Dr Karin Kruger, BVSc, MSc, DACVIM
Equine Specialist Physician
7 Nov 2015
Timing is Everything
Neonatal medicine can be extremely rewarding (although incredibly time consuming) if a diagnosis is made and appropriate treatments given timeously. In order to identify abnormalities as soon as possible, all valuable equine births should be observed by a competent person.
A normal foal will be born within 20 min of onset of stage 2 labour, stand within an hour and nurse within 2 hours.
The placenta should also be passed in its entirety by 3 hours. If the foal is not born within 30 min, immediate assistance must be given to save the foal’s life. If a foal does not stand on its own by 2 hours, or nurse by 3 hours veterinary intervention is indicated.
Valuable foals should be examined by a competent veterinarian at 12-24 hours of age. The mare can be checked at the same time for foaling injuries. Blood should be taken for determination of IgG, and a complete blood count and serum biochemistry performed if any abnormalities are detected.
Important history questions include:
• Is the mare uni/multiparous?
• Were there any complications, illnesses or medications used during pregnancy?
• Did the mare have any complications with previous foals?
• Did the udder develop prematurely, does she eat fescue grass?
• How long was the birthing process?
• How long until the foal stood, nursed, passed meconium and urinated?
• Was an IgG checked, the navel dipped and a 24h exam performed by a vet?
• Did they attempt to bottle feed and how?
• Treatments given by owners
• Onset of clinical signs
• Last time foal was seen standing and nursing
Physical examination of the neonate
Vital parameters can change dramatically over the first 24 hours of a foal’s life (see table below).
Heart Rate (beats/ min)
Respiratory Rate (breaths/min)
Body Temp (C)
Arrhythmias (APC, Afib, Vtach) can be normal in the first 15 min. of life. A continuous murmur is auscultated over the left heart base for the first 4-7 days until the ductus arteriosus closes. Variable systolic flow murmurs can also be heard under one week of age. On thoracic auscultation, end-expiratory crackles can often be heard in the dependent lung, but should resolve within a few minutes of standing.
Changes in the rate, effort or pattern of respiration can be more useful to detect abnormalities than auscultable changes. A foal should have an effective suck reflex within 10 min and should be able to sit in sternal without assistance. At 20 minutes, it should attempt to rise.
Mucous membranes should be light pink with a CRT <2 sec. Peripheral pulses should be strong and the distal extremities warm. It is important to note that cyanosis will only be seen in the mucous membranes once the PaO2 is <35-40 mm Hg and then only if the haematocrit is normal. Tissue damage will start once PaO2 drops below 60 mm Hg.
Due to central respiratory suppression, a foal with hypoxaemia may not have any changes in the respiratory rate or effort and therefore arterial blood gas analysis may be the only way to detect hypoxaemia.
Foals’ eyes tend to have slightly rounder pupils and slight, symmetrical ventromedial deviation is normal up until one month of age. They have decreased corneal sensitivity and are prone to entropion, which leads to ulceration if undetected. Fibrin in the anterior chamber or hypopyon may indicate in-utero bacterial exposure or sepsis.
A healthy, term foal is born with a mature small intestine, while large intestinal development continues after birth. Premature or dysmature foals may not have adequate intestinal function to sustain life and may require intensive intervention. The abdomen should be evaluated for intestinal borborygmi and the presence of umbilical, scrotal or inguinal hernias. Any passage of meconium should be evaluated.
A foal will urinate for the first time by 8-12 hours of age and frequently thereafter. Stranguria, decreased or delayed urination may indicate a ruptured bladder. Foal urine should be hyposthenuric (SG<1.008). Normal foals urinate, suckle and sleep frequently (at least hourly, but up to 7 times per hour).
The umbilicus can be palpated with a gloved hand and should be dipped regularly in an appropriate disinfectant until completely dry. The majority of the umbilical structures are however internal and it is not uncommon to find a severe internal umbilical infection with no external abnormalities. Ultrasound of the internal umbilical structures will detect any infections and abnormalities and should be performed in all critically ill foals.
The musculoskeletal system should be evaluated for congenital abnormalities such as cleft palate, brachygnathism, limb or tendon abnormalities, etc. In premature or dysmature foals, limbs should be radiographed to determine if cuboidal bones are completely ossified. The presence of fractured ribs and ruptured tendons should be noted. All joints should be palpated for heat or effusion that may be associated with sepsis.
Neurologically, foals have intact cranial nerve responses at birth. Withdrawal reflexes are present, but the menace response may be absent for several weeks. The gait is hypermetric, and a base wide stance normal. Foals also tend to have exaggerated responses to external stimuli.
Any abnormalities noted at birth may indicate in-utero acquired sepsis, neonatal maladjustment (dummy foal) or that the foal is premature or dysmature. Bradycardia is often associated with hypoglycaemia, hypothermia, hyperkalaemia, or tissue hypoxia. Decreased, absent or abnormal breathing (apneustic) is most commonly the result of central respiratory depression, and less commonly hypoglycaemia, hypothermia and prematurity. Additional diagnostic test may be warranted in at risk foals, or foals with abnormal physical examinations. These may include:
complete blood count, serum biochemistry and arterial blood gas analysis for detection of infection, organ dysfunction, integrity of pulmonary gas exchange and acid-base status
• urine SG and glucose monitoring
• blood cultures (3 different sites, 30 min apart)
• indirect blood pressure
• thoracic/abdominal ultrasound: assess organs, rib fractures, umbilicus
• radiography: fractures, thoracic, physes, NG tube placement, cuboidal bones
• MRI: congenital malformations, bony trauma, soft tissue or vascular disruption
In dealing with neonates, I live by two mantras:
1. Timing is everything
2. Any sick neonate is septic until proven otherwise
Prematurity / Dysmaturity
The normal gestation period for a mare is approximately 340 days. Foals are termed premature if they are born at <320 days gestation. Intrauterine growth retardation can however lead to foals with signs of prematurity after normal gestation periods. Overdue foals (>360 days) may also show similar abnormalities. Premature foals tend to have domed foreheads, sleek hair coats (or no hair depending on how early they are) and floppy ears.
They are weak, unable to regulate their body temperature and therefore at great risk of developing failure of passive transfer. They have lax tendons, increased range of joint motion and may have incompletely ossified carpal and tarsal bones. These cartilaginous bones can be crushed if foals are not supported and if exercise is not restricted, leading to permanent orthopaedic disease.
Lax tendons usually correct with time and controlled exercise. Light wraps can be applied to protect the skin if the foal is walking on its fetlocks. Heel extensions can be applied to assist the foal in standing on the solar surface of the hoof. Foals that are not strong enough to suckle unassisted should ideally be referred for intensive care.
It used to be thought that ‘dummy foals’ were the result of hypoxia during late gestation and birth. While a foal that experienced significant hypoxia during birth (e.g. dystocia) may have neurological deficits requiring treatment, it has now been proven that the classical ‘dummy’foal’ syndrome is caused by the presence of neuroactive progestogens that are not present in normal foals. Maladjusted foals can appear normal at birth and develop clinical signs at any time until 48 hours of age.
They have a lack of affinity for the dam and lose the suck reflex. These foals can be found aimlessly wandering around the stable. Without intensive care, failure of passive transfer, hypoglycaemia, hypothermia, hypoxia and sepsis may develop. This syndrome can frequently be reversed using the Madigan foal squeeze, but care must be taken to also treat any of the abovementioned complications.
Failure of Passive Transfer
Foals are born with a naïve immune system and derive all immunoglobulins from colostrum. If colostral transfer of immunity is inadequate, the foal will be at risk for developing sepsis. For this reason, immunoglobulins should be tested in all valuable foals between 12 and 24 hours of age and additional colostrum or plasma given (20ml/kg) if IgG <800 mg/dL.
Any sick foal is septic until proven otherwise. The diagnosis can be confirmed by blood culture, complete blood count and serum amyloid A or fibrinogen detection. After taking 3 samples for blood culture, I usually start my septic or at risk foals on ceftiofur sodium (5mg/kg BID IV/IM) until culture results are available. Any foal who is not suckling on its own should be referred for intensive care. Internal umbilical infections are common and can lead to septic arthritis if not treated with the appropriate antibiotic until resolution or surgical excision. Septic arthritis must be treated immediately if there is to be any athletic future for the horse.
The most common cause of colic in the early neonatal period in an otherwise healthy foal is meconium impaction. Foals assume a typical straining posture. Diagnosis can be confirmed using a gloved, lubricated little finger or an abdominal radiograph. Initial treatment consists of infusing 150-200ml warm soapy water through a lubricated foley catheter using gravity. If this is unsuccessful, a retention enema can be performed over 45 min. with 180 ml of the following solution (via gravity): 8g N-acetyl-L-cysteine, 1.5 tsp baking soda (22.5g), 200ml water
Intravenous and oral fluids may be used to keep foals well hydrated and assist in stool softening and analgesia should be administered as needed. I typically use small doses of flunixin meglumine (0.5- 1mg/kg) or buscopan. Refractory cases may require surgical intervention.
Neonatal isoerythrolysis occurs when the mare is exposed to a foreign red blood cell antigen during pregnancy. She then develops antibodies against this antigen, which attacks the foal’s red blood cells when transferred through colostrum. Foals are normal at birth and then develop the disease after ingesting colostrum within hours to days after birth.
Due to intravascular and extravascular haemolysis, foals become pale and icteric. They usually have haemoglobinaemia and haemoglobinuria, anaemia and can develop pigment nephrosis, colic, melaena and kernicterus. Differential diagnoses include sepsis, hepatic disease, piroplasmosis, and herpes virus.
Blood transfusions should be given using a universal donor or the mare’s washed red blood cells if the foal’s PCV is dropping rapidly and reaches 15%, or if it decreases to below 12%. The foal should be provided with ‘safe’ colostrum, and muzzled and fed a milk replacer until the gut barrier has closed. Multiple blood transfusions increases the risk of liver failure due to iron overload.
Birth or subsequent trauma can result in a ruptured bladder, urachus, or any other part of the urinary system. Foals develop severe systemic compromise within 24-36 hours of rupture. They are lethargic, have abdominal distention, stranguria and difficulty breathing.
Blood tests reveal azotaemia, hyperkalemia, hyponatremia and hypochloremia. Since many of these foals have concurrent sepsis, IgG and blood culture are often indicated.
A large amount of hypoechoic fluid on ultrasound and abdominocentesis will confirm the diagnosis. Since these foals are metabolically unstable, emergency treatment is indicated until the foal can be stabilized and the bladder repaired surgically. Intravenous fluids should not contain potassium (use 0.9% saline).
Intravenous glucose, bicarbonate and insulin can be used to decrease potassium and prevent fatal arrhythmias. Calcium is also cardioprotective in hyperkalemia. Urine can be drained from the abdomen using a sterile teat cannula or abdominal drain. Antimicrobials should be given to prevent and treat sepsis.
Flexural deformity of the carpus, fetlock or coffin joints may be congenital or acquired. Radiographs should be performed to determine whether there are any underlying bone abnormalities and concurrent problems such as ruptured extensor tendons ruled out. Early treatment is imperative and is accomplished through controlled exercise, bandaging with or without splints and intravenous oxytetracycline (44 mg/kg in 1L SLOW IV).
Toe extensions may assist in straightening fetlock and coffin joint contractures, but surgery needs to be performed timeously in refractory cases.
Angular Limb Deformity
Fully weight bearing dorso-palmar (plantar) radiographs should be taken to determine the pivot point. The practitioner must determine whether all bones are normal (crushed cuboidal bones?) and whether ligament laxity contributes to the angular limb deformity. For true angular limb deformity, the more distal the pivot point, the more rapid surgical interventions should be.