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Manual of Equine Neonatal Medicine
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Hypoglycemia

Author(s):
Madigan J.E.
In: Manual of Equine Neonatal Medicine by Madigan J.E.
Updated:
OCT 08, 2015
Languages:
  • EN
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    Read

    I. Foals at Risk

    Peracute or cardiac form

    1. Cesarean section or dystocia with anesthesia.
    2. Premature or small for gestational age.
    3. Neonatal Isoerythrolysis foals.
    4. Hypothermia.
    5. Asphyxia and hypoxia.
    6. Septicemia.
    7. Maladjustment syndrome.
    8. Inherited metabolic defects
    1. Lysosomal storage disease
    2. Glycogen Branching Enzyme deficiency (See Congenital Anomalies and Genetic Disorders)
    1. Previous bolus injections of glucose or rapid rate of glucose infusion and sudden cessation.
    1. "Rebound" hypoglycemia following bolus.
    2. When parenteral nutrition discontinued.
    1. Orphan foals.
    2. Liver failure - Tyzzer's disease.
    3. Hyperlipidemia.

    II. Symptoms

    1. Many foals merely look weak, or are floppy and falling when attempting to rise. It may manifest as decreased nursing, apathy or lethargic appearance.
    2. Seizures are not a consistent clinical sign even with prolonged hypoglycemia.

    III. Diagnosis

    1. Asymptomatic hypoglycemia.
    1. Suspect when dextrose stick is less than 60 mg/dl (3.3 mmol/l).
    2. Order Stat quantitative blood glucose.
    3. Diagnosis is glucose less than 40 mg/dl (2.2 mmol/l) in a presuckle foal and less than 80 mg/dl (4.4 mmol/l) in a foal >2 hours which has suckled.
    1. Symptomatic hypoglycemia is defined as symptoms that disappear with glucose infusion regardless of blood glucose level.

    IV. Therapy

    1. Draw pretreatment blood for quantitative glucose.
    2. Symptomatic foal: foal that has not nursed with no measurement - 8 mg/kg/min glucose (high end of the dose range) which translates to 200 ml/h of 10% dextrose in an isotonic crystalloid like LRS or Plasmalyte 148A for an average sized foal (which is a dose rate of 4 ml/kg/h of a 10 % dextrose solution) for the first hour, then decrease to 4 mg/kg/min after that (200 ml/h of 5% dextrose). Recheck glucose in 1 hour. (See section on Fluid therapy).
    3. Attempt to maintain blood sugar at 100-160 (80-180) mg/dl (4.4-10 mmol/l). Check serum Na to avoid hyponatremia.
    4. Begin oral feedings of milk or 10% dextrose or karo (corn) syrup in a syringe or by nasogastric tube.
    5. Correct predisposing causes and provide nursing care.
    6. Monitor glucose every 4 to 6 hours via dextrose sticks.
    7. Correct any concurrent acid base imbalance or hypoxemia.

    V. Prognosis is Poor to Guarded, Treatment Must Be Started Early to Be Beneficial

    1. Prolonged hypoglycemia can result in permanent neurologic defects.
    2. We have found a reasonable response to severe (10-15 mg/dl [0.6-0.8 mmol/l] blood glucose) hypoglycemias if correction of the concurrent initiating factors can be accomplished.
    3. A recent multicenter study evaluated the association between blood glucose and survival rates of critically ill neonatal foals. 29.1% of the study population had blood glucose concentrations within the reference range of 4-7 mmol/l (76-131 mg/dL) at admission, 36.5% were hyperglycemic, and 34.4% were hypoglycaemic. Foals with blood glucose concentrations <2.8 mmol/L (50 mg/dL) or >10 mmol/L (180 mg/dL) at admission were less likely to survive [1].
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    References

    1. Hollis AR, Furr MO, Magdesian KG, Axon JE, Ludlow V, Boston RC, Corley KT.: Blood glucose concentrations in critically ill neonatal foals. J Vet Intern Med. 2008 Sep-Oct; 22(5):1223-7. - PubMed -

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    About

    How to reference this publication (Harvard system)?

    Madigan, J. E. (2015) “Hypoglycemia”, Manual of Equine Neonatal Medicine. Available at: https://www.ivis.org/library/manual-of-equine-neonatal-medicine/hypoglycemia (Accessed: 10 June 2023).

    Affiliation of the authors at the time of publication

    School of Veterinary Medicine, University of California-Davis, CA, USA.

    Author(s)

    • John Madigan

      Madigan J.E.

      Professor of Medicine and Epidemiology
      MS DVM Dipl. ACVIM ACAW
      Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California
      Read more about this author

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