Fluid and electrolyte management

Transcription

1 281 Chapter Appendix 5B Fluid and electrolyte management Learning outcomes After reading this appendix, you will be able to: Describe the approach to the management of fluid and electrolytes in the seriously ill or injured child B.1 Introduction At birth, approximately 80% of a child s body weight is water. This percentage falls gradually during childhood, reaching 60% water by adulthood. Total body water is distributed between the intracellular, interstitial and intravascular spaces, moving from one compartment to another depending on various pressure and osmotic gradients. In illness and injury these fluid shifts may be rapid, with significant clinical consequences. B.2 Fluid balance Normally fluid balance is tightly controlled by thirst, hormonal responses and renal function: the quantities in Table B.1 provide a guideline to appropriate fluid intake. These formulae are based on an assumption of 100 kcal/kg/day of caloric intake, 3 ml/kg/hour of urine output and normal stool output. For example: A 6 kg infant would require 600 ml/day A 14 kg child would require = 1200 ml/day A 25 kg child would require = 1600 ml/day In critical illness or injury some or all of these mechanisms may be profoundly disrupted, and fluid therapy has to be tailored to the needs of the specific child. In the presence of anuria due to acute renal failure, fluid requirements may fall below 30 ml/kg/day, while in high output diarrhoea requirements may be as high as 400 ml/kg/day. Fluid intake is required to replace fluid losses and to enable the excretion of various waste products through the urine. Insensible losses (via respiration and sweat) generally amount to between 10 and 30 ml/kg/day. The actual volume of insensible fluid loss is related to the caloric content of the feeds, ambient temperature, humidity of inspired air, presence of pyrexia and quality of the skin. Insensible losses from a child on a ventilator in a cool environment with minimal caloric intake may be minimal. Usually between 0 and 10 ml/kg/day are lost in the stool (this will increase markedly in diarrhoea, where losses in excess of 300 ml/kg/day are not uncommon). Urinary losses are between 1 and 2 ml/kg/h (i.e. approximately 30 ml/kg/day). Advanced Paediatric Life Support: A Practical Approach to Emergencies, Sixth Edition. Edited by Martin Samuels and Sue Wieteska John Wiley & Sons, Ltd. Published 2016 by John Wiley & Sons, Ltd.

2 282 / Part 6 Appendices Table B.1 Fluid requirements in well, normal children Body weight Fluid requirement per day (ml/kg) Fluid requirement per hour (ml/kg) First 10 kg Second 10 kg 50 2 Subsequent kilograms 20 1 Dehydration and shock Concepts Dehydration does not cause death, shock does. Shock may occur with the loss of 20 ml/kg from the intravascular space, while clinical dehydration is only evident after total losses of >25 ml/kg As a guide, the child with dehydration and no shock can be assumed to be 5% dehydrated; if shock is present, then 10% dehydration or greater has occurred The treatment of shock requires the rapid administration of an intravascular volume of fluid that approximates in electrolyte content to plasma The treatment of dehydration requires a gradual replacement of fluids with an electrolyte content that relates to the electrolyte losses, or to the total body electrolyte content Pathology from electrolyte changes is related to either extreme levels, or rapid rates of change Administration of sodium bicarbonate is rarely indicated Overhydration is potentially as dangerous as dehydration The intravascular volume of an infant is c. 80 ml/kg, and of an older child 70 ml/kg. A rapid loss of 25% of this volume (i.e. 20 ml/kg) will cause shock unless that volume is replaced from the interstitial fluid at a similar rate. Clinical signs of dehydration (Table B.2) are only detectable when the patient is 2.5 5% dehydrated. Five per cent dehydration implies that the body has lost 5 g per 100 g body weight, i.e. 50 ml/kg. Clearly, shock may occur in the absence of dehydration, dehydration may occur in the absence of shock, or both may occur together all dependent on the rate of fluid loss and the rate of fluid shifts. Table B.2 Signs and symptoms of dehydration and shock (adapted from NICE, 2009) No clinically detectable dehydration Clinical dehydration Clinical shock Appears well Appears to be unwell Pale, lethargic or mottled Normal breathing pattern Normal or tachypnoea Tachypnoea Normal heart rate Normal or tachycardia Tachycardia Normal peripheral pulses Normal peripheral pulses Weak peripheral pulses Normal capillary refill time Normal or mildly prolonged capillary refill time Prolonged capillary refill time Normal blood pressure Normal blood pressure Hypotension Normal skin turgor Reduced skin turgor Normal urine output Decreased urine output Decreased urine output Alert and responsive Altered responsiveness (e.g. irritable, lethargic) Decreased level of consciousness Eyes not sunken Moist mucous membranes (except after a drink) Sunken eyes Depressed fontanelle* Dry mucous membranes (except for mouth breathers ) Warm extremities Warm extremities Cold extremities *Only useful in an infant if still patent and in the absence of disorders such as meningitis.

3 Appendix B Fluid and electrolyte management / 283 The priorities of management are to identify shock and treat it effectively and rapidly (see Chapter 6), identify dehydration and institute a treatment programme that will enable effective rehydration over hours, identify the presence and aetiology of acid base problems and correct these where necessary, and identify the presence and aetiology of electrolyte abnormalities and correct these gradually without precipitating complications. One factor remains unknown at the initiation of therapy, namely the ongoing fluid losses that will occur during therapy. Thus any plan of fluid management represents a starting point, and this will have to be modified in the light of data from constant monitoring. The critical clinical questions are therefore: Is the patient shocked? Is the patient dehydrated? Does the patient have a significant acid base abnormality? Are there significant electrolyte problems? Shock The treatment of hypovolaemic shock secondary to fluid loss (after securing the airway and providing high flow oxygen) is the rapid administration of crystalloid. The starting volume is 20 ml/kg, and this can be repeated if there is inadequate clinical response (with no evidence of intravascular overload). The fluids used should approximate in electrolyte concentrations to those of serum (options include 0.9% saline and Hartmann s solution, however the latter should be used with care in renal impairment as it contains potassium). The presence of hyper or hyponatraemia does not affect the choice of fluids during this phase of resuscitation. In the context of severe sepsis there is some concern about the use of fluid boluses for resuscitation. It seems reasonable to continue with fluid bolus administration with careful monitoring of the patient s response. Unless there is evidence of cardiac dysrhythmia or neurological abnormality, electrolyte abnormalities should be corrected gradually. Once shock has been adequately treated, attention can turn to management of hydration. Frequent reassessment remains necessary as the patient may well become shocked again if the underlying cause of the fluid shifts (e.g. gastroenteritis) is ongoing. Dehydration Many clinical signs of dehydration are individually unreliable (Table B.2) and have poor interobserver reproducibility, but taken together they provide a reasonable estimate of total body fluid losses. Weight is the only clinically available objective measure of total body fluid changes, and enables an accurate assessment of fluid balance over time (unfortunately initial fluid therapy must usually be based on a clinical assessment of hydration because the pre sickness weight is not often available). The measured weight loss or percentage dehydration: 5% dehydration lossof5mloffluidper100 gbody weight,or50 ml/ kg 10% dehydrated loss of 10 mlof fluidper100 gbodyweight, or100 ml/ kg Management of dehydration consists of the administration of calculated daily maintenance fluids in addition to calculated replacement fluids over a 24 hour period. Therapy should be monitored at 3 4 hourly intervals using weight as an objective measure, to ensure that the patient is gaining weight at an appropriate rate. If the calculated fluid administration rate is too slow or too fast, then the rate should be modified appropriately. See Table B.3 for the commonly available crystalloid fluids. When the gut is functioning, oral rehydration using standard solutions is preferred (the World Health Organisation (WHO) formulation provides 75 mmol sodium, 20 mmol potassium, 65 mmol chloride, 10 mmol citrate and 75 mmol glucose per litre; the formulations recommended in the UK have lower sodium concentrations of mmol/l). This fluid should be administered frequently in small volumes (a cup and spoon works very well for this process). Generally, normal feeds should be administered in addition to the rehydration fluid, particularly if the infant is breast fed.

4 284 / Part 6 Appendices Table B.3 Commonly available crystalloid fluids Fluid Na + (mmol/l) K + (mmol/l) Cl (mmol/l) Energy (kcal/l) Other Sodium chloride 0.9% Sodium chloride 0.45%, dextrose 5% Hartmann s solution Lactate Dextrose 5% Dextrose 10% When there is excessive vomiting or there are signs of damaged bowel, fluid therapy should be given intravenously. Unless there is bowel damage, attempt early and gradual introduction of oral rehydration therapy during intravenous fluid therapy. If tolerated, stop intravenous fluids and complete rehydration with oral rehydration therapy. Example A 6 kg child is clinically shocked and 10% dehydrated as a result of gastroenteritis. Initial therapy 20 ml/kg for shock = 6 20 = 120 ml of 0.9% saline given as a rapid intravenous bolus Estimated fluid therapy over the next 24 hours 100 ml/kg for 10% dehydration = = 600 ml 100 ml/kg for daily maintenance fluid = = 600 ml Rehydration + maintenance = 1200 ml Therefore start with an infusion of 1200/24 = 50 ml/h Application of fluid therapy Reassess clinical status and weight at 4 6 hours, and if satisfactory continue. If the child is losing weight increase the fluid rate, and if the weight gain is excessive decrease the fluid rate. Start giving more of the maintenance fluid as oral feeds if the child is tolerating the fluids. Fluid overload and overhydration In the same way that fluid losses may cause shock, dehydration or both, excessive fluid administration can cause intravascular fluid overload, overhydration or both. In the patient with nephrotic syndrome, fluid has leaked out of the intravascular space and into the tissues because of a low serum albumin. Such children may be grossly overhydrated, with diffuse severe oedema. However, many patients with nephrotic syndrome have a contracted intravascular space, and attempts to diurese these patients without first expanding the intravascular space with albumin may result in shock. By contrast the patient with myocardial dysfunction may have an intravascular compartment that is grossly overfilled. The clinical signs of intravascular overload may be present, and yet the patient (particularly if they have been on diuretics) may actually be total body fluid depleted and may appear dehydrated. Children with renal impairment may present with a combination of intravascular and total body fluid overload. Administration of further fluid can worsen fluid overload leading to pulmonary oedema. The treatment of fluid overload can be complex and the non specialist should seek expert advice.

5 Appendix B Fluid and electrolyte management / 285 Electrolyte abnormalities Table B.4 shows the normal electrolyte requirements. Table B.4 Water, electrolyte and energy requirements in well, normal children Body weight Water (ml/kg/day) Sodium (mmol/kg/day) Potassium (mmol/kg/day) Energy (kcal/day) Protein (g/day) First 10 kg Second 10 kg Subsequent kilograms Sodium Both low and high sodium levels are potentially dangerous. Severe hypernatraemia may be associated with brain damage, because brain tissue shrinks as a result of intracellular dehydration and blood vessels may tear or clot up. Too rapid correction of hypernatraemia may lead to cerebral oedema and convulsions. Similarly, rapid correction of hyponatraemia may also be associated with demyelination and permanent brain injury. The electrolyte losses during dehydration depend on the reason for dehydration. In gastroenteritis, sodium losses in diarrhoea stool range from approximately 50 mmol/l (rotavirus) to approximately 80 mmol/l (cholera and enteropathogenic Escherichia coli). In renal dysfunction sodium losses may be minimal (diabetes insipidus) or high (renal tubular dysfunction). Hypernatraemia Hypernatraemia in the dehydrated patient may be the end result of excessive loss of water (e.g. diabetes insipidus, diarrhoea), excessive intake of sodium (e.g. iatrogenic poisoning, non accidental injury), or a combination of both (e.g. children with gastroenteritis given excessive sodium in rehydration fluid). The electrolyte content of the replacement solution depends on the cause of the dehydration. Previously, 0.45% NaCl, containing 75 mmol/l NaCl, was considered a safe starting solution for intravenous rehydration. This was based largely on the electrolyte content of stool in diarrhoea. By contrast, patients with rare renal tubular dysfunction who lose excessive sodium and water through their kidneys may require 0.9% NaCl to replace the renal losses of sodium. Measurement of the sodium content of urine and stool may help direct replacement therapy. More recently, consensus guidelines have recommended starting with an isotonic solution such as 0.9% NaCl, or 0.9% NaCl with 5% glucose, for fluid deficit replacement and maintenance for hypernatraemic dehydration due to a number of children developing a rapid fall in sodium with hypotonic solutions. The principles in the treatment of hypernatraemia are: 1. Treat shock first. 2. Calculate the maintenance fluid and estimate the fluid deficit carefully. 3. Aim to lower the serum sodium at a rate of no more than 0.5 mmol/h. 4. Check other electrolyte levels such as calcium and glucose. 5. Monitor the electrolytes frequently obtain expert advice if correction is not improving. 6. Clinically assess hydration and weigh frequently. Hyponatraemia Hyponatraemia may be due to excessive water intake or retention, excessive sodium losses, or a combination of both. If the child is fitting from hyponatraemia, partial rapid correction of the serum sodium level will be necessary to stop the fitting. Administration of 4 ml/kg of 3% NaCl solution over 15 minutes will raise the serum sodium by approximately 3 mmol and will usually stop the seizures.

6 286 / Part 6 Appendices If hyponatraemia is due to excessive water intake or retention, and the patient is not symptomatic, the restriction of fluid intake to 50% of normal estimated requirements may be adequate therapy. If dehydrated and intravenous fluids are required then 0.9% NaCl is an appropriate fluid. The principles in the treatment of hyponatraemia are: 1. Treat the child s seizures with hypertonic 3% NaCl (seizure control should happen simultaneously). 2. Calculate the maintenance fluid and estimate the fluid deficit carefully. 3. Aim to raise the serum sodium at a rate of no more than 0.5 mmol/h. 4. Check other electrolyte levels such as calcium and glucose. 5. Monitor the electrolytes frequently obtain expert advice if correction is not improving. 6. Clinically assess hydration and weigh frequently. Potassium Unlike sodium, potassium is mainly an intracellular ion and the small quantities measurable in the serum and extracellular fluid represent only a fraction of the total body potassium. The intracellular potassium acts as a large buffer to maintain the serum value within a narrow normal range. Cardiac arrhythmias can occur at values outside this range. Thus hypokalaemia is usually only manifest after significant total body depletion has occurred. Similarly, hyperkalaemia represents significant total body overload, beyond the ability of the kidney to compensate, or massive break down of blood cells resulting in the release of potassium. The causes of hyper and hypokalaemia are given in Table B.5. Table B.5 Causes of hypo and hyperkalaemia Hypokalaemia Diarrhoea Alkalosis Volume depletion Primary hyperaldosteronism Diuretic abuse Hyperkalaemia Renal failure Acidosis Adrenal insufficiency Cell lysis Excessive potassium intake In the critically ill neonate, inadequate cardiac output must always be excluded as a cause Hypokalaemia Hypokalaemia is rarely an emergency and is usually the result of excessive potassium losses from acute diarrhoeal illnesses. As total body depletion will have occurred, large amounts are required to return the serum potassium to normal. Oral supplementation is the preferred route. In cases where this is not suitable, intravenous supplements are required. However, strong potassium solutions are highly irritant and can precipitate cardiac arrhythmias, thus the concentration of potassium in intravenous solutions ought not to exceed 40 mmol/l except when given centrally with close cardiac monitoring. Patients who are alkalotic or are receiving insulin or salbutamol will have high intracellular potassium stores. The hypokalaemia in these cases is the result of a redistribution of potassium into cells rather than potassium deficiency, and management of the underlying causes is indicated. Hyperkalaemia Hyperkalaemia is a dangerous condition. Although the normal range extends up to 5.5 mmol/l, it is rare to get arrhythmias below 7.5 mmol/l. Precise blood taking is critical as a squeezed sample lyses blood cells, raising potassium level spuriously. The most common cause of hyperkalaemia is renal failure either acute or chronic. Hyperkalaemia can also result from potassium overload, loss of potassium from cells due to acidosis or cell lysis, or endocrine causes such as hypoaldosteronism and hypoadrenalism. The immediate treatment of hyperkalaemia is shown schematically in Figure B.1. If there is no immediate threat to the patient s life because of an arrhythmia then a logical sequence of investigation and treatment can be followed. Beta 2 stimulants, such as salbutamol, are the immediate treatment of choice. They rapidly act within 30 minutes by stimulating the cell wall pumping mechanism and promoting cellular potassium uptake. They are easily administered by a nebuliser. The serum potassium will fall by about 1 mmol/l with these dosages.

7 Appendix B Fluid and electrolyte management / 287 Consider specific arrhythmia protocol Arrhythmia? Yes Calcium 0.1 mmol/kg IV No Nebulised salbutamol mg Repeat serum potassium Falling Calcium resonium 1 g/kg PO or PR PLAN DIALYSIS IF NECESSARY Remains After high bicarbonate Assess ph <7.34 Sodium bicarbonate 1 2 mmol/kg IV >7.35 Glucose 10% 5 ml/kg and insulin 0.05 units/kg/h IV Figure B.1 Algorithm for the management of hyperkalaemia Summary of emergency management of hyperkalaemia in children (Continued overleaf) Basics Stop K + intake Stabilise myocardium Shift K + into cells Definition: K + significantly above upper end of normal for age and/or rising ABC Monitoring: continuous ECG (first signs are tented T waves then loss of P waves), SaO 2, blood pressure, urine output, weight Recheck urea and electrolytes urgently hours may have elapsed since last sample. Sample may have haemolysed Consider the cause: high K + intake, high production or low output Stop any potassium in diet and in any fluids being infused Stop drugs that can cause hyperkalaemia, e.g. angiotensin converting enzyme inhibitor (ACE inhibitor), angiotensin II blockers and β blockers 10% calcium gluconate ml/kg IV over 5 min, max. 20 ml; give undiluted Give if ECG changes or K + significantly above upper end of normal for age or rising Effect occurs within minutes. Duration of action approx. 1 h, repeat within 5 10 min as necessary Nebulised salbutamol <2 year: 2.5 mg or 2 years: 5 mg; repeat 2 hourly as necessary Onset of action: within 30 min, max. effect at min Seek specialist advice The following strategies can be used depending on clinical situation: Shift K + into cells Sodium bicarbonate 1 2 mmol/kg IV over 30 min (1 mmol = 1 ml of 8.4% NaHCO 3, dilute 1:5 in 5% dextrose)

8 288 / Part 6 Appendices Glucose (± insulin): peripheral access: 10% glucose 5 10 ml/kg/h central access: 20% glucose ml/kg/h Maintain blood glucose at mmol/l. Physiological homeostasis should increase endogenous insulin production Add insulin after an hour if blood sugar >15 mmol/l Make up a syringe of 50 units insulin in 50 ml 0.9% NaCl (=1 unit/ml); commence infusion at 0.05 ml/kg/h Maintain blood glucose at mmol/l by adjusting infusion rate in 0.05 ml/kg/h steps Can cause severe hypoglycaemia. Measure blood sugar frequently (15 min after commencing or increase in dose, then every 30 min until stable) Remove K + from body Dialysis Calcium resonium: by rectum: 250 mg/kg (max. 15 g) 6 hourly, repeat if expelled within 30 min by mouth: 250 mg/kg (max. 15 g) 6 hourly Limited role for oral route as it is unpalatable. Takes 4 h for full effect In specialist environment Sodium bicarbonate is also effective at rapidly promoting intracellular potassium uptake. The effect is much greater in the acidotic patient (in whom the hyperkalaemia is likely to be secondary to movement of potassium out of the cells). The dosage is the same as that used for treating acidosis, and 1 2 ml/kg of 8.4% NaHCO 3 is usually effective. It is important to also check the serum calcium because hyperkalaemia can be accompanied by marked hypocalcaemia, particularly in patients with profound sepsis or renal failure. The use of bicarbonate in these situations can provoke a crisis by lowering the ionised calcium fraction rapidly, precipitating tetany, convulsions or hypotension and arrhythmias, so frequent blood monitoring is required. Insulin and glucose are the classic treatment for hyperkalaemia. They are not, however, without risk, and the use of salbutamol has reduced the requirement for such therapy. It is easy to precipitate hypoglycaemia if monitoring is not adequate. Large volumes of fluid are often used as a medium for the dextrose and, particularly in the patient with renal failure fluid overload, can then be a problem. Many children are quite capable of significantly increasing endogenous insulin production in response to a glucose load, and this endogenous insulin is just as capable of promoting intracellular potassium uptake. It thus makes sense to start treatment with just an intravenous glucose load and then to add insulin as the blood sugar rises. The above treatments are the fastest means of securing a fall in the serum potassium, but all work through a redistribution of the potassium into cells. Thus the problem is merely delayed rather than treated in the patient with potassium overload. The only ways of removing potassium from the body are with dialysis or ion exchange resins such as calcium resonium administrated via the gut. Dialysis can only be started when the patient is in an appropriate nephrology or critical care setting, but will be the most effective and rapid means of lowering the potassium. In an emergency situation where there is an arrhythmia (heart block or ventricular arrhythmia) the treatment of choice is intravenous calcium. This will stabilise the myocardium temporarily but will have no effect on the serum potassium. Thus the treatments discussed above will still be necessary. Calcium Some mention of disorders of calcium metabolism is relevant because both hyper and hypocalcaemia can produce profound clinical pictures. Hypocalcaemia Hypocalcaemia can be a part of any severe illness, particularly septicaemia. Other specific conditions that may give rise to hypocalcaemia are severe rickets, hypoparathyroidism, pancreatitis or rhabdomyolysis, and citrate infusion (in massive blood transfusions). Acute and chronic renal failure can also present with severe hypocalcaemia. In all cases, hypocalcaemia can produce weakness, tetany, convulsions, hypotension and arrhythmias. Treatment is that of the underlying condition. In the emergency situation, however, intravenous calcium can be administered. As most of the above conditions are associated with a total body depletion of calcium and because the total body pool is so large, acute doses will often only have a transient

9 Appendix B Fluid and electrolyte management / 289 effect on the serum calcium. Continuous infusions will also often be required, and most appropriately given through a central venous line as calcium is irritant to peripheral veins. In renal failure, high serum phosphate levels may prevent the serum calcium from rising. The use of oral phosphate binders or dialysis may be necessary in these circumstances. Hypercalcaemia Hypercalcaemia usually presents as long standing anorexia, malaise, weight loss, failure to thrive or vomiting. Causes include hyperparathyroidism, hypervitaminosis D or A, idiopathic hypercalcaemia of infancy, malignancy, thiazide diuretic abuse and skeletal disorders. Initial treatment is with volume expansion with normal saline and furosemide diuretic. Following this, investigation and specific treatment are indicated. B.3 Diabetic ketoacidosis Diabetic ketoacidosis (DKA) is a condition in which a relative or absolute lack of insulin leads to an inability to metabolise glucose. This leads to hyperglycaemia and an osmotic diuresis. Once urine output exceeds the ability of the patient to drink, dehydration occurs. In addition, without insulin, fat is used as a source of energy, leading to the production of large quantities of ketones and metabolic acidosis. There is initial compensation for the acidosis by hyperventilation and a respiratory alkalosis but, as the condition progresses, the combination of acidosis, hyperosmolality and dehydration leads to coma. DKA is often the first presentation of diabetes; it can also be a problem in known diabetics who have decompensated through illness, infection or non adherence to their treatment regimes. History The history is usually of weight loss, abdominal pain, vomiting, polyuria and polydipsia, although symptoms may be much less specific in under 5 year olds who also have an increased tendency to ketoacidosis. Examination Children may be dehydrated with deep and rapid (Kussmaul) respiration. They may also be drowsy with the smell of ketones on their breath. Salicylate poisoning and uraemia are differential diagnoses that should be excluded. Whilst rare, infection often precipitates decompensation in both new and known diabetics. Fever is not part of DKA. Suspect sepsis in the presence of fever, hypothermia, hypotension and a refractory acidosis or lactic acidosis. Management Assess: Airway Breathing Circulation Give 100% oxygen and place on a cardiac monitor Place on a cardiac monitor (observe for peaked T-waves from hyperkalaemia) Consider placement of a nasogastric tube Take blood for: Blood gases Urea and electrolytes, creatinine Glucose Ketones Take urine for: Sugar Take other investigations only if indicated: Full blood count (leucocytosis commonly occurs in DKA and is not necessarily a sign of infection) Chest X-ray Blood culture CSF Throat swab Urinalysis, culture and sensitivity

10 290 / Part 6 Appendices The principles of management of diabetic ketoacidosis are: 1. Fluid boluses are only to be given in DKA to reverse signs of shock and should be given slowly in 10 ml/kg aliquots. If there are no signs of shock, do not routinely give a fluid bolus. If a second saline bolus is needed, specialist advice should be sought. 2. To rehydrate after signs of shock have been reversed with 48 hours of replacement fluid. 3. The first 20 ml/kg of fluid resuscitation are given in addition to replacement fluid calculations and should not be subtracted from the calculations for the fluids for the next 48 hours. Resuscitation volumes over 20 ml/kg should be subtracted from the fluid volume calculated for the 48-hour replacement. 4. Discuss the use of inotropes with a paediatric intensive care specialist if a child in DKA has signs of hypotensive shock. When calculating the fluid requirement for children and young people with DKA, assume a 5% fluid deficit in mild to moderate DKA (indicated by a blood ph of 7.1 or above) or a 10% fluid deficit in severe DKA (indicated by a blood ph below 7.1). Replace this deficit over 48 hours Calculate the maintenance fluid requirement for children and young people with DKA using the following reduced volume rules: if they weigh less than 10 kg, give 2 ml/kg/h if they weigh between 10 and 40 kg, give 1 ml/kg/h if they weigh more than 40 kg, give a fixed volume of 40 ml/h These are lower than standard fluid maintenance volumes because large fluid volumes are associated with an increased risk of cerebral oedema The total replacement fluid to be given over 48 hours is calculated as follows: Hourly rate = (deficit/48 hours) + maintenance per hour 5. To replace insulin; start an intravenous insulin infusion 1 2 hours after beginning intravenous fluid therapy. Use a soluble insulin infusion at a dosage between 0.05 and 0.1 units/kg/h. 6. To return the glucose level to that approaching normal. 7. To avoid hypokalaemia, hypoglycaemia and rapid changes in serum osmolarity. 8. To treat the underlying precipitating cause of the DKA. The detailed management of DKA is complex. Advice should be sought from experienced local practitioners and published guidelines. Complications All of the complications in the box require intensive monitoring on an intensive care unit. Major complications of diabetic ketoacidosis Cerebral oedema Cardiac dysrhythmias Pulmonary oedema Acute renal failure Most important cause of death and poor neurological outcome. Attempt to avoid by slow normalisation of osmolarity with attention to glucose and sodium levels, and hydration over 48 h Monitor for headache, recurrence of vomiting, irritability, Glasgow Coma Scale score, inappropriate slowing of heart rate and rising blood pressure Treat with hypertonic (3%) saline 3 ml/kg or mannitol infusion ( mg/kg over 20 min), or alternatively hypertonic saline may be used Hyperventilation has been associated with worse outcomes Usually secondary to electrolyte disturbances, particularly potassium Careful fluid replacement may limit the occurrence of pulmonary oedema Uncommon because of high osmotic urine flow B.4 Summary You should now be able to: Describe the approach to the management of fluid and electrolytes in the seriously ill or injured child