NUTRITION
Malnutrition in critically ill
patients in intensive care units
Joanne Quirk
T
he objective of nutritional support is to
provide the basic materials for body
homeostasis via the alimentary tract
when oral feeding is not possible (Emery,
1991). This is not an uncommon requirement
in the intensive care unit (ICU), as the majority
of patients have either a serious illness, trauma
or have had major surgery and are therefore
unable to maintain their own nutritional needs.
The provision of artificial nutrition for crit-
ically ill patients has become a daily practice
in ICUs, yet many patients remain under-
nourished or even malnourished (Horwood,
1992). McCain (1993) estimates that malnu-
trition is prevalent in many mechanically ven-
tilated patients and suggests that the overall
incidence of malnutrition in ICU could be as
high as 50%. Severe protein-calorie malnutri-
tion is the main problem in many ICU
patients due to increased catabolic state often
associated with acute severe illness and the
frequent presence of previous chronic wasting
conditions (Webb et al, 1999).
Nutritional failure results when a patient’s
nutritional intake falls short of metabolic
requirements. If prolonged, this will lead to
malnutrition which is associated with an
increased morbidity and mortality (Verity,
1996). According to Webb et al (1999), the
signs of nutritional failure are insidious, and
the diagnosis is often only made when mal-
nutrition has become established. Failure to
feed critically ill patients in the first few days
of their admission to ICU will be more detri-
mental in the already malnourished patient;
the consequences may be much less marked in
the well-nourished (Zainal, 1994).
METABOLIC RESPONSE TO CRITICAL
ILLNESS
Metabolism refers to all of the chemical reac-
tions of the body. Tortora and Grabowski
(1996) have described it as the energy-balancing
act between catabolic (degradative) reactions
and anabolic (synthetic) reactions (Table 1).
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Abstract
The provision of artificial nutrition for critically ill patients is of great
importance as many are unable to maintain their own nutritional needs.
The administration of total parenteral nutrition (TPN) and enteral
nutrition (EN) has become a daily practice in intensive care units.
Despite this, many patients remain undernourished or even malnourished
and it is estimated that the incidence of malnutrition in intensive care
patients could be as high as 50% (McCain, 1993). The reasons by which
patients become or remain undernourished are multifactorial and range
from physiological to iatrogenic. In order to lessen the catabolic state
which results from the hypermetabolism associated with critical illness,
prompt and adequate nutritional support must be delivered. It is
essential that members of the multidisciplinary team caring for critically
ill patients are aware of the importance of nutrition and the deleterious
effects of malnutrition to achieve the best possible outcome for patients.
Catabolism is a chemical process which
breaks down complex organic compounds
into simple ones. These catabolic reactions
release chemical energy that can be used to
drive anabolic reactions. Some of the impor-
tant sets of catabolic reactions are those
occurring in glycolysis, the Krebs cycle and the
electron transport chain. Chemical reactions
that combine simple molecules and monomers
to make more complex ones and that form the
body’s structural and functional components
are collectively known as anabolism. An
example of an anabolic process is the forma-
tion of peptide bonds between amino acids,
thereby building up the amino acids into
Joanne Quirk is Senior Staff
protein portions of cytochromes, enzymes, Nurse, Intensive Care,
hormones and antibodies. Royal Halifax Infirmary,
During simple starvation metabolic adapta- Halifax, West Yorkshire
tion occurs with the aim of conserving essential Accepted for publication:
tissues. Glycogen reserves are only small and April 2000
are useful for just 24–36 hours. Consequently,
Table 1. The process of anabolism and catabolism
Anabolism A+B Combine AB
(synthesis) Atom, ion or molecule → New molecule
Catabolism AB Breakdown A+B
(decomposition) Atom, ion or molecule → Atom, ion or molecule
537
 NUTRITION
energy must be obtained by utilizing triglyc-
erides from fat stores and amino acids derived
from proteins (Tortora and Grabowski, 1996).
As starvation continues, the body adopts sever-
al protein-conserving measures such as the
reduction in basal metabolic rate, while nerve
cells adapt to using ketone bodies rather than
glucose as an energy source.
Sepsis initiates some of the most profound
physiological and metabolic abnormalities
observed in critically ill patients (Wiley et al,
1990). In severe injury the body is unable to
adopt the protective mechanisms seen in sim-
ple starvation (Garrard et al, 1996). Increases
in energy and protein metabolism are distinc-
tive of the hypermetabolic response to trauma,
major surgery and sepsis. The main character-
istics of hypermetabolism are a massive
increase in resting energy expenditure with an
associated increase in oxygen consumption,
cardiac output and carbon dioxide production.
In hypermetabolic states such as sepsis,
burns and severe trauma, muscle wasting
occurs due to a massive outflow of amino
acids from the muscles. Serum albumin levels
often decrease after major injury. Albumin
breakdown is accentuated after trauma and
hypoalbuminea is frequently seen despite
increased synthesis of all plasma proteins
including albumin (Oh, 1996).
Wiley et al (1990) maintain accelerated
proteolysis and increased negative nitrogen
balance are characteristic of sepsis and this
response pattern is often similar to that
described for injury. Feeding does not stop the
initial state of catabolism and negative nitro-
gen balance, but early feeding (providing pro-
tein and calories) minimizes body tissue
breakdown (Verity, 1996).
Table 2. The physiological effects of malnutrition
Weight loss, loss of fat and muscle wasting
Impairment of muscle function
Reductions in respiratory drive
Respiratory muscle weakness
Decreased heart rate, arterial and venous pressure, stroke volume
and cardiac output
Poor wound healing
Immunodeficiency
Decreased mobility and increased incidence of pressure sores
Source: Webb et al (1999)
538
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PHYSIOLOGICAL EFFECTS
OF MALNUTRITION
The obvious effects of malnutrition are reduc-
tion in weight, loss of fat and progressive mus-
cle wasting (Table 2). In addition to its effect
on body composition, malnutrition results in
severe impairment of muscle function which
can lead to reductions in respiratory drive, res-
piratory muscle weakness and therefore venti-
lator dependence (Garrard et al, 1996). It is
known that undernutrition is associated with
decreases in heart rate, arterial and venous
pressures, stroke volume and subsequently
cardiac output (Webb et al, 1999). In critical-
ly ill patients with already compromised car-
diac and respiratory function these additional
stresses may prove to be catastrophic. Protein
deficiency has been associated with poor
wound healing, diminished mobility and a
high incidence of bedsores (Viney, 1996).
Early nutritional support may be needed
for critically ill people who can develop com-
plications in days (Faraquar, 1993).
THE IMMUNE SYSTEM
A juxtaposition can be seen in the relation-
ship between nutrition and the immune sys-
tem and it is often difficult to separate the
effects of an illness from the immunodeficient
state (Webb et al, 1999). Nutritional deficien-
cy will impair the immune response, reducing
protection against infection. The resultant
infection can itself subsequently precipitate
malnutrition. Opportunistic infections occur
more frequently in malnourished patients,
which could be a direct result of immunosup-
pression (Verity, 1996). Poor nutritional sta-
tus is associated with a high incidence of sep-
sis, Gram-negative nosocomial pneumonia
and urinary tract infection in the presence of
an indwelling catheter (Garrard et al, 1996).
The use of specific nutrients as pharmaco-
logical modifiers of either the metabolic
response to trauma or sepsis, or to specific
metabolic responses have been investigated
(Adam, 1994). Combinations of these
immunonutrients are now added to nutrition-
al supplements given to critically ill patients.
Glutamine is the most abundant amino acid in
the body and is a specific nitrogen and energy
source for the gut and cells of the immune sys-
tem. Recent studies (Rennie, 1996) suggest
that if provided in small amounts, glutamine
BRITISH JOURNAL OF NURSING, 2000, VOL 9, NO 9
 MALNUTRITION IN CRITICALLY ILL PATIENTS IN INTENSIVE CARE UNITS
may contribute to the preservation of the gut
mucosal integrity and prevent bacterial
translocation. Arginine has been shown to
increase the body’s wound healing capabilities
by increasing the synthesis of collagen and the
release of growth hormone (Adam, 1994).
Fatty acids and in particular omega-3 fatty
acids enhance immune function by a range of
mechanisms. They are precursors for the
eicosanoids (thromboxane, prostaglandins
and leukotrienes) and, therefore, have a con-
siderable role in the immune response.
Clinical studies of other immune enhancing
enteral formulas suggest that the addition of
arginine and omega-3 polyunsaturated fatty
acids to feeds have beneficial effects on the
immune system (Heys et al, 1999). This may
contribute to the reduction of length of stay
in hospital, although there is no evidence at
present to support a reduction in mortality.
GUT INTEGRITY
Whenever gastrointestinal function is not
impaired, enteral feeding should be preferred
to parenteral nutrition (Zainal, 1994).
According to Raper and Maynard (1992), the
vast majority of critically ill patients are able
to tolerate enteral feeding. One of the factors
implicated in sepsis in critically ill and injured
people is diminished integrity of the gut
(Verity, 1996). Many researchers have
explored the immunological role of the gas-
trointestinal tract and have shown that a com-
promise of the gastrointestinal tract plays a
role in the pathogenesis of infection in the crit-
ically ill patient (Maynard and Bihari, 1991).
In health the stomach and small bowel are
essentially sterile, while the colon contains
hundreds of different enteric bacterial species
which are essential for the digestion of nutri-
ents. The gastrointestinal tract also serves as
a barrier to microorganisms, endotoxin and
other bacterial or digestive products. This
barrier is maintained by normal epithelial
cells and their tight junctions and is support-
ed by various immunological mechanisms. In
the critically ill, the effectiveness of this barri-
er is reduced, the main cause being mucosal
ischaemia (Hayland et al, 1993). This enables
the translocation of bacteria and endotoxin
into the portal circulation. According to
Anderson and Fearson (1995), translocation
plays a distinct part in sepsis and shock which
may progress to multiple organ failure.
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‘
The provision of enteral nutrition can Whenever
maintain mucosal integrity and reduce bacte-
rial translocation (Maynard and Bihari,
gastrointestinal
1991). There is substantial evidence that the function is not
gastrointestinal barrier function is worsened impaired, enteral
by the absence of nutrients in the gut
(Hayland et al, 1993). Also, the paracrine and
feeding should be
endocrine functioning of the gut, its contribu- preferred to
tion to the immune defences and its ability to parenteral
recover full absorptive capacity during reha-
bilitation were all worsened by the lack of
nutrition...One of
enteral nutrition (Rennie, 1996). the factors
Anderson and Fearson (1995) suggest that implicated in sepsis
it is possible that enteral nutrition reduces
colonization of the upper gastrointestinal
in critically ill and
tract and therefore reduces the incidence of injured people is
nosocomial pneumonia. diminished integrity
NUTRITIONAL ASSESSMENT
of the gut...Many
researchers...have
The assessment of the nutritional state in the shown that a
critically ill is difficult. Many parameters such
as clinical (serum and urinalysis) and anthro-
compromise of the
pometric measurements exist which are epi- gastrointestinal tract
demiologically useful and correlate with mor- plays a role in the
bidity and mortality (Garrard et al, 1996).
Unfortunately, no single measurement is of
pathogenesis of
consistent value in predicting malnutrition or infection in the
’
risk of complications in individual patients. critically ill
In the critically ill, a patient’s body weight is
not a very reliable sign of weight loss, as its
patient...
importance can be obscured by oedema.
The measurement of serum albumin levels is
also a relatively insensitive indicator of nutri-
tion status (Horwood, 1990) as a fall in levels
are usually the consequence of its metabolism,
and reflects the severity and duration of stress
rather than the nutritional status. Although it
is dependent on the iron status, transferrin has
a better response to nutritional repletion,
while pre-albumin and retinol-binding pro-
tein, both of which have short half-lives, are
useful for following the efficacy of nutritional
support (Webb et al, 1999).
Many empirical formulas and nomograms
exist for the calculation of basal metabolic rate
(BMR), the best known being the Harris-
Benedict equation, established from studies on
healthy adults and children (Table 3). The use
of such equations is associated with a number
of problems. The ideal height and weight is
infrequently known for the critically ill patient,
leading to errors in the baseline calculation.
It could be concluded that, to date, a reliable
hospital test to assess nutritional status does
539
 NUTRITION
not exist. Therefore, it is important to conduct
thorough assessments on every patient observ-
ing him/her for muscle wasting, oedema, skin
changes and inspecting the condition of the
patient’s mouth and hair. A nutritional history
may be obtained from the patient’s family,
which could provide information about weight
loss or gain, eating patterns, diet restrictions
and bowel habits (Zainal, 1994).
DELAYS IN FEEDING
There are a number of factors which may limit
the achievement of prescribed nutritional
intake. Byers and Block (1995) investigated the
predictive factors for critically ill patients unable
to take regular oral intake for five consecutive
days. He concluded that the positive risk factors
were the need for neurosurgery, endotracheal
intubation, pelvic fracture, laparotomy and
emergency surgery. Surprisingly, body mass
index had little effect. On admission to the ICU
the primary considerations are the heamody-
namic and oxygenation status of the patient.
Garrard et al (1996) suggest that even after the
patient has been stabilized, feeding may be
delayed for a further 12–48 hours for three
common reasons (Table 4).
The inadequate provision of artificial nutri-
tion may occur for a variety of reasons in ICUs.
Patients receiving either parenteral or enteral
feed may be subject to fluid restrictions and
therefore the rate of feed may be reduced to lev-
els which do not fulfil their nutritional require-
Table 3. Equation for calculating BMR (basal metabolic rate)
The Harris-Benedict equation
Men: EE = 66.5 + 13.7W + 5.00H – 6.78A
Women: EE = 66.5 + 9.56W + 1.85H – 4.68A
Injury factors Minor operation x 1.2
Trauma x 1.3
Sepsis x 1.6
Severe burns x 2.10
W = weight; H = height; A = age (years); EE = energy expenditure
Table 4. Common reasons for delays in feeding
A delay in the prescription of feed
Staff failure to recognize the importance of nutritional support
and unaware of the consequences of malnutrition
Late prescription of total parenteral nutrition when enteral nutrition
is poorly tolerated
540
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ments. A wide variety of commercially prepared
feeds are available which have different sources
and concentrations of protein, carbohydrate
and fat. Consequently, they differ in calorie den-
sity, ranging from 1 kcal/ml to 2 kcal/ml. High
density feeds should be considered for patients
in which feeding is frequently interrupted or dif-
ficult to establish (Buckley and MacFie, 1997).
CRITICALLY ILL PATIENTS
Critically ill patients, particularly if they have
had recent surgery or are sedated and artifi-
cially ventilated, are often thought to have a
paralytic ileus due to a decrease in gastric
absorption, which is caused by a reduction in
smooth muscle contraction. Raper and
Maynard (1992) suggest that the vast major-
ity of patients at their hospital were able to
tolerate nutrition by the nasogastric route or
directly into the small intestine, regardless of
the presence of bowel sounds.
Occasionally, patients may not absorb enter-
al feed and this may lead to abdominal disten-
sion, regurgitation, vomiting and possible pul-
monary aspiration because of high residual
gastric volumes (RGV). The causes of the delay
in gastric emptying include the administration
of opiate, the use of low dose dopamine and
possibly other catecholamine infusions, poor
gastric perfusion, electrolyte and fluid abnor-
mality and the response to stress and pain
(Goldhill, 1997). Nursing assessment of the
absorption of feed by monitoring RGV, vigi-
lance with regard to distension and reflux and
appropriate alteration in feed rates are impor-
tant factors in minimizing the complications of
feed intolerance (Viney, 1996).
The most frequently cited amount of RGV
that should cause concern in the critically ill
patient is 150–200 ml in gastric feeding and
100 ml with intestinal feeding (Adam, 1994). It
is suggested that the feed rate should be
reduced (10 ml/hr is the minimal rate necessary
for gastrointestinal mucosal protection; Hall et
al, 1996) and where regurgitation remains a
problem medical advice on the need for an
intestinal tube or total parenteral nutrition
should be sought. Gastrokinetic agents such as
cisapride, metoclopramide or domperidone can
be given in an attempt to speed the return of
gastric emptying.
The traditional nasogastric tube is placed
in one of the least tolerant areas of the gut,
the stomach. As previously stated, gastric
BRITISH JOURNAL OF NURSING, 2000, VOL 9, NO 9
 MALNUTRITION IN CRITICALLY ILL PATIENTS IN INTENSIVE CARE UNITS
motility is affected by many factors which
may cause dysfunction and intolerance of
feed. Nasojejunal feeding is becoming a more
popular practice, as it is a less sensitive area
of the gut, which is likely to absorb feed long
after gastroparesis occurs.
The onset of diarrhoea is often attributed
to the administration of enteral nutrition and
it is common practice in this situation to cease
enteral nutrition (Bowling et al, 1993).
Diarrhoea frequently occurs in critically ill
patients, but it should not be assumed to be
caused by feed intolerance, as there are many
other causes, e.g. antibiotic therapy or
hypoalbuminaemia. Therefore, until aetiolo-
gy has been clearly established feeding should
not be disrupted (Verity, 1996).
FUTURE INVESTIGATIONS
Whether nutritional support has a positive
effect on outcome in the critically ill has proved
to be difficult as the aetiology of the underlying
illness is frequently multifactorial (Hayland et
al, 1993). Thus, any controlled trials would
require a large number of patients with similar
underlying pathology. Further problems occur
in the stratification of patients, as it would not
be considered ethical to place patients in the ‘no
feeding’ category. However, a number of ran-
domized, controlled clinical trials have been
performed with regard to nutritional support,
but few were aimed specifically at the critically
ill, and the majority enrolled small sample sizes
(Lee et al, 1990; Kudst et al, 1992).
Despite a lack of data from randomized
clinical trials, significant insight can be drawn
from our understanding of the physiology of
starvation and nutrition in critical illness.
CONCLUSION
The provision of nutritional support should
be regarded as a quintessential aspect of the
management of critically ill patients. In order
to give critically ill patients the best possible
chance of survival, ICU staff need to be aware
of recent developments in clinical nutrition
and adopt a multidisciplinary approach to
nutrition to achieve the best possible outcome
for patients in ICU. The formation of a nutri-
tional support team comprising a doctor,
pharmacist, dietician and nurse would help to
highlight potential problems associated with
nutrition in each individual trust and offer
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strategies to overcome them (Lennard-Jones,
1992). It also would enable the importance of
nutrition to be brought to the attention of the
intensive care team.
Those caring for critically ill patients need
to question their own knowledge regarding
the physiology of malnutrition and the latest
developments and research that provide opti-
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