Serum
Ideally samples should be centrifuged in GP surgeries which will remove the possibility of spurious potassium results. Potassium results from un-centrifuged samples arriving in the laboratory greater than than 4 hours post collection, will carry a warning indicating there maybe a spurious result. Un-centrifuged samples arriving in the laboratory greater than 12 hours post collection will not be analysed.
mmol/L
Potassium is the major intracellular cation, with a 20 fold greater concentration in the cells than in the extracellular fluid. Only 2% of total body potassium circulates in the plasma. The sodium potassium ATPase pump is largely responsible for maintaining this important ratio. The kidneys are also important in regulating potassium balance. Proximal tubules reabsorb nearly all of the filtered potassium. Under the influence of aldosterone, additional potassium is secreted by the distal tubules and collecting ducts in exchange for sodium. Maintaining normal potassium levels is important for regulation of neuromuscular excitability, cardiac contractility and rhythm, extracellular volume, and acid base balance.
Hypokalemia is defined as a plasma potassium concentration less than 3 mmol/L. The primary mechanisms are excessive GI or urinary loss of potassium, increased cellular uptake, or inadequate dietary intake. GI loss results from vomiting, diarrhea, gastric suction, or intestinal fistula discharge. Diuretics, such as thiazides and furosemide, promote potassium secretion in the distal tubules. Kidney disorders, such as renal tubular acidosis, cause excessive urinary loss of potassium. Hyperaldosteronism leads to excessive urinary secretion of potassium and metabolic acidosis. Hypomagnesemia causes hypokalemia by promoting both urinary and fecal loss of potassium. Magnesium deficiency diminishes sodium potassium ATPase activity and enhances aldosterone secretion. Alkalemia and insulin are the two major causes of increased cellular uptake of potassium. Alkalemia promotes intracellular loss of hydrogen ion. To preserve electroneutrality, both potassium and sodium enter cells. Plasma potassium decreases by 0.4 mmjmol//L for every 0.1 unit rise in pH. Insulin promotes the entry of potassium into muscle and hepatocytes. Reduced dietary intake of potassium is a rare cause of hypokalemia, but may be an important factor in patients taking diuretics.
Hyperkalemia occurs frequently in hospitalized patients with a reported incidence of 1 to 10%.(Arch Intern Med 1998; 158: 917-24). Hyperkalemia was defined as a critical plasma potassium level of 6 mmmol/L or more. The incidence of hyperkalemia in this study was 2.3%. Approximately 2 hyperkalemic episodes occurred per day during the study period. Most of the elevated potassium levels fell between 6.0 and 7.1 mmol/L, but a few values were as high as 9.0 mmol/L. Further investigation revealed that most cases of hyperkalemia were multifactorial in origin.
| Cause | % of Cases |
| Renal failure | 77 |
| Hyperglycemia | 49 |
| Potassium supplements/ TPN | 15 |
| Medications | 63 |
| Cyclosporine/ Tacrolimus | 27 |
| Beta Blockers | 17 |
| Trimethoprim | 15 |
| ACE inhibitors | 15 |
| Digoxin | 14 |
| NSAID | 9 |
| K sparing diuretics | 5 |
| Heparin | 5 |
| Amphotericin | 2 |
| Succinylcholine | 2 |
| Pentamidine | 1 |
| Penicillin G | 1 |
| RBC transfusion | 10 |
| Rhabdomyolysis | 5 |
Renal failure was present in more than two thirds of the patients. Hyperglycemia was the second most common contributor to hyperkalemia. Medications contributed to the development of hyperkalemia in 63% of cases. The drugs most often implicated are listed in the table. Heparin causes hyperkalemia by suppressing aldosterone.
Another recent study revealed that 194 of 1818 (11%) medical outpatients using angiotensin converting enzyme (ACE) inhibitors developed hyperkalemia, which was defined as a potassium level above 5.1 meq/L (Arch Intern Med 1998; 158:26-32). The majority of patients had potassium levels between 5.1 and 5.5 mmol/L, but one fifth of the patients had higher levels. Independent risk factors for developing hyperkalemia included a raised serum creatinine level above 130 mmol/L, congestive heart failure, and the use of long acting ACE inhibitors.
Hyperkalemia can cause muscle weakness by decreasing the ratio of intra to extracellular potassium, which alters neuromuscular conduction. Muscle weakness does not usually develop until plasma potassium reaches 8 meq/L. Hyperkalemia disturbs cardiac conduction, which can cause arrhythmias. Plasma potassium levels between 6 and 7 mmol/L may alter the ECG, while levels greater than 10 mmol/L may precipitate cardiac arrest.
Factitious causes of hyperkalemia include:
Plasma is the preferred specimen for patients with platelet counts greater than 600,000/uL. Erroneously high potassium results are also produced by centrifugation of SST tubes in fixed angle centrifuges. Under these conditions, the separation gel does not form a complete barrier and potassium leaks out of red blood cells into the plasma during specimen storage
1 day
Local test
Can be added on to an existing request up to 4 days following sample receipt
Specimen Labelling Procedure
8210
