Garcés Chávez Cristian Geovanny1,2*, Paredes Luis1,3.
The myopathies produce impairment of the striated skeletal muscle in its
structure or development, distinguishing two categories: genetic myopathies
and acquired myopathies. COVID-19 has been categorized as a disease
which acute respiratory manifestation is caused by the SARS-CoV-2 virus. In
very severe cases, patients are admitted to Intensive Care Units (ICU), where
they receive invasive, complex, and long-term treatments that can have
negative consequences for recovery, making the risk-benet balance a
very complex factor. The purpose of this work is to address the relationship
between myopathy and COVID-19 in severely ill patients admitted to the ICU,
observing the set of factors that cause the conditions and the impact on the
clinical evolution of these patients. For the development of the project, a
search was carried out in the following databases: Medline, Scielo - Scientic
Electronic Library Online, Google Scholar and Redalyc, using appropriate
descriptors and selecting a total of 54 articles. It is concluded that myopathy
and COVID-19 are closely related in patients hospitalized in the ICU, also
showing the presence of neurological problems associated with multisystemic
involvement, among which are polyneuropathy in critical patients, myopathy
in critical patients, Guillain-Barré Syndrome, among others.
Las miopatías producen afectación del músculo esquelético estriado
en su estructura o desarrollo, distinguiéndose dos categorías: Miopatías
genéticas y miopatías adquiridas. La COVID-19 ha sido catalogada como
una enfermedad cuya manifestación respiratoria aguda es causada por el
virus SARS-CoV-2, en casos muy severos, los pacientes son ingresados en las
Unidades de Cuidados Intensivos (UCI), donde reciben tratamientos invasivos,
complejos y prolongados que pueden traer consecuencias negativas para
la recuperación, haciendo del balance riesgo benecio un factor muy
complejo. El objetivo de este trabajo es abordar la relación existente entre
la miopatía y COVID-19 en pacientes críticos internados en UCI, observando
el conjunto de condiciones que provocan las afectaciones y el impacto
en la evolución clínica. Para el desarrollo de la investigación se realizó una
búsqueda en las bases de datos Medline, Scielo – Scientic Electronic Library
Online, Google Académico y Redalyc, utilizando descriptores adecuados
y seleccionándose en total 54 artículos. Se concluye que la miopatía y
COVID-19 están estrechamente relacionados en pacientes internados en
UCI, evidenciándose además la presencia de problemas neurológicos
asociados con afectación multisistémica dentro de los que se encuentran
la polineuropatía del paciente crítico, la miopatía del paciente crítico, el
Síndrome de Guillain-Barré, entre otros.
Revista Médica Vozandes
Volumen 32, Número 2, 2021
Palabras clave: COVID-19, Myopathies, Intensive Care Unit, Treatment, Consequences. (Mesh).
Forma de citar este artículo: Garcés CC,
2021; 32 (2): 41 - 47
1 Universidad Central del Ecuador, Facultad de Cien-
cias Médicas, Posgrado de Medicina Crítica y Terapia
Intensiva. Quito – Ecuador
2 Hospital General IESS Riobamba. Médico del servicio
de Terapia Intensiva. Riobamba – Ecuador.
3 Hospital General Enrique Garcés. Médico del servicio
de Terapia Intensiva. Quito – Ecuador.
Garcés Chávez Cristian
Paredes Luis
Este artículo está bajo una
licencia de Creative Com-
mons de tipo Reconocimien-
to – No comercial – Sin obras
derivadas 4.0 International.
DOI: 10.48018/rmv.v32.i2.6
*Corresponding author: Garcés Chávez Cristian
Received: 16 – Jul – 2021
Accepted: 12 – Sep – 2021
Publish: 20 – Dic – 2021
Article history
Conflict of interest: The authors declare no conict
of interest.
Financial disclosure: The authors have no nancial
relationships relevant to this article to disclose.
Authors’ contribution: All the authors reviewed and
approved the nal manuscript.
Keywords: COVID-19, Miopatías, Unidad de Cuidados Intensivos, Tratamiento, Secuela. (Mesh).
42 Revista Médica Vozandes
Volumen 32, Número 2, 2021
Myopathies are considered neuromuscular diseases
characterized by the impairment of the striated skeletal muscle
in its structure or development, distinguishing two categories:
genetic myopathies (inherited) and acquired myopathies (1). The
rst data in the literature referring to inherited myopathies (IM) was
in 1852, where Edward Meryon described granular degeneration
in postmortem muscle. Idiopathic inammatory myopathies (IIM)
directly affect skeletal muscle and can sometimes involve the
skin and other organs to varying degrees (2).
Weakness associated to critical illness is a general term describing
neuromuscular disorders related to a severe disease such as
COVID-19. It is divided into three groups depending on the
damage location: polyneuropathy due to critical illness (CIP),
myopathy due to critical illness (CIM) and, polyneuromyopathy
due to critical illness (CIPNM) (3).
Although it has been described in the literature that among the
clinical symptoms caused by the SARS-CoV-2 virus are respiratory
manifestations, fever, gastrointestinal problems, among others,
since the beginning of the pandemic, neurological symptoms
such as headache, anosmia, myalgia, insomnia and confusion
have also been observed (4).
ICUs are part of the last step in the integrated patient care
system and their main objective is the diagnosis and treatment
of critically ill patients, those with very deteriorated health
conditions and high risk of suffering severe complications in
the short and medium term (5). The consequences of admission
to the ICU may be the result of the different and aggressive
treatments or secondary to other aspects of the disease itself,
such as fatigue, asthenia, weight loss, cognitive shortcomings,
myopathy and polyneuropathy (6).
The current relationship between myopathy and COVID-19 in
critical patients admitted to the ICU, observing the
set of conditions that cause the impairment and
functional decline in these patients has particular
importance given the current circumstances, and
constitutes a relevant aspect for future research.
An unstructured search was carried out in the
following databases: Medline (https://www., Scielo Scientic
Electronic Library Online (http://www.scielo.
org), Académic Google (
es) y Redalyc (,
using descriptors and key words: “COVID-19”,
“COVID-19, Myopathies , “Intensive Care Unit”,
“Treatment”, “Consequences”.
A total of 147 related articles were obtained;
giving emphasis on those of an original nature,
specically systematic reviews, case studies and
experimental studies; 63 publications prior to
2012 were rejected, resulting in 84 articles in the
sampling phase, 12 were not relevant or were
duplicates, for a total of 72 to choose from. Finally,
the 54 most updated and best documented
publications were selected (Figure 1).
Literature Review
While CIM, CIP and CIPNM are similar in their
clinical presentation, there are important
differences in their pathophysiology. CIP
is a sensorimotor axonal polyneuropathy
characterized by the loss of individual nerve
bers, whereas the weakness in CIM is attributed
Identication Database articles
Items excluded and unavailable
Non-relevant and duplicate articles
Excluded articles
Chosen articles
Articles analyzed
Selected articles
Figure 1 . Flow chart for articles selection.
Source: Author.
Revista Médica Vozandes
Volumen 32, Número 2, 2021
to a decrease in thick myolaments leading to the death
of skeletal muscle myobers (7).
CIP shows worse results when compared to CIM (8).
Although substantial progress has been made to improve
understanding of the mechanisms related to these
conditions, age and length of ICU stay are important
indicators of long-term outcomes (9).
ACE2 receptors serve as a protective molecule, maintain
physiological homeostasis, and prevent the development of
numerous diseases. Binding of SARS-Cov2 to ACE2 not only
initiates the entry of the virus into the human body, but also
disrupts the protective action of ACE2 in affected organs.
Therefore, it is important to re-evaluate the impact of ACE2
in modulating organ function and human health (10).
Skeletal muscle plays an extremely important role in the
regulation of the motor system and metabolic homeostasis.
Through activation of the classical RAS pathway, the ACE-Ang
II-AT1 axis participates in muscle pathogenesis by promoting
disturbances in the motor system and insulin sensitivity, that
is, muscle wasting accompanied by pathological muscle
remodeling or insulin resistance, respectively (11).
Regarding the ACE2-Ang 1-7 pathway as a counter-
regulatory system of the ACE-Ang II-AT1 axis, previous studies
in skeletal muscle mention a protective role of Ang 1-7 in
pathological muscle remodeling and insulin resistance (12),(13).
Riquelme et al. investigated the role of ACE2 in the
existing pathological muscle modulation, suggesting that
ACE2 activity and protein levels in skeletal muscle
were increased by genetic induction of muscular
dystrophy, which could imply a compensatory
mechanism of the RAS protective pathway against
muscle injury (14),(15).
Myopathy can be caused by several factors such as:
direct viral damage to skeletal muscle or secondary
disorders such as motor neuron involvement,
malnutrition, systemic inammatory response,
prolonged bed rest and insufcient O2 supply (16),(17).
Atrophy and brosis are caused by pathological
muscle remodeling of skeletal muscle, secondary to
endothelial dysfunction in the microcirculation and
RAS system in the musculature (18).
Muscle atrophy is caused by an imbalance in protein
metabolism, especially by inhibition of the IGF-1-AKT-
mTOR pathway due to the alteration caused by
AngII in muscle protein synthesis, which can indirectly
induce cell apoptosis (13). This damaged or atrophied
muscle tissue directly inuenced by AngII is replaced
by connective tissue producing muscle brosis with a
subsequent decrease in skeletal muscle (19).
To shorten, it can also be mentioned that SARS-COV2
can induce muscle atrophy through dysregulation
of the renin-angiotensin-aldosterone system (RAS)
in interaction with other processes secondary to
hospitalization in the ICU (Figure 2) (20),(11).
Figure 2 . Summary of the etiopathogenesis of COVID myopathy – 19
Source: Author
44 Revista Médica Vozandes
Volumen 32, Número 2, 2021
During the COVID-19 pandemic, neuromuscular complications
have been evident (21). Between 30% and 50% of ICU patients
present during hospitalization neuromuscular weakness
apparently secondary to CIM and CIP or their combination,
causing an increase in the number of days of mechanical
ventilation and ICU stay (22).
Mao et al. (2020) stated that 36.4% of patients had neurological
manifestations that were directly related to the severity of the
clinical picture of COVID-19 (23),(24).
Markussen et al. (2019) state that it is predictable and logical
that patients who have been hospitalized in the ICU for a
longer period of time will present physical consequences, such
as myopathy, polyneuropathy, musculoskeletal retractions,
among others (25),(26).
Authors such as Céspedes et al. (2021) report that in the
advanced phase of COVID-19, there is clinical manifestations
related to peripheral nerve involvement, dysautonomias and
myopathies (27). Muscle weakness due to post-ICU immobility has
been considered as the sequela that most affects the quality of
life and recovery time of these patients. (Figure 3) (28).
A large number of patients with COVID-19 require admission
and long-term stay in intensive care units (UCI) (29), therefore,
the chance of complications and the development of CIM was
highly possible (30),(31).
•Guillain Barré syndrome (GBS) andCOVID-19
GBS is one of the most common causes of paralysis worldwide,
manifesting as an acute inammatory polyradiculoneuropathy.
Among the usual clinical features are symmetrical ascending
weakness, painful paresthesias, decreased
or absent osteotendinous reexes, alteration
of cranial nerves and in severe cases even
respiratory muscle weakness may occur (32). It
can appear as a heterogeneous disease and
different variants have been reported (33).
Gigli et al. (2021) reported 47 patients with
classical GBS or its variants in patients diagnosed
with COVID-19, suggesting a marked increase
in its frequency during the pandemic (34).
Zuberbuhler et al. (2021) assume that respiratory
failure in patients with COVID-19 is secondary to
the relationship between muscle weakness and
viral lung infection (35).
•Transverse myelitis and encephalomyelitis in
Transverse myelitis leads to the destruction of
the myelin of nerve cells causing the interruption
of the messages that the spinal cord sends
throughout the body via the peripheral nerves,
resulting in pain, muscle weakness, paralysis,
sensory problems or bladder and bowel
dysfunction (36). SARS-CoV-2 has clinical features
that are not only limited to the respiratory tract,
but also involve the nervous system. Several
authors have studied the indirect and direct
mechanisms involved in the complications
and neurological manifestations reported in
COVID-19 and have identied the possible
mechanisms of direct invasion of SARSCoV-2
into the CNS (36). This is why isolated cases of
encephalopathy, encephalitis, encealomyelitis,
necrotizing hemorrhagic encephalopathy,
among others, have been described (37).
•Cerebrovascular disease (ECV) and COVID-19
Figure 3 . Consequences of COVID-19 in patients admitted to the ICU
Source: Author
Revista Médica Vozandes
Volumen 32, Número 2, 2021
Related to the prothrombotic phenotype of severe
COVID, ischemic cerebrovascular events have been
reported with an incidence that can reach up to 5% of
hospitalized patients (38).
Another mechanism that has been mentioned is
endothelial dysfunction, SARS-CoV-2 binds and invades
vascular endothelial cells through ACE2 present in the
endothelium, triggering endothelial inammatory cell
death (pyroptosis) (39),(40).
CIP, CIM and CIPNM are usually diagnosed during the
recovery phase of the disease and while all are known to
share common clinical signs, the diagnosis also depends
on the correct interpretation of those data related to the
clinical presentation and electrodiagnostics, with standard
laboratory tests showing little signicance (3).
Sagging and generally symmetrical weakness are aspects
found in CIP, CIM and CIPNM, a potential differentiating
factor may be no or diminished response to pain, vibration
or temperature sensitivity in those with CIP, whereas
these functions would be seen in CIM (41). Muscle atrophy
is generally more evident in CIM, which is difcult to
diagnose due to the condition of critically ill patients. In
awake patients, muscle strength can be assessed using the
Medical Research Council (MRC) scale, which rates muscle
weakness in six muscle groups, giving a score between 0
(no contraction) and 5 (normal strength). CIPNM is dened
when the total MRC score is less than 48, other causes of
weakness having been previously ruled out (3).
Laboratory tests are not considered indispensable for
the diagnosis of CIAW, however, it has been recognized
that plasma IL-6 is an early marker of membrane
dysfunction for CIM (3). GDF-15 is a critical disease
mediator stimulated by the stress of muscle atrophy
and is considered a potential biomarker candidate;
however, further studies will be needed to conrm
its usefulness (8).
Needle electromyography can help clarify the
diagnosis, among the ndings are described:
early recruitment and small amplitude polyphasic
waves in the different affected muscles (biceps
brachii, rectus femoris and tibialis anterior muscles),
reduced amplitude and duration of the motor
unit potential and sometimes the presence of
brillations and fasciculations (42).
Muscle biopsy in the case of CIP shows atrophy due
to denervation of muscle bers type 1 and 2. In CIM,
atrophy of myobers, focal or diffuse loss of thick
laments, angulated bers, fatty degeneration, and
necrosis are described.
With imaging techniques such as computed
tomography and nuclear magnetic resonance it
is possible to observe the degree of muscle loss
and the infiltration of muscle by adipose tissue.
It also allows the evaluation of deeper muscle
groups; however, among the main disadvantages
of these techniques are described their high cost,
exposure to radiation and the need to transport
the patient out of the ICU (30).
Treatment model provides for minimization of
associated risk factors, symptom management and
physical rehabilitation (26).
Figure 4 . Therapeutics recomended to myopathy
Source: Author
46 Revista Médica Vozandes
Volumen 32, Número 2, 2021
Some authors state that there are no recommended
pharmacological treatments to prevent or treat CIAW (43).
However, euglycemia has been shown to improve some
outcomes in critically ill patients. Insulin therapy greatly reduced
CIP and CIM rates, including mechanical ventilation time,
hospitalization days, and mortality rate (44).
Functional electrical stimulation (FES) is reported to be
benecial in patients who have not been admitted to the
ICU by promoting increased muscle strength (45),(46).
However, there is discordance among the results, so more
and better studies are needed to support its efcacy (47),(48).
Early passive and active mobilization plus sedation breaks may aid
recovery, especially in patients admitted to the ICU for COVID-19
(49), being relevant, safety from a procedural point of view with
a low risk of adverse events (50). Zhou et al. (2014) report that
early mobilization leads to a lower incidence of CIAW, improving
functional capacity and increasing the ability to stand upright (51).
The proposals studied have focused on: transfers (from supine to
sitting), walking and cycloergometry adjacent to the bed (22).
Yang et al. (2018) mention that malnutrition is the leading
cause of “critical illness polyneuropathy,” emphasizing
the harmful effects of parenteral nutrition in
critically ill patients and supporting early enteral
feeding (52).
McGlory et al. (2020) report that omega-3
fatty acid supplementation improved skeletal
muscle anabolism (53), also showing strong anti-
inammatory properties (54).
Myopathies are an important aspect to consider
for the development of complications and
consequences associated with COVID-19 in
critically ill patients admitted to the ICU. Among
the most important neurological problems
associated with COVID-19 with multisystemic
involvement are polyneuropathy in the critically
ill patient, myopathy in the critically ill patient
and Guillain-Barré syndrome, so there is a close
relationship between myopathy and COVID-19,
an aspect of particular importance in the
present circumstances.
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