Warning: mkdir(): Permission denied in /home/virtual/lib/view_data.php on line 81 Warning: fopen(/home/virtual/e-apem/journal/upload/ip_log/ip_log_2022-10.txt): failed to open stream: No such file or directory in /home/virtual/lib/view_data.php on line 83 Warning: fwrite() expects parameter 1 to be resource, boolean given in /home/virtual/lib/view_data.php on line 84 The Author Reply: Endocrine and metabolic emergencies in children: hypocalcemia, hypoglycemia, adrenal insufficiency, and metabolic acidosis including diabetic ketoacidosis
Ann Pediatr Endocrinol Metab Search


Ann Pediatr Endocrinol Metab > Volume 21(2); 2016 > Article
Kim: The Author Reply: Endocrine and metabolic emergencies in children: hypocalcemia, hypoglycemia, adrenal insufficiency, and metabolic acidosis including diabetic ketoacidosis
To the editor:
I thank Dr. Rosival, who provided the interests and comments on my paper "Endocrine and metabolic emergencies in children ...."1). Dr. Rosival questioned about absolute and relative insulin deficiency of the patients with diabetic ketoacidosis (DKA), and why bicarbonate therapy should be sparing for patients with DKA.

1. Insulin deficiency

Dr. Rosival commented on serum insulin level of the patients with DKA citing several references. Of course, the patient who shows normal concentration of serum insulin could be developed full-blown DKA. Even if insulin levels were checkable, it meant relative insulin deficient status, because those levels of insulin itself couldn't overcome the overwhelming hyperglycemic effects of counter regulatory hormones (cortisol, epinephrine, growth hormone, and glucagon) during stress (infection, trauma, and surgery)1). The basic underlying mechanism for DKA is a reduction in the net effective concentration of circulating insulin, coupled with a concomitant elevation of counter regulatory stress hormones2). In patients with DKA, the deficiency in insulin can be absolute, or it can be insufficient relative to an excess of counter regulatory hormones2).
Also, a lot of new patients have been diagnosed as type 1 diabetes mellitus initially through DKA due to absolute insulin deficiency3). DKA has been increasingly noted in newly diagnosed obese type 2 diabetic patients4).

2. Bicarbonate therapy

Bicarbonate therapy should be considered in severe acidosis (pH<6.9) due to DKA1). Acidosis of the patients with DKA is reversible by fluid and insulin replacement. Insulin stops further ketoacids production and allows ketoacids to be metabolized, which generates bicarbonate. Treatment of hypovolemia improves tissue perfusion and renal function, increasing the excretion of organic acids. Controlled trials have shown no clinical benefit from bicarbonate administration5,6,7,8), and there are well recognized adverse effects of bicarbonate therapy, including paradoxical central nervous system acidosis9) and hypokalemia from rapid correction of acidosis9). Failure to account for the sodium being administered and appropriately reducing the NaCl concentration of the fluids can result in increasing osmolality9). Nevertheless, there may be selected patients who may benefit from cautious alkali therapy. These include patients with severe acidemia (arterial pH<6.9), in whom decreased cardiac contractility and peripheral vasodilatation can further impair tissue perfusion, and patients with life-threatening hyperkalemia10). Therefore, routine bicarbonate administration for patent with DKA is not recommended unless the acidosis is profound.
I was trying to describe condensing a bunch of essential facts of the clinically important contents of endocrine emergencies into a short paper1), which is readable than tedious longer one. It has, therefore, short explanation of pathophysiology of DKA. Dr. Rosival pointed out 2 issues (insulin and bicarbonate) and led us to consideration of the core pathogenesis of DKA.


Conflict of interest: No potential conflict of interest relevant to this article was reported.


1. Kim SY. Endocrine and metabolic emergencies in children: hypocalcemia, hypoglycemia, adrenal insufficiency, and metabolic acidosis including diabetic ketoacidosis. Ann Pediatr Endocrinol Metab 2015;20:179–186. PMID: 26817004.
crossref pmid pmc
2. Umpierrez GE, Kelly JP, Navarrete JE, Casals MM, Kitabchi AE. Hyperglycemic crises in urban blacks. Arch Intern Med 1997;157:669–675. PMID: 9080921.
crossref pmid
3. Maniatis AK, Goehrig SH, Gao D, Rewers A, Walravens P, Klingensmith GJ. Increased incidence and severity of diabetic ketoacidosis among uninsured children with newly diagnosed type 1 diabetes mellitus. Pediatr Diabetes 2005;6:79–83. PMID: 15963034.
crossref pmid
4. Musey VC, Lee JK, Crawford R, Klatka MA, McAdams D, Phillips LS. Diabetes in urban African-Americans. I. Cessation of insulin therapy is the major precipitating cause of diabetic ketoacidosis. Diabetes Care 1995;18:483–489. PMID: 7497857.
crossref pmid
5. Hale PJ, Crase J, Nattrass M. Metabolic effects of bicarbonate in the treatment of diabetic ketoacidosis. Br Med J (Clin Res Ed) 1984;289:1035–1038.
crossref pmid pmc
6. Morris LR, Murphy MB, Kitabchi AE. Bicarbonate therapy in severe diabetic ketoacidosis. Ann Intern Med 1986;105:836–840. PMID: 3096181.
crossref pmid
7. Okuda Y, Adrogue HJ, Field JB, Nohara H, Yamashita K. Counterproductive effects of sodium bicarbonate in diabetic ketoacidosis. J Clin Endocrinol Metab 1996;81:314–320. PMID: 8550770.
8. Green SM, Rothrock SG, Ho JD, Gallant RD, Borger R, Thomas TL, et al. Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emerg Med 1998;31:41–48. PMID: 9437340.
crossref pmid
9. Assal JP, Aoki TT, Manzano FM, Kozak GP. Metabolic effects of sodium bicarbonate in management of diabetic ketoacidosis. Diabetes 1974;23:405–411. PMID: 4208463.
crossref pmid
10. Lever E, Jaspan JB. Sodium bicarbonate therapy in severe diabetic ketoacidosis. Am J Med 1983;75:263–268. PMID: 6309004.
crossref pmid


Browse all articles >

Editorial Office
#510, DoosanBearstel 381, Gangnam-daero, Seocho-gu, Seoul 06620, Korea
Tel: +82-2-3471-4268    Fax: +82-2-3471-4269    E-mail: kspe.editor@gmail.com                

Copyright © 2022 by Korean Society of Pediatric Endocrinology.

Developed in M2PI

Close layer
prev next