While many of
the metabolic changes due to injury are useful, the catabolic process
can be detrimental to repair and recovery. The severe catabolism leads
to muscle wasting and loss of weight, poor wound healing, impaired immunity,
respiratory distress and increased morbidity. It is generally
considered that losses of 20% of weight increase susceptibility to
stress and losses of 30% increase mortality appreciably.
The patients with severe head injury, SAH, intracerebral
hematoma or chronic spinal conditions are liable to both the
inconvenience of not being able to achieve a reasonable daily intake
and the additional insult of active nutritional and metabolic
depletion. They often require a well planned nutritional support.
Addressing the balance of metabolic and nutritional
demands during illness is a long term effort with little prospect of
normalizing all the factors. Rather, goal should be individually
tailored and attempts made to reverse trends in metabolic parameters. Optimal
nutritional intervention may provide an optimal environment for
neuronal sprouting and regeneration.
Metabolic aspects following a neural
Studies suggest that a comatose, head injured patient’s
energy requirement is equivalent to that of a patient with 20-30%
burns. The hypermetabolism, which follows head injury, is often
increased out of proportion to the severity of tissue injury, over 170%
of RME (resting metabolic expenditure). The paralyzed, sedated and
intubated patient’s requirements may approach basal levels when
compared to predicted values.
Muscular activity is a major component of energy
expenditure. In the patients with spinal cord injuries the expenditure
is about 20% less than that normally calculated, more so in
As in any acute injury, there is a sympathetic discharge
that causes massive release of catecholamines from the adrenals. This
alters the pattern of metabolism in many tissues, such as,
gluconeogenesis in liver, nitrogen release in muscle and triglycerides
and free fatty acid from adipose tissue. The increased catecholamines,
in addition, increase the RME and body temperature and may also be
responsible for the cerebral vasoconstriction so often seen in severe
There is an apparent association between raised ICT and
gastric hypersecretion resulting in the ‘stress ulcer’.
Hyperamylasaemia has also been noted in severe head injury as compared
to other trauma. The role of gut hormones in these is not known. It has
been suggested that the autonomic centers around the 4th
ventricle and the hypothalamic-pituitary axis are important.
There is a rise in blood glucose, as in any illness or
injury and a relative resistance to insulin effect with a decrease in
glucose consumption in brain and muscle. There is associated increased
lactate turnover due to incomplete oxidation of glucose and the failure
of mitochondrial oxidative metabolism. High glucose levels together
with the failure of oxidative glucose metabolism combine to produce
excess lactate, which may account for poor neurological outcome.
In association with increased blood glucose, there is
breakdown of fats and release of fatty acids and triglycerides and
lipaemia providing energy. Cholesterol and phospholipids are increased
to a lesser extent.
Protein and nitrogen metabolism:
The ‘catabolic hormones’ (glucagon, cortisol and
the catecholamines) are prime mediators in the mobilization of glucose
and the deamination of skeletal muscle to form primary amino acids. At
first there is hypoalbuminaemia. Later, there is progressive
conservation of visceral protein at the expense of the somatic muscle
mass. Nitrogen loss can be reduced to some extent with administration
of carbohydrates with exogenous insulin, if required. The liver
utilizes principally glutamine and alanine for gluconeogenesis. These
amino acids represent some 35% of the total output from muscle protein.
The ‘non-essential’ arginine cannot be synthesized during stress.
Decreased arginine impairs immunity. In addition, there is increased
hepatic synthesis of fibrinogen, caeruloplasmin, C-reactive protein,
complement fractions and coagulation factors.
In the spinal cord injured, a massive wasting of nitrogen
occurs in the first 10 days, exceeding the levels found in the head
injured. At some point in the chronic phase, nitrogen excretion
falls well below normal.
There is activation of platelets, perhaps, due to release
of the vast stores of thromboplastins in the brain. High levels of
fibrin degradation products are often associated with brain injury,
suggesting diffuse intravascular coagulation and widespread consumption
of platelets. Coagulation parameters have been used to predict the
The aim is to optimize support until
homeostasis is re-established as the illness subsides.
Overfeeding is to be avoided.
For periods longer than few
days, the help of a qualified dietician is mandatory.
In acute illness, nutritional support should be introduced
when surgery has finished, though hyperglycemia should be controlled.
Early start reduces the number of septic episodes complicating major
illness. The main disadvantage is exacerbation of hyperglycemia, which
is associated with poor outcome after brain injury and stroke. Hence
some would prefer to feed late, risking failure of immunological
If surgery is elective, prophylactic hyperalimenation is
Energy requirements at rest are determined by age, sex,
and body surface area. The women need less and there is a 10% increase
in metabolic expenditure per degree centigrade rise in body
temperature. Energy requirements of the injured patients are expressed
as a percentage of expected, based on a normal person of the same age,
sex, and body surface area. Body weight may be the most valuable index
and most often used along with skin fold thickness.
For obvious reasons, body weight measurement is difficult
in neurologically compromised patients. Biochemical measures of liver
and renal function are readily available. The short half-life proteins,
transferrin, C-reactive protein (CRP) and retinal binding protein (RBF)
are useful for early assessment. Albumin, having a longer half-life, is
more useful for weekly and monthly monitoring.
A resting normal individual requires about
It is recommended that the spinal injured require 10 to
15% less than the normal. Obviously associated injuries must be taken
into account. In the brain injured, those with GCS of 6-7 require about
20% more and those with GCS of 4-5 require about twice the normal
requirement. Those with GCS of more than 8, those on a ventilator, paralyzed
and the uncomplicated post craniotomy patients may not need additional
It is not so well quantified. About 10-15% of the
energy needs are required in normal individuals.
It is suggested that a protein intake of 2 to 2.5 gm
/kg/day is adequate, both in head injury and spinal injury. The aim
should be to reduce daily nitrogen losses to below 10gm. The type of
protein may need attention. Protein composed of a large percentage of
BCAA (branched chain amino acids ) seems to improve nitrogen retention.
BCAAs are oxidized by the skeletal muscles. Infusion of BCAAs decrease
skeletal muscle catabolism. Alanine and glutamine are available
endogenously at the expense of muscle protein and are used for increased
synthesis of new proteins for host defense, coagulation, wound healing
and gluconeogenesis. In addition, glutamine is the primary energy
source for the gut. Enhanced efflux of glutamine from skeletal muscle
as well as increased use of glutamine causes a decrease in the
intracellular gradient sepsis, burns and trauma. Albumin is important
in oncotic pressure maintenance, drug transport and enteral feeding
In India, about 20% of energy may usefully be derived from
fats. At all levels of calorie intake, invisible fat furnish about 9%
energy and visible fat 10%. This would come to 10-20 gms of fat per
day. Dietary fats are important because they serve as stored energy
reserves and as carriers of essential fatty acids and fat-soluble
vitamins and has protein sparing action. The type of lipid administered
may also play a role. Fish oil, which is rich in omega-3 fatty acids is
Vitamins and minerals:
Vitamins and trace elements are added, especially in
prolonged parenteral nutrition.
Vitamin E supplementation, as a membrane targeted
scavenger of lipids peroxyl radicals, may protect against neural
induced oxidative injury. Vitamin C is an antioxidant like vitamin
Magnesium maintains normal intracellular sodium and
potassium gradients and plays a role in the regulation of various
neurotransmitter and neuro chemical reactions. Magnesium administration
immediately after brain injury result in a dose a dose dependent
improvement in motor function.
Zinc deficiency has been correlated to T-cell dysfunction.
Zinc supplementation has significantly improved visceral protein
levels, a trend towards less mortality and improvement in GCS scores.
Salt restriction is avoided in the brain injured to avoid
For most neurosurgical diseases, the gut remains
functional and should preferentially be used. Simple oral supplements
may be enough to enhance calorie intake and a good balance of nutrients
can be maintained.
Where the level of consciousness is decreased or bulbar
function impaired, a nasogastric tube may be used. A Ryles tube is
satisfactory. A fine bore tube is a better alternative, if the feeding
is to continue beyond 10 days to avoid nasal and esophageal pressure
injury. The positioning of the tube must be checked clinically and
radiologically. In a restless patient the tube may get displaced and
aspiration before each feed is a must. Continuous feeding is the norm
to prevent a post-prandial hyperglycemia. Bolus feeding may be useful
in the ambulant. Rarely a feeding jejunostomy is required for long term
feeding as in a vegetative state.
Most preparations are egg and milk based. Egg is the most
biologically available protein source. In general, the greater the amount
of essential amino acids, the more biologically available is a protein.
Vegetable oils make up the fat component and sucrose and cornstarch
constitute the carbohydrate sources of most preparations.
It is to be noted the patients on morphine will have impaired
gastric emptying and those on broad-spectrum antibiotics may develop
There is no evidence to suggest that enteral nutrition is
superior to parenteral one. However, enteral nutrition is recommended
wherever possible to avoid the risk of infection associated with
The entire support can be given parenterally as in Total
Parenteral Nutrition (TPN ) or a part of it can be given
enterally with the remaining being supplemented as in Partial
Parenteral Nutrition ( PPN ).
In acute stage, there may be ileus, warranting a
parenteral route. Total parenteral nutrition (TPN) provides guaranteed
intake and is easy to administer, but requires a central venous line as
the preparations are hyper tonic. Associated risk of infection is a
real problem. 3 liters bag may help to some extent. TPN may also be
associated with hepatic cholestasis, electrolyte imbalance and defects
in calcium and phosphorous metabolism.
One potential contraindication to parenteral nutrition is
Some studies suggest that multi organ failure is commoner
in TPN as it translocate endotoxins form the gut, facilitated by the
poor blood flow and ischaemic conditions in the gut. Other study
shows that enteral nutrition does not reduce the incidence of multi