Question of the Week # 158

158) A 55 year old man comes to the Emergency Room complaining of left upper quadrant discomfort. His physical examination reveals Splenomegaly. Laboratory investigations were sent but there was a significant delay in sending the specimen to the laboratory after collection. Laboratory investigations reveal a WBC count of 110,000/µl with neutrophilia,  basophilia and eosinophilia and Serum potassium of  3.0/µl. Leucocyte Alkaline Phosphatase level is low. A bone marrow biopsy is obtained and the results are pending. The most likely explanation of the patients hypokalemia :

A) Delay in specimen transport to lab

B) Marked Leucocytosis and Delay in specimen transport

C) Tumor Lysis

D) Splenomegaly

E) Renal loss

8 Responses

  1. bbbbbbbbbb

  2. E

    CML may lead to blast crisis which increase tumor burden eventually lead to lysozymuria and precipitate loss of K+ from kidney ?

    can anyone add in to that ?? i would really like to know the real trick to answer this question . 🙂

  3. tough one!! can anyone answer?

  4. B, There is transcellular shift of potassium into the large number of leukemia cells. This is pseudohypokalemia from transport delay. The patient does not truly have this deficiency. Pseudo- hypokalemic is prevented by in Vivo potassium homeostasis. In this specimen, delay in transport should have released cellular potassium to cause hyperkalemia – But sometimes leukemia cells (if they are >100000/uL), consume the potassium in vitro especially if they are still capable of metabolically active processes in a favorable in vitro specimen (for example one that is loaded with B12 and folic acid, glucose, thiamine, insulin, and low effective cytotoxic agent activity). There is also a more debatable or controversial explanation. Leukemic cells can also cause pseudohypokalemia if they have among them lymphoid line of progenitor cells with CD 34+ expression. These cells can sustain tumor cell population by their indefinite replication potential. (If the cells are still replicating in vitro, they will consume the available potassium in the specimen just like our normal newly formed cells do in Vivo after an injection of vitamin B 12.)
    This second reason is still subject to debate and research.
    In summary, metabolically active leukemic cells >100000/uL can consume potassium after a transport delay.


  5. B. I think the key is that blood sample has sat in room temp for too long in a pt with leukemia. This can acuse false drop in serum K. In any case, if this pt had very high serum K this could still be false elevation so repeating blood test is necessary (as we usually do in real life).

  6. Factitious hypokalemia may be seen in patients with a high WBC count (> 100,000/µL [100 × 109/L]) in acute leukemia when the blood samples have been allowed to stand at room temperature.[51] This phenomenon is related to transcellular potassium shift into the leukemic cells. Pseudohypokalemia should not be confused with true hypokalemia, which may be seen in patients with acute myeloid leukemia, especially with monocytic differentiation. The mechanism in this case is related to lysozymuria, which promotes renal tubular excretion of potassium.
    Answer is B. Question states that there was a significant delay to send the sample to the lab. so It can be pseudohypokalemia. repeat the blood test again, make sure not to delay the transport to lab. If still have the problem, it is true hypokalemia and E is correct.

  7. E. CML: high levels in all cell lines, splenomegaly, DECREASE leukocyte alkaline phosphatase ( which differentiates it from Leucemoid Reaction ). Hypokalemia, renal tubular excretion due to lysozymuria.

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