EVALUATION OF NASAL OBSTRUCTION

Apr 5, 2009

History and Physical Exam

History
  • Character of Nasal Obstruction: onset and duration, constant versus intermittent, unilateral (tumors, normal nasal cycle) versus bilateral obstruction, associated mouth breathing, snoring, anosmia/hyposmia/taste disturbances, tearing (nasolacrimal duct obstruction or allergy)
  • Contributing Factors: potential toxin and allergen exposure, known drug allergies, medications (see Table 1–1), history of immunodeficiency, asthma, sinusitis, otitis media, allergy, sleep disturbances, facial trauma or surgery
  • Associated Symptoms: allergic component (sneezing, itchy and watery eyes, clear rhinorrhea), sinus involvement


  • Antihypertensives
  • Psychotropic Medications
  • Oral Contraceptives
  • Chronic Nasal Decongestants: rhinitis medicamentosa
  • Cocaine: local vasoconstriction
  • Tobacco: irritates mucosa and impairs ciliary clearance
  • Antithyroid Medication
  • Aspirin: activates peripheral chemoreceptors
  • Marijuana

headaches), acute infection (fevers, malaise, purulent or odorous nasal discharge, pain)
Other Head and Neck (H&N) Symptoms: sore throat, postnasal drip, cough, ear complaints, halitosis, ocular pain, hoarseness
Think “KITTENS” for differential diagnosis (see Table 1–2)

Physical Exam
  • External Nasal Exam: external deformities (firmness, tenderness on palpation), nasal flaring, nasal airflow
  • Anterior Rhinoscopy/Nasal Endoscopy: examine twice (with and without topical decongestion), quality of turbinates (hypertrophic, pale, blue), quality of nasal mucosa, nasal septum, osteomeatal complex obstruction, foreign bodies, nasal masses, choanal opening
  • Quality of Nasal Secretions: purulent or thick (infectious), watery and clear (vasomotor rhinitis, allergy), salty and clear (CSF leak)
  • H&N Exam: facial tenderness, tonsil and adenoid hypertrophy, cobblestoned posterior pharynx, cervical adenopathy, otologic exam

Ancillary Tests
  • Allergy Evaluation: (see below)
  • Paranasal Plain Films: may be considered for screening, largely been replaced by CT/MRI
  • CT/MRI of Paranasal Sinus: indicated if obstruction may be secondary to nasal masses, polyps, or complicated sinusitis

Tabel 1-2 Differential diagnosis of Nasal Obstruction

(K) Congenital

Infectious & Idiopathic

Toxins & Trauma

Tumor
(Neoplasia)

Endocrine

Neurologic

Systemic

Neurogenic tumors

Infectious rhinitis

Nasal and septal fractures

Papillomas

Diabetes

Vasomotor rhinitis

Granulomatous
diseases

Congenital nasopharyngeal cysts

Rhinoscleroma

Medication side effects (rhinitis medicamentosa)

Nasal Polyps

Hypothyroidism


Vasculitis

Teratoma

Chronic sinusitis

Synechia

Hemangiomas

Pregnancy


Allergy

Choanal atresia

Adenoid hyperplasia

Environmental irritants

Pyogenic granulomas



Cystic fibrosis

Nasoseptal deformities


Septal hematomas

Foreign bodies

Juvenile nasopharyngeal
angiofibromas

Malignancy






  • Biopsy: indicated for any mass suspect for malignancy, avoid biopsy of vascular neoplasms (juvenile nasopharyngeal angiofibroma, sarcomas) or encephaloceles
  • Rhinomanometry: provides an objective measurement of airway resistance, largely not utilized in clinical practice since highly time consuming, not cost effective, and inaccurate
  • Ciliary Biopsy and Mucociliary Clearance Tests: electronmicroscopy and ciliary motility studies for ciliary defects
  • Nasal Secretion Protein and Glucose: evaluate for CSF leak if suspected
  • Culture and Sensitivity: surgically obtained cultures usually indicated for complicated acute rhinosinusitis and resistant chronic sinusitis
  • Pulmonary Function Tests: suspect reactive airway disease component
  • Olfactometry: qualitative and quantitative testing of olfactory substances

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Physiology of the Nasal Airway

Mar 13, 2009

Nasal Cycles and Respiratory Airflow
  • nasal airflow is regulated through the volume of the venous sinusoids (capacitance vessels) in the nasal erectile tissue (located primarily in the inferior turbinate and to a lesser extent in the anterior septum)
  • the hypothalamus continuously stimulates a sympathetic tone (via the superior cervical sympathetic ganglia) to maintain a level of nasal vasoconstriction
  • inspired air is warmed to body temperature and is humidified to almost 100% humidity
  • Sneeze Reflex: induced by allergens, ammonia, viral infections, exercise, and other irritants which stimulates trigeminal afferents, complex efferent input results in a slow inspiratory phase, glottic and velopharyngeal closure (increases subglottic pressure), followed by a sudden glottic opening (sneeze)
  • Regulation Response Types
  1. Asymmetrical Congestive Response (The Nasal Cycle): normal physiological congestion/decongestion cycle alternating between nasal sides every 2–7 hours
  2. Symmetrical Congestive Response: temporary bilateral congestion induced by exercise, changes in body position, hyperventilation, cold air, sulfur, histamine, and other irritants; lasts 15–30 minutes

Microvasculature
  • regulates nasal volume, humidity, and heat exchange
  • Resistance Vessels: arterioles and precapillary sphincters, regulate blood flow to the nasal mucosa
  • Subepithelial Capillaries: fenestrated vessels allow for transport of solutes and fluids
  • Venous Sinusoids: capacitance vessel, determines blood volume and nasal congestion
  • Arteriovenous Anastomoses (AVA): regulate nasal blood flow by allowing blood to flow directly from the resistance vessels to the venous sinusoids

Regulation of Nasal Microvasculature
  • Sympathetic Innervation: provides vasoconstrictor tone to arteries and capacitance veins, mediated through Norepinephrine (primary neurotransmitter), Neuropeptide Y (a weak vasoconstrictor, enhances effects of norepinephrine), and Avian Pancreatic Polypeptide (APP)
  • Parasympathetic Innervation: controls secretions and dilates resistance vessels, mediated through Acetylcholine (primary neurotransmitter), Vasoactive Intestinal Peptide (VIP), and Peptide Histamine Isoleucine (PHI)

Nasal Valves
  • External Nasal Valve (Nasal Vestibule): anterior nostril (nasal alar cartilage, columella, and nasal sill), potential cause of obstruction during inspiration
  • Internal Nasal Valve (Limen Nasi): bordered by septum, anterior edge of the inferior turbinate, and caudal edge of upper lateral cartilage; narrowest segment (50% of total nasal resistance), potential site of obstruction secondary to Bernoulli’s principle (narrowed segment accelerates nasal airflow resulting in a decrease in intraluminal pressure)

Mucociliary System
  • Function: humidification, cleaning of inspired air, eliminating debris and excess secretion from paranasal sinus and nasal airway
  • Mucociliary Flow: mass motion of mucous layer in the paranasal sinus of the mucous blanket at 1 cm/min (eg, migration in the maxillary sinus begins at the floor of maxillary sinus natural ostium nasal cavity nasopharynx)
  • Components
  1. Ciliated, Pseudostratified Columnar Epithelium: anterior border begins at limen nasi
  2. Double Layered Mucous Blanket: deep, less viscous, serous periciliary fluid (sol phase) and superficial, more viscous, mucous fluid (gel phase)
  3. Mucous Producing Glands: goblet cells (columnar cells, basal nucleus, secretory granules at lumen end), deep and superficial seromucinous glands (serous or mucous acini with cuboidal duct complexes), and intraepithelial glands (20–50 mucous cells around a single duct)

  • Major Composition of Nasal Mucus: 95% water, 3% glycoproteins (mucin), 2% salts, immunoglobulins (IgA), lysozymes (bacteriolytic), and lactoferrin (bacteriostatic)


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Prosthetic Rehabilitation of Cancers Involving the Face

Feb 21, 2009

Cancers that involve the facial structures such as the eye, ear, and nose, may require removal of a portion or all of the involved structures. In such cases, a removable prosthesis can be made to restore the appearance of these structures. After evaluation by a head and neck surgeon, the patient is referred to a dental oncologist for examination prior to surgery. Photographs and facial impressions may be made prior to surgery to document existing facial contours. An explanation of the procedures and the time required to make the prosthesis is discussed with each patient before surgery. Pictures of patients with similar diseases before and after surgery are available to view and discuss.


After an appropriate period allowing for healing, the patient is scheduled for initiation of the prosthesis fabrication process. This takes approximately five to seven visits, and in some cases, these appointments can last several hours. Special types of skin adhesives retain most prostheses. Implants similar to dental implants can be used to retain the prosthesis in some cases. These prostheses are made of silicone and require removal and cleaning every week. The average lifetime of a facial prosthesis is approximately two years.

Some prostheses can be remade in the laboratory and sent to the patient in the mail while others will require the patient to make an appointment with the dentist for evaluation before a new prosthesis can be made. In some instances surgically removed tissues can be reconstructed with compatible tissues from other parts of the body. In this case, a prosthesis may or may not be indicated or needed. When indicated, the reconstructed tissue may need surgical revision before a prosthesis is constructed. Treatments such as radiotherapy and chemotherapy can delay the fabrication of a facial prosthesis. These delays are necessary to allow proper healing of the tissues that will support and retain the prosthesis.

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Radiation Therapy and Your Mouth

Radiation therapy is a common type of treatment for cancer of the head and neck region. There are several important glands in this region called salivary glands. The major function of these important glands is the production of moisture (saliva) in the mouth. When the salivary glands are included in the treatment area, they may be damaged, limiting the amount of saliva produced. This is important because saliva is responsible for a number of important functions in the mouth. As far as teeth are concerned, saliva helps to prevent tooth decay. It also lubricates soft tissues such as the tongue, cheeks, and lips, which helps prevent irritation, which may occur during the normal process of speaking, eating, and swallowing.

Radiation therapy can also affect the jawbones by reducing the size of blood vessels supplying blood to them. Since blood vessels carry cells responsible for defense against bacteria, this can decrease the ability of the jaws to fight infection. Another very important side effect of radiation therapy is that it may cause scar tissue to form in the muscles and joints (temporomandibular joint-TMJ). If this occurs you may not be able to open your mouth to eat normal bites of food or adequately clean your mouth.

These side effects can be classified as short and long term problems. Short-term problems may include infection (bacterial, fungal, or viral), change in taste, pain, bleeding, and inflamed oral tissues commonly called mucositis. Mucositis is similar to a sunburn on your skin. In some patients this may become painful and interfere with eating. Long-term problems include permanent dryness (xerostomia), tooth decay (caries), decrease in the ability to open the mouth wide (fibrosis).

An infection in the jaws called osteoradionecrosis can result in a loss of a portion of bone and tissue covering the bone (ORN, osteoradionecrosis). How severe these problems become is related to the radiation dose, size of the treatment field, degree of mouth dryness, and the quality of the patient's oral hygiene. Prevention and treatment of the complications are discussed in separate areas of this web page (see Oral care Instruction Sheet and Physiotherapy Instruction Sheet).


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Special Devices Used During Radiation Therapy

Special treatment devices, known as radiation stents, may provide significant benefit to the patient and radiotherapist by assisting in the delivery of the radiation to precise local areas and thereby limiting complications following therapy. Not all patients undergoing head and neck radiation therapy will have a stent fabricated. The need for a radiation device is determined by the treating radiotherapist. If a stent is to be made, it can be used to protect (shield) or displace vital structures outside the treatment field, place diseased tissues within a daily repeatable position during treatment, position the beam, or maintain radioactive material at the tumor site.


At the first appointment, impressions are usually made of the upper and lower jaws and stone models are subsequently made from those impressions. A jaw registration composed of wax is made to approximate the upper and lower jaws in the treatment position. The stone models are placed into the wax registration and mounted onto an instrument so that the jaw relationship is reproduced. The radiation device is initially prepared in wax and verified in the patient's mouth prior to it being finalized. The completed radiation stent is usually made of an acrylic resin and may or may not contain a shielding lead alloy, depending upon several conditions: type of radiation given, condition of the diseased hard and soft tissues, oral opening ability, and the needs of the treating radiotherapist. Although use of these devices is usually confined to the head and neck region, they are occasionally of advantage in other accessible areas.

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Supracricoid Partial Laryngectomies

The Supracricoid Partial Laryngectomies (SCPL) are a subset of surgical procedures that are available to the Head and Neck Surgeon for the management of selected cancers of the larynx. The SCPLs are a subset of conservation laryngeal operations.

SCPL refers to the resection of the diseased or affected part of the larynx that is removed at the time of operation. The defect in the larynx is then reconstructed at the time of operation with what is known as a crico-hyoidal impaction. The specific type of impaction is either a cricohyoidoepiglottopexy, a cricohyoidopexy, or a tracheocricohyoidoepiglottopexy. Exactly which reconstruction is used is determined by the location of the patient’s cancer, the extent of involvement of the tumor and the patient's overall condition. The SCPLs are all alike in that the anterior component of the vocal cords is removed bilaterally in addition to the immediate area above and below the vocal cords. If the tumor then extends either above or below the actual vocal cords (or glottis), then either of the above reconstructions is performed. In addition, one of the arytenoids (the cartilage that controls the vocal cords) can also be removed.

The benefits of the SCPLs are that rather large tumors can be effectively removed from the larynx while still preserving swallowing, speech and the airway functions of the larynx. While the patient's voice will never be normal after any of the supracricoid partial laryngectomies, the patient is able to communicate readily without the aid of any prosthesis or electronic device, and most importantly, the vast majority of patients do not need a permanent tracheostomy. A tracheostomy is necessary in the immediate post-operative period, but we are usually able to remove this in the few days after surgery, before the patient even leaves the hospital. Then, as the surgery and tracheostomy sites heal, the patient relearns how to speak and swallow. Obviously then, if we can avoid the permanent hole in the neck needed with more traditional laryngeal surgeries, then the patient can lead a more normal and active life with fewer, if any, restrictions.

The SCPLs do, however, have some contraindications. Not everyone is a candidate for conservation laryngeal surgeries, and very specific criteria have to be met to be able to perform the resection and reconstruction while still removing the entire tumor. Obviously, the first goal of any cancer operation is to remove all of the cancer. In addition, pulmonary function must be assessed before performing any of the above surgeries. While patients recuperate from their surgery, there is often a moderate amount of aspiration of saliva and even diet into the airway. While the patient relearns to swallow in usually no more than seven to ten days, it is important that he have healthy lungs so that he can tolerate this small degree of aspiration. In addition, SCPLs do not give patients a normal voice. Patients are, however, able to communicate readily and without the use of any assisted devices.

Once a patient is found to have cancer of the larynx, it is then up to his treating surgeon to assess the extent of the disease and consider the patient's surgical options. If SCPL is an option, then we like to use it as we feel that not only is the patient’s long-term function significantly improved as compared to traditional therapy but also long-term cancer control is not sacrificed.

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TNM Staging

Traditionally, patients have had the impression that tumors are staged on a scale I (best prognosis) through IV (worst prognosis). While this has been true in the past, it has also been found that generic terms like stage I, II, III, or IV are not useful in planning treatment nor does it give enough information to all the members of the healthcare team who may participate in a patient's care. Therefore, in 1988, a committee called the American Joint Committee on Cancer was established to address this issue. This committee created a new method of staging for cancers throughout the body and fine tuned the staging methodology for the head and neck. TNM staging can still be converted to the traditional stage I-IV, but most physicians now talk of tumors in terms of their TNM staging.

The T in TNM stands for tumor. Tumors are graded on a scale of 0-4. T0 means that there is no evidence of the primary tumor at the time of diagnosis (an unusual but not uncommon occurrence). T4 usually refers to later, more invasive and larger tumors which involve adjacent structures, including the muscles, neck, etc. The "T-staging" varies for different parts of the head and neck. For example, tumors of the oral cavity (the region in the mouth from the lips to the tonsils) are staged as T1 if the tumors are 0 to 2 cm. in size, T2 if they are 2-4 cm. in size, T3 if they are greater than 4 cm. in size, and T4 if there is nerve involvement, involvement of bone, or extensive spread of tumor. However, this cannot be applied to all regions of the head and neck.

The N in TNM refers to node status. The "N-staging" is used for all types of head and neck cancers. The "N-staging" ranges from N0 (no evidence of nodal metastasis) to N3 (extensive nodal disease usually greater than 6 cm. in size). N1 refers to metastasis into lymph nodes which are on the same side as the primary tumor and which are smaller than 3 cm. N2 refers to tumors that are 3 to 6 cm. in size. The N2 classification is further broken down to A, B, and C. N2A refers to tumors on the same side as the primary tumor, measuring 3-6 cm. in size. N2B refers to tumors with nodes in several different areas of the neck but none greater than 6 cm. and all on the same side as the primary tumor. N2C refers to lymph nodes on the opposite side of the neck from the primary tumor or on both sides of the neck. N3, then, generally refers to massive nodal disease, which usually signifies a late stage or extensive nodal metastasis.

The M in TNM staging refers to metastasis or distant metastasis. M0 means that there is no evidence of distance metastasis at the time of initial presentation and M1 means that there is evidence of metastasis to any other site in the body outside of the head and neck.

The TNM staging, while sometimes quite difficult for the lay person to understand, is very useful to practicing head and neck oncologists in that it provides a common language for head and neck oncologists to communicate with when discussing cancer patients. It is still possible to break down the TNM staging into the traditional stage I-IV tumor staging system for patients; however, most patients will most likely hear their tumors described with TNM staging. The prognosis for each TNM stage varies based on the location of the primary. For each "T-stage", however, the presence or absence of nodal disease is highly significant in the prognosis. The worst prognostic sign in cancers of the head and neck (and most commonly squamous cell carcinoma) is the presence of nodal metastasis. While the presence of nodal metastasis is by no means a hopeless situation, lymph node metastasis does imply later disease, and more aggressive treatment is usually indicated.

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Tracheoesophageal Puncture

The tracheoesophageal puncture procedure for alaryngeal voice restoration is one method that a person who has had a total laryngectomy can use to talk following removal of the larynx. TE speech is often chosen because of its similarity to normal laryngeal speech. The method involves the creation of a tracheoesophageal puncture (TEP) at the time of the laryngectomy, or later when the patient is well healed. The opening is maintained by a prosthesis that acts as a one-way valve by allowing lung air to pass into the esophagus for sound production when the stoma is covered. At the same time, it prevents food and liquid from entering the trachea. When TEP is done after the laryngectomy, it usually involves a minor surgery that can be done on an outpatient basis.

The operation involves the creation of a small opening in the wall that separates the trachea (windpipe) and the esophagus. After the surgeon has performed the puncture, a small red rubber catheter is placed in the puncture to keep it from closing and to allow it to form adequately before the voice prosthesis is placed. The catheter is usually left in place 3-7 days before it is removed and the TE voice prosthesis is fit. Most patients do not complain of any discomfort while the catheter is in place and go about their daily routine without difficulty. During this short period of time, patients are usually able to eat and drink normally without problems.

There are many different kinds of prostheses. Selection depends upon the physical characteristics and comfort level of the patient. Most of the time, 3-5 visits are required to properly size, fit, and teach the TE speaker to manage and use the voice prosthesis. The TE speaker usually covers the stoma with a finger or a thumb to divert pulmonary air through the prosthesis into the esophagus for sound production. The actual sound is produced by the vibration of the walls of the esophagus. The sound is then shaped by the movement of the articulators, lips, tongue, teeth, etc. to form words and conversation just as the normal laryngeal speaker does. Some tracheoesophageal speakers are successful using a tracheostomal breathing valve instead of a finger to occlude the stoma. With this device, normal breathing is uninhibited, but the valve closes automatically during exhalation for speech production, enabling the patient to speak with both hands free.

Most patients are evaluated prior to TE puncture by a trained speech pathologist who assumes the responsibility for or participates with the physician in evaluating the potential of the esophagus for sound production to ensure TE speech success. Once the appropriate prosthesis has been fit, the TE speaker is taught to clean, remove, and reinsert the prosthesis. He or she is also shown how to apply and remove the tracheostoma valve should this device be used.

Care and maintenance of the prosthesis is not difficult. Most patients independently remove and replace it without problems. Other patients prefer to have their prosthesis replaced by their speech pathologist or physician. The average TE voice prosthesis lasts 2-3 months before it is removed, and a new one is reinserted. However, some patients are able to wear the prosthesis for much longer periods of time, up to and in some instances, beyond one year, before they need to remove it. Other patients find that they need to remove the prosthesis sooner. Again, the speech pathologist assists the TE speaker in selecting the appropriate prosthesis and developing a management routine to maximize the longevity of the voice prosthesis and to avoid problems.

The key to tracheoesophageal speech candidacy is good sound production. Usually the only contraindication to tracheoesophageal puncture is continued alcohol abuse and impaired cognitive-mental functioning. Pulmonary function must be adequate to support sound generation. Manual dexterity and good vision are important but not absolutely imperative for those patients who rely on the speech pathologist, physician or significant other to replace the prosthesis. The use of adaptive devices such as the tracheostoma breathing valve provide automatic diversion of airflow, thereby eliminating the need for digital occlusion for some patients.

There are several factors that are not considered contraindications to tracheoesophageal puncture procedures. These include diabetes, unilateral or bilateral neck dissections, and radiation therapy. The patient's medical status and surgical requirements should always be evaluated by the physician prior to tracheoesophageal puncture so as to ensure success postoperatively. Patients who have had extended surgical procedures including removal of other structures as well as the larynx may also be candidates. Good preoperative evaluation will determine appropriate candidacy.

The method of tracheoesophageal speech restoration offers many laryngectomees the potential for spontaneous, effortless speech production. It is important, however, that patients be evaluated properly and discuss their options with trained medical professionals prior to puncture to ensure postoperative TE speech success and avoid communicative frustration.

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Videostroboscopy of the Larynx

Videostroboscopy is a clinical evaluation tool, which allows one to directly observe the apparent motion of the larynx. This examination provides valuable information beyond that which the naked eye can see. It gives the clinician information regarding vocal fold vibration as well as an immediate and magnified image of the presence or absence of pathology. It can also document small changes in the vibratory capacity of the larynx as a result of a specific treatment modality. The presence of abnormal vibration may be detected using videostroboscopy long before the actual pathology becomes visually detectable to the naked eye. Videostroboscopy also provides a permanent record for documentation and comparison. Videostroboscopy has been found to be a valuable means for evaluating the degree of infiltration by cancerous lesions. Stroboscopy is also a very useful way to evaluate patients with vocal fold paralysis, because the onset of any improvement can often be observed earlier and with greater accuracy than with the eye or the ear.

Videostroboscopic evaluation of laryngeal functioning is routinely and easily performed in a clinic setting using either a rigid or flexible fiberoptic endoscope. In order to perform rigid oral endoscopy, the patient is asked to protrude the tongue and the clinician holds the tongue as a rigid tube is inserted into the mouth. The tube or scope, projects a high intensity light at a predetermined angle illuminating the structures to be observed and recorded. The advantages of this method are high illumination, a wide field of view, and excellent imaging capability. The disadvantages are that the procedure does interfere with normal speech production and there is some minor patient discomfort associated with the natural gag mechanism. However, the patient's discomfort is minimized with the use of a topical anesthetic spray.

Flexible fiberoptic endoscopy is performed with a flexible tube which is inserted through the nasal passage. Again, a high intensity light is transmitted through the flexible scope, which illuminates the structures to be viewed by the clinician, and/or recorded. In this procedure, one advantage is the excellent image of the vocal folds along with other structures of the oral cavity and throat. Since the small flexible scope is inserted through the nose, it does not interfere with the patient's ability to speak during the examination. The disadvantages are that the image is smaller than the image provided by rigid endoscopy, and the brightness of the image may be reduced. Again, possible patient discomfort is minimized with the use of a topical anesthetic spray administered into the nasal cavity. Both procedures allow the patient to go about their daily routine following completion of the evaluation.

The entire examination takes approximately 3-5 minutes, depending upon the experience of the examiner and the cooperation of the patient. Correct interpretation of the results requires knowledge and familiarity with the anatomy and physiology of the larynx, phonation, and the effect of potential pathologies on the vibratory functioning of the larynx. The technique is only one part of a clinical examination and is a valuable supplement to other currently used diagnostic procedures.

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Xerostomia

Dry mouth (Xerostomia) is caused by a lack of normal salivary function, through either a reduction in salivary flow or alteration of salivary composition. Three pairs of major salivary glands (parotid, submandibular, and sublingual) and an abundance of minor salivary glands scattered throughout the oral cavity produce saliva. The combined product of these glands provides a complex fluid, consisting of antibodies, electrolytes, proteins, glycoproteins, and lipids. Many studies have shown that saliva plays a significant role in the health of the teeth and oral mucosa.

Individuals who have had a decrease in the amount of saliva can exhibit many problems with their teeth and oral mucosa. Such manifestations can include increased dental caries, dehydration of the mucosa (mucositis), and oral infections, which will lead to discomfort and difficulty in chewing, swallowing, and speaking.

The most common causes of xerostomia include medical treatments and systemic disorders. The medical treatments that interfere with salivary function are medications, radiotherapy, surgery and trauma. Radiation therapy for head and neck cancer causes permanent salivary gland damage and is an important cause of xerostomia. The severity of xerostomia depends on the volume of tissue irradiated, length of therapy, radiation dose, and the amount of salivary gland tissue involved. Xerostomia may also be associated with a variety of systemic disorders, particularly Sjögrens syndrome (an autoimmune disorder that affects salivary and lacrimal functions as well as connective tissue), diabetes, scleroderma, and graft-versus-host disease as seen in bone marrow transplant patients. Many drugs, including analgesics, antidepressants, antihypertensives, and antihistamines can cause xerostomia.

Complications arising from dry mouth, such as increased dental caries, difficulty in swallowing, chewing and speaking, and an increased incidence of oral infection, can lead to nutritional deficiencies, and an overall decline in the quality of life. Additionally, patients with xerostomia have difficulty in wearing removable prostheses due to the dry mucosa and increased incidence of frictional denture sores.

The management of patients suffering from xerostomia can be a challenging dilemma for both dentist and patient. Xerostomia may be an early manifestation of a physiological disorder or an underlying salivary gland disease. Therapeutic options for relief of the symptoms of xerostomia is largely palliative, as reversal of the primary cause is often not possible. There can be a poor correlation between subjective reports and actual gland function as well as a large variation in degrees of salivary function found with xerostomia. Treatment is aimed initially at restoring the flow of saliva using mechanical means such as chewing sugar-free gum, taste stimulants, or systemic salivary gland stimulants (sialogogues). Artificial saliva substitutes and mouth wetting agents may be used, although the majority provide only short term relief of symptoms, and can cause irritation of oral tissues during long-term use.

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METABOLICALLY ACTIVE TUMORS

Feb 7, 2009

Tumors that arise from cells within the endocrine glands may secrete normal hormones in abnormal amounts. These cells derive from neural crest, neural ectoderm, or placodal ectodermal tissue that secrete monoamine (e.g., serotonin) or polypeptide (e.g., insulin) substances. These tumors are referred to as APUDomas (i.e., amine precursor uptake and decarboxylation) or neurocrinopathies. Tumor types include islet cell tumors, medullary carcinoma from the thyroid C cells, pheochromocytomas from adrenal chromaffin cells, and carcinoid tumors from Kulschitsky or enterochromaffin cells found in almost every organ of the body.

Carcinoid tumors are the most common of the APUDomas. They occur most frequently in the ileum and bronchus and have a high incidence of synchronous and metachronous neoplasms, whether carcinoid or other types of neoplasms. The active tumors secrete serotonin, although other substances (e.g., histamine, dopamine, substance P) have been suggested. The carcinoid syndrome includes flushing, diarrhea, cardiac valve disease, and occasionally wheezing. The mainstay of diagnosis is the 24-hour urinalysis for 5-HIAA, the major metabolite of serotonin. Treatment is surgical removal or pharmacotherapy to control the diarrhea and flushing using serotonin antagonists (e.g., cyproheptadine, methasergide), parachlorophenylalanine, or natural or synthetic somatostatin.

Pheochromocytomas are associated with “spells” and hypertension, either episodic (50%) or sustained (50%), which is difficult to differentiate from essential hypertension. The spells include a variety of symptoms, such as headache and acute anxiety or panic attacks with sweating. The rule of 10s applies: 10% are malignant, 10% occur bilaterally, and 10% are extraadrenal, occurring anywhere along the sympathetic chain from the skull base to the gonads. These types of tumors are usually called paragangliomas. Active tumors secrete norepinephrine alone (i.e., paragangliomas) or norepinephrine combined with epinephrine (i.e., adrenal tumors).

Tumors are diagnosed using 24-hour urinalysis for vanillylmandelic acid, computed tomography, 131I-metaiodobenzylguanadine, or ultrasound. All patients must be prepared for surgical excision with 7 to 14 days of a-adrenergic blockers. Phenoxyabenzamine is used orally beginning at a dose of 10 mg given four times each day and gradually increased to 300 mg daily until postural hypotension develops. A b-adrenergic blocker may be added 48 hours before surgery if the patient has tachycardia or arrhythmia or if the catecholamine profile shows excess epinephrine secretion. Propranolol is given in doses of 10 mg four times a day. Both medications are given the morning of surgery, and large amounts of intravenous fluid are used intraoperatively after tumor removal to counteract the marked increase in intravascular capacity, which can cause an acute fall in blood pressure. This occurs because the adrenergic stimulation is precipitously removed as the secreting tumor is removed.

Multiple Endocrine Neoplasia Syndromes

Several neoplastic syndromes involving multiple endocrine glands have been described. Currently, the favored nomenclature for the most well-established yndromes and their most commonly encountered neoplasias are listed. These syndromes are typically inherited in an autosomal dominant pattern; however, penetrance is variable.

MEN I is characterized by parathyroid, pancreatic, and pituitary neoplasias. The most common parathyroid neoplasia is multiglandular hyperplasia. Gastrin-producing islet cell tumors account for over half of the pancreatic tumors in MEN I and become the greatest source of morbidity in affected individuals. The most frequent pituitary neoplasm is a prolactinoma. Other endocrine tumors are unusual in patients with MEN I but may occur. The genetic mutation responsible for the syndrome occurs in the tumor suppressor gene, menin, and has been mapped to chromosome 11.

The distinguishing features of MEN IIa are medullary thyroid carcinoma (MTC), pheochromocytomas, and parathyroid tumors. MTC develops in hyperplastic C cells of the thyroid and is nearly universal in MEN IIa. Treatment consists of total thyroidectomy in all known cases and in unaffected carriers identified through prospective screening. Pheochromocytomas occur in over half of individuals and are typically bilateral and multicentric. They typically develop much later than MTC; however, when both are present, the pheochromocytoma should be removed first. Parathyroid hyperplasia is less frequent compared with MEN I, occurring in 10% to 35%. The genetic abnormality responsible for MEN IIa is a mutation of the RET proto-oncogene on chromosome 10. There is a 100% correlation between the presence of the RET mutation and MEN II and hereditary MTC. Thus, suspected carriers and family members are now being screened based on polymerase chain reaction techniques to identify carriers of the mutated RET proto-oncogene .

MEN IIb is characterized by MTC, pheochromocytomas, and mucosal neuromas. The mucosal neuromas are universal and predominantly involve the oral cavity and can involve other sites of the gastrointestinal tract and the conjunctiva, cornea, and eyelid. MTC in these patients is more aggressive than in MEN IIa, with metastatic disease developing in some children before age 1. The incidence of pheochromocytomas and their clinical course is similar to that of MEN IIa. Hyperplasia of the parathyroid glands is rare. The genetic mutation is also found in the RET proto-oncogene on chromosome 10; however, the specific point mutation is distinct from that causing MEN IIa.

Endocrine Emergencies

Hypercalcemic Crisis

Severe hypercalcemia, or hypercalcemic crisis, predominantly occurs in patients with advanced previously diagnosed malignancy. Serum calcium levels are typically elevated at least to 3.5 mmol/L (14 mg/dL); however, symptom severity also correlates with the rapidity of the calcium elevation. Ionized calcium levels are preferred for diagnosis and follow-up, as this is the physiologically active fraction. Clinical findings in emergent cases include hypovolemia, mental status changes, and gastrointestinal symptoms. Cardiac arrhythmias and renal dysfunction may also complicate the initial course.

Two separate mechanisms for malignancy-associated hypercalcemia are currently accepted. First, many solid tumors secrete a PTH-related protein (PTHrP) that has similar activity to PTH, although its production is unregulated. Squamous cell carcinoma of the lung, head and neck, cervix, esophagus, vulva, and skin, in addition to breast cancer, renal cell, and bladder cancer, are most commonly found to secrete PTHrP. Second, metastatic and hematogenous tumors produce local intercellular mediators that stimulate osteoclast activity. These cytokines (tumor necrosis factor beta, interleukin-6, etc.), once secreted by the tumor cells, act on the local osteoclast population to mediate bone resorption and calcium liberation.

Regardless of the underlying etiology, acute symptomatic hypercalcemia requires aggressive treatment. Initial efforts focus on rehydration. Volume contraction is universal and results from the osmotic diuresis and decreased glomerular filtration rate, which accompany uncontrolled hypercalcemia. Fluid replacement with isotonic saline should be started at 2 to 4 L/day. The use of loop diuretics to stimulate calciuresis is not performed routinely. Bisphosphonates (e.g., pamidronate) are osteoclast inhibitors and are considered first-line therapies for hypercalcemic crisis. Volume expansion and bisphosphonate therapy can normalize most patients’ serum levels. However, the rate of response with the bisphosphonates is 3 to 6 days for calcium normalization. In the critically ill patient, a more rapid response is desired. Calcitonin reduces calcium levels within hours by direct osteoclast inhibition, and its ability enhances renal calcium excretion. Its main drawback is its short-lived effectiveness. Gallium nitrate and plicamycin are no longer considered first-line therapy because the bisphosphonates have significantly better toxicity profiles. Glucocorticoids and dialysis are indicated in specific circumstances.

Hypocalcemia

Acute or emergent hypocalcemia is uncommon. The typical presentation centers around the neuromuscular irritability that predominates the clinical picture. Numbness, paresthesias, cramps, tetany, and seizures are often seen. Laryngeal tetany and cardiac arrhythmias can result in mortality if not treated immediately. When complicated or emergent hypocalcemia is suspected, intravenous elemental calcium should be administered until clinical improvement is observed. Preferably, 100 to 300 mg of calcium gluconate is given over 10 minutes. Ionized calcium levels should be obtained and followed until normalization occurs. Ideally, the underlying etiology will be identified and treated. The most common etiology in the practice of otolaryngology is hypocalcemia from sudden PTH deficiency, seen after parathyroid or thyroid surgery. Intravascular ionized calcium levels typically reach their lowest 24 to 48 hours after surgery. Additional causes of hypocalcemia include rapid intravascular protein binding, vitamin D deficiency, and PTH resistance. Several anions may also complex with ionized calcium to decrease the concentration precipitously, such as citrate, bicarbonate, and phosphate. One other scenario is the hungry bone syndrome most commonly seen after removal of larger adenomas in elderly patients.

Once the acute situation has been temporized, long-term calcium supplementation is instituted and may be enhanced with vitamin D, depending on the underlying etiology and the initial response to oral calcium therapy. Difficult cases may benefit from evaluation of serum phosphate and magnesium levels, because abnormal levels will complicate the diagnosis and treatment of hypocalcemia.

Thyroid Storm

Thyrotoxic crisis is an uncommon complication of thyrotoxicosis. It has become a rare complication in the surgical patient, and most commonly occurs in medical patients with known Grave’s disease and a precipitating event that leads to an acceleration or decompensation of their hyperthyroid state. Clinically, patients present in a severe hypermetabolic state. Fever, tachycardia, and sweating are nearly universal. Arrhythmias are common, and heart failure and shock may ensue. Motor restlessness and mental status changes are common. If unrecognized or untreated, stupor, coma, and hypotension develop, and the course ends in fatality.

Common precipitating events include other acute illnesses, infections, trauma, and emergent surgeries. Others include radioiodine therapy, parturition, toxemia of pregnancy, and diabetic ketoacidosis. Not all cases have identifiable precipitating events; however, they must be sought to properly treat the patient and avoid additional morbidity.

Diagnosis is based on the history and clinical presentation. Once the diagnosis is anticipated, treatment should begin before confirmation with laboratory testing. A scoring system has been devised for grading patients on the severity of their crisis.

There are three goals of therapy. First, treatment must focus on controlling the hyperthyroid state. Propylthiouracil is used first to prevent further synthesis of thyroid hormone and to limit the peripheral conversion of T4 to the more physiologically active T3. Iodide is used to block the release of preformed hormone stores from the thyroid gland. Lithium may be used in cases where iodide is contraindicated. Glucocorticoids are used routinely and are associated with improved survival. Definitive treatment of the hyperthyroidism occurs after reaching an euthyroid state with either radioactive 131I ablation or surgical excision. The second object of therapy is reestablishing a normal homeostatic state. Many of the acute manifestations can be controlled with b-adrenergic blocking agents. Propranolol has been used most extensively, but B1-selective agents have theoretic advantages in certain patients (e.g., heart failure, asthma, etc.). Other measures include volume reexpansion, electrolyte normalization, glucose monitoring, and treating the hyperthermia. Salicylates should be avoided because they increase the basic metabolic rate and displace bound thyroid hormone, thereby increasing serum levels. Cardiac arrhythmias may require pharmacotherapy and anticoagulation. The final goal of therapy is identifying and treating the precipitating trigger. Mortality from thyroid storm is still significant (15% to 20%), despite earlier diagnosis and aggressive treatment.

Myxedema Coma

Myxedema coma is the end result of chronic untreated hypothyroidism. It is typically seen in elderly women during the winter months. Most cases are initiated by a precipitating event such as an infection (35%), medications (e.g., sedatives), cold exposure, or an exacerbation of another chronic illness. Patients develop symptoms insidiously, and diagnosis may be delayed. Major clinical findings include hypothermia, altered mental status, and respiratory suppression. Typical skin changes include periorbital edema, peripheral edema, dry skin, and signs of anemia. Bradycardia is common. Progressive depression of the sensorium may result in coma. Early diagnosis is essential to limit morbidity and mortality. Once the diagnosis is suspected, treatment should begin. Confirmation with laboratory testing will reveal depressed T4 levels and elevated TSH.

Initial treatment may require respiratory assistance with mechanical ventilation. In addition, underlying illnesses need attention (pneumonia, heart failure, urinary tract infection, etc.). Thyroid replacement begins with an intravenous T4 bolus, followed by daily maintenance doses. Glucocorticoids are given routinely to prevent the potential complication of adrenal crisis. Passive measures are used to rewarm the patient, thereby avoiding rapid vasodilation and possible vascular collapse, which may accompany aggressive warming measures. Typically, a hyponatremia similar to SIADH is present and should be treated with free water restriction. Volume expansion should be accomplished with isotonic crystalloids or whole blood. Response to therapy occurs within the initial 24 hours and is evident by improvement of hypothermia, bradycardia, and mental status. Prolonged respiratory assistance is not uncommon. Mortality rates have improved to approximately 15% to 20% with aggressive treatment.

Diabetic Emergencies

Many of the complications of diabetes are true medical emergencies, including diabetic ketoacidosis, nonketotic hyperglycemic–hyperosmolar coma, and hypoglycemia. Additional characterization and therapeutic protocols for these conditions is beyond the scope of this chapter, and the reader is directed to the chapter on perioperative management issues.

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PANCREAS

Physiology

Pancreatic islet cells produce insulin, glucagon, human pancreatic polypeptide, and somatostatin. Insulin, derived from proinsulin, consists of an alpha and beta chain connected by a C peptide. The basal secretion level is raised in a biphasic response to stimulation. The rapid phase may release stored preformed insulin in response to glucose, amino acids, glucagon, and some gastrointestinal hormones. With continuous glucose administration, both preformed and new insulin is released in the delayed phase. Release is stimulated by the vagal nerve and b-adrenergic receptors and inhibited by b-adrenergic blockers, sympathomimetic amines (e.g., epinephrine, norepinephrine), and somatostatin, which also inhibits glucagon. Stress triggers the release of glucagon, glucocorticoids, GH, and catecholamines, which are antagonists to insulin, resulting in glycogenolysis, gluconeogenesis, ketogenesis, lipolysis, and nitrogen wasting. Stress also affects wound healing, electrolyte and fluid balance, and susceptibility to infection.

Dysfunction

There are two types of diabetes mellitus with seemingly different causes, but they are both associated with similar complications. Type I (i.e., juvenile onset) usually appears in patients younger than 25 years who are insulin deficient, ketosis prone, and usually not obese. The cause is thought to be an autoimmune response to beta cells triggered by infection. The insulin levels of these patients are generally difficult to control. Type II (i.e., adult onset) has a more gradual onset. Patients are generally obese, over 40 years old, ketosis resistant, and more stable and easier to control. It is thought to be the more inheritable form of diabetes. Obesity reduces the number of insulin receptors on insulin-responsive cells, altering glucose tolerance. With fasting and weight loss, the number of receptors increases to normal levels.

In addition to random fasting blood sugar levels, screening for diabetes is accomplished with the 2-hour postprandial glucose tolerance test, using a fixed amount of glucose after a 3-day period of carbohydrate loading. Serum glucose determinations are 10% to 15% higher than whole blood determinations; therefore, it is important to know which test is performed.

Surgical diabetic patients under stress or anesthesia are thought to undergo hormone imbalances, causing glucose intolerance. They are also at greater perioperative risk due to disease-impaired cardiovascular, renal, and neurologic systems. Before surgery, careful assessment of these systems is important, as is assessing glucose control and modifying the patient’s regimen if necessary.

Symptoms of angina, which must be sought, may be absent. Autonomic dysfunction presents with orthostatic hypotension, nocturnal diarrhea, early satiety, or difficulties with erections and ejaculations in the male patient. Nocturia, dry mouth, blurred vision, weakness, palpitations, hunger, and nightmares are symptoms related to poor glucose control. The effects associated with hypoglycemia may be masked by neuropathies or b-adrenergic blockers (e.g., propranolol).

A thorough examination of the heart and peripheral pulses is necessary with an examination for bruits and orthostasis. An electrocardiogram should be obtained preoperatively and postoperatively to detect a silent myocardial infarction. Laboratory data should include preoperative fasting glucose, electrolytes, blood urea nitrogen, creatinine, chest radiograph, and clean-catch urinalysis. Long-term control can be assessed with the hemoglobin A1C determination, which is elevated with high glucose levels due to incorporation of glucose into the hemoglobin molecule. Levels remain elevated for 4 to 6 weeks, the lifespan of an erythrocyte. Before surgery, the patient in ketoacidosis should be stabilized as much as possible or surgery should be delayed to establish better glucose control or clear up bacteria in the urine. Diabetics are at increased risks for diseases with a predilection for immunocompromised patients, such as invasive fungal and bacterial infections. In addition, they suffer from poor wound healing, as may be evident after surgical procedures.

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ADRENAL GLAND

Anatomy and Physiology

The adrenal gland consists of the cortex and the medulla. The adrenal medulla is made of chromaffin cells that secrete norepinephrine and epinephrine in response to fear, anger, or stress. These hormones result in increased heart rate, raised blood pressure, vasoconstriction, and altered carbohydrate metabolism. The adrenal cortex is further divided into three zones that secrete five groups of steroids: corticosteroids, aldosterone, androgens, estrogens, and progesterone. All are derived from cholesterol. The outer region, the zona glomerulosa, secretes the main mineralocorticoid, aldosterone. Most of the glucocorticoids, androgens, and progesterone are secreted by cells in the middle, the zona fasciculata. The inner zona reticularis is responsible for the remainder of the steroids secreted by the cortex. This area atrophies in older males and enlarges with pregnancy and in the summer in women of childbearing age. Unlike the medulla, removal of the cortex is incompatible with life. The glucocorticoids are bound to transcortin, carrying 70% of the circulating cortisol.

Aldosterone secretion, the serum potassium level, and ACTH are controlled mainly by angiotensin II. It acts on the collecting duct of the kidney, the salivary glands, and the gut mucosa, causing the excretion of hydrogen and potassium ions in exchange for sodium ions.

Dysfunction

Hyperadrenocorticism

Hyperadrenocorticism causes Cushing’s syndrome, characterized by centripetal obesity with moon facies and buffalo hump, hirsutism, easy bruisability, amenorrhea, manic behavior or psychosis, osteopenia, muscle weakness, and violaceous striae of the abdomen, hips, and breasts. Excess of glucocorticoids leads to increased volume and blood pressure, hypokalemia, negative nitrogen balance, and glucose intolerance because they are insulin antagonists. The causes include pharmacologic administration of glucocorticoids or ACTH and pathologic conditions, such as an ACTH-producing pituitary adenoma, adrenal hyperplasia, adrenal adenomas or carcinomas, or secondary ectopic ACTH production in some lung, thymus, or pancreatic tumors. Presentation of ectopic ACTH production may be atypical, including hyperpigmentation due to the stronger melanocyte-stimulating hormonelike properties. Cushing’s syndrome usually presents in the third to sixth decade of life and occurs more commonly in women. At surgical exploration, 75% to 90% of these cases are due to corticotropic cell adenomas with autonomous secretion and are therefore not under hypothalamic control. In the other 10% to 25%, no pituitary tumor is found.

Adrenocortical Insufficiency

Primary adrenocortical insufficiency (i.e., Addison’s disease) may be due to destruction of the gland from autoimmune disease, tumors, infection, hemorrhage, or metabolic failure in hormone production. Secondary causes are hypopituitarism or suppression by exogenous steroids, ACTH (e.g., autonomous tumors), or endogenous steroids. The disease is characterized by fatigability, weakness, anorexia, nausea and vomiting, weight loss, hyperpigmentation, hypotension, and occasionally hypoglycemia. In women, the loss of adrenal androgens causes a loss of axillary and pubic hair. The absence of glucocorticoid causes volume depletion with decreased cardiac output and function, leading to shock that is sometimes called addisonian crisis.

Overproduction of Aldosterone

Primary overproduction of aldosterone is due to an adenoma (i.e., Conn’s syndrome) or nodular hyperplasia of the zona glomerulosa and is associated with moderate hypertension, hypokalemia, alkalosis, and normal or slightly increased sodium levels. Symptoms include muscle weakness, nocturnal polyuria, and cramping of the hands. Secondary excess is seen in cirrhosis, ascites, the nephrotic syndrome, and with diuretic use if the patient is volume depleted. In primary overproduction, tests show elevated aldosterone levels with severely suppressed plasma renin levels that do not respond to volume depletion; in secondary overproduction, one finds renin levels that are not suppressed and that may rise using various methods. Congenital or infantile forms of hypoaldosteronism are due to an enzyme defect in production. In the elderly, the condition is thought to be caused by an intrinsic renal problem, causing inadequate renin production. Many patients are diabetic and present with moderate renal insufficiency and serum potassium levels that are much higher than expected.

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THYROID GLAND

A detailed discussion regarding the thyroid gland and its associated diseases can be found in Chapter 114. The following discussion focuses on the endocrinology of the thyroid gland.

Physiology

Thyroid hormone affects the metabolic rate and plays a critical role in thermogenesis from increased energy release and higher oxygen consumption required by the stimulation of various processes. These processes include actions involved in fetal and neonatal growth, especially of the brain; glucose, amino acid, and electrolyte transport into the cell; oxidative phosphorylation; and protein, carbohydrate, and lipid metabolism. Thyroid hormone increases production of lipogenic enzymes and induces production and storage of fat in times of excess carbohydrate ingestion.

The thyroid gland converts iodine into thyroid hormone by organification. Oxidized iodine attaches to the 3 and 5 positions of tyrosine in the thyroglobulin molecules, which then couple by oxidation, forming tetraiodothyronine or T4 10 times more abundantly than T3. The hormone–thyroglobulin complex is stored as the colloid at the center of the cluster of thyroid follicle cells. To release thyroid hormone, thyroid follicular cells form pseudopodia, creating vesicles by endocytosis. These contain lysosomes that hydrolyze the thyroglobulin using hydrogen supplied by reduced glutathione, freeing thyroid hormone for release into the circulation by exocytosis. Organification is blocked by propylthiouracil and reducing substances used to treat hyperthyroidism. Release is inhibited by iodine, which affects production of glutathione reductase.

TSH from the pituitary stimulates the synthesis and release of thyroid hormone from the thyroid gland, which then exerts feedback inhibition directly on the pituitary thyrotropic cell by competing with thyrotropin-releasing hormone from the hypothalamus. After release into the circulation, thyroid hormone is bound to thyroid-binding proteins, mostly T4-binding globulin (70% to 80%), albumin, and transthyretin, to keep the hormone soluble in plasma and assist with distribution to the cells. A minute amount circulates freely in the plasma. It is this part that diffuses into the cell and is carried to the nucleus by binding proteins. Here it stimulates DNA transcription, resulting in the formation of messenger RNA and the production of various proteins. T4 binds with 10 times higher affinity to the thyroid-binding globulin, and T3 binds preferentially to intracellular sites. Therefore, most T4 is found in the circulation, and most T3 is found within the cells. The amount of free hormone can be affected by drugs that displace bound hormone (e.g., aspirin in high doses, phenytoin, carbamazepine) and severe nonthyroidal illness, which reduces the ability to bind thyroid hormone. Binding proteins are elevated by acute hepatitis, elevated estrogen (e.g., pregnancy, birth control pills, postmenopausal estrogen), or methadone and are reduced by anabolic steroids, nephrotic syndrome, or decreased production due to an inherited disorder.

Most T4 is secreted by the thyroid gland. It is functionally a prohormone but may have some metabolic activity itself. Conversion to T3, the more metabolically active form, occurs by monodeiodination in the liver, kidney, and possibly other organs, which accounts for 80% of the circulating T3. During stress or nonthyroid illness, T4 preferentially converts to inactive reverse T3 to conserve the body’s metabolism by removal of an iodide from the inner ring, instead of the outer ring as in T3. The deiodinase system is inhibited by fasting, systemic illness, kidney or liver disease, acute psychiatric illness, severe vomiting of pregnancy, and drugs (e.g., propylthiouracil, glucocorticoids, propranolol, iodine-containing agents), leading to the accumulation of reverse T3 and a fall in T3 levels. Large amounts of T4 are stored in the thyroid gland and bound in the circulation to thyroid-binding globulin, thereby prolonging the time for hormone deficiencies to manifest themselves clinically. Inflammation may cause injury to the gland with leakage of thyroglobulin, causing elevated levels of T4, T3, thyroglobulin, and other iodinated products in the serum.

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PARATHYROID GLANDS

Parathyroid anatomy and physiology and its pathologic states are discussed thoroughly in Chapter 115. The following discussion highlights the role of PTH in the regulation of calcium metabolism.

Calcium Metabolism

Calcium homeostasis depends on the release of PTH and on small amounts of vitamin D and calcitonin. The function of the parathyroid glands is to maintain calcium and phosphorus homeostasis. Calcium is important for the formation of intercellular ground substance, teeth, and bone. At the membrane level, it affects neuromuscular irritability, muscular contractility, and cardiac rhythmicity. Lack of extracellular calcium causes tetany and death if not corrected.

PTH is a peptide of 84 amino acids with an active amino-terminal end and an inactive carboxy-terminal end. Its secretion by the parathyroid glands is enhanced by a low ionized serum calcium and a high phosphate level.

Calcitonin, a peptide of 32 amino acids, is produced by the parafollicular C cells of the thyroid and contributes to calcium homeostasis by suppressing osteoclastic activity in bone and decreasing the amount of calcium available to the extracellular space. Calcium circulates in the extracellular compartment in three forms: 47% is ionized and is the free and active form that is readily used; 47% is bound to albumin and globulin and fluctuates with the serum protein level; and 6% is bound to anions such as bicarbonate, phosphate, and citrate.

Calcium is pumped from the extracellular compartment into the intracellular space. When serum calcium falls, the parathyroids release PTH, which increases osteoclastic activity, causing resorption of bone and release of calcium; increases resorption of calcium at the renal tubular cell; increases absorption of calcium from the gastrointestinal tract; stimulates renal-1-hydroxylase, which allows 1-hydroxylation of vitamin D in the kidney; and increases excretion of phosphorus in the urine, decreasing the serum phosphorus level.

Vitamin D is produced from exposure to sunlight or is obtained from the diet. Dietary calcium is provided by dairy products, green vegetables, nuts, fish, and calcium supplements. Approximately 1 g of calcium is ingested each day, and most of this is absorbed in the duodenum and upper jejunum. 1,25-Dihydroxyvitamin D increases the uptake of calcium at the brush border of the intestine by increasing cellular ATP and alkaline phosphatase content. At the other end of the cell, calcium is extruded into the extracellular fluid in exchange for sodium. The inactive vitamin D is transported by carrier protein to the liver, where it is 25-hydroxylated. It is then transported to the kidney, where 1-hydroxylation takes place, and it becomes activated to perform its function in maintaining calcium homeostasis by increasing calcium absorption and increasing calcium release from bone by osteoclastic activity.

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SURGICAL ANATOMY OF THE HEAD AND NECK

Anatomy is the basic science of all surgery. Surgery in the region of the head and neck cannot be considered safe unless the surgeon thoroughly understands the anatomy of this area and its important variations. Although anatomic structures and the relations between them do not change, our knowledge of anatomy must be continually updated to meet the challenge of new surgical techniques and approaches. This chapter is overview of surgical anatomy of the head and neck with a focus on the major regions. It is not a substitute for thorough anatomic knowledge, which can be gained only through intensive study in a cadaver laboratory and an operating room.
THE CRANIUM
Scalp
The cranium is covered by the hair-bearing scalp, which is divided into layers of skin and subcutaneous tissue, galea aponeurotica, loose connective tissue, and periosteum or pericranium covering the calvarial vault. The blood supply of the scalp comes from the paired supraorbital and supratrochlear arteries anteriorly, the terminal branches of the superficial temporal arteries laterally, and the occipital vessels posteriorly. This rich vascularity provides a network on which small scalp flaps can be based and rotated, as in the management of male pattern baldness. Sensation to the scalp is provided by branches of cranial and spinal nerves.
Calvaria
The bony vault of the cranium, the calvaria, consists of the unpaired frontal bone, the paired parietal bones, and the unpaired occipital bone (Fig. 1.1). In the lateral aspect, the greater wing of the sphenoid bone and the temporal bone complete the cranium. There is a rich layer of diploic bone between the inner and outer tables of the calvaria. This is a source for split-thickness calvarial bone grafts, which often are used in head and neck reconstruction. The calvarium is thickest at the external occipital protuberance and in the parietal region. It is thinnest over the temporal region. This allows ready access for neurotologic operations on the middle fossa. The venous circulation of the calvaria is provided by diploic veins, which drain to the veins of the scalp or into the dural venous sinuses. In some instances the diploic veins are connected to each other, and this communication allows osteomyelitis that originates in the frontal sinus to involve the frontal bone, scalp, and dura.
Cranial Fossae
The intracranial cavity is roughly divided into three fossae. The anterior or frontal cranial fossa contains the paired frontal lobes and provides access to the nasal cavity for the olfactory nerves through the cribriform plate. The crista galli provides superior midline extension of the nasal septum. The middle cranial fossa contains the temporal lobes. In this important junction of the cranial cavity, the middle meningeal artery arises from the foramen spinosum, and the trigeminal nerve enters through the superior orbital fissure (V1), the foramen rotundum (V2), and the foramen ovale (V3). Cranial nerves II, III, IV, and VI, which traverse the cavernous sinus and enter the orbit, also course through the middle cranial fossa. The internal carotid artery is in its place in the carotid siphon as it traverses the cavernous sinus in this region. The posterior cranial fossa contains the paired cerebellar hemispheres and the brainstem. In this location, the internal auditory meatus is associated with the seventh and eighth cranial nerve complex. The jugular foramen, transverse sinus, and foramen magnum are the major landmarks of the posterior cranial fossa.
EYELID, ORBIT, AND EYE
Eyelids

The upper and lower eyelids are similar in structure, although the upper eyelid is more mobile and has features not found in the lower eyelid. The space between the eyelids is known as the palpebral fissure, which is limited medially and laterally by the canthi. At the medial canthus is the lacrimal caruncle, where there is a small lake of tears and the tiny papillae of the lacrimal duct system. The conjunctiva is a thin mucous membrane layer that covers the inner aspects of the eyelids and extends onto the surface of the globe.
Tarsus
The upper tarsal plate provides rigidity to the upper eyelid and is larger than the lower tarsus (Fig. 1.2). Each eyelid consists from without inward of skin, subcutaneous tissue, voluntary muscle of the orbicularis oculi, orbital septum, tarsus, smooth muscle, and conjunctiva. The more freely mobile upper lid receives the insertion of the levator palpebrae superioris muscle. The orbicularis oculi is the sphincteric muscle of the upper and lower eyelids. It attaches at a medial palpebral ligament and spreads in an arc laterally and inferiorly to provide a sphincteric muscle to the eye. It receives innervation from the temporal and zygomatic branches of the facial nerve. This muscle interdigitates with the frontalis muscle and the corrugator supercilia.
Blood Supply
The arterial supply of the eyelids is provided by the angular branch of the facial artery, which forms an anastomotic network with the supraorbital and supratrochlear artery and shares a small contribution from the superficial temporal vessels. The veins of the eyelids are larger and more numerous than are the arteries and drain into the ophthalmic and angular veins medially and the superficial temporal vein laterally. Accompanying the peripheral arterial arcade of the upper eyelid, the veins of the small venous plexus drain into the ophthalmic vein, which drains posteriorly to the cavernous sinus. The veins in this region of the face do not have valves and may propagate septic emboli posteriorly. This is a particularly dangerous situation for patients who have infections in the areas of the eyelids or periorbital abscess. These patients are at risk of cavernous sinus thrombosis.
Lacrimal System
The lacrimal apparatus consists of a secretory portion, the lacrimal gland, its ducts, the drainage apparatus, the lacrimal canaliculi and sac, and the nasolacrimal duct (Fig. 1.3). The lacrimal gland is partially divided into two portions by the lateral horn of the aponeurosis of the levator palpebrae. The larger orbital portion of the gland lies in a shallow fossa on the frontal bone and is in contact anteriorly with the orbital septum. The excretory ductules of the lacrimal gland run through the orbital part of the gland, run through or close to the posterior part of the palpebral portion, and are joined by ducts from this portion. Removal of the palpebral portion can destroy the drainage of the entire gland.
Movement of the eyelid distributes tears over the surface of the eye, and any excess tends to accumulate in the lacrimal lake. This structure drains into the paired superior and inferior canaliculi and from there into the lacrimal sac. The lacrimal sac is housed in the bony lacrimal fossa of the medial orbital wall. This drains into the nasal lacrimal duct and eventually into the inferior meatus of the nose.
Orbit
The bony orbit consists of the medial wall occupied largely by the ethmoid bone, lacrimal bone, and a portion of the nasal process of the maxilla (Fig. 1.4). The floor of the orbit consists of the roof of the maxilla. The inferior orbital fissure is at its lateral extent. The zygomatic bone and greater wing of the sphenoid form the lateral orbital wall and join the frontal bone superiorly to complete the pyramidal bony orbit. On its medial aspect are the paired ethmoidal foramina, which provide a route to the orbit for the anterior and posterior ethmoidal arteries. The optic canal posteriorly transmits the optic nerve and ophthalmic artery. The superior orbital fissure transmits cranial nerves III, IV, V, and VI and provides an aperture for the ophthalmic vein.
Eye
The eye consists of the cornea and sclera in the anterior aspect. The anterior chamber protrudes as a second sphere on the structure of the orbit. The lens and iris form the posterior portion of the anterior chamber. Contained within the substance of the eye is the vitreous. The retina rests on the choroid. The fovea centralis is the focal point of the eye. Asymmetric to the structure of the orbit is the insertion of the optic nerve and ciliary arteries.
The seven voluntary muscles of the orbit are the levator palpebrae superioris; the superior, inferior, medial, and lateral rectus muscles; and the superior and inferior oblique muscles (Fig. 1.5). The smooth muscles of the orbit are the orbitalis muscle, the superior and inferior tarsal muscles, and ciliary and iridial muscles within the eye. The superior oblique is supplied by cranial nerve IV, the lateral rectus by cranial nerve VI, and the other voluntary muscles of the orbit by cranial nerve III. The tarsal and orbital muscles (of Müller) are supplied by sympathetic fibers derived from the carotid plexus and from the superior cervical ganglion. The dilator pupillae, the sphincter pupillae, and the ciliary muscle are supplied by parasympathetic fibers through the oculomotor nerve (III).

The primary blood supply to the orbit is through the ophthalmic artery. The primary drainage is through the ophthalmic vein, which drains directly into the cavernous sinus. An additional anastomotic network is present on the anterior aspect of the face in the form of an arcade of vessels around the eyelids and through the pterygoid plexus.
THE EAR
The development and the anatomic and physiologic features of the ear are discussed in Chapter 128 and Chapter 129.
NOSE AND PARANASAL SINUSES
External Nose

The external part of the nose is a roughly pyramidal shape. The skeleton of the external nose is partly bony and partly cartilaginous and membranous. The nasal bones, which are usually narrow and thicker above, wider and thinner below, articulate firmly above with the nasal part of the frontal bone and with each other laterally with the nasal process of the maxilla (Fig. 1.6). Attached to the inferior aspect of the nasal bones are the upper lateral cartilages. These are continuous with the cartilaginous septum. In the inferior aspect, the lobule of the nose is formed mostly by the lower lateral cartilages, which consist of a medial and lateral crus. There are several small cartilages within the nasal ala. The chief arterial supply of the nose is from the facial artery through the angular artery and superior labial arteries. Venous drainage is similar, with a component gaining access to the ophthalmic vein through draining vessels from the trochlear and angular veins.
Nasal Cavity
The nasal cavities are also known as the nasal fossae. The nasal septum consists of the nasal septal cartilage, the nasal crest of the maxilla, the nasal crest of the palatine bone, the vomer, and the perpendicular plate of the ethmoid bone. The lateral nasal wall is formed by the prominent nasal turbinates. The meatus are situated below the corresponding turbinates (Fig. 1.7). The inferior meatus provides drainage for the nasolacrimal duct. The middle meatus provides drainage for the anterior nasal sinuses, namely the frontal sinus, anterior ethmoid sinuses, and the maxillary sinus. The superior meatus provides drainage for the posterior sinuses, namely the posterior ethmoid and sphenoid sinuses.
The arterial supply of this region is from internal carotid sources through the anterior and posterior ethmoid arteries and from an external carotid source through the sphenopalatine artery. Contributions also may exist from the greater palatine vessels and the septal branch of the superior labial artery. These form an important anastomotic network in the anterior septum known as the Kiesselbach plexus, which accounts for most nosebleeds.
Sinuses
The paranasal sinuses consist of the paired frontal, ethmoid, maxillary, and sphenoid sinuses (Fig. 1.8). The frontal sinus develops as one of several outgrowths from the region of the frontal recess. Two, three, or even more frontal sinuses on a side have been reported, and some persons have no frontal sinus. The degree of pneumatization of the frontal sinuses varies. Pneumatization may extend into the roof of the orbit and laterally into the frontal bone as far as the sphenoid wing. The frontal sinuses drain into the anterior aspect of the middle meatus.

Ethmoid Sinuses
The ethmoid sinuses consist of a variable number of separate cavities that honeycomb the ethmoid bone between the upper part of the lateral nasal wall and the medial wall of the orbit. The anterior ethmoid cells are divided into frontal recess cells, which open into the frontal recess of the middle meatus; infundibular cells, which open into the ethmoid infundibulum; and bullar or middle ethmoid cells, which open directly into the middle meatus on or above the ethmoid bulla. There may be one to seven posterior ethmoid cells. The bullae and posterior ethmoid cells may encroach on each other and overlap, the bullar cells spreading backward or the posterior cells forward. The posterior ethmoid cells drain into the superior meatus.
Sphenoid Sinus
The sphenoid sinus usually opens into the sphenoethmoidal recess above and behind the superior nasal concha. The ostium usually is in the posterior wall of the recess, but sometimes it is on its lateral wall. The degree of pneumatization of the sphenoid sinus varies. This variation is an important factor in surgical approaches to the pituitary gland. The relations of the sphenoid sinus are important because of the surrounding anatomic structures. The optic nerves are superior to the sinus, and the internal carotid artery is lateral to the sinus within the cavernous sinus. The maxillary nerve lies in the inferior lateral portion of the sinus in the anterior aspect. The hypophysis lies within the posterior superior portion of the sphenoid sinus and can be approached through transsphenoidal hypophysectomy.
Maxillary Sinus
The maxillary sinus usually is the largest of the paranasal sinuses and is situated in the body of the maxilla. Its anterior wall is the facial surface of this bone, and its posterior wall is the infratemporal surface. Its medial wall is that of the nasal cavity. The roof of the maxillary sinus is also the floor of the orbit, and it also may be affected in blowout fractures of the orbit. The maxillary sinus drains into the middle meatus of the nasal cavity. The roots of the posterior molar teeth may extend into the sinus. The maxillary sinus is bounded posteriorly by the pterygomaxillary fossa, through which course the terminal branches of the internal maxillary artery. These vessels can be approached through the maxillary sinus for relief of epistaxis.
THE FACE
Facial Bones and Muscles

The bones of the face include the frontal and nasal bones and the facial bones proper—maxilla, mandible, zygomatic, and palatine bones. The facial and mimetic muscles are divided into five chief groups concerned with the mouth, nose, orbit, ear, and scalp (Fig. 1.9). The platysma muscle in the neck also belongs to the facial group. The chief action of these muscles is on skin into which they insert. All these muscles are innervated by the facial nerve.
Parotid Gland
The parotid gland, which is anterior to and below the lower part of the ear, extends subcutaneously backward over the anterior portion of the sternocleidomastoid muscle, forward over the masseter muscle, and deeply behind the ramus of the mandible to lie between the mandible and the external acoustic meatus and mastoid process (Fig. 1.10). The gland is roughly divided into a lateral and medial portion by the course of the facial nerve. Related to the parotid gland are several periparotid and intraparotid lymph nodes, which may swell. The parotid gland drains through the parotid duct. It is innervated by the auriculotemporal nerve from the otic ganglion.
Facial Nerve
The anatomic characteristics of the facial nerve vary in the extracranial portion of the nerve. Identification of the nerve depends on marking the position of the posterior belly of the digastric muscle, the external meatal cartilage, the tympanomastoid suture line, and the styloid process.
ORAL STRUCTURES
Maxilla

The maxilla is the chief component of the upper jaw (Fig. 1.11). In addition to housing the dental apparatus and the maxillary sinus, it is related posteriorly to the medial and lateral pterygoid plates. The hard palate unites the paired maxilla and forms the bony roof of the oral cavity. Sensation to the upper teeth is provided by the maxillary nerve through the posterior superior and anterior superior alveolar nerves. The infraorbital nerve, another branch of V2, provides sensation over the face of the maxilla and soft tissues.
Palate
The palate intervenes between the nasal and oral cavities (Fig. 1.12). It consists of the maxilla, the horizontal process of the palatine bone, and the pterygoid plates. Soft tissues covering this area form the hard and soft palates of the roof of the mouth. The skeletal core of the soft palate is the palatine aponeurosis. The most superficial muscle fibers on the pharyngeal surface of the soft palate are those of the palatopharyngeus muscle. The levator veli palatini, tensor veli palatini, and uvular muscle complete the structures of the soft palate.

Mandible
The mandible, or lower jaw, consists of the tooth-bearing body and the ramus that extends upward from the angle of the mandible. The ramus, including the angle, is covered externally by the masseter muscle, which is crossed by the facial nerve and parotid duct. Between the ramus and the medial pterygoid muscle are the inferior alveolar and lingual nerves. Overlapping the posterior border of the ramus is the parotid gland, and within and paralleling this border is the upper portion of the external carotid artery. The superficial branch of this artery emerges from the parotid gland behind the temporomandibular joint, and its internal maxillary branch runs transversely deep to the ramus. Inferiorly and medially, the angle and posterior part of the body of the mandible are related to the submandibular gland, and medially, the anterior part of the mandible is adjacent to the sublingual glands. The musculature most intimately concerned with the mandible and its movements consists of the masseter, temporal, and two pterygoid muscles (Fig. 1.9). These muscles govern mastication and are innervated by the third division of the trigeminal nerve.
Hyoid Bone and Tongue
The hyoid bone, to which are attached infrahyoid and suprahyoid muscles, effectively separates the anterior suprahyoid and infrahyoid fascial compartments. The suprahyoid muscles are the digastric and stylohyoid muscles, the mylohyoid and the geniohyoid muscles, and the muscles of the tongue (Fig. 1.13). The extrinsic muscles of the tongue are the genioglossus, the hyoglossus, and the styloglossus. The intrinsic muscles of the tongue are complicated bundles of interlacing fibers, among which are connective tissue septa. The midline septum lies between and effectively separates the muscles, nerves, and vessels of the two sides. It is an almost bloodless midline plane.
Submandibular Gland
The submandibular gland occupies most of the submandibular triangle and expands beyond this area over the superficial structures of the anterior and posterior bellies of the digastric muscle (Fig. 1.14). Its posterior border is close to the lower part of the parotid gland at the angle of the jaw, where it is separated from this gland by the stylomandibular ligament. The submandibular gland is crossed superficially by the facial vein and sometimes by the ramus mandibularis branch of the facial nerve. The larger submandibular lymph nodes lie along the superficial upper border of the gland, between it and the mandible. The anterior portion of the submandibular gland lies directly against the mylohyoid muscle and the mylohyoid nerve. Medial to the mandible and above the level of the submandibular gland is the lingual nerve in its course toward the tongue. When the submandibular gland is removed, the facial vein is sacrificed, but the ramus mandibularis branch of the facial nerve is preserved to avoid disruption of the corner of the mouth. The facial artery passes across the upper surface of the gland, usually grooving it deeply before rounding the lower border of the mandible, and must be sacrificed in removal of the gland. The submandibular and sublingual glands are innervated from the submaxillary ganglion fibers that accompany the sensory fibers of the lingual nerve. These fibers originate in the chorda tympani and pass into the submandibular ganglion.
PHARYNX AND LARYNX
The wall of the pharynx consists of mucosa and voluntary muscle. The mucosal structure of the pharynx varies. That of the nasal part is ciliated and resembles the mucosa of the nose. In the rest of the pharynx, the epithelium is stratified squamous tissue. The muscular wall of the pharynx with its thin covering of buccal pharyngeal or visceral fascia is separated from the prevertebral fascia by an area of loose connective tissue that constitutes the retropharyngeal space.
Nasopharynx
The nasal part of the pharynx, the nasopharynx, is continuous anteriorly through the choana with the nasal cavities (Fig. 1.15). The floor is the upper surface of the soft palate. The fornix or roof, the mucosa of which is attached close to the base of the skull, slopes downward and backward to become continuous with the posterior wall. The eustachian tubes are prominent on the lateral aspect of the nasal pharynx. There may be adenoid tissue in the superior recess of the nasopharynx.
Oropharynx
The oropharynx is continuous anteriorly through the fauces, or oral pharyngeal isthmus, with the oral cavity. The boundaries of the fauces are the posterior border of the soft palate above, the palatine arches laterally, and the dorsum of the tongue. Below the fauces, the anterior wall of the pharynx is the posterior or pharyngeal dorsum of the tongue. On the posterior parts of the dorsum of the tongue lie irregular nodules of tissue known as the lingual tonsils. The lateral wall of the passageway of the fauces houses the large palatine tonsils. The lingual tonsils in the anterior aspect, the palatine tonsils in the lateral aspect, and the pharyngeal tonsils or adenoids in the posterior and superior aspects form a ring of lymphoid tissue known as the Waldeyer ring.
Hypopharynx
The laryngeal part of the pharynx, or hypopharynx, extends from just above the level of the hyoid bone superiorly to the lower border of the cricoid cartilage inferiorly, narrowing rapidly to become continuous with the esophagus. The anterior wall is formed laterally by mucosa on the medial surface of the thyroid cartilage and centrally or medially by the larynx and its appendages. Above is the epiglottis and the aditus of the larynx. Below the aditus, the anterior wall of the pharynx is also the posterior wall of the larynx. Lateral to the epiglottis are the lateral glossoepiglottic folds that form the anterolateral boundary between the oral and laryngeal parts of the pharynx. Below these folds, the hypopharynx extends forward around the sides of the larynx between this area and the thyroid cartilage. These bilateral expansions are the piriform recesses or sinuses.
The intrinsic portion of the larynx consists of the epiglottis, false vocal folds, laryngeal ventricles, paired true vocal folds, and arytenoid cartilages in the posterior aspect. Contained within the aryepiglottic folds are the paired corniculate and cuneiform cartilages. The space between the two vocal folds is the glottis.
The muscles of the pharynx are the superior, middle, and inferior constrictors. These muscles look like ice cream cones inserted into one another. They gradually merge to form the cricopharyngeus muscle at its inferior extent and then the esophagus. Each constrictor inserts with the corresponding muscle of the opposite side and the midline into a posterior midline raphe. These muscles are innervated by cranial nerve X through the pharyngeal plexus. Dehiscence in the pharyngeal constrictors may give rise to Zenker diverticula. Immediately lateral to the pharyngeal muscles are the great vessels of the neck and cranial nerve X.
Larynx
The major structural elements of the larynx are the shield-shaped thyroid cartilage and cricoid cartilages (Fig. 1.16). They join through the cricothyroid joint. The superior cornua of the thyroid ala articulate through several small cartilages with the hyoid bone. Overlying the structure of this skeletal framework are the infrahyoid muscles, which include the paired sternohyoid, sternothyroid, omohyoid, and thyrohyoid muscles.
The epiglottis is formed of fibroelastic cartilage and has multiple perforations that allow free access of lymphatic drainage or tumor to the preepiglottic space. The preepiglottic space is a C-shaped space bounded superiorly by the median glossoepiglottic ligament, inferiorly by the thyroid cartilage, anteriorly by the thyrohyoid membrane, and posterolaterally by the epiglottis and aryepiglottic folds. Free dissemination of tumor can occur within the preepiglottic space. The paired arytenoid cartilages provide an attachment for the vocal ligament and movement of the vocal folds. The intrinsic muscles of the larynx are innervated by the recurrent laryngeal nerve. The exception is the cricothyroid muscle, which is innervated by the superior laryngeal nerve. The recurrent laryngeal nerve enters inferiorly and laterally to the cricothyroid articulation through the Killian-Jamieson area. The recurrent laryngeal nerve on the left originates over the aortic arch and ascends in the neck to innervate the larynx. On the right, this structure goes around the subclavian artery.
THE NECK
Cervical Triangles

The prominent landmarks of the neck are the hyoid bone, the thyroid cartilage, the trachea, and the sternocleidomastoid muscles (Fig. 1.17). The sternocleidomastoid muscles divide each side of the neck into two major triangles, anterior and posterior. The anterior triangle of the neck may be further delimited by the strap muscles into the superior and inferior carotid triangles. The posterior triangles or lateral triangles of the neck are formed by the posterior border of the sternocleidomastoid muscle anteriorly, the clavicle inferiorly, and the anterior border of the trapezius muscle posteriorly. The omohyoid muscle divides this triangle of the neck into a small inferior subclavian triangle and a larger posterior occipital triangle. Deep to these muscles are the scalenes, which form much of the muscle mass of the posterior and lateral portions of the neck. The brachial plexus and subclavian artery course between the anterior and middle scalene muscles. The subclavian vein courses anteriorly to the anterior scalene muscle.
Inferior Portion of the Neck
In the inferior root of the neck and closely associated with the brachial plexus are the paired phrenic nerves that course medially to innervate the diaphragm (Fig. 1.18). These nerves originate in the ventral rami of the cervical plexus of the third, fourth, and fifth cervical nerve rootlets. The subclavian artery gives rise to the thyrocervical trunk. The transverse cervical and suprascapular arteries typically course laterally over the surface of the phrenic nerve. This relation allows identification of these structures. The vagus nerve lies further medially and is contained within the carotid sheath. It shares the sheath with the common, internal, and external carotid arteries and jugular vein. Posterior to the carotid sheath lies the cervical sympathetic nerve. On the surface of the carotid sheath lie the ansa hypoglossi nerves.
Lateral Portion of the Neck
The dominant structure of the lateral cervical triangle is the spinal accessory nerve. It emanates from the posterior border of the sternocleidomastoid muscle in close association with the splay of nerves of the cervical sensory plexus. It innervates the trapezius muscle on its inferior aspect in close association with the transverse cervical artery or suprascapular artery, which variably supplies the trapezius muscle.
Arterial Supply
The two common carotid arteries differ in length because the right carotid usually arises from the brachycephalic artery behind the sternoclavicular joint, and the left arises from the arch of the aorta (Fig. 1.19). Both arteries end by bifurcating into the internal and external carotid arteries. Over the lateral aspect of these arteries course the paired hypoglossal nerves. The internal carotid artery is situated more posteriorly and has no branches. The external carotid artery has branches and lies slightly anteriorly. This information can be crucial in differentiating the two vessels for ligation. From its origin, the internal carotid artery ascends directly toward the carotid canal and is crossed laterally, in ascending order, by the hypoglossal nerve, occipital artery, posterior belly of the digastric and associated stylohyoid muscle, and the posterior auricular artery. Still higher and close to the base of the skull, the external carotid artery is anterolateral to the internal carotid artery, and the stylopharyngeus muscle and associated glossopharyngeal nerve, the pharyngeal branch of the vagus, and the stylohyoid ligament all pass laterally to the internal carotid, between it and the external carotid artery.
After its origin in the carotid triangle, the external carotid artery passes upward, deep to the posterior belly of the digastric and stylohyoid muscles, crosses the styloglossus and the stylopharyngeus muscles on their lateral aspects, and parallel to the ramus of the mandible passes into the deeper portion of the parotid gland. The external carotid artery has branches to the superior thyroid, lingual, facial, ascending pharyngeal, occipital, posterior auricular, maxillary, transverse facial, and superficial temporal arteries.
Venous Supply
The veins of the neck vary considerably in their connections with each other and in their relative sizes (Fig. 1.20). Those conducting blood downward from the head and face include the external jugular, anterior jugular, internal jugular, and vertebral veins. At the base of the neck are the suprascapular and transverse cervical veins and the subclavian vein, which unites with the internal jugular vein to form the brachycephalic or innominate vein. The subcutaneous veins and the external and anterior jugular veins are especially variable in size and course.
Lymphatic Vessels
The lymphatic system of the neck consists of numerous lymph nodes intimately connected with each other by lymphatic channels and the terminations of the thoracic and right lymphatic ducts. The deep cervical lymph nodes are numerous and prominent, and many of them are large. They form a chain embedded in the connective tissue of the carotid sheath. Most are in that portion of the sheath around the internal jugular vein. They extend from the base of the skull to the base of the neck. Two nodes that deserve particular attention are the superior jugulodigastric node at the junction of the internal jugular vein and the posterior belly of the digastric and the inferior juguloomohyoid node at the junction of that muscle and the internal jugular vein. Block resection of the neck in a standard radical or modified manner relies on reproducible and consistent lymphatic drainage pathways for success.
Viscera
The visceral structures of the neck include the thyroid and parathyroid glands, a portion of the pharynx, the larynx, the trachea, the esophagus, and sometimes portions of the thymus (Fig. 1.21). The thyroid gland lies below and on the side of the thyroid cartilage covered anteriorly by the infrahyoid muscles. A pyramidal lobe of the thyroid may extend superiorly from the isthmus that connects the two lobes of the thyroid gland. On the posterior surface of the thyroid gland lie the paired parathyroid glands. Successful parathyroid exploration and thyroidectomy depend on accurate identification and preservation of the recurrent laryngeal nerves and identification of the parathyroid glands. Landmarks that are used successfully to locate these structures include the trachea, common carotid artery, and inferior thyroid artery, which form a triangle within which the surgeon usually finds the recurrent laryngeal nerve. Lymphatic drainage occurs along the peritracheal nodes. Venous drainage similarly is directed inferiorly along the inferior thyroid veins.
The four or more parathyroid glands develop from the dorsal extremities of the third and fourth pharyngeal pouches. As the thyroid and thymus and their associated parathyroid glands move caudally from the region in which they originate, the thymus normally descends beyond the level at which the thyroid halts. The parathyroids from the fourth pouches (superior parathyroid glands) typically are situated more craniad than the thyroid gland, and those derived from the third pouches (inferior parathyroid glands) are typically freed from the thymus and become associated with the thyroid gland at its lower pole. Both sets of parathyroid glands usually are situated on the posterior aspect of the lateral lobes of the thyroid gland, but there are many exceptions. Because of the manner in which they arise and migrate into the neck, the glands often are displaced and may be situated in other portions of the thyroid gland or lie above or below it.

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