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Manual of Equine Neonatal Medicine
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Assessment of Maturity - Prematurity

Author(s):
Madigan J.E. and
Magdesian K.G.
In: Manual of Equine Neonatal Medicine by Madigan J.E.
Updated:
MAR 31, 2014
Languages:
  • EN
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    Editor's Comment - While there have been a greater number of successful outcomes from critical care of foals, the premature foal remains the most difficult condition to manage. Outcomes of very premature foals admitted to intensive care reveal a poor rate of survival (4060%). Of those surviving, limb angulation, lack of calcification of bones in carpus and tarsus, and poor growth continue to cause complications. When determining if a foal is premature, physical signs and hematology are more reliable than using gestational age.

    I. Gestational Length

    1. Normal range = 320-360 days, no difference for sex, or time of year.
    2. Less than 320 days considered premature.
    3. Gestation length is poor indicator of individual readiness for birth.
      Terms "Immature" and "dysmature" indicate gestational age is normal, but foal has signs, behavior and physiology of a premature foal.
    4. Foals that are small for gestational age (term) due to in utero growth retardation.
    1. May or may not show signs of prematurity.
    2. Causes: in utero infections, twins or twin which was resorbed or mummified in early gestation, placentitis, malnutrition, other maternal uterine abnormalities.

    II. Clinical Signs of Immaturity - Unreadiness for Birth [1]

    1. Weaker, take longer to rise and depressed sucking ability.
    2. Smaller size and reduced birth weight.
    3. Silky hair over back and rear quarters.
    4. Hooves do not dry out and separate from the "golden hoof".
    5. Domed forehead and soft lips.
    6. Floppy ears, red tongue.
    7. Hyperextension (hypoflexion) of fetlock joints.
    8. Reduced tolerance to oral feedings.
    9. Reduced body temperature and susceptibility to hypothermia.
    10. Incomplete ossification of carpal and tarsal bones. May predispose to angular limb deformity.
    11. Respiratory rate may increase following birth with some evidence of respiratory distress.

    III. Laboratory Findings in Unreadiness for Birth

    1. Adrenocortical insufficiency.
    1. Seen as narrow neutrophil/lymphocyte ratio of 0.5-1:1 due to a neutropenia. Normal foals have a 2:1 ratio 3 hours following birth.
    2. Lymphocyte counts are higher than term foals (3500 5000/ul).
    3. Low plasma cortisol and no rise following administration of ACTH.
    1. Normal foals have a wider neutrophil/lymphocyte change in response to IM ACTH within 3 hours of birth.
    2. 0.01 mg cosyntropin (low dose) or 0.1 mg (high dose) (short-acting) IM total [2,3].
    3. Foals without HPA (hypothalamic-pituitary-adrenal axis) dysfunction should have a significant rise in plasma cortisol levels 30 minutes after administration [3].
    4. Increased plasma Vasopressin and ACTH concentrations in septic foals were associated with higher mortality in one study. Several septic foals had increased vasopressin/ACTH and ACTH/cortisol ratios, which indicates relative adenohypophyseal and adrenal insufficiency [4].
    1. Respiratory system compromise and blood gas abnormalities.
    1. Signs of hypoventilation - Decreased PaO2 increased PaCO2.
    2. Venous pH <7.25 (normal foal >7.3) and tendency for pH to decrease.
    3. May have decreased functional surfactant and respiratory distress.
    1. Depressed blood glucose 2 hours post foaling (<60 mg/dl; 3.3 mmol/l).
    2. Decreased absorption of colostral immunoglobulin. Overall immune function is decreased.
    3. Increased susceptibility to infection.

    IV. Outcome of Premature Foals - Based on Induced Parturition Model [5]

    1. Survival rates of foals from induced parturition before 320 days gestation is poor.
    2. Spontaneous births in Thoroughbreds between 280-322 days gestation have 73% survival. Fetus is prepared for delivery and final maturation processes develop
    3. Correlation of post foaling behavior and outcome w/o treatment [2].
    1. If the foal does not establish righting reflexes and has weak sucking - Will die.
    2. If foal becomes sternal and has good head and neck tone, strong sucking reflex, but took 2 hours to stand, will do well for 24 hours and then fade and die unless intervention provided.
    3. If foal appears viable at birth and has normal righting reflexes at delivery, can stand and suck - Prognosis is better but a degree of fading still occurs in this group, 1-7 days following birth.

    V. Diagnostic Evaluation

    1. Conduct physical exam.
    2. Complete blood count.
    3. Measure venous acid base.
    4. To assess respiratory maturity and function
    1. Administer face mask oxygen (10 L/min) and measure arterial oxygen after 5 minutes. PaO2 should be >200 mmHg. If less, have shunt or atelectasis.
    1. Monitor serum glucose levels.
    2. Assess serum IgG. Recommend giving supplemental colostrum and 1 liter plasma IV before assessment of IgG at 18 hrs because of the common finding of failure of passive transfer.

    VI. Treatment [1]

    1. Supporting the foal by environmental temperature control, nutrition, circulatory and respiratory support with oxygen, or ventilation may be required.
    2. Adrenal insufficiency support.
    1. Depot long acting ACTH (Synacthen Depot®, Novartis) may provide stimulation after several days.
    1. 0.4 mg IM total dose. Repeat 6 and 12 hours with 0.2 mg IM total dose.
      Editor's Comment - This is from older literature.
    1. Hydrocortisone -Sodium succinate (Cortelan® Glaxo Laboratories) or 50 mg BID Solu-Delta-Cortef® (Upjohn) has been used.
    1. Avoid pharmacological doses to prevent disruption of immune system.
    2. A short tapering course of hydrocortisone sodium succinate (Pfizer, New York) (1.3 mg/kg/day for 48h, 0.65mg/kg/d for 24h then 0.33mg/kg/d for 12h; total doses given in 6 doses as an IV bolus q4h) has potentially beneficial anti-inflammatory effects without significantly impairing innate immune function [7].
    1. Surfactant replacement and chemical closure of ductus arteriosus (flunixin-meglumine daily for 48 hrs) are now being attempted to increase survivability.
    2. Daily nursing care and maintenance as per the critical foal.
    1. Watch for entropion.
    2. These foals tolerate oral feeding very poorly initially.
    3. Start total parental nutrition early.
      Editor's Comment - This can greatly increase survival.
    1. Prevention and control of sepsis.
    2. Therapy for limbs - MUST assess by radiography the degree of ossification of carpus and tarsus. Foals body weight must be supported during early ambulation.
    1. Heel extensions taped or glued on foot have provided increased support (See Cardiac Catheterization Pressure Measurements)
    2. Support wraps should not normally be used because they cause tendon relaxation.
    3. Radiograph carpus and tarsus and limit activity in foals with minimum ossification.
    4. Provide optimal nutrition up to 30% of BW per day in milk while confining foal and limiting movement.
    5. Many foals survive and then have damaged joints.
    1. Complete non weight bearing may be needed initially.

    VII. Nutrition Support (See Parenteral Nutrition and Enteral Nutrition)

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    References

    1. Vaala WE. Diagnosis and treatment of prematurity and neonatal maladjustment syndrome in newborn foals. Compend Cont Educ Pract Vet 8:S211-S222, 1986.

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    About

    How to reference this publication (Harvard system)?

    Madigan, J. E. and Magdesian, K. G. (2014) “Assessment of Maturity - Prematurity”, Manual of Equine Neonatal Medicine. Available at: https://www.ivis.org/library/manual-of-equine-neonatal-medicine/assessment-of-maturity-prematurity (Accessed: 05 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
    • K. Gary Magdesian

      Magdesian K.G.

      Professor
      DVM Dipl ACVIM Dipl ACVECC Dipl ACVCP
      Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California
      Read more about this author

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