Adenoidectomy - technical. This operation is also known as pharyngeal tonsillectomy
The adenoids are considered a collection of lymphoid tissue positioned on the posterior nasopharyngeal surface. They are anatomically linked to Waldeyer’s ring which includes the palatine and lingual tonsils. Adenoidectomy refers to the surgical excision of this tissue, which is done to treat a variety of disease processes. Although adenoidectomy suggests complete excision of adenoid tissue, most surgical techniques shave off the superficial adenoid tissue.
Adenoid hypertrophy or chronic adenitis may cause significant problems related to craniofacial morphology in the growing child, excessive snoring, obstructive sleep apnea (OSA), and poor oral intake. Removal of adenoid tissue is performed to improve the quality of life and reduce the negative sequelae associated with these problems. It is generally a well-tolerated procedure with a fairly low risk profile and the majority of patients have significant improvement in symptoms following the operation. Because adenoid hypertrophy is often associated with tonsillar hypertrophy, the tonsils and adenoids are often removed together, in a procedure referred to as a T&A (tonsillectomy and adenoidectomy).
Inflammatory and infectious processes involving the adenoids and the tonsils are very prominent in the pediatric population, and often result in two of the most common operations in young children: tonsillectomy and adenoidectomy. The adenoids are a triangular-shaped tuft of tissue in the posterior nasopharynx and were first described in 1868 by the Danish physician Meyer (Curtin 1987). He reported a case of a young woman who complained of nasal obstruction and decreased hearing. He discovered that her nasopharynx was obstructed with soft tissue which he called “adenoid vegetations.” He constructed a ring knife which he passed through the nose to excise the adenoids. Seventeen years later in 1885, Gottstein described the first use of an adenoid curette. In the early 1900s, tonsillectomy and adenoidectomy were commonly performed to treat problems such as anorexia, mental retardation, and enuresis, or simply to promote good health (McClay 2008).
The adenoid tissue forms the central part of Waldeyer’s ring, which also includes the palatine and lingual tonsils to form a ring of lymphoid tissue around the upper end of the pharynx. The adenoid develops during the third to seventh month of gestation as a midline structure resulting from the fusion of two lateral primordia. The adenoid tissue continues to grow until approximately the fifth year of life, in response to various antigenic challenges, and then typically regresses by puberty. The blood supply is from the ascending pharyngeal artery, the ascending palatine artery, the pharyngeal branch of the maxillary artery, the artery of the pterygoid canal, and the tonsillar branch of the facial artery. Venous outflow occurs via the pharyngeal plexus which ultimately drains into the internal jugular and facial veins. Nerve supply is via the pharyngeal plexus which is supplied by both the glossopharyngeal and vagus nerves. Lymphatic drainage of the adenoids goes to the retropharyngeal and pharyngomaxillary space lymph nodes (Bailey et al. 2005).
The anatomic location of the adenoids as well as the relationship to surrounding structures has major implications in terms of the pathophysiology of disease processes related to adenoid hypertrophy. Obstruction of the Eustachian tubes, which are located laterally, plays a significant role in middle ear disease. Adenoid enlargement and inflammation are also significant in chronic sinusitis as well as allergic rhinitis. Given their location in the nasopharynx, adenoid hypertrophy also results in nasal obstruction, mouth breathing, nasal voice, and obstructive sleep apnea. Chronic mouth breathing due to nasal obstruction during the age when the facial bones are developing can produce a high arched palate and narrowing of the midface. This results in elongation of the face with predominance of the upper teeth, the so-called adenoid facies (Bailey et al. 2005).
The adenoids are a predominantly B-cell organ, and are involved in inducing secretory immunity and regulating secretory immunoglobulin production. Immunoglobulins produced by the adenoids include IgA, IgM, IgG, and IgD. Despite their clear role as secondary lymphatic organs, the overall effect of adenoidectomy on the immune system appears to be minimal. There have been some reports of decreased nasopharyngeal IgA production against polio vaccine following adenoidectomy and increased rates of Hodgkin’s disease following tonsillectomy and adenoidectomy, but these claims have been unsubstantiated by more in-depth studies. Many different organisms can cause adenoid inflammation, from viruses and yeasts to anaerobes and aerobes. Most infections are polymicrobial because the oropharynx is colonized with many bacteria, which can also make it difficult to distinguish between organisms which are colonizers versus invaders. However, hypertrophied and chronically infected adenoids have been shown to have more beta-lactamase producers than non-diseased adenoids (Bailey et al. 2005).
Historically, the adenoids were removed using sharp instrumentation, such as curettes. Although this technique remains in use, several other techniques have gained favor in recent years, including thermal, microdebrider, and bipolar radiofrequency (CoblatorTM) reduction. The CoblatorTM utilizes a system of radiofrequency bipolar electrical current which passes through a field of normal saline and results in the production of a plasma field of sodium ions which are able to break down intracellular bonds and vaporize tissue. The CoblatorTM can be used for adenoidectomy and works well for fairly small adenoid pads, but is not as effective in larger adenoid pads. The microsurgical debrider consists of a rotating blade, which has a suction incorporated into it and, therefore, effectively shaves tissue. It is a very efficient and effective method of removing adenoid tissue, and is particularly useful for removing adenoid tissue that extends through the choanae into the nasal cavity (Flint et al. 2010).
Adenoidectomy is most commonly performed in conjunction with tonsillectomy but can be performed alone. After induction of general anesthesia, the patient is placed in Rose’s position, and a mouth gag is placed to expose the oropharynx. The soft and hard palate are then visualized and palpated for any evidence of submucous cleft palate. Typically, a red rubber catheter is passed through one or both nares, brought back out through the oral cavity, and used to suspend the soft palate to allow better visualization of the nasopharynx.
A nasopharyngeal mirror is then used to assess the adenoid pad and guide placement of the curette, which is placed high in the nasopharynx, along the margin of the vomer. It is then drawn downward with mild pressure to remove the adenoid tissue, with care being taken not to penetrate into the prevertebral fascia and not to disturb the Eustachian tube orifice (Thiessing et al. 2010). Smaller curettes or a nasopharyngeal punch can then be used to remove residual adenoid tissue in the choanae. If a microdebrider is used, the exposure is the same, and the mirror is used to guide the microdebrider and shave down the adenoid tissue. Once all desired tissue has been removed, the nasopharynx is packed, and then possibly suction electrocautery is used to achieve hemostasis. (Flint et al. 2010) Some prefer to perform adenoidectomy with thermal reduction alone using suction monopolar cautery.
Indications for adenoidectomy
The most common indication for tonsillectomy and adenoidectomy in the pediatric population is obstructive sleep apnea, which has a reported incidence of 1–3% (Flint et al. 2010). Airway obstruction typically results from the tonsils and adenoids filling the area of the oropharynx and nasopharynx, thus obstructing airflow. This can lead to intermittent complete airway obstruction, particularly during sleep, owing to the effects of gravity and relaxation of the surrounding oropharyngeal and nasopharyngeal soft tissue. Obstructive adenoid hyperplasia is diagnosed by clinical history and physical examination. A triad of obligate mouth breathing, snoring, and hyponasal speech are seen. Rhinorrhea and post-nasal drip may also be seen, but these symptoms are less specific and must be differentiated from allergic rhinitis. Polysomnography should be performed to determine the degree of obstruction.
Obstructive sleep apnea, if untreated, results in severe and potentially life-threatening consequences including pulmonary hypertension and cor pulmonale (Sargi and Younis 2007). Apneic events and associated oxygen desaturations are typically short and associated with a brief period of arousal, during which the patient repositions himself and opens the airway. However, in severe cases, the apnea can be prolonged, resulting in significant oxygen desaturation, which puts significant stress on the cardiovascular system.
Adenoid hypertrophy can also be associated with failure to thrive, dysphagia, speech abnormalities, and craniofacial growth abnormalities. The presence of any of these, even in the absence of sleep apnea, is an indication for adenoidectomy. Failure to thrive in these patients is thought to be secondary to disruptions in growth hormone secretion during REM sleep in patients with OSA (Lieberman et al. 2006). The most common speech abnormality seen in these patients is hyponasal speech, which typically improves significantly following adenoidectomy. Craniofacial abnormalities associated with adenoid hypertrophy include the “adenoid facies” described above, as well as occlusion abnormalities.
Children with middle ear disease also benefit from adenoidectomy. The close proximity of the adenoid tissue to the orifice of the Eustachian tubes is significant in the pathogenesis of middle ear disease. Eustachian tube dysfunction can result in chronic otitis media with effusion as well as recurrent acute otitis media. Removal of the adenoid tissue has been shown to be effective in resolving both of these disease processes, regardless of the size of the adenoids. The mechanism of the adenoids role in middle ear pathology is unclear, but it has been postulated that either the bacteria harbored in the adenoids cause irritation of the Eustachian tube lining resulting in Eustachian tube dysfunction, or the harbored bacteria cause a chronic infection of the middle ear space.
Finally, patients with a history of chronic recurrent sinusitis may also benefit from adenoidectomy. A recent study showed that biofilms are prominent in the adenoids of children who have chronic sinusitis (Coticchia et al. 2007). Adenoids removed for OSA were compared to adenoids removed for chronic sinusitis, and showed that 95% of the surface of the adenoids of sinusitis patients was covered in biofilms, compared to only 2% of the surface in OSA adenoids.
There are no absolute contraindications to adenoidectomy, but there are several relative contraindications. The most commonly recognized contraindication to adenoidectomy is the presence of palatal abnormalities. These patients are at increased risk of developing velopharyngeal insufficiency, one of the most dreaded complications of adenoidectomy where there is nasal escape of speech or food. It is important to include a complete palatal examination as part of the preoperative work-up, to determine the presence of a submucosal cleft palate or bifid uvula. Patients with a history of cleft palate or evidence of an occult cleft palate should not undergo adenoidectomy unless absolutely necessary, and a conservative adenoidectomy should be performed, taking care to preserve the lower portion of the adenoid pad (Ruben and Weg 1975).
Children with a history of nasal regurgitation or hypernasal speech are also at increased risk of postoperative VPI. These patients should be carefully evaluated, and adenoidectomy only performed if absolutely necessary. Another group in which adenoidectomy should be performed cautiously are patients with neuromuscular disorders. These patients frequently have Eustachian tube dysfunction, and adenoidectomy is performed in the hope of improving their middle ear disease. However, the Eustachian tube dysfunction is often directly related to their hypotonicity rather than the adenoids, so this should be investigated preoperatively (Ruben and Weg 1975).
Adenoidectomy significantly improves symptoms in a majority of patients. In conjunction with tonsillectomy, adenoidectomy significantly improves symptoms of OSA, and reduces the risk of cardiac and pulmonary sequelae associated with severe OSA. In patients who already have ventricular dysfunction, T&A results in rapid improvement of ventricular function. Many patients with OSA also have failure to thrive, and reports have shown catch-up growth following T&A in these patients (Lieberman et al. 2006). Given its simplicity, low risk profile, and effectiveness, adenoidectomy is considered a first-line treatment for a variety of disease processes related to adenoid hypertrophy/infection.
Most patients tolerate adenoidectomy fairly well, although there are potential serious postoperative complications. These complications are primarily related to pain, bleeding, airway obstruction, postoperative pulmonary edema, velopharyngeal insufficiency, and nasopharyngeal stenosis. Advances of modern surgical technique and anesthesiology have significantly reduced the number of complications related to adenotonsillectomy.
The most serious complication of adenotonsillectomy is postoperative hemorrhage, with rates reported from 0.5% to 10% (Flint et al. 2010). Bleeding can occur intraoperatively, immediately postoperatively or in the delayed postoperative period. Intraoperative hemorrhage may be related to an underlying coagulopathy or major arterial damage. Steps to control intraoperative bleeding include suction cautery, and if needed, the placement of packing in the tonsillar fossa and oversewing the tonsillar pillars to provide pressure in the fossa. Suture ligatures should be used with caution, as they may damage the underlying arterial vessels, thereby worsening the bleeding, or predisposing to postoperative bleeding. In severe cases, ligation of larger arteries or embolization may be necessary, but this is extremely uncommon. Postoperative bleeding in the immediate postoperative period following adenoidectomy can be initially controlled with topical decongestant nasal sprays. If the bleeding is severe, these patients should be taken back to the operating room for examination of the nasopharyngeal pad. Patients and parents should be made aware of the risk of delayed postoperative bleeding, and instructed to return to the emergency room immediately if there is any evidence of bright red bleeding from the nose or mouth, as this can be fatal if not managed appropriately. Patients with delayed bleeding should be taken to the operating room for examination of the tonsillar fossa and adenoid bed.
Postoperative airway obstruction may occur secondary to edema of the tongue, nasopharynx, and palate. Intravenous corticosteroids may be given intraoperatively to reduce this complication. In patients with a history of obstructive sleep apnea and long-term upper airway obstruction, pulmonary edema may arise after adenotonsillectomy. Therefore, patients with a prolonged history of severe OSA or patients who have evidence of cor pulmonale should be observed closely after surgery with pulse oximetry. Patients with postoperative hypercapnia sometimes require mechanical ventilation until their hypercapnia resolves.
Velopharyngeal insufficiency, or hypernasality, is a relatively uncommon complication related to adenoidectomy, with an estimated incidence of around 0.1% (Flint et al. 2010). A family history of VPI or personal history of hypernasal speech or nasal regurgitation as an infant may predispose patients to postoperative VPI. The incidence of VPI is increased in patients with palatal anomalies, and therefore adenoidectomy should be performed conservatively in this cohort of patients. Patients with VPI should be evaluated by a speech pathologist. Most cases are transient and resolve over time; however, in some situations surgical intervention, such as a pharyngeal flap, sphincter pharyngoplasty, or posterior pharyngeal wall augmentation, may be necessary.
Nasopharyngeal stenosis is the result of excessive cauterization or laser application with subsequent mucosal destruction of the nasopharynx, lateral nasopharyngeal wall, and posterior tonsillar pillars. This can result in scarring of the soft palate to the posterior pharyngeal wall and can result in significant obstruction of the nasal airway. This requires surgical repair, typically using a combination of skin flaps, mucosal flaps, stents, and skin grafts, and often requires multiple surgical procedures to repair (Mankekar 2010). Cotton describes a laterally based pharyngeal flap in which an incision is made laterally through the scar tissue into the pharyngeal wall (Cotton 1985). The mucosa is then elevated to allow for scar tissue removal, and the entire posterior pharyngeal wall is elevated as a laterally based pharyngeal flap which is elevated as a mucomuscular flap at the plane of the prevertebral fascia. The inferior limit of the flap is dissected posteriorly as far as possible, and the flap is mobilized and sewn into position. Bivalved flaps as well as transnasal endoscopic approaches have also been described.
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