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2 BJNN/Stroke Association Suppl ement April/May 2020
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COMMENT
Malnutrition in acute stroke:
whatarewe treating?
Priya Baby
Stroke is a leading cause of
death and disability worldwide
(Katan and Luft, 2018). It is
estimated that by 2030, deaths
from stroke will increase to
12million per year (Feigin et al, 2014).
Malnutrition in acute stroke is identied
as an important factor associated with
poor outcomes, including: functional
dependence; increased rate of infections,
such as pneumonia and urinary
infections; pressure ulcers; length of
hospital stay; and mortality (Gomes
et al, 2016). A quarter of patients
with stroke become malnourished
in the acute phase (Royal College
of Physicians Intercollegiate Stroke
Working Party, 2016). Several factors
contribute to a high risk of malnutrition
after stroke (National Institute for
Health and Care Excellence (NICE),
2017). Increased metabolism associated
with acute illness is one such factor.
Nurse clinicians often nd it difcult
to assess and treat malnutrition in
patients with acute stroke, and in my
experience, ghting malnutrition in
these patients is a major challenge
for nurses working in stroke units.
Hence, it is relevant for nurses to
understand the pathophysiology
of malnutrition in acute stroke and
appraise various methods to assess it.
The clinical studies undertaken to assess
and treat malnutrition should also
consider its pathophysiology to derive
meaningfulconclusions.
Understanding malnutrition
inacute stroke
The state of malnutrition results from
an imbalance between energy intake
and requirement. Either the intake
can be low, as in a state of starvation,
or there could be a major rise in the
requirement. In starvation, the body
enters a hypometabolic state, with
minimised catabolism (McCue, 2012).
Unlike this, the acute phase of stroke
is a hypermetabolic state, due to the
high response of the immunological
and endocrine systems of the body to
the acute illness. The inammatory
response of the body to acute stroke
leads to the release of excessive
inammatory cytokines, such as
tumour necrosis factor-alpha (TNF-α),
interleukin1 (IL-1) and interleukin
6 (IL-6), both in the brain and in
the systemic circulation (Anrather
and Iadecola, 2016). This promotes
dysregulation of the neuroendocrine
axes, especially the hypothalamic–
pituitary–adrenal (HPA) axis (Barugh
et al, 2014; Preiser et al, 2014), in acute
stroke. In addition, stroke itself can
cause damage to the HPA inhibitory
areas of the brain (Barugh et al, 2014).
The activation of the HPA axis causes
the release of cortisol, which is a
counter-regulatory hormone to insulin
and growth hormone (Figure1). A surge
of cortisol is largely responsible for
increased catabolism (Wang et al, 2006).
In addition to increased catabolism,
the acute phase of the illness is
also marked by a halt in anabolism
(which is the constructive aspect of
metabolism in which the body builds
complex molecules from simple ones)
by peripheral inactivation of anabolic
pathways (Van den Berghe et al,1998).
These neuroendocrine-mediated
changes in the body are responsible for
the hypermetabolic state reected in
acute stroke. When the stroke is severe,
involving large areas of the brain and
causing high disability, the amount of
cortisol released is proportionately high
(Barugh et al, 2014).
In the initial period after an acute
stroke, patients may have reduced food
consumption, especially due to anorexia
which is secondary to inammation
(Don and Kaysen, 2004), dysphagia,
motor and sensory impairments, feeding
dependence and depression, as well as
other focal decits, such as apraxia and
neglect, that affect eating (Bouziana and
Tziomalos, 2011). These will affect their
nutritional status (NICE, 2017)
Indicators for malnutrition
inacute stroke
There are several indicators used to
demonstrate malnutrition in stroke.
These include biochemical measures,
ABSTRACT
Malnutrition is an important concern in
patients with acute stroke. It is a major
factor contributing to poor outcome.
There are several factors that are
associated with malnutrition in acute
stroke. Hypermetabolism, associated
with acute illness, is one of the major
factors. I have examined the metabolic
changes after acute stroke and the
methods of assessing malnutrition in
the light of the literature. The
pathophysiological background of how
the metabolic changes in acute stroke
contribute to altered indices of nutrition
has also been examined. The tools
available for marking malnutrition in
acute stroke are appraised on the basis
of the pathobiology.
Key Words malnutrition; acute stroke;
protein energy malnutrition; nutrition
assessment
Author Priya Baby, Lecturer, College of
Nursing, National Institute of Mental Health
and Neurosciences, Bangalore, India
Correspondence priam19@gmail.com
Accepted January 2020
This article has been subject to double-blind
peer review.
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anthropometric measures, and history-
based and physical examination-based
tools. The common biochemical
measures used include serum albumin,
prealbumin and transferrin. The
common anthropometric indices used
include mid-arm muscle circumference
(MAMC) and triceps skinfold thickness
(TSF) (Saikaley et al, 2018; Zhang et al,
2015). Tools which use a combination
of history and physical examination,
such as Mini Nutritional Assessment
(MNA), Malnutrition Universal
Screening Tool (MUST) and Subjective
Global Assessment (SGA), are also
used in the assessment of malnutrition
in acute stroke.
The changes in biochemical and
anthropometric indices during an
acute stroke are inuenced by the
inammatory and neuroendocrine
Figure 1. Dysregulation of the hypothalamic–pituitary–adrenal axis in acute stroke
ACTH, adrenocorticotropic hormone; CRH, coorticotropin-releasing hormone; HPA, hypothalamic–pituitary–adrenal
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responses. These changes are directly
reective of the inammation and
severity of the illness.
Biochemical markers
ofmalnutrition
Serum albumin is commonly used as
an indicator of nutrition in stroke. It
is an abundant protein in the body
with various physiological functions.
Serum albumin levels are inuenced
by several factors, such as renal
loss, gastrointestinal loss, decreased
production of albumin in liver diseases
and reduced plasma volumes (Gounden
and Jialal, 2018). It is also inuenced
by the body’s inammatory response
(Nazha et al, 2015). Hypoalbuminaemia
is strongly associated with systemic
inammation. Patients with acute stroke
have a coexisting inammatory state
and they develop hypoalbuminaemia
due to inammation (Dziedzic et al,
2007). Inammation results in increased
fractional catabolic rate, causing a faster
drop in the serum levels of albumin
(Don and Kaysen, 2004). Contrary
to the general notion that acute
malnutrition causes hypoalbuminaemia,
serum albumin and prealbumin levels
are not changed, even after several
weeks of experimental starvation (Lee
et al, 2015). A drop in albumin levels
during the acute phase of illness should
be attributed to the redistribution of
albumin between the extravascular
and intravascular space in response
to acute inammation (Soeters et al,
2019). Patients with acute stroke and
with low serum albumin were found
to have high cortisol levels, signifying
the association between cortisol level
and albumin (Dziedzic et al, 2012).
Hence hypoalbuminaemia should be
considered as an expression of the
Table 2. History-based and physical examination-based tools for assessing malnutrition
Tools Parameters used
Mini Nutritional Assessment (Short Form) ■ BMI (body mass index)
■ History of reduced food intake
■ History of weight loss
■ Mobility
■ Acute disease or psychological stress
■ Presence of dementia or depression
Malnutrition Universal Screening Tool ■ BMI (body mass index)
■ History of weight loss
■ Acute disease effect
Subjective Global Assessment History
■ Weight loss
■ Dietary intake
■ Gastrointestinal symptoms
■ Functional capacity
Physical examination
■ Muscle wasting
■ Loss of subcutaneous fat
■ Oedema
Table 1. Commonly used biochemical markers of nutritional status
Commonly used biochemical
markers of nutrition
Limitations
Albumin ■ Negative acute phase protein: concentration falls in acute phase of illness (has an inverse
relation to inammation)
■ Has a half-life of 20 days
■ Only 5% of the total albumin is synthesised by the liver on a daily basis. Hence, daily intake is
not reected in the serum level
Prealbumin ■ Negative acute phase protein: concentration falls in acute phase of illness (has an inverse
relation to inammation)
■ Is affected by kidney and thyroid functions
Transferrin ■ Negative acute phase protein: concentration falls in acute phase of illness (has an inverse
relation to inammation)
■ Is affected by iron deciency/overload in the blood
■ Is affected by renal function and intake of oestrogen preparations
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inammatory process and the severity
of illness rather than merely being
attributed to to reduced food intake.
Similarly, prealbumin and transferrin
are also negative acute phase proteins
whose concentrations relate inversely to
inammation in acute illness (Davis et
al, 2012); Bharadwaj et al, 2016; Lacy
et al, 2019). Thus, similar to albumin,
their use as nutritional markers in
acute stroke is jeopardised (Table 1).
In acute disease conditions, the use of
these serum markers for nutritional
adequacy is confounded by multiple
parameters, such as kidney function,
thyroid function and iron deciency
states, rendering them inefcient for
assessing and diagnosing malnutrition
(Bharadwaj et al, 2016). Hence nurses
may not be able to use these markers to
identify malnutrition.
Anthropometric indices as
markers of nutrition
Anthropometric indices, such as TSF
(which denotes fat loss) and MAMC
(which denotes muscle loss), are
also used to mark nutritional status.
The TSF is measured to the nearest
millimetre in the right arm using a
skinfold caliper. MAMC is calculated
from the mid-arm circumference
(MAC) and TSF using a standard
formula: MAMC=MAC–(3.14×TSF).
The MAC is the circumference of the
right arm at the mid-point between the
olecranon process and the acromion. It
is measured in centimetres, using a non-
stretchable tape.
As discussed earlier, the high-stress
response of the body in acute stroke
causes increased levels of cortisol,
leading to a shift in the metabolism
and increased mobilisation of fat
(Vanhorebeek and Van den Berghe,
2006), which results in loss of TSF
thickness. Loss of muscle tissue in the
acute phase of stroke is signicantly
correlated with stroke severity and
positive C-reactive protein (CRP),
signifying the inuence of inammation
(Nozoe et al, 2016). The storm of
catabolic factors, reduced anabolic
stimuli and systemic inammation lead
to muscle loss (Phillips, 2017). Thus the
anthropometric changes in the acute
phase of stroke are a reection of the
inammation and stress response of
thebody.
Nutrition-focused
physicalexamination
As marking nutritional status in
the acute phase of stroke can be
confounded by many variables,
nutrition-focused physical examination
is a viable option to identify patients
who are malnourished (Bharadwaj et
al, 2016). A recent meta-analysis has
shown that malnutrition on admission
is one of the strongest risk factors for
worsened nutritional status later in the
course of illness (Chen et al, 2019). The
validated tools, such as MNA, MUST
and SGA, that use history-based and
physical examination-based data, can
identify malnourished patients on
admission and later (Foley et al, 2009).
The MNA includes 18 self-reported
questions derived from general,
anthropometric, dietary and self-
assessment. The short form of the
MNA (MNA-SF) is a screening tool
consisting of six questions (Montejano
Lozoya et al, 2017). The MUST uses
history-based and physical examination-
based parameters to calculate the
overall risk of malnutrition (Todorovic
et al, 2003). The SGA uses history-
based and physical examination-
based sub-criteria. An overall rating
for nutritional status is determined
on the basis of sub-criteria rating
assessment (Lim et al, 2016) (Table2).
NICE guidelines recommend the
use of MUST for initial and weekly
screening of patients with acute stroke.
This eliminates the bias of using only
biochemical or anthropometric indices
in assessing malnutrition. The history-
based and physical examination-based
tools consider the overall risk of
malnutrition based on the effect of the
acute illness itself.
Protein and energy
supplementation in acute stroke
Enteral supplementation of protein in
stroke does not show any improvement
in serum protein markers (Rabadi
et al, 2008; Geeganage et al, 2012).
Anthropometric indices have also
shown deterioration, despite aggressive
nutritional supplementation, in patients
with acute stroke (Nozoe et al, 2016;
Ha et al, 2010). A Cochrane analysis
of studies on enteral supplementation
in acute stroke has failed to show any
reduction in mortality or poor outcome
(Geeganage et al, 2012). NICE (2017)
and the Royal College of Physicians
Intercollegiate Stroke Working Party
(2016) do not recommend routine oral
supplementation in patients after acute
stroke. Only patients who are identied
as malnourished should be given
supplemental nutrition (NICE, 2017).
Recommendations and
futuredirections
Malnutrition should be identied and
treated. In the acute phase of stroke,
rather than individual markers of
KEY POINTS
■ Acute stroke causes increased
activation of the hypothalamic–
pituitary–adrenal (HPA) axis, resulting
in large amounts of cortisol release
■ The neuroendocrine and inammatory
responses of the body in acute
stroke result in hypermetabolism
■ The commonly used biochemical and
anthropometric markers of
malnutrition are inuenced by the
inherent metabolic changes in the
acute phase of illness
■ Protein and energy supplementation
during the acute phase of a stroke
may not be enough to combat the
changes in biochemical and
anthropometric markers
ofmalnutrition.
CPD reective questions
■ What is the reason for increased
metabolism in the acute phase
ofstroke?
■ How does acute stroke result
inhypoalbuminemia?
■ How are the anthropometric indices
inuenced by increased stress and
inammation in the acute phase
ofstroke?
■ Enteral supplementation of protein
and energy in the acute phase of
stroke does not adequately manage
the altered indices of malnutrition.
Explain the reason.
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COMMENT
malnutrition, history-based and physical
examination-based tools should be used
to identify malnourished patients.
Recent research in malnutrition
opens a new arena of treatment. It
focuses on the cause of malnutrition
rather than the markers of it. In the
case of acute events, such as stroke,
ghting resistance to anabolism and
hypercatabolism is the preferred
option (De Bandt, 2015). Multifaceted
interventions that may include anti-
inammatory diets, glycemic control,
physical activity, appetite stimulants,
anabolic agents, anti-inammatory
agents, anticytokines and probiotics,
will be necessary to blunt undesirable
aspects of inammatory response to
preserve body cell mass (Jensen, 2006;
Coelho Junior et al, 2016). In my
opinion, this area of nutrition needs
more evidence to translate into practice.
Conclusion
Acute stroke is an active inammatory
state, which has important implications
in nutrition. The immediate response
of the body to this acute event is highly
protective, allowing the homeostatic
mechanisms to ensure survival.
This can lead to changes in various
biochemical markers, such as albumin,
prealbumin and transferrin, that are
commonly used to denote malnutrition.
The anthropometric indices, such as
TSF and MAMC, are also affected
by the catabolic effects of the acute
response of the body to illness. Thus,
reduced food intake may not be the
only reason for malnutrition in acute
stroke. It can be recommended that
nurses should pay cautious attention
while interpreting altered biochemical
markers and anthropometric indices in
patients with acute stroke as markers
of malnutrition. History-based and
physical examination-based tools such
as MUST should be used for assessment
of malnutrition in acute stroke.
In general, future research in the
area of nutrition in acute stroke should
appreciate the importance of the acute
stress response and inammation,
and their confounding effects on the
nutritional interventions. bjnn
Acknowledgement: The author would like to thank
Gouripriya Jayasuryan, Nursing Ofcer at the
National Institute of Mental Health and
Neurosciences, Bangalore, India, for her help with
this study.
Declaration of interest: The author of this article
declares no conicts of interest.
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