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Surgical patients are subject to a variety of major stressors that make massive demands on the body’s ability to maintain physiological equilibrium and sustain life. Examples of such stressors include:
Major operations —tissue trauma, blood and fluid loss, anaesthesia (particularly Trendelenburg head-down position + pneumoperitoneum for laparoscopic surgery), healing and repair
Major trauma including fractures and burns; head, abdominal and chest injuries
Major cardiovascular events, for example, myocardial infarction, pulmonary embolism, stroke
Haemorrhage and fluid infusion including blood; fluid and electrolyte abnormalities
Infection, inflammation and sepsis
Hypoxia and hypotension
Direct and indirect tissue trauma
Fall in intravascular volume, leading to a fall in cardiac output and reduced peripheral perfusion and hypoxia
Excess intravenous fluids, particularly 0.9% NaCl, causing interstitial oedema
Local and spreading inflammation and infection
Systemic inflammatory responses and sepsis
Pain
Psychological stress
Excess heat loss
Secondary effects on the blood
Starvation
The way the body responds to major systemic insults depends on several factors: the physiological reserve of the patient’s vital 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.
The aim is always to recognise problems early by regular clinical observation, and to correct abnormal physiology rapidly and accurately to prevent intrinsic compensatory mechanisms becoming overwhelmed. If this happens in one organ system without correction, escalating decompensation of other organ systems follows.
Management requires careful monitoring, often in a high-dependency or intensive care unit, with repeated investigations of organ function and dysfunction. In most elective operations, many of the responses discussed subsequently can be mitigated by good preoperative assessment, preoperative optimisation, appropriate perioperative fluid management, ensuring oxygenation, adequate analgesia, reducing psychological stress, preventing infection and using best operative technique to minimise tissue trauma, blood loss and complications. Enhanced recovery programmes (Enhanced Recovery After Surgery Programmes [ERAS] have been introduced which give special attention to these factors before, during and after operation and benefits accrue with attention to each of many small details ( Table 2.1 ). A list of ERAS society guidelines is given at: http://erassociety.org.loopiadns.com/guidelines/list-of-guidelines/ . ‘Prehabilitation’ exercise training has been used but has so far failed to translate into improved outcomes.
Enhanced Recovery Protocols | ||
---|---|---|
When | Component | Rationale |
Well in advance | Structured preoperative information, education and counselling, including psychological assessment and treatment for depression and anxiety | Reduce fear and anxiety |
Stopping smoking and excessive alcohol consumption | Reduce complications | |
Day of surgery | No prolonged fasting. Preoperative fluid and carbohydrate loading | Reduce insulin resistance and improve recovery |
No routine bowel preparation | Reduce dehydration and ileus | |
Prophylaxis against thromboembolism | Reduce thromboembolic complications | |
Preoperative antibiotic prophylaxis against infection | Reduce rate of infection | |
No premedication | More alert patient postoperatively | |
Intraoperative | Short-acting anaesthetic agents | More rapid recovery |
Midthoracic epidural for analgesia | Reduce need for opioid analgesics | |
No drains or rapid removal | Less discomfort and greater mobility | |
Goal directed fluid therapy | Avoid water and salt overload | |
Postoperative | Epidural analgesia continues postoperatively | |
No nasogastric tubes | Less discomfort and greater mobility | |
Anticipate and treat nausea and vomiting | Improve comfort | |
Continue goal directed fluids | Avoid overload | |
Early oral nutrition to stimulate gut motility | Improved nutrition and recovery of bowel function | |
Early removal of urinary catheter | Improve comfort | |
Nonopioid analgesics (e.g., NSAIDs) | Avoid complications of opioids | |
Early mobilisation | Restore strength; vary pressure on pressure points | |
Regular audit of compliance and outcomes | Ensure ERAS is maintained |
The individual variables responsible for potentially excessive systemic responses to severe injury or major surgery are summarised in Box 2.1 .
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 there is tissue ischaemia.
This is a key factor in initiating systemic responses. Hypovolaemia results from:
Excess fluid loss ( Box 2.2 )
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 (septicaemia) —massive peripheral vasodilatation and third space losses caused by 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. Restricted oral intake also explains the mild tachycardia commonly seen in postoperative patients. Compensation is most effective in young fit individuals, but decompensation can be sudden and rapid. Catecholamines also have profound catabolic effect, 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.
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 by affecting venous return, systemic vascular resistance, and particularly cause myocardial dysfunction in elderly patients with cardiac disease. Major events, such as sepsis (septic shock), pulmonary embolism or myocardial infarction may precipitate cardiovascular collapse.
Pain causes increased catecholamine and adrenocorticotrophic hormone (ACTH) secretion. Perioperative blockade of pain (e.g., by regional anaesthesia, such as thoracic epidurals) greatly reduces the adverse systemic effects.
Psychological stress associated with injury, severe illness or elective surgery has an effect similar to pain on sympathetic function and hypothalamic activity.
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 particularly 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, covering the head (especially in babies as they lose heat more through the head), using warm air ‘bear-huggers’ and by warming fluids during intravenous infusion.
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. 48) may initiate widespread intravascular thrombosis, using up clotting factors and precipitating disseminated intravascular coagulation (DIC) , with failure of normal clotting.
Patients with major surgical conditions are often malnourished before operation (see Nutritional management , later). Many are starved for 6 to 12 hours preoperatively and often do not start eating for 12 to 24 hours after surgery. After major gastrointestinal (GI) surgery, starvation may be prolonged for several days, or much longer with complications such as anastomotic breakdown or fistula formation.
In severe trauma or extensive operative surgery, particularly if complicated by sepsis, the key factors in the systemic response are increased sympathetic activity plus 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 Fig. 2.1 .
The overall effect is rising blood glucose (levels may reach 20 mmol/L); often resulting in hyperglycaemia and a pseudo-diabetic 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.
In a normal healthy adult, nitrogen balance is constantly maintained. Protein turnover results in daily excretion of 12 to 20 g of urinary nitrogen which is made good by dietary intake. In a hypercatabolic state, nitrogen losses can increase three- or fourfold. Most importantly, this metabolic environment prevents proper use 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.
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 should be anticipated (see later).
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 for more than a day or two.
In general, patients who are unable to meet their fluid or electrolyte needs require maintenance replacement therapy equivalent to 25 to 30 mL/kg per day of water, 1 mmol/kg per day of sodium, potassium and chloride, and 50 to 100 g/day of glucose (noting that 5% glucose contains 5 g glucose per 100 mL).
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 later). These are best managed with the help of experienced anaesthetists and intensivists in high dependency or intensive care units, where monitoring and therapy can be rigorously managed.
The body of an average 70 kg adult contains 42 L of fluid, distributed between the intracellular compartment, the extracellular space and the bloodstream ( 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 L/day. About 1 L is lost insensibly from skin and lungs, 1300 to 1800 mL are passed as urine (about 60 mL/h or 1 mL/kg per h) and 100 mL are lost in faeces. About 100 to 150 mmol of sodium ions and 50 to 100 mmol of potassium ions are lost each day in urine and this is balanced by the normal dietary intake ( Table 2.2 ).
Normal Daily Intake | Normal Daily Output |
---|---|
Water | |
Diet 2300 mL Metabolism 200 mL |
Urine 1400 mL (minimum obligatory volume=400 mL) Skin loss 500 mL (obligatory diffusion and vaporisation) Note: sweating in pyrexia or a high ambient temperature can cause several litres extra loss each day Lung loss 500 mL (obligatory) Faecal loss 100 mL |
Sodium | |
Diet 150 mmol/day (range 50–300 mmol) | Stool 5 mmol/day Skin transpiration 5 mmol/day (in the absence of sweating) Urine 140 mmol/day (can fall down to 15 mmol/day if required) |
Potassium | |
Diet 100 mmol/day (range 50–200 mmol) | Stool 10 mmol/day (obligatory) Skin <5 mmol/day Urine 85 mmol/day (rarely falls below 60 mmol/day) |
For most patients, the daily water and sodium requirements are best met by using appropriate balanced quantities of normal saline solution (0.9% sodium chloride) and 5% dextrose (glucose) solution. Normal saline contains 154 mmol each of sodium and chloride ions per litre. One litre will thus satisfy the daily sodium requirement of uncomplicated patients. The additional requirement for water is made up with 2 to 2.5 L of 5% glucose ( Box 2.3 ). The small amount of glucose this contains contributes little to nutrition but renders the solution isotonic. This prescription is altered for patients with electrolyte abnormalities by varying the volume of normal saline given.
1000 mL 0.9% sodium chloride+20 mmol KCl
1000 mL 5% dextrose+20 mmol KCl
1000 mL 5% dextrose+20 mmol KCl
Total: 154 mmol sodium and 60 mmol potassium
1000 mL dextrose–saline (i.e., 4% dextrose+1.8% NaCl)+20 mmol KCl
1000 mL dextrose–saline+20 mmol KCl
1000 mL dextrose–saline+20 mmol KCl
Total: 90 mmol sodium and 60 mmol potassium
Note that Hartmann solution (or similar balanced electrolyte solutions, such as Ringer lactate) is often used as the sole fluid for intravenous infusion. This is more physiological and contains somewhat less chloride (111 mmol/L), some potassium (5 mmol/L) and insignificant amounts of calcium and lactate.
In children, water excretion is markedly reduced in the postoperative period as a result of increased ADH secretion. Maintenance fluids requirements can be based on published guidelines and formulae for example, https://www.nice.org.uk/guidance/ng29/ and https:// www.mdcalc.com/maintenance-fluids-calculations
Basic potassium requirements are met by infusing 60 to 80 mmol of potassium chloride in divided doses over each 24-hour period. Premixed intravenous fluids are generally available with 20 or 40 mmol of potassium chloride per 1000 mL infusion bags. If concentrations of potassium chloride greater than 40 mmol in 500 mL are required, they should be given via a central venous infusion in a critical care unit, with cardiac monitoring. Bolus injections of potassium chloride must never be given because rapid increases in plasma potassium can cause cardiac arrest.
Healthy kidneys are normally able to maintain fluid and electrolyte homeostasis in spite of large variations of fluid intake. The same also applies to fluid and electrolytes given intravenously.
The total blood volume in an adult male is about 5 L, of which about 55% to 60% is water (about 3.5 L). Falls in blood volume which are not too rapid or extensive can be compensated by fluid movement from the extracellular compartment, which has a volume of more than 10 L. A deficit of more than 3 L in whole body fluid volume cannot be sustained and intravascular volume inevitably becomes depleted. This is reflected in compensatory cardiovascular changes. Vasoconstriction causes cold peripheries: this is an important warning sign of hypovolaemia and more reliable than the early mild tachycardia, particularly in fit children and young adults as they compensate for a long time owing to good physiological reserves, before abrupt decompensation. When overall fluid deficit reaches about 3 L, the pulse rate becomes very rapid and hypotension and shock develop. Note that patients on beta-adrenergic blocking drugs or with cardiac conduction defects may not be able to increase heart rate and will therefore decompensate earlier. With 4 or more litres fluid deficit, the limit of cardiovascular compensation is reached and the patient develops hypovolaemic shock .
In neonates, children, the elderly and the chronically ill, cardiovascular compensation capacity is greatly reduced. A relatively small fluid and electrolyte imbalance may cause life-threatening complications.
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