Upper Digestive Tract

Anatomy and Physiology

The upper aerodigestive tract is a single conduit that must integrate and separate two very different vital functional systems: breathing and swallowing. In the healthy state, the anatomic structures and their neural substrates exquisitely coordinate each function through sensory-motor integration. The ability to swallow safely is critical for nutrition, hydration, and quality of life; however, its significance is often taken for granted when the physiology and pathophysiology are not fully appreciated. Understanding the anatomy and physiology of deglutition is not only required to properly evaluate and treat patients with dysphagia but also necessary to maximize functional outcomes after surgical interventions for head and neck cancer.

Dysphagia is not a disease, but rather a symptom or a collection of symptoms that broadly describe difficulty swallowing. Under the umbrella term dysphagia, finer distinctions are made that refer to the phase of swallowing where impairments exist. For example, patients may have oral, pharyngeal, oropharyngeal, pharyngoesophageal, or esophageal dysphagia. Dysphagia can also vary in terms of severity from mild to severe. However, it is unknown how much aspiration in a particular patient will result in pneumonia. Some patients can only tolerate a minimal amount of aspiration, while others tolerate larger amounts. The end point of dysphagia is pneumonia or airway obstruction. Unfortunately, to date, there is no universally accepted, standardized system that can be used to objectively define severity levels. In addition, the evaluation and treatment of dysphagia are often complicated by the fact that some patients are acutely aware of difficulty swallowing, while others may not perceive its presence or recognize the symptoms.

The swallowing difficulty can develop gradually from neurologic or respiratory disease, or be acquired suddenly as a result of injury or surgery. The multitude of different etiologies for dysphagia can often be delineated with a thorough history and physical examination. Instrumental assessments of swallowing function provide additional information that will further characterize swallowing function so that treatment can be planned. Effective therapeutic interventions are based upon each patient's specific physiology. Swallowing exercises can increase muscle strength and range of motion of swallowing structures. Skill training can instruct patients to use swallowing maneuvers such as breath-holding before drinking. Compensatory strategies such as changing head position can also be used to alter swallowing biomechanics. Diet alterations can be instituted so that unsafe food consistencies are eliminated. Surgical interventions, such as vocal fold augmentation or esophageal dilatation, may be required as the primary treatment, or in addition to swallowing therapy.

The ability to eat and drink safely and efficiently is fundamental to our quality of life. The wide variety of food and liquid that we enjoy throughout each day requires precise management because of the shared function of the upper aerodigestive tract. Indeed, modern research has shown that the pharyngeal swallow is not a stereotypic reflex as it was first described; rather, it is a patterned motor response to sensory input. As such, pharyngeal muscle force and contraction duration must rapidly and consistently adjust depending upon what is to be swallowed (1,2). To accomplish this feat, separate and overlapping phases of swallowing use sensory-motor integration Swallowing dysfunction can occur in each phase individually or collectively across them.

Anticipatory Phase

The anticipatory phase is often considered the first true step in swallowing because visual information, olfactory stimulation, and experience interact to form the initial motor plan (3). A common statement in the culinary profession is, "we eat with our eyes first." The adult has a well-developed motor plan for swallowing different types of food and drink that is based upon appearance (visual processing), consistency (tactile processing), taste (chemical processing), and bolus size (proprioceptive processing). Most have experienced a sudden awareness that an item placed in the mouth did not match what was expected. This observation can be viewed as practical evidence that a plan had been violated. Another example that illustrates this concept can be seen when we perceive a liquid to be very hot or a food is suspected of being very spicy. When experience indicates these possibilities, a slower presentation to the mouth will follow and care will be taken to ensure a smaller bolus size because of the anticipated negative effects.

It is also at the anticipator) level where distinctions between food and nonfood items are made and where palatability is determined. Oral intake may be avoided as a result of the information perceived and processed during this phase. If an individual is forced to eat or drink an item that he or she has predetermined (anticipated) is unsafe or undesirable, then gagging, coughing, and dysphagic symptoms may be observed. It is important to note that these are not behaviors that can be controlled; rather, they are in response to sensory stimulation. The anticipatory phase provides the initial sensory input to cortical swallowing structures. In patients with dementia or other cognitive impairments, the sensory processing of visual, olfactory, and experiential information can be altered. As such, the motor plan implemented to swallow may not match that of the bolus itself, putting the patient at risk for dysphagia.

Oral Preparatory Phase

Once solid and semisolid food is placed in the mouth, it must first be prepared for the pharyngeal phase. The combination of mastication and saliva production is considered to be the first step in digestion. Saliva from the submental, sublingual, and parotid glands flows into the oral cavity to mix with the bolus and begin the chemical process of food breakdown. The mandible closes to crush solid food and the rotatory motion of mastication enables the molars to shear and shred the food. The muscles of mastication are the masseter, temporalis, medial pterygoid, and lateral pterygoid muscles (Table 56.1). The masseter, temporalis, and medial pterygoid muscles elevate the mandible,

Summary Chart Of Peripheral Sensory And Motor Components Of Deglutition

Swallowing PhaseActionMuscleNerve

Oral preparatoryLabial closureOrbicularis orisFacial nerve (CN VII)

MasticationMasseter Temporalis Medial pterygoid Lateral pterygoid BuccinatorMandibular nerve (CN V3) Mandibular nerve (CN V3) Mandibular nerve (CN V3) Mandibular nerve (CN V3) Facial nerve (CN VII)

Bolus formationGenioglossus Hypoglossus Styloglossus PalatoglossusHypoglossal nerve (CN XII) Hypoglossal nerve (CN XII) Hypoglossal nerve (CN XII) Pharyngeal branch (CN X)

Tongue sensationAnterior two-third Posterior one-thirdLingual nerve (CN V3) Glossopharyngeal nerve (CN IX)

Tongue tasteAnterior two-third Posterior one-thirdChorda tympani nerve (CN VII) Glossopharyngeal nerve (CN IX)

PharyngealSoft palate depressionPalatoglossusPharyngeal branch (CN X)

Velopharyngeal closureLevator veli palatini Tensor veli palatini Palatoglossus Superior constrictorsPharyngeal plexus (CN X) Trigeminal nerve (CN V3) Pharyngeal branch (CN X) Pharyngeal plexus (CN X)

Vocal fold closureLateral cricoarytenoid

Interarytenoid

ThyroarytenoidRecurrent laryngeal nerve (CN X) Recurrent laryngeai nerve (CN X) Recurrent laryngeai nerve (CN X)

Laryngeal elevationMylohyoid

Anterior belly, digastric Stylohyoid

Posterior belly, digastric

Geniohyoid

ThyrohyoidTrigeminal nerve (CN V3) Trigeminal nerve (CN V3) Facial nerve (CN VII) Facial nerve (CN VII) Cervical 1 (CI)

Cervical 1 (CI) via hypoglossal nerve (CNXII)

EsophagealUpper esophageal segment relaxationCricopharyngeusPharyngeal plexus, recurrent laryngeal nerve (CN X)

while the lateral pterygoid depresses the mandible, thereby opening the mouth. Contraction of the masseter and medial pterygoid muscles also results in lateral mandible movements required for the rotary motions. Sensory and motor innervation to the muscles of mastication and salivary glands is provided by several branches of the trigeminal nerve. The cyclic motion of the mandible and motions of the tongue are mediated, in part, by a cortical central pattern generator (CPG). A CPG is essentially neural circuitry that generates rhythmic movement. It is important to remember that during this phase, the airway is open and active breathing continues. During mastication, respirator) rate becomes more rapid and irregular when compared to tidal breathing (4). If the bolus is not well controlled, solid food may fall into the open airway resulting in aspiration or asphyxiation. Also during mastication, the circular fibers of the orbicularis oris muscle work to actively close the lips and maintain the food or liquid within the oral cavity. An incompetent oral sphincter will result in drooling of saliva or loss of food and liquid out of the mouth. This circumstance is very embarrassing for patients and severely impacts the social aspects of meals. Neurologic diseases and surgical resections that prevent labial closure or impair sensation can cause anterior oral loss of food or liquid.

During mastication, the complex motions of the tongue move and guide prandial material by placing it between the molars, shifting food from side to side, and ultimately collecting it to form a single, cohesive, prepared bolus. Tongue motion is highly complex because it is composed of several intrinsic and extrinsic muscles that are oriented in multiple directions. The intrinsic lingual muscles are the superior and inferior longitudinal muscles, the transverse muscle (transverse lingualis), and the vertical muscle (vertical lingualis). Extrinsic lingual muscles are the genioglossus muscle that protrudes the tongue, the hypoglossus muscle to depress the tongue, and the styloglossus muscle that elevates and retracts the tongue. All of these muscles are innervated by the hypoglossal nerve (cranial nerve [CN] XII). The palatoglossus muscle is innervated by the pharyngeal branch of the vagus nerve (CN X) and elevates the back of the tongue to prevent premature spillage into the pharynx. In addition to muscle strength and coordination, adequate sensory input is necessary for safe swallowing.Sensor processing by the tongue and oral cavity is required to adequately prepare the bolus and maintain its cohesion. Tactile sensation to the anterior two-thirds tongue is mediated by the lingual nerve (CN V3) and taste sensation is provided to this region by the chorda tympani nerve (CN VII). The glossopharyngeal nerve (CN IX) provides both sensory and taste to the posterior one-third of the tongue. Oral sensation is also basic to proprioception because the oral structures and changing bolus characteristics must continually interact until the bolus is perceived to be fully prepared to swallow.Oral preparation through mastication essentially places everyone on a "pureed" diet, since humans do not swallow solid food whole. Difficulty swallowing pills can be attributed to both the anticipatory phase where fear and anxiety affect swallowing function in addition to volitional inhibition of mastication. Maintaining bolus cohesion and control is aiso needed for liquids and puree consistencies so that the next phase of swallowing can be accomplished.

Oral Transfer Phase

Once the bolus is prepared, it must be collected into a cohesive unit and moved to the posterior oral cavity. Oral transfer is accomplished by containing the bolus within the center of the tongue while the tongue tip contacts the alveolar ridge and pushes the bolus back across the hard palate using a wave-like propulsive force. During both the preparatory and transfer phases, sensor)' information is gathered in relation to bolus size and texture. Although it is not understood how humans have an intrinsic knowledge in relation to swallowing safety, the bolus will be subdivided if it is determined to be too large. Once the bolus reaches the posterior oral cavity, the lateral portions of the tongue press on the anterior facial pillars (innervated by CN IX) to terminate the oral phase and subsequently trigger the pharyngeal phase. Throughout the oral preparatory and transfer phases, the soft palate is pulled down and forward by the palatoglossus muscle (innervated by the pharyngeal branch, CN X) to maintain contact with the posterior tongue, thus sealing the oral cavity from the nasopharyngeal airway (Table 56.1). This mechanism allows maintenance of the bolus within the oral cavity while continuing to breathe through the nose (Fig. 56.1).

Oral dysphagia is present when the bolus is inadequately prepared or controlled. Poor dentition can lead to an inadequately prepared solid bolus that may have the potential to block the airway if aspirated. Failure to clear the oral cavity after a primary or secondary swallow can also result in aspiration after o; between swallows. Reduced posterior oral control and/or weak velar depression may produce premature loss or "premature spillage" of a bolus into the pharynx or larynx before the pharyngeal phase of swallowing is "triggered." If the bolus cannot be controlled or transferred, gavage feedings may be necessary in order to bypass the oral cavity. A significant delay or failure to elicit the pharyngeal phase is classified as oral dysphagia, regardless of bolus location, since it is the oral tongue that must trigger the pharyngeal response. Impaired cognitive function or poor sensation can cause patients to "forget" to elicit the pharyngeal swallow. Significantly reduced lingual range of motion, as a result of surgery or neurologic disease, can impair tongue strength or prevent the posterior tongue from reaching the facial arches to trigger the swallow. Oral dysphagia can occur in isolation or concomitant with pharyngeal dysphagia. It is important to always keep in mind that the airway remains open during the oral preparatory and transfer phases because the patient is breathing; therefore, prandial aspiration can occur both before and after the swallow.

Figure 56.1 Posterior oral containment of the bolus. Note velar depression and airway continuity from the nasal passages to the trachea (dotted line). B, bolus; V, velum; M, mandible; H, hyoid; A, arytenoid; P, posterior pharyngeal wall, *, UES; T, trachea.Pharyngeal PhaseThe pharyngeal phase begins with elevation of the soft palate to seal the nasopharynx from the oropharynx (Table 56.1). Mediated by the sensory and motor fibers that are primarily contained in the pharyngeal plexus, velopharyngeal closure is the result of elevation and tensing of soft palate and contraction of the palatopharyngeal muscles, combined with anterior motion of the posterior pharyngeal wall (Passavant ridge, superior pharyngeal constrictor muscle). 'I he adenoid pad and uvula may also aid in velopharyngeal closure. If the patient has velopharyngeal incompetence, they can experience nasal regurgitation during the swallow. Within milliseconds of velar elevation,

Figure 56.2 Elevation of the velum with subsequent closure of the nasopharynx. The hyoid and larynx are elevating. The arytenoids are about to approximate the petiole of the epiglottis to close the laryngeal aditus. B, bolus; V, velum; M, mandible; H, hyoid; A, arytenoid; P, posterior pharyngeal wall; *, UES; T, trachea.the posterior tongue lowers to enable the bolus to enter the oropharynx (Fig. 56.2). The base of tongue retracts and exerts the primary propulsive force on the bolus. The upright epiglottis protects the airway by dividing the bolus and directing it into the lateral channels of the pharynx toward the hypopharynx. The larynx begins to elevate, moving in a superior and anterior trajectory. Activation of the thyrohyoid muscle (innervated by the first cervical nerve via the hypoglossus nerve) and the suprahyoid musculature (mylohyoid, anterior and posterior digastrics, stylohyoid, and geniohyoid muscles) results in the superior and anterior thrust of the hyoid bone to the mandible. During laryngeal elevation, the true and false vocal folds adduct (lateral cricoarytenoid, interarytenoid, and thyroarytenoid muscles, all innervated by the recurrent laryngeal nerve, CN X) as the arytenoid cartilages are drawn forward (5). Vocal

Figure 56.3 The hyolaryngeal complex elevated, with complete closure of the airway. The bolus is about to enter the UES. B, bolus; V, velum; M, mandible; H, hyoid; P, posterior pharyngeal wall; *, UES; T, trachea.fold paralysis or severe vocal fold atrophy often results in glottic incompetence, which can result in aspiration during the swallow. The complex combination of base of tongue retraction, laryngeal elevation, and contraction of the aryepiglottic muscles creates contact between the arytenoids and the epiglottic petiole (Pig. 5G.3). This mechanism closes the laryngeal vestibule during pharyngeal bolus transit. Strong closure of the laryngeal entrance (aditus) can prevent aspiration and compensate for reduced glottal closure.

A common misconception is that the epiglottis inverts to protect the airway (6,7). In fact, the epiglottis has no motor innervation and cannot actively move An upright epiglottis protects the airway by capturing and containing material within the valleculae. Epiglottic inversion is then biomechanically created by the combination of the tongue

Figure 56.4 The inverted epiglottis within the bolus stream. The opaque circle is a coin, which is used to correct for magnification. B, bolus; M, mandible; H, hyoid; E, epiglottis; T, trachea; C, coin.base retraction, hyolaryngeal elevation, and the weight of the bolus (Fig. 56.4). The inverted epiglottis can enter the upper esophageal sphincter (UES) and may help to direct the bolus into the esophagus. When epiglottic inversion does not occur, it suggests the presence of base of tongue weakness and/or is often associated with reduced hyolaryngeal elevation. Sometimes, all that is needed to promote epiglottic inversion is to increase bolus size or to alter the biomechanics by having the patient tuck the chin toward their chest during the swallow.

For the bolus to enter the esophagus, the tonic muscle fibers of the UES must relax to allow the bolus to enter the esophagus. The superior and anterior motion of the hyoid and larynx during the pharyngeal phase creates a traction force that opens the lumen. Hyolaryngeal elevation must be of sufficient height and duration to allow the entire bolus to pass through to the upper esophagus (Fig. 56.5). If the LIES opening is limited in width and/or duration, truncation of the bolus and resultant residue in the post-cricoid region and/or pyriform sinuses (hypopharynx) can result. Aspiration of this residue can then occur alter the swallow when the airway reopens for breathing.

Following the tail of the bolus by several milliseconds is a sequential contraction of the pharyngeal muscles starting with the superior constrictor, followed by the middle constrictor and then the inferior constrictor. The wavelike motion of the pharyngeal constrictors is often mistaken for peristalsis; however, peristalsis can only be present in a circumferential "tube." The function of the sequential motion of the pharyngeal constrictors is to maintain a closed system within the pharynx during bolus transit (by contacting the tongue base) and to provide a "clearing wave" to assure that the entire bolus leaves the pharynx in anticipation of

Figure 56.5 A relaxed UES, with the opening into the esophagus maintained by hyolaryngeal elevation. B, bolus; V, velum; M, mandible; H, hyoid; P, posterior pharyngeal wall; T, trachea.airway opening. Patients who have had chemoradiation lor the treatment of cancer in this region often have inadequate clearing of material due to weakness and reduced range of motion of these muscles, putting them at risk for dysphagia. The pharyngeal phase of swallowing transpires in approximately 1 second or less. This rapid sequence of events is controlled by bilateral CPGs located within the brainstem.Esophageal Phase Active closure of the UES prevents air from entering the esophagus during breathing and also protects the airway from invasion by refluxate from the esophagus and/or stomach. The primary muscle of the UES is the cricopha-ryngeal (CP) muscle within the inferior constrictor muscles, with dual innervations from the glossopharyngeal nerve (CN IX) via the pharyngeal plexus and the recurrent laryngeal nerve (CN X) (Table 56.1). Once the bolus enters the esophagus, the circular and longitudinal muscles enable peristalsis to transport the bolus until it reaches the lower esophageal sphincter (LES) at the distal esophagus. The LES is a single muscle that, like the LIES, is tonic at rest. The EES relaxes with swallowing, enabling prandial material to enter the stomach. Esophageal dysphagia is present when either of the sphincter muscles (UES or LES) fails to open during deglutition (achalasia). Achalasia can be caused by a neurologic failure within the enteric nervous system scarring from radiation, or possibly repeated acid reflux.

A CP "bar" is a common finding on fluoroscopic swallowing studies but is not always a source of dysphagia unless it impedes bolus flow (Eig. 56.6). This finding can be due to hypertonicity and/or fibrosis of the muscle. This finding can also be the result of compensation to provide laryngeal protection in the face of esophageal dysmotility (esophageal-phalangeal rellux). High-resolution esophageal manometry may be helpful in characterizing different types of esophageal dysphagia.

Figure 56.6 A CP bar. Although the fibers have not relaxed fully, the bar diverts but does not obstruct bolus flow. B, bolus; T, trachea; CP, cricopharyngeal muscle.Breathing And Swallowing

The dual nature of the upper aerodigeslive tract necessitates central inhibition of respiratory muscles during each swallow. Cessation of breathing, combined with airway closure is called deglutitive apnea. Another common misconception is that babies can simultaneously breathe and swallow; nonetheless, vocal fold adduction and deglutitive apnea are also present in infants (8,9).

Several investigators have identified a preferred coordination between breathing and swallowing, finding that most swallows are timed to occur during mid to early exhalation (10,11). Exhalation has been reported to occur almost exclusively following every swallow, even those that occur during the inhalation phase. A target lung volume was recorded in healthy subjects who were found to consistently swallow between 51% and 56% of their vital capacity, irrespective of respiratory' pattern (12). hung volumes above functional residual capacity are associated with positive subglottic air pressures that are generated during each swallow (13,14). Lung-thoracic unit recoil creates the positive pressure by compressing the closed respiratory system during deglutitive apnea. Spontaneous changes in pharyngeal swallowing function have been measured in healthy adults when swallows are timed to occur at extremes in lung volume. Changes in lung volume are associated with changes in the amount of subglottic pressure that is generated, indicating that respi ratory signaling is also integrated into the sensory portion of each swallow. Emerging research points to the sensor)' receptors in the subglottis as the most likely structure that communicates the status of the respiratory system to the swallowing CPG (15-18). Due to the link between the respirator)' system and swallowing, pulmonary disease such as chronic obstructive pulmonary disease is considered to be a primary risk factor for dysphagia because of the additional demands that deglutition places on the respirator)'system (16,17)SummaryOropharyngeal swallowing is a multifactorial process that requires precise coordination of multiple muscles and nerves. The wide variety of consistencies that are consumed necessitates a high degree of sensor)' input to assure that the motor output will provide the safest and most efficient swallow. Sensory processing begins before food is placed in the mouth and continues in the oral and pharyngeal cavity. A portion of sensory input is also received from the respiratory system. Dysphagia can develop when there is a disruption at any level of sensory-motor integration. Therefore, knowledge of the anatomy and physiology of the upper aerodigestive tract in relation to swallowing is critical for the optimal care of patients.Highlight

Swallowing is not a stereotypic reflex, but rather a patterned motor response based upon the type of liquid or food to be swallowed.

Diseases and treatments of the head and neck, such as cancer, can alter die ability to swallow, and therefore a high index of suspicion is necessary for these patients.

Termination of the oral phase and triggering of the pharyngeal phase is created by the tongue contacting the facial pillars. Therefore, reduced tongue motion/strength could impair this transition to the next swallowing phase.

The epiglottis does not move independently but radier is moved by other structures. An upright epiglottis splits the bolus around the larynx into the pyriform sinuses. With base of tongue motion, hyolaryngeal elevation, and the weight of the bolus, the epiglottis inverts. The lack of epiglottic inversion points to a deficiency in one or more of the factors that lead to its movement.

Glottal incompetence can result in aspiration during the swallow. Strong closure of the laryngeal aditus superior to the level of the true vocal folds provides a layer of airway protection in this case.

The superior-anterior motion of the larynx creates opening of the LIES. Deficiencies in this movement due to surgery (such as suprahyoid release), scarring (such as chemoradiation), or neurologic deficiencies, will result in a shorting opening phase of the LIES, despite normal relaxation of the cricopharyn-geus muscle itself. This increases the possibility of postcricoid residue, which may be at risk of aspiration after the swallow is completed.

Proper coordination of breathing and swallowing can improve the strength, and therefore efficiency, of the swallow.

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