Pediatric Hypoglycemia Clinical Presentation

  • Author: Robert P Hoffman, MD; Chief Editor: Stephen Kemp, MD, PhD   more...
 
Updated: Aug 25, 2011
 

History

Glucose is normally the primary source for brain energy. The brain can also use ketones, but this transition is gradual. Symptoms of hypoglycemia reflect 2 major clinical pathways. The first pathway is caused by activation of the autonomic nervous system, which causes symptoms such as sweating, trembling, flushing, anxiety, heart pounding, and hunger. The second group of symptoms is due to neuroglycopenia and includes an inability to concentrate, confusion, tiredness, feeling tearful, difficulty speaking, behavioral changes, incoordination, weakness, and drowsiness. Nonspecific symptoms include mouth tingling, dry mouth, blurred vision, headache, and nausea. These symptoms, of course, vary according to the age of the patient.

Neonates

Symptoms of hypoglycemia in neonates include the following:

  • Tremulousness
  • Brisk Moro reflex
  • Lethargy
  • Poor feeding
  • Irritability
  • Hypothermia
  • Respiratory distress
  • Apnea
  • Bradycardia
  • Seizure
  • Coma
  • Sudden death

Older children

Symptoms of hypoglycemia in older children include the following:

  • Dizziness
  • Sweating
  • Hunger
  • Anxiousness
  • Confusion
  • Lethargy
  • Poor feeding
  • Irritability
  • Seizure
  • Coma
  • Sudden death
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Physical Examination

Hypoglycemic reactions are usually, but not always, accompanied by an increased heart rate with bounding pulse due to increased epinephrine secretion. Infants, if awake, may be irritable, tremulous, and cranky.

If the brain’s energy supply is severely impaired, the patient's mental status is likely to be impaired, with extreme inappropriate affect and mood, lethargy, seizure, or coma.

Large body size for age in the neonate or older child suggests hyperinsulinism, although some children with hyperinsulinism are born prematurely and are small for gestational age. Decreased subcutaneous fat suggests inadequate glucose stores. Poor linear growth may point to growth hormone deficiency, and midline facial and cranial abnormalities suggest pituitary hormone deficiencies. Liver size should be assessed for evidence of glycogen-storage diseases.

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Contributor Information and Disclosures
Author

Robert P Hoffman, MD  Associate Professor of Pediatrics, Department of Pediatrics, Ohio State University College of Medicine

Robert P Hoffman, MD is a member of the following medical societies: American Diabetes Association, American Pediatric Society, Christian Medical & Dental Society, Endocrine Society, and Pediatric Endocrine Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Karl S Roth, MD  Professor and Chair, Department of Pediatrics, Creighton University School of Medicine

Karl S Roth, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Nutrition, American Pediatric Society, American Society for Clinical Nutrition, American Society of Nephrology, Association of American Medical Colleges, Medical Society of Virginia, New York Academy of Sciences, Sigma Xi, Society for Pediatric Research, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London)  Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece; UNESCO Chair on Adolescent Health Care, University of Athens, Greece

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Endocrinology, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD  Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

References
  1. de Lonlay P, Giurgea I, Sempoux C, Touati G, Jaubert F, Rahier J, et al. Dominantly inherited hyperinsulinaemic hypoglycaemia. J Inherit Metab Dis. 2005;28(3):267-76. [Medline].

  2. Di Candia S, Gessi A, Pepe G, et al. Identification of a diffuse form of hyperinsulinemic hypoglycemia by 18-fluoro-L-3,4 dihydroxyphenylalanine positron emission tomography/CT in a patient carrying a novel mutation of the HADH gene. Eur J Endocrinol. Jun 2009;160(6):1019-23. [Medline].

  3. DePuy AM, Coassolo KM, Som DA, Smulian JC. Neonatal hypoglycemia in term, nondiabetic pregnancies. Am J Obstet Gynecol. May 2009;200(5):e45-51. [Medline].

  4. Tita AT, Landon MB, Spong CY, et al. Timing of elective repeat cesarean delivery at term and neonatal outcomes. N Engl J Med. Jan 8 2009;360(2):111-20. [Medline].

  5. Daly LP, Osterhoudt KC, Weinzimer SA. Presenting features of idiopathic ketotic hypoglycemia. J Emerg Med. Jul 2003;25(1):39-43. [Medline].

  6. [Guideline] Wight N, Marinelli KA. ABM clinical protocol #1: guidelines for glucose monitoring and treatment of hypoglycemia in breastfed neonates. Breastfeed Med. Autumn 2006;1(3):178-84. [Medline].

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Interpretation of the critical sample.
 
 
 
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