Introduction

Disorders of blood volume, body fluids, sodium, potassium and acid–base are common in acutely ill children. Always manage the airway and ventilation first, the ‘ABC’ principle of resuscitation, even in acute illness where shock and dehydration are dominant. In resuscitation of the circulation vigorous replacement of blood volume deficit is urgent, but correction of residual dehydration is not. Maintenance fluids are the last consideration.

Physiology

There are many physiological differences between adults and infants, and a few specific features that must be taken into account in managing fluid therapy. Infants have greater total body water, up to 70% of body weight compared with 60% in adults, the extra fluid being mostly extracellular, 30% of body weight compared with 20%^1,2 (Fig. 10.5.1). The ionic composition of intracellular and extracellular fluid is shown in Table 10.5.1. Small children drink more to accommodate a higher metabolic rate and excrete a higher solute load, and thus urine volume is greater.

Fig. 10.5.1 Body fluid compartments in children.

Source: Adapted from Henning, 1995.¹

Clinical assessment

In assessing the degree of dehydration, sequential body weight measurement is the most accurate measure of water loss. However, previous normal body weight is seldom available in the emergency department (ED).

Capillary refill times were studied in 32 children, aged 1–26 weeks, admitted to hospital with dehydration.⁴ The authors recommended a cut-off value of 2 seconds, below which minimal or no dehydration exists. A capillary refill time of 2–3 seconds suggests a 50–100 mL kg⁻¹ water deficit; 3–4 seconds 100–120 mL kg⁻¹, and over 4 seconds >150 mL kg⁻¹. However, ambient temperature affects capillary return.⁵

In children less than 4 years old clinicians overestimate the degree of dehydration by 3.2%.⁶ Other studies have suggested that the sensitivity of clinical examination for diagnosing dehydration is 74, 33 and 70% for mild, moderate and severe dehydration respectively.⁷ See Tables 10.5.2 and 10.5.3 for clinical signs associated with dehydration and electrolyte imbalance.⁸

Haemorrhagic shock

Clinical signs are of value in assessing degree of haemorrhage.⁹ See Table 10.5.4. Hypotension is a preterminal sign.

Source: Based on Morgan and O’Neill,1998.⁹

Fluid deficit

In the case of dehydration, once the percentage loss of body weight (PLBW) is estimated from clinical and laboratory tests the fluid deficit can be estimated.

Thus a 10 kg, 1- year-old who is 10% dehydrated has a fluid deficit of:

As this is an estimate, ongoing clinical parameters must be assessed including aiming for a urine output of >1.0 mL kg⁻¹ hr⁻¹.

Oedema

Oedema suggests that considerable water and salt retention has occurred. Mild sodium and water retention do not cause clinical oedema, nor does water retention without sodium retention, e.g. the syndrome of inappropriate antidiuretic hormone secretion rarely causes oedema. Oedema is most obvious in dependent and distensible subcutaneous tissue such as the genitalia, eyelids, lower legs and lower back. Firm pressure for at least 1 minute is needed to detect subtle cases. Causes include:

Investigations

Most children with gastroenteritis do not warrant an IV line or investigations. However, the following biochemical tests should be performed in children presenting with shock or significant problems of water and electrolyte imbalance that require intravenous treatment or where such disorders are expected, e.g. respiratory disease, renal disease, liver disease and encephalopathy:

Venous or intraosseous blood samples give a satisfactory measurement of electrolytes, and of respiratory and metabolic acid–base status.

A urine sample aspirated from a cotton wool ball placed at the perineum is satisfactory for all measurements except urine calcium.

Plasma osmolality can be calculated as well as measured in order to detect an osmolar gap.

If measured osmolality is greater than this figure by 5 mosmol kg⁻¹ or more, then an unmeasured solute is present such as an alcohol, e.g. ethanol or ethylene glycol. Ingestion of alcohols may cause a high anion gap ketoacidosis and hypoglycaemia.

Accurate timed urine collections are rarely possible in the ED. A useful indication of urine flow rate can be obtained from a spot urine sample, based on the relatively constant creatinine excretion between individuals. For example, a urine creatinine of 2000 μmol L⁻¹ represents urine flow of 2–4 mL kg⁻¹ hr⁻¹, and 8000 μmol L⁻¹ represents 0.5–1 mL kg⁻¹ hr⁻¹.

Fractional sodium excretion (FE_Na) is a useful diagnostic tool. It represents the proportion of filtered sodium that is not reabsorbed and is <1% in health. It is given by the formula:

A high FE_Na suggests any cause of natriuresis, including acute renal failure, a renal salt-wasting disorder or diuretics. Hyperosmolar urine with high urine creatinine and low FE_Na suggests dehydration of non-renal cause. Diabetes insipidus causes hypo-osmolar urine (often <100 mosmol kg⁻¹), low urine creatinine (often <1000 μmol L⁻¹) and plasma hyperosmolality. Plasma urea is high in most cases of dehydration because of reduced urea clearance.

Treatment

Replacement of circulating volume

Also called volume resuscitation, this is an urgent priority in any cause of hypovolaemic shock, e.g. haemorrhage, sepsis, burns, anaphylaxis and dehydration. It requires isotonic fluids (Table 10.5.5). Hypotonic fluids are inappropriate. Crystalloids are inexpensive and readily available. Colloids have a theoretical advantage of increasing the colloid oncotic pressure of plasma, thus helping to maintain fluid in the vascular space. However, in a capillary leak syndrome such as septic shock, the colloid may pass into the interstitial space. In practice, albumin in saline solution has been tested against 0.9% saline in adult intensive care patients. There was no difference in mortality or intensive care unit (ICU) stay between the two therapies. More saline was administered than albumin (ratio 1.38:1), suggesting that albumin may be superior in patients where excessive water administration may be harmful, e.g. pulmonary oedema, pulmonary hypertension and encephalopathy. There was a suggestion that albumin may be superior in sepsis but inferior in traumatic brain injury.¹⁰ A problem with saline is that it has no bicarbonate and relatively high chloride, so it can lead to hyperchloraemic acidosis. Hartmann’s and Ringer’s solutions are more physiological, containing buffer and calcium.^10–12

Table 10.5.5 Common crystalloid and colloid IV fluids

In dehydration, the loss of fluid and electrolytes is similar to the composition of extracellular fluid; this is predominantly where the loss comes from. Thus the deficit is best replaced with a solution that approximates extracellular fluid, i.e. 0.9% saline (normal saline).

However, as fluid replacement is not an exact science, and due to the fact that maintenance fluids also need to be given, a solution somewhere between 0.9% saline and 4% dextrose plus 0.18% saline is given. Saline (0.45%) with added glucose (2.5%) and sometimes potassium would be appropriate. Clinical parameters and serum biochemistry are sequentially measured and the fluid is adjusted accordingly.

An initial bolus or boluses of 20 mL kg⁻¹ to treat shock may be part of this initial fluid deficit.

Saline (but not Hartmann’s, Ringer’s and Plasmalyte) tends to cause a metabolic acidosis because of a dilution of bicarbonate by chloride, the principal extracellular buffer, and a relative hyperchloraemia.

Those containing lactate, gluconate or acetate are more physiological solutions, the buffer being rapidly metabolised to bicarbonate.

Glucose may be added to the sodium chloride preparations.

How much fluid?

Enough fluid should be given in shock to result in the improvement and disappearance of the signs of shock.

The blood volume of an infant is approximately 70–80 mL kg⁻¹. Decompensation in haemorrhagic shock starts to occur in class 3 haemorrhagic shock. At this stage it can be presumed that at least 30% or approximately 20 mL kg⁻¹ of blood has been lost.

Thus a bolus dose of 20 mL kg⁻¹ is a logical bolus dose of fluid with which to begin resuscitation.

However, in dehydration and sepsis much larger fluid losses and shifts have occurred and the total body water and extracellular fluid are likely to be depleted far more than 20 mL kg⁻¹. If crystalloid is given, not all of the fluid stays in the intravascular space. Capillary leakiness and third space losses in sepsis contribute to the ongoing loss of fluid from the vascular space.

Thus in dehydration repeated boluses may be necessary. Give a bolus, wait 10 minutes and reassess the patient again. Do not wait 10 minutes if it is clear that more than 20 mL kg⁻¹ will be required.^13–15

In severe sepsis such as meningococcaemia, 80–100 mL kg⁻¹ may be required. Good evidence exists that early and vigorous resuscitation improves morbidity and mortality in paediatric sepsis and meningococcaemia.¹⁶ The volume and the rapidity of resuscitation seems to be more important than the type of fluid used.^17–19

In haemorrhagic shock, boluses of 10 mL kg⁻¹ of whole blood or packed cells may be given. If fresh frozen plasma (FFP) is required this can also be given in 10 mL kg⁻¹ aliquots.

How to administer fluid in shock

Intravenous access is often difficult in a shocked young infant, but it is essential that this is achieved as soon as possible. If intravenous access has not been achieved within 90 seconds and/or three failed attempts have occurred, intraosseous access should be gained.

Poiseuille’s law states that the flow through a hollow tube is proportional to the radius to the power of four and inversely related to the viscosity of the fluid and length of the tube. The small radius can be overcome by applying a larger pressure differential across the tubing. Fluid can be drawn up in a 20 or 50 mL syringe and injected rapidly. It is harder to push fluid through a small cannula with a 50 mL syringe.

A three-way tap can be connected to a normal giving set attached to the IV fluid of choice. The tap can be turned off to the patient allowing fluid to be drawn into the syringe. The tap can then be turned off to the giving set and fluid can rapidly be injected into the patient.

Ideally, blood should be given through the largest cannula that can be inserted. As well as the usual complications of blood transfusion, the paediatric patient is at risk of hyperkalaemia from cell lysis through the small cannula.

Infants have a higher surface area to body weight ratio and lose heat more quickly. Overhead radiant warmers or fluid warmers are recommended for large rapid volume replacement when hypothermia is a risk.

Investigation and management of fluids in different conditions

Oral rehydration either by mouth or nasogastric tube is the method of choice for rehydration unless shock exists. It is safe, cheap and effective. It can be effective even in the case of vomiting.^21–26

Recommendations for oral and intravenous hydration in gastroenteritis as given by the American Academy of Pediatrics are contained in Table 10.5.7. Oral rehydration should occur with one of the recommended oral rehydration solutions (Table 10.5.8). No evidence exists to show that one formula is more effective than another.²² These fluids resemble 0.45% saline and 2.5% glucose with added potassium, a useful intravenous solution in this condition.⁸

∗ These recommendations cover children from 1 month to 5 years of age with no pre-existing comorbid conditions who live in developed countries. Specifically excluded are children who have diarrhoea lasting more than 10 days, diarrhoea associated with failure to thrive and/or vomiting in the absence of diarrhoea. If the physician is unsure of the dehydration category for a specific patient, the therapy for the more severe category should be used.

a The diet should emphasise complex carbohydrates, lean meats, yogurt, fruits and vegetables. Fatty foods, and foods and fluids that are high in simple sugars should be avoided.

b Replacement of ongoing fluid losses should include an amount for the estimated volume of emesis and 10 mL kg⁻¹ for each diarrhoeal stool.

Source: Based on Burkhart, 1999.⁸

Table 10.5.8 Oral rehydration solutions

Clear liquids or soft drinks are not to be encouraged. These may be high in carbohydrate and osmolality and lead to osmotic diarrhoea. Hyponatraemia may occur due to their low sodium content. Chicken broth is inappropriate as it may lead to hypernatraemia⁸ (Table 10.5.9).

Table 10.5.9 Electrolyte and carbohydrate content of common ‘clear liquids’

Some trials suggest frozen oral rehydration solution is better tolerated than the liquid form.²⁷ One study suggested that children with a serum bicarbonate greater than 13 mmol L⁻¹, and who were vomiting, could be treated with rapid intravenous rehydration (20–30 mL kg⁻¹ of isotonic crystalloid over 1–2 hours) in the ED.²⁸ They could then tolerate oral rehydration and be discharged home. Shorter stays in the ED were also enabled compared to times reported with oral rehydration solution.

Hypernatraemia and hypernatraemic dehydration

Hypernatraemia is usually caused by water depletion, or water plus sodium depletion in dehydration states where there is relatively more water depletion. Most causes of dehydration (see Table 10.5.5) can cause hypernatraemia. Rarely, hyperaldosteronism or salt poisoning cause sodium excess.

The clinical features are usually those of dehydration. Coma and seizures may occur, especially if plasma sodium is >160 mmol L⁻¹ at any time, and if there are rapid changes in circulating volume or plasma chemistry. Some neurological deficit may result from the encephalopathy of severe hypernatraemia.

Fractional sodium excretion is low because of a normal physiological response to dehydration, but may be high if the cause is an osmotic diuresis, excessive diuretic use or in salt poisoning. The urine is concentrated (osmolality >600 mosmol kg⁻¹) except in diabetes insipidus.

Shock is treated with isotonic fluids until haemodynamically stable, then 0.225–0.45% saline, with potassium as needed (40 mmol L⁻¹ if not hyperkalaemic). The estimated dehydration should be corrected over 48 hours with slow correction of plasma sodium at no more than 0.6 mmol L⁻¹ hr⁻¹ (15 mmol L⁻¹ day⁻¹).

If salt poisoning is suspected, obtain gastric fluid via nasogastric tube for sodium analysis. Features of dehydration are usually absent and FE_Na is high, often >10%. If there is salt excess without dehydration, then give less than maintenance water with no sodium, aiming for a very slow correction of plasma sodium, <0.6 mmol L⁻¹ hr⁻¹. A diuretic may be considered and, in extreme cases, dialysis.^29–31

Diabetes insipidus

Diabetes insipidus should be treated with glucose/water, replacing the previous hour’s urine volume plus 10–20 mL kg⁻¹ day⁻¹ for insensible losses. Hyperglycaemia may result. An intravenous vasopressin infusion may be needed, but only if the urine output is stable, which means usually after admission to a ward or ICU, and after consulting an endocrinologist.

Hyponatraemia and hyponatraemic dehydration

Hyponatraemia may be caused by water excess (e.g. water intoxication, inappropriate antidiuretic hormone (ADH)), water and salt retention where the water excess is greater than the sodium excess (e.g. nephrotic syndrome, heart failure, renal failure or liver failure), dehydration where sodium depletion is greater than the water depletion (e.g. renal loss, gastrointestinal loss, third-space loss, congenital adrenal hyperplasia, acute adrenal failure), or abnormal solute in extracellular fluid (e.g. glucose in uncontrolled diabetes) causing water shift from intra- to extracellular space.

Hyponatraemia may cause nausea, lethargy, depressed consciousness, raised intracranial pressure and seizures, especially if of rapid onset.

Urine osmolality and plasma urea are high in dehydration, but low in water intoxication. FE_Na is high in salt-losing states, inappropriate ADH and often in acute renal failure.

Treatment of shock is according to standard guidelines and can be instigated safely with normal saline. Severely symptomatic patients with plasma sodium less than 120 mmol L⁻¹, such as those with seizures or coma (which is likely to be associated with cerebral oedema), should have the sodium corrected rapidly to 125 mmol L⁻¹ (but no higher), using 3% saline (0.5 mmol mL⁻¹).

The following formula may be useful:

Excessive rapid correction of hyponatraemia can be associated with pontine or extrapontine myelinolysis, but it is not clear whether this relates to the severe hyponatraemia itself or the rapid correction. Convulsions and decreasing level of consciousness may occur at any time in treatment, especially if there are rapid changes in circulating volume or plasma chemistry. Some neurological deficit may result from the encephalopathy of severe hyponatraemia.

After treatment of shock, residual dehydration should be managed by replenishing extracellular space with 0.9% sodium chloride or one of the buffered isotonic solutions, slowly over 48 hours. Residual hyponatraemia should correct itself slowly.

Water intoxication needs water restriction to half maintenance and sodium supplementation if there is evidence of natriuresis.

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

This condition is over diagnosed. Plasma concentration of antidiuretic hormone, vasopressin, is elevated, despite physiological conditions which should suppress it, namely hypo-osmolality and water overload. Hyponatraemia and hypo-osmolality are accompanied by marked oliguria, but with high fractional sodium excretion and very high urine osmolality and sodium (often >200 mmol L⁻¹). The child is sodium depleted but water overloaded, so the management of choice is water restriction, the IV fluid being given as 0.9% saline. Furosemide causes a diuresis in SIADH and may contribute to management.

Pyloric stenosis

Shock is treated with 20 mL kg⁻¹ boluses of 0.9% saline. Saline (0.9%) with 40 mmol L⁻¹ of KCl is the appropriate rehydration solution. Glucose needs to be added. This remedies the loss of chloride and potassium, and slowly corrects the alkalosis.

Sepsis and meningococcal disease

There is no compelling argument for crystalloid or colloid.^18–21 A study of septic shock¹⁴ found that fluid resuscitation in excess of 40 mL kg⁻¹ in the first hour was associated with improved survival, decreased occurrence of persistent hypovolaemia and no increase in the risk of acute respiratory distress syndrome or pulmonary oedema. No restriction was placed on the type of resuscitation fluid used.

A study of severe meningococcaemia¹⁷ looked at 336 patients retrospectively and found a decreased mortality, both in the general population and in high-risk groups, when FFP was not used.

Thus, early vigorous fluid management is the key.

Haemorrhagic shock

Initial resuscitation can take place with crystalloid or colloid. Whole blood at 10 mL kg⁻¹ can be given and repeated as necessary until blood pressure is restored.

FFP should be thawed if a large transfusion is expected, and platelets requested. FFP only comes in adult-sized bags and doses of 10 mL kg⁻¹ are appropriate with repeating of coagulation times.⁹

Head injury

Vigorous treatment of shock should be undertaken to maintain cerebral perfusion pressure.³²

Interest has been generated in the use of 7.5% saline in head-injured patients. A prospective randomised study of 35 patients with head injury compared Ringer’s lactate with 7.5% saline.³³ Children treated with hypertonic saline had a statistically significant decrease in complications, intracranial pressure and ICU stay. There was no difference, however, in survival or duration of hospital stay. Neurological outcome was not well documented. More evidence is required.^33–35

Burns

The original Parkland formula of 3–4 mL kg⁻¹ per percentage burn is still applicable to burns patients. This is over the first 24 hours and starts at the time of the burn, not admission to ED.

Originally, 50% of this was to be given in the first 8 hours and the rest over the remaining 16 hours. However, recent evidence suggests that restoration of urinary output and vital signs occurs earlier if 50% is given in the first 4 hours. Many burns patients require more fluid than is provided by the Parkland formula. Aim for urine output greater than 1 mL kg⁻¹ hr⁻¹.³⁵

Some evidence also suggests that paediatric burns patients tolerate hypoalbuminaemia well and may not require albumin.³⁶

Diabetic ketoacidosis

Treatment of shock should include boluses of 20 mL kg⁻¹ of colloid or normal saline. Some solutions contain potassium and should ideally not be used in hyperkalaemic renal failure.

Rehydration over 48 hours is desirable so as to minimise the risk of cerebral oedema.

Cerebral oedema is almost exclusively a condition of the newly diagnosed young diabetic, with 95% of cases occurring under 20 years of age.

The fluid of choice is controversial. One article suggests that normal saline be used until restoration of glucose and then a change should be made to 0.45% saline. Potassium replacement should be started when the urinary output is adequate.³⁷

Hyperkalaemia

Hyperkalaemia is often discovered incidentally on routine chemistry, but may be suggested by ECG changes. It may be associated with renal failure, hypoxia-ischaemia or acidosis. There may not be potassium excess but rather potassium shift from intra- to extracellular fluid), β-blockers, rhabdomyolysis, haemolysis, potassium sparing diuretics, acute adrenal failure and potassium poisoning.

Mild hyperkalaemia may be asymptomatic but potassium levels >6 mmol L⁻¹, especially when acute, may cause weakness, peaked T-waves and wide PR interval on ECG, and then loss of P wave, heart block and asystole.

Investigations should include a blood gas, creatine kinase (CK) and glucose.

Any plasma potassium >6 mmol L⁻¹, or <6 but rising fast, demands urgent treatment. If K⁺ >7 mmol L⁻¹ or there are ECG changes, consider giving calcium 0.1–0.15 mmol kg⁻¹, which does not change plasma potassium but protects cell membranes. Beware of subcutaneous infiltration of the infusion. Sodium bicarbonate may also be given, especially if the child is acidotic, 1–3 mmol kg⁻¹ over 30–60 minutes, but its value is not certain. If plasma potassium is >6.5 mmol L⁻¹, consider arranging early dialysis. Discuss with the nephrology and intensive-care services.

Milder degrees of hyperkalaemia respond to 5–10 mcg kg⁻¹ IV salbutamol over a few minutes (or 2.5–5 mg of inhaled nebulised salbutamol if there is no IV cannula), to promote potassium entry into cells. This is more effective and longer lasting than glucose/insulin (0.1 U kg⁻¹ insulin plus 0.5 g kg⁻¹ glucose over 30–60 minutes).

Resonium, 1 g kg⁻¹ every 4–6 hours oral or rectal, may eliminate 1–2 mmol kg⁻¹ of potassium.

All cases of hyperkalaemia should be admitted with ECG monitoring.

Hypokalaemia

Hypokalaemia is often an incidental finding on blood chemistry and usually represents potassium depletion. Causes of potassium depletion include vomiting, diuretics, secretory diarrhoea, ureterosigmoidostomy, renal tubular acidosis, hyperaldosteronism, anorexia nervosa and diabetic ketoacidosis. Causes of hypokalaemia without depletion include salbutamol use, alkalosis and familial periodic paralysis.

Mild hypokalaemia is often asymptomatic but tachyarrhythmias, ileus, weakness and rhabdomyolysis may occur. Hypokalaemia associated with alkalosis usually corrects itself as the pH corrects.

Treat potassium depletion by slow potassium supplementation at 2 mmol kg⁻¹ day⁻¹ or greater. Never give 0.5 mmol kg⁻¹ in 1 hour without ECG monitoring and frequent repeat measurement. Concentration >40 mmol L⁻¹ of infusion fluid should be given into a central venous catheter.

Maintenance fluids

The concept of maintenance fluids refers to healthy children, where the kidneys are able to conserve or excrete water and salt over a wide range, in each case according to intake and non-renal losses. ‘Maintenance’ is a volume of water intake which maintains urine output in the middle of the normal range with an osmolality about that of extracellular fluid. However, changes in total body water and sodium and other electrolytes are common in many diseases. Insensible skin loss of water may be high because of fever and the higher surface area:weight ratio in infants. Maintenance is only relevant after restoration of circulating volume and total body water, and is therefore relevant to ongoing rather than ED care. A maintenance amount should be a starting amount. It may be excessive for any sick child where there may be diminished ability to excrete water.

Maintenance rates of 0.18% sodium chloride with 20 mmol L⁻¹ added potassium provide 40–100 mL kg⁻¹ day⁻¹ of water, 1.5–3 mmol kg⁻¹ day⁻¹ of sodium and 0.7–1.5 mmol kg⁻¹ day⁻¹ of potassium, which are normal quantities in healthy children.

A common formula for calculating ‘maintenance’ water requirements in a healthy child is as follows:

Reduce this by one-third initially, or even one-half if there is risk of cerebral oedema, e.g. in meningitis or brain injury, especially if hyponatraemia already exists. Less than ‘maintenance’ water should be given when water retention is likely, such as in sepsis and severe respiratory disease (0.7 × ‘maintenance’), cardiac failure (0.5 × ‘maintenance’), renal failure or other oliguric states without hypovolaemia (0.3 × ‘maintenance’ plus urine output) (Table 10.5.10). Greater than ‘maintenance’ is often advocated when water losses are expected, e.g. spontaneous hyperventilation or fever, but it is probably more appropriate to increase fluids only if urine output falls to 0.5 mL kg⁻¹ hr⁻¹. The most appropriate maintenance IV fluid in the acutely ill child is 0.45% saline because at half-‘maintenance’ rates this provides 1–3 mmol kg⁻¹ day⁻¹ of sodium, but separate consideration should always be given to sodium and other electrolyte requirements. Do not include dehydration deficit in maintenance; consider this separately and use 0.9% saline or a buffered isotonic solution for replacement.

Acid–base disorders

Disorders of physiological control of acidity of body fluids are common in acutely ill children. The system of defining acid–base state by changes in pCO₂ (respiratory) and standardised base excess (metabolic) according to the Copenhagen school remains the most familiar way of analysing acid–base disorders. Base excess is mostly bicarbonate deficit, but includes a small amount of buffering by albumin, and a larger amount by haemoglobin. Standardised base excess is provided by blood gas machines derived by microprocessor rather than the original nomograms. The philosophy of base excess has been challenged because it does not take into account the actual plasma albumin concentration and assumes a notional haemoglobin concentration of 50 g L⁻¹ across blood and extracellular fluid in all patients. It can be argued that the bicarbonate concentration alone is a sufficient measure of the degree of metabolic acidosis or alkalosis.

The anion gap remains a useful tool in determining whether any bicarbonate deficit is caused by organic acid (high anion gap) or by chloride excess (normal anion gap). It is obtained from the formula:

The normal is 16 mEq L⁻¹ and is essentially the negative charge on albumin and phosphate. Any excess is accounted for by abnormal unmeasured acid and/or lactate. Most modern laboratories, including blood gas machines, measure lactate. A more accurate way of determining the unmeasured component is from the formula:

Note that Mg²⁺ and Ca²⁺ are divalent and so are 2 × mmol L⁻¹.

The normal value for unmeasured anion is 5–6 mEq L⁻¹, including 1 mEq L⁻¹ of lactate. Any excess is abnormal. This may be lactate in hypoxia–ischaemia, acetoacetate or β-hydroxybutyrate in DKA, ketones in starvation, organic acids in inborn errors of metabolism or alcohol poisoning or toluene inhalation.

Most metabolic acid–base disturbances do not need treatment. Compensating mechanisms should generally not be treated, otherwise the primary disturbance is exacerbated. It is not necessary to restore pH to normal.

Slow sodium bicarbonate treatment may have a role in the management of normal anion gap acidosis where excessive chloride therapy would exacerbate hyperchloraemia. A suitable amount is 2 mmol kg⁻¹ day⁻¹. In diabetic ketoacidosis bicarbonate is not recommended acutely, even in severe acidaemia with pH < 7.0. However, ketoacids are excreted by osmotic diuresis in preference to chloride, so it may be helpful to include about a fifth of the sodium replacement as bicarbonate given just as slowly as the rest of the fluid. This may avoid hyperchloraemia and tachypnoea after the metabolic disorder is corrected. There is, however, no intravenous fluid preparation available that contains bicarbonate.

Correct hypoglycaemia. If an inborn error of metabolism is suspected give glucose at >8 mg kg⁻¹ min⁻¹, correct electrolyte imbalance, and partially correct acidosis with bicarbonate, giving this over at least 1 hour (see above).

Metabolic alkalosis

Metabolic alkalosis may be caused by chronic potassium and/or chloride depletion, e.g. vomiting, especially pyloric stenosis (accompanied by volume depletion) or renal (including diuretic use). It may be compensatory (chronic renal bicarbonate retention) in chronic respiratory failure, in which case it should not be treated. Acute alkalosis causing tetany by lowering plasma ionised calcium should be treated.

After correction of dehydration, chloride deficit is approximately 6 mmol kg⁻¹ for every 10 mmol L⁻¹ fall in plasma chloride. A suitable fluid for treating alkalaemic patients is 0.9% or 0.45% sodium chloride plus 40 mmol L⁻¹ potassium chloride with added glucose. Hypotonic solutions, which may exacerbate hyponatraemia, should not be used. Intravenous hydrochloric acid (or arginine hydrochloride) is indicated in rare severe cases when alkalosis may be depressing respiratory drive, and when the chloride deficit is not accompanied by sodium deficit. Give hydrochloric acid (150 mmol L⁻¹ solution) by central intravenous catheter. Give half-correction over at least 1 hour.

Acidifying diuretics such as acetazolamide may be indicated in metabolic alkalosis where there is sodium and water retention.

Controversies and future directions

There is debate about the use of albumin in sepsis and meningococcal disease.

There is continuing controversy about whether crystalloid or colloid is preferable in paediatric resuscitation, and which colloid, if any.

Hypertonic saline has been advocated in hypovolaemic shock but further research is required.