Disorders of fluids, electrolytes and acid–base

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10.5 Disorders of fluids, electrolytes and acid–base

Barry Wilkins, Wayne Hazell

Essentials

1 The most common causes of hypovolaemic shock in paediatric patients are sepsis, dehydration and trauma.
2 Vigorous restoration of the circulating volume reduces mortality in hypovolaemic shock.
3 Isotonic or near-isotonic fluids such as 0.9% saline, 4% albumin in 0.9% saline, blood products, Hartmann’s or Ringer’s solutions are appropriate for volume resuscitation. Hypotonic solutions including 5% glucose, 0.18%, 0.225% or 0.45% saline are inappropriate.
4 After resuscitation of circulating volume, residual dehydration should be corrected slowly with physiological solutions, such as Hartmann’s solution or 0.9% saline, or 0.45% saline in the presence of hypernatraemia.
5 The degree of dehydration is easily overestimated.
6 The concept of maintenance fluids applies only after resuscitation of circulating volume and repair of dehydration or water overload. Even then fluids must be individualised to the patient’s particular needs.
7 Hyponatraemia generally reflects water excess, and creates a risk for cerebral and pulmonary oedema. Hypotonic fluids are contraindicated until the plasma sodium is corrected. Cerebral oedema may develop rapidly in hyponatraemic children, especially after administration of hypotonic fluids.
8 Rapid correction of hyper- or hyponatraemia is contraindicated.
9 Hyperkalaemia with electrocardiogram (ECG) changes requires urgent potassium-lowering treatment.
10 Metabolic acidosis is common in sick children. The anion gap remains useful in determining the cause.
11 Treatment of acidosis is aimed at correcting the underlying cause. Alkali therapy is rarely indicated.
12 Metabolic alkalosis is caused by vomiting, especially pyloric stenosis, or as a compensation for chronic respiratory failure.

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.

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Fig. 10.5.1 Body fluid compartments in children.

Source: Adapted from Henning, 1995.1

Table 10.5.1 Ionic distribution of body fluid compartments

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The following physiological differences apply to children:1–3

• Infants are more dependent on heart rate for cardiac output.
• Infants have less ability to increase myocardial contractility.
• The infant’s ventricle is less compliant. Higher atrial pressures are required for the same degree of ventricular filling.
• The child is more dependent on the extracellular concentration of calcium.
• Storage and release of calcium from the sarcoplasmic reticulum in the infant’s myocardium is less efficient.
• The infant tolerates more tachycardia and hypotension.
• Degenerative diseases are uncommon in children.
• The capacity of the infant’s brain and heart for anaerobic metabolism is greater than the adult.
• The infant’s kidney is less able to concentrate urine and to handle a sodium load in the first 2 years of life. Thus infants are less able to compensate for fluid loss.
• Renal blood flow and glomerular filtration rate are less per unit body surface area.
• Infants have less capability to acidify the urine and are thus less able to deal with a hyperchloraemic acidosis caused by too much chloride administration.
• Total body water and extracellular fluid are proportionally higher in the first 6 months of life. In later childhood extracellular fluid declines and intracellular fluid increases due to cell multiplication.
• Limited glycogen stores exist. Hypoglycaemia frequently occurs in periods of stress in infants and young children.

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

Table 10.5.2 Degree of dehydration based on percentage of body weight lost∗

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Table 10.5.3 Signs of hypernatraemia and hypokalaemia in dehydration
Hypernatraemia
Cutaneous signs
Warm, ‘doughy’ texture
Possibly decreased skin-fold tenting in severe dehydration, thereby giving appearance of lower level of dehydration
Neurological signs
Hypertonia
Hyperreflexia
Lethargy common, but marked irritability
when touched
Hypokalaemia
Weakness
Ileus with abdominal distension
Cardiac arrhythmias

Source: Based on Burkhart, 1999.8

Plasma bicarbonate concentration may be the single most useful laboratory test; a level less than 17 mmol L−1 indicates moderate or severe dehydration. Addition of this to the clinical scale improves the sensitivity of diagnosing moderate and severe dehydration to 90 and 100% respectively. Plasma bicarbonate was a better predictor than plasma urea and creatinine.7

Shock is a disorder characterised by a decrease in end-organ oxygenation and/or perfusion. This does not solely depend on blood pressure and pulse rate. Blood pressure can be maintained in the infant with shock being present. Hypotension is a preterminal sign.

End-organ perfusion can best be assessed by the conscious state, capillary return, urine output and degree of metabolic acidosis.

Haemorrhagic shock

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

Table 10.5.4 Classes of haemorrhagic shock9
Class of haemorrhage Blood volume lost (%) Signs
I <15 Minimal, slight tachycardia
II 15–30 Tachycardia, tachypnoea, diminished pulse pressure, systolic BP unchanged, prolonged capillary refill, minimal decrease in urine output, anxiety
III 30–40 Tachycardia, tachypnoea, decreased BP, decreased urine output, mental status changes
IV >40 Hypotension, anuria, loss of consciousness

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.

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

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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:

• Heart failure
structural cardiac disease;
myocarditis;
cardiomyopathy;
arrhythmias, especially supraventricular tachycardia;
effusion.
• Liver disease
acute hepatic failure;
chronic hepatic failure.
• Renal disease
nephrotic syndrome.
• Protein-losing enteropathy
• Hereditary angio-oedema
• Excessive water and sodium intake
• Other causes of hypoalbuminaemia.

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:

• plasma sodium, potassium, urea, creatinine, osmolality, glucose, bicarbonate, lactate;
• plasma calcium, magnesium, phosphate, liver function tests, albumin;
• arterial and/or venous pH and gases if shocked.

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

• urine sodium, potassium, urea, creatinine, osmolality, glucose, and dipstick test for protein, red cells and casts (random spot sample).

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.

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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 (FENa) 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:

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A high FENa suggests any cause of natriuresis, including acute renal failure, a renal salt-wasting disorder or diuretics. Hyperosmolar urine with high urine creatinine and low FENa 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

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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.

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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.

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