The way the body responds to major systemic insults depends on several factors—the physiological reserve of the patient’s chief organ systems (i.e. basic fitness), the nature of the injurious process, the severity of physiological disruption, the duration of delay before resuscitation, and the virulence of any microorganisms involved. Most patients are remarkably resilient given good basic care but in a deteriorating patient, several physiological systems are likely to be impacted upon simultaneously, evoking a range of complex homeostatic mechanisms.

Management of the deteriorating patient

The aim is always to recognise problems early by regular clinical observation, and to correct abnormal physiology rapidly and accurately in order to prevent intrinsic compensatory mechanisms becoming overwhelmed. If this happens in one organ system without correction, snowballing decompensation of other systems follows.

Management requires careful monitoring, often in a high-dependency or intensive care unit, and repeated checks on organ function and dysfunction. In most elective operations, many of the responses discussed below can be mitigated by good preoperative preparation, accurate fluid replacement, ensuring oxygenation, adequate analgesia, reducing psychological stress, preventing infection and using careful operative technique to minimise tissue trauma, blood loss and complications. Enhanced recovery programmes are gradually being introduced which give special attention to these factors before, during and after operation (see: NHS Enhanced Recovery Partnership Programme document: Delivering enhanced recovery—Helping patients to get better sooner). The individual variables responsible for potentially excessive systemic responses to severe injury or major surgery are summarised in Box 2.1.

Stressors in the surgical patient

Direct and indirect tissue trauma: Tissue disruption (whether surgical or traumatic) leads to activation of local cytokine responses more or less in proportion to the damage. Responses are exaggerated if wounds are contaminated (e.g. debris, foreign bodies, faeces) or associated with tissue ischaemia.

Fall in intravascular volume: This is a key factor in initiating systemic responses. Hypovolaemia results from:

• Excess fluid loss (see Box 2.2)

Box 2.2 Sources of excess fluid loss in surgical patients

• Blood loss—traumatic or surgical

• Plasma loss—burns

• Gastrointestinal fluid loss—vomiting, nasogastric aspiration, sequestration in obstructed or adynamic bowel, loss through a fistula or an ileostomy, diarrhoea

• Inflammatory exudate into the peritoneal cavity—generalised peritonitis or acute pancreatitis

• Sepsis syndrome (septicaemia)—massive peripheral vasodilatation and third space losses due to increased capillary permeability causing relative hypovolaemia

• Abnormal insensible loss—fever, excess sweating or hyperventilation

• Interstitial sequestration of fluid as oedema in damaged tissues and generally as a result of systemic hormonal responses. This process is amplified in systemic sepsis

• Restricted oral intake during any perioperative period or whilst in intensive care

Falling intravascular volume stimulates sympathetic activity by removing baroreceptor inhibition in an attempt to maintain blood pressure by increasing cardiac output and peripheral resistance. This also explains the mild tachycardia commonly seen in postoperative patients. Compensation is most effective in young fit individuals, but decompensation is often sudden and rapid. Catecholamines also have profound metabolic effects, increasing the turnover of carbohydrates, proteins and lipids. Falling renal perfusion activates the renin–angiotensin–aldosterone system, increasing renal reabsorption of sodium and water. A centrally mediated increase in antidiuretic hormone (ADH) secretion promotes further conservation of water.

Reduced cardiac output and peripheral perfusion: Circulatory efficiency may be impaired by hypovolaemia, and myocardial contractility may be depressed by anaesthetic agents and other drugs. Anaesthetic drugs generally cause peripheral dilatation and positive-pressure ventilation impairs venous return. Head-down positioning and artificial pneumoperitoneum for laparoscopic surgery further stress cardiovascular physiology. Major events such as sepsis (septic shock), pulmonary embolism or myocardial infarction may precipitate cardiovascular collapse.

Systemic inflammatory responses and sepsis (see Ch. 3):

Pain: Pain causes increased catecholamine and adrenocorticotrophic hormone (ACTH) secretion. Perioperative blockade of pain (e.g. by regional anaesthesia) greatly reduces the adverse systemic effects.

Stress: Psychological stress associated with injury, severe illness or elective surgery has an effect similar to pain on sympathetic function and hypothalamic activity.

Excess heat loss: This can occur during long operations and after extensive burns. Heat loss imposes enormous demands upon energy resources; if body core temperature falls, physiological processes such as blood clotting are impaired. Small babies are very vulnerable to heat loss. Heat loss in the operating theatre is counteracted as far as possible by raising the ambient temperature, insulating exposed parts of the body, using warm water underblankets or warm air ‘bear-huggers’ and by warming fluids during intravenous infusion.

Blood coagulation changes: General metabolic responses to injury activate thrombotic mechanisms and initially depress intrinsic intravascular thrombolysis. Thus the patient is in a prothrombotic state and may suffer intravenous thrombosis and consequent thromboembolism.

If substantial haemorrhage occurs, clotting factors eventually become exhausted, causing failure of clotting. The systemic inflammatory response syndrome (SIRS, see Ch. 3, p. 51) may initiate widespread intravascular thrombosis, using up clotting factors and precipitating disseminated intravascular coagulation (DIC), with failure of normal clotting.

Starvation and stress-induced catabolism: Patients with major surgical conditions are often malnourished before operation (see Nutritional management, below). Most are starved for 6–12 hours preoperatively and often do not start eating for 12–24 hours after surgery. After major GI surgery, food may be withheld for several days, or much longer with complications such as anastomotic breakdown or fistula formation.

Metabolic responses to pathophysiological stress

In severe trauma or extensive operative surgery, particularly if complicated by sepsis, the key factors in the systemic response are increased sympathetic activity together with increased circulating catecholamines and insulin. Cytokine responses signal other cells to prepare for action (e.g. polymorphs, T and B cells), to compensate for starvation, provide additional energy and building blocks for tissue repair, and conserve sodium ions and water.

Glucose production is massively increased by gluconeogenesis under the influence of catecholamines. There is also enhanced secretion of ACTH, glucocorticoids (cortisol), glucagon and growth hormone, all contributing to the general catabolic response. Insulin acts as an antagonist of most of these and is secreted in increased amounts from the second or third day after injury.

The sum of these factors is to cause inevitable catabolism and potentially extreme changes in fluid balance and electrolytes. These metabolic changes are shown in Figure 2.1.

Fig. 2.1 Metabolic responses to major systemic insults

Effects on carbohydrate metabolism: The overall effect is rising blood glucose (levels may reach 20 mmol/L), often resulting in hyperglycaemia and a pseudodiabetic state, and glucose may appear in the urine. This is in marked contrast to simple fasting, in which glucose levels are normal or low and glycosuria does not occur.

Effects on body proteins and nitrogen metabolism: In the normal healthy adult, nitrogen balance is constantly maintained. Protein turnover results in daily excretion of 12–20 g of urinary nitrogen which is made good by dietary intake. In a hypercatabolic state, nitrogen losses can increase three- or four-fold. Most importantly, the metabolic environment prevents proper utilisation of food or intravenous nutrition. There is therefore huge destruction of skeletal muscle. This state of negative nitrogen balance contrasts markedly with simple starvation in which body protein is preserved.

Effects on lipid stores and metabolism: The effects of major body insults on lipid metabolism are little different from simple starvation; most of the energy requirements are met from fat stores.

Surgical catabolism reverses only as the patient recovers from the illness and therefore early parenteral nutrition has little effect, although carbohydrate administration may spare some protein loss.

Note that when patients have been severely ill, carbohydrate metabolism is minimal and energy comes from catabolism of protein and fat. Once feeding recommences, there is a danger of refeeding syndrome which must be anticipated (see below).

Fluid, electrolyte and acid–base management

Introduction

Fluid, electrolyte and acid–base derangements can be minimised if high-risk patients are assessed before operation and closely monitored before, during and after operation. If abnormalities do develop, the diagnosis and management can be worked out with reasoning and common sense. Plasma urea and electrolytes should be checked at least daily in patients undergoing major surgery or those receiving intravenous fluids.

Severely ill patients with abdominal infection, sepsis and fistulae and patients with severe burns are likely to suffer major problems of fluid balance (and nutrition, see below). These are best managed with the help of experienced anaesthetists in intensive care or high-dependency units, where monitoring and therapy can be rigorously managed.

Normal fluid and electrolyte homeostasis

The body of an average 70 kg adult contains 42 litres of fluid, distributed between the intracellular compartment, the extracellular space and the bloodstream (see Fig. 2.2). Fluid input is mainly by oral intake of fluids and food but about 200 ml/day of water is produced during metabolism. Normal adult losses are between 2.5 and 3 litres/day. About one litre is lost insensibly from skin and lungs, 1300–1800 ml are passed as urine (about 60 ml/hour or 1 ml/kg/hour) and 100 ml are lost in faeces. About 100–150 mmol of sodium ions and 50–100 mmol of potassium ions are lost each day in urine and this is balanced by the normal dietary intake (see Table 2.1).

Table 2.1

Summary—normal daily fluid and electrolyte input and output

Fig. 2.2 Distribution of fluid content in the body compartments

In patients with a distended and taut abdomen, measuring abdominal compartment pressure can help early recognition. Treatment involves reopening the abdomen and leaving it open until the risk of rising pressure subsides.

Problems of fluid and electrolyte depletion

Loss of whole blood or plasma: Rapid and copious blood loss in traumatic injury or operative surgery initially depletes the intravascular compartment and loss of only 1 litre may cause hypotension or even hypovolaemic shock. When haemorrhage is less rapid, there is time to replace fluid loss from the extracellular compartment, so greater volumes can be lost before the cardiovascular system becomes compromised, although losses still need to be restored physiologically or by transfusion.

If blood loss has ceased, the need for transfusion is based on estimated or measured volume lost and on known haemoglobin concentration. Acute blood loss of 500–1000 ml is usually treated by transfusing crystalloids. Larger volume losses are best replaced by transfusion of whole blood or packed red cells supplemented by normal saline. Slow chronic blood loss, e.g. from a peptic ulcer or hookworm infestation, does not cause fluid balance problems but may cause symptoms and signs of anaemia; transfusion is not usually required.

In severe burns, the amount of plasma likely to be lost is easily underestimated and should be calculated using a standard formula based on the burnt area to guide fluid replacement (see Ch. 17).

Gastrointestinal fluid loss: Between 5 and 9 litres of electrolyte-rich fluid is normally secreted into the upper GI tract each day as saliva, gastric juice, bile, pancreatic fluid and succus entericus (small bowel secretions; see Table 2.2). Most of the fluid is reabsorbed in the large intestine.

Table 2.2

Daily gastrointestinal secretions and electrolyte composition

Huge volumes of water and electrolytes may be lost as a result of vomiting, nasogastric aspiration, diarrhoea, sequestration of fluid in obstructed or adynamic bowel or drainage to the exterior via a fistula or an ileostomy. If there is widespread bowel inflammation causing diarrhoea as in gastroenteritis or ulcerative colitis, inflammatory exudate may greatly increase the total fluid lost.

Cholera and other infective diarrhoeal diseases can cause the loss of up to 10 litres of electrolyte-rich fluid in one day and this fluid loss is a frequent cause of death, particularly in children.

Abnormal fluid losses in hospital must be measured or estimated accurately and recorded on a fluid balance chart. In addition, observations should be regularly made for signs of fluid depletion including pulse rate, blood pressure, periodic urine output and, if necessary, central venous pressure (CVP). These measures enable intravenous replacement to be predicted and the adverse consequences of fluid and electrolyte depletion to be prevented.

From Table 2.2, it can be seen that vomitus, nasogastric aspirate and diarrhoea are variably rich in sodium and potassium. As a general rule, GI fluid losses should be replaced by an equivalent volume of normal saline, with potassium chloride added as needed. In intestinal obstruction or adynamic ileus, fluid sequestrated in bowel is replaced in a similar manner, although volume requirements have to be estimated. Fistulae and overactive ileostomies cause chronic loss of fluid that is high in chloride and bicarbonate.

Intra-abdominal accumulation of inflammatory fluid: Severe intra-abdominal inflammation may cause several litres of fluid rich in plasma proteins and electrolytes to be lost into the peritoneal cavity. This typically occurs in peritonitis or acute pancreatitis and often in the context of the systemic inflammatory response syndrome (SIRS). This is best replaced (as well as can be estimated) by physiological saline or other suitable crystalloids.

Systemic sepsis (SIRS and multiple organ dysfunction syndrome): Systemic sepsis is associated with widespread endothelial damage and a large increase in capillary permeability mediated by a range of cytokines and other circulating mediators. The result is extensive loss of protein and electrolyte-rich fluid from the circulation into the extravascular space (‘third space loss’), which, combined with loss of peripheral resistance, results in cardiovascular collapse and shock.

The required fluid volume is difficult to estimate and replacement is usually given so as to maintain cardiovascular stability (pulse rate and blood pressure) and urinary output (at least 0.5 ml/kg body weight/hour) whilst avoiding fluid overload and cardiac failure. In the severely ill patient, in whom the volume requirements are particularly difficult to judge, a central venous pressure line or transoesophageal Doppler provide a more accurate method of assessing precise fluid replacement needs (see Enhanced recovery programmes, below).

Abnormal insensible fluid loss: Abnormal insensible fluid loss can greatly increase overall fluid loss, particularly in the seriously ill or elderly patient and must be included in the fluid balance equation. Pyrexia increases insensible loss by approximately 20% for each degree Celsius rise in body temperature, mainly in the form of exhaled water vapour. A pyrexia of 38.5°C for 3 days would therefore cause an extra litre of fluid loss. Sweating causes loss of sodium-rich fluid which can be easily overlooked in patients with fever and when the ambient temperature rises.

Preventing acute renal failure: Maintaining fluid balance in surgical patients depends on anticipating problems before they cause adverse effects and risk acute renal failure. Acute renal failure is a serious complication with a high mortality in surgical patients. Prevention involves similar strategies in all patients at risk, namely:

• Observing changes in vital signs—pulse rate, blood pressure and CVP if appropriate

• Checking hourly urine output is adequate

• Measuring fluid losses to guide replacement

• Seeking clinical signs of fluid imbalance (both dehydration and overload)

• Regularly estimating plasma urea and electrolytes

In patients with cardiac failure or shock, monitoring and treatment is best carried out in an intensive care or high-dependency/critical care unit, using invasive monitoring to help determine the required volume of fluid replacement.

Common fluid and electrolyte problems

Intermediate elective operations and uncomplicated emergency operations

Most operations fall into this category. Patients are generally in fluid and electrolyte equilibrium before operation, although diuretic therapy (for cardiac failure, hypertension or chronic renal failure) may cause problems. For these, plasma urea and electrolytes should be checked before operation. Note that loop and thiazide diuretics may cause hypokalaemia whilst potassium-sparing diuretics such as spironolactone may cause hyperkalaemia. If serious abnormalities are found, operation must be postponed until the problem is corrected. Hypokalaemia can usually be treated by oral potassium supplements or by adding a potassium-sparing diuretic. Hyperkalaemia is usually corrected by substituting a loop or thiazide diuretic.

Mild renal dysfunction (plasma urea up to about 15 mmol/L and creatinine up to about 170 mmol/L) is not usually a contraindication to surgery. These patients tend to be mildly dehydrated, however, and oral fluid intake should be strongly encouraged.

Introduction to management

For elective surgery, the patient is often kept ‘nil by mouth’ for 6–12 hours before operation, although most can take clear fluids by mouth up to 3 hours before operation. The patient is likely to take very little oral fluid for up to 6 hours after operation and a fluid deficit of 1000–1500 ml is therefore common. Mild fluid deficits can usually be quickly made up once the patient is drinking normally and intravenous fluid replacement is rarely required. For patients with mild renal failure, an infusion should be set up at the outset of the ‘nil by mouth’ period to prevent acute-on-chronic renal failure. Occasionally, and despite the use of anti-emetics, patients vomit after operation and intravenous fluids should be employed if vomiting is prolonged.

Children and especially infants and neonates are much more vulnerable to fluid deprivation because of their small total body fluid volume and disproportionate insensible losses. Even relatively minor operations can cause dehydration and intravenous fluids may be necessary, with the rate and volume calculated according to body weight and measured blood loss.

As a rule, the sooner the body can assume control over its own fluid and electrolyte homeostasis the better. Intravenous fluids should be discontinued as soon as normal oral intake has been resumed and urine output is satisfactory.

Major operations

Major elective or emergency operations, especially those involving bowel, pose particular problems with fluid management. The principal reasons are:

• Patients are often elderly and are likely to have a diminished cardiovascular reserve. They may have pre-existing fluid and electrolyte abnormalities

• Preoperative vomiting and restricted fluid intake may have caused dehydration and electrolyte abnormalities

• Blood loss during and after operation may be substantial

• Operations may take several hours with consequent insensible losses from the open wound

• Third space losses of 500–1000 ml can occur after major surgery or trauma as a result of systemic responses to trauma

• The recovery period when oral intake is nil or restricted may become extended—several days following complicated bowel surgery or peritonitis (e.g. perforated diverticulitis or an anastomotic leak)

Careful pre- and postoperative assessment of patients is crucial so problems can be anticipated. This should include clinical examination for dehydration (dry mouth and loss of normal skin turgor) or overhydration (elevated jugular venous pressure or cardiac failure). Plasma urea and electrolytes, creatinine and full blood count should be measured daily. Elevated urea concentration with little elevation of creatinine is characteristic of dehydration. An abnormally high haemoglobin concentration (providing polycythaemia is not present) also indicates dehydration, especially if it was normal beforehand.

Enhanced recovery programmes

In recent years, clinicians in surgery have been attempting to shorten hospital stays and reduce complication rates by developing structured systems that reduce the stress response to enhance recovery. These involve attention to all facets of surgical care, so-called ‘multimodal optimisation’ or ‘fast track recovery’. This includes special attention to perioperative fluid management, the use of minimal access surgical techniques and mechanisms to preserve postoperative organ function, including:

• Preoperative assessment and improved education and preparation of patients so that they understand what will happen and cope with planned early discharge

• Home care arrangements to cope with early discharge

• Improved methods of calculating fluid replacement that ensure the patient remains normovolaemic within narrow limits, preventing central hypovolaemia and fluid overload. NICE have recommended the use of transoesophageal Doppler ultrasound monitoring of left ventricular stroke volume to enable intraoperative assessment of fluid status and provide individualised goal-directed fluid therapy. Trials have shown this can reliably shorten hospital stays and reduce complication rates

• Planned and assisted early postoperative mobilisation

• Early enteral nutrient challenge and the use of gut-specific nutrients such as glutamine, antioxidants and synbiotics (nutritional supplements that improve the balance of intestinal microflora). Methods that enable earlier return of gut function may be fundamental to rapid recovery. Gastrointestinal gut-associated lymphoid tissue (GALT) forms more than half the body’s immunological cell mass and is believed to play a key role in stress responses to surgery. Sustaining nutrition of the small bowel wall from within the lumen may prevent breakdown of intestinal barrier function. Healthy bowel function enables earlier tolerance of food, less postoperative ileus and less postoperative nausea and vomiting

• Avoiding opiates by using epidural or regional analgesia

• Delivering high concentrations of inspired oxygen

Abnormalities of individual electrolytes

(see Table 2.3 for a summary of causes and effects)

Table 2.3

Causes and effects of sodium and potassium deficiency and excess

Abnormalities of plasma sodium concentration: Plasma sodium abnormalities are usually discovered incidentally on regular measurement of electrolytes.

Hyponatraemia: A low plasma sodium level may be real or spurious. Spurious results commonly arise when blood is taken from an arm receiving an intravenous infusion; less commonly, false laboratory results can occur if there is lipaemia resulting from parenteral nutrition. If in doubt, the test should be repeated with appropriate precautions.

In hyponatraemia (except in severe hyperglycaemia or infusion of mannitol), the plasma becomes hypotonic. This causes cellular overhydration which in severe cases results in cerebral oedema. Mild hyponatraemia is symptomless but when the plasma sodium falls below about 120 mmol/L, patients often become confused. Convulsions and coma occur when concentrations fall below about 110 mmol/L. If hyponatraemia is confirmed biochemically, the next step is to clinically assess the state of hydration (i.e. the extracellular fluid volume) and this will guide therapy.

There are three possibilities:

• Water deficit with a larger sodium deficit (clinical signs—dry mouth, poor skin turgor, poor urine output, high urine osmolality): sodium insufficiency is usually due to diuretic therapy, vomiting, diarrhoea or other excessive losses of body fluids with inadequate replacement. Treatment involves rehydration with appropriate sodium-containing intravenous fluids

• Sodium normal with a larger water excess (clinical signs—weight gain, ankle swelling, raised jugular venous pressure): this usually results from organ dysfunction. Cardiac failure is the most common cause, followed by renal, liver and respiratory failure. Overhydration is compounded by excessive intravenous fluid administration. Management is based primarily on treating the organ failure, e.g. diuretics for cardiac failure

• Water excess: this is uncommon and is usually due to inappropriate antidiuretic hormone (ADH) secretion. This is rare on a surgical ward except for TUR syndrome in which excess fluid is absorbed during transurethral resection of the prostate. It can also occur following head injury or neurosurgery, or may occur in pneumonia, empyema, lung abscess or oat-cell carcinoma of the lung. Excess ADH increases water reabsorption by the renal tubules independently of sodium. The result is water overload and dilutional hyponatraemia. Inappropriate ADH secretion is the most likely diagnosis if the urine osmolality is found to be high and the plasma osmolality low. Hyponatraemia caused by inappropriate ADH secretion is managed by restricting fluid intake to 1 litre per day

Hypernatraemia: This is uncommon and is often iatrogenic in the surgical patient. The usual cause is either excess administration of sodium via intravenous fluids or inadequate water replacement. Hypernatraemia is more likely to occur after operation because increased aldosterone secretion causes sodium to be conserved by the kidney. Very rarely, hypernatraemia is caused by Conn’s syndrome (primary hyperaldosteronism).

Treatment involves encouraging the patient to drink more water, or infusing fluids with a low sodium content.

Abnormalities of plasma potassium concentration: Acid–base abnormalities (see below) can have a profound effect on plasma potassium concentration but are likely to correct spontaneously as the acid–base problem is treated.

Hypokalaemia: In the preoperative patient, hypokalaemia usually results from poor dietary intake, diuretic therapy, chronic diarrhoea, losses from a malfunctioning ileostomy or, rarely, excess mucus secretion from a rectal villous adenoma. Rarely, hypokalaemia may be caused by primary hyperaldosteronism (Conn’s syndrome).

Postoperatively, hypokalaemia is usually caused by inadequate potassium supplementation in intravenous infusions. The lack of intake is compounded by increased urinary losses from stress-induced secondary hyperaldosteronism.

Hypokalaemia causes skeletal muscle weakness and reduces GI motility, with paralytic ileus in extreme cases. When severe, there is also a risk of sudden cardiac arrhythmias or even cardiac arrest. Hypokalaemia can usually be corrected with oral potassium supplements (effervescent or slow-release tablets). For patients on intravenous fluids, potassium supplements are added as appropriate. The infusion rate should not generally exceed 15–20 mmol per hour, but larger quantities may be required following operations involving cardiopulmonary bypass.

Hyperkalaemia: This is less common than hypokalaemia in surgical patients but may require urgent correction. In the preoperative patient, it is most commonly caused by chronic renal failure, high doses of ACE inhibiting drugs or potassium-sparing diuretics. Occasionally, non-steroidal anti-inflammatory drugs cause hyperkalaemia. Postoperative hyperkalaemia is usually iatrogenic, caused by excessive intravenous potassium administration, although it may be associated with acute renal failure or blood transfusion.

Hyperkalaemia is asymptomatic in its early stages but there is a high risk of sudden death from asystole when plasma potassium concentration reaches about 7.0 mmol/L. The emergency management of hyperkalaemia is shown in Figure 2.3.

Fig. 2.3 Emergency management of hyperkalaemia

Acid–base disturbances (see Fig. 2.4 and Table 2.4)

Major acid–base abnormalities are rare in uncomplicated surgery and usually arise in seriously ill patients. In a nutshell, when breathing is inadequate, carbon dioxide builds up and combines with water to produce carbonic acid (‘respiratory acid’) which contributes to an acidic pH. Treatment is to lower the PCO₂ by assisted breathing. In addition, when normal metabolism is impaired, oxidative metabolism declines and lactic acid accumulates. Treatment is directed at the cause of metabolic impairment, e.g. sepsis, together with organ support therapy, e.g. oxygen, intravenous fluids and antibiotics.

Table 2.4

Acid–base disorders

Fig. 2.4 Interpretation of blood gas analyses in the patient with acid–base disturbances

Metabolic acidosis: Metabolic acidosis usually follows an episode of severe tissue hypoxia resulting from hypovolaemic shock, myocardial infarction or systemic sepsis. The most common cause is inadequate tissue oxygenation leading to accumulation of lactic acid. In surgical patients, the onset of metabolic acidosis is often an indicator of serious intra-abdominal problems such as an anastomotic leak. Metabolic acidosis is also seen in acute renal failure and uncontrolled diabetic ketoacidosis. Clinically, patients have rapid, deep, sighing ‘Kussmaul’ respirations as they hyperventilate to blow off carbon dioxide (a respiratory compensatory mechanism). Arterial blood gas estimations show the characteristic picture of raised hydrogen ion concentration and low standard bicarbonate with a low arterial PCO₂. Plasma potassium concentration is elevated because of a shift from the intracellular compartment to the extracellular compartment. Treatment is directed at the underlying cause.

Respiratory acidosis: This results from carbon dioxide retention in respiratory failure. The usual causes in surgical patients are underlying chronic respiratory disease made worse by postoperative chest complications or prolonged respiratory depression due to sedative, hypnotic or narcotic drugs. Plasma hydrogen ion concentrations and PCO₂ are elevated but standard bicarbonate is initially normal. A degree of metabolic compensation may occur as the kidneys excrete excess hydrogen ions and retain bicarbonate. Treatment is directed at the underlying cause and to providing assisted ventilation.

Metabolic alkalosis: Metabolic alkalosis is usually caused by severe and repeated vomiting or prolonged nasogastric aspiration for intestinal obstruction. The latter classically occurs in pyloric stenosis with gross loss of gastric acid. The patient becomes severely dehydrated and depleted of sodium and chloride ions; the condition is thus known as hypochloraemic alkalosis. The kidney attempts to compensate by conserving hydrogen ions but this occurs at the expense of potassium ions lost into the urine. Patients become hypokalaemic not only from excess urinary loss but also because potassium shifts into the cells in response to the alkalosis. Treatment of hypochloraemic hypokalaemic alkalosis involves rehydration with normal saline infusion including potassium supplements; large volumes (up to 10 litres) are often required. Renal excretion of bicarbonate ions eventually corrects the alkalosis.

Respiratory alkalosis: This occurs when carbon dioxide is lost via excessive pulmonary ventilation. The usual cause in surgical practice is prolonged mechanical ventilation during general anaesthesia or in the intensive care unit without adequate monitoring.

Nutritional management in the surgical patient

Essential principles

Malnutrition is a wasting condition resulting from deficiencies in energy (i.e. calorie), protein and sometimes vitamins and trace elements. Recognising and treating pre-existing malnutrition and preventing postoperative starvation are important aspects of surgical management that are often neglected. Basic evaluation for malnutrition should be a standard part of assessing surgical patients (see Box 2.4) because untreated malnutrition predisposes to a range of problems that substantially increase morbidity and mortality rates and delay recovery (see Box 2.5).

Box 2.4 Assessing patients for malnutrition

Clinical assessment

• Lack of nutritional intake for 5 days or more

• Clinical appearance (‘end-of-bedogram’)—does the patient look malnourished?

• Unintentional weight loss of more than 10% from usual body weight within previous 6 months indicates malnutrition. More than 20% is likely to represent severe malnutrition

• Body mass index (BMI)—less than 18.5 suggests malnutrition

Anthropometric assessment

• Triceps skin fold thickness—technically difficult to perform but provides a good proxy for body density and hence overall fat content

• Mid arm circumference—unreliable because of technical measurement artefact and lack of dependable data upon which to base measurements

• Hand grip strength—easy to perform but lack of reproducible baseline data limits application to research projects

Blood indices

• Reduced plasma albumin, prealbumin or transferrin. In critically ill patients, plasma albumin of less than 35 g/L is associated with a five-fold increase in complications and a 10-fold increase in death rate. Note that low plasma albumin alone is not an accurate marker of malnutrition but may be caused by other metabolic abnormalities

• Reduced lymphocyte count. If plasma albumin and lymphocyte count are both low, there is a 20-fold increase in death rate

Box 2.5 Adverse effects of protein/calorie depletion in surgical patients

• Protein deficiency leads to impaired wound healing and higher rates of wound breakdown

• Protein depletion seriously impairs immune function and the ability to combat infection

• Skeletal muscle mass is lost, reducing muscular strength and general physical activity as well as causing fatigue. This increases the risk of thromboembolism and pressure sores

• Thoracic muscle mass depletion depresses respiratory efficiency and increases risk of pneumonia

• Albumin becomes depleted leading to generalised oedema

• Small bowel mucosal atrophy reduces its ability to absorb nutrients and may lead to bacterial translocation into the bloodstream because of loss of mucosal integrity

• Impaired mental function leads to apathy, depression and low morale

• Postoperative complication rates are higher—twice the rate of minor complications, three times the rate of major complications and three times the mortality compared with well-nourished patients

• Combinations of these factors lead to prolonged recovery times and longer hospital stays

Causes of malnutrition include reduced food intake (anorexia, fasting, pain on swallowing, physical or mental impairment), malabsorption (impaired digestion or absorption, or excess loss from gut) and altered metabolism (trauma, burns, sepsis, surgery, cancer cachexia). Patients with any of these predisposing factors need to be scrutinised more thoroughly for malnutrition.

In practice, most surgical patients have no special nutritional requirements and easily withstand the short period of starvation associated with their illness and operation. All hospitalised patients should be screened using a recognised screening tool and their nutritional state optimised preoperatively as far as is feasible. In any case, optimal nutritional support should be provided after operation.

Nutritional support in hospital is usually provided by a dedicated team and input ranges from encouraging the patient to eat regularly through offering easily prepared but tasty oral diets (e.g. liquidised normal food), through concentrated sip feeds (e.g. Fortisip) and various types of supplementary enteral nutrition given via tube, to managing long-term total parenteral nutrition (TPN) for patients unable to absorb nutrients from the gastrointestinal tract.

Recognising the patient at risk

Malnutrition is common in surgical patients and often goes unrecognised. Studies have shown that as many as 50% of surgical inpatients suffer from mild malnutrition and 30% from severe malnutrition. Simple clinical assessment is the best determinant of the state of nutrition, although other indices can also be used (see Box 2.4).

For patients found to be malnourished, studies have shown that simple pretreatment with regular proprietary sip feeds can stave off postoperative muscle weakness, reduce fatigue and markedly lessen complication rates. However, the evidence of clinical benefit is weak for more complex and prolonged endeavours to improve nutrition by the parenteral route (for example, in oesophageal cancer). Even if it is impracticable to improve the preoperative nutritional state, malnutrition still needs to be recognised and attention given in the postoperative period. The duration of starvation should be kept as short as possible and appropriate nutrition provided. This contributes to healing, improves resistance to infection and reduces complications caused by muscle weakness (see Box 2.5).

Effects of starvation

Simple starvation: During simple starvation (i.e. in the absence of illness or trauma), blood glucose concentration is maintained by lowering of insulin secretion and increasing glucagon production. Liver glycogen becomes exhausted within 24 hours but gluconeogenesis in liver and kidneys is enhanced, utilising amino acids from protein breakdown and glycerol from lipolysis as substrates. Much of the glucose thus produced is used by the brain, as most other tissues are able to metabolise fatty acids and ketones derived from adipose tissue. Overall energy demands fall in simple starvation and energy is obtained largely from body fat. Protein is conserved until a late stage.

Trauma, surgery or sepsis: In severe trauma or major surgery, and particularly in sepsis, energy requirements increase by 20–100% of normal. As in simple starvation, lipid becomes a major fuel source; this decreases glucose utilisation, but fatty acids other than glycerol cannot be used for glucose synthesis. Hepatic glucose production increases, but peripheral glucose utilisation is impaired, often leading to hyperglycaemia.

Skeletal muscle proteolysis and urinary nitrogen excretion increase enormously compared with the fasted state. Protein from skeletal muscle is catabolised to release amino acids (particularly alanine), lactate and pyruvate. The stimulus for proteolysis is likely to be macrophage cytokines (e.g. IL1, IL6, TNF). IL1 reduces hepatic albumin synthesis in favour of more urgently needed acute-phase proteins and gluconeogenesis. Amino acids are also used directly in wound healing and in haemopoiesis.

In sepsis, there is a progressive inability at mitochondrial level to fully oxidise substrates for energy generation, leading to a fall in oxygen consumption as sepsis worsens. Fatty acids are increasingly mobilised from adipose tissue, manifesting as hypertriglyceridaemia; mobilisation is governed by raised levels of glucagon, catecholamines, cortisol and TNF. Fatty acids are oxidised for adenosine triphosphate (ATP) production in order to fuel synthesis of new glucose and proteins. If liver failure develops, amino acid clearance deteriorates and plasma concentrations rise. Some amino acids are then metabolised into false neurotransmitters which promote the vasodilatation and hypotension seen in sepsis and cause septic encephalopathy.

Supplementary nutrition

Supplementary nutrition other than liquidised diets and sip feeds is a complicated and sometimes expensive process with distinct risk of complications. It should not be undertaken without proper assessment. Deciding whether a patient is likely to benefit from supplementary nutrition depends on determining:

• That the patient is malnourished or will be deprived of nutrition for at least 5 days

• That the patient is likely to benefit—certain conditions make supplemental nutrition ineffective (e.g. enteral feeding in high output enterocutaneous fistula)

• Whether there is an appropriate route for administration, e.g. suitable gut function

Nutritional support is generally recommended in well-nourished patients who are unable to tolerate oral feeding for 7–10 days, or 5–7 days if already malnourished.

Methods of giving supplementary nutrition: Box 2.6 summarises the range of nutritional regimens and their main surgical indications. The gastrointestinal tract should be used whenever possible because any form of enteral feeding is intrinsically safer than parenteral nutrition and is much cheaper. In addition, the small intestinal mucosa tends to atrophy when not used. Enteral feeding supports the gut-associated immunological shield and prevents microorganisms translocating into the circulation, reducing the chances of blood-borne infection. Contraindications to enteral feeding include intestinal obstruction, high-output intestinal fistula, intractable vomiting or diarrhoea, and severe malabsorption.

Box 2.6 Special methods of nutrition and their indications

1. Selective diets for specific indications, e.g. diabetic, low-protein (renal and liver failure), low-fat (gallstones), high-fibre (constipation, diverticular disease) or weight reducing (obesity)

2. Liquidised normal diet—for patients with partial oesophageal obstruction (e.g. stricture, tumour or oesophageal intubation for cancer)

3. High-protein, high-calorie dietary supplements ‘sip diet’—for chronically malnourished patients capable of a normal diet or debilitated convalescent patients

4. Polymeric liquid diet via tube—short chain peptides, medium chain triglycerides and polysaccharides plus vitamins and trace elements These contain the full range of nutritional requirements often including fibre. Used for nutritional support of patients unable to eat or drink such as the unconscious, ventilated and seriously ill patient in intensive care or patients unwilling to take adequate nutrition following major surgery or trauma

5. Elemental diet via tube, containing L-amino acids and simple sugars requiring no digestion and minimal absorptive capacity—for patients with minimal remaining bowel after massive resection. These are expensive and unpalatable and the high osmolarity can cause diarrhoea

6. Peripheral parenteral nutritional support for patients unable to have tube feeding but needing specific energy or protein supplementation

7. Total parenteral nutrition (TPN), i.e. comprehensive intravenous nutrition—for patients with prolonged ileus or a very proximal fistula

Sip feeds: If the patient is able to eat, fluid diets (total or supplementary) can be given orally. Proprietary sip feeds containing easily absorbed calories, protein, minerals and vitamins are available in a variety of formulations and flavours and are well tolerated.

Tube feeds: Certain patients are unsuitable for sip feeding but can be fed by one of several tube feeding routes. Indications include patients with swallowing difficulties (including overspill and lack of cooperation), anorexia, lack of palatability of liquid feeds, the need for a higher volume of feed than the patient can comfortably manage and anticipated substantial delay in resuming oral feeding after operation.

Even if the patient is unable to swallow (for example, because of bulbar palsy, unconsciousness or facial fractures), complete enteral nutrition can be delivered by means of a fine-bore nasogastric or nasojejunal tube, the latter for those who require post-pyloric enteral feeding, e.g. in acute pancreatitis). An individual fluid diet is formulated and is delivered at a controlled rate using a pump, often overnight.

Feeding tubes can also be placed percutaneously into stomach or jejunum, either at operation (if feeding problems are anticipated) or with endoscopic or laparoscopic help. Gastrostomies are often employed in patients after stroke or in those with upper gastrointestinal anastomoses or obstructing lesions. The usual technique nowadays is by percutaneous endoscopic gastrostomy (PEG), combining gastroscopy and percutaneous placement. PEG tubes are contraindicated in peritonitis, ascites and prolonged ileus.