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Management of shock, fluid management and blood transfusion


Fluid and electrolyte balance

Normal water and electrolyte balance

Water forms about 60% of total body weight in men and 55% in women. Approximately two-thirds is intracellular and one-third is extracellular. Extracellular water is distributed between the plasma and the interstitial space ( Fig. 4.1A ).

Fig. 4.1, Distribution of fluid and electrolytes between the intracellular and extracellular fluid compartments.

The differential distribution of ions (and water) across cell membranes is essential for normal cellular function. The principal extracellular ions are sodium, chloride and bicarbonate. The major intracellular ions are potassium, magnesium, phosphate and sulphate ( Fig. 4.1B ).

The osmolality (tonicity) and volume of extracellular fluid (ECF) are tightly regulated. The osmolality of ECF (normally 275–295 mOsmol/kg) is determined primarily by sodium and chloride ion concentrations. As changes in chloride are largely determined by changes in sodium, it is the amount of sodium in the ECF that is the most important determinant of tonicity. When ECF osmolality rises, antidiuretic hormone (ADH, also known as vasopressin) is released from the posterior pituitary. This stimulates thirst and water retention by the kidney, which lowers osmolality. Conversely, when plasma osmolality falls, ADH secretion is suppressed ( Fig. 4.2A ).

Fig. 4.2, (A) Figure showing increased osmolality triggering thirst and release of ADH. (B) The renin–angiotensin–aldosterone system. ACTH, Adrenocorticotrophic hormone.

A fall in ECF volume stimulates the release of renin from the juxtaglomerular apparatus of the kidney and activation of the renin-angiotensin system. This leads to production of angiotensin II, a potent vasoconstrictor that stimulates thirst and the release of adrenocorticotrophic hormone (ACTH) from the anterior pituitary and aldosterone from the adrenal cortex. Aldosterone increases both sodium and water reabsorption in the renal tubules ( Fig. 4.2B ). Conversely, expansion of ECF volume (hypervolaemia) leads to atrial distension and release of atrial natriuretic peptide from the heart, stimulating sodium and water excretion.

The distribution of fluid between the intra- and extravascular compartments is dependent on the oncotic pressure of plasma and the permeability of the endothelium, both of which may change as a consequence of illness or following surgery. Plasma oncotic pressure is primarily determined by albumin.

Maintenance fluid requirements

In healthy people ( Table 4.1 ):

  • Between 2500 and 3000 mL of fluid is lost every 24 hours from the kidneys and gastrointestinal tract, and through evaporation from the skin and respiratory tract

  • Fluid losses are largely replaced through eating and drinking

  • A further 200 to 300 mL of water is provided endogenously every 24 hours by the metabolic oxidation of carbohydrate and fat.

Table 4.1
Normal daily losses and requirements for fluids and electrolytes
Volume (mL) Na + (mmol) K + (mmol)
Urine 2000 80 60
Insensible losses from skin and respiratory tract 700 – –
Faeces 300 – 10
Less water created from metabolism 300 – –
Total 2700 80 70

In adults, the normal daily maintenance fluid requirement is ∼20 to 25 mL/kg (∼2000 mL/day). Newborn babies and children contain proportionately more water than adults. The daily maintenance fluid requirement at birth is about 75 mL/kg, increasing to 150 mL/kg during the first weeks of life. After the first month of life, fluid requirements decrease and the ‘4/2/1’ formula can be used to estimate maintenance fluid requirements: the first 10 kg of body weight requires 4 mL/kg/h; the next 10 kg requires 2 mL/kg/h; thereafter, each kg of body requires 1 mL/kg/h. The estimated maintenance fluid requirements of a 35-kg child would therefore be:


( 10 × 4 ) + ( 10 × 2 ) + ( 15 × 1 ) = 75 mL / h .

In the absence of sweating, almost all sodium loss is via the urine. Under the influence of aldosterone, this can fall to 10 to 20 mmol/24 hours. Potassium is also excreted mainly via the kidney, with a small amount (10 mmol/day) lost via the gastrointestinal tract. In severe potassium deficiency, losses can be reduced to about 20 mmol/day, but increased aldosterone secretion, high urine flow rates and metabolic alkalosis all limit the ability of the kidneys to conserve potassium and predispose to hypokalaemia.

In adults, the normal daily requirement for both sodium and potassium is approximately 1 mmol/kg.

Assessing losses in the surgical patient

In addition to reduced oral fluid intake in the perioperative period, fluid and electrolyte balance may be altered in the surgical patient for several reasons:

  • ADH and aldosterone secretion

  • Loss from the gastrointestinal tract (e.g., bowel preparation, ileus, stomas, fistulae)

  • Insensible losses (e.g., sweating secondary to fever)

  • ‘Third-space’ losses, as described later

  • Surgical drains

  • Medications (e.g., diuretics)

  • Underlying chronic illness (e.g., cardiac failure, portal hypertension)

An understanding of the causes and nature of fluid losses encountered in the surgical patient, together with careful monitoring of fluid balance, is essential in the management of fluids and electrolytes perioperatively ( Table 4.2 ).

Table 4.2
Fluid loss
A. Source of Fluid Loss in Surgical Patients
Typical losses per 24 hours Factors modifying volume
Insensible losses 700–2000 mL ↑ Losses associated with pyrexia, sweating and use of nonhumidified oxygen
Urine 1000–2500 mL ↓ With aldosterone and antidiuretic hormone secretion; ↑ with diuretic therapy
Gut 300–1000 mL ↑ Losses with obstruction, ileus, fistulae and diarrhoea (may increase substantially)
Third-space losses 0–4000 mL ↑ Losses with greater extent of surgery and tissue trauma

B. Nature of Fluid Loss Following Surgery and Trauma
Nature of fluid Mechanism Contributing factors
Blood Haemorrhage Site and magnitude of tissue injury
Poor surgical haemostasis
Abnormal coagulation
Electrolyte-containing fluids Vomiting Anaesthesia/analgesia (e.g., opioids)
Obstruction or ileus
Nasogastric drainage Ileus
Gastric surgery
Diarrhoea Antibiotic-related infection
Enteral feeding
Sweating Pyrexia
Water Evaporation Prolonged exposure of viscera during surgery
Plasma-like fluid Capillary leak/sequestration in tissues Acute inflammatory response
Infection
Burns
Ischaemia–reperfusion syndrome

Insensible fluid losses

Hyperventilation increases insensible water loss via the respiratory tract, but this increase is not usually large unless the normal mechanisms for humidifying inhaled air (the nasal passages and upper airways) are compromised. This occurs in intubated patients in the intensive care unit or in those receiving nonhumidified high-flow oxygen. In these situations, inspired gases should be humidified routinely.

Sweating may increase fluid loss by up to 1 L/h, but these losses are difficult to quantify. Pyrexia increases water loss from the skin by approximately 200 mL/day for each 1°C rise in temperature. High ambient temperatures in tropical countries will also significantly increase losses from sweat. Sweat also contains significant amounts of sodium (20–70 mmol/L) and potassium (10 mmol/L).

The effect of surgery

Fluid-conserving measures of stress response

Decreased circulating volume and the neuroendocrine response to hypovolaemia are common after major surgery and may persist even after normal circulating volume has been restored. The net result is oliguria, together with sodium and water retention – primarily due to the release of ADH and aldosterone.

Secretion of ADH promotes the retention of free water (without electrolytes) by cells of the distal renal tubules and collecting ducts, and is increased in response to:

  • Afferent nerve impulses from the site of injury

  • Atrial stretch receptors (responding to reduced volume) and the aortic and carotid baroreceptors (responding to reduced pressure)

  • Increased plasma osmolality (principally the result of an increase in sodium ions) detected by hypothalamic osmoreceptors

  • Input from higher centres in the brain (responding to pain, emotion and anxiety).

Aldosterone increases the reabsorption of both sodium and water by distal renal tubular cells with the simultaneous excretion of hydrogen and potassium ions into the urine. Aldosterone secretion is increased by:

  • Activation of the renin–angiotensin system. Renin is released from afferent arteriolar cells in the kidney in response to reduced blood pressure, tubuloglomerular feedback (signalling via the macula densa of the distal renal tubules in response to changes in electrolyte concentration) and activation of the renal sympathetic nerves. Renin converts circulating angiotensinogen to angiotensin (AT)-I. AT-I is converted by angiotensin-converting enzyme (ACE) in plasma and tissues (particularly the lungs) to AT-II, which causes arteriolar vasoconstriction and aldosterone secretion.

  • Increased adrenocorticotropic hormone (ACTH) secretion by the anterior pituitary in response to hypovolaemia and hypotension via afferent nerve impulses from stretch receptors in the atria, aorta and carotid arteries. ADH also increases ACTH secretion.

  • Direct stimulation of the adrenal cortex by hyponatraemia or hyperkalaemia.

Increased ADH and aldosterone secretion following injury usually lasts 48 to 72 hours, during which time urine volume is reduced and osmolality increased. Typically, urinary sodium excretion decreases to 10 to 20 mmol/24 hours (normal 50–80 mmol/24 hours) and potassium excretion increases to >100 mmol/24 hours (normal 50–80 mmol/24 hours). Despite this, hypokalaemia is relatively rare because of a net efflux of potassium from cells. This typical pattern may be modified by fluid and electrolyte administration.

‘Third-space’ losses

If tissue injury is severe, widespread and/or prolonged, the loss of water, electrolytes and colloid particles into the interstitial space can amount to many litres, significantly reducing circulating blood volume.

Fluid accumulation in the interstitial space contributes to oedema. Excess fluid moves from this space into the lymphatics only up to a point. Formation of ‘oedema fluid’ is largely dependent on the net balance of hydrostatic and oncotic pressures inside the capillary and the interstitium. The hydrostatic pressure on the arteriolar side of the capillary falls from 37 mm Hg to 17 mm Hg on the venular side. The colloid oncotic pressure throughout the lumen of the capillary is 25 mm Hg. The hydrostatic pressure is 1 mm Hg in the interstitium. There is a net outward pressure on the arteriolar side (37 − 1 − 25 = 11) and a net inward pressure (25 − 17 − 1 = 9) on the venular side.

This normal balance becomes disturbed, with an accumulation of excess interstitial fluid, if the hydrostatic pressure increases on the venular side (e.g., heart failure), the colloid oncotic pressure falls (e.g., liver or kidney disease) or endothelial permeability is increased (e.g., sepsis and/or injury).

In recent years, the role of the endothelial glycocalyx in the homoeostasis of transvascular fluid exchange has been recognised. The glycocalyx is a web of membrane-bound glycoproteins on the luminal side of endothelial cells. This forms a dynamic interface ∼2 μm thick between blood and the capillary wall. It appears that the integrity of the glycocalyx may be compromised by the rapid infusion of intravenous fluids and in a range of systemic inflammatory states, such as sepsis, surgery and trauma. This contributes to capillary leak.

Minimising ‘third-space losses’ may increase rates of recovery following surgery. For very sick patients, such as those with sepsis and multiple organ failure in the intensive care unit, there is evidence that positive overall fluid balance may delay recovery or increase mortality. The goal of fluid therapy is therefore to provide sufficient fluids to replace losses and maintain an adequate intravascular circulating volume but avoid excessive replacement that increases localised or generalised oedema formation.

Loss from the gastrointestinal tract

The magnitude and content of gastrointestinal fluid losses depends on the site of loss ( Table 4.3 ):

  • Intestinal obstruction. In general, the higher an obstruction occurs in the intestine, the greater the fluid loss because fluids secreted by the upper gastrointestinal tract fail to reach the absorptive areas of the distal jejunum and ileum.

  • Paralytic ileus. This condition, in which propulsion in the small intestine ceases, has numerous causes. The most common is probably handling of the bowel during surgery and usually resolves within 1 to 2 days of operation. Occasionally, paralytic ileus persists for longer, and in this case, other causes should be sought and corrected if possible. During paralytic ileus the stomach should be decompressed using nasogastric tube drainage and fluid losses monitored by measuring nasogastric aspirates.

  • Intestinal fistula. As with obstruction, fistulae occurring high in the gut are associated with the greatest fluid and electrolyte losses. As well as volume, it may be useful to measure the electrolyte content of the fluid lost to estimate the fluid and electrolyte replacement required.

  • Diarrhoea. Patients may present with diarrhoea or develop it during the perioperative period. Fluid and electrolyte losses may be considerable.

Table 4.3
The approximate daily volumes (mL) and electrolyte concentrations (mmol/L) of various gastrointestinal fluids a
Volume Na + K + Cl − HCO 3 −
Plasma – 140 5 100 25
Gastric secretions 2500 50 10 80 40
Intestinal fluid (upper) 3000 140 10 100 25
Bile and pancreatic secretions 1500 140 5 80 60
Mature ileostomy 500 50 5 20 25
Diarrhoea (inflammatory) – 110 40 100 40
Mixed gastric aspirate – 120 10 – –

a If gastrointestinal loss continues for more than 2 to 3 days, samples of fluid and urine should be collected regularly and sent to the laboratory for measurement of electrolyte content. For calculation of electrolyte replacement, mixed gastric aspirate composition can be used for ease of calculation. For example, replacement of 2 litres of nasogastric aspirate would require an additional supply of 240 mEq of Na + and 20 mEq of K + in addition to the daily requirement.

Intravenous fluid administration

When choosing and administering intravenous fluids ( Table 4.4 ), it is important to consider:

  • What fluid deficiencies are present

  • The fluid compartments requiring replacement

  • Any electrolyte disturbances present

  • Which fluid is most appropriate

Table 4.4
Composition of commonly administered intravenous fluids
Na + (mmol/L) K + (mmol/L) Cl – (mmol/L) HCO 3 − (mmol/L) Ca 2+ (mmol/L) Mg 2+ (mmol/L) Oncotic pressure (mmH 2 O) Typical plasma half-life pH
5% dextrose – – – – – 0 – 4.0
0.9% NaCl 154 0 154 0 0 0 – 5.0
0.18% NaCl/4% dextrose 31 0 31 0 0 0 0 – 4.0
Ringer lactate (Hartmann solution) 131 5 112 Lactate 28 a 1 1 0 – 6.5
Plasma-Lyte 148 140 5 98 Acetate 27 b
Gluconate 23 b 		0 1.5 0 – 7.4
Haemaccel (succinylated gelatin) 145 5.1 145 0 6.25 0 370 5 hours 7.4
Gelofusine (polygeline gelatin) 154 0.4 125 0 0.4 0.4 465 4 hours 7.4
Human albumin solution 4.5% 150 0 120 0 0 275 – 7.4
Bicarbonate cannot be directly added to the solutions because it is unstable (tends to precipitate).

a The lactate present in Ringer lactate solution is rapidly metabolised in the body. This generates bicarbonate ions.

b The acetate and gluconate present in Plasma-Lyte 148 is rapidly metabolised in the body. This generates bicarbonate ions.

Types of intravenous fluid

Crystalloids

Dextrose 5% contains 5 g of dextrose ( d -glucose) per 100 mL of water. This glucose is rapidly metabolised, and the remaining free water distributes rapidly and evenly throughout the body’s fluid compartments. So, shortly after the intravenous administration of 1000 mL 5% dextrose solution, about 670 mL of water will be added to the intracellular fluid compartment (IFC) and about 330 mL of water to the EFC, of which about 70 mL will be intravascular ( Fig. 4.3 ). Dextrose solutions are therefore of little value as resuscitation fluids to expand intravascular volume. Dextrose 5% is an isotonic solution in contrast to more concentrated dextrose solutions (10%, 20% and 50%), which are hypertonic. These solutions are an irritant to veins, and their use is normally limited to the protocolised management of diabetic patients or patients with hypoglycaemia.

Fig. 4.3, Distribution of different fluids in the body fluid compartments 30 to 60 minutes after rapid intravenous infusion of 1000 mL.

Sodium chloride 0.9%, Hartmann solution and Plasma-Lyte 148 are isotonic solutions of electrolytes in water. Sodium chloride 0.9% (also known as normal saline) contains 9 g of sodium chloride dissolved in 1000 mL of water; Hartmann solution (also known as Ringer lactate) has a more physiologic composition of sodium, potassium, chloride and calcium. Plasma-Lyte 148 contains physiologic concentrations of sodium, chloride and magnesium but does not contain calcium or potassium. All three fluids have an osmolality similar to that of ECF (about 290–300 mOsm/L), and after intravenous administration, they distribute rapidly throughout the EFC ( Fig. 4.3 ). Isotonic crystalloids are appropriate for correcting EFC losses (e.g., gastrointestinal tract losses or sweating) and for the initial resuscitation of intravascular volume, although only about 25% remains in the intravascular space after redistribution (which typically occurs within 30–60 minutes).

Balanced solutions, such as Hartmann and Plasma-Lyte 148, more closely match (or balance) the composition of ECF by providing physiologic concentrations of sodium and chloride. These solutions do not contain bicarbonate because this is unstable in solution and may precipitate during storage. The solutions contain a substrate that the body can metabolise to generate bicarbonate ions as part of the metabolic pathway. For Ringer lactate, lactate is the substrate. For Plasma-Lyte 148, acetate and gluconate are the substrates. These solutions decrease the risk of hyperchloraemia, which can occur following large volumes of fluids with higher sodium and chloride concentrations, such as sodium chloride 0.9%. Hyperchloraemic acidosis can develop in these situations. This has been associated with renal impairment in some studies. Plasma-Lyte 148 is increasingly used as the first-line crystalloid for resuscitation because the risk of hyperchloraemic acidosis is reduced, and it does not contain potassium (minimising the risk of hyperkalaemia, especially when renal failure or hyperkalaemia may be present). The use of acetate/gluconate, rather than lactate, is also an advantage because lactate is used as an index of shock severity and response to resuscitation, and will be altered by the lactate in Ringer lactate solution.

Hypertonic saline solutions have an osmolality greater than ECF and induce a shift of fluid from the IFC to the EFC, thus reducing brain water and increasing intravascular volume and serum sodium concentration. Potential indications include the treatment of cerebral oedema and raised intracranial pressure, hyponatraemic seizures and ‘small-volume’ resuscitation of hypovolaemic shock.

Mannitol is filtered freely by the kidney and acts as an osmotic diuretic, increasing urinary loss of both sodium and water. Given as a 10% to 20% hypertonic solution, mannitol is used for the acute management of cerebral oedema (raised intracranial pressure) and angle-closure glaucoma (raised intraocular pressure). There is no evidence-based role for the use of mannitol to prevent acute kidney injury.

Dextrose–saline solutions

A number of dextrose–saline solutions are available. The isotonic solution of 4% dextrose/0.18% sodium chloride is widely used as a solution for maintenance of fluid status when replacement of losses rather than resuscitation is needed, because this combination can provide appropriate replacement of sodium, chloride and glucose in a single fluid (see maintenance fluids). Importantly, it reduces the risk of excessive sodium and chloride replacement. ‘Half-normal saline’ is a commonly used (hypertonic) crystalloid and contains 0.45% sodium chloride in 5% dextrose. Commercially available 5% dextrose with 0.9% normal saline in 500 mL is a hypertonic solution (twice the osmolarity of plasma) and should be used with caution.

Colloids

Colloid solutions contain particles that exert an oncotic pressure and may occur naturally (e.g., albumin) or be synthetically modified (e.g., gelatins, hydroxyethyl starches [HES], dextrans). When administered, colloid remains largely within the intravascular space until the colloid particles are removed by the reticuloendothelial system. The intravascular half-life is usually between 6 and 24 hours, and such solutions are therefore appropriate for fluid resuscitation. Thereafter, the electrolyte-containing solution distributes throughout the EFC.

Albumin solutions, such as human albumin, are prepared from pooled human plasma with solutions pasteurised to minimise risks of infection transmission. Albumin solutions do not contain iso-agglutinins and can be given independent of the recipient’s blood group. Commonly used solutions are iso-osmolar (5% albumin) or hyperosmolar (20%). There is no evidence to support the use of albumin simply to increase a patient’s serum albumin, and there is little evidence of clinical benefit above crystalloid for its routine use in the resuscitation of shock. Some clinicians advocate the use of iso-osmolar albumin solutions in patients with a limited response to crystalloid or those with severe sepsis or septic shock, but this remains controversial as there is currently only limited evidence to support this practice. Hypertonic albumin solutions (typically 100 mL 20% albumin) are used in more specialist contexts to expand intravascular volume in patients who may be intravascularly deplete but with an excess of total body water and/or low serum albumin, such as those with chronic liver disease or severe pancreatitis. There is little evidence to support this practice.

Synthetic colloids are more expensive than crystalloids and have variable side effect profiles. Recognised risks include coagulopathy, reticuloendothelial system dysfunction, pruritus and anaphylactic reactions. HES in particular appear to be associated with increased mortality and renal failure and are no longer recommended.

The theoretical advantage of colloids over crystalloids is that, as they remain in the intravascular space for several hours, smaller volumes are required. Some clinicians advocate the use of colloids, particularly albumin, in patients with a limited response to crystalloid or in patients with hypoalbuminemia. However, current evidence suggests that crystalloids and colloids are equally effective for the correction of hypovolaemia with comparable patient outcomes ( EBM 4.1 ). As colloids are not associated with improved survival and are more expensive than crystalloids, it is difficult to justify their use in routine surgical practice.

Lewis SR et al. Colloids versus crystalloids for fluid resuscitation in critically ill people. Cochrane Database of Systematic Reviews 2018, Issue 8. Art. No.: CD000567.
EBM 4.1
Crystalloid versus colloid

‘Using colloids (gelatins; starches; dextrans; or albumin or FFP) compared with crystalloids for fluid replacement probably makes little or no difference to the number of critically ill people who die. It may make little or no difference to the number of people who die if gelatins or crystalloids are used for fluid replacement.’

FLOAT NOT FOUND

Maintenance fluid requirements

Under normal conditions, adult daily sodium requirements (80 mmol) may be provided by the administration of 500 to 1000 mL of 0.9% sodium chloride. The remaining water requirement to maintain fluid balance (2000–2500 mL) is typically provided as 5% dextrose. An alternative is to use 0.18% NaCl/4% dextrose solutions (2000–3000 mL per 24 hours according to size and estimated fluid losses). Daily potassium requirements (60–80 mmol) are usually met by adding potassium chloride to maintenance fluids, but the added amount can be titrated to measured plasma concentrations. Potassium should not be administered at a rate greater than 10 to 20 mmol/h except in severe potassium deficiency, and, in practice, 20-mmol aliquots are added to alternate 500-mL bags of fluid.

An example of a suitable 24-hour fluid prescription for an uncomplicated patient is shown in Table 4.5 ; the process of adjusting this for a hypothetical patient with an ileus is shown in Table 4.6 .

Table 4.5
Provision of normal 24-hour fluid and electrolyte requirements by intravenous infusion
An alternative approach is to use 0.18% NaCl/4% dextrose solution with addition of potassium as required. The total fluid requirements per 24 hours vary according to patient weight and fluid losses but are typically 2000 to 3000 mL per 24 hours
Intravenous fluid Additive Duration (hours)
500 mL 0.9% NaCl 20 mmol KCI 4
500 mL 5% dextrose – 4
500 mL 5% dextrose 20 mmol KCI 4
500 mL 0.9% NaCl – 4
500 mL 5% dextrose 20 mmol KCI 4
500 mL 5% dextrose – 4

Table 4.6
Estimating fluid (mL) and electrolyte (mmol/L) requirements in a patient with ileus a
Volume (mL) Na + K +
Urine 1500 80 60
Nasogastric aspirate 2000 240 20
Insensible loss 800 – –
Minus endogenous water –300 – –
Net losses/requirements 4000 320 80
2 L of normal saline would supply 300 mmol of Na + .
2 L of 5% dextrose would supply water.
The required 60–80 mmol of K + could be added as 20 mmol to alternate 500-mL bags.
Note: The 1500 mL of urine is not an abnormal loss. It shows that, during this 24-hour period, hydration has been adequate. Urine output need not be replaced. The abnormal loss (nasogastric aspirate 2000 mL) + normal daily requirement (shown in Table 4.5 ) = 5000 mL is the requirement. The insensible loss and endogenous water have been accounted for in the normal daily requirement.

a Assuming that the patient is in electrolyte balance and is losing 2 L/day as nasogastric aspirate and 1.5 L/day as urine, 24-hour losses can be calculated as shown.

In patients requiring intravenous fluid replacement for more than 3 to 4 days, supplementation of magnesium and phosphate may also be required as guided by direct measurement of plasma concentrations. The provision of total parenteral nutrition should also be considered in this situation.

Treatment of postoperative hypovolaemia and/or hypotension

Hypovolaemia is common in the postoperative period and may present with one or more of the following: tachycardia, cold extremities, pallor, clammy skin, collapsed peripheral veins, oliguria and/or hypotension. Hypotension is more likely in hypovolaemic patients receiving epidural analgesia as the associated sympathetic blockade disrupts compensatory vasoconstriction. Intravascular volume should be rapidly restored with a series of fluid boluses (e.g., 250–500 mL crystalloid) with the clinical response assessed after each bolus. Although the evidence in favour of balanced solutions is currently uncertain, Plasma-Lyte 148 or equivalent solutions are widely considered the optimum first-line crystalloid solution for bolus resuscitation of hypovolaemia.

Shock

Shock is an imbalance between oxygen delivery and oxygen demand. This results in cell dysfunction and ultimately cell death and multiple organ failure.

Definition

Shock exists when tissue oxygen delivery fails to meet the metabolic requirements of cells. An imbalance between oxygen delivery (D O 2 ) and oxygen demand can result from:

  • a global reduction in oxygen delivery

  • maldistribution of blood flow

  • impaired oxygen utilisation

  • an increase in tissue oxygen requirements

  • a combination of these factors

Shock is initially reversible but must be recognised and treated promptly to prevent progression. Left uncorrected, shock will result in a fall in oxygen consumption (V O 2 ), anaerobic metabolism, tissue acidosis and cellular dysfunction, in turn leading to multiple organ dysfunction and ultimately death. Although shock is sometimes considered to be synonymous with hypotension, it is important to understand that tissue oxygen delivery may be inadequate even though the blood pressure and other vital signs remain normal.

Classification of shock

There are four broad categories of shock:

  • 1.

    Distributive shock characterised by peripheral vasodilation, a fall in systemic vascular resistance (SVR) and blood pressure, e.g., septic shock. This can occur in the context of a normal or even high cardiac output (CO).

  • 2.

    Hypovolaemic shock due to reduced intravascular volume and a fall in CO.

  • 3.

    Cardiogenic shock caused by intracardiac causes of cardiac pump failure and a fall in CO, e.g., myocardial infarction or arrhythmia.

  • 4.

    Obstructive shock caused by extracardiac cardiac pump failure and a fall in CO, e.g., pulmonary embolus, cardiac tamponade or tension pneumothorax.

A more useful classification widely used in clinical practice characterises shock on the basis of the underlying aetiology:

Hypovolaemic shock

This is probably the most common and readily corrected cause of shock encountered in surgical practice, which results from a reduction in intravascular volume secondary to the loss of blood (e.g., trauma, gastrointestinal haemorrhage), plasma (e.g., burns) or water and electrolytes (e.g., vomiting, diarrhoea, diabetic ketoacidosis) ( Table 4.7 ).

Table 4.7
Causes of hypovolaemic shock
Gastrointestinal haemorrhage

  • Oesophageal varices

  • Oesophageal mucosal (Mallory–Weiss) tear

  • Acute erosive gastritis

  • Gastric and duodenal ulceration

  • Cancer

  • Diverticula

Trauma
Ruptured aneurysm
Obstetric haemorrhage

  • Ruptured ectopic pregnancy

  • Placentia praevia

  • Placental abruption

  • Postpartum haemorrhage

Pulmonary haemorrhage

  • Pulmonary embolus

  • Cancer

  • Cavitating lung lesions, e.g., tuberculosis, aspergillosis

  • Vasculitis

Major blood loss during surgery

Septic shock

Septic shock results from circulatory and cellular abnormalities that occur as part of a dysregulated host response to infection. These changes impair tissue oxygen delivery and are associated with significantly increased mortality (>40%). The 1992 consensus definitions of sepsis provided a degree of categorisation of the host response (systemic inflammatory response syndrome [SIRS], sepsis, severe sepsis and septic shock), but these have been shown to lack sensitivity and specificity. New consensus definitions (Sepsis-3) have been published. In the Sepsis-3 criteria, the quick sepsis-related organ failure assessment (qSOFA) score is used to assess the presence of three symptoms: altered mental status, low blood pressure (<100 mm Hg) and tachypnoea (respiratory rate >22 breaths per minute). If a patient with infection has two or more of these criteria (‘qSOFA-positive’), they should be assumed to have sepsis. Patients with septic shock can be identified as those with sepsis, persisting mean arterial blood pressure (MAP; <65 mm Hg) and an elevated serum lactate (>2 mmol/L) despite adequate fluid resuscitation (∼30 mL/kg) ( Fig. 4.4 ). Importantly, qSOFA-positive status should prompt clinicians to investigate organ dysfunction and escalate therapy, including critical care referral, as appropriate.

Fig. 4.4, The interrelationship between sepsis and septic shock. Based on third international consensus definition Sepsis-3.

4.1
Summary

Sepsis—1992 Consensus definitions ∗

∗ American College of Chest Physicians & Society of Critical Care Medicine Consensus Conference Committee definitions 1992.

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