Managing physiological change in the surgical patient

Published on 11/04/2015 by admin

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Managing physiological change in the surgical patient

Systemic responses

Factors responsible for systemic responses (Box 2.1)

Surgical patients are subject to a variety of major injuries and catastrophes that make massive demands on the body’s ability to sustain life and maintain physiological equilibrium. Examples of such stressors include:

Box 2.1   Factors responsible for systemic responses to severe injury or major surgery

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

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

• 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.

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.

Fluid, electrolyte and acid–base management

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).

Maintenance of water and sodium

For most patients, the daily water and sodium requirements are best met by using appropriate 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 2–2.5 litres of 5% glucose (see 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.

Box 2.3   Sample daily intravenous fluid regimens as a substitute for oral intake in uncomplicated cases

Note that Hartmann’s solution (or similar balanced electrolyte solutions such as Ringer’s lactate) is often used as the sole fluid for intravenous infusion. This is more physiological and contains 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 are based on published guidelines and formulae (see: http://www.nda.ox.ac.uk/wfsa/html/u19/u1914_01.htm).

Limits of compensatory mechanisms

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 litres, of which about 55–60% is water (about 3.5 litres). 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 litres. A deficit of more than 3 litres 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 children. When overall fluid deficit reaches about 3 litres, 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 of fluid deficit, the limit of cardiovascular compensation is reached and the patient develops hypovolaemic shock. Note that fit young people are able to sustain normal vital signs longer but when they do decompensate, they do so abruptly.

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.

Physiological changes in response to surgery and trauma

The stresses of trauma or surgery cause a rise in circulating catecholamines. Stress also stimulates the hypothalamo–pituitary–adrenal axis, which increases secretion of cortisol and aldosterone. These hormones promote renal conservation of sodium and water and cause a reduction in urine volume and urine sodium concentration.

Effects of a fall in renal perfusion: Any substantial reduction in effective circulating volume may cause a fall in renal perfusion. In addition, aortic surgery involving aortic clamping may alter the dynamics of renal artery flow, whilst raised intra-abdominal pressure (see Abdominal compartment syndrome, below) disrupts renal blood flow.

A fall in renal perfusion activates the renin–angiotensin–aldosterone mechanism to sustain the blood pressure. As glomerular filtration falls, renin release is stimulated from the renal juxtaglomerular apparatus and this catalyses the conversion of angiotensin I to angiotensin II in the lungs. Angiotensin II has a powerful pressor effect on the peripheral vasculature, counteracting hypotension, as well as stimulating aldosterone release from the adrenal cortex. Aldosterone promotes active reabsorption of sodium ions from the distal convoluted tubules of the kidney, accompanied by passive reabsorption of water. Sodium reabsorption is linked to increased excretion of potassium and hydrogen ions.

The net effect is that in conditions causing renal perfusion to fall, the urine output falls by several hundred millilitres per day, and the urine that is produced is low in sodium (less than 40 mmol/L), high in potassium (greater than 100 mmol/L) and acidic. The loss of hydrogen ions causes a degree of metabolic alkalosis.

Other factors in water conservation: Water conservation is further enhanced by stress-mediated secretion of antidiuretic hormone (ADH), also known as vasopressin, from the posterior pituitary (neurohypophysis). Loss of water alone increases the plasma osmolality, stimulating ADH release, mediated by osmoreceptors in the hypothalamus. ADH binds to receptors in the distal renal tubules and promotes reabsorption of water. Release of ADH is also stimulated by falls in blood pressure and volume, sensed by stretch receptors in the heart and large arteries. Changes in blood pressure and volume are not nearly as sensitive a stimulator as increased osmolality, but are potent in extreme conditions (e.g. loss of over 15% volume in acute haemorrhage). Stress and pain probably also promote ADH release via other hypothalamic pathways.

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