Key Points
Always clinically assess patients before ordering any tests.
Only order tests that could directly change patient management.
Laboratory tests are more useful for monitoring than diagnosis.
Laboratory tests should be interpreted in the context of the patient’s state.
If the laboratory result looks wrong, then it probably is.
Statistically 5 per cent of all normal test results will be outside of the reference range.
Be aware that different laboratories may use different methods for some tests, for example, cardiac troponin can be measured as troponin T or troponin I, and there are multiple methods available.
The laboratory is always available for help and advice, so get to know them and they will be able to help you when something unusual occurs.
Introduction
This chapter focusses on routine clinical biochemistry investigations, including those recommended in the NICE 2003 guidelines, preoperative tests: the routine preoperative tests for elective surgery (www.nice.org.uk/guidance/cg3). The guidelines, simplified in Table 16.1, recommend electrolytes, renal function, blood glucose, urine analysis and blood gas analysis, dependent on surgery grade and patient health. Pregnancy testing should also be considered in female patients of reproductive age.
Table 16.1 Summary of the Nice 2003 preoperative assessment guidelines. (www.nice.org.uk/guidance/cg3)
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For any laboratory investigation, 5 per cent of the population will have a ‘normal’ result outside the reference range. The more tests requested, the greater probability a result will be ‘abnormal’. Results must always be interpreted in their clinical context and a totally unexpected result (potassium of 15mmol/L) is likely to be erroneous and should be treated as such. Spurious or inaccurate results may be attributable to one or more factors: sample collection, sample transport, sample storage or sample processing.
Where possible, UK harmonised reference ranges have been quoted (www.pathologyharmony.co.uk). For analytes without a harmonised reference range, a local hospital range has been quoted to help orientate the reader, although care should be taken as ranges may differ between laboratories.
Renal Profile
Renal profiles include sodium, potassium, urea and creatinine.
Sodium
(133–46mmol/L) is the major cation in the extracellular fluid (ECF). Its concentration is dependent on total body sodium and water balance.
Hyponatraemia is one of the most commonly encountered abnormalities in biochemical tests and is caused by an excess of water in relation to sodium. It can be further classified (Table 16.2) according to volume status (hypovolaemia, euvolaemia, hypervolaemia), which although useful to delineate its aetiology, requires additional clinical evaluation and further tests.
Osmolality
(serum: 275–95mmol/kg) is a measure of the number of particles dissolved in a kilogram of fluid. Paired urine and serum samples for osmolality and sodium should be interpreted together. In true hyponatraemia, serum osmolality is reduced. The urine/plasma osmolality ratio indicates whether there is net water retention (>1) or water loss (<1). A urine sodium >20mmol/L suggests renal sodium loss and <10mmol/L suggests sodium retention due to low effective circulating blood volume; functional with raised ECF volume (heart failure, liver cirrhosis plus ascities, nephrotic syndrome) or actual with a reduced ECF volume (fluid and/or electrolyte loss).
The syndrome of inappropriate antidiuretic hormone (SIADH) is a diagnosis of exclusion and should be diagnosed only once abnormal thyroid, adrenal and cardiac function have been excluded.
Hyponatraemia can be classified as mild (>130mmol/L), moderate (120–30mmol/L) or severe (<120mmol/L). In the majority of cases the hyponatraemia is mild and no further action is required, but moderate cases warrant further investigation and treatment. The most frequent cause is diuretic therapy.
For treatment of hyponatraemia, please refer to Chapter 8 of this volume.
Pitfalls.
Samples taken from a drip arm cause spuriously low sodium concentrations. Samples with a raised serum osmolality produce a dilutional hyponatraemia by redistributing water from the intracellular to the extracellular compartment. This can be detected directly if the substance is easily measureable (glucose in hyperosmolar diabetes mellitus) or indirectly by calculating the osmolar gap (measured osmolality – 2 × sodium + urea + glucose). An elevated value (>10) indicates the presence of an osmotically active substance. Pseudohyponatraemia (where serum osmolality is normal) is due to reduced water volume in the measured sample from either raised serum triglycerides or protein. If suspected, sodium concentration should be measured on a blood gas analyser, which is not affected by water volume in the sample.
Hypernatremia is water depletion relative to sodium. Water loss is compensated for by the total body water pool, so signs of reduced extracellular fluid volume may be absent. Hypernatremia is almost always due to dehydration. Causes include inadequate intake (limited access to water, inability to drink), excessive loss through the kidneys (increased osmotic load, renal tubular disorders, diabetes insipidus), skin (sweating), lungs (hyperventilation) and gut (vomiting, diarrhoea). Excessive sodium intake is uncommon apart from inappropriate intravenous sodium treatment (some IV drugs contain significant sodium content, normal saline contains 155mmol/L of sodium, and beware of hypertonic saline).
Potassium
(3.5–5.3mmol/L) is tightly regulated through renal excretion, modulated by aldosterone, rate of urine flow and supply of sodium to the distal tubule. Acute changes in serum potassium occur with changes in pH due to exchange of hydrogen ions in the extracellular compartment for potassium in the intracellular compartment. Acidosis is accompanied by a rise in serum potassium and alkalosis by a fall. Catecholamines and insulin cause acute changes in potassium values when administered, but insulin is not the primary regulatory hormone for serum potassium levels.
Hypokalaemia is usually caused by renal loss (diuretics the commonest cause) or gastrointestinal tract loss (diarrhoea, vomiting). Hyperaldosteronism as a cause of hyperkalaemia does occur, but is rare. Aldosterone and renin should be measured only following normalisation of the potassium and cessation of any interfering antihypertensive drugs.
Hyperkalaemia is commonly caused by renal impairment or drugs, rarely increased intake (usually with complicating factors).
Pitfalls.
Spurious hyperkalaemia is the commonest type of hyperkalaemia found in routine clinical practice. Causes include: haemolysis due to poor venepuncture technique (taking samples with a syringe and injecting them into a vacutainer is the worst of all); potassium EDTA contamination of the sample due to inappropriate tube use or order of blood draw (this is detected in the laboratory by very low calcium, magnesium and alkaline phosphatase values); prolonged storage and delayed separation (especially if the sample is refrigerated at 4°) and cold weather.
Urea
(2.5–7.8mmol/L) is freely filtered at the glomerulus, but the rate of production varies with protein intake and turnover (urea is raised by a high-protein diet or a gastrointestinal bleed) and liver function. Urea varies depending on hydration level and dehydration is the commonest cause of a raised urea. Urea is elevated in renal dysfunction, although should not be used in isolation. The relative proportion of urea and creatinine increase is a useful tool to distinguish causes of renal failure. Urea is raised disproportionally to creatinine in pre-renal renal failure (dehydration).
Creatinine
(local range: 60–106umol/L) is produced at a constant rate from muscle breakdown and is freely filtered at the glomerulus; however, its concentration is dependent on diet (level of meat consumption) and muscle mass.
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