Tavera HM, Coyote EN

Language: Spanish
References: 17
Page: 180-187
PDF size: 111.08 Kb.

ABSTRACT

Diabetic ketoacidosis (DKA) is one of the most serious acute complications of diabetes mellitus. It consists of the biochemical triad of hyperglycemia › 300 mg/dL, metabolic acidosis pH ‹ 7.3, HCO₃ › 15 mmol/L, and ketonemia with ketonuria › 3 mmol/L. All patients with diabetes, regardless of type, can present diabetic ketoacidosis at the time of diagnosis, with non-compliance of insulin treatment, or in association with a febrile illness. Diabetic ketoacidosis is caused by insulin deficiency, either relative or absolute and to excessive secretion of counterregulatory hormones that promote ketogenesis and acidosis. The clinical picture can be serious, including extreme dehydration, electrolitic disturbance, hypotension and altered mental status. May be clinically confused with acute abdomen. Diagnosis is confirmed in the presence of hyperglycemia › 300 mg/dL, acidemia and ketosis. General principles in the management include correction of fluid deficits and electrolyte disturbances, interrupting ketoacid production and lowering plasma glucose with insulin therapy. Rapid correction of metabolic abnormalities should be avoided to decrease the risk for precipitating cerebral edema.

REFERENCES

1. Laffel L. Acute complications of diabetes in children. Endocrinol Metab Clin North Am 2000; 29: 707.

2. Chiasson JL, Aris-Jilwan N, Belanger R, Bertrand S, Beauregard H, Ekoe JM,Fournier H, Havrankova J. Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state. CMAJ 2003; 168 (7): 859-66.

3. Magee M, Bhatt B. Endocrine and metabolic dysfunction syndromes in the critically ill. Management of decompensated diabetes. Crit Car Clin 2001; 17: 1.

4. Coyote N, Dorantes LM. Cetoacidosis diabética. Urgencias en pediatría. Hospital Infantil de México Federico Gómez. 5a ed. México: McGraw-Hill-Interamericana, 2002; 93-99.

5. Pizarro D. Alteraciones del equilibrio hidroelectrolítico y ácido base. Alteraciones hidroelectrolíticas en pediatría. México: Ediciones Médicas del Hospital Infantil de México Federico Gómez, 1991: 57-58.

6. Kitabchi A, Umpierrez G, Murphy M, Barrett E, Kreisberg R, Malone J. Management of hyperglicemic crises in patients with diabetes. Diabetes Care 2001; 24: 131-153.

7. Brandenburg MA, Dire DH. Comparison of arterial and venous blood gas values in the initial emergency department evaluation of patients. Ann Emerg Med 1998; 31: 459-465.

8. Chavarría B. Diabetes mellitus en el niño y el adolescente. México: Librería de Medicina, 1978; 79-94.

9. Felig B. Endocrinología y metabolismo. México: Mc Graw-Hill, 1983; 902-909.

10. Gardner LI. Endocrine and Genetic Disease of childhood and adolescence. London. 1975; 946-963.

11. Kalamazoo. Diabetes. Michigan: Upjohn Company, 1965; 85-87.

12. García E. Tratamiento hemodinámico del paciente grave: Cristaloides, coloides, inotrópicos y vasodilatadores. Terapia intensiva. México: McGraw-Hill-Interamericana, 1998; 271-272.

13. Lifshitz F. Diabetic ketoacidosis. In: Pediatric Endocrinology. New York: Marcel Dekker, 1996: 631-642

14. Umpierrez G, Cuervo R, Karabell A, Latif K, Freire A, Kitabchi A. Treatment of diabetic ketoacidosis with subcutaneous insulin aspart. Diabetes Care 2004; 27: 1873-1878.

15. Umpierrez G, Latif K, Stoever J, Cuervo R, Park L, Freire A. Efficacy of subcutaneous insulin lispro versus continuous intravenous regular insulin for the treatment of patients with diabetic ketoacidosis. Am J Med 2004; 117: 291-296.

16. Van Der Meulen JA, Klip A, Grinstein S. Possible mechanism for cerebral edema in diabetic ketoacidosis. Lancet 1987; 8: 306-308.

17. Glaser N, Barnett P, McCaslin I, Nelson D, Trainor J, Louie J et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med 2001; 344: 264-269.