Resumo

NARES-TORICES, Miguel Ángel; GONZALEZ-MARTINEZ, Armando; MARTINEZ-AYUSO, Francisco Agustín  e  MORALES-FERNANDEZ, Manuel Orlando. Hypoglycemia: Time is brain. What are we doing wrong?. Med. interna Méx. [online]. 2018, vol.34, n.6, pp.881-895. ISSN 0186-4866.  https://doi.org/10.24245/mim.v34i6.2040.

Acute complications of diabetes account for approximately 20 to 30% of adult patients hospitalized in the emergency department. Approximately 90% of all patients recei-ving insulin experience at least one episode of hypoglycemia. As serum glucose levels decrease, a series of responses in the body occurs in a staggered fashion. The first triggered mechanism of defense is the cessation of insulin production in pancreatic B cells, appearing at approximately 80 mg/dL. Second, increased glucagon secretion appears around 68 mg/dL. Brain tissue consumes approximately 25% of total body consumption in its post-absorptive state. Serum glucose crosses the blood-brain barrier through the capillaries by diffusion facilitated by the GLUT-1 transporter. The most sensitive areas to decreased glycemic intake are the cortex, hippocampus and striatum. This article provides an overview of hypoglycemia pathophysiology, with emphasis on its deleterious effects on brain tissue, as well as its approach to physicians in the emergency department.

Palavras-chave : Hypoglycemia; Brain death; Glucose; Glucagon.

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