Neurosensory dysphagia in a COVID-19 patient.

Dear Sirs,

We describe the case of a 72-year-old man admitted to the hospital with COVID-19 pneumonia. The neurological history and exam were unremarkable.

Due to respiratory worsening, oro-tracheal intubation and repeated courses of pronation became mandatory after 1 week. As gas exchanges improved, the patient weaned from the ventilator and self-extubated after 14 days. We performed a bedside fibro-endoscopic evaluation of swallowing (FEES) on the day after, documenting poor control of the oral and oropharyngeal phases, laryngeal penetration, and inhalation by gravity (Penetration- Inhalation Scale, [PAS] 8) [11]. The patient immediately initiated dry swallow rehabilitation. Feeding was administered exclusively through a nasogastric tube (NGT) or intravenously (after the patient removed it, on day 26).

Bedside FEES was repeated after one month, but despite a substantial improvement of the oral and oropharyngeal phases, the patient still presented inhalation for solids and liquids–(PAS 8) (Fig. 1). The bronchoscope touch induced neither laryngeal sensitivity nor cough reflex, and the instrument could easily cross vocal folds. Absolute fasting was confirmed, and percutaneous endoscopic gastrectomy (PEG) was suggested.

Fig. 1

FLAIR (a) and T2-weighted (b) brain images on MRI, showing mild non-specific periventricular hyperintensities (*). Images from the FEES, disclosing a normal anatomy before deglutition (c), bolus stasis in glosso-epiglottic valleculae and pyriform sinuses (d), initial penetration (e) and inhaled material reaching the trachea and right main stem bronchus (f). Panel G represents the mechanism of infection, starting with the binding between the spike protein of SARS-CoV-2 and ACE-2 receptor and TMPRSS2, which are expressed by the olfactory epithelium, the oral mucosae and the pharingolaryngeal surface cells. Created with BioRender.com. MRI Magnetic Resonance Imaging; FLAIR Fluid Attenuated Inversion Recovery; FEES Fibro-Endoscopic Evaluation of Swallowing; NGT Naso Gastric Tube; SARS-CoV-2 Severe Acute Respiratory Syndrome Corona Virus 2; ACE-2 Angiotensin-Converting Enzyme 2; TMPRSS2 Transmembrane Protease Serine 2

The neurological examination did not reveal deficits in the cranial nerves, excepted for absent gag reflex. Brain MRI disclosed small non-specific periventricular white matter hyperintensities on T2-weighted sequences (Fig. 1). After gadolinium administration, neither lesions nor other brain structures showed contrast-enhancement.

In physiological conditions, swallowing results from sensorimotor coordination of more than thirty muscles and six cranial nerves [4].

After Acute Respiratory Syndrome Disease (ARDS), about 30% of intubated patients develop dysphagia with a consequent risk of aspiration pneumonia, delayed oral feeding, weight loss, and increased mortality [2, 6, 9].

In this patient, post-intubation dysphagia might be due to pharyngolaryngeal trauma, neuromuscular weakness, and altered sensitivity (neurosensory dysphagia) [6].

Pharyngolaryngeal trauma usually affects the oral and pharyngeal phases of swallowing and resolves within few days [6], possibly explaining the alterations of the first FEES. Conversely, neuromuscular weakness usually depends on muscle atrophy following prolonged intubation [10], which is not our case.

In line with our experience, neurosensory dysphagia manifests with aspiration consequent to impaired control of the bolus from the oral to the pharyngeal phase but resolves in one week [6].

Patients with Severe Acute Respiratory Syndrome Corona Virus 2 (SARS-CoV-2) infection can experience long-lasting neurological symptoms, including loss of smell (anosmia) and taste (ageusia) [8]. The olfactory epithelium and the oral mucosae express the Angiotensin-Converting Enzyme 2 (ACE-2) receptor and Transmembrane Protease Serine 2 (TMPRSS2) proteins, which are entry route for the virus [12]. Interestingly, both the pharynx and larynx surface cells express these proteins [12] (Fig. 1) and have a mutual sensory innervation through the superior laryngeal branch of the vagus nerve [1].

Against this background, the atypical duration of neurosensory dysphagia and the documentation of dysphagia cases during COVID-19 infection [5] might suggest a common pathogenic background of anosmia, ageusia, and neurosensory dysphagia.

Therefore, early evaluation of swallowing is mandatory in COVID-19 extubated patients to recognize possible neurological damage (and consequent slower recovery) [3].

When abnormal findings are present, bedside FEES could be the most appropriate second-level examination [5], even if at high-risk for generating SARS-CoV-2 aerosols [7].

In our opinion, the best timing for FEES could be 7–10 days after the extubation of COVID-19 patients. In this time window, most dysphagia causes resolve spontaneously (i.e., laryngeal paresis, pressure ulcers) [6], and the virus clearance might be complete.

If post-intubation dysphagia is confirmed, a NGT can be a useful measure, but it can delay swallowing rehabilitation in the presence of reduced sensitivity. In these patients, PEG positioning could be the best option. After discharge, serial FEES can detect deglutition improvements and lead to prompt PEG removal.