Abstract: PO1126
Pseudohyperkalemia with Concurrent Hyperkalemia
Session Information
- Salt, Potassium, and Water Balance: Clinical
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolyte, and Acid-Base Disorders
- 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Ismail, Momen M., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
- Hamid, Akbar H., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
- Mahmoud, Yasmin N., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
- Mallappallil, Mary C., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
- Oh, Man S., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
- John, Sabu, SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
- Salifu, Moro O., SUNY Downstate Health Sciences University Department of Medicine, New York, New York, United States
Introduction
In sickle cell patients, acute hemolytic crisis and sickle cell nephropathy are relatively common. Risk of hyperkalemia increases with hemolysis and tubular dysfunction. Sepsis can also worsen the complication of hemolytic crisis with significant thrombocytopenia, a well-known cause of pseudohyperkalema. We report a case of concurrent true hyperkalemia and pseudohyperkalemia in the setting of thrombocytosis due to acute sickle cell crisis.
Case Description
A 36 year old African American male with history of sickle cell disease, asthma and DVT presented with bilateral shoulder, knee, and back pain. In ED, he was hypotensive, and tachycardic. Labs were notable for leukocytosis, anemia, reticulocytosis, renal failure, and elevated lactate dehydrogenase. Chest x-ray showed left base atelectasis. He was admitted for acute sickle cell crisis and fluctuant right thigh abscess, which was surgically drained and managed with antibiotics. Platelet level was 585 K/uL; serum potassium was 4.7 mmol/L; and creatinine was 1.78 mg/dL with normal urine output. Potassium level steadily rose and peaked at 6.5 mmol/L with sinus bradycardia but no other ECG changes. At the same time, platelet level peaked to 1105 K/uL.
Discussion
In our patient with significant thrombocytosis, pseudohyperkalemia was suspected. Degranulation of platelets during clotting releases about 50% of potassium inside platelets. For platelet count of 1000 K/uL with normal MPV, serum potassium level is expected to be higher than plasma potassium level by about 0.7 mmol/L. Serum-plasma potassium differences in our patient were within the expected range. In our patient, as shown below, mild concurrent true hyperkalemia is also noted likely due to sickle cell nephropathy, a known cause of hyperkalemia due to hyporeninemic hypoaldosteronism. Due to potassium release from platelets during clotting, serum potassium is always higher than plasma potassium in all normal persons by 0.2 to 0.3 mmol/L. With thrombocytosis, the difference becomes larger, and serum potassium is likely to reach hyperkalemic level if the baseline potassium is already higher than usual due to concomitant impairment of renal potassium excretion.
| Platelet (K/uL) | Plasma Potassium (mmol/L) | Serum Potassium (mmol/L) |
| 1105 | 5.3 | 6.1 |
| 942 | 4.9 | 5.8 |
| 464 | 4.3 | 4.9 |