is significant. 

Tonsillar fossa lesions have a higher risk of lymph node involvement compared to lesions of the anterior tonsillar pillar. Similar lymph node distribution occurs as with the anterior tonsillar pillar. Although primary lesions of the posterior tonsillar pillar are rare their lymph node metastatic direction also would be more posterior, with involvement of the high cervical as well as the spinal accessory and upper posterior triangle nodes. 
Symptoms may include sore throat, increasing pain, trismus, bleeding, and referred otalgia. Primary lesions of the tonsillar fossa are quite large before symptoms manifest possibly because of decreased sensitivity. Bimanual palpation is mandatory to determine the extent of the lesions. 

Generally, early T1 and T2 lesions are treated by irradiation or surgery. Radiation therapy locally fails to cure approximately 20% of T2 lesions and 30% - 50% of T3 lesions. In these moderately advanced lesions, surgery is recommended if the primary lesion fails to show adequate regression at 5000 rads. Combined modalities is best for management of lesions that extend beyond the confines of the tonsillar fossa; many recommend combined therapy if clinically positive neck nodes appear initially. Generally a composite resection is performed followed by postoperative radiation therapy. Planned preoperative radiation therapy usually is recommended only if large fixed nodes are found at the initial examination. The status of the neck nodes affects survival rates. Survival may drop by 50% with positive nodes. 

Socioeconomic Issues
The number of adenotonsillectomies peaked in the 1930's at approximately 1,000,000 surgeries per year and has slowly decreased since due to the advent of antibiotics, definitive surgical indications, and improved understanding of the pathophysiology of the disease process. Today approximately 200,000 - 300,000 adenotonsillectomies are performed with the trend increasing towards outpatient surgery. Therefore accurate records are difficult to come by to know the exact amount of surgeries being performed. 

No practice involving health care for children in the 20th century has excited more heated controversy among health professionals than has surgical removal of the tonsils and adenoids. Long the most common major operation carried out on children, adenotonsillectomy continues to constitute a treatment whose benefits in relation to costs and risks have yet to be thoroughly assessed and whose indications have begun to clarified only in the past decade. Nonetheless, the persistently high rate of performance of adenotonsillectomy, despite apparent substantial declines in recent years, attests to its hold on the minds of many physicians and parents as a treatment of importance and value. Annual expenditures for tonsil and adenoid surgery in the United States probably exceeds half a billion dollars. 

Discussion by Dr. Ronald Deskin:

Indications for tonsillectomy and adenoidectomy for upper airway obstruction are usually clear cut and absolute indications based on airway obstructions symptoms and physical findings. A sleep study is not necessary unless the history and the physical findings do not agree or there is some suspicion of a central apnea component. Indications for recurrent tonsillitis are based on the individual patient but in general the numbers of infection per year as stated in the grand rounds text are adhered to. A child who has fewer episodes than stated in the text but who has severe illness with each infection requiring long term bed rest, school absence or hospitalization might be considered for surgery with fewer numbers of acute episodes. 

Post-operative sedation and strong analgesia should be avoided in small children who have tonsillectomy and adenoidectomy for upper airway obstruction. Tylenol generally is adequate and codeine may be used carefully for children over 5 to 6 years of age. 

The use of Beta-Lactamase stable antibiotics should be considered for treatment of recurrent acute tonsillitis and for cases of chronic tonsillitis. Beta-Lactamase producing bacteria may be inactivating the penicillin antibiotic and making the strep throat persist or recur quickly. 

A reasonable laboratory work-up for routine tonsillectomy and adenoidectomy in children would include a hematocrit level. Knowing that the child is not anemic is important in pre-operative planning and provides a baseline should post-operative bleeding occur and a post-operative hematocrit is being evaluated.

Posted 10/09/1996

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