Bailey & Love Bailey & Love Bailey & Love
19
Bailey & Love Bailey & Love Bailey & Love
Chapter
Nutrition and fluid therapy
Learning objectives
To understand:
•• The causes and consequences of malnutrition in the
surgical patient
•• Fluid and electrolyte requirements in the pre- and
postoperative patient
INTRODUCTION
Malnutrition is common. It occurs in about 30% of surgical
patients with gastrointestinal disease and in up to 60% of those
in whom hospital stay has been prolonged because of postop-
erative complications. It is frequently unrecognised and con-
sequently patients often do not receive appropriate support.
There is a substantial body of evidence to show that patients
Figure 19.1  Severely malnourished patient with wasting of fat and
muscle.
Carl Ferdinand Cori, 1896–1984, Professor of Pharmacology and later Biochemistry, Washington University Medical School, St Louis, MI, USA and his wife
Gerty Theresa Cori, 1896–1957, also Professor of Biochemistry at the Washington University Medical School. In 1947, the Coris were awarded a share of the
Nobel Prize for Physiology or Medicine for their discovery of how glycogen is catalytically converted.
03_19-B&L27_Pt3_Ch19.indd 278
•• The nutritional requirements of surgical patients and the
nutritional consequences of intestinal resection
•• The different methods of providing nutritional support
and their complications
who suffer starvation or have signs of malnutrition have a
higher risk of complications and an increased risk of death
in comparison with patients who have adequate nutritional
reserves.
Long-standing protein–calorie malnutrition as seen in
cachexia or general frailty is easy to recognise (Figure 19.1).
Short-term undernutrition, although less easily recognised,
frequently occurs in association with critical illness, major
trauma, burns or surgery, and also impacts on patient recov-
ery. The aim of nutritional support is to identify those patients
at risk of malnutrition and to ensure that their nutritional
requirements are met by the most appropriate route and in a
way that minimises complications.
PHYSIOLOGY
Metabolic response to
starvation
After a short fast, lasting 12 hours or less, most food from the
last meal will have been absorbed. Plasma insulin levels fall
and glucagon levels rise, which facilitates the conversion of
liver glycogen (approximately 200 g) into glucose. The liver,
therefore, becomes an organ of glucose production under fast-
ing conditions. Many organs, including brain tissue, red and
white blood cells and the renal medulla, can initially utilise
only glucose for their metabolic needs. Additional stores of
glycogen exist in muscle (500 g), but these cannot be utilised
directly. Muscle glycogen is broken down (glycogenolysis)
and converted to lactate, which is then exported to the liver
where it is converted to glucose (Cori cycle). With increasing
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ve duration of fasting (>24 hours), glycogen stores are depleted
and de novo glucose production from non-carbohydrate pre-
cursors (gluconeogenesis) takes place, predominantly in the
liver. Most of this glucose is derived from the breakdown of
amino acids, particularly glutamine and alanine as a result of
catabolism of skeletal muscle (up to 75 g per day). This pro-
tein catabolism in simple starvation is readily reversed with
the provision of exogenous glucose.
With more prolonged fasting, there is an increased reli-
ance on fat oxidation to meet energy requirements. Increased
breakdown of fat stores occurs, providing glycerol, which can
be converted to glucose, and fatty acids, which can be used as
a tissue fuel by almost all of the body’s tissues. Hepatic pro-
duction of ketones from fatty acids is facilitated by low insulin
levels and, after 48–72 hours of fasting, the central nervous
system may adapt to using ketone bodies as their primary fuel
source. This conversion to a ‘fat fuel economy’ reduces the
need for muscle breakdown by up to 55 g per day.
Another important adaptive response to starvation is a
significant reduction in the resting energy expenditure, pos-
sibly mediated by a decline in the conversion of inactive
thyroxine (T4) to active tri-iodothyronine (T3). Despite
these adaptive responses, there remains an obligatory glucose
requirement of about 200 g per day, even under conditions of
prolonged fasting.
Summary box 19.1
Metabolic response to starvation
●● Low plasma insulin
●● High plasma glucagon
●● Hepatic glycogenolysis
●● Protein catabolism
●● Hepatic gluconeogenesis
●● Lipolysis: mobilisation of fat stores (increased fat oxidation) –
overall decrease in protein and carbohydrate oxidation
●● Adaptive ketogenesis
●● Reduction in resting energy expenditure (from approximately
25–30 kcal/kg per day to 15–20 kcal/kg per day
Metabolic response to trauma and
sepsis
This is described in full in Chapter 1 and summarised in Sum-
mary box 19.2.
From a nutritional point of view, two factors deserve
emphasis. First, in contrast to simple starvation, patients
with trauma have impaired formation of ketones, and the
breakdown of protein to synthesise glucose (gluconeogen-
esis) cannot be entirely prevented by the administration of
glucose. Second, although it is generally accepted that the
metabolic response to trauma and sepsis is always associated
with ‘hypermetabolism’ or hypercatabolism’, these terms are
ill defined and do not indicate the need for very high-energy
intakes. There is no evidence to show that the provision
de novois Latin for ‘from the beginning’.
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Nutritional assessment 279
Summary box 19.2
Metabolic response to trauma and sepsis
●● Increased counter-regulatory hormones: adrenaline,
noradrenaline, cortisol, glucagon and growth hormone
●● Increased energy requirements (up to 40 kcal/kg per day)
●● Increased nitrogen requirements
●● Insulin resistance and glucose intolerance
●● Preferential oxidation of lipids
●● Increased gluconeogenesis and protein catabolism
●● Loss of adaptive ketogenesis
●● Fluid retention with associated hypoalbuminaemia
of high-energy intake is associated with an amelioration of
the catabolic process and it may indeed be harmful; there is
mounting evidence for the benefits of permissive underfeed-
ing in critically ill surgical patients.
NUTRITIONAL ASSESSMENT
Laboratory techniques
There is no single biochemical measurement that reliably
identifies malnutrition. Albumin is not a measure of nutri-
tional status, particularly in the acute setting. Although a low
serum albumin level (<30 g/L) is an indicator of poor prog-
nosis, hypoalbuminaemia invariably occurs because of alter-
ations in body fluid composition and because of increased
capillary permeability related to ongoing sepsis. Malnutri-
tion is associated with defective immune function, and mea-
surement of lymphocyte count and skin testing for delayed
hypersensitivity frequently reveal abnormalities in malnour-
ished patients. Immunity is not, however, a precise or reliable
indicator of nutritional status, nor is it a practical method in
routine clinical practice.
Body weight and anthropometry
A simple method of assessing nutritional status is to esti-
mate weight loss. Measured body weight is compared with
ideal body weight obtained from tables or from the patient’s
usual or ­premorbid weight. Unintentional weight loss of more
than 10% of a patient’s weight in the preceding 6 months is
a good prognostic indicator of poor outcome. Body weight is
­frequently corrected for height, allowing calculation of the
body mass index (BMI, defined as body weight in kilograms
divided by height in metres squared). A BMI of less than 18.5
indicates nutritional impairment and a BMI below 15 is asso-
ciated with significant hospital mortality. Major changes in
fluid balance, which are common in critically ill patients, may
make body weight and BMI unreliable indicators of nutritional
status.
Anthropometric techniques incorporating measurements
of skinfold thicknesses and mid-arm circumference per-
mit estimations of body fat and muscle mass, and these are
indirect measures of energy and protein stores. These mea-
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280 CHAPTER 19  Nutrition and fluid therapy

surements are, however, insufficiently accurate in individual FLUID AND ELECTROLYTES

patients to permit planning of nutritional support regimens.
Similarly, use of bioelectrical impedence analysis (BIA) per- Fluid intake is derived from both exogenous (consumed liq-
mits estimation of intra- and extracellular fluid volumes. uids) and endogenous (released during oxidation of solid
These techniques are only useful if performed frequently on a foodstuffs) fluids. The average daily water balance of a healthy
sequential basis in individual patients; in this respect, trends adult is shown in Table 19.1.
are much more important than absolute impedance figures.
All of these techniques are significantly impaired by the pres- TABLE 19.1  Average daily water balance of a healthy
ence of oedema. adult in a temperate climate (70 kg).
Output Volume (mL) Intake Volume (mL)
Clinical Urine 1500 Water from 200
The possibility of malnutrition should form part of the beverage
workup of all patients. A clinical assessment of nutritional Insensible 900 Water from food 1000
status involves a focused history and physical examination, losses
an assessment of risk of malabsorption or inadequate dietary Faeces 100 Water from 300
intake and selected laboratory tests aimed at detecting spe- oxidation
cific nutrient deficiencies. This is termed ‘subjective global
assessment’ and encompasses historical, symptomatic and Fluid losses occur by four routes:
physical parameters. Recently, the British Association of
Parenteral and Enteral Nutrition introduced a malnutrition 1 Lungs. About 400 mL of water is lost in expired air
universal screening tool (MUST), which is a five-step screen- each 24 hours. This is increased in dry atmospheres or in
ing tool to identify adults who are malnourished or at risk of patients with a tracheostomy, emphasising the importance
undernutrition (Figure 19.2). of humidification of inspired air.

The MUST tool

(iii) Acute disease effect
(i) BMI (kg/m2) (ii) Weight loss in 3–6 months
Add a score of 2 if there
0 = 20.0 0 = 5% has been or is likely to be
1 = 18.5–2.0 1 = 5–10% no or very little nutritional
2 = 18.5 2 = 10% intake for 5 days

Add scores

Overall risk of undernutrition*

0 1 2 or more
Low Medium High

Routine clinical Observe Treat

care†
Repeat screening
Hospital – every week
Care homes – every month
Community – every year for
special groups, e.g. those
75 years
Hospital – document dietary
and fluid intake for 3 days
Care homes (as for hospital)
Community – repeat screening,
e.g. from 1 month to 6 months
(with dietary advice if necessary)
Hospital – refer to dietician or
implement local policies.
Generally food first followed
by food fortification and
supplements
Care homes (as for hospital)
Community (as for hospital)

*If height, weight or weight loss cannot be established, use documented or recalled
Figure 19.2  The malnutrition uni-
values (if considered reliable). When measured or recalled height cannot be
versal screening tool (MUST) for
obtained, use knee height as a surrogate measure.
adults (adapted from Elia M (ed.).
If neither can be calculated, obtain an overall impression of malnutrition risk
The MUST Report. Development
(low, medium, high) using the following: and use of the ‘malnutrition uni-
(i) Clinical impression (very thin, thin, average, overweight); versal screening tool’ (MUST) for
(iia) Clothes and/or jewellery have become loose fitting; adults. A report by the Malnutrition
(iib) History of decreased food intake, loss of appetite or dysphagia up to 3–6 months; Advisory Group of the British Asso-
(iic) Disease (underlying cause) and psychosocial/physical disabilities likely to cause weight loss. ciation for Parenteral and Enteral
† Involves treatment of underlying condition, and help with food choice and eating Nutrition. Report No. 152, 2003,
when necessary (also applies to other categories). ISBN 1 899467 70X).

Marinos Elia, contemporary, Head of the Adult Clinical Nutrition Group, The Medical Research Council, Cambridge, UK.

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Nutritional requirements 281

2 Skin. In a temperate climate, skin (i.e. sweat) losses are examination to assess hydration status (peripheries, skin
between 600 and 1000 mL/day. turgor, urine output and specific gravity of urine), urine
3 Faeces. Between 60 and 150 mL of water are lost daily in and serum electrolytes and haematocrit.
patients with normal bowel function. ●● Estimation of losses already incurred and their nature: for
4 Urine. The normal urine output is approximately 1500 mL/ example, vomiting, ileus, diarrhoea, excessive sweating or
day and, provided that the kidneys are healthy, the specific fluid losses from burns or other serious inflammatory con-
gravity of urine bears a direct relationship to volume. A ditions.
minimum urine output of 400 mL/day is required to excrete ●● Estimation of supplemental fluids likely to be required
the end products of protein metabolism. in view of anticipated future losses from drains, fistulae,
Maintenance fluid requirements are calculated approxi- nasogastric tubes or abnormal urine or faecal losses.
mately from an estimation of insensible and obligatory losses. ●● When an estimate of the volumes required has been made,
Various formulae are available for calculating fluid replace- the appropriate replacement fluid can be determined from
ment based on a patient’s weight or surface area. For example, a consideration of the electrolyte composition of gastro-
30–40 mL/kg gives an estimate of daily requirements. intestinal secretions. Most intestinal losses are adequately
The following are the approximate daily requirements of replaced with normal saline containing supplemental
some electrolytes in adults: potassium (Table 19.3).
●● sodium: 50–90 mM/day;
●● potassium: 50 mM/day; TABLE 19.3 Composition of gastrointestinal secretions
●● calcium: 5 mM/day; (mmol/L).
●● magnesium: 1 mM/day. Na K Cl HCO3
The nature and type of fluid replacement therapy will be Saliva 10 25 10 30
determined by individual patient needs. The composition of Stomach 50 15 110 –
some commonly used solutions is shown in Table 19.2.
Duodenum 140 5 100 –
Note that Hartmann’s solution also contains lactate
29 mmol/L. Dextrose solutions are also commonly employed. Ileum 140 5 100 30
These provide water replacement without any electrolytes Pancreas 140 5 75 115
and with modest calorie supplements (1 litre of 5% dextrose Bile 140 5 100 35
contains 400 kcal). A typical daily maintenance fluid regimen
would consist of a combination of 5% dextrose with either
Hartmann’s or normal saline to a volume of 2 litres.
There has been much controversy in the literature NUTRITIONAL REQUIREMENTS
regarding the respective merits of crystalloid versus colloid Total enteral or parenteral nutrition necessitates the provi-
replacement. There is no consensus on this topic and the sion of the macronutrients, carbohydrate, fat and protein,
usual advice is to replace like with like. If the haematocrit together with vitamins, trace elements, electrolytes and
is below 21%, blood transfusion may be required. There is water. When planning a feeding regime, the patient should
increasing recognition, however, that albumin infusions are be weighed and an assessment made of daily energy and pro-
of little value. tein requirements. Standard tables are available to permit
In addition to maintenance requirements, ‘replacement’ these calculations.
fluids are required to correct pre-existing deficiencies and Daily needs may change depending on the patient’s condi-
‘supplemental’ fluids are required to compensate for antici-
tion. Overfeeding is the most common cause of complications,
pated additional intestinal or other losses. The nature and
regardless of whether nutrition is provided enterally or
volumes of these fluids are determined by:
parenterally. It is essential to monitor daily intake to provide
●● A careful assessment of the patient including pulse, blood an assessment of tolerance. In addition, regular biochemical
pressure and central venous pressure, if available. Clinical monitoring is mandatory (Table 19.4).

TABLE 19.2  Composition of crystalloid and colloid solutions (mmol/L).

Solution Na K Ca Cl Lactate Colloid
Hartmann’s 131 5 2 111 29
Normal saline (0.9% NaCl) 154 154
Dextrose saline (4% dextrose in 0.18% saline) 30 30
Gelofusine 150 150 Gelatin 4%
Haemacel 145 5.1 <1 145 Polygelin 75 g/L
Hetastarch Hydroxyethyl starch 6%

Alexis Frank Hartmann, 1898–1964, paediatrician, St Louis, MO, USA.

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282 CHAPTER 19  Nutrition and fluid therapy
TABLE 19.4 Monitoring feeding regimes.
Daily Body weight
Fluid balance
Full blood count, urea and electrolytes
Blood glucose
Electrolyte content and volume of urine
  and/or urine and intestinal losses
Temperature
Weekly (or more Urine and plasma osmolality
frequently if Calcium, magnesium, zinc and phosphate
clinically indicated) Plasma proteins including albumin
Liver function tests including clotting factors
Thiamine
Acid–base status
Triglycerides
Fortnightly Serum vitamin B12
Folate
Iron
Lactate
Trace elements (zinc, copper, manganese)
Macronutrient requirements
Energy
The total energy requirement of a stable patient with a normal
or moderately increased need is approximately 20–30 kcal/kg
per day. Very few patients require energy intakes in excess of
2000 kcal/day. Thus, in the majority of hospitalised patients in
whom energy demands from activity are minimal, total energy
requirements are approximately 1300–1800 kcal/day.
Carbohydrate
There is an obligatory glucose requirement to meet the needs
of the central nervous system and certain haematopoietic
cells, which is equivalent to about 2 g/kg per day. In addition,
there is a physiological maximum to the amount of glucose
that can be oxidised, which is approximately 4 mg/kg per
minute (equivalent to about 1500 kcal/day in a 70-kg person),
with the nonoxidised glucose being primarily converted to
fat. However, optimal utilisation of energy during nutritional
support is ensured by avoiding the infusion of glucose at rates
approximating physiological maximums. Plasma glucose
levels provide an indication of tolerance. Avoid hyperglycae-
mia. Provide energy as mixtures of glucose and fat. Glucose is
the preferred carbohydrate source.
Fat
Dietary fat is composed of triglycerides of predominantly four
long-chain fatty acids. There are two saturated fatty acids
(palmitic (C16) and stearic (C18)) and two unsaturated fatty
acids (oleic (C18 with one double bond) and linoleic (C18
with two double bonds)). In addition, smaller amounts of lin-
olenic acid (C18 with three double bonds) and medium-chain
fatty acids (C6–C10) are contained in the diet.
The unsaturated fatty acids, linoleic and linolenic acid,
are considered essential because they cannot be synthesised
in vivo from non-dietary sources. Both soybean and sunflower
in vivois Latin for ‘in a living thing’.
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oil emulsions are rich sources of linoleic acid and provision of
only 1 litre of emulsion per week avoids deficiency. Soybean
emulsions contain approximately 7% alpha-linolenic acid
(an omega-3 fatty acid). The provision of fat as a soybean
oil-based emulsion on a regular basis will obviate the risk of
essential fatty acid deficiency.
Safe and non-toxic fat emulsions based upon long-chain
triglycerides (LCTs) have been commercially available for
over 30 years. These emulsions provide a calorically dense
product (9 kcal/g) and are now routinely used to supplement
the provision of non-protein calories during parenteral nutri-
tion. Energy during parenteral nutrition should be given as
a mixture of fat together with glucose. There is no evidence
to suggest that any particular ratio of glucose to fat is opti-
mal, as long as under all conditions the basal requirements for
glucose (100–200 g/day) and essential fatty acids (100–200
g/week) are met. This ‘dual energy’ supply minimises meta-
bolic complications during parenteral nutrition, reduces fluid
retention, enhances substrate utilisation (particularly in the
septic patient) and is associated with reduced carbon dioxide
production.
Concerns have been expressed about the possible immu-
nosuppressive effects of LCT emulsions. These are more
likely to occur if the recommended infusion rates (0.15 g/kg
per hour) are exceeded. Nonetheless, these concerns have
prompted the development of newer emulsions based upon
medium-chain triglycerides, omega-3 fatty acids and, most
recently, structured triglycerides, which combine long and
medium-chain triglycerides in the same emulsion. The evi-
dence of clinical benefit for these emulsions compared with
conventional LCTs is tenuous, particularly if infusion rates
are appropriate and hypertriglyceridaemia is avoided.
Protein
The basic requirement for nitrogen in patients without
pre-­existing malnutrition and without metabolic stress is
0.10–0.15 g/kg per day. In hypermetabolic patients the nitro-
gen requirements increase to 0.20–0.25 g/kg per day. Although
there may be a minority of patients in whom the requirements
are higher, such as after acute weight loss when the objec-
tive of therapy is longterm repletion of lean body mass, there
is little evidence that the provision of nitrogen in excess of
14 g/day is beneficial.
Vitamins, minerals and trace elements
Whatever the method of feeding, these are all essential com-
ponents of nutritional regimes. The water-soluble vitamins
B and C act as coenzymes in collagen formation and wound
healing. Postoperatively, the vitamin C requirement increases
to 60–80 mg/day. Supplemental vitamin B12 is often indi-
cated in patients who have undergone intestinal resection or
gastric surgery and in those with a history of alcohol depen-
dence. Absorption of the fat-soluble vitamins A, D, E and K
is reduced in steatorrhoea and the absence of bile.
Sodium, potassium and phosphate are all subject to signi­
ficant losses, particularly in patients with diarrhoeal illness.
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Their levels need daily monitoring and appropriate replace-
ment.
Trace elements may also act as cofactors for metabolic
processes. Normally, trace element requirements are met
by the delivery of food to the gut and so patients on long-
term parenteral nutrition are at particular risk of depletion.
Magnesium, zinc and iron levels may all be decreased as part
of the inflammatory response. Supplementation is necessary
to optimise utilisation of amino acids and to avoid refeeding
syndrome.
FLUID AND NUTRITIONAL
CONSEQUENCES OF
INTESTINAL RESECTION
Up to 50% of the small intestine can be surgically removed
or bypassed without permanent deleterious effects. With
extensive resection (<150 cm of remaining small intestine),
metabolic and nutritional consequences arise, resulting in the
disease entity known as short bowel syndrome. The clinical
presentation of patients with short bowel syndrome is depen-
dent upon the site and extent of intestinal resection.
Small bowel motility
Small bowel motility is three times slower in the ileum than
in the jejunum. In addition, the ileocaecal valve may slow
transit. The adult small bowel receives 5–6 litres of endog-
enous secretions and 2–3 litres of exogenous fluids per day.
Most of this is reabsorbed in the small bowel. In the jeju-
num, the cellular junctions are leaky and jejunal contents are
always isotonic. Fluid absorption in this region of bowel is
inefficient compared with the ileum. It has been estimated
that the efficiency of water absorption is 44% and 70% of
the ingested load in the jejunum and ileum, respectively. The
corresponding figures for sodium are 13% and 72%, respec-
tively. It can be seen, therefore, that the ileum is critical in
the conservation of fluid and electrolytes.
Ileum
The ileum is the only site of absorption of vitamin B12 and
bile salts. Bile salts are essential for the absorption of fats and
fat-soluble vitamins. The enterohepatic circulation of bile
salts is critical to maintain the bile salt pool. Following resec-
tion of the ileum, the loss of bile salts increases and is not met
by an increase in synthesis. Depletion of the bile salt pool
results in fat malabsorption. In addition, loss of bile salts into
the colon affects colonic mucosa, causing a reduction in salt
and water absorption, which increases stool losses.
Colon
Transit times in the colon vary between 24 and 150 hours.
The efficiency of water and salt absorption in the colon
exceeds 90%. Another important colonic function is the
fermentation of carbohydrates to produce short-chain fatty
acids. These have two important functions: first, they enhance
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Fluid and nutritional consequences of intestinal resection 283
water and salt absorption from the colon and, second, they are
trophic to the colonocyte.
Effects of resection
Resection of proximal jejunum results in no significant alter-
ations in fluid and electrolyte levels as the ileum and colon
can adapt to absorb the increased fluid and electrolyte load.
Absorption of nutrients occurs throughout the small bowel,
and resection of jejunum alone results in the ileum taking over
this lost function. In this situation, there is no m
­ alabsorption.
Resection of ileum results in a significant enhancement
of gastric motility and acceleration of intestinal transit. Fol-
lowing ileal resection, the colon receives a much larger vol-
ume of fluid and electrolytes and it also receives bile salts,
which reduce its ability to absorb salt and water, resulting
in diarrhoea. Even the loss of 100 cm of ileum may cause
steatorrhoea, which can necessitate the administration of
­
oral cholestyramine to bind bile salts. With larger resections
(>100 cm) dietary fat restriction may be necessary. Regular
parenteral vitamin B12 is required.
The most challenging patients are those with short bowel
syndrome who have had in excess of 200 cm of small bowel
resected together with colectomy. These patients will usually
have a jejunostomy. They are conveniently divided into two
groups termed ‘net absorbers’ and ‘net secretors’. Absorbers
characteristically have more than 100 cm of residual jejunum
and they absorb more water and sodium from the diet than
passes through the stomach. These patients can be managed
without supplementary parenteral fluids.
Secretors usually have less than 100 cm of residual jeju-
num and lose more water and sodium from their stoma than
they take by mouth. These patients require supplements.
Their usual daily jejunostomy output may exceed 4 litres per
24 hours. The sodium content of jejunostomy losses or other
high-output fistulae is about 90 mmol/L. Jejunal mucosa is
leaky and rapid sodium fluxes occur across it. If water or any
solution with a sodium concentration of less than 90 mmol/L
is consumed, there is a net efflux of sodium from the plasma
into the bowel lumen. It is therefore inappropriate to encour-
age patients with high-output jejunostomies (secretors) to
drink large amounts of oral hypotonic solutions. Treatment
begins with restricting the total amount of hypotonic fluids
(water, tea, juices, etc.) consumed to less than 1 litre a day.
Patients should be encouraged to take glucose and saline
replacement solutions, which have a sodium concentration of
at least 90 mmol/L. The World Health Organization (WHO)
cholera solution has a sodium concentration of 90 mmol/L
and is commonly used.
Complications of short bowel syndrome include peptic
ulceration related to gastric hypersecretion, cholelithiasis
because of interruption of the enterohepatic cycle of bile
salts and hyperoxaluria as a result of the increased absorption
of oxalate in the colon predisposing to renal stones. Some
patients with short bowel syndrome develop a syndrome of
slurred speech, ataxia and altered affect. The cause of this syn-
drome is fermentation of malabsorbed carbohydrates in the
colon to d-lactate and absorption of this metabolite. Treat-
ment necessitates the use of a low carbohydrate diet.
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284 CHAPTER 19  Nutrition and fluid therapy
Anti-secretory drugs reduce the amount of fluid secreted
from the stomach, liver and pancreas. These include
H2-receptor antagonists, proton pump inhibitors and the
somatostatin analogue octreotide. Octreotide also reduces
gastrointestinal motility, while proton pump inhibitors lower
gastric pH sufficiently to decrease the need for neutralisation
of acid in the duodenum and proximal jejunum. This results
in significant lowering of high jejunostomy outputs and dos-
age should be titrated against stoma effluent pH for optimal
results. Anti-motility drugs include loperamide and codeine
phosphate, which also decrease water and sodium output from
the stoma by about 20%.
ARTIFICIAL NUTRITIONAL
SUPPORT
The indications for nutritional support are simple. Any
patient who has sustained 5 days of inadequate intake or who
is anticipated to have no or inadequate intake for this period
should be considered for nutritional support. The periods may
be less in patients with pre-existing malnutrition. This con-
cept is important because it emphasises that the provision of
nutritional support is not specific to certain conditions or dis-
eases. Although patients with Crohn’s disease or pancreatitis,
or those who have undergone gastrointestinal resections, may
frequently require nutritional support, it is the fact that they
have had inadequate intakes for defined periods that is the
indication rather than the specific disease process.
Nasogastric/
duodenal/jejunal
tube
Whole food
PPN TPN
by mouth
Gastrostomy
tube
Jejunostomy
tube
Figure 19.3  Techniques used for adjuvant nutritional support. PPN,
partial parenteral nutrition; TPN, total parenteral nutrition. Redrawn
with permission from Rick Tharp, rxkinetics.com.
ad libitumis Latin for ‘freely or as much as you wish’.
John Alfred Ryle, 1889–1950, Regius Professor of Medicine, Cambridge U
­ niversity and later Professor of Social Medicine, Oxford University, Oxford, UK, intro-
duced the Ryle’s tube in 1921.
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Enteral nutrition
The term ‘enteral feeding’ means delivery of nutrients into
the gastrointestinal tract. The alimentary tract should be
used whenever possible. This can be achieved with normal
food, oral supplements (sip feeding) or with a variety of tube-
feeding techniques delivering food into the stomach, duo­
denum or jejunum.
A variety of nutrient formulations are available for enteral
feeding. These vary with respect to energy content, osmolar-
ity, fat and nitrogen content and nutrient complexity; most
contain up to 1–2 kcal/mL and up to 0.6 g/mL of protein.
Polymeric feeds contain intact protein and hence require
digestion, whereas monomeric/elemental feeds contain nitro-
gen in the form of either free amino acids or, in some cases,
peptides. These are less palatable and are used much less fre-
quently than in previous years. Newer feeding formulations
are available that include glutamine and fibre to optimise
intestinal nutrition, or immunonutrients such as arginine and
fish oils, but these are expensive and their use is controversial.
Sip feeding
Commercially available supplementary sip feeds are used in
patients who can drink but whose appetites are impaired or
in whom adequate intakes cannot be maintained with ad
libitum intakes. These feeds typically provide 200 kcal and
2 g of nitrogen per 200 mL carton. There is good evidence
to demonstrate that these sip-feeding techniques are associ-
ated with a significant overall increase in calorie and nitrogen
intakes without detriment to spontaneous nutrition. The evi-
dence that these techniques improve patient outcomes is less
convincing.
Tube-feeding techniques
Enteral nutrition can be achieved using conventional naso­
gastric tubes (Ryle’s), fine-bore feeding tubes inserted into
the stomach, surgical or percutaneous endoscopic gastros-
tomy (PEG) or, finally, postpyloric feeding utilising nasoje-
junal tubes or various types of jejunostomy (Figure 19.3).
The choice of method will be determined by local circum-
stances and preference in many patients. Whichever method
is adopted, it is impor­tant that tube feeding is supervised
by an experienced dietician who will calculate the patient’s
requirements and aim to achieve these within 2–3 days of the
instigation of feeds. Conventionally, 20–30 mL are admin-
istered per hour initially, gradually increasing to goal rates
within 48–72 hours. In most units, feeding is discontinued for
4–5 hours overnight to allow gastric pH to return to normal.
There is some evidence that this might reduce the incidence
of nosocomial pneumonia and aspiration. There is good evi-
dence to confirm that feeding protocols optimise the toler-
ance of enteral nutrition. In these, aspirates are performed
on a regular basis and if they exceed 200 mL in any 2-hour
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Artificial nutritional support 285

period, then feeding is temporarily discontinued or the rate of

feed administration is diminished.
Tube blockage is common. All tubes should be flushed
with water at least twice daily. If a buildup of solidified diet
occurs, instillation into the tube of agents such as chymotryp-
sin may salvage a partially obstructed tube. Guidewires should
not be used to clear blockages as these may perforate the tube
and cause contiguous damage.
Nasogastric tubes are appropriate in a majority of patients.
If feeding is maintained for more than a week or so, a fine-
bore feeding tube is preferable and is likely to cause fewer gas-
tric and oesophageal erosions. These are usually made from
soft polyurethane or silicone elastomer and have an internal
diameter of <3 mm.

Fine-bore tube insertion

The patient should be semi-recumbent. The introducer wire is
lubricated and inserted into the fine-bore tube (Figure 19.4).
The tube is passed through the nose and into the stomach via
the nasopharynx and oesophagus. The wire is withdrawn and
the tube is taped to the patient. There is a small risk of mal-
position into a bronchus or of causing pneumothorax. The
position of the tube should be checked using plain abdominal
radiography (Figure 19.5). Confirmation of position by pH Figure 19.5 Radiograph of a tube similar to that in Figure 19.4
testing is possible but limited by the difficulty of obtaining a inserted beyond the duodenojejunal flexure.
fluid aspirate with narrow lumen tubes.

Figure 19.6  Percutaneous endoscopic gastrostomy tube.

endoscopic control using local anaesthesia, known as PEG

Figure 19.4  A fine-bore feeding tube with its guidewire.
Gastrostomy
The placement of a tube through the abdominal wall directly
into the stomach is termed ‘gastrostomy’. Historically, these
were created surgically at the time of laparotomy. Today,
the majority are performed by percutaneous insertion under
(percutaneous endoscopic gastrostomy) tubes (Figure 19.6).
Two methods of PEG are commonly used. The first is
called the ‘direct-stab’ technique in which the endoscope is
passed and the stomach filled with air. The endoscopist then
watches a cannula entering the stomach having been inserted
directly through the anterior abdominal wall. A guidewire is
then passed through the cannula into the stomach. A gastros-
tomy tube (commercially available) may then be introduced
into the stomach through a ‘peel away’ sheath. The alterna-
tive technique is the transoral or push-through technique,
whereby a guidewire or suture is brought out of the stomach
by the endoscope after transabdominal percutaneous inser-
tion and is either attached to a gastrostomy tube or the tube
is pushed over a guidewire. The abdominal end of the wire

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 PART 3 | PERIOPERATIVE CARE
286 CHAPTER 19  Nutrition and fluid therapy
is then pulled, advancing the gastrostomy tube through the
oesophagus and into the stomach. Continued pulling abuts it
up against the abdominal wall.
If patients require enteral nutrition for prolonged periods
(4–6 weeks), then PEG is preferable to an indwelling nasoga-
stric tube; this minimises the traumatic complications related
to indwelling tubes. PEG does have procedure-specific com-
plications, although these are uncommon. Necrotising fasci-
itis and intra-abdominal wall abscesses have been recorded.
Sepsis around the PEG site is more common and may necessi-
tate systemic antibiotics or repositioning. A persistent gastric
fistula can occur on removal of a PEG if it has been in place
for prolonged periods and epithelialisation of the tract has
occurred. This necessitates surgical closure.
Jejunostomy
In recent years, the use of jejunal feeding has become increas-
ingly popular. This can be achieved using nasojejunal tubes
or by placement of needle jejunostomy at the time of lapa-
rotomy. Some authorities advocate the use of jejunostomies
on the basis that postpyloric feeding may be associated with
a reduction in aspiration or enhanced tolerance of enteral
nutrition. In particular, there are many advocates of jejunos-
tomies in patients with severe pancreatitis, in whom a degree
of gastric outlet obstruction may be present, related to the
oedematous head of pancreas. In most patients it is appropri-
ate to commence with conventional nasogastric feeding and
progress to postpyloric feeding if the former is unsuccessful.
Nasojejunal tubes often necessitate the use of fluoros-
copy or endoscopy to achieve placement, which may delay
commencement of feeding. Surgical jejunostomies, even
using commercially available needle-insertion techniques, do
involve creating a defect in the jejunum, which can leak or
be associated with tube displacement; both of these complica-
tions result in peritonitis.
Complications
Most complications of enteral nutrition can be avoided with
careful attention to detail and appropriate infusion rates.
Patients should be nursed semi-recumbent to reduce the
possibility of aspiration. Complications can be divided into
those resulting from intubation of the gastrointestinal tract
and those related to nutrient delivery. The former are more
frequent with more invasive means of gaining access to the
intestinal tract (see above under Enteral nutrition). The latter
include diarrhoea, bloating and vomiting. Diarrhoea occurs
in more than 30% of patients receiving enteral nutrition
and is particularly common in the critically ill. Up to 60%
of patients in intensive care units may fail to receive their
targeted intakes. There is no evidence that the incidence of
diarrhoea and bloating is reduced by the use of half-strength
feeds. It is important to introduce normal feeds at a reduced
rate according to patient tolerance. Metabolic complications
associated with excessive feeding are uncommon in enterally
fed patients. There have been reports of nosocomial enteric
infections associated with contamination of feeds, which
03_19-B&L27_Pt3_Ch19.indd 286
Summary box 19.3
Complications of enteral nutrition
●● Tube-related
Malposition
Displacement
Blockage
Breakage/leakage
Local complications (e.g. erosion of skin/mucosa)
●● Gastrointestinal
Diarrhoea
Bloating, nausea, vomiting
Abdominal cramps
Aspiration
Constipation
Metabolic/biochemical
●●
Electrolyte disorders
Vitamin, mineral, trace element deficiencies
Drug interactions
●● Infective
Exogenous (handling contamination)
Endogenous (patient)
should be kept in sealed containers at 4°C and discarded once
opened. In all patients, it is essential to monitor intakes accu-
rately as target intakes are often not achieved with enteral
nutrition.
The complications of enteral nutrition are summarised in
Summary box 19.3.
Parenteral nutrition
Total parenteral nutrition (TPN) is defined as the provision
of all nutritional requirements by means of the intravenous
route and without the use of the gastrointestinal tract.
Parenteral nutrition is indicated when energy and protein
needs cannot be met by the enteral administration of these
substrates. The most frequent clinical indications relate to
those patients who have undergone massive resection of the
small intestine, who have intestinal fistula or who have pro-
longed intestinal failure for other reasons.
Route of delivery: peripheral or
central venous access
TPN can be administered either by a catheter inserted in the
central vein or via a peripheral line. In the early days of paren-
teral nutrition, the only energy source available was hypertonic
glucose, which, being hypertonic, had to be given into a cen-
tral vein to avoid thrombophlebitis. In the second half of the
last century, there were a number of important developments
that have influenced the administration of parenteral nutri-
tion. These include the identification of safe and non-toxic
fat emulsions that are isotonic; pharmaceutical developments
that permit carbohydrates, fats and amino acids to be mixed
in single containers; and a recognition that the provision of
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energy during parenteral nutrition should be a mixture of glu-
cose and fat and that energy requirements are rarely in excess of
2000 kcal/day (25–30 kcal/kg per day). These changes enabled
the development of peripheral parenteral nutrition.
Peripheral
Peripheral feeding is appropriate for short-term feeding of up
to 2 weeks. Access can be achieved either by means of a dedi-
cated catheter inserted into a peripheral vein and manoeuvred
into the central venous system (peripherally inserted central
venous catheter (PICC) line) or by using a conventional short
cannula in the wrist veins. The former method has the advan-
tage of minimising inconvenience to the patient and clinician.
PICC lines have a mean duration of survival of 7 days. The
disadvantage is that when thrombophlebitis occurs, the vein
is irrevocably destroyed. In the alternative approach, intrave-
nous nutrients are administered through a short cannula in
wrist veins, infusing the patient’s nutritional requirements on
a cyclical basis over 12 hours. The cannula is then removed
and resited in the contralateral arm. Peripheral parenteral
nutrition has the advantage that it avoids the complications
associated with central venous administration, but suffers the
disadvantage that it is limited by the development of throm-
bophlebitis (Figure 19.7). Peripheral feeding is not indicated
if patients already have an indwelling central venous line or
in those in whom long-term feeding is anticipated.
New cannula inserted
Cannula removed Endothelial damage
Extravasation/pain
Venoconstriction
PVT cycle
Thrombus
(vein occlusion)
Drug/infusion
administered
Inflammation/thrombosis (further
venoconstriction)
Inflammatory and vasoactive
mediators
Figure 19.7 Cycle of causes of peripheral vein thrombophlebitis
(PVT) (after Payne-James J, Grimble G, Silk D (eds). Artificial nutri-
tion support in clinical practice, 2nd edn. London, Greenwich Medical
Media, 2001).
Central
When the central venous route is chosen, the catheter can
be inserted via the subclavian or internal or external jugular
vein. There is good evidence to show that the safest means
of establishing central venous access is by insertion of lines
John Jason Payne-James, contemporary forensic physician and medical writer, Leigh-on-Sea, Essex, UK.
Robert O Hickman, b.1929, formerly paediatric nephrologist, Seattle Childrens’ Hospital, Seattle, WA, USA.
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PART 3 | PERIOPERATIVE CARE
Artificial nutritional support 287
Figure 19.8  Infraclavicular subclavian line.
under ultrasound guidance; however, this will not be prac-
ticable for all cases. Most intensive care physicians and
­anaesthetists favour cannulation of internal or external jug-
ular veins as these vessels are easily accessible. They suffer
the disadvantage that the exit site is situated inconveniently
on the side of the neck, where repeated movements result in
disruption of the dressing with the attendant risk of sepsis.
The infraclavicular subclavian approach is more suitable for
feeding as the catheter then lies flat on the chest wall, which
optimises nursing care (Figure 19.8).
For longer-term parenteral nutrition, Hickman lines are
preferable. These are often inserted by a radiologist with flu-
oroscopic guidance or ultrasound. They incorporate a small
cuff, which sits at the exit site of a subcutaneous tunnel. This
is thought to minimise the possibility of line dislodgement and
reduce the possibility of line sepsis. Whichever technique is
employed, a postinsertion chest x-ray is essential before feed-
ing is commenced to confirm the absence of pneumothorax
and that the catheter tip lies in the distal superior vena cava,
to minimise the risk of central venous or cardiac thrombosis.
Multilumen catheters can be used for the administration of
TPN; one port should be employed for that sole purpose and
strict protocols of aseptic care employed.
An alternative technique for central intravenous access
allows the PICC technique under ultrasound guidance to can-
nulate the cephalic vein in the arm, which facilitates passage of
a catheter into the bracheocephalic vein or superior vena cava.
This has many advantages as it minimises the risks of insertion
and ensures distance between the site of skin entry and the tip
of the catheter. Thrombophlebitis, however, can occur.
Complications of parenteral
nutrition
The commencement of TPN may precipitate or accentuate
underlying nutrient deficiency by encouraging anabolism.
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288 CHAPTER 19  Nutrition and fluid therapy
Common metabolic complications include fluid overload,
hyperglycaemia, abnormalities of liver function and vitamin
deficiencies. Fluid overload can be avoided by daily weigh-
ing of the patient. A weight change of >1 kg/day normally
­indicates fluid retention. Hyperglycaemia is common because
of insulin resistance in critically ill patients. Even modest rates
of glucose administration may be associated with hyperglycae-
mia. Hyperglycaemic patients undergoing surgery are known
to run a substantially higher risk of infectious complications.
Abnormalities of liver enzymes are common in patients
who are receiving TPN. Although the precise mechanisms
are unclear, intrahepatic cholestasis may occur and hepatic
steatosis and hepatomegaly have been reported. Reducing the
fat content or infusion of fat-free TPN may be required. If
liver enzymes continue to deteriorate, TPN should be tempo-
rarily discontinued. In addition, overfeeding is a major factor
in hepatic and other metabolic complications associated with
TPN. Supplemental parenteral glutamine during parental
nutrition should be considered, particularly in the critically
ill patient.
Catheter-related sepsis occurs in 3–14% of patients. It
may occur at the time of line insertion or afterwards by migra-
tion of skin bacteria along the external catheter surface. Some
studies suggest that manoeuvring of the catheter hub due to
frequent manipulation is a common cause. Contamination
of the infusate is rare. Seeding on the catheter at the time
of bacteraemia from a remote source may also cause catheter
infection.
Diagnosis of catheter-related sepsis requires that the same
organism is grown from the catheter tip as is recovered from
blood and that the clinical features of infection resolve on
removal of the catheter. Traditional methods of confirming
line sepsis have necessitated removal of the line with subse-
quent bacteriological assessment. An alternative approach is
to use an endoluminal brush passed down the catheter and
withdrawn into a polythene sheath. The brush tip is cultured
at the same time as performing blood cultures. Catheter sep-
sis is confirmed if identical organisms are cultured from brush
and blood. A second alternative is to culture blood withdrawn
through the catheter and compare this with peripheral blood
cultures. If the colony count from the catheter sample is five
or more times higher than that from peripheral blood, then
line sepsis is probable.
Some of the complications of TPN may not be a direct
result of the provision of nutrients by the intravenous route,
but rather a consequence of the absence of luminal nutrients.
This may cause a shift in the mucosa-associated intestinal
microbiome, an increased mucosal proinflammatory state
and the loss of epithelial barrier function leading to bacterial
translocation of enteric organisms. The gut origin of sepsis,
mediated by bacterial translocation, may be significant in
critical illness and multiorgan failure.
The complications of parenteral nutrition are summarised
in Summary box 19.4.
Refeeding syndrome
This syndrome is characterised by severe fluid and electrolyte
shifts in malnourished patients undergoing refeeding. It can
03_19-B&L27_Pt3_Ch19.indd 288
Summary box 19.4
Complications of parenteral nutrition
●● Related to nutrient deficiency
Hypoglycaemia/hypocalcaemia/ hypophosphataemia/
hypomagnesaemia (refeeding syndrome)
Chronic deficiency syndromes (essential fatty acids, zinc,
mineral and trace elements)
●● Related to overfeeding
Excess glucose: hyperglycaemia, hyperosmolar
dehydration, hepatic steatosis, hypercapnia, increased
sympathetic activity, fluid retention, electrolyte
abnormalities
Excess fat: hypercholesterolaemia and formation of
lipoprotein X, hypertriglyceridaemia, hypersensitivity
reactions
Excess amino acids: hyperchloraemic metabolic acidosis,
hypercalcaemia, aminoacidaemia, uraemia
●● Related to sepsis
Catheter-related sepsis
Possible increased predisposition to systemic sepsis
●● Related to line
On insertion: pneumothorax, damage to adjacent artery,
air embolism, thoracic duct damage, cardiac perforation or
tamponade, pleural effusion, hydromediastinum
Long-term use: occlusion, venous thrombosis
occur with either enteral or parenteral nutrition, but is more
common with the latter. It results in hypophosphataemia,
hypocalcaemia and hypomagnesaemia. These electrolyte dis-
orders can result in altered myocardial function, arrhythmias,
deteriorating respiratory function, liver dysfunction, seizures,
confusion, coma, tetany and death. Patients at risk include
those with alcohol dependency, those suffering severe malnu-
trition, anorexics and those who have undergone prolonged
periods of fasting. Treatment involves matching intakes with
requirements and assiduously avoiding overfeeding. Calorie
delivery should be increased slowly and vitamins adminis-
tered regularly. Hypophosphataemia and hypomagnesaemia
require treatment.
Nutrition support teams
Multidisciplinary nutrition teams ensure cost-effective and
safe nutritional support, irrespective of how this is adminis-
tered. The incidence of catheter-related sepsis is significantly
reduced.
SUMMARY
Fluid therapy and nutritional support are fundamental
to good surgical practice. Accurate fluid administration
demands an understanding of maintenance requirements and
an appreciation of the consequences of surgical disease on
fluid losses. This requires knowledge of the consequences of
surgical intervention and, in particular, intestinal resection.
Malnutrition is common in hospital patients. All patients
who have sustained or who are likely to sustain 5 days of
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inadequate oral intake should be considered for nutritional
support. This may be dietetic advice alone, sip feeding or
enteral or parenteral nutrition. These are not mutually
exclusive. The success or otherwise of nutritional support
should be determined by tolerance to nutrients provided
and nutritional end points, such as weight. It is unrealistic
to expect nutritional support to alter the natural history of
disease. It is imperative that nutrition-related morbidity is
kept to a minimum. This necessitates the appropriate selection
of feeding method, careful assessment of fluid, energy and
protein requirements, which are regularly monitored, and the
avoidance of overfeeding.
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Further reading 289
ACKNOWLEDGEMENTS
With thanks to Marcel Gatt and Clare McNaught.
FURTHER READING
British Association Parenteral and Enteral Nutrition. BAPEN. Avail-
able from: (www.bapen.org.uk/res_pub.html).
Elia M, Ljungqvist O, Stratton R, Lanham SA (eds). Nutrition Society
textbook: clinical nutrition, 2nd edn. Oxford: Wiley-Blackwell, 2012.
Nice guideline: Nutrition support for adults: oral nutrition support,
enteral tube feeding and parenteral nutrition. Clinical guidelines
(CG32). Feb 2006.
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