NEONATAL SYNDROMES

INTRODUCTION

In this section we have attempted to provide a useful overview of the major syndromes of the foal based upon the presenting signs. Included at various relevant points are descriptions of some of the major causes for these. This cannot possibly be definitive but provide at least some indication of the more common clinical entities.

One of the most important aspects of neonatal medicine is to establish whether a foal is suffering from a congenital (inherited or non-inherited) disorder or from an acquired disorder. Certain diseases are obviously in one or other category but others may be less easily categorized. For example, a newborn foal that has significant difficulty with swallowing may have a cleft palate or cleft soft palate or even a subepiglottic cyst. A foal that is dull from a few hours old may be affected by a septicemic disease acquired before or during birth.

A careful clinical examination is obligatory in every foal presented. The value of a prepared form for the recording of the findings cannot be overstated (see p. 476).

PREMATURITY AND DYSMATURITY

Most Thoroughbred or purebred mares have certified service dates and where this information is available the length of the gestation can usually be accurately calculated. Paddock or naturally bred mares are more difficult (or impossible) to predict and every effort should be made to identify dates of service by careful observation and recording of estrus behavior.

It is important to assess both the gestational age and the clinical appearance together as the normal gestational length is variable in the horse and foals may be obviously abnormal at full or even extended gestational age. This makes for very unpredictable results from induced parturition.¹ Generally an induced delivery should not be regarded as normal even when the induction is performed for purely elective reasons in a full term mare. A 365-day gestation can be normal in some horses whereas in others it is the result of persisting placental insufficiency and the results of the pregnancy are equally unpredictable. Although the terms ‘prematurity’ and ‘dysmaturity’ are applied to different circumstances relating to the duration of gestation, the clinical signs of the two states are for all practical purposes the same. These two ‘conditions’ can therefore be grouped together under the term ‘unreadiness for birth’.^2,³ Survival rates for premature or dysmature foals are lower than normal in spite of the extra effort that can be brought to bear. Premature foals (gestational age 300–320 days) have a 70–75% survival rate.⁴

The definitions of prematurity and dysmaturity are:

• Prematurity: a foal born prior to 320 days is classified as premature.

Note:

• The accepted limit of viability for foals is taken to be 300 days’ gestation. This has sometimes been exceeded.⁵ Placentitis may switch on the fetus prematurely and can be a good prognostic indicator.

• However, in general, the survival of any foal with a gestational age < 320 days has a poor chance of survival even in the best circumstances.

• Most very early foalings are best regarded as abortions.

• It is unwise to offer a better prognosis than is realistic.

• Dysmaturity: a foal born within the normal gestational range (320–345 days) but showing the signs normally associated with prematurity. These foals are often termed ‘immature’ or ‘unready for birth’ in that they are apparently have little ability to maintain body homeostasis and show slow adaptation to extrauterine conditions. Foals may even have a prolonged gestational age (> 350 days).

• For the most part, foals that do not establish normal righting reflexes and a normal suck reflex will die without intensive care.

• Those that show normal righting and a strong suck reflex will often progress satisfactorily until 24 hours and then will rapidly fade and die unless strong intervention is applied.

• If the foal can stand and suckle within 2–3 hours of birth the prognosis is better but such a foal may need intensive care if it is to survive normally.

• The detailed management of a dysmature or premature foal is described on pages 158 and 405.

These foals usually require critical care (see p. 409), supportive treatment and support of adrenocortical function. Nursing is critical; without this there is little or no point in simply administering drugs.

Specific therapy

If the foal’s adrenal gland appears unresponsive to the ACTH stimulation test then exogenous cortisol needs to be administered – a single dose of hydrocortisone should be given immediately (0.5 mg/kg i.v. or i.m.). Many clinicians continue corticosteroid therapy alongside the depot ACTH treatment (below). This therapy is controversial because (a) it has unknown efficacy, (b) it may have a negative feedback on the ACTH stimulated endogenous cortisol production and (c) any corticosteroid use has a risk of inducing gastric ulcers and immunosuppression. However, if the adrenal gland has been shown to be unresponsive to ACTH stimulation then it would appear logical that some exogenous corticosteroid administration is essential until adrenal function improves. In practice, the same regimen is used as that for treatment of cerebral oedema (see p. 166) is used for this purpose and has appeared helpful – dexamethasone given at a dose of 4 mg total dose/50 kg foal i.m. q 12 h, and maintained for several days. The dose should be tailed off.

Depot ACTH (Synacthen^® Depot, Tetracosactrin acetate, Alliance Pharmaceuticals, Wiltshire, UK; Cortrosyn^®, Organon Pharmaceutical, USA) is usually given at 0.4 mg total dose to a 50 kg foal i.m., then 0.2 mg total dose i.m. repeated at 6–12 h for up to 4 days.

Respiratory support: because the majority of premature foals develop some degree of pulmonary dysfunction, appropriate respiratory support is often critical, including:

• intranasal oxygen if hypoxemic (see p. 385)

• maintenance in sternal recumbency, regular turning from side to side and encouragement to stand

• the efficacy of artificial and natural surfactant products (used for hyaline membrane disease in human premature babies) is debatable and most of the products are restrictably expensive.

Colostral intake and monitor efficiency of absorption should be ensured. The gastrointestinal tract of the premature foal is often intolerant of oral feedings. However, the caloric requirements of the premature foal are probably great and, therefore, a combination of enteral and parenteral nutrition is usually required (see p. 427). In addition, the premature foal often has incomplete skeletal ossification and, although no specific data exist, it may be wise to supplement premature foals with calcium and phosphorus (e.g. FoalAide, Equine Buckeye Nutrition, Baileys Horse Feeds, W. Yorks, UK).

Antibiotics are very important either prophylactically or to treat existing infection. Every effort to identify the bacteria responsible must be made, by cultures of blood, tracheal aspirates, intravenous catheter tips, etc. For guidelines on antibiotic choice see page 193. It is best to have a completely normal WBC count and differential and plasma fibrinogen/ serum amyloid A level before discontinuing antibiotics. It is not unusual for hematology to remain abnormal for as long as 2 to 4 weeks. Closely monitor the foal for nosocomial infections. If a fever spike is noted, if the WBC count changes dramatically, or if there is clinical deterioration, additional bacterial cultures are warranted and a change in antibiotic therapy may be necessary.

Management of limb deformities is discussed on page 289. Exercise must be limited if hypoplasia of the carpal or tarsal bones is present.

Supportive treatment

Maintain warm environment: blankets, lamps, heating pads, etc. Give general nursing care (see p. 411).

Note: Non-surviving premature foals commonly follow a more-or-less predictable course:

• Usually a deceptively satisfactory first 18 hours, with some improvement.

• Decline in awareness and convulsions commonly develop.

• Poor suckle and seeking reflexes and loss of dam recognition.

• Increasing respiratory acidosis and increased respiratory effort.

• Abdominal distention and failure of gastric emptying (possible spontaneous gastric reflux).

• Pulse quality deteriorating and reduced urine output.

• Death at 48–72 hours of age.

Prognosis

This tends to be poor and frequently foals develop secondary complications such as sepsis or longer-term developmental bone disease (see p. 197). These foals often do well for 24–48 hours and then fade, and respiratory maturation is often a crucial factor such that atelectasis is often limiting.

No single parameter should be used to obtain a prognosis – rather the whole range should be employed and those with several ‘unfavorable’ signs are usually in need of intensive care and may need to be moved to a hospital situation (see Table 6.1).

Table 6.1

Prognostic indicators for prematurity and dysmaturity ^a

Parameter	Favorable	Unfavorable
Placenta	Normal, placentitis^b	Chronic changes e.g. villous atrophy
Delivery	Normal, spontaneous, unassisted	Induced parturition, dystocia
Mare’s health	Normal	Colic, surgery, endotoxemia, aged
Foal’s neurological status (at 24 h)	Normal	Poor suckle reflex, deteriorating awareness, seizures
Leukocyte count (× 10⁹/L)	5.0 – rising	< 5.0 persistently
Neutrophil:lymphocyte ratio	≥ 2	< 2 persistently
Plasma fibrinogen (g/L) at birth	> 4	1–3
Blood pH	> 7.3	< 7.3 persistently
Plasma cortisol (ng/mL)	> 120	< 30
Response to aqueous ACTH (0.125 mg i.v. or i.m.)	Widening of N:L ratio, threefold increase in plasma cortisol	No/little change in either N:L ratio or plasma cortisol

^a After Koterba 1990.⁸

^b Note that placentitis can be seen as a favorable parameter because several studies^5,9 have now shown that placentitis may switch on the fetal adrenal gland prematurely allowing sufficient cortisol production for extrauterine survival of these premature foals.

Prevention

In order to limit the potentially devastating effects of premature delivery it is important to attempt to prevent it developing in the first place. By far the best method of prevention of prematurity is obviously to prevent early delivery, but this is far easier to say than to do!

Avoid induction of parturition unless necessary, as readiness for birth may be difficult to predict.

Measures that result in a reduction in placental insufficiency will result in an improved chance of a normal gestation and a normal foal. However, it is important to balance the threat of a deteriorating placental environment with the risks of early delivery. Repeated careful prenatal assessment of the foal by combinations of ultrasonographic, electrocardiographic and clinical assessment (of fetal movement and size) can be helpful (see p. 25). It is probably a sensible precaution to make these assessments in all high risk mares. An abnormal placenta can sometimes be detected with transabdominal ultrasonographic examination.¹⁰ Other aspects of the fetus that are suggestive of fetal stress include the heart rate and size, fetal movement and the volume and character of the allantoic fluid.

Various treatments have been described to prevent impending abortion, for example tocolytic drugs to delay parturition (Clenbuterol, Ventipulmin^®, Boehringer Ingelheim Ltd., Berks, UK), progesterone therapy of the mare (Regumate^®, Intervet Ltd., Bucks, UK) and ACTH (Depot ACTH (Synacthen^® Depot, Tetracosactrin acetate, Alliance Pharmaceuticals, Wiltshire, UK; Cortrosyn^®, Organon Pharmaceutical, USA)) to encourage fetal maturation.

SEIZURES, WEAKNESS AND ABNORMAL BEHAVIOR

Abnormal behavior patterns are an important aspect of neonatal clinical medicine. The signs may range from subtle changes in behavior such as a loss of maternal affinity, abnormal postures and reduced suckle reflexes to the more dramatic signs of obvious depression, weakness (myasthenia) aimless wandering and seizures. Neurologic disease can produce these signs in combination or individually but it is also possible that some of them can be encountered in foals without neurological conditions. Weakness and depression in the neonate have many causes and the signs associated with abnormal behavior can be primary (due to neurological disease) or secondary (due to disease of other body systems in which there are neurological effects). The differentiation of definite neurological disease and the effects of some metabolic disturbances such as hypoglycemia and electrolyte disturbances can be difficult. Severe liver failure and azotemia can, for example, cause secondary neurological signs; simply managing the obvious signs may not help to solve the underlying problem. Critically ill foals are very often depressed, weak, recumbent and may show abnormal behavior and the first objective of the clinician is to establish whether the neurological signs are the result of primary neurological disease or secondary to another disease.

Young foals have an inherently low seizure threshold ¹¹ and premature and dysmature foals have a high tendency to seizures.¹² A single seizure should not be taken necessarily to indicate serious disease or a longer-term problem. Seizures are much more commonly secondary to other disorders. Septic foals, maladjusted foals and those affected by neonatal hypoxia–ischemia syndrome or intracranial traumas also have an increased tendency to seizures.

The particular difficulties of a detailed clinical examination of foals make it essential that a meticulous clinical and a specific neurological examination are performed (see p. 476). It is frequently necessary to perform sequential examinations to establish progression of signs and in some cases the subtle signs may become more obvious on a second occasion. The interval between examinations needs to be relatively short and repeated clinical assessments at 1–2-hour intervals can be a valuable help. Undue delays between the examinations can, however, be catastrophic because some conditions will change rapidly. Supportive tests including hematology and biochemistry are invariably required. Most clinicians will always perform a blood culture in aerobic and anaerobic conditions. Analysis of cerebrospinal fluid is useful but collection is problematical and so this is seldom performed outside specialized hospital conditions (see p. 387).

Etiology

Abnormal behavior patterns include variations of one or more of the following:

1. Seizures: a seizure (convulsion, fit or ictus) is an abnormal behavioral manifestation of abnormal electrical activity in the forebrain that result in involuntary, spontaneous, paroxysmal muscular activity and varying degrees of unconsciousness.

2. Depression: this signifies involvement of the forebrain. Mentation and demeanor are the main features to use in diagnosis. Conditions may be primary or secondary.

3. Recumbency: this may be a result of musculoskeletal problems but if the foal has no orthopedic reason to be recumbent then weakness is usually the cause. Weakness has a number of neurological and metabolic causes. For example a hypoglycemic foal or a profoundly anemic foal will be very weak and will become tired rapidly. Usually a weak foal can stand, but only for a short time, and its exercise tolerance is very limited.

4. Collapse (syncope).

5. Loss of awareness (usually first manifested as loss of maternal recognition or off-suck).

6. Blindness.

Abnormal behavior that is present from birth can be due to congenital conditions (see p. 131) but a larger proportion is the result of potentially critical acquired disease. Birth asphyxia syndrome, infections and trauma are probably the commonest causes of abnormal behavior in newborn foals. A significant number of foals have signs that are either neurological or resemble neurological disease but recover spontaneously. These may be associated with adaptive changes or be due to immaturity of development. For example, some foals are born blind but vision becomes normal within a few hours of birth. The attendant may not even notice that there was anything ‘wrong’ at birth.

Diagnosis

The neurological examination of the foal carries special problems. Details of a suitable protocol are shown in Figure 6.2. The value of a full and thorough examination cannot be overstated. In the assessment of any neurological disease the ‘time versus sign’ graph is a useful aid to both the prognosis and the assessment of therapy. This graph represents the change in the severity of a particular sign (or the combination of signs if a syndrome is being assessed) with advancing time; its use depends heavily on the repeated critical and detailed neurological examination and to this end a prepared form can be a significant advantage (see p. 483).¹³