Pseudohyperkalemia is a rise in serum potassium concentration by more than 0.4 mEq/L than the normal potassium concentration. In vitro clotting results in the release of potassium from the elements of blood which gives a falsely elevated serum potassium level. It has been routinely observed with thrombocytosis, leukemia and myeloproliferative syndromes. It is important to note reactive thrombocytosis is a common occurrence secondary to malignancy. Potassium release from platelets is a universal phenomenon during coagulation and more potassium is released if more platelets are present. An 85 year old female with history of colon cancer and known liver metastasis was admitted for nausea, vomiting, and watery diarrhea. Her serum potassium on admission was 5.8 mEq/L and her renal functions remained normal. An active search for the cause of her hyperkalemia failed to define a source of hyperkalemia. Pseudohyperkalemia was presumed as a diagnosis and was confirmed by plasma potassium of 4.6 mEq/L. Failure to identify this well known but frequently overlooked cause of hyperkalemia may have resulted in life threatening hypokalemia due to a potassium lowering agent. This indicates that treating the patient as a whole is much more important than treating laboratory values.
An 85 year old female presented to the emergency department with 1-2 episodes of non bloody non bilious emesis per day for three days, watery stools, and severe dehydration. The patient was diagnosed with colon cancer with liver metastasis 1.5 years ago and had also undergone a subtotal colectomy one year after diagnosis. In the ED, her platelets measured 566K/mm3 and her potassium 5.8mEq/L. Subsequently she was given hydroxyurea and various potassium lowering agents.
Repeat platelet measurements were consistently above the upper limit of normal of 450K/mm3. Repeat serum potassium after the initial treatment and had dropped to 4.7mEq/L and then later to 4.3mEq/L. She was admitted to the floor to manage her other conditions, including SIRS, hyponatremia, and megaloblastic anemia.
After extensive research and laboratory tests, it was discovered that her hyperkalemia was secondary to reactive thrombocytosis associated with colon cancer. Pseudohyperkalemia was presumed as the diagnosis and was confirmed by plasma potassium of 4.6mEq/L versus elevated serum potassium upon admission of 5.8mEq/L. This case indicated the importance of treating the patient and not the lab values as the continued use of potassium lowering agents could have dangerously decreased the patients’ plasma potassium level.
Hyperkalemia is a life threatening emergency that can lead to fatal arrhythmias. Normal serum potassium is 3.5-5.0mEq/L, mild hyperkalemia ranges from 5.1-6.1 mEq/L, moderate between 6.2-7.0 mEq/L and severe above 7.0 mEq/L.
Hyperkalemia can be the result of ineffective elimination, excessive release from cells, or excessive intake. Ineffective elimination of potassium occurs in renal failure, mineralcorticoid deficiency or resistance states, or various medications including angiotensin converting enzyme inhibitors, nonsteroidal anti-inflammatory drugs, and potassium sparing diuretics. Excessive potassium release from cells occurs in rhabdomyolysis, massive hemolysis or shifts in and out of cells secondary to acidosis, low insulin levels, or beta blocker therapy. Excessive intake of potassium can occur with potassium containing dietary supplements or KCl injections.
The signs and symptoms of hyperkalemia are due to the hyper excitability of tissues. Patients present with cardiovascular abnormalities including dysrythmias, wide complex tachycardia, and fatal ventricular fibrillation. Fortunately for clinicians, potassium values correlate to ECG changes. Peaked T waves are the first manifestation, followed by loss of P waves, and widening and slurring of the QRS complexes. Patients can also present with neuromuscular irregularities including muscle cramps, parenthesis, tetany, and focal neurological deficits.
Hyperkalemia management consists of numerous treatments. Cardioprotection is of primary concern and is accomplished by stabilizing the membranes using calcium gluconate or calcium chloride. Potassium can also be pushed intracellular using a beta-agonist, insulin, or hydrogen bicarbonate. Excretion of potassium is accomplished by intravenous fluids, loop diuretics, or hemodialysis. Chronic hyperkalemia can be treated with slower acting agents such as ion exchange resins that act in the gastrointestinal tract. Most popularly used is kayxelate (sodium polystyrene sulfonate).
As noted in the case above, there is a commonly overlooked cause of hyperkalemia. An increase of blood elements such as platelets can cause in-vitro clotting and a release of potassium resulting in a falsely elevated serum potassium level termed pseudohyperkalemia. Reactive thrombocytosis is a common phenomenon in malignancies of the colon, lung, and malignant mesothelioma.
As seen in this case, it is important as clinicians to understand why lab values are the way they are and it is important to treat the cause not the value. If pseudohyperkalemia was not determined, than this patient would have been treated with more potassium lowering agents and could have entered into a fatal state of hypokalemia. It has been shown that the plasma potassium is a much more accurate assessment of body potassium than serum potassium and should be ordered in all patients with hyperkalemia and colon, lung, or mesothelioma malignancies.