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17 Pharmaconutrition in Critical Care 189
Use of Probiotics in Clinical Practice?
A good summary of current studies is provided by the meta-analysis by Sharif and
colleagues. They included 65 RCT in their meta-analysis to answer the main
questions about use of probiotics. After analysing 65 RCT, they concluded that
administration of probiotics or symbiotic reduces the risk for VAP (RR 0.72, 95% CI
0.59–0.89) and healthcare-associated pneumonia (RR 0.70; 95% CI 0.55–0.89). In
addition, no significant difference was found in mortality (RR 0.94, 95% CI
0.87–1.04) or frequency of diarrhoea (RR 0.98; 95% CI 0.85–1.12), but shorter
length of stay in the ICU or hospital and shorter duration of mechanical ventilation.
Serious adverse events, on the other hand, were more frequently associated with
probiotic use than with placebo. Considering that there are only two RCT-reported
events, the risk of potential side effects associated with probiotics administration
cannot be conclusively answered because of limited reporting and reporting quality
[
49]. Thus, evidence on side effects is currently based on case series reporting a
possible association between probiotic administration with Saccharomyces and
diagnosed fungemia [50, 51].
From this current study situation, the national and inte rnational scientific socie ties
derive similar conclusion. For example, the American Society of Parenteral and
Enteral Nutrition (ASPEN) does not advocate the general use of probiotic in critical
care, but a selective use for special patient groups (polytrauma, liver transplantation,
pancreatitis) can be considered as long as RCTs have been able to demonstrate safety
and benefit for the specific probiotics [30].
On the other hand, the guideline of the European Society for Clinical Nutrition
and Metabolism on clinical nutrition in ICU does not make recommendations on
probiotics [32]. Overall, the available studies are too heterogeneous with partly low
methodology quality, so that further research is needed to verify the promising
results on probiotic use.
References
1. Gianotti L, Nespoli L, Sandini M. Pharmaconutrition: which substrates? Eur J Surg Oncol.
2022;50:106798. https://doi.org/10.1016/j.ejso.2022.12.003.
2. Berger MM, Chioléro RL. Antioxidant supplementation in sepsis and systemic inflammatory
response syndrome. Crit Care Med. 2007;35:S584–90.
3. Pierre JF, Heneghan AF, Lawson CM, Wischmeyer PE, Kozar RA, Kudsk
KA. Pharmaconutrition Review: Physiological Mechanisms. J Parenter Enter Nutr. 2013;37:
51S–65S.
4. Practical recommendations for immune-enhancing diets. Elsevier Enhanced Reader. https://doi.
org/10.1093/jn/134.10.2868S.
5. Dupertuis YM,
pharmaconutrition: a gigantic challenge. Curr Opin Clin Nutr Metab Care. 2009;12:398.
6. Manzanares W, Dhaliwal R, Jiang X, Murch L, Heyland DK. Antioxidant micronutrients in the
critically ill: a systematic review and meta-analysis. Crit Care. 2012;16:R66.
Meguid
MM, Pichard C. Advancing from immunonutrition to a
190 A. Cotoia et al.
7. Marik PE, Zaloga GP. Immunonutrition in critically ill patients: a systematic review and
analysis of the literature. Intensive Care Med. 2008;34:1980–90.
8. Beale R, Bryg D, Bihari D. Current literature: immunonutrition in the critically ill: a systematic
review of clinical outcome. Nutr Clin Pract. 2000;15:312–4.
9. Preiser J-C, Malherbe C, Santacruz CA. Pharmaconutrition in the critically ill patient. In:
Ichai C, Quintard H, Orban J-C, editors. Metabolic disorders and critically ill patients. Cham:
Springer International Publishing; 2018. p. 421–9.
10. Saito H. Immunonutrition. Nihon Geka Gakkai Zasshi. 2004;105:213–7.
11. Jones NE, Heyland DK. Pharmaconutrition: a new emerging paradigm. Curr Opin
Gastroenterol. 2008;24:215–22.
12. Cruzat V, Macedo Rogero M, Noel Keane K, Curi R, Newsholme P. Glutamine: metabolism
and immune function, supplementation and clinical translation. Nutrients. 2018;10:1564.
13. Cotoia A, Cantatore LP, Beck R, Tullo L, Fortarezza D, Marchese F, Ferrara G, Cinnella
G. Immunological effects of glutamine supplementation in polytrauma patients in intensive care
unit. J Anesth Analg Crit Care. 2022;2:41.
14. Novak F, Heyland DK, Avenell A, Drover JW, Su X. Glutamine supplementation in serious
illness: a systematic review of the evidence*. Crit Care Med. 2002;30:2022–9.
15. Heyland DK, Wibbenmeyer L, Pollack JA, et al. A randomized trial of enteral glutamine for
treatment of burn injuries. N Engl J Med. 2022;387:1001–10.
16. Garrel D, Patenaude J, Nedelec B, Samson L, Dorais J, Champoux J, D’Elia M, Bernier
J. Decreased mortality and infectious morbidity in adult burn patients given enteral glutamine
supplements: a prospective, controlled, randomized clinical trial*. Crit Care Med. 2003;31:
2444.
17. Wischmeyer PE, Dhaliwal R, McCall M, Ziegler TR, Heyland DK. Parenteral glutamine
supplementation in critical illness: a systematic review. Crit Care. 2014;18:R76.
18. Stehle P, Ellger B, Kojic D, Feuersenger A, Schneid C, Stover J, Scheiner D, Westphal
M. Glutamine dipeptide-supplemented parenteral nutrition improves the clinical outcomes of
critically ill patients: a systematic evaluation of randomised controlled trials. Clin Nutr ESPEN.
2017;17:75–85.
19. Holecek M. Side effects of long-term glutamine supplementation. J Parenter Enter Nutr.
2013;37:607–16.
20. Stechmiller JK, Childress B, Cowan L. Arginine supplementation and wound healing. Nutr Clin
Pract. 2005;20:52–61.
21. The pharmacodynamics of L-Arginine1,2,3. Elsevier Enhanced Reader. https://doi.org/10.
1093/jn/137.6.1650S.
22. Griffiths RD, Allen KD, Andrews FJ, Jones C. Infection, multiple organ failure, and survival in
the intensive care unit: influence of glutamine-supplemented parenteral nutrition on acquired
infection. Nutrition. 2002;18:546–52.
23. Martínez-Arnau FM, Fonfría-Vivas R, Cauli O. Beneficial effects of leucine supplementation
on criteria for sarcopenia: a systematic review. Nutrients. 2019;11:2504.
24. Bear DE, Rooyackers O. HMB and leucine supplementation during critical illness and recovery.
Curr Opin Clin Nutr Metab Care. 2022;25:88.
25. Martin JM, Stapleton RD. Omega-3 fatty acids in critical illness. Nutr Rev. 2010;68:531 – 41.
26. Wichmann MW, Thul P, Czarnetzki H-D, Morlion BJ, Kemen M, Jauch K-W. Evaluation of
clinical safety and benefi cial effects of a fish oil containing lipid emulsion (Lipoplus, MLF541):
data from a prospective, randomized, multicenter trial*. Crit Care Med. 2007;35:700.
27. Mizock BA. Nutritional support in acute lung injury and acute respiratory distress syndrome.
Nutr Clin Pract. 2001;16:319–28.
28. Turner KL, Moore FA, Martindale R. Invited review: nutrition support for the acute lung injury/
adult respiratory distress syndrome patient: a review. Nutr Clin Pract. 2011;26:14–25.
29.
Langlois PL,
critically ill patients with acute respiratory distress syndrome: a systematic review and metaanalysis. Nutrition. 2019;61:84–92.
D’Aragon F, Hardy G, Manzanares W. Omega-3 polyunsaturated fatty acids in
17 Pharmaconutrition in Critical Care 191
30. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of
nutrition support therapy in the adult critically ill patient. J Parenter Enter Nutr. 2016;40:159–
211.
31. Heyland D, Dhaliwal R, Drover J, Gramlich L,
for nutrition support in mechanically ventilated, critically ill adult patients. J Parenter Enter
Nutr. 2003;27:355–73.
32. Singer P, Blaser AR, Berger MM, et al. ESPEN guideline on clinical nutrition in the intensive
care unit. Clin Nutr. 2019;38:48–79.
33. Heyland DK, Novak F, Drover JW, Jain M, Su X, Suchner U. Should immunonutrition become
routine in critically ill patients? A systematic review of the evidence. JAMA. 2001;286:944.
34. Alonso de Vega JM, Díaz J, Serrano E, Carbonell LF. Oxidative stress in critically ill patients
with systemic inflammatory response syndrome. Crit Care Med. 2002;30:1782–6.
35. Preiser J-C, Van Gossum A, Berré J, Vincent J-L, Carpentier Y. Enteral feeding with a solution
enriched with antioxidant vitamins A, C, and E enhances the resistance to oxidative stress. Crit
Care Med. 2000;28:3828–32.
36. Kahn SA, Beers RJ, Lentz CW. Resuscitation after severe burn injury using high-dose
ascorbic acid: a retrospective review. J Burn Care Res Off Publ Am Burn Assoc. 2011;32:
110–7.
37. Tanaka H, Matsuda T, Miyagantani Y, Yukioka T, Matsuda H, Shimazaki S. Reduction of
resuscitation fluid volumes in severely burned patients using ascorbic acid administration: a
randomized, prospective study. Arch Surg. 2000;135:326–31.
38. Berger MM, Shenkin A, Schweinlin A, et al. ESPEN micronutrient guideline. Clin Nutr.
2022;41:1357–424.
39. Schrezenmeir J, De Vrese M. Probiotics, prebiotics, and synbiotics—approaching a definition.
Am J Clin Nutr. 2001;73:361s–4s.
40. Wang J, Ke H, Liu K-X, Qu J-M. Effects of exogenous probiotics on the gut microbiota and
clinical outcomes in critically ill patients: a randomized controlled trial. Ann Palliat Med.
2021;10:1180190–1190.
41. Isolauri E, Sütas Y, Kankaanpää P, Arvilommi H, Salminen S. Probiotics: effects on immunity.
Am J Clin Nutr. 2001;73:444s–50s.
42. Sánchez B, Delgado S, Blanco-Míguez A, Lourenço A, Gueimonde M, Margolles
A. Probiotics, gut microbiota, and their influence on host health and disease. Mol Nutr Food
Res. 2017;61:1600240.
43. Walker WA. Mechanisms of action of probiotics. Clin Infect Dis. 2008;46:S87–91.
44. Alberda C, Marcushamer S, Hewer T, Journault N, Kutsogiannis D. Feasibility of a Lactoba-
cillus casei drink in the intensive care unit for prevention of antibiotic associated diarrhea and
Clostridium difficile. Nutrients. 2018;10:539.
45. Alberda C, Gramlich L, Meddings J, Field C, McCargar L, Kutsogiannis D, Fedorak R, Madsen
K. Effects of probiotic therapy in critically ill patients: a randomized, double-blind, placebocontrolled trial. Am J Clin Nutr. 2007;85:816–23.
46. Oami T, Chihade DB, Coopersmith CM. The microbiome and nutrition in critical illness. Curr
Opin Crit Care. 2019;25:145–9.
47. Hayakawa M, Asahara T, Henzan N, et al. Dramatic changes of the gut flora immediately after
severe and sudden insults. Dig Dis Sci. 2011;56:2361–5.
48. Cotoia A, Paradiso R, Ferrara G, et al. Modifications of lung microbiota structure in traumatic
brain injury ventilated patients according to time and enteral feeding formulas: a prospective
randomized study. Crit Care. 2023;27:244.
49.
Sharif S,
analysis of randomized controlled trials. Crit Care Med. 2022;50:1175.
Greer A, Skorupski C, et al. Probiotics in critical illness: a systematic review and meta-
Dodek P. Canadian clinical practice guidelines
192 A. Cotoia et al.
50. Roy U, Jessani LG, Rudramurthy SM, Gopalakrishnan R, Dutta S, Chakravarty C, Jillwin J,
Chakrabarti A. Seven cases of Saccharomyces fungaemia related to use of probiotics. Mycoses.
2017;60:375–80.
51. Kara İ, Yıldırım F, Özgen Ö, Erganiş S, Aydoğdu M, Dizbay M, Gürsel G, Kalkanci
A. Saccharomyces cerevisiae fungemia after probiotic treatment in an intensive care unit
patient. J Mycol Médicale. 2018;28:218–21.
Chapter 18
Physical and Functional Recovery
of Critically Ill Patients
Roberto Martinez-Alejos, Joan-Daniel Martì, Paolo Pelosi,
and Denise Battaglini
Introduction
Critically ill patients admitted to the intensive care unit (ICU) often develop physical
and functional dysfunction, usually exacerbated and perpetuated by long-term
mechanical ventilation, ICU therapies, and prolonged bed immobilization.
ICU-acquired weakness (ICUAW) is defined as neuromuscular dysfunction with
no plausible etiology other than the critical illness [1]. The median prevalence of
ICUAW
proxi
ocular muscles.
scarce and of low quality, limiting generatability. Mobilization and physical early
rehabilitation are successful interventions to reduce the burden of sedatives and
analgesics and to increase muscular strength in critically ill patients [3–6].
physical function and recovery in critically ill patients who experience ICUAW.
is 43% [2]. ICUAW generally affects respiratory and limb muscles, with
mal muscles being more affected than distal, whereas sparing the facial and
Information on outcomes of rehabilitation and physical function after ICUAW are
The aim of this chapter is to discuss the main progresses in the assessment of
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_18.
R. Martinez-Alejos
Research Methodology
Montpellier, France
J.-D. Martì
Cardiovascular Surgery ICU, Hospital Clinic, Barcelona, Spain
P. Pelosi · D. Battaglini (
Dipartimento di scienze Chirurgiche e Diagnostiche Integrate, Università degli studi di Genova,
Genoa, Italy
IRCCS Ospedale Policlinico San Martino, Genoa, Italy
© The
Author(s), under exclusive license to Springer Nature Switzerland AG 2024
A. Cotoia et al. (eds.), Nutrition, Metabolism and Kidney Support,
https://doi.org/10.1007/978-3-031-66541-7_18
Department, Montpellier Tranning School of Physiotherapy,
✉)
193
194 R. Martinez-Alejos et al.
Pathophysiological Mechanisms, Risk Factors, and Clinical Implications
Pathophysiological Mechanisms of ICUAW
ICUAW is a bundle of multifactorial disorders whose physiopathology remains not
clearly elucidated. ICUAW can be attributed to complex structural and functional
alterations within the central nervous system, as well as the peripheral nerves and the
myofibers [
dysfunction. (1) Muscle atrophy is driven by a catabolic status, characterized by a
reduction in anabolic effector hormones and an increase in catabolic hormones,
which often aggravates critical illnesses. This resulting imbalance contributes to a
marked muscle wasting, which is primarily of myogenic origin [6]. This muscle loss
is enhanced by an altered protein balance where protein breakdown is faster than
protein synthesis, due to the activation of proteolytic systems like the ubiquitinproteasome pathway [6]. Additionally, mechanical unloading due to immobilization
or denervation can exacerbate this phenomenon. Clinically, this atrophy happens
rapidly; we can estimate a loss of muscular mass up to 2% decrease per day during
the first week in ICU, with patients with multi-organ failure losing more muscle mass
than those without [
(2) Muscle dysfunction is driven by multiple factors, in particular [8]:
6]. The main alterations include (1) muscle atrophy and (2) muscle
7].
(a) Microcirculatory disturbances can compromise tissue perfusion and oxygen
delivery, potentially leading to neuronal injury, axonal degeneration, and
chronic membrane depolarization of terminal motor axons. Nevertheless, the
impact of edema-induced compression damage to muscles and nerves on microcirculatory changes remains controversial.
(b) Bioenergetic dysfunction of mitochondria is commonly associated with reduced
oxygen supply and subsequent impairment of energy production, and it is
primarily attributed to impaired oxygen utilization resulting from direct mitochondrial damage, which is further exacerbated by inflammation, hyperglycemia, and free radicals. These factors lead to dysfunction in the electron transport
chain, impairing mitochondrial respiration and oxidative phosphorylation,
which are necessary for efficient energy production. Dysfunctional mitochondria
also generate excessive amounts of reactive oxygen species and free radicals,
which further damage cellular macromolecules and organelles. This selfperpetuating cycle of damage and dysfunction can significantly impair cellular
function and contribute to the pathogenesis of ICUAW [
(c)
Membrane and
pathogenesis of muscle dysfunction. The inactivation of sodium channels plays a
significant role in inducing a rapid and reversible hypo-excitability or
inexcitability of the nerve and muscle membranes in ICUAW patients. Furthermore, altered intracellular calcium homeostasis has been shown to contribute to
ion channel alterations are other possible factors acting in the
6, 8].
18 Physical and Functional Recovery of Critically Ill Patients 195
impaired muscle contractility by disrupting excitation-contraction coupling, a
critical process in muscle function [7].
Risk Factors Associated with Physical and Functional Recovery in Critically Ill Patients
Several risk factors have been reported independently associated with ICUAW.
Severity of the critical ill condition seems to be the main factor reported by the
literature. Indeed, higher severity illness scores, sepsis, inflammation, and multiple
organ failure are associated with ICUAW. Similarly, patients presenting higher
Acute Physiology and Chronic Health Evaluation (APACHE) score show higher
ICUAW rates [
neuromuscular blockers agents seem to be as well independently associated with
ICUAW; however, the effect of these drugs is controversial with mixed results in
RCTs which may suggest that their association and ICUAW is more complex and
depends on other factors such as dose, rates, timing, and concomitant glycemic
control. Nevertheless, longer periods with continuous sedation seem to have a
deeper effect on muscle atrophy and weakness than patients with a rapid decrease
and discontinuation of sedation [10].
Regarding the respiratory function, a longer time spent on mechanical ventilation
and length of ICU stay are predictors of ICUAW development. Some studies point
that respiratory muscle weakness is associated with infection or sepsis, disease
severity, and peripheral weakness [11]. Moreover, the phrenic nerve and diaphragm
present electrophysiological abnormalities like those of the peripheral nerves and
muscles, suggesting that respiratory weakness is part of ICUAW. The relationship
between mechanical ventilation, ICUAW, and diaphragmatic dysfunction can be
bidirectional. Prolonged mechanical ventilation has been associated with an
increased risk of developing these conditions, as it can lead to muscle atrophy and
weakness, particularly in the diaphragm [11, 12]. This weakness can then lead to a
prolonged need for mechanical ventilation and difficult weaning from it. Conversely,
ICUAW and diaphragmatic dysfunction can also contribute to prolonged mechanical
ventilation and failed weaning.
Finally, some anthropometric variables seem to be more related to ICUAW as we
find a higher risk of muscular weakness in women and in older patients, while some
others are pending confirmation, such as obesity [8].
9]. Higher levels of lactates and the use of corticosteroids and
Clinical Impact of Poor Physical and Functional Recovery in Critical Illnesses
Recovery seems to be directly impaired in ICUAW patients. Indeed, prolonged
weaning and weaning failure are common situations in these patients. In a review
196 R. Martinez-Alejos et al.
published in 2007, 12 out of 13 studies observed an independent association between
ICUAW and prolonged weaning [13], and one study indicated that ICUAW was the
only significant predictor of weaning failure in septic patients (OR 15.4, 95% CI
5.6–52.3) [14
]. However, more recent data showed that despite 80% of ICUAW
patients presenting diaphragmatic dysfunction measured with bilateral
supramaximal magnetic twitch stimulation of the phrenic nerves (median 14.2
(IQR = 13.2–17.5) cmH
median 4.7 (IQR = 3.2–7.2) cmH
O in patients without diaphragmatic dysfunction vs
2
O in patients with diaphragmatic dysfunction,
2
p < 0.05), this dysfunction seems to not be associated with weaning failure, with
50% of ICUAW patients succe
4–13) cmH
O weaning success patients versus median 4.3 (IQR = 3–9) cmH2O
2
ssfully extubated within 72 h median 6.8 (IQR =
weaning failure patients; p = 0.08) [15].
Regarding physical outcomes,
ICUAW can have lasting consequences on
patients’ physical functioning and activity limitations. Up to 65% of patients who
require prolonged mechanical ventilation for more than 7 days show activity limitations at hospital discharge. Among older patients who develop ICUAW, activity
limitations may persist for up to 1 year post-discharge [16]. Additionally, acute
respiratory distress syndrome (ARDS) survivors often experience higher muscle
weakness and activity limitations 1 year after the onset of the condition. Moreover,
6-minute walk test scores seem to remain significantly below predicted values (70%
of predicted values) even 5 years after the ICU stay [17]. A recent systematic review
in 11,693 patients with ARDS concluded that ICU survivors can experience physical
and mental health impairment (without differences between those with or without
COVID-19), sometimes not completely recovering up to 5 years after ICU
discharge [18].
Finally, it should be highlighted that COVID-19 patients developing ICUAW
seem to present lower hand-grip measurements and Medical Research Council
(MRC) score than non-COVID-19 patients, which may impact negatively on
outcomes [19].
These findings
highl
ight the need for rehabilitation and physical therapy interventions to address the long-term functional outcomes of patients who have undergone prolonged mechanical ventilation and critical illness. It is critical to focus on
promoting physical recovery to improve patients’ overall quality of life and reduce
the risk of persistent activity limitations [20].
How to Assess Physical and Functional Recovery in Critical Illnesses
Physical and functional function in critical illnesses can be assessed using a variety
of tools, including severity and functional status scores, as well as imaging techniques. The choice of assessment tool often depends on the conscious status of the
18 Physical and Functional Recovery of Critically Ill Patients 197
patient and their level of cooperation, as there is no consensus on which tool is
preferred [1].
Among the scale s used, the 6-grade MRC scale is a valuab
le tool for the overall
estimation of motor function. Relevant muscle impairment is typically defined by a
cutoff of 48 points, while severe impairment is set at 36 points [21]. The 4-grade
MRC scale has not demonstrated clear superiority in diagnosing ICUAW and still
requires validation [22, 23]. Additionally, there are other less commonly used but
interesting tools such as the Scored Physical Function in Intensive Care Test, the
Functional Status Score for the ICU, and the Chelsea Critical Care Physical Assessment Tool [24–26].
The 6-minute walk test (6-MWT) was not included in the Delphi consensus of
core outcome measures (COMS) for patients with acute respiratory distress syndrome (ARDS), although it has been proposed as a good measure of physical
function [27]. However, this tool has been included in the consensus guidelines of
COMS for patients with neurological diseases, along with the 10-meter walk
20].
test [
Recently, the sit-to-stand test (STST) has been suggested as a feasible and safe
option to assess physical function in ICU patients, and it is easier to implement than
the 6-MWT. The STST can be evaluated at ICU discharge by performing as many
repetitions as possible within 30 seconds or by completing five repetitions as rapidly
as possible [28, 29]. Both options have shown high inter- and intra-rater reliability in
assessing function in moder ately ill ICU patients. See Fig.
18.1 for a summary of the
main diagnostic scales used for functional evaluation during rehabilitation in the
ICU (Fig. 18.2 and Table 18.1).
There are several diagnostic tests available for the assessment of physical func-
tion and recovery in critically ill patients.
Handheld dynamometry allows for the measurement of quadriceps strength [32],
although its use in the critical care setting is not well documented.
Electromyography (EMG) is a useful tool for unconscious patients and can be
used to investigate nerve conduction. Its utility is even greater in patients who can
cooperate by providing voluntary muscle contractions [33, 34].
Ultrasound has gained popularity in the last few decades for assessing muscle
strength and function. It is a repeatable, low-cost, and bedside-available technique
that allows for the assessment of muscle quality and quantity. Ultrasound is used to
assess contractile dysfunction of respiratory muscles, diaphragm thickness and
thickening, and muscle wasting in limb muscles such as the rectus femoris [33].
Near-infrared spectroscopy (NIRS) is a novel tool that provides information
about catabolism, inactivity, and the loss of lean body mass. It assesses skeletal
muscle oxidative capacity [35, 36].
Both m
ic resonance imaging (MRI) and computed tomography (CT) can
agnet
provide information on adipose tissue and quantify lean body mass. However, they
require specialized personnel for interpretation and software [37].
Bioelectrical
impedance analysis (BIA) and bioelectrical impedance vector anal-
ysis (BIVA) are safe and low-cost techniques that can estimate body fat and muscle
198 R. Martinez-Alejos et al.
<48 points: relevant
MRC scale
Shoulder abductors Left Right
Elbow flexors Left Right
Wrist extensors Left Right
Hip flexors Left Right
Knee extensors Left Right
Foot dorsiflexors Left Right
6-MWT
STTS
Grade 5: Normal
Grade 4: Movement against gravity and resistance
Grade 3: Movement against gravity over (almost) the full range
Grade 2: Movement of the limb but not against gravity
Grade 1: Visible contraction without movement of the limb (not existent for hip flexion)
Grade 0: No visible contraction MRC grade for each muscle (given in full numbers)
The patient walks as far as possible for six minutes, turning around.
Put a sign every 3 m with a minimum distance of 30 m before turning around.
Measure arterial pressure, heart rate, and ask for dyspnea using the Borg scale
before starting. Peripheral oxygen saturation during 6-MWT is also suggested.
The patient sit and stand up as much times as possible in 30 seconds or
as fast as possible five times.
Sitting on a chair with 43 cm (cm) of seat height.
Each participant cross their arms over their chest (if possible) and sit
with their back against the backrest of the chair
muscle impairment
<36 points: severe
muscle impairment
In healthy subjects
ranges betw een
400 – 700 m
Treshold of functional
independance:
Median 15 rep in 30”
females
Median 17 rep in 30” males
12 s (11–15 s) for five rep
Fig. 18.1 Main diagnostic scales for assessment of functional status during rehabilitation in ICU
Fig. 18.2 Early protocol stepwise. (Adapted from [30, 31]. ICU intensive care unit, MRC Medical
Research Council score, NMES neuromuscular electrical stimulation, RASS Richmond Agitation
Sedation Score)
mass. They involve electrodes and measure resistance and reactance after injecting
an alternating sinusoidal electric current [33].
Muscle and nerve biopsies can provi
although they are invasive and have limitations [
de additional information on muscle status,
1].