Vol.18, No.
12 December 1996 V HEINZ SYMPOSIUM 1996
Continuing Education Article
FOCAL POINT
★Nutritional intervention is seldom
addressed early enough in the
management of sick or injured
patients.
KEY FACTS
■ Metabolic rate slows during
protracted simple starvation,
but critically ill patients are
typically in a hypermetabolic
state.
■ Sepsis may cause critical illness
or result from the accompanying
atrophy of the gastrointestinal
tract and translocation of
bacteria.
■ Critically ill patients may have
hyperinsulinemia despite glucose
intolerance in tissue.
■ Critically ill patients should not
be allowed to lose weight, even
if they are obese.
■ Veterinarians should be more
concerned about the energy
needs of critically ill patients and
less concerned about vitamins
and minerals.
Nutritional Needs of
Critically Ill Patients
Virginia Tech
Craig D. Thatcher, DVM, PhD
A norexia is a common problem in veterinary patients, especially among
the critically ill. Many animals that are presented to the veterinarian
may not have eaten properly for a prolonged period.
Nutrition for critically ill or injured animals should be addressed early in case
management. With all the concern about diagnostics, fluid therapy, and thera-
peutic regimens, it is easy to overlook the animal’s need for nutritional support
at first. Nevertheless, early attention to the patient’s nutritional needs can have
an important impact on outcome.
There are several pressing reasons to emphasize nutritional support. One of
the most important is ethical: The veterinarian is deciding whether to support
the patient nutritionally or to let it continue to be anorectic. Veterinarians
have an ethical responsibility to ensure that hospitalized patients are properly
fed.
Nutritional support of human patients has been shown to contribute dra-
matically to the medical outcome of a case.1,2 The earlier the intervention, the
better the outcome usually is.
Finally, many types of nutritional support—even most methods of tube feed-
ing—are easy and practical. Some can become routine in a hospital setting.
Others, especially parenteral nutrition, are somewhat more difficult. Neverthe-
less, many veterinarians could institute parenteral feeding in a practice setting.
Providing such services could represent an opportunity for practice growth and
additional practice income.
Nutritional support includes assessment of the animal’s nutritional require-
ments relative to its physiologic state and assessment of the current diet, in-
cluding intake and feeding method. The nutritional plan involves not only the
diet to be fed and the amount to be fed but also the route of administration. If
the animal will not eat, the practitioner must decide whether the nutrients will
be provided enterally through a tube or via a parenteral route.
MALNUTRITION VERSUS STARVATION
Much of the information on the nutritional status of hospitalized animals
has been extrapolated from studies of humans. Nevertheless, many of the find-
ings have been successfully applied to the care of dogs, cats, and other veteri-
nary species. Between 30% and 50% of hospitalized human patients are
Small Animal The Compendium December 1996

malnourished.3,4 The incidence of malnutrition among tion.13,14 Nutritional intervention is intended to prevent
hospitalized veterinary patients is probably also high. these problems. Again, much of this information has
The box lists disorders that may increase the risk of come from the human medical literature. Nevertheless,
malnutrition. the same effects are probably occurring in veterinary
Malnutrition is common in hospitalized patients patients.
because metabolism is altered as a result of disease. Mal-
nutrition worsens infection as well as surgical complica- Simple Starvation
tions. 2,5–10 Thus, malnutri- Glucose Homeostasis
Disorders That May tion increases morbidity and Simple starvation differs somewhat from the me-
tabolism that occurs in critically ill animals.15 During
Increase the Risk of mortality rates among hu-
man patients and probably starvation, the animal initially tries to maintain its
Malnutrition does so among veterinary pa- blood glucose levels. The first metabolic consequence
tients. of simple starvation is therefore increased hepatic gly-
Disorders That Alter
Malnutrition has many cogenolysis and increased gluconeogenesis. Glycogen
Loss of Protein and
causes. Nutrient intake may stores, however, are depleted within 24 hours.16
Electrolytes
be altered; and the animal Hormonal changes that accompany food deprivation
■ Vomiting may be less able to digest, include a change in insulin response.17 As simple starva-
■ Draining wounds absorb, or metabolize nutri- tion progresses, the blood glucose level decreases. In-
■ Burns ents. The animal’s ability to sulin secretion decreases initially because of the low
■ Ileus eliminate wastes may also be blood glucose. The increase in glycogenolysis implies
■ Diarrhea impaired. Nutrient require- increased glucagon secretion; low blood glucose
ments are different for crit- increases glucagon production, thus stimulating
■ Abscesses
ically ill animals than for glycogenolysis and gluconeogenesis. So in simple star-
■ Malassimilation healthy dogs and cats.11 The vation, glucagon increases initially in an attempt to
nutritional status and nutri- maintain blood glucose levels.
Disorders That Alter
ent intake of high-risk hos- As glucagon increases, lipolysis (the breakdown of
Nutrient Requirements
pitalized patients should be body fat) increases. This increases levels of glycerol, free
■ Trauma monitored. Their intake fatty acid, and ketone bodies. As starvation proceeds,
■ Blood loss must be compared with their more ketone bodies (e.g., β-hydroxybutyrate) are pro-
■ Liver disease nutritional requirements. duced, thus resulting in mild acidosis. During pro-
■ Sepsis Many hospitalized patients longed starvation in humans, ketones are utilized as an
■ Drug–nutrient have no oral intake of food, energy source by the brain.17 Free fatty acids increase
and others eat less than usu- and eventually level off. Glucose concentration should
interactions
al. Sick animals may be selec- also stabilize over time.
■ Burns tive in what they will eat and
■ Multiple surgical therefore may eat inappro- Metabolic Changes
procedures priate, unbalanced diets In simple starvation, the animal down-regulates its
■ Chronic renal disease (e.g., a patient that will only metabolism and becomes hypometabolic to conserve its
■ Fever eat cooked chicken). A pa- body stores of protein and fats. Therefore, the basal
tient’s nutrient stores can metabolic rate decreases in starving animals.17–19
■ Cancer
rapidly be depleted if the pa- In simple starvation, hepatic gluconeogenesis increas-
tient’s intake is not meeting es. After hepatic glycogen is depleted, amino acids are
its requirements. The veterinarian must estimate the used for gluconeogenesis.18,20–23 These amino acids are
patient’s nutritional requirements and its nutrient in- derived from the breakdown of both skeletal muscle
take and develop a plan to address the deficit. The nu- and visceral body proteins, many of which have very
tritional intervention must then be implemented and short half-lives (e.g., prealbumin, retinal binding pro-
adapted as the animal’s condition changes. tein, fibronectin, and transferrin).18,20 The levels of
Malnutrition can impair humoral and cell-mediated these proteins might become valuable in monitoring
immunity.12 Cutaneous hypersensitivity reactions are the nutritional status of critically ill animals. However,
delayed. The complement cascade and the opsonic these tests are not routinely available in veterinary
function of plasma can be affected, as can the function medicine.
of polymorphonuclear lymphocytes. Malnutrition can Currently, serum albumin is used to aid in the moni-
also delay wound healing or cause organ dysfunc- toring of nutritional status; but serum levels of proteins

UNBALANCED DIETS ■ IMMUNE FUNCTION ■ GLUCAGON

The Compendium December 1996
with short half-lives might provide better information.
Hepatic gluconeogenesis also uses secretory proteins
(e.g., immunoglobulins and lymphokines).11,20 Thus,
these proteins eventually become depleted in starving
animals.
As mentioned, the metabolic rate decreases with
chronic starvation. Conversion of thyroxine (T4) to tri-
iodothyronine (T3) decreases. Consequently, the active
T3 level decreases and oxygen consumption declines.17
As starvation progresses, fat oxidation increases and
protein breakdown decreases because of the decreased
metabolic rate. The brain adjusts by using ketone bod-
ies for energy because the glucose requirements of the
central nervous system decrease.20 As starvation contin-
ues, the site of gluconeogenesis shifts from the liver to
the kidneys.17,18 In cases of prolonged simple starvation,
ketosis occurs. Ketone bodies accumulate in the blood,
and metabolic acidosis results.
Much of the information on the metabolic changes
described above was derived from studies of humans.
Dogs and cats show somewhat different responses.
Dogs show a milder ketosis. Fat mobilization progresses
more slowly in dogs than in humans. 24 Cats have
increased fat metabolism compared with dogs. This
difference is important because starving cats with en-
hanced fat oxidation may be predisposed to hepatic
lipidosis.25–27
Critical Illness
Although metabolic rate decreases in starving ani-
mals, critically ill or injured animals are typically in a
hypermetabolic state. The consequences are somewhat
different from those of simple starvation.
Hypermetabolism
In hypermetabolic states, the neuroendocrine system
is typically activated because of local tissue injury or
changes in homeostasis. Many critically ill animals have
had some local tissue injury and may also have hypo-
volemia because of intractable vomiting, diarrhea, de-
hydration, or other problems. Hypoglycemia and aci-
dosis progress rapidly in critically ill animals because of
activation of the neuroendocrine pathway. Such stress
has many metabolic consequences.12,15,20,28,29
When the neuroendocrine system is activated by crit-
ical illness or acute injury, the sympathetic nervous
system responds. Epinephrine and norepinephrine are
released. The stimulation of the sympathetic nervous
system is positively correlated with the severity of the
stressor.18,20 The more severe the stress, the greater the
stimulation of the sympathetic nervous system and
consequently the greater the hypermetabolism.
Simultaneously, there is an increase in the counter-
FAT MOBILIZATION ■ NITROGEN BALANCE ■ RESPIRATORY QUOTIENT
Small Animal
regulatory hormones: Glucagon is released, and cortisol
levels increase.28 The increases in these counterregulato-
ry hormones have several results.28,30 The animal may
rapidly deplete its nitrogen and therefore enter negative
nitrogen balance. Potassium levels will also be depleted.
Because of the cortisol response, the animal becomes
glucose intolerant; hyperinsulinemia occurs despite the
glucose intolerance in tissue.
Consequently, ill or injured animals are in a hyper-
metabolic state and have marked nitrogen losses (which
will result in a negative nitrogen balance). The body is
in negative nitrogen balance when nitrogen losses (e.g.,
via urine, feces, and skin) exceed dietary nitrogen in-
take. Nitrogen balance reflects the body’s protein bal-
ance. Protein losses are also proportional to the stress
that the animal has received.
Researchers in human medicine have estimated the
increase in metabolic rates in humans with various dis-
orders.31 Humans with long-bone fractures have an in-
crease in metabolic rate of somewhere between 15%
and 30%. The metabolic rate may be increased by up
to 50% if the person has multiple injuries. Burn pa-
tients exhibit the highest increase in metabolic rate—
sometimes as high as 100%. Critically ill animals prob-
ably have similar increases in metabolic rate.12,32
The hypermetabolic state in humans depends on
mediators of inflammation as well as on hormonal re-
sponses. Both components must be present for hyper-
metabolism.33 Documented mediators of inflammation
include interleukin-1 and tumor necrosis factor.33,34
Both are probably increased when an animal is in a
hypermetabolic state.
Sepsis
Sepsis, which is common in critically ill animals, may
have a serious impact on metabolism. In particular,
oxygen consumption, metabolic rate, and cardiac index
are higher in septic humans than in nonseptic pa-
tients—and the respiratory quotient is lower. The lower
respiratory quotient means that fat is being used as the
primary energy source. Respiratory quotient reflects the
relative quantity of energy produced by carbohydrate,
fat, and protein.17,35 When critically ill patients have
sepsis, their risk of multiple organ failure may be in-
creased.
Sepsis may cause critical illness, but prolonged
anorexia may also contribute to sepsis. When a hyper-
metabolic critically ill animal is not receiving nutrition-
al support, the gastrointestinal tract atrophies and its
walls become thinner. Thus, the gastrointestinal walls
become more permeable to bacteria and toxins that are
normally present in the lumen. The bacteria and toxins
can then translocate into the bloodstream; thus, they
Small Animal
may contribute to sepsis.36 Other factors related to criti-
cal illness, such as decreased immune response, may
also contribute.11,20
Nutritional support of critically ill animals may be
important in preventing sepsis. Enteral nutritional
support helps to protect the integrity of the gastroin-
testinal tract.37 The animal should be fed enterally if
possible. Even a small amount of enteral feeding can
have an important protective effect in the gastrointesti-
nal tract.
Protein intake is crucial for maintaining the integrity
of the gastrointestinal tract. Protein deficiency decreases
bowel weight, increases epithelial perforation, and de-
creases crypt depth in the gastrointestinal tract.38 These
changes are related to atrophy of the gastrointestinal
tract.
ASSESSMENT
All too often, veterinarians wait to address the criti-
cally ill patient’s nutritional status until the animal has
been ill for several days. The earlier that nutritional in-
tervention is undertaken, the better the outcome will
be.
Currently, veterinarians can use many sources of
information when assessing an animal’s nutritional sta-
tus.32,39,40 Assessment of the nutritional status of dogs
and cats is a structured process that includes review of
the history and medical record, physical examination,
laboratory evaluation, and an estimation of nutritional
allowances based on physiologic status. Sometimes the
decision to institute nutritional support is based on
clinical impression rather than objective data. The first
step is to obtain as much information as possible on the
animal’s history. The veterinarian should ask the owner
not only about medical history, but also about dietary
history, including the animal’s usual diet and eating
habits.
The medical records should also provide some im-
portant objective information that may provide clues to
the animal’s current nutritional status. Physical exami-
nation and laboratory evaluation can certainly be help-
ful. All of the foregoing information helps in assessing
the animal’s nutritional requirements. If a diagnosis of
illness is made, it can also help guide nutritional inter-
vention, especially if the animal can benefit from a diet
with an altered nutrient profile.
Once the initial assessment is complete, the veteri-
narian must formulate a nutritional plan. The plan
then must be implemented and monitored and the
client educated.
Body Weight
An animal’s nutritional requirements depend largely
GASTROINTESTINAL INTEGRITY ■ MONITORING ■ BODY CONDITION
The Compendium December 1996
on its physiologic state. Body weight is an important
indicator of the need for nutritional support. Nutri-
tional support is indicated if the patient has recently
lost more than 10% of usual or optimum body weight.
This indication applies to animals that are ill from any
cause, not just to critically ill animals. Even if a patient
is obese, it should not be placed on a weight-reduction
diet when it is critically ill. Obesity should only be ad-
dressed after the critical illness has resolved.
Body weight of critically ill patients should be moni-
tored daily. Monitoring body weight can aid in evaluat-
ing the success of nutritional intervention. An animal
that is receiving nutritional support to meet its nutri-
tional requirements should not continue to lose body
weight. Nevertheless, body weight is only one indicator
of the animal’s nutritional status.
Clinical Condition
Restricted food intake for 3 days is not cause for
much concern. However, animals that have been
anorectic for longer than 3 days may benefit from nu-
tritional intervention. So do animals with illnesses that
result in nutrient loss. Chylothorax, for example, can
cause tremendous losses of protein into the thorax. An-
imals that are receiving antinutrients (i.e., medications
that interfere with nutrient absorption or metabolism)
or catabolic drugs can also benefit from nutritional in-
tervention. Nutritional support may be indicated if the
patient has received intravenous fluids for longer than 3
days if therapy that causes catabolism, anorexia, or dys-
phagia is required.
Some illness and treatment regimens (e.g., some
cancer chemotherapies) predictably cause anorexia. In
these cases, the veterinarian should anticipate the need
for nutritional support.
Other indicators of the animal’s nutritional status in-
clude muscle mass and the condition of haircoat, claws
or nails, and skin. Thin, dry, and scaly skin and easily
depilated haircoat may indicate undernutrition. The
practitioner should examine each body system to iden-
tify any problems related to nutrition.
Body condition scoring, which is a subjective evalua-
tion of the animal’s fat cover, may suggest that an ani-
mal needs nutritional support. The animal’s fat cover is
scored from one to five: 1 is very thin and 5 is grossly
obese. A score of 3 represents the optimum body con-
dition. The fat over the ribs, down the topline or over
the spinous processes, and over the lumbar transverse
process is visually assessed and palpated. The area
over the tuber coxi and tuber ischii is also evaluated.
Fat tends to accumulate around the tailhead in dogs.
Obesity is also typically evident in the animal’s ventral
silhouette.
Small Animal
Laboratory Assessment
No single diagnostic or laboratory test accurately
depicts the nutritional status of dogs and cats, but a
combination of tests can provide additional informa-
tion. Chronically ill animals typically are hypoalbu-
minemic. Animals with hypoalbuminemia generally
benefit from nutritional support. Lymphocyte count
and packed cell volume may serve as objective indica-
tors of nutritional status. Serum glucose is important in
the assessment of hypercatabolic, severely stressed ani-
mals. Serum alkaline phosphatase, hemoglobin levels,
and biochemical profiles indicative of liver, kidney, or
other organ problems can be helpful in assessing the
animal’s nutritional status.
Low serum albumin may indicate depletion of viscer-
al protein; however, serum albumin levels change slow-
ly (i.e., over days) because of that protein’s long half-
life. Tests for the levels of proteins with very short
half-lives are currently used to monitor nutritional
status and the effects of nutritional support in human
medicine. These levels may, however, reflect the prima-
ry disease process rather than nutrient depletion. The
tests to monitor levels of proteins with very short half-
lives are not yet available for veterinary use.
In human patients, hypoalbuminemia correlates
with increased morbidity and mortality rate and longer
hospital stays. Hypoalbuminemia also correlates with
a higher incidence of infection and lower body cell
mass.41 Similar relationships probably occur in veteri-
nary patients.
The diagnosis of hypoalbuminemia can aid in the se-
lection of patients that are at high risk for malnutrition.
Certainly, animals that have protein-losing enteropathy
or nephropathy and are losing large amounts of protein
may benefit from nutritional intervention.
REQUIREMENTS
The practitioner must consider the patient’s physio-
logic state, the nature of the disease or injury, and envi-
ronmental factors in determining the animal’s nutrient
requirements. After deciding that a critically ill patient
might benefit from nutritional support, the veterinari-
an estimates the patient’s nutrient requirements.12,32,39
Water is the nutrient that has the highest priority for
the animal. Next is energy, especially in the form of fat
and carbohydrate. Protein can certainly contribute to
meeting the animal’s caloric requirements but is also
essential for wound healing and tissue repair. The re-
quirements for vitamins and minerals are the least
urgent, yet these requirements are often the first ones
addressed by the veterinarian.
Critically ill patients have lower metabolic rates and
energy requirements than those of healthy dogs and
SERUM ALBUMIN ■ BIOCHEMICAL PROFILES ■ ENERGY REQUIREMENTS
The Compendium December 1996
cats. The caloric requirements are less, primarily be-
cause critically ill patients have decreased physical activ-
ity. A summary of the various equations that have been
used to calculate the energy requirements of sick dogs
and cats has been published.12
The resting energy requirement (RER) is calculated
as follows:
RER (kcal) = 30 (body weight [kg]) + 70
Another formula is as follows:
RER (kcal) = 70 (body weight [kg])0.75
The energy requirements of critically ill animals are at
or greater than RER but rarely exceed maintenance en-
ergy requirements. Factors to multiply RER for esti-
mating energy requirements in a wide variety of ill-
nesses have been extrapolated from human respiration
calorimetry studies for use in veterinary patients.39
After estimating the animal’s requirements, the vet-
erinarian must choose the diet to be fed and the
method of nutrient delivery. Whenever enteral feeding
is possible, it is preferable to parenteral nutrition. En-
teral nutrition is more physiologic, less expensive, and
easier to accomplish than parenteral delivery. Some-
times, however, the animal can only be supported
through the parenteral routes. The veterinary literature
describes numerous techniques for enteral and par-
enteral nutrition.32,39,42,43
For enteral feeding, food dosage (g/day) is deter-
mined by the daily caloric requirement of the patient
(kcal/day) divided by the caloric density of the diet
(kcal/g):
Total daily energy requirement
Food dosage =
Diet caloric density
Commercially available diets usually contain nonenergy
nutrients properly balanced to the caloric density of the
product. Thus, all of the animal’s nutrient needs will be
met if its energy needs are met.
About the Author
Dr. Thatcher is Head of the Department of Large Animal
Clinical Science, Virginia-Maryland Regional College of
Veterinary Medicine, Virginia Tech, Blacksburg, Virginia,
and is a Diplomate of the American College of Veterinary
Nutrition.
Small Animal
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