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 4^th 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.

Coagulation:

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.

Assessment:

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.