Fluid replacement therapy

6.1 Fluid replacement therapy



Trevor Duke, Sarah McNab


Safe management of the fluid and electrolyte needs of unwell children requires knowledge of body water and electrolyte composition, fluid requirements during health and illness, an ability to recognize signs of dehydration and overhydration, an understanding of composition of fluid replacement, and monitoring.



Body fluid composition


Body fluids are separated into two main compartments, intracellular (ICF) and extracellular (ECF) fluid. ECF is further separated into intravascular and interstitial fluid. The proportion of body weight that is water falls from about 78% in a term newborn to 60% in adults (Table 6.1.1). Intracellular water accounts for about 40% of body weight. Intravascular fluid (plasma) accounts for only about 5% of body weight. Interstitial fluid is proportionately higher than intravascular fluid in infants, with an interstitial to plasma volume ratio of 5 : 1, compared with 3 : 1 in adults. Large changes in body weight over 24  hours or less usually reflect changes in total body water (TBW), because it takes a much longer period for substantial weight change due to growth or subcutaneous tissue wasting. In the first few days of life, there is a shift of water from ECF to ICF, accompanied by a 7% loss of TBW, so this is a very vulnerable period for dehydration with illness. Body fat contains only 20% water, so obesity implies a relative reduction in percentage of body weight as water. Conversely, malnourished children may have up to 80% of body weight as water. The clinical consequences are that:



• the severity of dehydration may be underestimated in obese children


• nutritional wasting is easily confused with dehydration as the clinical signs are similar


• fluid loads are poorly tolerated in severe malnutrition.



Table 6.1.1 Body water distribution

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Water balance depends on intake, output and usage for metabolism. Water is normally lost from skin, lung, intestine and kidney. Fluid and energy requirements as a proportion of body weight decrease from infancy to adult life, so infants and children have higher metabolic requirements than adults and smaller absolute fluid stores, making them more vulnerable to dehydration.


ECF has relatively high sodium and chloride content. ICF has high potassium, phosphate, magnesium and protein concentrations (Fig. 6.1.1). Small intestinal secretions are high in sodium, diarrhoea fluid is high in potassium, gastric fluid is high in chloride and pancreatic secretions are high in bicarbonate (Table 6.1.2).


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Fig. 6.1.1 Electrolytes in body fluids.



Table 6.1.2 Typical composition of body fluids in children (mmol/L)

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Cell membranes are relatively permeable to water, potassium and chloride, and relatively impermeable to sodium, phosphate and protein. Sodium is actively transported out of cells by energy-dependent sodium pumps. There is equilibrium in tonicity, hydrostatic and colloid osmotic pressure between plasma and interstitial fluid. Water leaves the arterial end of the capillary under hydrostatic pressure and is drawn into the venous end of capillary beds by plasma oncotic pressure.



Regulation of extracellular fluids


The plasma osmolality, being the concentration of solute particles, remains almost constant between 285 and 300 mOsmol per kg H2O. The osmolality of plasma is controlled through a finely regulated feedback system in the hypothalamus, the posterior pituitary and the collecting duct of the nephron, which contain osmoreceptors and volume receptors.


In health, the intake of water is regulated by thirst. This is controlled by a centre in the mid-hypothalamus, which responds to changes in circulating blood volume, via stretch and baroreceptors in the cardiovascular system, or small changes (as little as 1–2%) in plasma osmolality.


In the kidney, nephrons regulate water and electrolyte excretion. The nephron comprises the proximal tubule, the hypertonic medulla and ascending loop of Henle, the distal tubule and the collecting duct. The precise regulation of fluids and electrolytes in the ECF occurs by reabsorption of the glomerular filtrate into capillaries, secretion into the tubule lumen and eventual excretion in the urine.


Each day normal adult kidneys filter 180 litres water, 25 000  mmol sodium, 5000 mmol bicarbonate and 700 mmol potassium. Under normal circumstances most of this is reabsorbed. Approximately two-thirds of the filtered sodium is reabsorbed in the proximal convoluted tubule. Another 25% is reabsorbed in the loop of Henle, which is used to create a concentration gradient for the countercurrent multiplier system, allowing the production of concentrated urine. In adults, urine osmolality can vary from a maximal dilution of 100 mOsmol/kg to a maximal concentration of 1400 mOsmol/kg; newborns and young children have a more limited ability to concentrate and dilute urine. The distal tubule reabsorbs only 5% of the filtered sodium, but the electrical gradient generated is used for potassium and hydrogen ion excretion into the distal tubule. Renal sodium retention also occurs via the renin–angiotensin–aldosterone system.


Water retention is regulated via antidiuretic hormone (ADH) released from the posterior pituitary. The primary action of ADH is to increase the permeability of the renal collecting ducts to water. A rise in plasma osmolality is corrected by increased ADH secretion, resulting in a reduced volume of urine, which is concentrated. This allows the body to conserve free water to reduce plasma osmolality. Conversely, a fall in plasma osmolality inhibits ADH secretion, resulting in excretion of an increased volume of dilute urine.


Circulating blood volume is contained in arteries (10%), the venous system (55%), and heart, lungs and capillary bed (35%). The volume and distribution within the circulation is controlled by rapid feedback loops. Baroreceptors and stretch receptors in the heart and large vessels detect changes in venous tone and stimulate ADH secretion or inhibition and changes in venous tone, cardiac output and arteriolar resistance via the autonomic nervous system. Volume depletion is the dominant stimuli to thirst and ADH release, and so may stimulate water retention and oral intake at the expense of hypotonicity.


There are also non-osmotic drivers of ADH secretion, which allows ADH to be released despite normal or low plasma osmolality. Many of these stimuli are present in sick children and include intracranial pathology (e.g. meningitis, head injury), respiratory disease (pneumonia), surgery and pain. The potential for non-osmotic ADH stimuli must be considered when prescribing fluid replacement. ADH reduces the body’s ability to excrete free water and may lead to hyponatraemia if an inappropriately hypotonic fluid is given.



image Practical points




• Antidiuretic hormone (ADH) helps maintain intravascular volume and osmolality.


• In unwell children, ADH secretion may occur despite normal or low osmolality. This decreases water excretion, further decreasing plasma osmolality.


• This must be taken into consideration when considering the volume and composition of fluid replacement.



Oedema


Oedema is increased interstitial fluid and occurs by several mechanisms:



• increased hydrostatic pressure in the capillaries: venous obstruction, congestive heart failure


• decreased plasma oncotic pressure: hypoproteinaemic states such as nephrotic syndrome, protein-losing enteropathy, severe liver disease, and severe protein-energy malnutrition or kwashiorkor


• increased capillary permeability: this can occur locally from insect bites, or in one organ, such as cerebral oedema from traumatic brain injury, brain infection or other brain injury, or generally as in capillary leak syndrome from severe septicaemia.


Oedema may also occur if interstitial lymphatic vessels are poorly developed (Turner syndrome) or obstructed (e.g. filariasis, lymph node obstruction from tuberculosis).



Assessment of dehydration



Clinical history and examination


A detailed history and examination is essential for the assessment of any child with suspected dehydration, overhydration or electrolyte imbalances. The symptoms listed below are relevant to different cases, although they may not always be available or reliably elicited on history-taking.



History




• Diarrhoea: duration, frequency, basic estimate of volume (small, large, profuse), presence of blood, mucus


• Vomiting: duration, frequency, volume, presence of bile or blood, whether projectile


• Eating and drinking: frequency, thirst, type of fluid intake (e.g. breast milk, oral rehydration solution, cordials, hypercaloric feed supplements)


• Urine output: frequency, number of wet nappies


• Associated symptoms: fever, cough, shortness of breath, abdominal pain, seizures, rashes, etc.


• Nutritional status: view the child’s growth chart including trend in values. Check skin folds on triceps and buttocks for presence of wasting. Also check weight for height, and height for age (low height for age in a malnourished child is stunting, which suggests chronic undernutrition).



Examination




• General condition: drowsy, restless or irritable


• Vital signs: temperature, pulse volume and heart rate, respiratory rate, blood pressure


• Eyes: sunken, no tears on crying


• Mouth and tongue: dry mucous membranes


• Skin: skin turgor reduced or central capillary refill time increased


• Muscle tone: weak, floppy or unable to hold head up


• Chest: deep acidotic breathing


• Abdomen: distended or tender, palpable masses.


The signs of dehydration are listed in Table 6.1.3. Precise estimation of percentage of dehydration is not possible using clinical signs, but an indication of the degree of dehydration, sufficient for formulating a plan for fluid management, is possible. Combinations of these signs are more specific than any individual sign. Clinical signs may be combined to classify a child as having mild (3–5%) dehydration (usually accompanied by few, if any, clinical signs), moderate (6–9%) dehydration, or severe (> 10%) dehydration.



Table 6.1.3 Signs of dehydration

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Weight change


When available, weight change from the immediate premorbid state is the most accurate way of estimating the degree of dehydration. If the child has been weighed accurately in the last few days, the percentage weight loss will be approximately equal to the percentage dehydration. Another way of thinking of this is that the weight loss in grams is approximately equal to the fluid deficit in millilitres. However, the weights (premorbid and when sick) should be done using a comparable method: similar scale accuracy, unclothed, etc. If the premorbid weight was recorded more than a couple of weeks previously in young infants, the interpretation is less reliable and must take account of the weight gain expected because of growth.



image Practical points



Clinical evidence on assessing dehydration




• A change in weight, where available, is the most accurate way to assess the degree of dehydration.


• Clinical signs will allow an estimation of dehydration, with combinations of signs performing better than individual signs.


• This classification is most reliable:


• no signs of dehydration (usually less than 5% dehydrated)

• some signs of dehydration (typically 6–9% dehydrated)

• many signs of dehydration/signs of severe dehydration (10% dehydrated or more).

• Additional history and laboratory tests (e.g. bicarbonate) may be helpful in selected cases.



Fluid requirements


Before administering fluid replacement, five questions need to be addressed:



1. Why am I giving fluid?


Reasons for giving fluid can be broadly grouped into:


• resuscitation

• deficit

• maintenance

• ongoing losses.

2. How will I give the fluid?


Options include:


• oral

• nasogastric/percutaneous endoscopic gastrostomy (PEG) tube

• intravenous.

3. What type of fluid should I use?


4. How much fluid should I give?


5. How will I monitor the child receiving fluid replacement?


The fluid requirements of acutely unwell children are dynamic, and frequent monitoring of clinical signs, weight, urine output and some laboratory tests are essential so that appropriate modifications to fluid administration can be made.



Resuscitation for shock


Fluid resuscitation involves the rapid restoration of intravascular volume and is needed where shock is present. The clinical signs of shock are poor peripheral perfusion, cool pale extremities, tachycardia with low-volume pulses, low blood pressure, high blood lactate levels or large base deficit. Although hypotension is a sign of shock, this is usually a late sign in children; the absence of hypotension should not delay appropriate treatment. Children with more than one of these cardiovascular signs require intravenous fluid resuscitation. If an intravenous cannula cannot be inserted in a child needing fluid resuscitation, use the intraosseous route to the circulation. A volume of 20 mL/kg of an isotonic fluid should be administered as a bolus (i.e. run through as rapidly as possible). As this fluid will replace intravascular volume, its osmolality should be similar to that of plasma. Examples of appropriate fluids are: 0.9% sodium chloride (also known as normal saline) or Hartmann’s solution (also known as Ringer’s lactate solution) (Table 6.1.4). In severe septic shock in adults and in severe malaria in children, there is some evidence that outcomes are better when albumin is used compared with crystalloids. If there is no improvement, a further 20 mL/kg should be administered. Any child receiving fluid resuscitation should be monitored closely and reassessed immediately after giving the fluid. If signs of hypovolaemia persist despite two 20 mL/kg boluses of fluid, the child should be monitored in an intensive care unit. Check for signs that are suggestive of an underlying cause of shock (e.g. sepsis, cardiogenic, metabolic, diabetic ketoacidosis, intussusception, poisoning).



Table 6.1.4 Types of intravenous fluid available

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Replacing the fluid deficit


A patient’s fluid deficit refers to the degree of dehydration at the time of presentation (see assessment of dehydration above and Table 6.1.3). If shock is present, this should be corrected first as described above.


If a recent premorbid weight is available, the volume of fluid deficit in millilitres is equal to the weight lost in grams. When a recent weight is unavailable, the percentage of dehydration must be approximated using the guidelines for assessment outlined above. The volume of fluid deficit may then be calculated using the following formula:



image



(e.g. 7% dehydration in a 12 kg child = 7 × 12 × 10 = 840 mL deficit).


Deficits can be replaced either orally, via a nasogastric (or PEG, where there is one present) tube or intravenously, depending on the severity of illness and other factors.


Oral rehydration salts are the mainstay of treatment of dehydration from gastroenteritis for the majority of children. Specific oral rehydration solutions (ORS) can be suggested (for further information on ORS, see Fluid and electrolyte problems in specific illnesses – gastroenteritis, below). Where vomiting is present, oral rehydration is best achieved by offering small volumes of fluid frequently. This may be achieved by offering fluid via a syringe every 10 min or by using ORS icy-poles, which are available commercially. In general, aim for 10 mL/kg every hour.


ORS can be given via a nasogastric tube where adequate oral fluid is not tolerated and the child has moderate to severe dehydration, even if the child is vomiting. Nasogastric tubes can be unpleasant and carry a risk of pulmonary aspiration. After insertion, the position of a nasogastric tube needs to be checked. This is indicated by the presence of acidic gastric fluid aspirated from the nasogastric tube. Deficit can be rapidly replaced with ORS via a nasogastric fluid running at 25 mL per kg per h for up to 4 h or until the deficit is replaced. Where there is significant vomiting, the rate of nasogastric replacement may be reduced and, if the vomiting is due to gastroenteritis, ondansetron, an antiemetic, may be considered. A deficit should be replaced more slowly (over approximately 6–8 h) in young infants or those with significant abdominal pain.


Where oral or nasogastric fluid replacement is not tolerated or is contraindicated (e.g. suspected appendicitis), intravenous fluids are used. A fluid deficit primarily involves loss of extracellular fluid and, as such, should be replaced with an intravenous fluid with a similar osmolality to the extracellular space (e.g. Hartmann’s solution or 0.9% sodium chloride). Hypotonic fluids (containing significantly less sodium than plasma) such as 4% dextrose with 0.18% sodium chloride should never be used. These fluids can lead to hyponatraemia, seizures and cerebral oedema.


When replacing a deficit intravenously, the rate of administration depends on the underlying condition. In general, where the deficit has occurred rapidly (e.g. acute gastroenteritis, appendicitis), it may be replaced rapidly (over approximately 4–8 h). Where the deficit has occurred over a longer period of time or there is significant electrolyte imbalance, the volume should be replaced more cautiously (over 24–48 h). In these circumstances, the ongoing requirement for maintenance hydration must also be taken into consideration (i.e. the maintenance requirement should be given in addition to the deficit replacement), plus additional fluid if there are ongoing abnormal losses such as persisting diarrhoea or vomiting.


Any child receiving fluid rehydration for a pre-existing deficit should be monitored closely. They should be weighed and clinically assessed prior to commencing therapy and after 6 h of rehydration. Those who are severely dehydrated should be assessed prior to this. Where the deficit is being replaced intravenously, serum electrolytes should be repeated after 6 h of therapy (sooner if there is an electrolyte imbalance). See “Assessment of dehydration” for important features to note on clinical assessment. Examining a child for signs of fluid overload is also important once fluid therapy has been instituted. All children should be reassessed after the deficit therapy is replaced to determine their ongoing fluid requirements.

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Aug 4, 2016 | Posted by in PEDIATRICS | Comments Off on Fluid replacement therapy

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