DISCUSSION
SSNHL is mostly defined as a sensorineural hearing loss of at least 30
decibels (dB) at three consecutive frequencies, occurring within a
timeframe of 72 hours. It can affect any age group, but mostly occurs in
patients aged 40-60 years. In the majority of cases, adequate
investigation does not reveal any underlying cause (e.g. vestibular
schwannoma, stroke, malignancy, exposure to noise or ototoxic
medication), so that the SSNHL is considered as
idiopathic.(9,10) However, multiple etiologies have
been proposed.
First, SSNHL has often been associated to viral infection. Serological
techniques such as PCR and immunoglobulin detection have previously been
used to confirm viral load in patients with SSNHL. However, a direct
causality between acute viral infection and SSNHL remains uncertain
since in vivo sampling of inner ear fluid is potentially harmful.
Second, vascular impairment is suggested as a cause of SSNHL. Both
cardiovascular risk factors and virally induced hypercoagulability or
inflammatory edema can theoretically lead to cochlear ischemia with
subsequent hearing loss.(10)
Thus, how about the specific SARS-CoV-2 infection and occurrence of
hearing loss? Interestingly, the audiological profile of patients with
asymptomatic SARS-CoV-2 infection was examined, showing significantly
worse high frequency pure-tone threshold amplitudes and transient evoked
oto-acoustic emissions in these patients compared to non-infected
subjects. This finding suggests a damaging effect on cochlear outer hair
cell function.(11)
It is known that SARS-CoV-2 affects cells through the angiotensin
converting enzyme 2 (ACE2) receptor. This receptor is expressed in
various cell types, such as lung respiratory epithelium and the
sustentacular cells of the olfactory neuroepithelium. On the one hand,
viral infection of the auditory nervous system could induce symptoms in
a similar way as infection of the olfactory nervous system is believed
to contribute to the pathophysiology of
COVID-anosmia.(1,12) On the other hand, coagulopathy
with high incidence of thrombotic events is well-described in COVID-19
patients.(13) ACE2 receptors are expressed in
endothelial cells in various organs as well. The important findings of
Varga et al. taught us that SARS-CoV-2 promotes the induction of
endotheliitis. The team detected SARS-CoV-2 elements in endothelial
cells, with evidence for the induction of endothelial dysfunction and
cell apoptosis.(14) Hence, as hypothesized by
Harenberg et al., hearing loss in COVID-19 patients could be a result of
endothelial cell dysfunction with micro-thrombosis at the level of the
auditory center in the temporal lobe, the auditory nerve or the
cochlea.(12) In the case of Degen et al. however, the
sudden hearing loss is described as a neurological complication of viral
meningitis.(4)
COVID-19 is postulated to be the cause of SSNHL in our case. The risk of
a false association, in particular because of the unclarified
pathophysiology of SSNHL, should however be stated. Therefore, we agree
with and applied the criteria of Satar et al. before proposing the
relationship between SARS-CoV-2 infection and occurrence of SSNHL in our
case.(15) First, the infection was
laboratory-confirmed. Second, pathological ipsilateral Video Head
Impulse Testing assigns for vestibular involvement, although our patient
did not complain of associated symptoms. Next, other causes of SSNHL
have been excluded anamnestically, serologically and by magnetic
resonance imaging. Last, the temporal concordance between SARS-CoV-2
infection and onset of SSNHL remains unresolved. Four out of the nine
cases did not report the onset of SSNHL. All five cases that did mention
the onset of hearing loss, describe occurrence between at least 12 and
47 days after the first COVID-19 symptoms. We could therefore
hypothesize that SSNHL in SARS-CoV-2 infection is more likely to appear
in the downward phase of the infection, however, three patients were
only able to notice their hearing loss when released from the Intensive
Care Unit.
CONCLUSION This case report adds new well-founded evidence to the association
between COVID-19 and hearing loss. We hope it will contribute to the
prompt recognition of both SSNHL and SARS-CoV-2 infection. Based on this
case and literature review, we advise to include PCR testing in the
diagnostic work-up of patients presenting with SSNHL during the ongoing
pandemic. Whether the sudden hearing loss is the result of endothelial
cell dysfunction with micro-thrombosis in the cochlea or central
auditory pathways remains unclear.