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Dysphagia: dysphagia is a distressing symptom, which can have far-reaching effects on a patient's life.

Dysphagia is the general term for disordered swallowing. The inability to swallow safely will have an impact on the ability to maintain both hydration and nutrition at an adequate level. Additionally, not being able to meet and socialise over a meal or a drink, or enjoy a family meal together has vast ramifications on one's enjoyment of life and social interaction.

This article provides a simple overview of the swallowing process and common clinical problems and a review of some of the current evaluations, treatments and rehabilitation options available to patients with dysphagia.

It is estimated that between 6 and 15 million adults and an unknown number of children in the USA alone are affected by dysphagia. (1) Despite its common prevalence, few patients receive a formal diagnosis (2) and as such, many of these patients develop serious complications.

Stages of swallow

Swallowing can be divided into 3 functional phases:

* oral phase

* pharyngeal phase

* oesophageal phase.

While this is a very practical classification, it should be emphasised that all phases are functionally connected and that dysfunction in one phase will have a significant impact on function in all the others.

The process of swallowing needs to be considered as part of a pressure-generating system. The bolus will always move from one highpressure chamber to the next low-pressure chamber, with muscles compressing and expanding the various compartments and their associated valves. Any anatomical or neuromuscular dysfunction in one area will result in a loss of the pressure gradient and as a result, transit of the bolus may be slowed or inco-ordinated. The path a bolus takes (Fig. 1)

The bolus is introduced to the oral cavity; thereafter there is interaction between orbicularis oris, buccinator and the muscles of mastication to adequately prepare the bolus for the pharyngeal stage.

[FIGURE 1 OMITTED]

This stage of swallowing, the oral phase, is entirely under voluntary control via the cortical and subcortical areas of the brain.

Once sensory information reports the bolus to be adequately prepared, the bolus will be moved posteriorly. As the bolus passes the posterior faucal (tonsil) arches the swallow becomes reflexive under the control of the brainstem. It should be noted that in the over-60s, the swallow may only become reflexive as the bolus reaches the vallecula (between the back of the tongue and epiglottis). Simultaneously, velopharyngeal closure occurs, i.e. the soft palate lifts and closes the posterior nasal space to prevent movement of the bolus into the nasal cavity. The lips should remain tightly closed, the teeth closely approximated and the tongue in contact with the palate for pressure in the oral chamber to be maintained. Failure of these processes will result in pocketing of food and residuals being left in the oral cavity. Oral-pharyngeal seal is completed by the full retraction of the tongue base onto the posterior pharyngeal wall.

A number of processes assist in the transit of the bolus into the pharynx. Firstly, elevation and forward movement of the hyoid creates a negative sucking pressure in the hypopharynx. Secondly, closure of the airway and an apnoeic interval during the pharyngeal phase prevents the bolus being sucked towards the negative pressure within the airway and finally, the sequential stripping action of the superior, middle and inferior pharyngeal constrictors moves the bolus into the upper oesophagus. Dysfunction in the pharyngeal phase can lead to multiple problems in the safe transit of the bolus, the most crucial being the increased likelihood of penetration or aspiration.

Elevation and protraction of the hyoid has also been shown to play a crucial role in the opening of the upper oesophageal sphincter (UES) through the anatomical stretch that occurs with the up-and-forward movement of the larynx. Failure of UES to open adequately is a major cause of aspiration and penetration and contributes significantly to a dysfunctional swallow.

Once the bolus has entered the oesophagus, the UES must be closed and remain closed to counteract the increased pressures that come about through the stripping action of the oesophageal musculature. The lower oesophageal sphincter needs to be open for the bolus to leave the oesophagus and enter the stomach.

Neural control of swallow

In the past, the swallow was thought to be a pure reflex but has now been shown to be a pattern-elicited response. (3) The oral phase is controlled primarily by cortical and subcortical areas. The reflexive pharyngeal and oesophageal stages are under brainstem control and require bilateral innervation due to the need for the two sides to work in unison in order to provide the pressure gradient required.

Fig. 2 shows a brief overview of the cranial nerves and their involvement in the swallow process.

Who is at risk for dysphagia?

Many patients with dysphagia are overlooked, so be sure to consider this diagnosis in someone with recurrent episodes of pneumonia, dehydration and weight loss. There are numerous causes of dysphagia; some of the more common ones have been summarised in Table I.

Signs and symptoms

* Coughing during or after swallowing

* Choking on food or liquid

* Voice change ('gurgly' vocal quality) during meals

* Sensation of food getting stuck in the throat

* Sensation of having a lump in the throat

* Painful swallowing

* Recurrent chest infections of unknown origin

* Weight loss and fatigue.

[FIGURE 2 OMITTED]

How to evaluate and investigate a patient with dysphagia

Bedside clinical evaluation

The main purpose of a clinical swallowing evaluation is to identify patients who are at risk for dysphagia and who may require either further investigations or a referral for specialist management or rehabilitation. The swallowing evaluation should include a careful history, clinical examination and possibly additional imaging studies.

Daniels et al. identified six clinical features associated with an increased risk of aspiration in stroke patients. The presence of any two of these six features correctly identified the risk of aspiration with 92% accuracy. (4) The indicators listed in Table II should form the basis of a simple bedside examination.

Although aspiration and penetration remain the most life-threatening signs, they are not the only signs that should qualify the patient for further investigations and referral for treatment.

Diagnostic swallowing evaluations

The primary purpose of any imaging examination should be to directly evaluate the kinesiology of the swallowing mechanism, determine swallowing safety and identify the effects of possible compensatory strategies. Contrary to common practice, the primary function of any imaging evaluation should not be to solely determine whether aspiration or penetration is taking place. The investigations should determine the cause and area of dysfunction, so that the most appropriate treatment can be employed.

The main two imaging tools used to evaluate dysphagia are:

* modified barium swallow (MBS) using videofluoroscopy

* video-endoscopy

* flexible endoscopic evaluation of swallowing (FEES)

* flexible endoscopic evaluation of swallowing with sensory testing (FEEST).

There are advantages and disadvantages to each modality and it is difficult to determine the superiority of either technique in the evaluation of dysphagia (Table III). A thorough working knowledge of the processes and timing of normal swallow mechanisms is necessary for the interpretation of either examination.

When performing a MBS study, it is best conducted with a suitably experienced speech therapist, radiographer and radiologist. The patient is tested against a recommended protocol involving the use of varying quantities and viscosities of liquid and solid boluses. If swallowing dysfunction is evident during the instrument evaluation, therapeutic intervention must be attempted during the diagnostic study in order to assess the efficacy of the intervention relative to the particular swallowing impairment.

Management of dysphagia

The dysphagia patient is best managed in a multidisciplinary team environment, including speech therapists and physiotherapists. The employment of a treatment strategy must be specific to the actual biomechanical disorder and not merely applied in a random fashion.

Acute management of dysphagia must consider the following first and foremost:

* hydration

* nutrition

* the impact of limiting the swallow through nasogastric feeds or nil per os orders.

Medical treatment

There are very few good randomised clinical trials that have been conducted into the effectiveness of various medical and surgical interventions. Medical treatments generally involve the management of symptoms as well as treating the underlying cause, e.g. Parkinson's or gastro-oesophageal reflux disease (GORD).

Surgical treatment

Surgical interventions must be directed towards the specific deglutition dysfunctions. They are primarily aimed at addressing anatomical dysfunctions or at dealing with the nutritional requirements of the patient, e.g. percutaneous endoscopic gastrostomy (PEG) insertion. PEG should only be considered when long-term oral feeding is deemed unsafe. Studies looking at the PEG decision-making process concluded that the decision to insert a PEG tube was often made in a time of crisis, with incomplete information and no reasonable alternative to tube feeding being perceived. (5)

PEG-related complications are reported in up to 70% of patients and are a considerable cause of morbidity and mortality. Aspiration pneumonia is reported in about 20-30% of PEG-fed patients and is frequently a terminal event. (6,7)

Other surgical procedures that can be considered include:

* tracheostomy

* vocal fold medialisation

* surgical management of cricopharyngeal dysfunction (CPD) or spasm

* dilatation

* Botox injection

* cricopharyngeal myotomy

* laryngotracheal separation (for severe life-threatening aspiration).

Rehabilitative treatment

The primary goal of the rehabilitation therapist should be to keep the patient swallowing safely for as long as possible or to restore the swallow as quickly as possible.

The majority of muscle fibres involved in the swallowing process are type II fibres, which can lose up to 10% of their muscle bulk in a 24-hour period. If nasogastric (NG) feeding is to be introduced, it should always be accompanied by a referral to a rehabilitation therapist who can start the strengthening or compensatory strategies earlier rather than later so as to limit disuse atrophy and muscle weakness.

At this stage it may also be appropriate to consider the introduction of the Frazier Free Water Protocol. While it is a commonly held belief that the aspiration of clean water is harmful, this is untrue. The Frazier Free Water Protocol allows people with dysphagia free access to water under specific conditions, thereby maintaining active swallowing for longer periods.

The therapeutic management of dysphagia (Table IV) can be subdivided into:

* treatment techniques to improve the strength and co-ordination of the swallow

* compensatory techniques.

In a nutshell

* A thorough working knowledge of the normal swallowing mechanism is the basis for understanding and treating dysphagia.

* All phases of swallowing are functionally connected and problems in one area will impact on other areas.

* Dysphagia is best managed within a multidisciplinary team environment.

* Any decision to substantially alter or stop a patient's oral feeding should be done in consultation with or referral to a speech therapist.

* Diagnostic imaging studies need to assess swallowing dysfunction and the effect of compensatory strategies and not merely the presence of aspiration or penetration.

References

(1.) ECRI. Diagnosis and treatment of swallowing disorders in acute-care stroke patients. Agency for Health Care Policy and Research Publication No 99-E.24. July 1999.

(2.) Ekberg O, Hamdy S, Woisard V, Wuttge-Hannig A, Ortega P. Social and psychological burden of dysphagia: its impact on diagnosis and treatment. Dysphagia 2002; 17: 139-146.

(3.) Jean A. Brainstem control of swallowing: Neuronal network and cellular mechanisms. Physiol Rev 2001; 81: 929-969.

(4.) Daniels SK, McAdam CP, Brailey K, Foundas AL. Clinical assessment of swallowing and prediction of dysphagia severity. Am J Speech Lang Pathol 1997; 6: 17-24.

(5.) Mitchell SL, Berkowitz RE, Lawson FME, Lipsitz LA. A cross-national survey of tube feeding decisions in cognitively impaired older persons. J Am Geriatr Soc 2000; 48: 391-397.

(6.) American Gastroenterological Association Technical Review on tube feeding for enteral nutrition. Gastroenterology 1995; 108: 1282-1301.

(7.) Gomes GF, Pisani JC, Macedo ED, Campos AC. The nasogastric feeding tube as a risk factor for aspiration and aspiration pneumonia. Curr Opin Clin Nutr Metab Care 2003; 6: 327-333.

ALAN McCULLOCH, MB BCh, FCS (SA) ORL ENT Surgeon in private practice, Sandton Medi-Clinic, Johannesburg

Alan McCulloch is a member of the multidisciplinary Dysphagia Treatment Unit at RehabMatters Therapy Centre in Rivonia, Johannesburg. E-mail: alanent@gmail.com
Table I. Common causes of dysphagia

* Neurological diseases--stroke, Parkinson's amyotrophic lateral
sclerosis, multiple sclerosis, traumatic brain injury

* Head and neck tumours and malignancies

* Sequelae of radiotherapy

* Autoimmune diseases--lupus, myasthenia gravis, Sjogren's

* Laryngopharyngeal reflux

* Infectious diseases--Haemophilus, Streptococcus, fungal

* Thyroid diseases

* Vascular abnormalities--aberrant vessels and compressive rings

* Congenital abnormalities--palatal/laryngeal clefts

* Psychogenic--developmental, conditioned dysphagia, primary
conversion reaction, secondary conversion reaction

* Disorders of oral, pharyngeal, oesophageal motility

* Upper oesophageal sphincter dysfunction

* Pharyngeal, oesophageal diverticulae/pouches, rings and webs

Table II. Basic indicators of a simple bedside examination for
dysphagia

Indicator Finding

Abnormal volitional A weak response, verbalised response,
 (voluntary) cough or no response on command to cough
Abnormal gag reflex Either absent or weakened velar (soft
 palate) or pharyngeal wall contraction,
 unilateral or bilateral, in response to
 tactile stimulation of the tongue base,
 faucal (tonsil) arches or posterior pharyngeal
 wall
Dysphonia Voice disorder reflected by impaired
 vocal quality, pitch, or intensity
Dysarthria Speech disorder reflected by impaired
 respiration, articulation, phonation,
 resonance or prosody
Cough after swallow Cough immediately or within 1 min of
 ingestion of calibrated water volumes
 (5, 10, 20 ml presented in duplicate)
Voice change after Alteration in voice quality from baseline
 swallow following ingestion of calibrated
 water volumes

Table III. Comparison of MBS and FEES/FEEST studies

Only MBS can

* Visualise bolus during oral and oesophageal stages

* Assess completeness of tongue base retraction

* Assess completeness of upper oesophageal sphincter opening

* Assess completeness of hyo-laryngeal elevation and protraction

* Assess extent of aspiration

Only FEES/FEEST can

* Visualise secretions

* Directly assess sensation

* Identify mucosal anomalies

* Identify the effect of altered anatomy on bolus flow, glottic
closure and airway protection

* View location of bolus within hypopharynx

Table IV. Therapeutic management of dysphagia

Treatment techniques

* Myofascial techniques

* Exercises

* Swallow manoeuvres

* Sensory stimulation techniques

* Electrical stimulation (NMES)

* Biofeedback

Compensatory techniqes

* Modify sequence of delivery

* Alteration of bolus volume, texture, taste or
temperature

* Modify rate of delivery

* Alter positioning--head turn, chin tuck

* Advice on procedure of swallow, e.g.
multiple swallows

* Alter method of food/liquid delivery

* The use of neuromuscular electrical stimulation (NMES) in the
management of dysphagia is a relatively new therapy and is now
available in South Africa through a number of VitalStim-certified
therapists. VitalStim([R]) therapy is an FDA-approved
method to promote swallowing therapy through the application of
NMES to the swallowing muscles with the goal of strengthening and
re-educating the muscular system and improving motor control of
the swallowing mechanism. This is not a stand-alone therapy and
should form part of a well-planned exercise and biofeedback-based
programme. It is most suited to dysphagias associated with upper
motor neuron lesions.
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Author:McCulloch, Alan
Publication:CME: Your SA Journal of CPD
Geographic Code:1USA
Date:Aug 1, 2009
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