Pathological Aspect of Dysphagia

#### **Chapter 2**

## Pathology of Nonneoplastic Lesions of the Vocal Folds

*Nil Çomunoğlu, Şebnem Batur and Ayşe Mine Önenerk*

#### **Abstract**

Nonneoplastic vocal fold lesions are common that can cause hoarseness and voice change. Reactive lesions of Reinke's space can be observed in all ages and genders and comprise the majority of the benign nonneoplastic vocal fold lesions. Although clinically different terms are used to define reactive lesions of Reinke's space, they share the same histopathologic features. In order to differentiate vocal fold polyp and nodule and Reinke's edema, clinical findings should be considered. Epithelial changes such as pseudoepitheliomatous and verrucous hyperplasia may cause diagnostic challenge due to resemblance of squamous cell carcinoma. Evaluation of the invasion border and cellular atypia may aid in correct diagnosis.

**Keywords:** vocal fold nodule, vocal fold polyp, Reinke's edema, contact ulcer, keratosis

#### **1. Introduction**

The vocal folds, also known as vocal cords, extend through the laryngeal cavity bilaterally and are primarily responsible for voice production. The thyroarytenoid muscle, deep lamina propria, intermediate lamina propria, superficial lamina propria, and squamous epithelium comprise the vocal folds [1–3]. The superficial lamina propria, which is also called Reinke's space, consists of loose fibrous or elastic components and provides a gelatinous surface for vocal folds to vibrate upon. The deep and superficial lamina propria forms the vocal ligament. Madruga et al. demonstrated that type I collagen is abundant in the superficial lamina propria which forms a narrow band. The intermediate lamina propria essentially contains type III collagen, and the deep lamina propria is rich from both type I and type III collagen [4].

In a study of Chandramouli et al., nonneoplastic lesions of the larynx comprise 80% of the benign lesions diagnosed [5]. The etiology of the nonneoplastic vocal fold lesions is usually multifactorial, including phonotrauma (excessive loudness and cough, excess tension while speaking or singing, etc.), laryngeal trauma (endotracheal intubation), hypothyroidism, cigarette smoking, alcohol abuse, and gastroesophageal reflux (GERD) [6–10].

#### **2. Exudative lesions of Reinke's space**

Vocal fold nodules and polyps and Reinke's edema are exudative vascular-stromal lesions involving Reinke's space. The similarities and distinct features of these lesions have long been studied [11]. Although some discriminating features have

been emphasized, most of the literature concludes that these lesions share the same histopathologic features which prevent a definitive diagnosis [11, 12].

#### **2.1 Reinke's edema**

Reinke's edema is one of the most common causes of hoarseness and approximately comprises 10% of the laryngeal pathologies [13, 14]. It is the result of fluid accumulation in Reinke's space that lies beneath the surface epithelium of the true vocal cords [13]. Smoking, vocal abuse, upper respiratory tract infection, and gastroesophageal reflux (GERD) have been associated with Reinke's edema [13, 15–17]. Marcotullio revealed that the occurrence and recurrence of Reinke's edema depend on the number of cigarettes daily used [15]. Zeitels et al. showed that increased subglottic aerodynamic driving pressure is the underlying mechanism of edema [18]. It has been hypothesized that vocal hyperfunction along with the underlying conditions such as reflux, smoking, etc. is more prone to Reinke's edema [13]. Vecerina et al. classified Reinke's edema into transparent and livid type [19]. Hypothyroidism is stated not to be related with Reinke's edema [13, 20–22]. Majority of the patients are adults (aged between 20 and 60 years). Most of the patients experience Reinke's edema unilaterally (74%). Only a small group of the patients has bilateral edema (26%) [13].

Most of the time, serous fluid is observed upon incision in macroscopic evaluation. However, if the condition persists longer, a jellylike fluid can be seen [13]. Patients are treated with vocal rehabilitation and surgery after eliminating the underlying conditions. Cessation of cigarette smoking is an important factor in long-term treatment [23, 24]. Histopathologic features include subepithelial edema and expansion of the intercellular space, especially the basal membrane. Few blood vessels can be observed [25]. The overlying epithelium is normal most of the time [13]. Duflo et al. showed that antioxidant gene expression is increased in Reinke's edema compared to the vocal fold polyps [26]. In addition, Branski et al. demonstrated that heme oxygenase is increased in vocal fold fibroblasts [27]. Collagen and elastin fiber configuration alterations are demonstrated in Reinke's edema [28, 29]. Dikker et al.'s stated that increased fibrin, hemorrhage, and thickening of the basement membrane are related with Reinke's edema [30].

#### **2.2 Vocal fold nodule and polyp**

Vocal fold nodules and polyps are polypoid lesions of the vocal folds sharing the same histopathologic features. They are usually differentiated by clinical findings. A polypoid lesion larger than 3 mm is often regarded as a polyp, whereas smaller lesions are classified as a nodule [31]. Vocal fold nodules are usually bilateral lesions involving anterior or middle vocal fold and located superficially to the free edge of the vocal fold [32]. They are slightly more common in women and in young age [10, 33]. Vocal polyps occur more commonly at the anterior portion of the vocal fold, and in more than 90% of the patients, they are unilateral [31]. There is no age and gender predilection for vocal polyps. Vocal abuse is the leading etiologic factor for vocal fold nodules and polyps; singers, lecturers, and coaches are more prone to developing these lesions due to excessive and loud voice use [6, 10]. Infection, hypothyroidism, GERD, cigarette smoking, and allergy are the other frequent causes [7–9, 34]. Patients present with hoarseness and change in voice quality.

Grossly, vocal cord polyps and nodules present as sessile or polypoid lesions with nodules presenting as few millimeters and polyps up to few centimeters in size [5]. They can be white or bright red, and their consistency varies from firm to soft with a mucoid or glistening cut surface [32].

*Pathology of Nonneoplastic Lesions of the Vocal Folds DOI: http://dx.doi.org/10.5772/intechopen.88735*

Although previous studies have attempted to identify histopathologic features which may aid in the differential diagnosis, it is now widely accepted that vocal fold nodules/polyps cannot be differentiated on the histopathologic basis [11, 31, 32, 35]. Epithelial hyperplasia, basement membrane thickening, edema, and vascular proliferation can be seen both in nodules/polyps and Reinke's edema [25, 31, 36]. Ancillary studies such as Verhoeff-van Gieson, Masson trichrome, and Alcian blue did not reveal any difference among these entities [31].

Histopathology represents primarily the extent of the vascular damage and the temporal stage of the lesion [37]. Vocal abuse causes vascular injury and increased vascular permeability. If the damage is minimal, then increased permeability causes only edema, and the microscopic evaluation reveals hypocellular myxoid stroma which is defined as edematous myxoid-type vocal fold nodule/polyp according to some authors (**Figure 1**). When this lesion is not removed or resolved, it undergoes fibrosis, and fibrous-type polyp/nodule evolves. Oval and spindle cells are observed embedded in a fibrous stroma (**Figure 2**). Rarely atypical cells can be detected in this type which is not related with an aggressive behavior [36, 38, 39]. However, if the vascular injury is severe enough for fibrin escape to the subepithelium and interstitium at the beginning of the injury, then hyaline-type polyp/nodule occurs which is characterized by a hypocellular/acellular eosinophilic stroma. By the time capillary proliferation occurs, it progresses to a vascular-type nodule/polyp. This subtype shows ectatic vascular channels in a hypocellular stroma (**Figure 3**). Although, these classification and staging are helpful in understanding the

**Figure 1.** *Polyp with hypocellular myxoid stroma (H&E, ×100).*

**Figure 3.** *Polyp stroma shows ectatic vasculature with a hypocellular stroma (H&E, ×200).*

histopathologic spectrum, it is clinically insignificant. In addition, mixed features are seen in a single lesion most of the time. The overlying squamous epithelium may be normal, atrophic, or hypertrophic, and keratosis can be seen.

Differential diagnosis includes amyloidosis, myxoma, and contact ulcer. Differentiation of hyaline-type vocal fold nodule/polyp from amyloidosis can be made by observing the distribution of eosinophilic material carefully. In hyaline-type nodule/polyp, it is more homogenous, whereas in amyloidosis there is perivascular and periglandular accentuation of the deposit. Histochemical stains like Congo red and crystal violet can be helpful in identifying the nature of the amorphous material. Myxoma has been rarely reported in the larynx, and it has characteristic stellate spindle cells embedded in an avascular, basophilic, gelatinouslike matrix [40, 41]. Contact ulcer has an ulcerated and fibrin-coated surface and usually involves the posterior portion of the vocal folds.

Surgery has a limited value for these lesions as they are reactive changes to an underlying injurious condition which must be managed. Not surprisingly, voice therapy may result in resolution in most of the patients [42, 43]. Also, treatment of the exact underlying condition such as hypothyroidism can be helpful in the treatment of vocal fold polyps/nodules.

#### **3. Contact ulcer**

Contact ulcer is an ulcerated granulation tissue due to vocal abuse, endotracheal intubation, and GERD. Men are more commonly affected than women except that postintubation-related ulcers are more common in female patients. Clinically patients present with hoarseness, cough, dysphonia, habitual coughing, and throat cleaning [44].

Contact ulcers are generally bilateral ("kissing ulcer") and involve the posterior part of the vocal fold. Grossly they present as an ulcerated, tan-white to erythematous polypoid lesion up to 3 cm in diameter. Microscopic evaluation reveals ulceration underlying a fibrin and/or fibrinoid necrosis and capillary proliferation that is oriented perpendicularly to the mucosal surface (**Figure 4**). Central and base part of the lesion contains hemosiderin-laden macrophages. Usually a dense inflammatory infiltration accompanies. Re-epithelization, mucosal hyperplasia, and fibroblastic proliferation can be observed in chronic phase of the lesion [45].

Clinicopathologic correlation is important in the correct diagnosis as histopathologic features are somewhat nonspecific. Differential diagnosis includes vasculartype vocal cord polyp/nodule, Kaposi sarcoma, Wegener granulomatosis, and

*Pathology of Nonneoplastic Lesions of the Vocal Folds DOI: http://dx.doi.org/10.5772/intechopen.88735*

#### **Figure 4.**

*Ulceration, necrosis, and granulation tissue formation. Capillaries oriented perpendicular to surface (H&E, ×200).*

infectious agents. Wegener granulomatosis can be differentiated from contact ulcer with features of vasculitis and necrotizing granulomas. Also, laboratory findings, such as cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA) positivity, support a diagnosis of Wegener granulomatosis over contact ulcer. Kaposi sarcoma may rarely involve the larynx, and histopathologic evaluation reveals spindle cells with intracellular spheroid hyaline globules forming slit-like spaces and anastomosing vascular channels. Immunohistochemical staining with human herpes virus 8 (HHV8) reliably confirms the diagnosis as Kaposi sarcoma.

Like vocal polyps/nodules, contact ulcer is treated with voice therapy, anti-GERD medication, and behavioral modifications in order to decrease habitual coughing and throat clearing [44].

#### **4. Amyloidosis**

Amyloidosis is the deposition of an extracellular, acellular, fibrillar, and amorphous material in various sites of the body. It can be primary (associated with plasma cell neoplasms) or secondary (associated with chronic systemic diseases such as familial Mediterranean fever, rheumatoid arthritis, etc.). Primary amyloidosis can be classified as systemic or localized. The larynx is the most common site for localized amyloidosis [46, 47]. It may also be associated with "mucosa-associated lymphoid tissue" (MALT) lymphoma or a neuroendocrine tumor. Laryngeal amyloidosis generally affects adults at the sixth decade. Patients present with hoarseness and voice changes because of mass effect [45]. Grossly it presents as a firm polypoid lesion up to 4 cm covered by normal-appearing mucosa. Cut surface may be firm and starch-like and gray or yellow-orange in color. Localized laryngeal amyloidosis can involve the larynx diffusely or present as a nodule. Microscopic examination reveals diffuse subepithelial or discrete nodular lesion consisting of amorphous, fibrillary, and hyaline-like eosinophilic substance deposition. Usually the distribution of the deposition is more pronounced in perivascular and periglandular areas. Lymphoplasmacytic infiltration and foreign body giant cells can be seen but usually sparse.

Differential diagnosis includes hyalinized-type vocal fold polyps/nodules and lipoid proteinosis which are negative with Congo red and crystal violet. Most importantly as amyloid can be associated with multiple myeloma, laryngeal neuroendocrine tumors, and medullary thyroid carcinoma, a systemic evaluation of the patient is necessary.

#### *Voice and Swallowing Disorders*

If amyloidosis is limited to the larynx, patients are treated with surgical removal of the lesion. However, other treatment options will be applied if the patient has an underlying neoplastic condition or chronic inflammatory disease.

#### **5. Cysts of the larynx**

Nonneoplastic cysts of the larynx consist of laryngocele, saccular, and ductal cysts [48–50].

#### **5.1 Laryngocele**

Laryngeal ventricles are the spaces between the true and false vocal cords which extend upward and form the laryngeal saccule bilaterally. Laryngocele can be defined as a symptomatic dilation of the laryngeal saccule with air entrapment [51]. An important feature of laryngocele is that the lumen of the cyst communicates with the laryngeal cavity. Radiography reveals an air-filled cystic enlargement. They are usually unilateral, may occur over a wide age range, and are more frequent in males. Occupations such as glassblower or wind instrumentalists are at increased risk of developing laryngocele due to repetitive increase in intralaryngeal pressure. Patients present with hoarseness and foreign body or globus sensation.

Clinically it can be divided as internal, external, or combined. Internal laryngocele is confined to the endolarynx and presents as a supraglottic submucosal lesion. In contrast external laryngocele extends through the thyrohyoid membrane. However, in combined laryngocele, the cyst herniates through the thyrohyoid membrane and presents as an anterior neck mass [51–53]. Patients present with hoarseness, dyspnea, and chronic cough. In histopathologic examination, the respiratory epithelium is identified as the lining of the cyst wall.

Differential diagnosis includes other laryngeal cysts. However, laryngocele is the only air-filled cyst of this region and communicates with the laryngeal cavity—an important finding in differentiation.

Symptoms may resolve with the expulsion of trapped air from the cyst lumen. Treatment of laryngocele is simple excision or marsupialization of the cyst wall.

#### **5.2 Saccular cyst**

Saccular cyst is a mucin-filled cyst due to obstruction of the laryngeal saccule. It can be acquired or congenital [49, 50]. If it extends medially, it may obscure the anterior vocal fold. Lateral saccular cysts are similar to the external laryngoceles, herniated through the thyrohyoid membrane, and may present as a neck mass [37].

Saccular cysts are usually lined by respiratory-type epithelium. Squamous or oncocytic lining can be observed in some cases. Cyst lumen is filled with mucin or acute inflammatory exudate.

Differential diagnosis includes laryngocele and thyroglossal ductus cyst. It is differentiated from laryngocele by mucin content, and it does not communicate with the laryngeal cavity. It is difficult to discriminate a thyroglossal cyst from a saccular cyst when it invades through the pre-epiglottic space and histopathologically lacks the thyroid tissue. When this is the situation, investigation of the anatomic localization of the cyst is a reliable finding in the differentiation of these cysts. Thyroglossal ductus cysts are related with the hyoid bone and located in the midline of the neck.

*Pathology of Nonneoplastic Lesions of the Vocal Folds DOI: http://dx.doi.org/10.5772/intechopen.88735*

#### **5.3 Ductal cysts (squamous, tonsillar, oncocytic)**

Ductal cysts are the most common type of laryngeal cysts. Cyst lining epithelium can be squamous or oncocytic [49, 54] (**Figures 5** and **6**). When a squamous lined cyst is surrounded by lymphoid tissue, it is called a tonsillar cyst. Tonsilar cysts are more common in the vallecula which contains tonsillar remnants.

#### **5.4 Other cysts**

Rarely epidermal, dermoid, and branchial cleft cysts may occur in the endolarynx.

#### **Figure 5.**

*The right side of the figure represents a squamous cell lined cyst. On the left cyst lining cells appear oncocytic (H&E, ×400).*

**Figure 6.** *Ductal cyst with lining oncocytic cells (H&E, ×400).*

#### **6. Hyperplastic lesions of the larynx**

Hyperplastic lesions of the larynx are a result of a reparative process. Clinical terms such as leukoplakia (white plaque), erythroplakia (red plaque), erythroleukoplakia (red and white changes), or pachydermia (extensive thickening of the mucosa) are used to describe the lesion macroscopically, and they are not histologic entities [55].

Keratosis of the larynx is synonymously used with simple hyperplasia and squamous hyperplasia [56]. Singers and other occupations that lead to an individual to use his/her voice excessively and cigarette smokers are at risk of keratosis. Hoarseness is the leading complaint. Laryngoscopy identifies leukoplakia. Microscopic evaluation reveals a thickened squamous epithelium without cellular or architectural atypia [55]. Generally, a hyperkeratotic layer overlies the epithelium. Lesions with warty configuration are referred as verrucous keratosis [56, 57].

Pseudoepitheliomatous hyperplasia (PEH) is a reactive proliferation of the squamous epithelium which develops in response to infections, trauma, or neoplasia. Histologically these lesions are downward thickening of the epithelium (**Figure 7**). Due to a less well-defined epithelial stromal interface and the tendency of anastomosing epithelial tongues entrapping the submucosa, the lesion may mimic squamous cell carcinoma [58]. However, in PEH, the hyperplastic epithelium forms large bulbous projections, and basement membrane is always preserved.

**Figure 7.** *Downward proliferation of benign appearing surface epithelium (H&E, ×200).*

**Figure 8.** *Parakeratosis and verrucous hyperplasia of the surface epithelium (H&E, ×100).*

*Pathology of Nonneoplastic Lesions of the Vocal Folds DOI: http://dx.doi.org/10.5772/intechopen.88735*

Verrucous hyperplasia is a verrucous and keratotic form of squamous hyperplasia which may show varying degrees of cytological atypia (**Figure 8**). The presence of cellular atypia and a relatively regular epithelial-stromal border supports a diagnosis of verrucous hyperplasia over verrucous squamous cell cancer (SCC) [59].

#### **7. Conclusions**

Voice change or hoarseness of voice and nonneoplastic vocal fold lesions lead to a high percentage of vocal fold biopsies. Both clinical and histopathologic features should be considered in order to differentiate lesions involving Reinke's space and also hyperplastic epithelial lesions from squamous cell carcinoma.

#### **Author details**

Nil Çomunoğlu1 \*, Şebnem Batur1 and Ayşe Mine Önenerk<sup>2</sup>

1 Pathology Department, Istanbul University Cerrahpasa, Cerrahpasa Medical Faculty, Istanbul, Turkey

2 Pathology Department, Karaman State Hospital, Karaman, Turkey

\*Address all correspondence to: nilcomunoglu@gmail.com

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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[58] Gnepp DR. Diagnostic Surgical Pathology of the Head and Neck. 2nd ed. Philadelphia: Saunders Elsevier; 2009

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Section 3

## Dysphagia in Stroke Patients

#### **Chapter 3**

## Swallowing Disorders in Patients with Stroke

*Aiko Osawa and Shinichiro Maeshima*

#### **Abstract**

Swallowing disturbance often causes by stroke and may predispose patients to malnutrition and dehydration, as well as increases the risk of such complications as suffocation and aspiration pneumonia. As an initial evaluation, the water swallowing test can be easily carried out, but not all of the aspiration can be excluded. Therefore, videofluorography (VF) and videoendoscopic examination (VE) of swallowing should be performed to find a safety method of oral intake for providing visualization of the pharynx and larynx dysfunction. Clinical severity scale is important because once the severity is determined, the treatment strategy is also known. Swallowing training can be divided into indirect training without food (basic training) and direct training with food (eating training). In general, it is important to select conditions and training diets that are easy to swallow and have a low risk of aspiration while using indirect training and direct training that aim at gradually improving the level of oral intake.

**Keywords:** stroke, dysphagia, swallowing assessment, pneumonia, videofluorography

#### **1. Introduction**

Stroke is a group of diseases associated with sudden disturbance of consciousness and motor or cognitive dysfunctions induced by cerebrovascular disorder. Pathological conditions are roughly classified into three categories according to the causes: stroke occurred due to cerebrovascular occlusion, stroke induced by rupture of small cerebral vessels, and subarachnoid hemorrhage associated with rupture of brain aneurysm, etc. According to the reports of the National Stroke Association, incidence of stroke is one person every 40 s; about 800,000 and 290,000 persons develop stroke every year in the USA [1] and Japan [2], respectively.

Medical management for stroke has changed remarkably in many ways such as rearrangement of emergency medical system, improvement of treatment methods including thrombolytic therapy and endovascular treatment of the brain, formation of medical teams in a stroke unit, and preparation of guidelines for stroke treatment, resulting in improvement of survival rate [3, 4]. More than a half of the survived patients however suffer from disabilities to a certain extent such as motor paralysis, sensory or visual impairment, cognitive disturbances including aphasia and unilateral neglect, and dysphagia, which all affect the patients' activities of daily living.

#### **2. Incidence and features of dysphagia due to stroke**

It has been reported that dysphagia is observed in 39–81% of stroke patients during the acute phase [5, 6], and the results obtained from videofluoroscopic examination of swallowing (VF) or videoendoscopic examination of swallowing (VE) may reveal that even more patients are complicated by dysphagia [7]. However, it improves promptly, most of the time, in a few days or few weeks after the onset, and sever disorders may persist until the chronic stage in about 10% of the patients [7–9]. These show how important it is, for management of stroke, to prevent aspiration pneumonia and let patients regain ability to swallow safely during the acute phase.

Pathology of dysphagia varies according to the sites of the central nervous system being affected [7, 10]. The cause of dysphagia after stroke is roughly categorized into two mechanisms: pseudobulbar palsy associated with disturbance of upper motor neurons toward nuclei in the medulla oblongata and bulbar palsy associated with lower motor neurons from nuclei in the medulla oblongata in the brain stem. In patients with pseudobulbar palsy induced by cerebrovascular events in cerebral lesions, symptoms and signs such as delayed swallowing reflex during the pharyngeal phase of swallowing, reduced laryngeal elevation, and residual food in the vallecula or pyriform sinus are observed. While in patients with bulbar palsy induced by brain stem lesions, loss of swallowing reflex and insufficient opening of the esophageal orifice are observed. In either case, patients are often complicated by disturbance of consciousness or cognitive disorder, and swallowing is also affected during the anticipatory, preparatory, and oral phases as described below.

#### **3. Swallowing process model**

There are two major systematic models known for normal swallowing dynamics (**Figure 1**). The first one is liquid swallowing model which consists of five phases including the anticipatory phase in addition to four other stages: preparatory, oral,

#### **Figure 1.**

*Five stage and process models for swallowing. Two paradigmatic models are commonly used to describe the physiology of normal eating and swallowing: the five-stage model for drinking and swallowing liquid and the process model for eating and swallowing solid food.*

#### *Swallowing Disorders in Patients with Stroke DOI: http://dx.doi.org/10.5772/intechopen.88341*

pharyngeal, and esophageal phases [11]. During the anticipatory phase (recognition phase), characteristics of food are recognized, the posture and the way to eat are determined, and saliva secretion is induced. During the preparatory phase, mastication occurs to make the food easy to swallow (into a food bolus). During the oral phase, the food bolus is transferred to the pharynx by the tongue movement. The pharyngeal phase begins when the food bolus formed in the vallecula starts moving downward through the pharyngeal cavity until it reaches the esophageal orifice. This is an involuntary action which occurs unconsciously. Contraction of the suprahyoid muscle and thyrohyoid muscle induces elevation of the hyoid bone and larynx. The epiglottis descends and blocks the laryngeal aperture to prevent aspiration of the food. Along with contraction of the pharyngeal muscles, the food bolus is sent to the esophageal orifice. Once the food bolus enters the esophagus during the esophageal phase, the cricopharyngeus muscle (upper esophageal sphincter) contracts to close the esophageal orifice so that food reflux will not occur.

The second one is a process model which involves mastication [12, 13]. Solid food is transported to a molar region by the tongue (Stage I transport). The food is grounded by mastication and transported actively to the oropharynx with the tongue movement (Stage II transport). Then, a food bolus is formed. Food transport occurs repeatedly even during mastication. The bolus is formed inside the oral cavity if it is command swallow of liquid food. However, if it is chew-swallow of solid food, the bolus is formed in the area between the oropharynx and the vallecula. If the bolus contains liquid, some of it reaches the pyriform sinus before swallowing reflex begins. Thus, it is important to understand that there are two different types of swallowing dynamics before making assessments.

### **4. Assessment of dysphagia**

In assessment of dysphagia, the cause and onset mechanism of the condition should be revealed to understand pathology. The physical findings include observation of the level of consciousness and respiratory conditions. Neurological findings (especially on trigeminal, facial, glossopharyngeal, vagus and hypoglossal nerves), the level of cognitive functions, nutritional state, dehydration status, as well as the current status and past history of pneumonia, should be assessed. In addition, food residues inside the oral cavity, furred tongue, dental caries, characteristics of saliva, denture, and gingivitis should also be examined.

There is a risk of food aspiration whenever food or fluid is put inside the mouth. Therefore, assessment of swallowing functions should be performed if possible before ingesting food. Even if meals have already been started, ask patients and families detailed questions whether or not the patients have symptoms associated with aspiration.

#### **4.1 Interviews and observational assessments**

Characteristics of dysphagia are likely to be observed in the activities of daily living. Dysphagia can be suspected by asking simple questions to patients and their families. The question items may be associated with increase of cough and sputum after meals, sputum containing food, change in voice quality after meals, pharyngeal discomfort, decreased appetite, tired feeling during meals, prolongation of meal time (over 45 min), change in the type of meals, and the way to eat, loss of weight, and fever.

#### *4.1.1 Eating assessment tool (EAT-10)*

This is a standardized questionnaire form which is easy to use [14]. The assessment using a questionnaire form consists of 10 questions regarding pleasure of eating meals, loss of weight, effort of swallowing, etc. which are evaluated by scores between 0 (no problem) and 4 (serious problem). The maximum score is 40.

#### *4.1.2 Mann assessment of swallowing ability (MASA)*

This is a highly reliable and valid assessment performed in stroke patients during the acute phase based on psychostatistic evaluations on consciousness, cooperative actions, auditory comprehension, etc. [15]. It consists of 24 items including alertness, cooperation, auditory comprehension, respiration, dyspraxia, saliva, and tongue movement, and the maximum score is 200. Allocation of scores varies according to the level of importance for each item. The risk for dysphagia or aspiration and the degree of dysphagia are evaluated by the total score to determine the food form to be recommended. No special device is required, and the assessment can be performed within 15–20 min.

#### **4.2 Bedside swallowing assessment**

The swallowing assessments are performed at the bedside after confirming that the level of alertness is satisfactory (<10) and that the patient's general condition is stable without any progression of stroke.

#### *4.2.1 Dry swallowing*

It is a basic movement to swallow saliva, demonstrating whether or not the patient is able to swallow before conducting a screening test [16].

#### *4.2.2 Repetitive saliva swallowing test (RSST)*

In this test, an examiner asks a patient to swallow saliva while palpating the hyoid bone and thyroid cartilage with the index finger and the middle finger, respectively, and counts how many times the patient swallows within 30 s [17, 18]. It is considered positive when <3.

#### *4.2.3 Water swallowing test (WST)*

The examiner asks a patient to swallow 30 ml of water at the room temperature as usual and observes how many times he/she swallows and if he/she ever gets choked [19]. It is considered positive if the patient could swallow at once without getting choked within 5 s.

#### *4.2.4 Modified water swallowing test (MWST)*

The examiner asks a patient to swallow 3 ml of cold water and observes if he/ she ever gets choked and if the voice or respiratory state changes. The maximum score is 5 for this test [18, 20]. If possible, the examiner asks the patient to swallow twice more. The test can be performed up to three times, and the worst swallowing activity is evaluated. It is considered abnormal when the score is <3 (swallowing present, respiration satisfactory, choking present, and/or wet hoarseness).

*Swallowing Disorders in Patients with Stroke DOI: http://dx.doi.org/10.5772/intechopen.88341*

#### *4.2.5 Food test (FT)*

In this test, the examiner asks a patient to ingest a tea spoon of flan (about 4 g) [18, 21]. The content of the assessment is the same as in MWST except that there is another assessment of residual food inside the oral cavity after swallowing in this test.

#### *4.2.6 Simple swallowing provocation test (SSPT)*

The examiner inserts a transnasal catheter 5 Fr into the epipharynx in the supine position and injects distilled water at room temperature to induce swallowing [22]. At first, the examiner injects 0.4 ml of distilled water and observes for 3 s. If the patient does not swallow, 2 ml is additionally injected. If no swallowing was observed within 3 s, it is considered that the patient has a risk of aspiration pneumonia.

#### **4.3 Comprehensive clinical two-step swallowing assessment scales**

There are existing clinical assessment scales which combined clinical symptoms and WST as below. Comprehensive clinical evaluations rather than simple WSTs demonstrate higher sensitivity and specificity.

#### *4.3.1 Two-step thickened water test (TTWT)*

With this method proposed by Smithard et al. [23], WSTs of 5 ml (for three times) and 30 ml are performed after obtaining clinical findings such as the alert level, trunk control, soft palate movement, and voluntary coughing.

#### *4.3.2 Toronto Bedside Swallowing Screening Test (TOR-BSST)*

This is a comprehensive WST focusing on evaluation of dysphagia of the oropharynx in addition to assessment of three items: voice quality, tongue movement, and pharyngeal sensation [24].

#### *4.3.3 Gugging swallowing screen (GUSS)*

Prior to the assessment, posture control is evaluated. An examiner assesses clinical findings including the state of consciousness, coughs (wet hoarseness), and dry swallowing (saliva swallowing) (5 points), followed by assessments of the swallowing state, presence or absence of choking or drooling, and change of voice after ingesting three food forms: semisolid, liquid, and solid (15 points) [25]. The food form is determined according to the score (20, normal food; 15–19, soft food; 10–14, dysphagia food; 0–9, indirect training).

All these tests can be easily performed to assess swallowing functions. However, not all aspirations can be detected. Simultaneous assessments using VF and WST or FT under the X-ray [26, 27] revealed that the higher the amount of fluid, the more aspirations are observed with VF, while the detection rates for choking, coughing, and wet hoarseness were not that high (**Figure 2**). In patients with decreased cognitive or physical functions and patients with brain stem lesions, silent aspiration cannot be denied even if there is no clinical finding of choking, coughing, or wet hoarseness [28]. VF and VE should be performed as much as possible in case where dysphagia is strongly suspected in physical examinations or BSA or when there is no effective strategy established for the treatment.

#### **Figure 2.**

*Clinical and VF findings of the food test. Simultaneous assessments using VF and WST or FT under the X-ray revealed that the higher the amount of fluid, the more aspirations are observed with VF, while the detection rates for choking, coughing, and wet hoarseness were not that high.*

#### **4.4 Videoendoscopy (VE) and videofluorography (VF)**

#### *4.4.1 Videoendoscopy (VE)*

Using a laryngeal fiberscope, the pharynx and larynx are primarily observed using real food (**Figure 3**). Although the moment of swallowing cannot be observed, early pharyngeal penetration of saliva or food bolus, timing of inducing swallowing reflex, pharyngeal residue, and laryngeal penetration/aspiration can be directly observed. This is a useful method which enables observation of the pharynx and larynx using actual food without irradiation. This can be used at the bedside as it does not require any large-scale devices [29].

**Figure 3.** *Videoendoscopy (VE). Videoendoscopy can be performed on patients at bedside.*

#### *Swallowing Disorders in Patients with Stroke DOI: http://dx.doi.org/10.5772/intechopen.88341*

VE can be performed without irradiation and is highly portable. In addition, it enables direct observation of mucosal and saliva conditions as well as assessment of actual meal settings. However, there is a risk of inducing pain or nasal bleeding when inserting the fiber, and it is difficult to observe oral cavity during mastication, bolus formation, and food transportation to the proximal part of the tongue; it becomes blurry at the moment of swallowing; hence, it is difficult to understand the details of laryngeal penetration/aspiration.

#### *4.4.2 Videofluorography (VF)*

Swallowing functions are assessed using an X-ray device. With this method, a patient is asked to ingest fluid (water) or solid/semisolid food (imitation food) which contain contrast medium (barium sulfate), and movement of the oral cavity, pharynx, and esophagus as well as structural abnormalities and movement of the food bolus are assessed [30]. The diagnostic value of this test is high as it can reveal formation of the food bolus and its transportation to the pharynx in the oral phase, the timing and the level of laryngeal elevation in the pharynx phase, and bolus passing at the esophageal orifice and the presence/absence or the level of aspiration (**Figure 4**). It also clarifies conditions where the risk of aspiration and pharyngeal residue is low and determines the safest food form, the method of ingestion, and the posture. Moreover, it also enables us to try various compensation methods and make detailed observations on dysphagia. Hence, this test should be considered as a gold-standard swallowing function assessment which can provide very important information to establish treatment strategy according to the findings of the observation [30].

#### *4.4.3 Swallowing CT scan*

With excellent spatial resolution (0.5 mm square) and time resolution (10 frames per second), 320 Area Detector CT (320-ADCT) enables us to precisely and quantitatively observe the swallowing movement in 3D. It presents 3D images of various organs from arbitrary directions; hence, it can precisely quantify swallowing dynamics [31, 32].

#### **4.5 Assessment of severity in swallowing**

Taking into consideration the functional diagnosis, causative disease, and general condition of the patient, the level of feeding is determined as the final overall evaluation of swallowing. Swallowing Performance Scale [33] and Functional Oral Intake Scale (FOIS) [34] are seven-level scales used in overseas countries to assess oral feeding status during the meals. While in Japan, Dysphagia Severity Scale (DSS) [35] is often used. This is a comprehensive assessment using the ordinal scale of seven levels, which can suggest a management method to a certain extent if the severity level is determined. VF and VE are not necessarily required in an evaluation using DSS. An evaluation made on clinical findings or a screening test by a highly experienced nurse can be equivalent to the evaluation made on DSS using VE [36]. Dysphagia Outcome and Severity Scale (DOSS) is a simple and easy-to-use point scale developed only to systematically evaluate the functional level of severity. With this scale, recommendations on feeding levels can be prepared based on objective evaluations [37].

#### **5. Treatment of dysphagia**

There are two types of dysphagia rehabilitation: indirect training which does not require feeding and direct training which requires feeding. For a patient with severe dysphagia, rehabilitation should be started with the indirect training, and then the direct training can be added according to the progress. Likewise, for a patient who can start rehabilitation with the direct training, the indirect training may be added if necessary [38, 39].

#### **5.1 Indirect training**

Indirect trainings which are typically used include pharyngeal cooling stimulation (ice massage), Mendelsohn maneuver with which the upper esophageal sphincter is mechanically opened by keeping the positions of the larynx and the hyoid bone elevated, blowing, supraglottic swallow (swallow while holding breath), Shaker exercise (head lift exercise), cervical anterior flexion exercise, balloon dilatation method, and pharyngeal electrical stimulation. At the same time, it is essential to conduct oral care. If a patient does not ingest food, the amount of saliva secretion decreases, and as a consequence, self-cleansing action of oral cavity with saliva decreases as well. In such cases, patients often have dry mouth covered by biofilm as seen with the furred tongue, which need to be removed by brushing. These trainings are conducted primarily by speech-language-hearing therapists and nurses. However, the concomitant use of pulmonary respiration therapy conducted by physiotherapists or trainings to improve the ability of performing daily activities conducted by occupational therapists is also very effective to prevent/relieve aspiration pneumonia and improve feeding ability. Hence, it is important to treat patients with the entire team in the rehabilitation approach for dysphagia.

#### **5.2 Direct training**

In the direct training, feeding is started as soon as safety conditions for feeding were established based on detailed evaluations. The patient is observed for 3–7 days to check if there is any sign of aspiration or pneumonia, and the meal condition is upgraded accordingly. In stroke patients, swallowing functions are likely to change

#### *Swallowing Disorders in Patients with Stroke DOI: http://dx.doi.org/10.5772/intechopen.88341*

according to the alert level, and facial palsy is frequently observed. As their masticatory functions have been generally decreased due to facial and lingual palsy, the patients are unable to produce a smooth and appropriately sized food bolus with adequate mastication. The poor pharyngeal clearance is likely to induce formation of food residues inside the pharynx. As the residual food may cause aspiration or suffocation, it is dangerous to offer meals which require mastication to patients with stroke in the acute phase. Therefore, it is considered safer to start feeding with a single food type such as food paste in patients suspected to have dysphagia, even if it is mild.

Once the feeding started, special attention should be paid on increase of saliva/ drooling and sputum, increase of coughs, tiredness after eating meals, fever, voice change (wet hoarseness) during meals, and residual food inside the oral cavity. Aspiration can occur without choking. Therefore, if there is any sign as listed above, auscultation of the chest and vital sign assessment should be performed along with chest X-ray and blood collection, if necessary. In addition, chest CT scan should also be considered if the patient is suspected to have pneumonia in the posterior side of the lung as it is often difficult to obtain remarkable findings on chest X-ray in such cases. If aspiration pneumonia is detected in these tests, direct training should be suspended for a moment, and pneumonia should be treated immediately. Once the treatment is completed, swallowing function assessments should be performed at the bedside along with VE and VE, if necessary, to reevaluate the conditions. Special attention is required especially in elderly patients with bilateral lesions who have neurological manifestations as they are likely to develop aspiration pneumonia [40, 41].

#### **6. Conclusions**

In assessment and treatment of dysphagia, "not choking" and "safe feeding" are not necessarily the same in meaning. It is necessary to conduct the swallowing function assessments and understand the patients' conditions along with the level of consciousness and physical state. Safe feeding can be achieved in stroke patients only by selecting appropriate food materials according to their pathological conditions at the optimal timing with appropriate feeding posture and efforts.

#### **Conflict of interest**

The authors declare that they have no competing interests.

*Voice and Swallowing Disorders*

### **Author details**

Aiko Osawa1 and Shinichiro Maeshima<sup>2</sup> \*

1 National Center for Geriatrics and Gerontology, Obu, Japan

2 Kinjo University, Hakusan, Japan

\*Address all correspondence to: shinichiromaeshima@gmail.com

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

*Swallowing Disorders in Patients with Stroke DOI: http://dx.doi.org/10.5772/intechopen.88341*

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Section 4
