CHAPTER 10. INTRAVENOUS FLUIDS AND COMMONLY PRESCRIBED INFUSIONS
Dr Thomas Aitchison Latta (circa 1790–1833) pioneered the use of intravenous saline as fluid resuscitation for cholera victims in 1832 using a small silver tube attached to a syringe.
INTRODUCTION
Fluid balance and the prescription of intravenous fluids is one of the most common duties performed by a hospital doctor. A detailed explanation of the physiology underlying fluid balance is beyond the scope of this text, but it is imperative that fluid prescriptions are based upon the individual requirements of that patient; there is no such thing as a standard fluid regimen. The patient should have their fluid status assessed through clinical history and examination prior to determining their management (Table 10.1).
| Hypovolaemia | Fluid overload | |
|---|---|---|
| Symptoms | Thirst Headache Dark concentrated urine Oliguria | Dyspnoea Orthopnoea Frothy (white/pink) sputum |
| Signs in order of frequency and reliability | Tachycardia Hypotension Cool peripheries Prolonged capillary refill time (>2 seconds) Postural hypotension (systolic drop of >20 mmHg on rising) Low jugular venous pressure Dry mucous membranes Increased skin turgor Sunken eyes | Tachypnoea Tachycardia Relative hypertension Low oxygen saturations Raised JVP Bilateral crepitations (initially bibasal but rising depending upon the degree of pulmonary oedema) Third heart sound (gallop rhythm) Peripheral oedema (dependent areas such as ankles and sacrum. Not reliable in the presence of concomitant hypoalbuminaemia) |
| Investigations | High urine specific gravity (concentrated urine) Oliguria/anuria Raised urea (initially) and creatinine (later) Raised serum osmolality Rising base deficit | Chest X-ray features of pulmonary oedema |
A strictly documented fluid balance chart, if accurate, might be helpful in assessing the prescription of intravenous fluids. However, third-space sequestration, gastrointestinal losses and febrile illnesses, for example, may lead to a gross underestimate of losses and what may appear to be a positive balance on paper due to modest fluid administration can in fact be very misleading. Remember a patient’s clinical signs never lie, and should be relied upon in preference to a fluid balance.
Furthermore, the clinical assessment should be made in the context of the patient’s acute disorder and chronic co-morbidities:
• Some common causes of hypovolaemia include:
— insensible losses, e.g. febrile illness and lack of fluid intake
— third space losses, e.g. bowel obstruction, sepsis, ascites
— acute losses, e.g. profuse diarrhoea (especially secondary to Clostridium difficile), vomiting, haemorrhage
— excessive diuresis, whether drug-induced or secondary to diabetes mellitus or insipidus.
• Chronic co-morbidities requiring judicious fluid input:
— left ventricular failure
— end-stage renal failure
— ascites.
DEHYDRATION VERSUS HYPOVOLAEMIA
While dehydration is commonly a term used to mean hypovolaemia the two are different. Dehydration is a relative loss of water that will lead to hypernatraemia and hyperuricaemia, while hypovolaemia is loss of circulating volume regardless of the fluid loss (blood, sequestration due to sepsis, GI fluid losses, etc.) and may or may not be associated with sodium and urea changes. The mechanism for urea change in hypovolaemic patients is as much related to renal hypoperfusion as it is to the composition of the fluid loss. Only the respiratory system leads to a pure water loss while diarrhoea leads to a relatively increased water loss.
Furthermore, it is possible for a patient to be normovolaemic and dehydrated or hypovolaemic and dehydrated. The former is often seen in hospitalized patients whose insensible losses are only replaced with saline. Consequently it is important for management purposes to be clear when describing dehydration, hypovolaemia or both.
INTRAVENOUS FLUIDS
Intravenous fluids can be divided into two types, namely crystalloids and colloids.
Crystalloids
Crystalloid solutions are aqueous solutions containing electrolytes that pass freely across semipermeable membranes. Crystalloids have no oncotic pressure, and so distribute readily from the intravascular compartment to the interstitium and beyond. For this reason crystalloids such as normal saline are commonly used for maintenance intravenous fluid replacement. The type of maintenance fluids prescribed needs to be tailored to the individual requirements of the patient taking into account both their volume status and electrolyte requirements (Table 10.2).
| Na+ | K+ | Cl– | Ca2+ | lactate | |
|---|---|---|---|---|---|
| Normal saline (NaCl 0.9%) | 154 | – | 154 | – | – |
| NaCl 0.45% | 77 | – | 77 | – | – |
| Dextrose–saline (NaCl 0.18%, dextrose 4%) | 30 | – | 30 | – | – |
| Dextrose 5% | – | – | – | – | – |
| Hartmann’s solution | 131 | 5 | 111 | 2 | 29 |
| Ringer’s solution | 130 | 4 | 109 | 1.5 | 28 |
• 5% dextrose is an isotonic solution that can effectively be thought of as intravenous water, because once infused the dextrose is metabolized. The dextrose serves to maintain tonicity and therefore prevents immediate red blood cell haemolysis. In effect the solution provides pure water and therefore will reduce urea and sodium concentrations. It is distributed throughout the whole body water (intracellular and extracellular). Consequently it is the least efficient fluid for intravascular volume replenishment.
• Hartmann’s solution contains less chloride than normal saline, 5 mmol/L of potassium and 29 mmol/L of lactate, which is later converted in the liver to bicarbonate. Thus Hartmann’s solution is more representative of plasma and so is described as being more ‘physiological’. This solution is distributed to the extracellular space (i.e. the interstitial and intravascular compartments).
• Normal saline is also exclusively distributed to the extracellular space and is as effective as Hartmann’s solution for restoring intravascular volume. If used exclusively it will lead to a rise in serum sodium and because of the chloride content produce hyperchloraemia, which displaces bicarbonate and thus may be responsible for a mild metabolic acidosis.
Colloids
In comparison to crystalloids, colloids are large molecules that contribute to oncotic pressure and do not cross semi-permeable membranes. In reality colloids simply remain within the intravascular compartment for longer than crystalloids, hence the use of solutions containing colloid for the rapid and acute expansion of intravascular volume (e.g. haemorrhage). In situations of increased capillary permeability, such as sepsis, colloids will eventually leak across the capillary membrane causing interstitial oedema through raising the interstitial oncotic pressure.
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