Basic concepts of fluid and electrolyte therapy 2nd edition – Part 2
8 September 2023
BJS Academy is delighted to host the second edition of the textbook ‘basic concepts of fluid and electrolyte therapy’, by Lobo, Lewington and Allison.
The authors have kindly divided the book into four easily digestible sections, and then some multiple choice questions at the end. This is the second section.
Surgeons sometimes focus a little too much on the technical aspects of their work, but without a sound knowledge of fluid and electrolyte management, their efforts in the operating theatre may easily be undone.
All surgeons will benefit from reading this book and gaining an understanding of how best to optimise fluid management in their patients.
Director, BJS Academy
The authors have made every eﬀort to ensure that drug dosages in this book are in accordance with current recommendations and practice at the time of publication.
However, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions.
The ﬁrst edition of this book was published in 2013 with the aim of improving understanding and clinical practice in the ﬁeld of ﬂuid and electrolyte therapy. Studies at that time suggested that, even though ﬂuid and electrolyte preparations are the most commonly prescribed medications in hospitals, management of ﬂuid and electrolyte disorders was suboptimal, possibly due to inadequate teaching, causing avoidable morbidity and even mortality. It should not be forgotten that ﬂuid therapy, like other forms of treatment, has the capacity to do harm as well as good unless administered with care and based on sound knowledge.
A second edition was felt appropriate in the light of further advances in knowledge and practice over the last 9 years. We have updated the book, adding new chapters, ﬁgures, tables and ﬂow charts to help the reader. New chapters include Ageing and Fluid Balance, Chronic Kidney Disease, Fluid Overload and the De-escalation Phase, and Perioperative Fluid Therapy and Outcomes. We have also tried to maintain consistency with published national and international guidelines, where available. References have now been cited in the text. To limit the number of references, we have tried, as far as possible to cite important review articles from which original studies may be sourced. However, relevant original works have been referred to when appropriate. We have included multiple choice questions so that readers may test their knowledge after reading the book.
The subject of ﬂuid balance in paediatrics is not addressed and this book should be regarded as relevant to adults only. It is still not our intention to write a comprehensive textbook dealing with complex problems, but to provide a basic hand-book for students, nurses, trainee doctors and other health care professionals to help them to understand and solve some of the most common practical problems they face in day to day hospital practice. We hope that it will also stimulate them to pursue the subject in greater detail with further reading and practical experience. In diﬃcult cases, or where there is uncertainty, trainee health care professionals should never hesitate to ask for advice from senior and experienced colleagues.
Dileep N. Lobo
Andrew J. P. Lewington
Simon P. Allison
List of Abbreviations
ASSESSMENT, MEASUREMENT AND MONITORING
As in all clinical conditions, assessment of ﬂuid and electrolyte status begins with a careful history and examination, followed by bedside and laboratory tests. The key features of assessment and monitoring of ﬂuid balance are summarised in Table 5.1.
This gives the initial clue to the likely abnormality and the type and degree of deﬁcit, e.g. a background of poorly controlled diabetes, a story of vomiting and/or diarrhoea, diuretics in an elderly patient who is confused, blood loss, burn injury, etc. All possible sources of ﬂuid and electrolyte gain or loss should be explored.
It is also important, in the initial assessment of any patient, that careful attention be paid to drug pre- scription cards as a number of drugs may aﬀect salt and water balance (e.g. diuretics, corticosteroids, laxatives, etc.) while others may contain signiﬁcant amounts of sodium, potassium or chloride (e.g. some antibiotics which are sodium salts) (see Chapter 6). Also 0.9% saline is often used as a diluent or vehicle for administration of drugs and this may contribute to sodium and chloride overload. Each ml of 0.9% saline provides 0.15 mmol of sodium and chloride.
Physical signs of ﬂuid deﬁcit are indicative but not speciﬁc, and no conclusion should be drawn from any single feature (Table 5.1). The ﬁrst indication of a falling intravascular volume is a decrease in central venous pressure (CVP), as evidenced by a fall in JVP. With progressive severity, pulse rate increases (Fig. 5.1), followed by a fall in blood pressure with pallor and sweating. The full-blown picture is called ‘shock’. In contrast, pink warm peripheries, with rapid capillary reﬁll after pressure and a negative passive leg raising test, are usually suggestive of an adequate circulation. Serial assessments of JVP, pulse, blood pressure and urine output are suﬃcient to monitor most patients, but in complex cases or in critical ill- ness, bedside examination may need to be supported by invasive techniques for assessing cardiovascular function.
It should also be remembered that shock states due to volume depletion, cardiac causes, or sepsis share many similar features which require expert assessment to distinguish.
Dependent oedema is not necessarily due to salt and water overload but, particularly in the elderly, may be gravitational in origin due to prolonged sitting and immobility.
Examination of the jugular ﬁlling with the patient reclining at 45° should be routine. If the level is elevated above the clavicle, this may signify intravascular over-expansion by administered ﬂuids, congestive heart failure, or both. If, however, no jugular ﬁlling is observed, then lower the patient slowly until ﬁlling is observed. If ﬁlling is still not seen or only seen with the patient nearly horizontal, then this may signify an intravascular volume deﬁcit. This manoeuvre is valuable in assessing patients still receiving intravenous ﬂuids some days after the acute phase of their illness has subsided and in whom recovery is slow or accompanied by complications. Such patients may have an expanded interstitial ﬂuid space with oedema due to excess crystalloid administration, but a diminished blood or plasma volume due to continuing leak of blood, protein or serous ﬂuid into wounds or inﬂamed areas. These ﬁndings may indicate the need for colloid (e.g. 20% salt-poor albumin) to expand the intravascular volume, improve renal blood ﬂow and allow the excretion of the salt and water overload. If, on the other hand, the jugular venous pressure (JVP) is elevated, then immediate cessation of crystalloid administration, with or without diuretics, will correct the underlying imbalance.
MEASUREMENTS AND INVESTIGATIONS
As described above, the volume and concentration of urine are important indicators of renal function. Oliguria may be physiological postoperatively or indicative of intravascular or ECF deﬁcit. If this is ac- companied by a concentrated urine and a rising blood urea, it is termed pre-renal AKI, correctable by appropriate ﬂuid replacement. A persisting low volume and concentration combined with a rising blood urea and creatinine suggest AKI due to intrinsic tubular damage has now developed, necessitating some form of renal replacement therapy (e.g. haemoﬁltration or haemodialysis). Changes in urine volume must, therefore, be interpreted in the light of accompanying features and circumstances.
In some acutely ill and postoperative patients urinary catheters may be required to monitor hourly urine output. However, they should not be used routinely because of the increased risks of urinary tract infection and catheter-related sepsis.
Nurses are often instructed to call junior doctors if the postoperative urine output falls below 30 ml/h. Consequently, the doctor often prescribes extra saline “just to be on the safe side”. This commonly results in salt and water overload. In fact, such “oliguria” is usually a physiological response to surgery. While it is important to identify the patient who has become hypovolaemic and is in need of resuscitation, it is unlikely that a patient who appears well with warm pink peripheries and no tachycardia or tachypnoea needs volume expansion. Urine output in such patients should be averaged over four to six hours and interpreted in combination with serial trends in vital signs of circulatory adequacy. A recent study has shown that a perioperative urine output target of 0.2 ml/kg/h (i.e. 14 ml/h in a 70 kg patient) is not inferior to the standard target of 0.5 ml/kg/h (i.e. 35 ml/h in a 70 kg patient). This strategy reduces the volume of intravenous ﬂuid administered without increasing the risk of developing AKI47.
Fluid balance charts
These provide useful information about changes in urine output and abnormal losses, e.g. gastric aspirate, but they have inherent inaccuracies. With great care in measurement and recording, they may be helpful in assessing ﬂuid balance over 24 hours. However, an assumption has to be made concerning insensible loss, and errors in measurement and recording are common. The cumulative error over several days can, therefore, be considerable. A suggested format for ﬂuid balance charts is shown in Fig. 5.2.
There is no substitute for daily weighing as an accurate measure of external water balance. Yet, this is seldom practised outside renal units. As it is a major safeguard against clinically important errors in ﬂuid volume administration, it is worth the extra eﬀort and resources required, particularly in complex postoperative cases. It does, of course, only measure external balance, which may conceal signiﬁcant changes in internal balance between ﬂuid compartments (e.g. in the presence of ileus or intestinal obstruction large volumes of extracellular ﬂuid may be pooled in the gut and, therefore, be functionally inert). Weight is, therefore, unchanged despite this clinically important ﬂuid shift, which reduces eﬀective ECF volume and necessitates salt and water replacement. Like any other parameter, weight measurements require intelligent interpretation in their clinical context and in the light of all the other information available.
Non-invasive assessment of the intravascular volume status can be performed using point of care ultrasound. It can also be used to assess a patient’s response to intravenous ﬂuid therapy by measuring the size and respiratory change in the diameter of the inferior vena cava. Ultrasound examination of the lungs can be useful in demonstrating the presence of pulmonary oedema.
Invasive techniques such as insertion of central venous catheters, arterial lines, ﬂow-guided monitoring (e.g. transoesophageal Doppler, Lithium Dilution Cardiac Output [LiDCO], plethysmography or Photonic Integrated Circuits Using Crystal Optics [PICCO]) to measure cardiovascular parameters are useful to help direct ﬂuid therapy in more complex patients48,49. These methods are for the expert rather than the novice.
The haematocrit (Hct) is a measurement of the proportion of blood that is made up of cells. Changes in ﬂuid balance can cause an increase or decrease in the concentration of red cells, e.g. in the acute phase of burn injury, plasma loss may be monitored by frequent haematocrit measurements which, therefore, help to guide ﬂuid replacement. Loss of ECF due to gastroenteritis or other causes similarly increases haematocrit. Conversely ﬂuid overload causes a fall in haematocrit due to dilution50,51.
This is expressed as g/L of whole blood (Table 5.2). Like the haematocrit, it is elevated in polycythaemia and in ﬂuid depletion. It is reduced in anaemia of any cause and following haemorrhage once the compensatory expansion of plasma volume has occurred. Infusion of intravenous ﬂuid boluses can also cause a fall in haemoglobin as well as haematocrit50,51.
In response to ﬂuid deﬁcit or excess the albumin concentration behaves in the same way as the haematocrit. Indeed, dilution by infused crystalloids is one of the main causes of hypoalbuminaemia in surgical patients50,51. Another major cause is the increased albumin escape rate from the circulation in response to proinﬂammatory cytokines7 (see Chapter 1).
This is expressed as a concentration, i.e. the proportion of sodium to water in the ECF. It is not a measure of the absolute amount of sodium in the body or the need for a higher or lower intake. In fact, the commonest cause of hyponatraemia is dilution by overenthusiastic administration of hypotonic ﬂuids (e.g. 5% dextrose or 0.18% saline in 4% dextrose). If, however, water balance is known from daily weighing, then changes in plasma sodium can usually be interpreted in terms of sodium balance. For example, if weight is unchanged, a fall in plasma sodium usually implies that sodium balance is negative and that intake should be increased in the next prescription. On the other hand, if weight has increased by 2 kg and the plasma sodium has fallen, the balance of water is positive and hyponatraemia is dilutional. The next prescription should, therefore, include less water and the same sodium intake as before.
An alternative approach to sodium balance is to measure intake and the sodium content of all ﬂuids lost. This, however, is diﬃcult to do accurately and is more demanding on staﬀ time and resources.
A falsely low serum sodium concentration may be caused by hypertriglyceridaemia, since triglycerides expand the plasma volume but contain no sodium. Similarly, hyponatraemia occurs in the presence of hyperglycaemia as in decompensated diabetes, since glucose also acts as an osmotic agent holding water in the ECF. This eﬀect disappears as soon as insulin treatment causes cellular uptake of glucose and lowering of its concentration in the blood.
The normal serum potassium concentration lies between 3.5 and 5.3 mmol/L. Concentrations rising above 5.5 mmol/L increase the risk of death from cardiac arrest and require urgent treatment which may include extra ﬂuids, intravenous glucose and insulin, bicarbonate, calcium gluconate (to stabilise the myocardium), intrarectal calcium resonium and even renal replacement therapy. Conversely, concentrations below 3.0 mmol/L increase the risk of arrhythmias and indicate the need for potassium supplementation by the oral or intravenous route (see Chapter 14).
Despite the fact that serum chloride measurements do not increase the cost of biochemical screening, many laboratories do not report serum chloride concentrations. However, in the diﬀerential diagnosis of acidosis, particularly in patients receiving 0.9% saline (with its high chloride content in relation to plasma)50-52, it is important for the detection of hyperchloraemic acidosis, in which the serum chloride is elevated and bicarbonate reduced. Hypochloraemic alkalosis may occur due to chloride losses from vomiting and in patients with high nasogastric tube aspirates.
Venous or arterial bicarbonate concentrations indicate acid-base status as described in Chapter 4.
With renal impairment due to either ﬂuid deﬁcit (pre-renal AKI) or intrinsic tubular AKI, blood urea con- centration rises, the rate of increase being greater in the presence of post injury catabolism. Urine output measurements are important but are subject to misinterpretation unless other parameters are also considered. It is useful to combine measurement of urine volume with plasma and urinary urea or osmolality to assess renal function. The urine :plasma urea ratio has been used in the past to measure renal concentrating function and in normal health can be as high as 100 in the presence of dehydration. With a rising blood urea and creatinine, accompanied by oliguria, urine:plasma urea ratio of <15 can be helpful in deﬁning the transition from pre-renal to intrinsic tubular AKI.
Creatinine is a breakdown product generated from normal muscle metabolism and from meat protein in the diet. Therefore, a 120 kg muscular man will generate more creatinine than a 70 kg elderly man. The kidneys ﬁlter and secrete creatinine from the blood into the urine at a constant rate. The concentration of serum creatinine, therefore, is inversely proportional to renal function, and rises in the presence of AKI. However, the serum creatinine does not usually rise above the lower limit of normal until the GFR has fallen by 50%. Increases in creatinine are used to deﬁne and stage AKI. The majority of hospitals in the UK have adopted an AKI warning system based on a modiﬁed algorithm of the KDIGO AKI deﬁnition and staging classiﬁcation38. The AKI warning is triggered in any patient who has two serum creatinine concentrations that demonstrate a rise in the creatinine consistent with the deﬁnition of AKI (see Chapter 10).
Glomerular ﬁltration rate
Glomerular ﬁltration rate (GFR) is the ﬂow rate of ﬁltered ﬂuid through the kidneys and is approximately 120-130 ml/min/1.73 m2, which equates to the daily ﬁltration of 170-180 litres of water and unbound small molecular weight constituents of blood. It is the most accurate measure of renal function. In reality the measurement of the true GFR is time consuming and requires the administration of radionuclides. It is, therefore, rarely measured except in the assessment of renal function in potential live kidney donors. In every day clinical practice serum creatinine and estimated GFR (eGFR) are used to estimate renal function.
Creatinine clearance provides an estimate of the GFR. The calculation of the creatinine clearance requires a 24-hour urine collection and the measurement of creatinine in the blood and urine. It is now rarely used in clinical practice and the eGFR is used instead.
Cockroft and Gault equation
The Cockcroft-Gault equation53 provides an estimate of creatinine clearance. This formula is not adjusted for body surface area and may be less accurate in obese patients. The Cockroft-Gault equation overestimates creatinine clearance by approximately 10 to 30%.
Age in years, weight in kg and serum creatinine (SCr) in mg/dl
Estimated glomerular ﬁltration rate (eGFR)
The eGFR is commonly calculated from the modiﬁed diet in renal diseases (MDRD) formula54 based on age, sex and serum creatinine concentration. It is a good estimate of renal function in the steady state, but should not be used to estimate kidney function in the setting of AKI. The eGFR value approximates to the percentage of kidney function (e.g. an eGFR of 60 ml/min/1.73 m2 would approximate to 60% kidney function). It is used to stage CKD and is not validated in patients less than 18 years of age, in pregnancy or obesity or in very muscular patients.
Urinary osmolality >500 mOsm/kg is indicative of pre-renal AKI and <350 mOsm/kg suggests intrinsic tubular AKI. Urinary and serum osmolalities are also used in the diagnosis and monitoring of diabetes insipidus and in the monitoring of hyper- and hypo-osmolal states. This ensures that treatment is controlled carefully to avoid too rapid changes in serum osmolality and consequent risks of central nervous system damage.
Serial data charts
The sticking of individual reports in the back of notes makes it diﬃcult to detect clinically important trends. The only satisfactory way of monitoring patients with ﬂuid and electrolyte problems is the use of serial data charts (Fig. 5.3) on which important data are recorded daily, so that changes and trends can be seen at a glance. In our own practice we used to record daily weight, serum biochemistry, haematology, etc. on charts which were kept by the patient’s bedside. However, this information is now stored in the digital patient record from which it can be retrieved easily.
PROPERTIES OF INTRAVENOUS CRYSTALLOIDS AND COLLOIDS
A variety of crystalloids containing salt and/or glucose and of artiﬁcial colloids is available for use in intravenous ﬂuid therapy.
To expand the intravascular volume during resuscitation current practice is to use a combination of salt containing crystalloids (preferable balanced electrolyte solutions) and colloids (the use of hydroxyethyl starch is discouraged for critically ill patients and those with sepsis and burns in most European countries because of possible renal toxicity). The properties of some commonly used crystalloids are summarised in Table 6.1 and must be borne in mind when choosing the most appropriate ﬂuid for any particular situation.
The ability of a solution to expand the plasma volume is dependent on its volume of distribution and the metabolic fate of the solute, so that while colloids are mainly distributed in the intravascular compartment, dextrose containing solutions, once the dextrose is metabolised, are distributed through the total body water and hence have a very limited and transient capacity to expand the blood volume (Fig. 6.1, Table 6.2). Solutions like 5% dextrose and dextrose saline are not meant for resuscitation, but are a means of providing free water when this is appropriate.
Isotonic sodium-containing crystalloids are distributed throughout the ECF (including the plasma) and classical textbook teaching suggests that such infusions expand the blood volume by a third of the volume of crystalloid infused. In practice, however, the capacity of these solutions to expand the plasma volume is only 20-25% of the volume infused, the remainder being sequestered in the interstitial space. Although these solutions are used successfully for this purpose, the price paid for adequate intravascular ﬁlling is overexpansion of the interstitial space and tissue oedema. This residual excess of salt and water has then to be excreted once the acute phase of illness has passed (see Chapter 13). Solutions of dextrose or of hypotonic saline can cause signiﬁcant hyponatraemia (Na+ <130 mmol/L), and care should be taken to avoid this potentially harmful eﬀect, particularly in children and the elderly. Compared with balanced crystalloids, 0.9% saline produces a hyperchloraemic acidosis because of its high chloride con- tent compared with plasma (Table 6.1). This causes a reduction in the strong ion diﬀerence ([Na+] + [K+] – [Cl–]) and also results in reduced renal blood ﬂow and glomerular ﬁltration (Fig. 6.2)56, as well as gastrointestinal mucosal acidosis and ileus, cellular dysfunction, impairment in mitochondrial function, oedema and worse outcome55,57. These eﬀects are described in more detail in Chapter 16. For these reasons balanced electrolyte solutions are preferred to 0.9% saline in most instances, unless there is chloride deﬁciency (e.g. from vomiting or gastric aspiration)55.
Colloids are homogenous non-crystalline large molecules or ultramicroscopic particles dispersed through a ﬂuid, usually a crystalloid. Colloidal particles are large enough to be retained within the circulation and, therefore, to exert an oncotic pressure across the capillary membrane. The ideal colloid should be readily available, have a long shelf life, have no special infusion or storage requirements and be relatively inexpensive. It should be suspended in an isotonic solution, have a low viscosity, be iso-oncotic with plasma and be distributed exclusively in the intravascular compartment, with a half-life of 6-12 h. The colloid should be metabolised or excreted and should not accumulate in the body. It should not be toxic, pyrogenic, allergenic or antigenic and should not interfere with organ function (e.g. renal or coagulation) or with acid base balance. There is no ideal colloid, that completely fulﬁls all these criteria, and the colloids used for volume replacement are either naturally occurring (human albumin solution, plasma protein fraction, fresh frozen plasma, and immunoglobulin solutions) or semisynthetic (gelatins, starches and dextrans). In the UK, commonly used colloids include succinylated gelatin (e.g. Gelofusine), urea-linked gelatin (e.g. Haemaccel) and albumin (for selected indications). Older preparations of hydroxyethyl starch are suspended in 0.9% saline while the newer preparations (Volulyte, Tetraspan) and gelatins (Gelofusine, Gelaspan and Haemaccel) are suspended in solutions containing lower amounts of chloride, making them more physiological. All currently available semisynthetic colloids contain 140- 154 mmol Na+ and therefore, contribute to the positive sodium balance seen in surgical patients.
Recent large randomized controlled trials have demonstrated that, in critically ill or septic patients, hydroxyethyl starch has an adverse eﬀect on renal function, and in some cases on mortality, when com- pared with crystalloids58-60. The Pharmacovigilence Risk Assessment Committee of the European Medicines Agency considered this evidence and initially issued cautionary guidance on the use of hydroxyethyl starch61. In January 2018, PRAC recommended suspending the marketing authorisations of hydroxyethyl starches. However, in July 2018, a controlled access programme was implemented to ensure that only accredited hospitals will be supplied with these medicines. This accreditation would require that relevant healthcare professionals receive training on the safe use of hydroxyethyl starches61. Albumin solutions are monodisperse as they contain particles of uniform molecular weight (69 kD) while synthetic colloids contain particles of varying sizes and molecular weights in an attempt to optimise the half-life (which is directly proportional to particle size) and plasma volume expanding capacity (which is proportional to the number of particles suspended) of the solutions.
With the moratorium on hydroxyethyl starches, albumin is now being used for resuscitation, especially in patients with sepsis62. Concentrated (20-25%) salt poor albumin may also be useful in patients in the post-acute phase of illness who are oedematous due to salt and water overload, but who still have a plasma volume deﬁcit, as it helps draw ﬂuid from the interstitial space into the intravascular space and improves renal perfusion allowing excretion of excess salt and water63. Albumin is also used in patients with hepatic failure and ascites64. However, the prescription of this expensive preparation should be conﬁned to senior clinicians.
Although, in theory, those colloids that are isooncotic with plasma should expand the blood volume by the volume infused, in practice, their volume expanding capacity is only 60-80%. Nevertheless, a given volume of colloid results in greater volume expansion and less interstitial oedema than an equivalent volume of crystalloid (Table 6.3). The advantages and disadvantages of colloids are summarised in Table 6.4. Although, in practice in the UK, we use a combination of crystalloids and colloids for resuscitation, there is, in fact, no ﬁrm evidence that the use of colloids rather than crystalloids in the acute phase of injury results in better outcome.
There are good theoretical grounds for using colloids for plasma volume expansion as they cause less salt and water overload and oedema than crystalloids. In practice, however, we tend to use a combination of the two in varying proportion according to the circumstances. There are very few indications for using 0.9% saline (except in cases of chloride deﬁciency, e.g. from vomiting) and balanced crystalloids are preferred in most circumstances. Although hydroxyethyl starch is still being used in some countries, its use in Europe has been recommended with caution by European Medicines Agency because of reports of renal toxicity61. The colloids currently in use in Europe include albumin and gelatins.
PRESCRIPTION AND ADMINISTRATION
Fluid and electrolytes may be administered orally, enterally, subcutaneously, or intravenously (peripherally or centrally), depending on the clinical situation. Before any prescription is written it is important to ask a number of questions:
Question 1. Does the patient need any prescription at all today?
If the patient is eating and drinking, the answer is usually no. In the case of a postoperative patient, for example, any intravenous ﬂuids should be discontinued as soon as possible. Intravenous ﬂuids are often continued unnecessarily, leading to ﬂuid overload as well as increased risk of cannula-site thrombophlebitis and infection. Nasogastric tubes are only indicated for drainage in the presence of true ileus or gastric dysfunction (e.g. delayed gastric emptying after pancreatic surgery). In the majority of cases, morbidity from nasogastric tubes exceeds any beneﬁt. Gastrointestinal function returns more rapidly postoperatively than assumed previously. The absence of bowel sounds per se does not mean that food and drink will not be tolerated. In the past, a combination of nasogastric tubes and excess intravenous ﬂuids has frequently caused unnecessary delay in re-establishing oral intake, increased risk of complications and a prolonged length of stay57,65,66.
Patients receiving artiﬁcial nutrition (parenteral or enteral) usually receive an adequate amount of water and electrolytes via the feed and most do not require additional intravenous ﬂuids. It is a common mistake to prescribe intravenous maintenance requirements in addition to the water and electrolyte con- tent of the feed, leading to avoidable ﬂuid overload.
Question 2. If so, does the patient need this for
b. replacement of losses, or
c. merely for maintenance?
This question is crucial. Many patients are ﬂuid overloaded because prescriptions based on resuscitation are continued thoughtlessly when maintenance ﬂuids are all that is required. Tables 1.1 and 1.2 show how low such maintenance requirements are. For example, 1 litre of 0.9% saline contains enough salt to meet 2 days’ normal maintenance requirements for sodium. Intravenous ﬂuid therapy may be needed for resuscitation, replacement or maintenance, depending on the stage of the illness (Fig. 7.1).
Resuscitation: In the event of blood loss from injury or surgery, plasma loss e.g. from burns or acute pancreatitis, or gastrointestinal or renal losses of salt and water, a resuscitation regimen is needed to restore and maintain the circulation, tissue perfusion and the function of vital organs. In this situation, patients should receive a rapid infusion of 500 ml (250 ml if risk of cardiac failure) of a balanced crystalloid (e.g. Hartmann’s solution, Ringer’s lactate, Plasmalyte 148 or Sterofundin). Two randomised trials have shown that if the initial resuscitation of patients in the emergency department was performed with balanced crystalloids, the incidence of major adverse kidney events was signiﬁcantly lower than if resuscitation was performed with 0.9 saline in both critically ill patients67 and those who were not critically ill68. If hyperkalaemia is present (K+ >5.5 mmol/L) or suspected oliguric AKI or rhabdomyolysis 0.9% saline is preferred initially (no potassium in this crystalloid). However, there is no evidence that administration of crystalloids containing 3-5 mmol/L of potassium worsen the hyperkalaemia69,70. The clinical response should be assessed immediately following administration of the ﬂuid bolus in terms of im- proved peripheral perfusion, decreased pulse rate, rise in blood pressure, rise in JVP and increase in urine output. Further administration will depend on the response (Fig. 7.2). If 0.9% saline has been used initially, conversion to a balanced crystalloid can be considered once potassium concentrations are known and good urine output has been established.
In the case of intravascular ﬂuid losses, colloids or a combination of colloids and crystalloids may be appropriate. However, in the light of reports of adverse events caused by infusion of hydroxyethyl starch in critically ill patients58-60, the Pharmacovigilence Risk Assessment Committee of the European Medi- cines Agency (EMA)61 made the following recommendations about the use of hydroxyethyl starches:
- They are contraindicated in patients with sepsis, burns or critical illness.
- They should only be used for the treatment of hypovolaemia caused by acute blood loss when crystalloids alone are not considered suﬃcient.
- They should be used at the lowest eﬀective dose for the shortest period of time.
- They should not be used for more than 24 h and patients’ kidney function should be monitored for 90 days.
However, this guidance has now been changed and the recommendation is to use hydroxyethyl starches with caution in accredited hospitals61. Albumin solutions may be of beneﬁt when used to resuscitate patients with sepsis. Gelatins are used frequently, but the risk of anaphylaxis is greater with gelatins than starches.
Large volumes of 0.9% saline are best avoided, except after gastric losses, because of the risk of producing hyperchloraemic acidosis and its undesirable sequelae55. In the case of major blood loss it is also necessary to cross match and to give packed cells. Early and adequate treatment of the underlying cause of ﬂuid loss, e.g. control of bleeding, is vital. In the severely injured patient, replacement of blood loss with packed cells, fresh frozen plasma and platelets in a ratio of 1:1:1 has been shown to be more beneﬁcial than packed cells alone, as this helps correct the associated coagulation defects71.
Algorithms for the initial resuscitation of the patient in haemorrhagic shock, as recommended by the Committee on Trauma of the American College of Surgeons72 and the patient in septic shock, as recommended by the Surviving Sepsis Campaign40 are shown in Figs. 7.3 and 7.4 respectively. It must be remembered that these are complex situations and senior help should be sought as soon as possible. Further details for management of the patient with haemorrhagic shock can be accessed from the Advanced Trauma Life Support® Manual72 and for the patient with sepsis from the Guidelines of the Surviving Sepsis Campaign40.
Once resuscitation has been achieved as judged by normalisation of vital signs and urine output or of parameters from more invasive measurements, the prescriber should switch to a maintenance regimen with accurate replacement of any continuing losses. Exceeding such requirements, in the mistaken belief that the patient will excrete any excess, delays recovery and impairs outcome.
Replacement: Any ﬂuid prescription should incorporate not only daily maintenance requirements, but replacement of any ongoing abnormal losses. In the case of a patient with losses from any particular part of the gastrointestinal tract (e.g. from a ﬁstula), the ﬂuid prescription should include the daily maintenance requirements plus like-for-like water and electrolyte replacement of any losses. In order to achieve this, the prescriber should be aware of the approximate electrolyte content of ﬂuid at diﬀerent levels of the gastrointestinal tract (see Table 1.3).
Maintenance: Maintenance prescriptions should aim to replace insensible loss (500-1000 ml), provide suﬃcient water and electrolytes to maintain the normal status of body ﬂuid compartments, and suﬃcient water to enable the kidney to excrete waste products 500-1500 ml (Tables 1.2 and 1.3). The average person requires 25-30 ml/kg water, 1 mmol/kg sodium and 1 mmol/kg potassium per day. Examples of how to provide this maintenance requirement are summarised in Table 7.1. Some drugs contain appreciable amounts of sodium, especially if diluted and administered in 0.9% saline (see Chapter 6). This additional sodium load should be taken into account when planning ﬂuid prescriptions. Table 7.2 gives some examples of the sodium content of drugs, but is not comprehensive. If in doubt, the hospital pharmacist should be consulted.
Question 3. What is the patient’s current ﬂuid and electrolyte status and what is the best estimate of any current abnormality?
The answer to this question is summarised in Chapter 5. Decision making should be achieved by using all the information available, including history, examination, vital signs, measurements and tests including urine output and concentration and serum biochemistry, ﬂuid balance charts, weight changes, and an understanding of the likely pathophysiological changes. It should not be based just on casual bedside assessment of unreliable and non-speciﬁc signs such as dry mouth or diminished skin turgor. Remember, serial weighing is the most accurate measure of external water balance.
Question 4. Which is the simplest, safest, and most eﬀective route of administration?
The most appropriate method of administration should be the simplest and safest that is eﬀective (Chapter 8). The oral route should be used whenever possible. In acute situations and in the presence of gastrointestinal dysfunction or large deﬁcits, the intravenous route is the most appropriate. However, intravenous ﬂuid administration should be discontinued at the earliest opportunity. Administration of ﬂuid by enteral tubes may be appropriate where swallowing is the major problem. Subcutaneous infusions (hypodermoclysis)73 should be considered, particularly in the elderly, for the management of chronic or recurrent problems (see Chapter 8).
Question 5. What is the most appropriate ﬂuid to use and how is that ﬂuid distributed in the body?
The most appropriate ﬂuid to use is that which most closely matches any previous or ongoing losses. Recent evidence favours the use of balanced electrolyte solutions rather than 0.9% saline to replace salt and water deﬁcits55,56, except in the case of losses of gastric juice with its high chloride content. Colloids should be used cautiously and in accordance with the recommendations described above. Blood and blood products should be used appropriately when indicated (see above).
It is important to be clear about the objective of any ﬂuid prescription whether it be resuscitation, replacement or maintenance to avoid giving too little or too much, since both will have an adverse eﬀect on outcome. The distribution of any infused ﬂuid in the body water compartments should be understood and the contribution of any additional electrolyte (e.g. sodium content of drugs) should be taken into account in any calculation of ﬂuid and electrolyte balance. Fluid should be administered in the simplest way possible and intravenous ﬂuids discontinued as soon as adequate oral intake is established.
ROUTES OF FLUID ADMINISTRATION
ORAL OR ENTERAL
The use of oral rehydration solutions to treat diarrhoeal disease in both children and adults is one of the most commonly used treatments worldwide, particularly in low- and middle-income countries. They can also be useful in the management of short bowel or inﬂammatory bowel disease in hospital or at home.
These preparations are based on the principle that salt absorption in the small bowel is linked to that of carbohydrate and is, therefore, enhanced by glucose, glucose polymers, and starch (e.g. rice water)74. Some preparations also contain potassium and an alkalising agent to counter acidosis. In developing countries, they can be made using locally available materials, with simple measuring devices to ensure the correct proportions of salt, sugar or rice starch, and boiled water. In the UK commercial preparations are available (see British National Formulary), 5 sachets of Dioralyte (Sanoﬁ, Guildford, UK), for example, reconstituted in 1 litre of water, give Na+ 50 mmol, K+ 20 mmol, Cl– 50 mmol, citrate 10 mmol, and glucose 90 mmol. The WHO formula contains 75 mmol/L Na+. These are suitable for diarrhoeal diseases in children and most adults, although, in short bowel syndrome or inﬂammatory bowel disease in adults, a more concentrated solution may be required and can be obtained mixing more sachets per litre.
Fluid and electrolytes may also be administered via enteral tubes (nasogastric, percutaneous gastrostomy or jejunostomy) where oral administration is diﬃcult. Monitoring of oral or enteral ﬂuid treatment follows the same general principles as outlined in Chapter 5. One of the advantages of oral and enteral over intravenous administration is that, owing to the regulatory mechanisms of the gastrointestinal tract, it is diﬃcult to give excess ﬂuid. On the other hand, when ﬂuid losses are very great, or in the presence of gastrointestinal failure, the intravenous route may be necessary for resuscitation and replacement or to maintain balance.
In patients receiving nutritional support by whatever route, the ﬂuid and electrolyte content of the feed should be included when calculating ﬂuid and electrolyte balance and writing ﬂuid prescriptions.
Most ﬂuids are infused via a peripheral venous cannula. Such cannulae should be inserted and maintained using meticulous care, technique and protocols, since their potential for causing morbidity and even mortality from infection is often underestimated. Each hospital should have clear guidelines, as part of clinical governance, to ensure optimal care of peripheral cannulae (Fig. 8.1). Insertion sites should be inspected daily and cannulae removed or resited at the earliest sign of any inﬂammation. In any case, it is good policy to resite cannulae at least every 72 h75.
Modern single or multi lumen polyurethane or silastic lines inserted via the internal jugular or subclavian vein have even greater potential than peripheral cannulae to cause morbidity and mortality unless inserted and maintained by skilled staﬀ observing standard protocols. Ideally, they should be inserted using ultrasound guidance76 and strict aseptic precautions should be observed while inserting and using them. Hypertonic glucose solutions or those with high potassium concentrations should be given by the central rather than the peripheral route in order to prevent phlebitis.
SUB-CUTANEOUS ROUTE (HYPODERMOCLYSIS)
This method has been used in paediatrics and health care of the older adult for many years. It is particularly eﬀective for replacing small or medium ﬂuid and electrolyte losses in patients unable to maintain balance by the oral route and deserves wider use. One of its advantages is that patients or their carers can be taught to manage it at home. We have found it particularly useful for domiciliary use in adult and elderly patients with salt and water losses from gastrointestinal diseases73.
As an example, 0.9% saline (500-2000 ml daily) or 5% dextrose (500 ml) containing up to 20 mmol K+ and/or 4 mmol Mg2+ per litre may be infused over 3-4 hours via a ﬁne butterﬂy cannula inserted into the subcutaneous fat, usually over the torso.
The intraosseous route for ﬂuid infusion directly into the marrow of a long bone has been primarily used as an alternative in children with diﬃcult intravenous access and military combat casualty care. However, in the last two decades, this route has also been established for the resuscitation of adults in emergency situations. The usual sites for insertion of an 18G needle with trocar (or proprietary device) are the anteromedial surface of the proximal tibia, 2-3 cm below the tibial tuberosity; the distal tibia, proximal to the medial malleolus; and the distal femur. Contraindications to the intraosseous route include, among others, proximal ipsilateral fracture, ipsilateral vascular injury and osteogenesis imperfecta. Intraosseous infusion should be limited to emergency resuscitation and discontinued when other venous access has been obtained.
When ﬂuid is delivered by either the enteral or parenteral route, what is prescribed is not necessarily what is delivered, and patients may receive either too much or too little as a result of inaccuracies in delivery rates. It is now recommended that ﬂuids should be delivered using infusion pumps set at predetermined rates (Table 8.1), which can be up to 999 ml/h. This increases the accuracy of ﬂuid delivery. Nevertheless, delays in changing ﬂuid bags once they are empty may still lead to errors.
In planning ﬂuid therapy it is important to select the safest, simplest and most appropriate route and to monitor this carefully to avoid over- or under-treatment and any potential complications of the method. The aphorism, ‘if the gut works, use it’ is as appropriate in ﬂuid therapy as it is in nutritional care.
In health a normal diet generates about 600 mOsm/day of solute waste products that need to be excreted in the urine. With normal renal function and maximal antidiuretic hormone stimulation a minimum urine volume of 500 ml/day is required for this purpose (the volume obligatoire of Claude Bernard)1,2. Oliguria is, therefore, deﬁned as a urine output <0.5 ml/kg/h. However, it is important to determine whether it is physiological, i.e. a normal response to surgery/injury or pathological, e.g. secondary to hypovolaemia and/or sepsis, resulting in hypoperfusion of the kidneys and AKI (see chapter 10).
Oliguria, occurring soon after uncomplicated surgery, is usually part of the normal physiological response to injury (see Chapter 1), conserving salt and water in an attempt to maintain intravascular volume. Isolated oliguria in the ﬁrst 48 hours after uncomplicated surgery, therefore, does not necessarily reﬂect intravascular hypovolaemia, although it may do so if conﬁrmatory features are present, e.g. tachycardia, hypotension, low central venous pressure (CVP), decreased capillary reﬁll, etc. (Table 9.1).
The key clinical question, therefore, is whether or not the oliguria is pathological, i.e. due to signiﬁcant intravascular hypovolaemia requiring treatment. It is, therefore, essential that the patient’s volume status is assessed carefully (Table 9.1). Remember that serial changes give more information than single observations. Also remember the importance of charting data in a serial manner and in a way that is easily accessible to the clinician. In diﬃcult cases, particularly intra-operatively, invasive monitoring may be required to guide optimal treatment77.
Urine output should be interpreted in the light of these clinical signs and measurements before giving ﬂuid treatment, which, in the absence of hypovolaemia, may not only be unnecessary, but also deleterious. Unnecessary ﬂuid therapy not only expands the blood volume excessively but also overexpands the interstitial ﬂuid volume, causing oedema and weight gain. The metabolic response to surgery further impairs the patient’s ability to excrete the additional saline load, making interstitial oedema worse and compromising organ function, increasing the risk of morbidity and mortality. Other consequences are dilution of the haematocrit and serum albumin concentration50,51 (See Chapter 5).
OLIGURIA SECONDARY TO AKI
Although it is important not to give excess ﬂuid, giving too little also has serious consequences66. Failure to recognize and treat intravascular hypovolaemia (and pre-renal AKI) adequately may compromise organ perfusion and result in the development of intrinsic AKI. There is evidence that patients with oliguric AKI have more severe tubular damage and a worse outcome.
Once a diagnosis of AKI has been made, the underlying cause must be established (see Chapter 10). The most common causes are hypovolaemia and/or sepsis leading to hypoperfusion of the kidneys. Clinical examination must be performed to establish the patient’s volume status and the source of sepsis must be identiﬁed and treated promptly. If the patient is hypovolaemic, then appropriate ﬂuid therapy must be given according to a documented management plan, which requires regular review and deﬁned endpoints78,79 (Fig. 9.1).
In a patient with hypovolaemia and oliguric AKI
- consider inserting a urinary catheter (not routine and may introduce infection) to aid with the assessment of volume status particularly if the patient is confused or incapacitated due to the severity of the acute illness
- resuscitate with IV ﬂuids (ﬂuid challenge)
- stat ﬂuid bolus of 500 ml (250 ml if in cardiac failure) of balanced crystalloid (0.9% saline if hyperkalaemic) or colloid
- assess clinical response to ﬂuid in terms of
- capillary reﬁll time
- pulse (reduction in pulse rate if tachycardic)
- jugular venous pressure (rise in JVP)
- blood pressure (rise in BP)
- pulmonary oedema (if present stop iv ﬂuids)
- urine output
- if there is a clinical response to a ﬂuid bolus, continue with replacement ﬂuids and discuss further ﬂuid therapy plans with a senior member of the team
- if there is no clinical response and no pulmonary oedema, administer a further 500 ml of crystalloid, reassess clinically and discuss with a senior member of the team. Remember to consider the possibility of postoperative bleeding as a cause for the hypovolaemia and failure to respond to a ﬂuid challenge.
- if the patient has volume unresponsive oliguric AKI, continue with iv ﬂuids cautiously, matching urine output and at the same time monitoring for signs of respiratory distress (rising respiratory rate, pulmonary oedema or falling oxygen saturations). Refer to the renal team.
Oliguric AKI secondary to hypovolaemia is either volume responsive or unresponsive. In patients who are ﬂuid responsive, further ﬂuid replacement can be prescribed as hourly ﬂuid input equal to the previous hour’s output plus 30 ml, with continuous monitoring and frequent review. In some cases, despite apparently adequate intravascular volume replacement the patient remains oliguric and unresponsive to any further ﬂuid challenge. At this point it is important to avoid precipitating pulmonary oedema and no further intravenous ﬂuid should be administered. If the patient remains hypotensive, treatment with vasopressors should be considered and the advice of the critical care team sought. If the patient is haemodynamically stable but the AKI continues to progress, refer to the renal team.
In addition to the risk of pulmonary oedema, excessive ﬂuid administration has been associated with a worse outcome. A number of studies in surgical patients have demonstrated that a ﬂuid regimen that causes less than 2 kg weight gain, reduces the number of postoperative complications including anastomotic leak, sepsis, and bleeding requiring transfusion9,57,65. On the other hand, a positive ﬂuid balance greater than 2.5 kg is associated with increased morbidity9,57,65.
A common clinical question with oliguric AKI is whether the administration of loop diuretics (frusemide, bumetanide) improves renal recovery by increasing urine output. Studies have demonstrated that the use of high-dose loop diuretics to increase urine output in patients with established AKI does not decrease the need for renal replacement therapy or improve survival80-82. However, they may have a short-term role in managing ﬂuid overload and pulmonary oedema. In these patients, they may be used cautiously to try and establish a diuresis and treat the pulmonary oedema. If the patient fails to respond, referral to the renal team is recommended. It must be remembered that high doses of loop diuretics are not without side-eﬀects and may cause permanent hearing loss.
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