Read Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice Online
Authors: Simon Paterson-Brown MBBS MPhil MS FRCS
Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice (78 page)
William G. Simpson and
Steven D. Heys
The importance of nutrition in all fields of clinical practice has become well recognised and none more so than in the management of patients who are undergoing surgery and/or are faced with critical illness. Despite this increasing understanding of the importance of nutrition in health, up to 40% of hospitalised patients can be classified as being malnourished and many of these patients are not recognised clinically as having this problem. In patients undergoing gastrointestinal surgery, for example, the prevalence of ‘mild’ and ‘moderate’ malnutrition has been estimated to be approximately 50% and 30%, respectively.
The clinical significance of this is vitally important because when patients are malnourished, disturbances in function at the organ and cellular level can manifest as the following:
altered partitioning and impairment of normal homeostatic mechanisms;
muscle wasting and impairment of skeletal muscle function;
impaired respiratory muscle function;
impaired cardiac muscle function;
atrophy of smooth muscle in the gastrointestinal tract;
impaired immune function;
impaired healing of wounds and anastomoses.
The key point, therefore, is that as a result of these malnutrition-induced changes, patients have an increased risk of postoperative morbidity and mortality. To further complicate the situation with respect to nutrition, patients undergoing surgery will also be fasted for varying periods of time (preoperatively and/or postoperatively). Moreover, if patients then experience postoperative complications (e.g. sepsis), these effects may be further potentiated and the disturbances of cellular and organ function occurring in malnutrition then made even more complex.
In this chapter the following areas, which are important for surgical practice, will be outlined:
the principles of the metabolic responses to feeding, trauma and sepsis;
nutritional requirements for surgical patients;
identification of patients who are malnourished or are at risk;
nutritional support principles for surgical practice and modifications in defined common clinical situations;
modulation of nutritional support with key nutrients – application to clinical practice.
In order to maintain the health of cells, tissues and organs, the metabolism must adapt to changes in nutritional intake, trauma and sepsis.While a detailed knowledge of complex biochemical pathways is not necessary, it is important to understand the principles of these metabolic and biochemical changes, and the metabolic response when a patient experiences trauma, undergoes surgery or develops sepsis. This forms the basis for understanding nutrition and nutritional support in critically ill patients.
A major advance in understanding occurred more than 80 years ago when Sir David Cuthbertson described the loss of nitrogen from skeletal muscle that occurred following trauma.
1
Cuthbertson concluded that the response to injury could be considered as occurring in two phases (
Fig. 17.1
):
Figure 17.1
Diagrammatic representation of the ebb and flow phases in the metabolic response to injury.
Reproduced from Broom J. Sepsis and trauma. In: Garrow JS, James WPT (eds) Human nutrition and dietetics, 9th edn. Edinburgh: Churchill Livingstone, 1993; pp. 456–64. With permission from Elsevier.
the ‘ebb’ phase, which is a short-lived response associated with hypovolaemic shock, increased sympathetic nervous system activity and reduced metabolic rate;
the ‘flow’ phase, which is associated with a loss of body nitrogen and resultant negative nitrogen balance.
These changes result in the following:
Ebb phase
decreased resting energy expenditure;
increased gluconeogenesis;
increased glycogenolysis.
Flow phase
increased resting energy expenditure;
increased heat production, pyrexia;
increased muscle catabolism and wasting and loss of body nitrogen;
increased breakdown of fat and reduced fat synthesis;
increased gluconeogenesis and impairment of glucose tolerance.
If the changes of the ‘ebb phase’ are not replaced by the ‘flow phase’, then despite any advances in surgery, anaesthesia and intensive care support, death of the patient is the inevitable outcome.
The central nervous system and the neurohypophyseal axis play key roles in regulating these metabolic changes following trauma, utilising a range of hormones and cytokines. Afferent nerve impulses also stimulate the hypothalamus to secrete hypothalamic releasing factors that, in turn, stimulate the pituitary gland to release prolactin, arginine vasopressin (antidiuretic hormone, ADH), growth hormone and adrenocorticotrophic hormone (ACTH). The changes in hormone levels in plasma following trauma are outlined in
Box 17.1
, with the stress hormones (adrenaline, cortisol, glucagon) playing pivotal roles.
Box 17.1
Changes in hormone levels in plasma following trauma
Catecholamines
Rapid increases in concentrations of adrenaline and noradrenaline within a few minutes of injury due to increased activity of sympathetic nervous system. Levels return to normal within 24 hours
Glucagon
Rises within a few hours; maximal levels 12–48 hours post-trauma
Insulin
Initially plasma levels are low following trauma, but rise to above normal levels and reach a maximum several days after the injury
Cortisol
Rapid increase in cortisol (due to stimulation by ACTH), returning to normal 24–48 hours later; may remain elevated for up to several days. Has ‘permissive’ effects with other hormones such as catecholamines
Growth hormone
Levels increased following trauma; usually return to normal levels within 24 hours
Thyroid hormones
Following trauma, the biochemical features of ‘sick euthyroid syndrome’ may be present: thyroid-stimulating hormone (TSH) levels normal or low, levels of free thyroxine (T
4
) and tri-iodothyronine (T
3
) normal, whereas the total levels are altered because of changes in binding protein concentration. In addition, reverse T
3
is generally high. These effects may be prolonged for some weeks
Other disturbances of thyroid function may, however, be present, including ‘transient hyperthyrotropinaemia of illness’ – a transiently raised TSH, not to be confused with hypothyroidism
Renin, aldosterone
Aldosterone levels increased after trauma, returning to normal within 12 hours. Its secretion is stimulated by renin, which in turn is produced in response to reduced renal perfusion
Testosterone
Plasma levels fall after trauma and may remain low for up to 7 days
Vasopressin/antidiuretic hormone
Plasma levels rise following trauma and may remain elevated for several days
Prolactin
Secretion increased following trauma but function in trauma is unknown
Cytokines
Increased secretion of interleukin (IL)-2, IL-6, tumour necrosis factor, etc.; inter-relationship between these changes leads to differential responses seen in trauma and sepsis
Amino acids are required for:
synthesis of proteins necessary for growth, function and structural repair;
energy substrates for gut, lymphocytes and other rapidly proliferating tissues (mostly glutamine), also as fuel in muscle;
hepatic gluconeogenesis – glucose is produced from alanine, which itself is produced by transamination reactions from other amino acids;
maintenance of renal acid–base balance (arginine);
production of proteins with specific roles in repair – immunological, endocrine, etc.
In the well-fed state, proteins are synthesised at a rate exceeding breakdown, whereas in the fasting state breakdown predominates. Following prolonged fasting for 1–2 weeks, breakdown still predominates but at a lower rate as the metabolism adapts to starvation. In contrast, following trauma or sepsis, breakdown exceeds synthesis regardless of whether the patient is fed or fasted; this response is, however, impaired if the metabolism is already adapted to starvation.
2
The magnitude of the nitrogen loss is proportional to the degree of operative trauma or the severity of the sepsis, and the major site of protein breakdown is skeletal muscle (contains 80% of the body's amino acid pool, with 60% being glutamine).
3
Glucose is the main fuel used by many different tissues, being essential for some. In the well-fed state it is available for absorption from the gastrointestinal tract and, mostly driven by insulin, any excess is converted to glycogen (glycogenesis) in both liver and muscle, and to fatty acids (lipogenesis), the latter predominating when glycogen stores are replete. On fasting, insulin levels are lower, with an associated reduction in peripheral utilisation of glucose, and it is endogenously produced from glycogen (glycogenolysis) or other precursors (gluconeogenesis), e.g. amino acids and fatty acids. Initially, glycogenolysis predominates, but after a number of hours (dependent on demands), gluconeogenesis predominates (colloquially referred to as ‘getting your second wind’). Following trauma, there is an increase in hepatic glycogenolysis (caused by increased sympathetic activity),
4
with these stores being substantially depleted within 24 hours.
5
Insulin antagonists are also involved in this metabolic response (see
Box 17.1
), and the insulin resistance is accompanied by a rise in insulin concentration. The circulating insulin level usually reaches a maximum several days after the injury, before returning towards normal levels.
In general, the carbohydrate response is to produce hyperglycaemia both in the immediate ‘shock’ (‘ebb’ phase) and later ‘flow’ phase of the metabolic response. The origin of the increased glucose differs between these two phases – while reduced peripheral utilisation of glucose is common to both phases, the glycogenolysis of the ebb phase must be replaced by gluconeogenesis in the flow phase. In the critically ill patient the advent of hypoglycaemia is an indication of major problems – glycogenolysis has slowed with depletion of glycogen stores, but gluconeogenesis is not yet adequate.
In the healthy, resting, fed state, triacylglycerol, being energy dense, is used by the metabolism to efficiently store energy. When fasting, lipolysis of triglyceride releases free fatty acids, which can be used as respiratory fuel for most cells other than brain and red blood cells, and glycerol that can be converted to glucose by hepatic gluconeogenesis.
6
Fatty acids are also metabolised in the liver to form ketone bodies, which are used as a preferential fuel source by many tissues (humans cannot use fatty acids for gluconeogenesis). Lipolysis is stimulated by glucagon during short-term fasting, by ACTH once the metabolism is adapted to starvation, or by adrenaline during exercise and stress. Following trauma, there is therefore an increase in the turnover of fatty acids and glycerol, although raised levels of lactate, for example in hypovolaemic shock, induce re-esterification leading to raised plasma triglyceride levels.
Changes in fluid compartments, minerals and micronutrients (micronutrients are broadly defined as substances required in amounts of < 1 g daily) are beyond the scope of this chapter, but it is worth re-emphasising that measured serum concentrations rarely reflect body status, and this is even more pronounced in starvation and illness; for example, hyponatraemia is more often associated with an excess of water than with a deficiency of sodium; hypocalcaemia does not indicate a deficiency of calcium, but can suggest a deficiency of magnesium. It is therefore essential to consider the effect of illness before trying to interpret laboratory results.
7
The metabolic response to sepsis is also characterised by alterations in protein, carbohydrate and fat metabolism, but the following are key differences:
8
The breakdown of skeletal muscle and nitrogen losses can be substantial (more than 15–20 g per day).
There is increased production of glucose by the liver (both gluconeogenesis and glycogenolysis), resulting in an elevated plasma glucose.
In contrast to the situation following trauma, there is an increased rate of glucose uptake and oxidation by peripheral tissues.
Decrease in the peripheral uptake of triacylglycerols and defective ketogenesis in the presence of sepsis (in contrast to the situation occurring after trauma) lead to hypertriglyceridaemia.
A significant abnormality in the patient with sepsis is the disruption of the microstructure of the hepatocyte mitochondria, particularly of the inner membrane. There is a block in energy transduction pathways, with consequent reduction in the aerobic metabolism of both glucose and fatty acids. The body therefore depends on the
anaerobic
metabolism of glucose, which also results in lactate production. It is essential, therefore, that there is an adequate supply of glucose from gluconeogenic pathways. If this is impaired or inadequate, then hypoglycaemia (and death) may ensue. The development of hypoglycaemia during sepsis is an indicator of an extremely poor prognosis and is usually associated with inevitable mortality.