Foal: neonatal maladjustment syndrome
Synonym(s): Dummy, Barker, Wanderer, Hypoxic-ischemic encephalomyelopathy (HIE)
Introduction
- Cause: uncertain. Has historically been associated with probable CNS hypoxial ischemia, secondary to placental dysfunction, external pressure in the birth canal, cardiovascular and/or respiratory dysfunction, metabolic disturbances; possibly systemic illness in utero → inability to adjust to extra-uterine life. More recent research suggests that it may be caused by the post-partum persistence of neuroactive steroids which normally keep the foal relatively quiescent during pregnancy.
- Signs: neurologic signs - poor or absent suckling reflex, convulsions, disorientation, inco-ordination, weakness or inability to stand, failure to seek out the udder or follow the mare. Some foals may exhibit abnormal 'barking' type vocalization, hence the synonym 'barkers'.
- Diagnosis: history and signs. History may be either consistent with lack of oxygen or (it's increasingly thought) of a notably rapid parturition
- Treatment: anticonvulsant therapy; cerebral decompression; thermoregulation; oxygen; nursing; ACTH for premature or dysmature foals.
- Prognosis: immediately guarded. Can be good in the long-term if foal survives the neonatal period.
Presenting signs
- Disorientation, lack of affinity for mare.
- Mild to moderate depression
- Convulsions.
- 'Barking' (rare).
- Failure to suckle normally.
- May be recumbent for longer periods than a normal foal.
Age predisposition
- Neonate within days of birth.
Pathogenesis
Etiology
Postulated causes
- Asphyxia/hypoxia: historically this was believed to be the main cause of neonatal maladjustment syndrome.
- Most recently, the post-partum persistence of neuroactive steroids (allopregnanolone and pregnanolone, androstenedione, dehydroepiandrosterone and epitestosterone) has been suggested as a cause:
- It is postulated that the normal pressures experienced by a foal as it passes through the birth canal of the mare for about 20 min during stage 2 of normal parturition may act to signal the transition from the in utero unconscious state to the post-partum conscious state, and that if birth is so rapid that squeezing is insufficient to trigger this signal neuroactive steroids may persist in the circulation of the neonatal foal and cause neonatal maladjustment syndrome.
- In healthy neonatal foals, the concentrations of neurosteroids decline steadily to very low concentrations within 24 h of birth compared to those of foals with NMS.
- Other factors which may be associated/concurrent with neonatal maladjustment syndrome (though not necessarily causes of it) include:
- Intrauterine growth retardation.
- Sepsis Foal: neonatal septicemia syndrome.
- Septic meningoencephalitis.
- Equine herpesvirus 1 infection Abortion: EHV-1.
- Electrolyte/osmolality disturbances.
- Acid-base imbalance Acid-base imbalance.
- Hepatic Liver disease: overview and renal disease.
- Vascular disorders.
- Trauma.
- Prematurity/dysmaturity Reproduction: prematurity / dysmaturity.
Definitions
- Prematurity: <320 days gestation, hypoflexion of limbs ('floppy') and inability to stand and suck within 2 h of birth, <45 kg birthweight (Thoroughbred).
- Dysmaturity: delivered at term but with signs of prematurity; associated with placental pathology and precocious mammary development in the mare.
Predisposing factors
General
- Lack of oxygen during pregnancy and/or parturition.
- Post-partum persistence of neuroactive steroids in the neonatal circulation.
Pathophysiology
- If cause by hypoxia, the following may contribute to hypoxia during pregnancy, during parturition, or in the immediate post-partum period:
- Placental problems:
- The equine placenta is of the diffuse epitheliochorial → extensive circulation of 300-400 cm between cardiac output and return → vulnerability to ischemia.
- Placental size correlates with fetal size at term.
- Factors affecting placental growth and size:
- Nutrition.
- Environmental temperature.
- Loss of attachment.
- Uterine and umbilical blood flow.
- Maternal size.
- Placental growth rate is determined early in pregnancy.
- Some compensatory growth following a period of retardation can occur but is severely limited as gestation progresses.
- Growth restricted placenta → growth-restricted fetus → hypoxemia and hypoglycemia plus other endocrine alterations (insulin, thyroid hormones, catecholamines and cortisol) → physiological alterations persist in neonate and older animal.
- Intra-uterine growth retardation → respiratory dysfunction and potentially decreased muscle mass at maturity.
- Pulmonary function:
- ?Inadequate duct density at termination of airways.
- Prolonged recumbency (post-partum) → atelectasis → loss of pulmonary dead space → right to left shunt develops → respiratory distress and hypoxemia.
- Dysmaturity:
- Placental pathology → fetal stress → precocious adrenocortical maturation → range of subtle effects on endocrine maturation and function.
- If caused by the post-partum persistence of neuroactive steroids:
- Pathophysiology seems to involve a more rapid than usual parturition, eg the normal pressures experienced by a foal as it passes through the birth canal of the mare (for about 20 min during stage 2 of normal) do not occur. Consequently, the signal which these pressures normally provide to trigger the transition from the in utero unconscious state to the post-partum conscious state does not occur.
- Neuroactive steroids may consequently persist in the circulation of the neonatal foal and cause neonatal maladjustment syndrome.
- Whatever the cause of the neonatal maladjustment syndrome, cerebral dysfunction → convulsions and/or failure to suck → lack of energy, weight loss, dehydration → rapid decline. The fact that the foal does not suck normally / take in adequate colostrum means that it is predisposed to failure of passive transfer Foal: failure of passive transfer (IgG) and at high risk of infection and septicemia.
- Placental problems:
Timecourse
- May be evident immediately/soon after birth or may become evident in the few days after birth.
- 'Dummy' foals may seem normal soon after birth and have a suck reflex at the time but become increasingly disorientated and lose the suck reflex.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- Aleman M, Weich K & Madigan J E (2017) Survey of veterinarians using a novel physical compression squeeze procedure in the management of neonatal maladjustment syndrome in foals. Animals 7 (9), 69 VetMedResource.
- Aleman M, Pickles K J et al (2013) Abnormal plasma neuroactive progestagen derivatives in ill, neonatal foals presented to the neonatal intensive care unit. Equine Vet J 45, 661-665 WileyOnline.
- Diesch T J & Mellor D J (2013) Birth transitions: Pathophysiology, the onset of consciousness and possible implications for neonatal maladjustment syndrome in the foal. Equine Vet J 45, 656-660 WileyOnline.
- Estell K E, Aleman M et al (2013) Clinical signs, neurobehavioral score, and electroencephalography recordings associated with infusion of a pregnenolone derivative to induce neonatal maladjustment syndrome. J Vet Intern Med 27 (3), 663-664.
- McCue P M & Ferris R A (2012) Parturition, dystocia and foal survival: A retrospective study of 1047 births. Equine Vet J 44 (S41), 22-25 WileyOnline.
- Madigan J E, Haggett E F et al (2012) Allopregnanolone infusion induced neurobehavioral alterations in a neonatal foal: Is this a clue to the pathogenesis of neonatal maladjustment syndrome? Equine Vet J 44 (S41), 109-112 WileyOnline.
- Toth B, Aleman M et al (2012) Evaluation of squeeze-induced somnolence in neonatal foals. Am J Vet Res 73 (12), 1881-1889 PubMed.
- McSloy A (2008) Hypoxic ischaemic encephalopathy: Recognising and treating the dummy foal. UK Vet 13 (9), 4-8 VetMedResource.
- No authors listed (1998) Third Dorothy Russell Havemeyer Foundation Third International Workshop on Equine Perinatology: comparative aspects. Proceedings. Equine Vet J 30 (6), 455-466 PubMed.
- Rossdale P (1993) Clinical view of disturbances in the equine fetal maturation. Equine Vet J 14, 3-7 PubMed.
- Drummond W H (1988) Neonatal maladjustment syndrome, its relationship to perinatal hypoxic-ischemic insults. Equine Vet J Suppl 5, 41-43 Wiley Online Library.
Other sources of information
- Neurology Research Group (online) Instructions to Use the Madigan Foal Squeeze Method. School of Veterinary Medicine, University of California, Davis, USA. Website: https://compneuro.vetmed.ucdavis.edu (pdf download).
- Madigan J E (2014) Gumshoe Sleuthing in the World of Infectious Disease and Neonatology: Discoveries that Changed Equine and Human Health. In: Proc Am Assoc Equine Pract. pp 101-131.
- Bernard W V (2003) Jump-Starting the Dummy Foal (Neonatal Maladjustment Syndrome/Hypoxic Ischemic Encephalopathy). In: Proc 49th AAEP Convention. pp 8-12.
- Bain F T (1999) How I Treat Neonatal Maladjustment Syndrome. In: Proc NAVC. pp 73.