Normal swallow physiology

In order to identify abnormal swallow, one needs to recognise the normal phases of swallowing. Normal swallow physiology can be divided into 3 phases:

• Oral Phase
• Pharyngeal
• Oesophageal

The detailed components of each phase are shown below:

Fig 1: Phases of normal swallowing.

Fig 2: Annotated diagrams of normal oral phase. Reference: Tan Tock Seng Hospital, Singapore

Fig 3: Normal oral phase (annotated). Reference: Tan Tock Seng Hospital, Singapore

Fig 4: Annotated normal pharyngeal phases. Reference: Tan Tock Seng Hospital, Singapore

Fig 5: Normal pharyngeal phase (annotated). Reference: Tan Tock Seng Hospital, Singapore

Fig 6: Annotated normal oesophageal phases. Reference: Tan Tock Seng Hospital, Singapore

Fig 7: Normal oesophageal phase (annotated). Reference: Tan Tock Seng Hospital, Singapore

Common swallowing abnormalities can be classified based on which phase of swallowing they occur in.

Oral phase

• Anterior loss

1. Contrast is seen spilling out anteriorly from the mouth.
2. Suggests weakness of orbicularis oris resulting in inadequate lip closure.
3. Causes inclue: facial nerve palsy, myotonic dystrophy and myasthenia gravis.

Fig 8: Anterior loss: contrast leaks out anteriorly from the mouth. Reference: Tan Tock Seng Hospital, Singapore

• Sublingual loss

1. Contrast is seen spilling below tongue.
2. In preparation for swallowing, food bolus is usually held between the superior surface of the tongue and palate.
3. Tongue weakness and loss of orolingual control results in poor control of the food bolus, resulting in sublingual loss.

Fig 9: Bolus held between tongue and palate in a patient with normal orolingual control (blue arrow). Sublingual loss occurs when contrast spills below the tongue (red arrow). Reference: Tan Tock Seng Hospital, Singapore

• Premature spillage

1. Contrast is seen spilling into the oropharynx before initiation of pharyngeal phase.
2. Tongue and soft palate forms a seal (palatoglossal seal) posteriorly to prevent food bolus from moving into the pharynx before swallowing.
3. Tongue weakness and loss of orolingual control can result in the inability to maintain the palatoglossal seal, resulting in premature spillage.

Fig 10: Containment of food bolus between tongue and palate with a normal palatoglossal seal (blue arrow). Premature spillage (red arrow) of the food bolus into the valleculae, indicating poor palatoglossal seal. Reference: Tan Tock Seng Hospital, Singapore

Fig 11: Demonstration of sublingual loss and premature spillage, both a result of tongue weakness and loss of orolingual control. Reference: Tan Tock Seng Hospital, Singapore

Pharyngeal phase

• Delayed onset

1. Hyoid bone remains in resting position although contrast bolus has reached pharyngeal lumen.
2. Increases the risk of penetration/aspiration due to an unprotected airway.
3. Attributed to reduced pharyngeal sensory perception.

Fig 12: The hyoid bone remains in the resting position (green arrow) despite contrast bolus seen in pharyngeal lumen (yellow asterix), indicating delayed pharyngeal phase. Reference: Tan Tock Seng Hospital, Singapore

• Reduced base of tongue to posterior pharyngeal wall apposition (BoT-PPW)

1. Seen as vallecular residue on the VFSS.
2. The BoT-PPW apposition is the most important driving force of pharyngeal swallow which pushes the bolus down the digestive tract.
3. If this is the primary abnormality, targeted therapy is viable (Masako manouevre).

Fig 13: Demonstration of reduced Bot-PPW and vallecular residue (yellow arrow). Reference: Tan Tock Seng Hospital, Singapore

• Reduced hyolaryngeal excursion 

1. Hyoid bone does not reach the inferior border of the mandible.
2. Results in reduced epiglottic retroflexion and poor airway protection.
3. Implies suprahyoid and pharyngeal elevator weakness. This can be further reduced in tracheostomy patients. Rehabilitation therapy can be performed (Shaker’s manouevre).

Fig 14: Reduced hyolaryngeal excursion in a patient with tracheostomy seen in-situ, resulting in penetration. Reference: Tan Tock Seng Hospital, Singapore

• Reduced/ delayed/ incomplete cricopharyngeus opening

1. Results in pyriform sinus residue, which increases the risk of aspiration when respiration resumes.

Fig 15: Reduced cricopharyngeus opening and pyriform sinus residue (orange arrow). Reference: Tan Tock Seng Hospital, Singapore

• Pyriform residue

1. Can be caused by pharyngeal-oesophageal sphincter (PES) dysmotility or mechanical obstruction.
2. The different pathophysiologies causing PES dysmotility is shown below:

Fig 16: Pathophysiology of pyriform residue.

Oesophageal phase

• Oesophageal dysphagia is best evaluated with:

1. VFSS – Subjective evaluation of oesophageal dysmotility
2. Manometry – Objective evaluation of oesophageal dysmotility
3. OGD – Rule out anatomical abnormalities

• VFSS provides a preliminary evaluation of oesophageal motility. Commonly seen oesophageal motility disorders on VFSS include:

1. Delayed oesophageal transit
2. Retrograde propulsion
3. Gastro-oesophageal reflux

Oesophageal phase abnormalities can be classified into functional and structural causes.

Functional Abnormalities

• Delayed oesophageal transit - Subjective assessment of food bolus transit time through the oesophagus.

1. The normal oesophageal transit is shown in Figure 17.
2. Delayed transit can be a result of oesophageal hold-up of bolus (Figure 18) and retrograde propulsion.
3. Cyclic ingestion can clear oesophageal hold up and improve transit time (Figure 19).

Fig 17: Normal oesophageal transit of food bolus. Reference: Tan Tock Seng Hospital, Singapore

Fig 18: Delayed oesophageal transit of food bolus. Reference: Tan Tock Seng Hospital, Singapore

Fig 19: Clearance of oesophageal hold-up with cyclic ingestion. (same patient as in Fig. 18) Reference: Tan Tock Seng Hospital, Singapore

• Gastro-oesophageal reflux - Reflux precaution advice should be given to the patient.

Structural Abnormalities

Dysphagia can be a result of structural abnormalities arising from anywhere between the oral cavity to the esophagus. Examples of these structural abnormalities include:

• Zenker’s diverticulum (Figure 20)
• Oesophageal diverticulum (Figure 21)
• Neck masses (Figure 22 and 23)

Fig 20: Zenker's diverticulum (orange outline) seen on fluoroscopy and CT Imaging. Reference: Tan Tock Seng Hospital, Singapore

Fig 21: Esophageal diverticulum seen on fluoroscopy and CT Imaging. Reference: Tan Tock Seng Hospital, Singapore

Fig 22: Patient with proven adenocarcinoma in bilateral thyroid cartilage laminae (likely metastasis). Reference: Tan Tock Seng Hospital, Singapore

Fig 23: Patient with proven adenocarcinoma in bilateral thyroid cartilage laminae (same patient as shown in Fig. 22) Reference: Tan Tock Seng Hospital, Singapore

Penetration and Aspiration

• Penetration occurs when food/liquid/contrast enters the larynx, but remains above the vocal cords.
• Aspiration occurs when food/liquid/contrast passes below the vocal cords.

Teaching Point: Penetration and aspiration are the end result of the various swallowing pathophysiologies.

Case Examples

Most patients present with a combination of swallowing pathologies across different phases of swallowing. It may be difficult to identify these pathologies as the process of swallowing occurs rapidly in real-time. Although identifying these pathologies in real-time can be done by experienced clinicians, it is helpful to review the study in slow motion in order to ensure that subtle abnormalities are not missed.  This is important in order to guide subsequent individualised rehabilitative therapy. 

As such, 3 annotated case examples are provided below in slow motion to guide the interpretation of a VFSS.

Fig 24: Oropharyngeal dysphagia showing (1) premature spillage (2) delayed pharyngeal phase onset (3) reduced tongue base to posterior wall apposition (4) reduced cricopharyngeus opening. Reference: Tan Tock Seng Hospital, Singapore

Fig 25: Oropharyngeal dysphagia showing (1) premature spillage (2) reduced tongue base to posterior wall apposition (3) reduced hyolaryngeal excursion (4) reduced cricopharyngeus opening. The above abnormalities result in penetration. Reference: Tan Tock Seng Hospital, Singapore

Fig 26: Oropharyngeal dysphagia showing (1) vallecular and pyriform sinus retention (2) reduced hyolaryngeal excursion and epiglottic retroflexion (3) reduced tongue base to posterior wall apposition (4) pyriform sinus build up. The above abnormalities result in aspiration. Reference: Tan Tock Seng Hospital, Singapore