Critical illness myopathy (CiM) is an acute primary myopathy, the spectrum of which ranges from pure

functional impairment with normal histology to muscle atrophy and necrosis.

Structural changes occur, such as myosin loss, and the proteolytic cascade involved in the breakdown of myosin and other
muscle proteins, such as titin, nebulin, and actin, seems up-regulated.37 This may reflect altered calcium homeostasis and
suggested by the increased expression of calpain, a calcium-activated protease in atrophic muscle fibers.38 However, any
comprehensive explanation of the pathogenesis of CIM needs to include altered gene expression, disordered muscle membrane
function, and proteolytic pathways involved in muscle protein breakdown (Zink, w. et al. Nat. Rev. Neurol. 5, 372–379 (2009))

Diagnosis

(Bird, 2007)

Faktor Resiko:
Hiperglikemia
Gangguan Elektrolit

Hiperosmolaritas

Nutrisi Parenteral

Hipoalbuminemia
Hiperlaktatemia

Electrolyte imbalance (OR, 2.48; 95%CI, 1.02-6.01),

Hyperosmolarity (OR, 4.8; 95%CI, 1.05-24.38),
Hyperglycaemia (OR, 2.86; 95%CI, 1.301-6.296),
Hyperglycaemia was identified as an independent risk factor for ICUAW. Increasing daily ICU insulin
dose was found to decrease risk of weakness. Besides, intensive insulin therapy demonstrated a
protective effect on the development of ICUAW, and blood glucose control (below 110 mg/dL)
reduced the incidence of ICUAW.

To avoid an increased risk of hypoglycaemia and critically ill patients’mortality, the current
recommendation for blood glucose levels that may safely reduce the incidence of ICUAW is 110-180
mg/dL
High lactate (OR, 2.18; 95%CI, 1.39-3.43),
Parenteral nutrition(OR, 5.11; 95%CI, 1.14-22.88)

Malnutrition occurs commonly in critically ill patients, and it predicts poor outcomes. It leads to muscle atrophy,41 impaired
muscle function and delayed weaning.42 It is essential to provide nutritional support for critically ill patients. However, parenteral
nutrition during the first week in the ICU was found to be associated with more muscle wasting43,44 because of inhibition of
autophagy, and parenteral nutrition was viewed as a significant risk factor of ICUAW.22 Optimized energy supplementation with early
enteral nutrition can improve critically ill patients’ outcomes by significantly reduced mortality,45 ventilator days,46 length of hospital
and ICU stay.47 Avoiding early parenteral nutrition and providing early enteral nutrition support may help to decrease the incidence
of ICUAW.
For patients with a high risk of ICUAW, such early and aggressive prevention measures as early treatment of sepsis and MOF,
blood glucose control, lung-protective ventilation, optimizing certain drugs use, early enteral nutrition support, maintaining water,
electrolyte and acid-base balance, may help to reduce the incidence of ICUAW.
Tao Yang et al. Risk factors for intensive care unit-acquired weakness:A systematic review and meta-analysis. Acta Neurol Scand. 2018;1–11.

In addition to issues with mobility, nutrition also needs to be addressed. In one small study of patients with
ICUAW transferred to a long-term care hospital (LTCH), anemia, hypoalbuminemia, and vitamin D deficiency
were identified, as were impairments in strength, balance, coordination, mobility, and endurance.45

Anamnesis:

Penurunan berat badan (ESPEN Guidelines)

Kapasitas fisik/fungsional sebelum sakit atau aktivitas sehari-hari sebelum sakit (ICU-Acquired Weakness.
Sarah E. Jolley, MD; Aaron E. Bunnell, MD; and Catherine L. Hough, MDCHEST 2016; 150(5):1129-1140)

Pemeriksaan Fisik:
Kapasitas Fungsional

Antropometri dan Komposisi Tubuh

Massa dan kekuatan otot (ESPEN)

Pemeriksaan Penunjang : (ESPEN)

Gula Darah
Blood glucose should be measured initially (after ICU admission or after artificial nutrition initiation) and at least
every 4 h, for the first two days in general.

Insulin shall be administered, when glucose levels exceed10 mmol/L.

Elektrolit

Pemeriksaan elektrolit (kalium, magnesium, fosfat) diukur setiap hari pada minggu pertama.

Albumin

Nitrogen Urea Urine

Terapi:

Pemeriksaan klinis menyeluruh, meliputi anamnesis, pemeriksaan berat badan, kapasitas

fisik/fungsional, pemeriksaan fisik, komposisi tubuh, massa dan kekuatan otot harus dilakukan untuk
menilai malnutrisi pada seluruh pasien penyakit kritis.

Setiap pasien penyakit kritis yang dirawat lebih dari 48 jam di ICU termasuk pasien berisiko malnutrisi.

Pemberian nutrisi secara oral harus diutamakan pada pasien yang mampu makan.

Jika asupan oral tidak memungkinkan, pemberian nutrisi enteral dini (dalam 48 jam) harus dilakukan.

Jika terdapat kontraindikasi oral dan pemberian nutrisi enteral, nutrisi parenteral diberikan dalam tiga
sampai tujuh hari. Pemberian nutrisi parenteral hanya dimulai jika seluruh strategi untuk
memaksimalkan nutrisi enteral telah dilakukan.

Pemberian kalori dihitung dengan rumus atau diberikan 25-20 kkal/kgBB/hari.

Pemberian nutrisi hipokalorik (di bawah 70% estimasi kebutuhan) diutamakan dibanding nutrisi isokalorik pada seminggu pertama perawatan
ICU.
Pemberian protein 1,2-2 g/kgBB/hari dan dapat lebih tinggi pada pasien dengan luka bakar atau trauma
multipel.
Pemberian karbohidrat tidak boleh melebihi 5 mg/kg BB/ menit.
Rekomendasi batas atas pemberian lipid intravena 1 g/kgBB/hari, maksimum 1,5 g/kg/hari.
Pemberian glutamin enteral dan parenteral tidak diberikan rutin, kecuali pada pasien luka bakar dan trauma.
Pemberian nutrisi enteral yang diperkaya asam lemak omega 3 dengan dosis nutrisional dapat diilakukan (500 mg EPA dan DHA)
Pemberian antioksidan dalam dosis aman (5-10X DRI).
ESPEN Intensive Care
1. Medical nutrition therapy shall be considered for all patients staying in the ICU, mainly for more than 48 h
2. A general clinical assessment should be performed to assess malnutrition in the ICU, until a specific tool has been validated.
3. Remark:
General clinical assessment could include anamnesis, report of unintentional weight loss or decrease in physical performance before
ICU admission, physical examination, general assessment of body composition, and muscle mass and strength, if possible.
4. Every critically ill patient staying for more than 48 h in the ICU should be considered at risk for malnutrition.
5. Oral diet shall be preferred over EN or PN in critically ill patients who are able to eat.
6. If oral intake is not possible, early EN (within 48 h) in critically ill adult patients should be performed/initiated rather than delaying
EN
7. If oral intake is not possible, early EN (within 48 h) shall be performed/initiated in critically ill adult patients rather than PN.
1. In case of contraindications to oral and EN, PN should be implemented within three to seven days.
2. To avoid overfeeding, early full EN and PN shall not be used in critically ill patients but shall be prescribed within three to seven days.
If predictive equations are used to estimate the energy need, hypocaloric nutrition (below 70% estimated needs) should be preferred over
isocaloric nutrition for the first week of ICU stay.
In patients who do not tolerate full dose EN during the first week in the ICU, the safety and benefits of initiating PN should be weighed on a
case-by-case basis.
PN should not be started until all strategies to maximize EN.
During critical illness, 1.3 g/kg protein equivalents per day can be delivered progressively tolerance have been attempted.
The optimal nutritional composition of macronutrients is defined by minimal requirements and upper limits.
For carbohydrates the upper limit should be 5 mg/kg body weight/min.
For intravenous lipids the upper recommendation is 1 g/kg body weight/day with a tolerance up to 1.5 g/kg/day.
Excessive
glucose based energy provision is associated with hyperglycemia,
enhanced CO2 production, enhanced lipogenesis, increased insulin
requirements and no advantage in protein sparing in comparison
with a lipid based energy provision
In ICU patients except burn and trauma patients, additional enteral GLN should not be administered.
EN enriched with omega-3 FA within nutritional doses can be administered.
High doses omega-3 enriched enteral formulas should not be given on a routine basis.
The International Society for the Study of FA and Lipids recommends a daily intake of 500 mg of eicosapentaenoic acid (EPA) þ
docosahexaenoic acid (DHA) for healthy humans [
Parenteral lipid emulsions enriched with EPAþDHA (Fish oil dose 0.1-0.2 g/kg/d) can be provided in patients receiving PN.
To enable substrate metabolism, micronutrients (i.e. traceelements and vitamins) should be provided daily with PN.
Antioxidants as high dose monotherapy should not be administered without proven deficiency showing a significant reduction of infectious
complications and of mortality, the 2016 ASPEN guidelines [41] recommend the provision of a combination of antioxidant micronutrients “in
safe doses” (i.e. 5e10 times Dietary reference intakes ¼ DRI).
Early EN should be performed in patients receiving neuromuscular blocking agents

Frailty is a clinical syndrome in which 3 or more of the

following criteria occur: 1. Unintentional weight loss, 2. Selfreported exhaustion, 3. Weakness (by grip strength), 4. Slow
walking speed and 5. Low physical activity
Frailty occurrence was also decreased in patients fed with EN enriched with the omega-3 FA EPA [312]. In patients receiving >1 g/kg per
day protein as 20% of the calories, frailty was less common. An ESPEN expert working group [313] recommend 1.2e1.5 g protein/
kg/day in older people who are malnourished or at risk of malnutrition because they have acute or chronic illness, with even high
protein intake for individuals with severe illness or injury

ASPEN
Based on expert consensus, in the absence of IC,
we suggest that a published predictive equation or a
simplistic weight-based equation (25–30 kcal/kg/d) be
used to determine energy requirements.
A4. Based on expert consensus, we suggest an ongoing
evaluation of adequacy of protein provision be performed.
Weight-based equations (eg, 1.2–2.0 g/kg/d) may
be used to monitor adequacy of protein provision by comparing
the amount of protein delivered with that prescribed, especially
when nitrogen balance studies are not available to assess
needs
We recommend that nutrition support therapy in
the form of early EN be initiated within 24–48 hours in the critically ill patient who is unable to maintain
volitional intake.
We suggest the use of EN over PN in critically ill
patients who require nutrition support therapy.
Based on expert consensus, we suggest that
patients who are at low nutrition risk with normal
baseline nutrition status and low disease severity (eg,
NRS 2002 ≤3 or NUTRIC score ≤5) who cannot
maintain volitional intake do not require specialized
nutrition therapy over the first week of hospitalization
in the ICU.
We suggest that sufficient (high-dose) protein should
be provided. Protein requirements are expected to be in
the range of 1.2–2.0 g/kg actual body weight per day and
170 Journal of Parenteral and Enteral Nutrition 40(2)
may likely be even higher in burn or multitrauma
patients
Use
of nitrogen balance or NPC:N (70:1–100:1) is of limited value
in the ICU.95
We suggest immune-modulating enteral formulations
(arginine with other agents, including eicosapentaenoic
acid [EPA], docosahexaenoic acid [DHA], glutamine, and
nucleic acid) should not be used routinely in the MICU.
Consideration for these formulations should be reserved
for patients with TBI and perioperative patients in the
SICU (see sections O and M).
We suggest that a combination of antioxidant
vitamins and trace minerals in doses reported to be safe
in critically ill patients be provided to those patients who
require specialized nutrition therapy.
[Quality of Evidence: Low]
Rationale: Antioxidant vitamins (including vitamins E and C [ascorbic acid]) and trace minerals
(including selenium, zinc,and copper) may improve patient outcome, especially in burns, trauma, and
critical illness requiring mechanical ventilation.
216,217 The aggregated results of 15 trials that met our
inclusion criteria (Figure 8) demonstrated that antioxidant and
trace element supplementation was associated with a significant
reduction in overall mortality (RR = 0.8; 95% CI 0.7–
0.92; P = .001).218–232 Infectious complications, ICU or hospital
LOS, and duration of mechanical ventilation were not significantly
different between patients placed on such antioxidant
multivitamin/trace element supplements and controls receiving
placebo. Most issues of administration, such as dosage, frequency,
duration, and route of therapy, have not been well standardized.
Renal function should be considered when
supplementing vitamins and trace elements.

We suggest that, in the patient at low nutrition risk

(eg, NRS 2002 ≤3 or NUTRIC score ≤5), exclusive PN be
withheld over the first 7 days following ICU admission if
the patient cannot maintain volitional intake and if
early EN is not feasible.
The risk/benefit ratio for use of PN in the ICU setting
is much narrower than that for use of EN
Based on expert consensus, in the patient determined
to be at high nutrition risk (eg, NRS 2002 ≥5 or NUTRIC
score ≥5) or severely malnourished, when EN is not
feasible, we suggest initiating exclusive PN as soon as
possible following ICU admission.
We recommend that, in patients at either low or high
nutrition risk, use of supplemental PN be considered
after 7–10 days if unable to meet >60% of energy and
protein requirements by the enteral route alone. Initiating
Figure 9. Enteral nutrition (EN) with glutamine vs EN with no glutamine, outcome mortality. ICU,
intensive care unit.
McClave et al 179
supplemental PN prior to this 7- to 10-day period in
critically ill patients on some EN does not improve
outcomes and may be detrimental to the patient.
We suggest that hypocaloric PN dosing (≤20 kcal/
kg/d or 80% of estimated energy needs) with adequate
protein (≥1.2 g protein/kg/d) be considered in
appropriate patients (high risk or severely malnourished)
requiring PN, initially over the first week of
hospitalization in the ICU.
H5. We recommend a target blood glucose range of 140 or
150–180 mg/dL for the general ICU population; ranges
for specific patient populations (postcardiovascular
surgery, head trauma) may differ and are beyond the
scope of this guideline.
Hyperglycemia is a common response to acute illness
and severe sepsis and may lead to poor outcomes. There
continues to be controversy regarding the lower point of the
range, with SCCM recommending 150–180 mg/dL,279 while
A.S.P.E.N. recommends 140–180 mg/dL

Tight
control of blood glucose using intensive insulin
treatment during the ICU stay may reduce the
incidence and severity of CIM and CIP.

Ascorbate and nitric oxide donors attenuate

platelet adhesion in septic capillaries and may
become novel adjuvant therapies to improve muscle
microcirculation during sepsis [47]—MOUSE
Secor D, Li F, Ellis CG, et al. Impaired microvascular perfusion in sepsis
requires activated coagulation and P-selectin-mediated platelet adhesion in
capillaries. Intensive Care Med 2010; 36:1928–1934.

The major findings from this study is that low vs. eucaloric parenteral nutrition had
no significant
effect on the size or force generating capacity (specific force) in single muscle fibers
and myosin:actin
ratios were not affected in either the slow-twitch soleus or the fast-twitch EDL
muscles in animals
exposed to a mimicked ICU setting over a period of 10–14 days

The Effect of Nutritional Status in the Pathogenesis

of Critical
Illness Myopathy (CIM)
Hannah Ogilvie 1 and Lars Larsson 1,2,* Biology 2014, 3, 368-382;
doi:10.3390/biology3020368

NUTRITIONAL
In critical illness, increased demand for anabolic glutamine
cannot be met by increased muscle protein proteolysis,
rendering this amino acid ‘conditionally essential’.
As glutamine is a precursor for glutathione, there is also a
conditional lack for antioxidants. Parenteral glutamine
[85] or glutathione supplementation [86] greatly reduced
complication and mortality rates. Despite increased need
for these compounds in critical illness some may not or
only modestly be present in conventional parenteral
nutrition solutions [16_].Curr Opin Clin Nutr Metab Care 9:403–409.

Nutritional and supplemental therapies include protein and

amino acid supplementation, antioxidant therapy, and hormonal
therapy. Studies examining nutritional supplementation
are difficult to extrapolate to the treatment of myopathies,
in that they typically focus on enhancement of the immune
system or other global outcomes and not the correction of
end-organ problems, such as myopathies.
Novak and colleagues (19) conducted a meta-analysis in
2002 to examine the relation of glutamine supplementation to
hospital length of stay, complication rates, and mortality in
both patients undergoing surgery and those with critical illness.
They focused on 14 randomized trials. Using aggregated
results, glutamine supplementation and mortality were associated
with a risk ratio (RR) of 0.78 (95% CI _ 0.58 –1.04). For
glutamine supplementation and complications from infection,
the RR was 0.81 (95% CI _ 0.64 –1.00). In addition, glutamine
supplementation was associated with a shorter hospital
length of stay (_2.6 d; 95% CI _ _4.5 to 0.7). A priori
defined subgroup analysis indicated that the greatest treatment
benefit was associated with parenteral, high-dose glutamine
supplementation, and hospital length of stay was affected most
favorably in surgical patients instead of critically ill patients.
Although this meta-analysis did not explore the effects of
glutamine supplementation directly, one could infer that patients
with a shorter length of stay might have a lower incidence
of ICU-acquired myopathies. Supplemental glutamine
in total parenteral nutrition was associated with a survival
benefit in ICU patients that apparently was sustained over a
6-mo trial period (20).
Garcia de Lorenzo and colleagues (21) examined 69 patients
with sepsis, divided into 3 groups that received 3 different
types of isocaloric total parenteral nutrition, each type
varying in the quality and quantity of amino acids. The short
half-life of plasma proteins increased in those patients treated
with high loads of BCAAs. In addition, there was a relation
among plasma concentrations of leucine, isoleucine, valine,
arginine, and BCAAs as part of a nutritional support regimen.
The primary outcome (and major finding) of this study was the
lower mortality observed in patients treated with high BCAA
loads (i.e., _0.5 g _ kg_1 _ d_1). Other investigators (3) studying
BCAA-rich total parenteral nutrition found these solutions
capable of correcting the plasma amino acid imbalance
that exists in sepsis. As mentioned previously, plasma BCAA
measurement may be used to quantify the efficacy of nutritional
replacement in critically ill patients (9). It must be
recognized, however, that the major role for BCAA metabolism
is to provide nitrogen for the formation of glutamine that
can then be utilized by cells of the immune system and used to
repair damaged muscle.
Arginine is another conditionally indispensable amino acid
for maintaining body protein homeostasis and nutrition after
burn injury or sepsis; nonetheless, outcomes in various types of
catabolic critical illness have been variable (22). In postsurgical
postsurgical,
moderately stressed subjects, parenteral nutrition supplemented
with arginine and glutamate improved nitrogen balance
and attenuated protein myofibrillar catabolism. This
amino acid is thought to be the primary stimulus for glutamine
generation (23).
Antioxidants might represent another type of nutritional
therapy of benefit to critically ill patients with myopathies.
Excess production of oxygen free radicals and diminished
endogenous antioxidant mechanisms have been implicated as
contributing to multiple organ failure in septic shock. Notably,
interactions among different endogenous antioxidant systems
imply that successful therapeutic strategies may depend on the
use of a combination of antioxidant agents, rather than a
single agent. Recent investigations have focused on one such
endogenous antioxidant, glutathione (GSH), the most abundant
thiol in the human body. The amino acid cysteine is a
critical and rate-limiting constituent of this tripeptide, with an
apparent increased requirement for this amino acid during
periods of catabolic illness (24,25). Muscle biopsies show decreased
GSH levels in parallel with low glutamine levels in
critically ill patients (26). Ortolani and colleagues (27) examined
critically ill patients with early septic shock receiving
standard therapy and either intravenous GSH or N-acetylcysteine
(NAC; a GSH precursor) and GSH. Oxidative stress
indices were substantially decreased at d 5 of treatment in the
GSH supplement group, and were even more marked in the
GSH and NAC group. Potentially, glutathione precursors,
such as NAC, may improve outcomes in critically ill patients
due to their ability to scavenge oxygen free radicals and replete
low glutathione stores. No trials to date have examined the
efficacy of this compound in treating or preventing myopathies,
but it bears noting that a sizable segment of the ICU
population, namely patients with a history of alcohol abuse or
with HIV disease, have profound plasma GSH deficiencies
compared to control subjects. Such patients may benefit from
supplementation with GSH or its

PPK Miopati Penyakit Kritis

Faktor Resiko Terkait Nutrisi:1

Hiperglikemia
Gangguan Elektrolit
Hiperosmolaritas
Nutrisi Parenteral
Hipoalbuminemia
Hiperlaktatemia

Anamnesis:
Riwayat penurunan berat badan2
Kapasitas fungsional sebelum sakit atau aktivitas sehari-hari sebelum sakit2,3
 Pemeriksaan Fisik2:
Kapasitas Fungsional
Antropometri dan Komposisi Tubuh
Massa dan kekuatan otot

Pemeriksaan Penunjang:
Gula Darah4
Elektrolit
Albumin
Nitrogen Urea Urin

Dukungan nutrisi:
 Pemeriksaan klinis menyeluruh, meliputi anamnesis, pemeriksaan berat badan, kapasitas fungsional,
pemeriksaan fisik, komposisi tubuh, serta massa dan kekuatan otot harus dilakukan pada seluruh pasien.2
 Pemberian energi
 Kebutuhan energi dapat dihitung dengan rumus misal Harris-Benedict yang ditambahkan dengan
faktor stress tergantung dari kondisi pasien.2
 Perhitungan kebutuhan energi juga dapat dilakukan dengan rule of thumb yaitu sebesar 25 – 30
kkal/ kgBB/hari.4
 Pemberian nutrisi hipokalorik (di bawah 70% estimasi kebutuhan) lebih disarankan dibandingkan
dengan pemberian nutrisi isokalorik pada seminggu pertama perawatan pasien penyakit kritis. 2
Keduanya tidak menunjukkan efek berbeda terhadap kejadian miopati penyakit kritis.5
 Pemberian makronutrien:
 Protein : 1,2-2 g/kgBB/hari dan dapat diberikan lebih tinggi pada pasien dengan luka
bakar atau trauma multipel.4
 Karbohidrat : - 50-60% total kalori
- Laju pemberian karbohidrat tidak boleh melebihi 5 mg/kg BB/ menit.2
 Lemak : Pemberian lipid intravena tidak boleh melebihi 1,5 g/kg/hari.2

 Pemberian mikronutrien dan nutrien spesifik:

 Pada miopati penyakit kritis diduga terjadi deplesi antioksidan di otot. Penelitian menunjukkan
bahwa biopsi otot pada penyakit kritis menunjukkan kadar glutation rendah. Namun belum terdapat
penelitian mengenai efek pemberian glutation dan antioksidan lain pada miopati penyakit kritis
secara langsung. Vitamin dan mineral antioksidan (vitamin A, vitamin C, vitamin E, selenium, zinc,
tembaga) dapat diberikan dalam dosis aman (lima hingga sepuluh kali angka kecukupan gizi).4,6
 Pada miopati penyakit kritis diduga terdapat defisiensi glutamin relatif. Biopsi otot pada penyakit
kritis menunjukkan kadar glutamin rendah. Namun belum terdapat penelitian yang secara langsung
meneliti efek suplementasi glutamin pada miopati penyakit kritis. Pemberian glutamin tidak
disarankan secara rutin. Glutamin dapat diberikan pada pasien dengan luka bakar atau trauma.2,6
  Pemberian nutrisi enteral yang diperkaya asam lemak omega 3 dengan dosis nutrisional dapat
dilakukan (500 mg EPA dan DHA).2

 Jalur pemberian nutrisi:

 Jika pasien masih dapat makan, pemberian nutrisi diutamakan melalui oral.
 Jika asupan oral tidak memungkinkan, pemberian nutrisi enteral dini (dalam 48 jam) harus
dilakukan.
 Pemberian nutrisi parenteral dilakukan apabila saluran cerna tidak berfungsi atau apabila
pemberian nutrisi oral dan enteral tidak dapat memenuhi kebutuhan nutrisi. Pemberian nutrisi
parenteral hanya dimulai jika seluruh strategi untuk memaksimalkan nutrisi enteral telah
dilakukan.2 Pemberian nutrisi parenteral dapat meningkatkan kejadian miopati penyakit kritis.

 Kadar glukosa dikontrol pada kadar 140-180 mg, jika perlu diberikan terapi insulin.4
 Koreksi albumin pada pasien dengan hipoalbuminemia.
 Koreksi elektrolit pada pasien dengan gangguan elektrolit.

REFERENSI:
1. Yang T, Li Z, Jiang L, Wang Y, Xi X. Risk factors for intensive care unit- ­ acquired weakness : A
systematic review and meta- - analysis. 2018;(May):1–11.
2. Singer P, Reintam A, Berger MM, Alhazzani W, Calder PC, Casaer MP, et al. ESPEN Guideline
ESPEN guideline on clinical nutrition in the intensive care unit. Clin Nutr [Internet]. 2018;
Available from: https://doi.org/10.1016/j.clnu.2018.08.037
3. Jolley SE, Bunnell AE, Hough CL. ICU-Acquired Weakness. Chest [Internet]. 2016;150(5):1129–
40. Available from: http://dx.doi.org/10.1016/j.chest.2016.03.045
4. Mcclave SA, Taylor BE, Martindale RG, Warren MM, Johnson DR, Braunschweig C, et al.
Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically
Ill Patient : Society of Critical Care Medicine ( SCCM ) and American Society for Parenteral and
Enteral Nutrition ( A . S . P . E . N .) Preliminary Remarks ( Intent of Guidelines ). 2016;
5. Ogilvie H, Larsson L. The Effect of Nutritional Status in the Pathogenesis of Critical Illness
Myopathy (CIM). 2014;368–82.
6. Hermans G, B DJ, Bruyninckx F, G VDB. Interventions for preventing critical illness
polyneuropathy and critical illness myopathy ( Review ). 2014;(1).