Nutrition in Neurosurgery: 


Dr. A. Vincent Thamburaj,   

Neurosurgeon, Apollo Hospitals,  Chennai , India.

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 injury:

Energy expenditure:

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 quadriplegics.

Hormonal response:

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 head injuries.

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.

Glucose metabolism:

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.

Fat metabolism:

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 outcome.

Nutritional support:

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 reserve.

If surgery is elective, prophylactic hyperalimenation is recommended.


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.  

Energy requirements: 

A resting normal individual requires about 26Kcal/kg/day. 

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 calories.

Nitrogen requirement 

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 tolerance.

Lipid requirements:

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 immuno stimulatory.

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 E. 

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 hyponatremia.

Enteral nutrition:

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 diarrhea.

Parenteral nutrition:

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 parenteral nutrition.

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 cerebral edema.

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 organ failure.



















































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