Voice production

The larynx also provides the basic phonatory sound upon which a voice can be produced. Adduction of the vocal cords produces a constricted area where the air pressure is reduced as it passes from the lungs to the pharynx (Bernoulli’s phenomenon). The vocal cord mucosa is consequently sucked together, producing a rise in the subglottic pressure which forces the cords apart again. This cycle is repeated to produce vibration and hence sound. Volume changes are effected by alteration of the subglottic pressure. Pitch alterations occur by modifying vocal cord length and tension. The quality of the raw basic laryngeal phonatory sound is further altered by the resonating cavities of the pharynx, mouth and nose. Speech is ultimately produced by the interaction of the articulators (teeth, tongue, lips) on this phonatory sound.

Oral cavity

The major signs and symptoms of oral disease include:

Pain

Dental disease is the most common cause of pain in the oral cavity. Carious teeth are tender if subjected to temperature changes and on chewing. Periodontal disease can cause pain on tooth brushing and is associated with halitosis due to accumulation of decaying food debris. Dentures may cause pain if improperly sized, or if they provide an abnormal bite. Atrophy of the teeth-bearing alveolar ridges may result in dentures causing pain, and is commonly seen in the elderly. Maxillary sinusitis may result in toothache if a tooth root is projecting into the sinus mucosa (Fig. 3.6). Pain due to malignant disease is severe and constant, and invariably leads to some degree of dysphagia.

Fig. 3.6 X-ray showing indentation of tooth roots in the maxillary antra.

Oral masses

Any complaint of a lump requires palpation of the site, even if a lesion is not visible. Virtually all lumps require biopsy to exclude cancer. Tongue masses are nearly always neoplastic. One exception is the rare, median rhomboid glossitis which presents as a red area on the dorsum of the tongue and is benign (p. 83).

Blockage of a duct of the sublingual salivary gland may give rise to a cystic lesion called a ranula in the floor of the mouth. An exostosis of the hard palate, ‘torus palatinus’, has a typical position in the midline and is hard to palpation (Fig. 3.7).

Fig. 3.7 The torus palatinus is an osteoma of the hard palate, usually located in the midline.

Pharynx

The precise symptoms are dependent on which region of the pharynx is primarily involved. The majority of pathologies in the oropharynx and hypopharynx, either inflammatory or neoplastic, will lead to some degree of dysphagia (p. 76) (Fig. 3.8). Deafness may occur due to obstruction of the Eustachian tube with nasopharyngeal pathologies. Progressive nasal obstruction and epistaxis with otological symptoms should alert the clinician to nasopharyngeal malignancy. Large oropharyngeal masses may cause a voice change (‘hot potato voice’) and respiratory obstruction.

Fig. 3.8 Symptoms of disease in the three regions of the pharynx.

The alteration in voice in hypopharyngeal neoplasia is due either to direct infiltration of the larynx, by involvement of the recurrent laryngeal nerve with development of vocal cord palsy. Secondary nodal neck masses are very frequent with pharyngeal neoplasia and may be the presenting feature. Pain in pharyngeal disease may be localized to the throat, but is more usually referred to the ear.

Larynx

An alteration in voice (dysphonia) is the predominant symptom in laryngeal pathology. Respiratory difficulties usually occur late. Pain, difficulty in swallowing (dysphagia) or a lump in the neck in association with dysphonia may represent laryngeal malignancy. Aspiration of solids and liquids may occur with an incompetent larynx due to vocal cord paralysis, but is invariable in neurological disease producing sensory loss of the supraglottis.

Salivary glands

Pain and swelling are the two cardinal symptoms of pathology in the major salivary glands. Characteristics of the pain may lead to a specific diagnosis. If associated with mastication and some temporary swelling of the gland, particularly the submandibular, it may be due to an obstructive lesion in the salivary ducts. Continuous pain of increasing severity should heighten the suspicion of malignant disease.

A permanent enlargement of the salivary gland is neoplastic unless proven to the contrary. Sjögren’s syndrome may produce swelling of one or all of the major salivary glands. Certain endocrine disease (e.g. myxoedema) and drugs (e.g. oral hypoglycaemics) may cause salivary gland hypertrophy. A weakness of the facial nerve in parotid gland disease signifies malignancy.

Neck lumps

Persistent neck lumps should be investigated. This should include fine needle aspiration cytology (FNAC), with ultrasound guidance if available. A full examination of the upper air and food passages should be carried out and biopsies taken if malignancy is suspected.

Imaging

The value of plain radiology of the oral cavity is limited to viewing dental disease. Otherwise, computed tomography (CT) or magnetic resonance imaging (MRI) scanning is superior. However, lateral X-rays of the pharynx are useful, and may show evidence of abnormal shadowing. Contrast swallow studies may provide information on hypopharyngeal and oesophageal pathology (Fig. 3.10). A variety of radiological investigations of the salivary glands are available and are selected according to the suspected pathology (Table 3.2).

Fig. 3.10 A barium swallow showing a large filling defect in the pharyngo-oesophageal region.

Table 3.2 Imaging techniques available in salivary gland pathology

Biopsy

Any persistent mass or swelling should be biopsied. In the oral cavity this may be possible with simple local anaesthesia. Masses sited in the pharynx often require full assessment under a general anaesthetic, and special instrumentation is required for biopsy. All laryngeal masses require biopsy. Swellings of a major salivary gland can be biopsied by fine needle aspiration, which can readily be performed as an outpatient procedure. Excision biopsies are required in all other circumstances.

Acute laryngitis

Acute laryngitis is very common and frequently associated with an upper respiratory tract infection. It may also be non-infective, occurring after vocal abuse, e.g. shouting. There is invariably some pain in the throat. Resolution is spontaneous, although a degree of symptomatic relief is produced by steam inhalations and voice rest. If symptoms continue for more than 3 weeks, referral to an ear, nose and throat (ENT) specialist is mandatory.

Polyps

Unilateral inflammatory polyps are not uncommon (Fig. 3.11). The history is similar to acute laryngitis, but resolution of hoarseness cannot occur until the polyp is removed under microlaryngoscopic control. Inhalation of fumes, whether from tobacco, smoke or chemicals, may result in acute dysphonia. All inflammatory lesions, either infection or traumatic, may produce a sufficient degree of oedema to cause respiratory embarrassment.

Fig. 3.11 A large polyp arising from the right vocal fold.

Chronic laryngitis

Chronic dysphonia is frequently due to chronic laryngitis. The risk factors are smoking, alcohol, laryngopharyngeal reflux and vocal abuse. The larynx may show hypertrophic epithelium and leukoplakia (Fig. 3.12). Such an appearance may herald neoplastic change, so biopsy is mandatory. If neoplasia has been excluded, management is directed to avoiding known aetiological factors.

Fig. 3.12 Chronic hyperplastic laryngitis. The white appearance is leukoplakia.

Laryngopharyngeal reflux

Gastro-oesophageal reflux disease (GORD) is due to reflux of stomach contents above the lower oesophageal sphincter. Reflux above the lower oesophageal sphincter is called laryngopharyngeal reflux (LPR). The refluxate contains acid, enzymes (pepsin) and bile salts. All of these can be damaging to the larynx. Conventional 24 hour pH studies may not be diagnostic for LPR as they only screen for prolonged reflux episodes with a pH below 4. Transient reflux or less acidic refluxate may not produce heartburn (‘silent reflux’) but still lead to laryngeal symptoms such as dysphonia, cough and throat clearing. LPR is also a risk factor for laryngeal pathology such as chronic inflammation, vocal granulomas and even mucosal metaplasia (Fig. 3.12).

Spasmodic dysphonia

Spasmodic dysphonia is primarily a neurogenic disorder, although a small percentage of cases may be psychogenic in origin. The most common form is characterized by gross hyperadduction of the vocal cords. The voice is distinctive and variously described as ‘strained’ or ‘strangled’. However, during singing, crying and laughing, the voice may be normal. In some patients, the onset of symptoms is related to a major life event, e.g. bereavement, family conflicts or road accidents.

Conventional speech therapy techniques are beneficial in treating those cases of psychogenic origin, but have little effect on those of neurogenic aetiology. Treatment involves regular injections of botulinum toxin into the vocal folds to abolish neuromuscular transmission at the motor end plate.

Acute non-infective laryngitis

Laryngitis can occur after an episode of aggressive singing, shouting or screaming. The cords are reddened, mild oedema may be present, and submucosal haemorrhages may occur. Treatment is directed at allowing the acute inflammation to resolve and correction of underlying poor vocal habits.

Vocal cord nodules

Nodules are more common in male children and adult women, particularly in personalities who vocalize aggressively.

The nodule is located at the junction of the anterior and middle third of the vocal cord (Fig. 3.16). This is the area of maximum trauma at higher pitch levels seen in activities such as screaming and singing. The dysphonia is breathy and husky with a low pitch quality due to the mass loading of the vocal cords.

Fig. 3.16 Vocal cord nodules.

With suitable voice therapy at reducing stress and improving vocal production, the majority of vocal cord nodules either resolve or are greatly improved. Only rarely is microlaryngoscopic excision required.

Vocal cord oedema and polyps

Oedema of the vocal cords is usually symmetrical and affects the whole length of the cord. It is due to accumulation of fluid in the subepithelial space of Reinke and is called Reinke’s oedema. Localization of the oedema to a circumscribed site will produce a polyp, usually sited in the anterior third of the vocal cord. Smoking is thought to be the principal risk factor for Reinke’s oedema owing to its effects on collagen synthesis and the microvascular circulation. Laryngopharyngeal reflux and hypothyroidism are the other risk factors.

Mild oedema of the cords may resolve with improvement in the voice. More severe forms, such as Reinke’s, are best treated by microsurgical removal of oedematous tissue, preserving the overlying mucosa (Fig. 3.17). Tissue should always be sent for histological diagnosis.

Fig. 3.17 Reinke’s oedema causing swelling of both vocal cords. There is also a vocal cord polyp in the subglottis anteriorly.

Chronic non-infective laryngitis

Epithelial changes in the vocal cords can occur owing to chronic vocal abuse coupled with irritant effects of long-term alcohol and tobacco use. The voice is described as a ‘gin and midnight voice’. The changes may be reversible with vocal therapy and alteration of life habits, but most patients will require surgical removal of the hyperplastic epithelium. Dysplasia or even frank neoplasia can occur in chronic hyperplastic laryngitis.

Contact ulcers

Vocal abuse due to hyperadduction of the vocal folds may result in erosion of surface mucosa; particularly susceptible is the junction of the middle and posterior third of the vocal cord (Fig. 3.18). These are termed contact ulcers and can be sited at the vocal process of the arytenoids. The reaction can sometimes lead to considerable granulation tissue with the formation of a contact granuloma (Fig. 3.19). Gastro-oesophageal reflux may exacerbate or perpetuate this problem.

Fig. 3.18 Contact ulcer on vocal process of left arytenoid.

Fig. 3.19 Vocal cord granuloma (x) arising from the vocal process of the left arytenoid cartilage.

A unilateral ulcer will require biopsy to exclude neoplasia. Bilateral cases without marked granulation may resolve with a combination of voice therapy, antibiotics, antireflux treatment and a reducing course of oral steroids. Surgical excision followed by medical treatment is rarely necessary.

Musculoskeletal tension disorders

Tension in individuals can be due to exogenous sources, e.g. overwork, worries or family life. Endogenous causes of tension include features such as overambition, perfectionism and uncontrollable anger. Such stresses may produce contraction of the intrinsic and extrinsic muscles of the larynx. This hypertonicity results in an audible and normal voice disorder, laryngoscopic examination.

The cardinal features are a dysphonia and the presence of discomfort or pain around the larynx. The clinician can reproduce the pain by palpating the larynx (Fig. 3.21). Occasionally patients may complain of feeling a foreign body in the throat and difficulty in swallowing.

Fig. 3.21 Laryngeal signs present in patients suffering with dysphonia secondary to musculoskeletal tension disorders.

The diagnosis is confirmed by an improvement in the voice if the larynx is massaged. Usually, counselling to reduce the causes of stress leads to rapid resolution of symptoms.

Ventricular dysphonia (dysphonia plicae ventricularis)

Ventricular dysphonia is a voice disorder that results from utilizing the false cords to produce vibration. It is usually seen in tense individuals. However, patients with lesions of the true cords may compensate by vocalizing with the false cords. The voice is harsh and frequently low pitched as if the patient is being strangled. Speech therapy is helpful in management.

Suitable speech therapy directed at muscular relaxation and correct vocalization produces good results.

Conversion voice disorders (hysterical voice disorder)

A conversion reaction is the production of physical symptoms without any underlying pathophysiological disease. If the larynx is chosen as the vehicle for the conversion reaction it can result in muteness, aphonia or dysphonia. A diagnosis of a conversion voice disorder can only be made if the larynx is normal in structure and function. In the majority of cases the conversion voice disorder is associated with a major emotional conflict or stress. The voice symptoms enable the patient to avoid emotional anguish.

The basis of treatment is to uncover the causes of the stress and assist the patient in coping with the events. Retrieval of the voice must be rapid, otherwise the risk of the conversion being resistant to therapy is high.

Mutational falsetto (puberphonia)

Mutational falsetto is the failure to change from a preadolescent high-pitched voice to the lower pitched voice of male adulthood. It is rarely due to immaturity of the larynx or vocal cords. Occasionally, chronic disorders, e.g. severe childhood asthma, may prevent or retard laryngeal development. In the majority of cases of puberphonia, the larynx is anatomically and physiologically normal.

The voice is characteristically high pitched, weak, breathy and monotonous and female in quality. It sounds immature and inadequately assertive. However, in sudden vocal outbursts, e.g. coughing or laughing, the voice may drop in pitch. Only a mature larynx can produce the low-pitched voice, enabling an aetiology of hypogonadism to be dismissed. Voice therapy usually produces a rapid resolution. In rare cases, long-term therapy is required to lower the fundamental speaking frequency.

Laryngeal papillomatosis

Laryngeal papillomata (Fig. 3.20) is a rare cause of dysphonia. It is caused by the human papilloma virus subtypes 6 and 11 and occasionally subtype 16 or 18. The virus is usually acquired in utero through an ascending infection through the mother’s cervix.

Fig. 3.20 Extreme laryngeal papillomatosis occluding the airway and obscuring the laryngeal inlet.

Symptoms range from none to dysphonia to dyspnoea with or without stridor. Treatment is aimed at inducing a remission. Human papilloma vaccination programmes do not include subtypes 6 and 11, so surgery is indicated in symptomatic individuals.

Laryngotracheobronchitis

Laryngotracheobronchitis is a viral infection, usually of the parainfluenza or respiratory syncytial type, occurring mostly between the ages of 6 months and 3 years. Clinical features include:

The airway problems are caused by the presence of tenacious secretions and mucosal swelling in the subglottis with risk of impaction of plugs of mucus.

Hospitalization is advisable in all except the mildest cases. The child is nursed in a croupette with humidified and warmed air to loosen thick secretions. Oxygen is administered to correct hypoxia. Nebulized or systemic steroids may be helpful.

Intubation is required in progressive and severe cases. Tracheostomy is reserved for airways that cannot be intubated. Regular saline suction and physiotherapy are performed postoperatively. In most cases, endotracheal intubation should only be necessary for 2–5 days.

Supraglottitis

Supraglottitis (acute epiglottitis) is caused by group B Haemophilus influenzae and is characterized by gross swelling in the supraglottis (Fig. 3.22). It is seen primarily in 3–7-year-olds, although adults may also be affected. Clinical features include:

Fig. 3.22 Supraglottitis. Diagnosis is clinical and the priority is to secure the airway. Physical examination of the throat may induce respiratory arrest and should be avoided unless facilities for immediate intubation or tracheostomy are available.

Supraglottitis is an emergency, as the time interval from stridor to total respiratory obstruction may be extremely short. Any distress to the child is to be avoided. Heliox and adrenaline (epinephrine) nebulizers may buy time until a senior anaesthetist and ENT surgeon are available. In most cases the anaesthetist is successful in intubating the child; however, the ENT surgeon is standing by to carry out an emergency tracheostomy if necessary. Intravenous third-generation cephalosporins are commenced and later changed depending on blood culture results. The patient is usually extubated a few days later when the condition has responded to treatment. Supraglottitis has become less common in children because of vaccination programmes.

Congenital tumours, webs and cysts

Subglottic haemangioma is the most common congenital tumour causing stridor. It is visualized on a lateral neck X-ray. The diagnosis is confirmed by endoscopy without biopsy. The condition is self-limiting as the tumours start to regress after the first year of life, but tracheostomy is occasionally necessary for airway obstruction. Laryngeal webs or cysts of any significant size may produce stridor, particularly if the airway is further compromised by an intercurrent infection.

Laryngomalacia (congenital laryngeal stridor)

Laryngomalacia is characterized by a weak supraglottic framework which collapses on inspiration, notably during exertion and crying. Severe stridor can supervene during respiratory infections. It is self-limiting and usually resolves by the age of 2 years. Surgery may be indicated if there is failure to thrive.

Subglottic stenosis

Subglottic stenosis may be congenital. Acquired cases are the result of the trauma of prolonged endotracheal intubation, particularly in premature births (Fig. 3.23). Clinical features include stridor on exertion, or with respiratory infection.

Fig. 3.23 Subglottic stenosis, seen here in a premature birth. The condition can be verified by a neck X-ray.

Tracheostomy may be necessary to secure the airway. The subglottis can be subsequently sized and decannulation attempted if the lumen enlarges satisfactorily with age. Laser excision or laryngeal reconstructive surgery may be required in severe cases.

Foreign body obstruction

Inhalation of foreign bodies is most common in children. In adults, the problem is usually associated with psychiatric illness or alcohol intoxication. Objects can lodge anywhere in the laryngotracheobronchial tree (Fig. 3.24), and may remain symptomless for long periods. Common symptoms include:

Fig. 3.24 Foreign body: chest X-ray in full expiration. A foreign body (peanut) lodged in the left main bronchus has produced ipsilateral hyperinflation and gross mediastinal shift to the right.

Foreign bodies can be radiolucent, so plain radiology may be misleading. Foreign bodies in the oesophagus can also produce stridor.

In a child, a foreign body may be dislodged by holding the patient up by the legs and giving a sharp slap on the back. The Heimlich manoeuvre can be used in both adults and children (Fig. 3.25). There should be a low threshold for tracheobronchoscopy in a child who has had a significant choking episode, even in the absence of clinical signs or radiological findings.

Fig. 3.25 The Heimlich manoeuvre: performed by applying a sudden bear hug, centred on the upper abdomen and xiphisternal region.

Retropharyngeal abscess

A now rare condition, retropharyngeal abscesses occur mostly in young infants and children. Inflammation and swelling in the retropharyngeal space, secondary to oropharyngeal infection, can cause respiratory embarrassment and severe dysphagia (Fig. 3.26). The child assists breathing by hyperextension of the neck, which is held rigid. Urgent parenteral antibiotics are administered and surgical drainage is performed to avoid spontaneous rupture with risk of inhalation of pus.

Fig. 3.26 Retropharyngeal abscess.

Respiratory papillomata

Respiratory papillomata are characterized by warty lesions appearing in the larynx caused by the human papilloma virus (Fig. 3.27). The trachea, bronchi and pharynx may be involved in florid cases. They are thought to be due to ascending uterine infection; however, acquired cases in adults may be due to genetic predisposition or be sexually acquired. Clinical features include stridor and hoarseness.

Fig. 3.27 Respiratory papillomata.

The carbon dioxide laser or sharp dissection under the microscope will minimize trauma to the underlying laryngeal mucosa.

If surgery needs to be repeated frequently for symptom control, then medical therapy, such as interferons, may be considered to try to induce remission. Tracheostomy is sometimes necessary in severe cases.

Acute laryngitis

Acute laryngitis results in marked inflammation of the vocal cords which can occur in respiratory infections or secondary to vocal abuse, tobacco smoke or ingestion of spirits. Clinical features include hoarseness and throat discomfort.

Treatment is symptomatic and includes voice rest, steam inhalation and avoidance of smoke and spirits.

Subglottic/tracheal stenosis

Subglottic stenosis can be congenital or acquired. The management of subglottic stenosis in children depends on the severity of the problem. Mild cases can be managed conservatively and may only require a tracheostomy until the airway has grown to an adequate size. Severe cases may require augmentation of the airway with cartilage grafts and are best managed in specialized units with a multidisciplinary approach.

Adult subglottic or tracheal stenosis is increasingly common and often misdiagnosed as asthma (Fig. 3.31). Advances in medical care mean that more patients are surviving periods of ventilation on intensive care units. However, injury is often sustained to the airway and one or more of the following factors may play a role:

Fig. 3.31 Acquired subglottic stenosis.

Management

It is sometimes possible to visualize a subglottic stenosis using a flexible laryngoscope. The site, degree and length of the stenosis can be determined using lateral neck X-rays. A CT scan is often more helpful (Fig. 3.32). Respiratory function tests will help to gauge the degree of disability related to the stenosis. However, some patients have a tracheostomy and these tests are not always possible.

Fig. 3.32 CT scan showing subglottic stenosis (arrow).

Tracheal or subglottic stenosis, if minor, may be treated with cruciate cuts using a knife or laser and dilatation. If the stenosis is more severe, it may require temporary stenting (Fig. 3.33).

Fig. 3.33 Silastic tracheal stent.

The topical application of mitomycin C (a cytotoxic antibiotic), if used in low concentrations, can inhibit fibroblast activity and restenosis. A more severely damaged airway may require anterior augmentation or, failing this, tracheal resection and end-to-end anastomosis.

Bilateral vocal cord palsy

Bilateral vocal cord palsy may be congenital or acquired. The vocal cords come to lie in the median or paramedian position. Although voice or cry may be good, there is usually stridor and dyspnoea. Congenital bilateral cord palsy will often recover as the child grows and the only treatment necessary may be a temporary tracheostomy. Acquired bilateral cord palsy is most commonly iatrogenic, following surgery on the neck or thorax, and the patient is usually reintubated or an emergency tracheostomy carried out. It is possible to remove the tracheostomy tube following a procedure on the vocal cords. The vocal cords can be lateralized surgically or an airway is lasered out from the back of one vocal cord (Fig. 3.34). The patient may subsequently be decannulated but will have a weak and ‘breathy’ voice.

Fig. 3.34 Laser cordectomy.

Glottic webs

Small glottic webs can produce dysphonia and, if more severe, dyspnoea. Small webs can be managed by dividing and applying mitomycin C. The procedure may need repeating several times because the web can reform.

Larger webs are also divided but, in addition, may require the insertion of a Silastic sheet into the anterior commissure or a laryngofissure approach and the insertion of a keel (Fig. 3.35).

Fig. 3.35 Anterior commissive injuries may lead to web formation. A keel, made of tantalum or Silastic, can be inserted through a laryngeal fissure to prevent this complication.

Life-threatening respiratory obstruction

Life-threatening respiratory obstruction is usually due to inhalation of foreign bodies or infections of the laryngotrachea. Children are more likely to be involved than adults. Wide-bore needles may be inserted directly into the trachea to provide temporary relief (Fig. 3.36) until either intubation or tracheostomy can be performed.

Fig. 3.36 Emergency methods to secure the airway in cases of life-threatening respiratory obstruction. (a) Needles inserted directly into the trachea. (b) The airway entered through the cricothyroid membrane (cricothyroidotomy; laryngotomy). In this instance a wide-bore venous cannula has been used.

A similar approach is feasible with the airway entered through the cricothyroid membrane (cricothyroidotomy) (Fig. 3.36). The membrane is easily palpable between the cricoid ring and inferior border of the thyroid cartilage. Any sharp object, e.g. a knife or scalpel, is inserted into the region and rotated once the airway is entered. Any available tube, e.g. a catheter or the barrel of a pen, is inserted to maintain the airway until intubation or a formal tracheostomy is performed.

It is rare nowadays to perform an emergency tracheostomy under local anaesthesia. Ongoing clinical assessment of the airway should allow it to be performed as an elective procedure.

Gradual-onset obstruction

It is imperative not to allow the clinical situation to deteriorate to one of life-threatening obstruction. Increasing stridor, the use of accessory muscles of respiration, tachypnoea, tachycardia and intercostal recession are worrying signs (see Table 3.6, p. 64).

In all age groups endotracheal intubation should be attempted only by an experienced anaesthetist (Fig. 3.37). This may require additional techniques with a rigid bronchoscope or flexible laryngoscope as aids in difficult intubations. An ENT surgeon should be standing by to perform a tracheostomy if intubation fails. Tracheostomy in children should, for a variety of reasons, be avoided (see Table 3.10, p. 70), except in an emergency.

Fig. 3.37 Endotracheal intubation can be routed through either the nose or the mouth.

Elective tracheostomy

The technique of elective tracheostomy is illustrated in Figure 3.38. The skin incision is made midway between the cricoid ring and suprasternal notch. The strap muscles are identified, running in the vertical plane, and separated in the midline. The thyroid isthmus should be divided and transfixed to avoid thyroid tissue falling into the tracheal window. In adults, a small window is then cut in the trachea between the second and third, or third and fourth tracheal rings. In children, a vertical incision is made to avoid transecting the trachea. The cricoid cartilage and the first tracheal ring must not be compromised, otherwise there is a high risk of late subglottic stenosis.

Fig. 3.38 Tracheostomy.

An appropriately sized tracheostomy tube with a high-volume low-pressure cuff should then be inserted. It is secured in position by tapes passed around the neck and tied. With the tracheostomy cuff inflated, the patient can continue to be ventilated.

Percutaneous tracheostomy tube insertion has gained popularity, especially on intensive care units. Relative contraindications to this technique include patients in whom it is difficult to palpate the larynx and trachea (overweight) and patients with coagulopathy.

There are several percutaneous tracheostomy kits available. All are based around insertion of a needle into the cervical trachea, which allows a guidewire to be passed. An opening into the airway, large enough to insert a tracheostomy tube, is created using serial dilators (Fig. 3.39) or using dilation forceps or a single dilation.

Fig. 3.39 Equipment required to perform a percutaneous tracheostomy.

The subsequent care of the tracheostomy should be meticulous in order to avoid severe complications. It is imperative to instruct the nursing staff appropriately (see Fig. 3.40, p. 70).

Fig. 3.40 Some important aspects of the postoperative care of tracheostomy.

Protection from bronchial secretions

With the development of medical techniques and the availability of high-dependency and intensive care units, many patients are kept alive longer than previously possible. Many patients in such units are at risk of sputum retention, e.g. chronic bronchitics or comatose patients without a cough reflex.

The modern technique is to manage these patients by inserting a percutaneous tracheostomy (Fig. 3.39). This method avoids an open procedure and may be performed by either critical care clinicians or ENT surgeons.

Protection from overspill and aspiration

The most frequent causes of overspill are neoplasia of the pharyngo-oesphagus, which prevents swallowing of food and drink, and saliva. Aspiration tends to be seen in cases of uncoordinated swallowing mechanism or secondary to laryngeal incompetence. The latter may be due to either loss of vocal cord movement, usually bilateral, or reduced laryngeal sensation.

A cuffed tracheostomy tube is required to prevent oropharyngeal contents from entering the laryngotrachea. In severe cases with no prospect of recovery of laryngeal competence, a laryngectomy may be necessary.

Acute sore throats

Infective conditions

Viral infections of the upper respiratory tract are frequently accompanied by the same pathology affecting the pharynx. Streptococcus is occasionally the primary causative organism rather than a secondary invader following a virus. Clinically the patient complains of a painful throat. Cervical lymphadenopathy and fever are common.

If viral in origin, there is invariably a runny nose and a productive cough due to chest infection. The presence of mucopus on the pharyngeal wall implies bacterial infection. Although throat swabs are not always helpful, they may rule out bacterial infection. The treatment is symptomatic. Oral analgesics and adequate fluid intake with bed rest are required for 3–4 days to allow the disease to resolve spontaneously. Antibiotics are administered only if bacterial infection is suspected. Acute tonsillitis is uncommon in adults in comparison to its frequency in children. The clinical approach is similar in both age groups (p. 73).

Candidal infection can give rise to a painful throat and is not uncommon in the immunocompromised, e.g. diabetics, and patients undergoing radiotherapy or chemotherapy, and those afflicted by lymphomata. The acquired immunodeficiency syndrome (AIDS) also increases the risk of such fungal infection. Diagnosis is made by noting the typical appearance and culture (Fig. 3.45). Treatment may be either local antifungal agents or parenteral administration if the patient also has systemic infection.

Fig. 3.45 Oropharyngeal involvement with Candida in a patient with HIV infection.

Peritonsillar abscess

A peritonsillar abscess is a condition in which pus forms between the tonsil capsule and the superior constrictor muscle. This will be preceded by a period of peritonsillar cellulitis. The patient has symptoms of severe unilateral sore throat causing dysphagia. This may lead to an inability to swallow even saliva, resulting in dribbling. The voice has a ‘hot potato voice’ quality. Trismus may be so prominent that visualization of the oropharynx is difficult. Ipsilateral otalgia and cervical adenopathy are other features. The most obvious clinical sign is a unilateral tonsillar inflammation causing deviation of the base of the uvula (Fig. 3.46).

Fig. 3.46 Gross swelling of the (right) tonsil due to a peritonsillar abscess. The uvula is pushed across the midline.

Peritonsillar cellulitis is treated by parenteral antibiotics. If an abscess is suspected, management involves incision and drainage of the abscess and parenteral antibiotics. As the β-haemolytic Streptococcus is the most frequent causative organism, penicillin is appropriate. Tonsillectomy may be advised in selected patients.

Chronic sore throats

Any patient with a chronic sore throat should be suspected of harbouring a malignancy in the oral cavity or pharynx. Associated cardinal symptoms, such as weight loss, dysphagia, hoarseness, and a history of smoking and excessive alcohol intake, make such a diagnosis more likely (see Fig. 3.54, p. 76).

The most common cause of a chronic sore throat in adults is chronic pharyngitis. This inflammation is multifactorial and non-infective (Fig. 3.47). Tobacco smoke and alcohol are particularly irritant to the pharyngeal mucosa. Chronically infected tonsils, characterized by infected white debris in the tonsillar crypts, can produce a discomfort in the throat. A hiatus hernia with acid reflux can also result in a constant sore throat due to pharyngeal inflammation. Management involves conservative measures to reduce or abolish the effect of irritating agents and tonsillectomy in selected cases.

Fig. 3.47 Chronic pharyngitis: potential aetiological factors producing chronic inflammation and the symptom of sore throat.

Acute sore throats

Tonsillitis

Acute tonsillitis presents a quite different clinical picture. The child is systemically unwell, there is dysphagia, halitosis, pyrexia, together with cervical lymphadenopathy. The diagnosis is apparent from the appearance of the tonsils (Fig. 3.48). Rare disorders that give a similar appearance may need to be excluded. Diphtheria (usually the tonsil is covered by a membrane) and haematological disorders should be included in the differential diagnosis. Throat swabs are generally unhelpful in management as the most common organism isolated is Streptococcus.

Fig. 3.48 Acute bacterial tonsillitis. Both tonsils are grossly enlarged and there is exudate on the surface. Glandular fever tonsillitis has a similar appearance.

Treatment of acute tonsillitis is with bed rest and administration of antibiotics such as penicillin, with maybe the first dose parenterally. Maintenance of fluid intake is important, and paracetamol provides suitable analgesia and acts as an antipyretic in lowering the temperature. Symptoms usually resolve within a few days. Tonsillectomy may be recommended in patients with severe recurrent infections (p. 74). Complications of tonsillitis are infrequent, but spread of infection may lead to abscess formation in the peritonsillar, retropharyngeal or parapharyngeal spaces (Fig. 3.49).

Fig. 3.49 Infection of the parapharyngeal space. This is usually due to spread from primary infection in the tonsils or teeth. There is a marked tender external swelling in the neck.

Indications

The indications for tonsillectomy are controversial (Table 3.13). Recurrent tonsillitis is probably the least controversial indication, as any child having more than three or four attacks a year may be spending upwards of 1–2 months off school every year. Chronic tonsillitis is not a straightforward diagnosis, and some would dispute it as a cause of a chronic sore throat in adults. Tonsillectomy for peritonsillar abscess (quinsy) is only recommended if there is a past history of recurrent tonsillitis. The tonsils are usually symmetrical so that tonsillectomy for unilateral enlargement is necessary if a diagnosis of neoplasia is being entertained. More recently it has become apparent that the tonsils, usually in association with the adenoids in children and the uvulopalatal area in adults, may be a cause of snoring and the more sinister obstructive sleep apnoea. In such cases tonsillectomy may be advised, in combination with adenoidectomy and palatal surgery as appropriate (p. 80). Tonsillar biopsy is also used as a screening test for new-variant Creutzfeldt–Jakob disease.

Table 3.13 Tonsillectomy: indications and contraindications

Contraindications

Contraindications to tonsillectomy are summarized in Table 3.13. The major operative risk is haemorrhagic so that any bleeding disorder should be corrected before surgery or permanent deferral may be necessary. Any recent inflammation will result in greater haemorrhage, so tonsillectomy should be avoided for 2–3 weeks after an acute infection. A child weighing less than 15 kg has a greater risk attached to the hazards of blood loss. In such cases the indications for surgery should be clear-cut and strong. Equally, a grossly overweight patient should be placed on a sensible weight-reduction diet before reconsidering tonsillectomy or any other elective surgical procedure.

Procedure

The tonsillectomy is performed under general anaesthesia by dissecting the tonsil from its bed. Haemostasis is achieved using surgical ties or bipolar diathermy.

Postoperative care and complications

Postoperatively the vital signs are monitored so that any reactionary haemorrhage is quickly recognized. The patient is nursed in the tonsil or coma position until the cough reflex has recovered. Food intake is encouraged as soon as possible so that the pharyngeal muscles are prevented from stiffening, but chewing also clears slough from the tonsil beds. Post-tonsillectomy pain is still difficult to manage outside hospital and patients should be encouraged to take regular oral analgesics; local anaesthetic mouthwashes may also be helpful.

Reactionary haemorrhage occurring within the first 24 hours after surgery is the most lethal complication. It should be picked up early provided the vital signs of blood pressure and pulse have been regularly and correctly recorded. In children the blood pressure may be well maintained owing to a rise in the pulse rate until the cardiovascular system suddenly decompensates. The patient is returned to the theatre to ligate the bleeding vessel. Blood transfusion may be required.

Secondary haemorrhage is due to infective slough separating from the tonsil bed and occurs about 5–10 days postsurgery. It invariably resolves with antibiotics, only rarely requiring formal vessel ligation or transfusion.

Symptoms of adenoidal infection or hypertrophy (Fig. 3.51)

Nasal symptoms

Large adenoids can cause severe nasal blockage resulting in mouth breathing. Other manifestations include nasal discharge due to chronic adenoidal infection. Snoring and sleep apnoea in children are invariably made worse by large adenoids.

Fig. 3.51 Symptoms of adenoid hypertrophy.

Signs and investigations of adenoidal disease

The nasal and otological signs of adenoidal disease are fairly obvious. A child with adenoids occluding the nasopharynx may have a hyponasal voice as the nose cannot act as a resonating chamber. The child speaks as if he or she has a constant cold, with a low-pitched, lifeless tone.

In children a paediatric flexible nasal endoscope is the most reliable way to assess the state of the adenoids. Where this is not available, a lateral X-ray of the nasopharynx may be helpful (Fig. 3.52). However, in most cases a clinical assessment of relevant symptoms is sufficient to consider adenoidectomy, and the size is assessed under general anaesthesia by finger palpation of the postnasal space or a postnasal space mirror.

Fig. 3.52 Lateral X-ray of the postnasal space showing a large pad of adenoidal tissue narrowing the airway.

Adenoidectomy

The indications and contraindications to adenoidectomy are summarized in Table 3.14. Traditionally, adenoids are curetted under general anaesthesia, a blind technique which may leave residual adenoidal tissue. Increasingly, adenoidectomy is performed, under vision, using a postnasal space mirror and suction diathermy ablation (Fig. 3.53). The postoperative care is similar to a child undergoing tonsillectomy.

Table 3.14 Adenoidectomy: indications and contraindications

Fig. 3.53 Suction diathermy and postnasal mirror used to ablate adenoidal tissue.

Complications include reactionary haemorrhage, which usually manifests as persistent nasal bleeding or occasionally haematemesis from swallowed blood, and is accompanied by a rising pulse rate. The child is returned to theatre and a postnasal tamponade effected by a postnasal pack. Secondary haemorrhage is rare but occurs about 5–10 days postoperatively and usually resolves on bed rest and antibiotic therapy. Hypernasality (rhinolalia aperta) of speech can result in patients with a short palate, in whom removal of the adenoids results in air escape as the nasopharynx cannot be closed off. Such a complication is more likely in patients with a cleft palate or submucous cleft, in whom adenoidectomy should be avoided.

Neuromuscular disorders

Dysphagia is invariably associated with other manifestations of the underlying pathology. Neurological lesions frequently cause sensory denervation of the larynx with a high risk of aspiration. Motor neurone disease results in a similar risk to the airway because of severe incoordination of the swallowing mechanism. Division of the cricopharyngeus (cricopharyngeal myotomy) may relieve dysphagia of neurological origin, as there is a failure of this segment of the lower pharynx to relax.

Intrinsic lesions of the digestive tract

Pharyngeal pouch

A pharyngeal pouch is a hernia of the pharyngeal mucosa through a potential weakness (Killian’s dehiscence) between the upper thyropharyngeus and lower cricopharyngeus fibres of the inferior constrictor muscle. Food debris collects in the pouch, which enlarges progressively. Regurgitation of undigested food particles is common and overspill may result in a chronic cough and pneumonitis. The pouch may increase in size to such an extent that it compresses the oesophagus to cause dysphagia. A barium swallow is usually diagnostic (Fig. 3.57). All but the smallest pouches will require either surgical excision and cricopharyngeal myotomy through the neck, or endoscopic stapling and division of the party wall between the pharynx and oesophagus.

Fig. 3.57 (left) A small pharyngeal pouch (arrows) that retains contrast medium during a barium swallow.

Oesophageal stricture

Strictures of the oesophagus may be due to malignancy or secondary to fibrosis induced by chronic reflux oesophagitis associated with a hiatus hernia. It is important to fully investigate all strictures with biopsy, to exclude neoplasia. Inflammatory strictures producing dysphagia are invariably accompanied by a long history of heartburn and epigastric discomfort. The typical stricture due to oesophageal reflux is seen in the lower third of the oesophagus (Fig. 3.58). Treatment comprises aggressive medical therapy to counteract the acid reflux, and possible dilatation of the stricture. Failure of conservative measures in patients with severe symptoms will necessitate surgical correction.

Fig. 3.58 (right) A stricture of the lower third of the oesophagus due to long-standing oesophageal reflux.

Achalasia of the oesophagus

Achalasia of the oesophagus is caused by a failure of relaxation of the cardia and abnormal oesophageal muscular tone during swallowing. This results in a stricture at the defective site, with gross proximal dilatation of the oesophagus. Besides dysphagia, regurgitation is common. A barium swallow has a typical appearance (Fig. 3.59). The majority of patients will require a cardiomyotomy (Heller’s operation) to divide the cardiac sphincter, as dilatation with bougies frequently fails to produce satisfactory relief.

Fig. 3.59 (left) Achalasia of the cardia. The oesophagus is grossly dilated containing food and liquid debris. The distal part of the oesophagus is extremely narrow.

Extrinsic lesions

The thyroid gland may narrow the oesophagus, either by compression in benign pathology, or by direct invasion in cases of malignancy. Vascular compression of the oesophagus can be produced by an aortic aneurysm or an aberrant right subclavian artery (dysphagia lusoria) (Fig. 3.60).

Fig. 3.60 (right) Dysphagia lusoria. This very rare cause of dysphagia is due to an aberrant right subclavian artery coursing posterior to the oesophagus, causing a spiral filling defect.

Psychosomatic causes

Globus pharyngeus, previously called globus hystericus, is a condition mainly of middle-aged women who complain of a feeling of lump in the throat. True dysphagia is not present. The patient usually volunteers that the symptoms are noted particularly during periods of anxiety. In such cases reassurance is all that is required. However, in those patients who appear to be psychologically well balanced, a barium swallow and a diagnostic oesophagoscopy should be performed to exclude neoplasia. It is now felt that in many cases of globus pharyngeus, acid reflux produces a reflex cricopharyngeal spasm leading to the symptom complex. It is therefore reasonable to give a trial of antireflux treatment, which may include simple antacids and proton pump inhibitors.

Swelling

The parotid gland territory is more extensive than most clinicians appreciate. Parotomegaly can affect the gland diffusely, or be localized to one area (Table 3.16). Extraparotid disease may present as parotid lumps (Fig. 3.61). A unilateral localized swelling is invariably neoplastic, of which 90% will be benign pleomorphic adenomas. Malignant parotid tumours are frequently accompanied by pain and facial nerve paresis, in addition to parotomegaly (see p. 113).

Table 3.16 Causes of swelling and pain of the parotid gland

Swelling and pain

Most patients who complain of pain in the parotid region invariably exhibit some degree of swelling. Most causes of parotid pain are exacerbated by chewing and this can be elicited by requesting the patient to chew a lemon-flavoured sweet.

Mumps

This used to be the most common cause of bilateral parotid swelling until the introduction of vaccination programmes (Fig. 3.62). Mumps-related parotomegaly is tender to touch and there is usually trismus and pyrexia. Treatment is symptomatic unless a bacterial infection supervenes to produce suppuration. Rare complications of mumps infection include orchitis and sensorineural deafness.

Fig. 3.62 Bilateral parotid enlargement due to mumps virus infection.

Neoplasia

Neoplasia, particularly if malignant, presents with parotid pain and swelling (p. 112). Secondary bacterial infection may produce features of a parotitis. The facial nerve is commonly affected, and there may be skin tethering (Fig. 3.63).

Fig. 3.63 Adenocarcinoma of the parotid gland.

Swelling

Painless diffuse enlargement of the submandibular gland is infrequent. In such cases, neoplasia should be excluded (Table 3.18).

Table 3.18 Causes of swelling and pain of the submandibular gland

Swelling and pain

The most common cause of swelling in the submandibular gland region is secondary to infection in the oral cavity. This is because the gland is associated with lymph nodes which become involved in the inflammatory response. Apical infection of the lower molars, gum disease and metastatic intraoral cancer may all produce swelling in this area.

Submandibular calculi

The most common primary disease of the submandibular gland causing pain and swelling is calculi. The symptoms are typically related to meal times. Usually the distal part of the duct is blocked so that many calculi are palpable in the floor of the mouth. Most stones are radio-opaque (Fig. 3.64). If located in the mouth they can be removed by an intraoral approach. More proximally sited calculi require excision of the gland.

Fig. 3.64 A stone in the submandibular duct.

Obstructive sleep apnoea

Snoring is invariably present. It is usually loud but interspersed with the apnoeic episodes when the pharynx is totally occluded. There is a struggle, with limbs thrashing in an attempt to shift air, and considerable movement of the thorax and abdomen is apparent. Symptoms due to sleep deprivation and secondary cardiac complications may occur.

The adult patient is often overweight and has a short neck, but routine examination may be normal. In children the tonsils may be so large that they meet or ‘kiss’ in the midline.

Central sleep apnoea

In contrast to OSA, there is no struggle in these patients. However, the features of sleep deprivation and any associated central nervous system (CNS) pathology may be present.

Rhinolaryngoscopy

Passage of a flexible rhinolaryngoscope (Fig. 3.66) allows a full examination of the upper respiratory tract to identify any obstructive pathology. It can also be used to observe whether the velopharyngeal lumen is compromised as a patient recovers from a short anaesthetic which mimics sleep nasendoscopy. A forced negative Valsalva manoeuvre (Müller manoeuvre) with visualization of the velopharynx also provides a measure of potential narrowing in this region.

Fig. 3.66 Examination with the flexible rhinolaryngoscope. A full examination of the upper respiratory tract may allow identification of the obstructive causes of snoring and sleep apnoea.

Radiology and CT scanning

Radiological investigation may be a simple lateral X-ray of the postnasal space to identify an adenoidal pad, and other views to check the position and size of the tongue in relation to the jaw. CT scanning can also be used to assess airway obstruction.

“STOP-BANG” Scoring System for Obstructive Sleep Apnoea

This is a simple questionnaire of 8 questions requiring a yes/no response e.g. degree of daytime sleepiness, Body Mass Index, evidence of nocturnal cessation of breathing … . A score above 3 indicates a strong likelihood of Obstructive Sleep Apnoea and should be referred for formal assessment including a sleep study.

Sleep studies

The routine investigations may be inconclusive, and a satisfactory screening evaluation should include a sleep study. During the sleep study it is possible to measure the following parameters (Fig. 3.67):

Fig. 3.67 Sleep study in obstructive sleep apnoea. Note the apnoeic episodes associated with severe hypoxaemia (SaO₂) and the elevated heart rate (HR). The chest and abdominal wall distortion increases with developing desaturation.

Surgery

In adults, nasal surgery may be required for nasal polyposis or a deflected septum. The velopharyngeal isthmus is also often the site of narrowing, and this is corrected by either a laser-assisted palatoplasty (LAPP) or a uvulopharyngopalatoplasty (UPPP) with a tonsillectomy (Fig. 3.68). The results of these procedures on snoring and sleep apnoea are variable. Some patients may be candidates for hyoid and jaw surgery to correct obstruction at other levels. In extreme cases of OSA, a tracheostomy may be life saving, as it provides a bypass to any obstruction.

Fig. 3.68 Surgical options for shortening and stiffening the palate in snoring and upper airway obstruction.

In children the usual site of narrowing is the oropharynx, caused by hypertrophy of the tonsils and adenoids. This is easily corrected by adenotonsillectomy. Sedative premedication must be avoided.

Cleft palate

The most common development defects of the palate are clefts. These may be complete and involve the lips, alveolus and palate. The repair of the cleft lip is performed as soon as possible after birth. The palatal defect is closed at about 6–12 months. The repair will also involve lengthening the soft palate so that the nasopharynx can be closed from the oropharynx to prevent nasal escape of air during speech, and nasal regurgitation of food and liquids during eating.

Recurrent oral ulceration

Recurrent ulceration is the most common cause of ulcers in the oral cavity. It may be due to aphthous ulceration which is of unknown aetiology, although nutritional and hormonal factors, as well as minor trauma, have been implicated. Herpes simplex eruptions have similar clinical features, although are more likely to involve the hard palate. Some patients with recurrent oral ulceration may have underlying vitamin B, folic acid or iron deficiencies. The lesions usually commence as a small vesicle which rapidly progresses to form ulcers. They may be of any size and number and occur anywhere in the mouth (Fig. 3.70). There is severe pain and the ulcers resolve spontaneously after 2–3 weeks. Various steroid preparations as pastes or pellets may be used orally to treat ulcers. Mouthwashes containing antibiotics or antiseptics give some pain relief, e.g. phenol gargles. Treatment with aciclovir may be employed in ulcers of herpetic origin.

Fig. 3.70 Aphthous ulceration of the tongue.

Infectious ulceration

Specific microorganisms may cause oral ulceration. Tuberculosis in the oral cavity is now rare. Syphilitic disease has oral manifestations. The primary chancre has a typical appearance. Snail-track ulcers may occur in the secondary stage and gummatous eruptions of the tertiary stage may affect the palate.

Acute ulcerative stomatitis (Vincent’s angina) is an infection with a spirochaete and an anaerobic organism. It is seen in patients with poor nutrition, low general resistance and inadequate oral hygiene. The ulceration occurs along the gingival margins but spreads and coalesces. There is a marked fetor. Treatment involves penicillin and metronidazole given intravenously, and attention to oral hygiene and nutrition.

Other causes of ulceration

Potential neoplastic causes of oral ulceration should never be overlooked, particularly if the ulcer persists, enlarges or is associated with cervical adenopathy.

Certain haematological diseases may cause intraoral ulceration. Agranulocytosis can present with an acute sore throat or tongue ulceration, and acute lymphatic leukaemia may be associated with haemorrhage and ulceration of the gum margins.

Autoimmune diseases can give rise to oral manifestations. Reiter’s syndrome produces arthritis, ocular lesions and oral ulceration. Behçet’s syndrome consists of orogenital ulceration and uveitis. The oral lesions in both conditions are treated with steroid preparations to reduce the inflammation and provide pain relief.

Geographical tongue

Geographical tongue (erythema migrans linguae) has a typical appearance. There are numerous red patches which gradually coalesce, but characteristically the patterns change with time. In the red areas there is an absence of filiform papillae. The condition is asymptomatic and usually remits spontaneously.

Median rhomboid glossitis

Median rhomboid glossitis appears as a smooth red patch over the mid-dorsum of the tongue. The area lacks papillae or taste buds and is sometimes associated with candidiasis.

Vitamin deficiencies

Deficiencies of vitamin B (riboflavin and nicotinic acid) produce pellagra. This results in smooth red lips (cheilitis) and a painful glossitis. Vitamin C deficiency gives rise to scarring which is associated with severe swelling and bleeding of the gums.

Scarlet fever

Scarlet fever may present in association with acute streptococcal tonsillitis. However, it may be accompanied by the ‘strawberry tongue’ with or without the skin rash.

Retention cysts

Retention cysts can occur owing to duct blockage of a minor salivary gland. They can reach considerable sizes, particularly if located in the floor of the mouth, when the term ‘ranula’ is applied (Fig. 3.72). A localized lymphangioma has an identical appearance.

Fig. 3.72 A mucous retention cyst (ranula) in the floor of the mouth.

Fordyce spots

Fordyce spots can occur in upwards of 50% of the population by adult life. They are small yellow spots, usually in the buccal mucosa, and are caused by heterotopic sebaceous glands.

Pemphigoid eruptions

Pemphigus and mucous membrane pemphigoid both cause transitory cystic lesions, but they are more likely to present as relapsing oral ulceration. The diagnosis is made by biopsy of the paraulcer tissue. Treatment involves systemic steroids.

Torus palatinus

A bony exostosis of the posterior portion of the hard palate, a torus palatinus (p. 58), may alarm a patient. They are benign and can be removed if affecting dentures.

Radiotherapy

A potent cause of intraoral problems is external beam radiotherapy. It can lead to a dried, inflamed and cracked oral mucosa, covered in thick tenacious secretion. The tongue can take on a smooth appearance due to loss of papillae.

Fissured tongue

A fissured tongue is frequently a congenital condition (Fig. 3.73). On rare occasions it is associated with iron-deficiency anaemia. Most cases are asymptomatic, but if food debris collects in the grooves it may give rise to soreness and halitosis. This is easily managed by regular oral hygiene.

Fig. 3.73 Fissured tongue.

Black hairy tongue

A black hairy tongue is caused by an overgrowth of filiform papillae on the dorsum (Fig. 3.74). Most sufferers are tobacco smokers and some cases have followed local application of antibiotics. The papillae may reach 1 cm in length and are treated by scraping and daily application of a toothbrush to the tongue.

Fig. 3.74 A severe case of black hairy tongue.

Intraoral lumps

Although most lumps in the oral cavity are diagnosed clinically, neoplasia may present as a mass rather than an ulcer. This is especially true of tongue lumps. Therefore, virtually all intraoral lumps should be biopsied.

Sites of impaction

Fish bones tend to lodge in the oropharynx (posterior tongue, vallecula and tonsil). Most other foreign bodies will tend to impact at sites of narrowing of the pharyngo-oesophagus (Fig. 3.77). These are the piriform fossa and postcricoid region, particularly at the level of the cricopharyngeus muscle. The aorta and left main bronchus constrict the mid-oesophagus and there is a relatively reduced diameter at the gastro-oesophageal junction.

Fig. 3.77 Sites of impaction of swallowed foreign bodies.

Visualization of foreign bodies

Most foreign bodies in the mouth and pharynx can be identified with the use of a head mirror and routine instruments, e.g. tongue depressors and laryngeal mirrors. The specific sites outlined in Figure 3.77 should be inspected. Fish bones frequently lodge in the tonsil and only a tiny length may project above the surface lining.

An oesophageal foreign body will be out of sight to routine examination, but commonly is associated with pooling of saliva in the piriform fossae. X-rays may be unhelpful because only radio-opaque objects will be visualized (Fig. 3.78), but soft tissue changes can be indicative.

Fig. 3.78 Radio-opaque bodies that have been swallowed. (a) A coin located in the lower oesophagus. (b) A lamb bone in the hypopharynx.

Treatment

In general, a foreign body visualized on routine examination can be removed with angled forceps. This is especially true of fish bones lodged in the tonsil or vallecula. It is kinder to apply topical anaesthesia prior to removal. All sharp foreign bodies should be extracted at the earliest opportunity because of the risk of perforation. In patients with persistent symptoms, despite normal examination and radiology, it is necessary to exclude a foreign body, so pharyngo-oesophagoscopy should be performed.

A food bolus impacted in the oesophagus may be left for 6–12 hours and sedatives can be administered to the patient to encourage the bolus to pass on. If bone or other solid objects are involved, they should be removed at the earliest opportunity as there is an increased risk of perforation.

In adults with pharyngo-oesophageal foreign bodies it is important to exclude underlying pathology (Fig. 3.79). This is particularly so in the lower oesophagus and in the region of the gastro-oesophageal junction.

Fig. 3.79 Potential underlying causes of impaction of a swallowed foreign body in adults.

Management after pharyngo-oesophagoscopy

It is vital to ensure that a proper regimen of patient care is given after a pharyngo-oesophagoscopy, whether a foreign body was found and removed or not.

Full-blown AIDS (WHO stage 4)

The diagnosis of AIDS is based on the presence of AIDS-defining illnesses, which include opportunistic infections and tumours indicative of cellular immune deficiency in individuals with no known cause for immune deficiency. The classic opportunistic infection is in the lungs and is caused by Pneumocystis jiroveci (Fig. 3.80). Candidal infection of the mouth and extending into the oesophagus is not infrequent, and results in severe dysphagia. Rhinosinusitis, causing postnasal discharge and sinofacial discomfort, is very common. PGL affecting lymphoid tissue in the nasopharynx can cause blockage of the Eustachian tube and subsequent secretory otitis media. Intraoral ulceration in AIDS may be due to herpes virus infection. It is similar in appearance to the usual benign variety, but does not resolve spontaneously. Of the neoplasias, the most common is Kaposi’s sarcoma. These appear as small, bluish, painless skin lesions, and the head, neck and oral cavity may be involved (Figs 3.81 and 3.82). Other tumours include non-Hodgkin’s lymphoma (B-cell type) and squamous cell carcinoma. Parotid enlargement can be an early presenting sign of HIV disease and is usually due to cystic change.

Fig. 3.80 Pneumocystis jiroveci lung infection.

Fig. 3.81 Kaposi’s sarcoma affecting the skin of the head and neck.

Fig. 3.82 Kaposi’s sarcoma presenting in the oral cavity.