How does ketoacidosis cause hyperkalemia




















Diabetes Res Clin Pract ; 34 : 23 — Lancet ; : — Iatrogenic hyperkalemia—points to consider in diagnosis and management. Nephrol Dial Transplant ; 13 : — Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.

Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Introduction. Severe hyperkalaemia in association with diabetic ketoacidosis in a patient presenting with severe generalized muscle weakness.

Milionis , Haralampos J. Oxford Academic. Google Scholar. George Dimos. Moses S. Cite Cite Haralampos J. Select Format Select format. Permissions Icon Permissions. Open in new tab Download slide. Diabetes Res Clin Pract. Nephrol Dial Transplant. Issue Section:. Download all slides. Comments 0. Add comment Close comment form modal. I agree to the terms and conditions. You must accept the terms and conditions.

Add comment Cancel. Submit a comment. Comment title. You have entered an invalid code. Submit Cancel. Thank you for submitting a comment on this article. Your comment will be reviewed and published at the journal's discretion. Please check for further notifications by email. View Metrics. Email alerts Article activity alert. Advance article alerts. New issue alert. Arterial blood gas analysis showed a pH of 6. Initial laboratory findings are shown in Table 1.

We did not measure plasma osmolality. Chest x-ray showed cardiac enlargement, and electrocardiography ECG revealed typical features associated with hyperkalemia, including absent P waves, prolonged QRS intervals and tented T waves Fig.

These physical and laboratory findings suggested DKA with marked hyperkalemia but no evidence of related total body fluid loss. It was thought that his body weight was increased due to the skip of hemodialysis, because he could not go to hemodialysis clinic.

Electrocardiography reveals features typically associated with hyperkalemia absent P waves, prolonged QRS interval and tented T waves.

We started an intravenous insulin infusion and hemodialysis to reduce the glucose and potassium levels. Fluid infusions were not given because there was no evidence of a fluid deficit.

The hyperkalemic changes disappeared from ECG. On hospital day 2, however, his right hemiplegia persisted. Head computed tomography demonstrated a low-density area in the left frontal lobe, indicating a left frontal cerebral infarction.

Although the insulin pump tube was fully filled with insulin, the infusion line was not properly placed into the abdominal skin. The patient underwent rehabilitation, but he was unable to manage his insulin pump because of the hemiplegia and higher cortical dysfunction induced by the cerebral infarction. We therefore removed the pump and switched to intermittent insulin therapy.

We performed brain CT scan twice, and there were no progression of the infarct area and brain edematous findings. On hospital day 40, he was transferred to another hospital for further rehabilitation. In patients with anuria on hemodialysis, DKA is generally rare, because urinary loss of water and electrolytes does not occur and regular hemodialysis improves metabolic acidosis 2. In this patient, extreme hyperkalemia of 9. In general, hyperglycemia is positively correlated with the serum potassium level 3 , but hyperkalemia to this extreme degree is rare.

In addition, reduced renal potassium excretion contributes to hyperkalemia in renal failure 4. This patient had a left frontal cerebral infarction resulting in right hemiplegia and higher cortical dysfunction, so we wondered if he had lost the ability to respond to hyperglycemia and handle his insulin pump properly.

The present episode likely depended on absolute lack of insulin action. In patients with diabetes who are anuric, there is a little reduction in weight and circulatory blood volume when the pathological state of DKA develops. This patient showed had some weight gain over his dry weight and cardiac enlargement on chest x-ray.

Normally, fluid infusion is essential for initial treatment of DKA 1. However, this could cause or worsen overhydration and pulmonary edema in patients with DKA who require chronic hemodialysis. Careful evaluation of body fluid volume and the serum potassium level are mandatory. If there is no volume depression, insulin treatment and prompt hemodialysis must be considered, but intravenous fluids should be minimized. Neurologic complications must also be assessed in patients with DKA who are on chronic hemodialysis.

Hemodialysis and insulin infusion may rapidly normalize serum potassium, and plasma tonicity, largely determined by glucose and sodium, improves with the decrease in plasma glucose. Some reports have shown that rapid alteration in plasma tonicity may cause seizures or prolonged loss of consciousness because a marked change in tonicity may produce cerebral edema 5 , 6.

Hence, careful follow-up is necessary to prevent brain damage associated with reduction of tonicity by hemodialysis. In this patient, brain edema progression was not found in successive brain CT scans after hemodialysis; however, there is a possibility that rapid reduction in hyperglycemia accompanying with a marked decrease in plasma osmolality by hemodialysis and insulin infusion may mimic the prolongation of conscious disturbance.

On the other hand, Daugirdas and coworkers noted that extracellular volume depletion in the central nervous system is less likely to occur in patients such as ours because hyperglycemia will not result in osmotic diuresis in an anuric patient 7.

The relationship between changes in plasma tonicity and central nervous system impairment is now controversial, and the management strategy is not well established for patients with DKA who are on chronic hemodialysis. Thus, we performed head computed tomography to assess the focal neurologic disorder. His severe hyponatremia was concomitantly improved after the reduction in plasma glucose, and we consider that hyponatremia was secondary induced by extreme hyperglycemia 8.

In summary, we have presented a patient with type 1 diabetes on chronic hemodialysis because of anuria. He had DKA with extreme hyperkalemia, which was resolved by rapid hemodialysis and intensive insulin therapy. Although hypokalemia is common in DKA, hyperkalemia is the more likely problem in patients on hemodialysis. The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector. H Yamada wrote the manuscript. H Yamada and S Funazaki managed this patient. All authors read and approved the final version of the manuscript. National Center for Biotechnology Information , U. Endocrinol Diabetes Metab Case Rep. Published online Sep 4.

Author information Article notes Copyright and License information Disclaimer. Corresponding author. Correspondence should be addressed to H Yamada; Email: pj. Received Jul 18; Accepted Jul This article has been cited by other articles in PMC. Abstract Diabetic ketoacidosis DKA is a critical complication of type 1 diabetes associated with water and electrolyte disorders.

Learning points: Patients with type 1 diabetes on hemodialysis may develop ketoacidosis because of discontinuation of insulin treatment. Background Diabetic ketoacidosis DKA is a very common endocrinology emergency.

Case presentation A year-old Japanese man with type 1 diabetes had been on chronic hemodialysis three times per week due to diabetic nephropathy since the age of 32 years. Open in a separate window. Figure 1.



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