Acute hyperkalemia induced by hyperglycemia in non-diabetic patient.

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Korean J Anesthesiol 2011 August 61(2): 175-176
http://dx.doi.org/10.4097/kjae.2011.61.2.175
Letter's to the Editor
Acute hyperkalemia induced by hyperglycemia in non-
diabetic patient
Sun Young Park, Tae Joon Kim, and Min Jung Kim
Department of Anesthesiology and Pain Medicine, Soonchunhyang University Hospital, Seoul, Korea
Corresponding author: Sun Young Park, M.D., Department of Anesthesiology and Pain Medicine, Soonchunhyang University Hospital, 657,
Hannam-dong, Yongsan-gu, Seoul 140-743, Korea. Tel: 82-2-709-9291, Fax: 82-2-790-0394, E-mail: sunnypark97@gmail.com
This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://
creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium,
provided the original work is properly cited.
CC
Hyperglycemia can induce hyperkalemia in diabetic
patients with insulin deficiency [1,2]. It is thus recommended
to monitor potassium concentrations in diabetic patients.
However, in healthy individuals, acute hyperglycemia appears
to lower or not affect the serum potassium concentration [3]
and hyperkalemia rarely occurs due to the kidney’s capacity
to excrete potassium. In this case, we describe a non-diabetic
patient who experienced acute severe hyperkalemia induced by
transient hyperglycemia during elective surgery.
A 49-year-old woman was admitted to hospital due to lipoma
on the abdomen and on the back and the fatty abdomen. The
patient had a history of hypertension, treated with angiotensin-
converting enzyme inhibitors (ACEi), for 5 years. Her random
blood glucose level was 121 mg/dl. The pre-operative fasting
glucose level was 109 mg/dl, the serum K+ level was 4.5 mmol/
L, BUN was 19.3 mg/dl, Cr was 0.7 mg/dl, and urine ketones
were negative. After excision of the lipoma over 2 h, the surgeon
began abdominal liposuction. Approximately 20 min later,
a T wave taller than the accompanying QRS complexes was
observed on the ECG. The blood pressure was 110/60 mmHg,
and the pulse rate was 61 beats/min. The blood loss was less
than 50 ml, and 760 ml of lactated ringer’s solution was infused.
There was no sign of dehydration. We performed an immediate
arterial blood analysis that revealed a K+ level of 8.07 mmol/
L, Na+ 140 mmol/L, pH 7.284, PaCO2 33.6 mmHg, PaO2 201.4
mmHg, HCO3 15.6 mmol/L, and an O2 saturation of 99.3%. The
blood sugar level was 327 mg/dl. We injected calcium gluconate
(300 mg) and regular insulin (5 units) intravenously and began
an infusion of 50% dextrose solution mixed with regular insulin
(25 units). The tall T waves disappeared within 5 min and the
patient was hemodynamically stable. Repeated arterial blood
analysis showed K+ levels of 5.16 mmol/L, Ca2+ 0.95 mmol/L,
pH 7.366, PaCO2 44.1 mmHg, PaO2 201.8 mmHg, HCO3 24.7
mmol/L, O2 saturation 99.0%, and a blood glucose level of 147
mg/dl. The operation proceeded uneventfully, and finished
within 3 h. The patient recovered with no specific complication.
In the post-anesthetic care unit, she was hemodynamically
stable, the serum K+ level was 3.9 mmol/L, and urine ketones
were negative. She did not complain of any symptom, such as
abdominal pain, nausea, vomiting, drowsiness, or weakness.
She did not have the previous symptoms of polyuria, polydipsia,
fever, chest pain, shortness of breath, or weight loss. The
postoperative BUN was 17 mg/dl, and the Cr was 0.6 mg/dl. The
serum K+ level was 4.4 mmol/L on the day after operation and
4.2 mmol/L on the following day. The blood sugar levels and K+
levels were maintained within the normal range. The highest
random blood glucose level was 147 mg/dl and the HbA1c was
5.3%. The patient was discharged on the 6th post-operative day,
with no complication.
Two major causes of hyperkalemia exist. The first is an
altered internal potassium balance, including acidosis, insulin
deficiency, hypoaldosteronism, and cell necrosis. The second
is an altered external balance, including the effects of ACEi.
Hyperkalemia can also occur as a response to blood cell lysis.
It is well-documented that the buffering of excess hydrogen
ions in cells leads to potassium movement into the extracellular
fluid, to maintain electoneutrality. This is true in metabolic
acidosis, caused by the accumulation of mineral acids, but
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Acute hyperkalemia induced by hyperglycemia in non-diabetic patient
Vol. 61, No. 2, August 2011
is less likely to occur in organic acidoses, such as diabetic
ketoacidosis (DKA) [2]. Although, we could not diagnose the
patient as having DKA, the acidemia would not explain the
severe hyperkalaemia noted in this patient.
In cases of severe volume depletion, the ability to handle
a potassium load is impaired due to decreased distal fluid
delivery, which can diminish potassium secretion [2]. In
our case, the patient did not display any sign or symptom of
hypovolemia. No evidence of hypoaldosteronism was observed.
The administration of an angiotensin-converting enzyme
inhibitor can limit aldosterone release, aggravating hyper-
kalemia. These drugs can reduce the concentration of
circulating angiotensin II and diminish intra-adrenal angio-
tensin II, which can mediate part or most of the stimulating
effect of hyperkalemia [2]. However, this was not true in the
present case, as the patient's plasma creatinine and urea levels
were normal, and the potassium, chloride and bicarbonate
levels were restored to normal [2,4].
We thus conclude that the hyperkalemia that developed
during surgery was induced by hyperglycemia in this case.
Mild-to-moderate hyperkalemia is common in patients with
hyperglycemic crises, such as in DKA. When circulating insulin
is low, as in DKA, K+ is released from cells, raising the plasma
potassium levels [2]. Furthermore, an elevation in plasma
osmolality causes osmotic water movement from the cells into
the extracellular fluid, which is paralleled by K+ release from
the cells. While the cell necrosis induced by the liposuction
process should be considered, we are aware of no report of
hyperkalemia during or after liposuction and this therefore
seems unlikely to explain the hyperglycemia observed [5].
In conclusion, our case report presents a non-diabetic
patient who, during a minor operation, became severely
hyperkalemic, apparently induced by hyperglycemia. Because
of its potentially fatal consequences, including skeletal muscle
weakness and cardiac manifestations, hyperkalemia exceeding
6 mEq/L should always be treated. We emphasize that acute
hyperkalemia can occur in various circumstances, as observed
in this unpredictable case, and should thus be monitored
carefully.
References
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induced hyperkalemia. Prevalence and possible origin. Intensive
Care Med 1986; 12: 416-8.
2. Milionis HJ, Dimos G, Elisaf MS. Severe hyperkalaemia in
association with diabetic ketoacidosis in a patient presenting with
severe generalized muscle weakness. Nephrol Dial Transplant 2003;
18: 198-200.
3. Goldfarb S, Cox M, Singer I, Goldberg M. Acute hyperkalemia
induced by hyperglycemia: hormonal mechanisms. Ann Intern
Med 1976; 84: 426-32.
4. Halperin ML, Kamel KS. Potassium. Lancet 1998; 352: 135-40.
5. Habbema L. Safety of liposuction using exclusively tumescent local
anesthesia in 3,240 consecutive cases. Dermatol Surg 2009; 35:
1728-35.