Physical Appearance and Bodyweight

The degree of physical maturity should be considered in relation to the estimated gestational age. This assessment should be made in light of the variable gestational length in horses. Typically, gestational length is calculated from the time of insemination through birth, which overestimates the true gestational period by as much as 7 days. The mean gestational period in thoroughbreds is approximately 340 to 342 days, with 95% of mares foaling at 327 to 357 days.¹² There are a number of factors that influence this period, including breed, gender, and the time of year. Colts on average have a gestational length that is approximately 1.5 to 2.5 days longer than that of fillies. They also are slightly heavier, are slower to stand, and have a heavier placenta.¹³ Mares that develop a pregnancy early in the breeding season have longer pregnancies than those that conceive late in the season. This can affect gestational length by as much as 10 days.^12,14 In some but not all breeds it has been suggested that dam, sire, and dam’s sire play a role in determining gestational period.¹⁵ Physical characteristics of immaturity include low birthweight, small body size, short and shiny hair coat, doming of the head, periarticular laxity, and droopy ears. Foals with a shortened gestational period and signs of physical immaturity are termed premature, whereas foals that are physically immature in the face of an appropriate gestational length are termed dysmature. Foals born after 356 days should be regarded as postterm. Such foals are distinguished from foals that are postmature, a condition of increased morbidity as a consequence of failing placental function.¹⁵ Postmature foals tend to have a lean and lanky physical appearance. Numerous factors influence a foal’s body weight at birth including breed, gender, gestational age, and intrauterine environment. Estimates of body weight for newborn thoroughbred foals for the purpose of drug calculation range between 40 and 55 kg, although many healthy foals may well exceed this range.

Foal Behavior

Normal foals achieve sternal recumbency with a raised head within minutes of birth. They also should be highly responsive to a range of tactile, visual, and auditory stimuli within 5 minutes of delivery.¹⁶ Attempts to rise should begin within 30 minutes. Initial attempts may be unsuccessful, but most foals are standing with control by 1 hour of age (mean 57 minutes; range 15 to 165 minutes).¹⁷ Initially the stance is characteristically wide-based, with moderate truncal swaying both forward and backward and from side to side. The suck reflex should be present within minutes of birth and should be vigorous by 30 minutes. After a period of adjustment the normal foal will eventually discover the mare’s udder and begin sucking. This is typically achieved before 2 hours (mean 111 minutes; range 35 to 420 minutes); most foals have sucked twice by 2½ hours of age. Sucking periods vary in duration between 1 and 5 minutes and are interspersed with periods of sleep that last approximately 7 minutes. A foal that spends long periods at the udder may not be getting an adequate intake of milk.

It is important to watch the foal during sucking to confirm appropriate teat contact and swallowing movements. The foal should also be observed after sucking for evidence of nasal regurgitation of milk. The normal neonatal foal spends approximately one third of its life recumbent; this is in contrast to the adult horse, which spends 5% to 10% of a 24-hour period in recumbency. An important part of the physical examination is assessment of the foal’s attitude. Normal foals are bright, alert, and very responsive to environmental stimuli. They should be curious and demonstrate frisky play at as early as 2 hours of age. Galloping can be observed by as early as 6 to 7 hours of age. Normal parameters for the foal are listed in Tables 17-1 to 17-3.

Table 17-1 Normal Physical Examination Parameters of the Neonatal Foal and Calf

Table 17-2 Normal Hematology Reference Values for Neonatal Foals

Table 17-3 Normal Serum Biochemical Reference Values for Normal-Term Postnursing Foals

AST, Aspartate aminotransferase (SGOT); BUN, blood urea nitrogen; GGT, γ-glutamyltransferase; LDH, lactate dehydrogenase; SDH, sorbitol dehydrogenase.

Recommendations to clients as to when veterinary intervention should be sought vary from practice to practice. The “1-2-3” rule is often quoted: the foal should be standing by 1 hour after birth, the foal should have sucked by 2 hours, and the placenta should be cleared by 3 hours. Some have translated this into a “2-4-6” rule for clients: seek veterinary attention if the foal has not stood by 2 hours, the foal has not sucked by 4 hours, or the placenta has not been clearedby 6 hours. These recommendations are used only as a rough guide and will obviously be influenced by peripartum conditions and client experience.

A potentially critical consequence to a delay in the onset of feeding is failure of passive transfer of maternal immunoglobulin. Foals should be supplemented with 20 mL/kg of good-quality colostrum by bottle or tube ideally before 6 hours of age. Measurement of serum immunoglobulin G (IgG) should be made between 12 and 18 hours of age. A normal foal that has consumed adequate amounts of colostrum will have a serum IgG measurement substantially greater than 800 mg/dL. Failure of passive transfer is generally defined as a serum IgG less than 400 mg/dL; partial failure of passive transfer is used when the serum IgG is between 400 and 800 mg/dL. Many authors have identified an association between low serum IgG and morbidity and mortality, most commonly caused by sepsis. Tetanus prophylaxis, in the form of antitoxin (1500 IU), should be administered to foals with untreated failure of passive transfer.

A modified Apgar score has been used in foals to semiquantitate the severity of signs that occur in response to peripartum asphyxia (Table 17-4).¹⁸ In human neonatal practice the acronym stands for activity, pulse, grimace, appearance, and respiration. The modification used in equine practice refers to appearance, pulse, grimace, attitude, and respiration. Appearance refers to oral mucous membrane color; pulse is self-explanatory and uses 60 beats per minute (bpm) as a cutoff; grimace is assessed in response to stimulation of the nasal mucosa, the inside of the pinnae, and the region over the thoracolumbar area adjacent to the spine; attitude reflects the degree of muscle tone; and respiration refers to ventilation rate and rhythm, with 30 breaths per minute as the cutoff. Each category is scored from 0 to 2 points, with a score of 10 being optimal. A score of 0 to 3 indicates marked depression; 4 to 6, moderate depression; and 7 to 8, mild asphyxial injury. Normal foals have a score of 9 or 10. Ideally the modified Apgar calculation should be made within the first minute after birth, but certainly within 15 minutes of delivery. Repeating the score 4 minutes later is recommended. Foals with low scores typically require aggressive resuscitation, whereas mildly affected foals may respond to vigorous rubbing, stimulation of the nasal mucosa, and limb movement.

Table 17-4 Apgar Score: Assessment of Neonatal Asphyxia¹⁹

Maternal Behavior

Any intervention should be made in consideration of the impact it may have on the relationship between the mare and the foal. Maternal behavior toward the foal is instinctive and can be modified or disturbed through excessive veterinary intervention. Maternal recognition is largely dependent on smell, and treatments may alter foal odor, thereby interfering with the normal bonding process. Separation of foal and mare may be unavoidable if necessary treatments are to be provided; however, maintenance of an environment in which the mare has continual access to her foal with respect to sight and smell is ideal. It is important to distinguish refusal to suck from true rejection; the latter commonly involves aggression toward the foal. Mares may be reluctant to allow the foal to suck if they are experiencing pain from udder edema, pelvic or perineal disease, or primary gastrointestinal problems. In addition, uterine contractions associated with passage of the fetal membranes may also cause transient discomfort in the mare. Management is dependent on recognition and treatment of the underlying problem. This may include provision of analgesia, local therapy of the udder (heat therapy, massage), and oxytocin (10 to 15 IU given intramuscularly [IM]) to facilitate milk letdown. Tranquilization with acepromazine may also be helpful.

Maiden mares commonly, and multiparous mares occasionally, demonstrate signs of confusion, fear, and anxiety with the arrival of a newborn foal. This usually results in sudden movement of the hindquarters away from the foal as it attempts to find the udder, mare squealing, and heightened sensitivity. Mares may attempt to bite or kick the foal if they are unable to escape. This is accentuated by placement into a busy or noisy environment, typical of many veterinary practices in spring. The most successful approach to managing anxious mares is through a combination of a low-stress environment, tranquilization, and patience. It is important to avoid threatening verbal or physical punishment, as this only heightens the mare’s anxiety. The use of a grazing muzzle or hobbles may be needed to reduce the risk to the foal from kicking or biting.

Risk factors for foal rejection include first birth, a history of previous rejection, disruption to the environment (e.g., forced separation, noise), and breed.^20,21 Rejection may occur more often in Arabian mares and more commonly within certain family lines within the breed.²¹

Body Temperature

Rectal temperature in foals reportedly ranges from 99° F to 102° F (37.2° C to 38.9° C) during the first 4 days after birth.¹⁷ The upper end of the normal range, which is approximately 1° F (0.6° C) above the upper end of the adult range, is strongly influenced by environment and exercise. Temperature can be variable in foals with systemic sepsis; in the early stages of sepsis the rectal temperature is commonly within the normal range or mildly elevated. Foals in septic shock usually have a low rectal temperature, and those with localized infection often are febrile.

Cardiovascular System

Physical assessment of the cardiovascular system includes examination of visible mucous membranes, palpation of peripheral arterial pulses, assessment of extremities for warmth, detection of limb or ventral edema, and cardiac auscultation. In the foal, preferred sites for subjective assessment of pulse rate, regularity, and strength include the dorsal metatarsal artery, the brachial artery, and the carotid artery. The dorsal metatarsal artery is easily palpated in healthy foals on the lateral aspect of the third metatarsal bone. The brachial artery is palpated at the level of the medial collateral ligament of the elbow joint. Reduced pulse pressure can be caused by a range of diseases including systemic sepsis, perinatal asphyxia, and prematurity. Indirect blood pressure monitoring is most commonly performed using an automated oscillometric device with a cuff positioned around the base of the tail or over the dorsal metatarsal artery.²² These devices reasonably reflect direct pressure measurements when used carefully with several repetitions. There are important limitations of indirect or direct blood pressure measurement in overall assessment of the cardiovascular system. In healthy foals the correlation between arterial blood pressure and cardiac output, one of the best available parameters to assess circulatory function, is acceptable but decreases significantly when there is altered systemic vascular resistance—a circumstance that is likely common to several common diseases. Recent descriptions of noninvasive methods to measure cardiac output, such as volumetric echocardiography, have shown good correlation with more robust but invasive techniques in anesthetized foals. The question remains if this correlation will be sustained in critically ill foals.

Cardiac auscultation is an important part of the physical examination of the newborn foal. This should include auscultation of both the left and right hemithorax. The heart rate can be highly variable in neonates and is dependent on age. Immediately after delivery the rate is around 60 bpm (range of 40 to 80 bpm), and it increases over the first several hours of life to approximately 120 bpm. This should stabilize to within a range of 80 to 100 bpm during the first week. Increases associated with activity and excitement should be expected. Cardiac arrhythmias occur commonly during the first hour after birth in apparently healthy neonatal foals; most arrhythmias are restricted to the initial 15 minutes of postpartum life. These include atrial premature contractions, paroxysmal atrial fibrillation, atrioventricular block, ventricular premature contractions, and ventricular tachycardia.^23-25 Most are attributable to hypoxia and high vagal tone. Cardiac arrhythmias after an hour of age should be considered abnormal.

Cardiac murmurs are also commonly auscultated in foals during the early neonatal period. The vast majority are localized to the left heart base and are considered to be physiologic rather than pathologic. The presence of a continuous murmur is consistent with patency of the ductus arteriosus. In most foals the systolic component of the murmur is louder and therefore more obvious than the diastolic component. The murmurs are therefore often described as holosystolic, with a point of maximal intensity on the left hemithorax, in the third intercostal space, and at the level of the scapulohumeral joint. Audible continuous murmurs are unlikely to persist for more than 3 days; however, the systolic component of the altered flow may linger for a week or longer in normal animals. It is commonly believed that many neonatal systolic murmurs with a point of maximum intensity over the left outflow tract may be a result of left ventricular ejection rather than flow through the ductus arteriosus. This would be similar to physiologic flow murmurs commonly heard in young adult horses. There are a number of observations that should prompt referral for echocardiographic assessment. These include persistence of any loud murmur, particularly if it is radiating or associated with a precordial thrill, and any signs of cardiac disease including weakness, cyanosis, pulmonary edema, ascites, or unexplained dependent edema. Bacterial endocarditis is rare in the neonate but certainly in older foals should be considered if the cardiac murmur is associated with fever, leukocytosis, and hyperfibrinogenemia. Many congenital heart defects have been reported in foals, with a wide variation in clinical signs and age of presentation. The most common congenital heart abnormality is a ventricular septal defect. Myocardial dysfunction has been reported in association with systemic sepsis in foals. Cardiac troponin I (cTnI) and the cardiac isoenzyme of creatine kinase (CKMB) are both elevated in foals with sepsis, although the elevation does not accurately predict survival.²⁶

Respiratory Tract

The respiratory rate, rhythm, and depth should be assessed as part of the physical examination of the neonate. The respiratory rate and tidal volume are markedly increased during the first 60 minutes of postnatal life. Rates approaching 80 breaths per minute are not uncommon during this time, after which there should be a steady decrease to approximately 30. Respiratory rhythm will vary with the level of consciousness. In foals with hypoxic-ischemic brain disease, periodic breathing patterns are common, including Cheyne-Stokes and erratic rhythms that may include lengthy apneic pauses, occasionally exceeding 30 seconds. Cheyne-Stokes respiration refers to periods of apnea and hypopnea that alternate with periods of hyperventilation. Both respiratory frequency and tidal volume are affected.²⁷ It is possible that periodic breathing may contribute to the pathology associated with the syndrome. Auscultation of the respiratory tract is an essential part of the examination but can be misleading. Moist rales are normally present throughout the respiratory cycle after birth because of residual fluid within the airways. Asymmetry of air movement and end-inspiratory crackles are also normal findings as a result of simple atelectasis of the dependent lung during lateral recumbency. These typically resolve within minutes of standing. Conversely, foals can have significant lung disease yet few abnormal findings on thoracic auscultation. Added to this problem is the absence of cough and nasal discharge in many neonates during the early phases of lower airway disease.

Thoracic trauma and rib fracture can occur as a complication of second-stage labor. Costochondral dislocation can occur in as many as 20% of births. Fractures of the rib shaft occur far less commonly and can on rare occasions cause significant clinical disease and death. This can include hemothorax, lung laceration and pneumothorax, and pericardial and myocardial puncture. Diagnosis is by observation of thoracic wall symmetry and synchrony, palpation, and imaging (ultrasound or radiography). Management is typically conservative unless displacement of shaft fragments is identified over key underlying structures.

Oral Cavity and Nasal Passages

Oral mucous membranes should be assessed for color, moisture, and refill time. Normal foals have membranes that are moist, are pale pink, and have a capillary refill time (CRT) of approximately 1.5 to 2 seconds. Given the importance of the intestinal system in the genesis of neonatal sepsis, it is recommended that the veterinarian have clean hands, or preferably be gloved, during this part of the overall examination. In the initial stages of systemic sepsis the membranes develop a bright red color with a brisk CRT. This is usually accompanied by episcleral congestion and reddening of the coronary bands. As septic shock ensues, the membranes darken and the refill time becomes prolonged. The presence of mucosal hemorrhages is most consistent with disseminated intravascular coagulation (DIC) associated with advanced systemic sepsis. A rare cause of mucosal petechial hemorrhages is neonatal alloimmune thrombocytopenia. Affected foals may demonstrate prolonged bleeding after routine venipuncture. A subset of affected animals may also have oral and lingual vesicles and ulcers and widespread ulcerative dermatitis with crusting. These foals are typically weak and are reluctant to suck from the dam because of oral pain. The condition appears to be self-limiting and resolves within 2 weeks, presumably because of removal of alloantibodies. Icterus of the oral mucous membranes can occur in association with bacterial or viral sepsis, as a consequence to hemolysis (as in neonatal isoerythrolysis or certain clostridial infections), or as a benign process, idiopathic neonatal hyperbilirubinemia. In hemolytic diseases of the newborn the yellow discoloration of the membranes is often superimposed on pale membranes. Blue or blue-gray discoloration of the membranes can occur with severe hypoxemia or circulatory collapse. Cyanosis can result from pulmonary or cardiac causes. The nasal passages should be examined for fluid or discharge. The presence of orange to brown fluid at the nares immediately after birth is consistent with meconium aspiration. Passage of meconium into the amniotic sac indicates prepartum stress.

Dental problems are uncommon in newborn foals with the exception of problems associated with facial deformities, such as maxillary prognathism, mandibular prognathism, and campylorrhinus. The central incisors usually erupt during the first 5 to 7 days of life. The middle incisors rise between 4 and 6 weeks of age, but the corner incisors do not erupt until 6 to 9 months. In miniature horses and ponies the eruption of the middle and corner incisors is delayed at 4 months and 12 to 18 months, respectively. The 12 temporary molars are present at birth or erupt within the first week of life. Maxillary prognathism or parrot mouth describes the condition in which the mandible is shorter than the maxilla, producing an overjet or overbite. The condition may affect the incisors, check teeth, or both. It is the most common congenital oral malformation of foals. The incidence has been reported to be 2% to 5%. Severe manifestations of the condition often coexist with other developmental abnormalities. A genetic basis is suspected (simple autosomal recessive) but has not been definitively established. Mandibular prognathism or sow mouth describes the condition in which the maxilla is shorter than the mandible, producing an underbite. It occurs less commonly than the maxillary equivalent. Campylorrhinus (wry nose, wry face) describes the condition in which the premaxilla and nasal septum are deviated laterally. The condition may occur singularly or in combination with other deformities, such as wry neck, cleft palate, and maxillary or mandibular prognathism. If the deviation is severe, the foal may have great difficulty in sucking from the mare. There may also be problems with breathing. However, in most foals the deviation is mild and represents a simple but obvious cosmetic defect. As with other facial deformities a heritable basis is possible; therefore breeding is not recommended. Cleft palate is an uncommon congenital defect of foals that results from incomplete fusion of the lip and/or secondary palate during the early gestational period. It has an estimated incidence of 0.1% to 0.2% of all births. Almost all clefts occur in the secondary palate, the horizontal partition dividing oral and nasal cavities. The secondary palate includes all of the soft palate and most of the hard palate, with the majority of the defects restricted to the soft palate. The basis of this congenital defect is not known but could include a heritable component and/or exposure of the developing fetus to infection, toxins, or nutritional disturbances.

The most common clinical sign is nasal regurgitation of milk immediately after sucking. Foals with small-palate defects may have intermittent milk drainage from the nostril and consequently escape diagnosis during the neonatal period. There are rare reports of cleft palates being initially diagnosed in adult horses. Most will develop an aspiration pneumonia that can be difficult to identify in its early stages because of immaturity of cough receptors. Surviving foals will typically be poorly grown and ill-thrifty. The diagnosis is usually straightforward and centers on an appropriate history and signalment. Confirmation is through palpation using the third finger or by direct inspection of the oral cavity. Smaller defects may be detected by endoscopic examination of the nasal passages or through the oral cavity under anesthesia. Oral palpation is recommended for all sick neonatal foals before commencing potentially costly treatment.

The presence of milk at the nares after feeding is not considered pathognomonic for a cleft palate. Many foals with this condition do not have the defect but rather delayed or altered coordination of the swallowing reflex. Clinical signs may be noted as early as a few hours of age and persist variably from hours through weeks. The basis of the condition is not known, but generalized weakness, hypoxic-ischemic brain disease, and nutritional myodegeneration (white muscle disease) have all been suggested as possible causes (Box 17-2). Soft-palate displacement may also occur in newborn foals as a result of a persistent frenulum between the ventral aspect epiglottis and base of the tongue or with hypoplasia of the epiglottis.²⁸ Chronically affected foals develop signs consistent with aspiration pneumonia, including cough, ill-thrift, and failure to grow. The diagnosis is confirmed through endoscopy of the nasopharynx; persistent dorsal displacement of a flaccid soft palate and dorsal collapse of the nasopharynx are typical findings. The palate will not replace during attempts to swallow. The procedure is important to rule out congenital defects of the palate and epiglottis, although endoscopy of the oral cavity under short-acting anesthesia may be necessary to rule out more obscure problems such as persistent frenulum or epiglottic hypoplasia. Radiography and ultrasound are useful diagnostic tests to confirm the presence and extent of a ventral consolidating pneumonia. Pharyngeal and subepiglottic cysts are uncommon in newborn foals but when present may be associated with dysphagia and nasal regurgitation of milk. Other clinical signs may include a respiratory noise, cough, and dyspnea. Diagnosis is by endoscopy and radiography. Treatment options include ablation using sharp dissection, laser ablation, or a snare.²⁹ Esophageal diseases are rare in the newborn foal. Reported conditions include congenital dilatation or ectasia, tubular or cystic esophageal duplication, megaesophagus, motor dysfunction, and stricture. Most descriptions are in foals outside of the neonatal period.

Eyes and Associated Structures

Several ocular features are unique to the newborn foal. These include a round pupil, reduced corneal sensitivity, prominent lens Y sutures, and persistence of blood in hyaloid artery remnants. The optic disc tends to be round rather than oval and has smooth margins. Normal newborn foals lack the ability to completely close their eyelids (lagophthalmos).³⁰ Entropion is one of the more common ocular problems in newborn foals. The condition primarily affects the lower lid and involves inward rolling of the lid margin such that the eyelid hairs may cause abrasion to the cornea. It rarely occurs as a primary event and is usually secondary to dehydration or emaciation. Temporary eversion using vertical mattress sutures or staples is highly effective at reducing the risk of corneal damage; a less preferred method involves subcutaneous injection of procaine penicillin into the lid. Surgical treatment for entropion is rarely indicated and should be reserved for older foals only. Corneal ulceration occurs commonly in sick neonatal foals. An important feature of the newborn foal is significantly reduced corneal sensitivity when compared with adult horses.³¹ This may in part explain why the signs of corneal disease in foals differ markedly from similarly affected adults. Cardinal signs of keratitis, including blepharospasm, photophobia, and excessive lacrimation, are often absent in the early stages of disease in neonates. There are a number of risk factors for corneal abrasion in foals, including the high prevalence of entropion, the propensity for prolonged recumbency, and the frequency of seizures and colic. The key to management is early recognition. In many hospital practices daily fluorescein staining is part of the routine management of most sick foals. The frequent use of lubricating ointments may also play an important prophylactic role in preventing eye disease.

Careful examination of the globe may reveal signs of iridocyclitis. This can be unilateral or bilateral and usually is regarded as an ocular manifestation of systemic sepsis. In very young foals the presence of fibrin or hypopyon may indicate in utero bacterial exposure, often caused by placental infection. Likely the most common cause of blindness during the neonatal period can be directly or indirectly linked to asphyxial brain injury. In many of these foals the loss of vision is attributable to cortical disease, as pupillary light reflexes are usually preserved. The prognosis for future vision is usually good. Cortical blindness can also result from prolonged generalized seizures. The menace response is not a reflex and is considered to be a learned behavior in newborn foals. The characteristic eyelid blink and ocular retraction may be absent during the first 1 to 2 weeks of postnatal life, but most foals still demonstrate head withdrawal in response to a threatening hand gesture, assuming an adequate level of alertness. Neonates should blink when a bright light is directed into the eye (bright light blink or dazzle reflex) and should have brisk direct and consensual pupillary light reflexes.

There may be a slight ventromedial rotation of the eyeballs in normal foals; this persists for the first month.¹⁶ Spontaneous nystagmus in any direction is abnormal, but vestibular nystagmus is present when the head is moved in a horizontal plane in healthy foals. The fast phase of the nystagmus is in the direction of head movement. Subconjunctival and scleral hemorrhage is a feature of foals born after dystocia. This can be an important warning sign of impending postasphyxial problems such as hypoxic-ischemic encephalopathy. The sclera should also be examined for signs of blood vessel congestion, a feature of sepsis, and for icterus. The differential diagnosis for neonatal icterus is discussed elsewhere. Most foals with an abnormally small globe (congenital microphthalmos) are blind, have a reduced palpebral fissure, and have a prominent nictitans.³⁰ The condition may be unilateral or bilateral, and it has been suggested that thoroughbred foals may be more commonly affected.³⁰ Foals are at increased risk for ulceration resulting from associated entropion. Microphthalmia has been reported to occur along with mandibular prognathism and cleft palate in foals exposed to griseofulvin during the second month of gestation.³² Congenital cataracts are relatively common eye defects in foals. Veterinarians should be careful not to misinterpret lens sutures as cataracts. These Y-shaped sutures may persist for up to a year. Assuming a normal retina, an absence of uveal tract inflammation, and an appropriate demeanor, most of these foals are candidates for surgery. Other abnormalities include atresia of the nasolacrimal system, dermoids, retinal dysplasia, and optic nerve hypoplasia.

Ears

Ear problems occur uncommonly in foals. It is, however, important to examine the inside of the pinnae for dermal ecchymotic or petechial hemorrhages. Foals with systemic sepsis may develop these lesions.

Thyroid Gland

Hypertrophy of the thyroid gland (goiter) can occur in response to deficient or excess dietary iodine. One of the more common reasons for thyroid gland enlargement in neonatal foals is excess iodine supplementation during pregnancy.³³ There are reports of neonatal goiter when seaweed was incorporated into the diet of broodmares³⁴ or when pellets that had been formulated with excessive iodine were fed to mares.³⁵ Dysmature foals with thyroid hyperplasia and concurrent musculoskeletal problems have been identified in western Canada and the northwestern United States.^36,37 The syndrome results in hypothyroidism and may be related to the feeding of diets that are high in nitrate or low in iodine to mares during pregnancy. Thyroid hormone is an important cofactor in maturation of the respiratory system, and hypothyroidism has been linked to respiratory failure in a newborn foal.³⁸ In older foals, enlargement of the thyroid has been associated with dietary iodine deficiency and low circulating levels of T₄.³³ Newborn foals have baseline T₃ and T₄ levels that are considerably greater than those of adult horses.³⁹ These levels decline over the first 12 days after birth. Normal day-old foals have a doubling of T₃ at 3 hours and a 16% increase in total T₄ at 6 hours after TSH administration.⁴⁰

Neck and Back

There are a number of congenital anomalies that affect the alignment of the vertebral column. These include atlantoaxial malformations, scoliosis, kyphosis, lordosis, and combined anomalies, such as kyphoscoliosis. Atlantoaxial malformations may occur with or without cervical scoliosis or signs of spinal cord compression. Arabian foals are most commonly affected, and a familial predisposition has been suggested.⁴¹ There may be palpable abnormalities of the atlas and axis and altered head carriage. The diagnosis is confirmed using radiography, with which a range of abnormalities is seen including atlantooccipital fusion, hypoplasia of the dens, and axis malformation. Prognosis is very poor, as many foals have signs of ataxia and paresis involving all four limbs at birth. Some animals may have normal neurologic function. Foals with severe kyphosis or kyphoscoliosis often have underlying malformation of the thoracic vertebrae.⁴²

Gastrointestinal Tract

Borborygmi should be easily heard in healthy neonates. Assessment of abdominal size and shape is part of the routine physical examination. This is critical in assessment of the foal with abdominal pain or decreased urine output. In contrast to small animals, in neonatal foals abdominal palpation is usually unrewarding. In small foals with relaxed abdominal muscles it may be possible to palpate meconium impactions and the urinary bladder. When abdominal distention is present, it is important to determine if it is a result of fluid or gas accumulation. Ultrasound has become an essential tool in the assessment of abdominal distention.

The routine administration of an enema is performed commonly in healthy newborn foals in an attempt to reduce the straining associated with the passage of meconium. Various methods are used, with commercial glycerine phosphate—based products the most common. These are relatively easy to administer, although care should be taken to avoid direct trauma to the rectal mucosa with the applicator tip. Most veterinary practices probably use gravity enemas of 400 to 800 mL of warm soapy water delivered through a soft tube, such as a canine stomach tube or male urinary catheter. Acetylcysteine retention enemas are not administered routinely, but rather in foals with resistant meconium impactions.

Coprophagy is observed in normal foals from birth through 5 to 6 months of age.^43-45 Most foals demonstrate coprophagy by 7 days of age. The consumption of feces is not driven by hunger, and foals have a selective preference to consume feces of their dams. The most likely basis for coprophagy is as a mechanism to populate the intestinal tract with bacteria, fungi, and protozoa essential for digestion of an herbivorous diet. Coprophagy precedes the passage of protozoa in foal feces and the development of the syndrome known as “foal heat diarrhea.” This is a benign diarrheal disease of newborn foals and should not require treatment.

Umbilicus

Breakage of the umbilical cord occurs naturally within 5 minutes of birth, with the natural break typically 2.5 to 7 cm beneath the body wall. Immediate postpartum transfusion of blood from the placenta to the foal is important, although the process is essentially complete within minutes, assuming establishment of a respiratory rhythm. Premature breakage of the cord can result in significant blood loss—up to one third of the circulating fetal blood volume.⁴⁶ Hemorrhage should therefore be controlled with a commercial clamp or umbilical tape. Prolonged attachment of the cord is unlikely to be a significant problem, although blood flow between the placental membranes and the foal is partly gravity dependent, such that blood could flow preferentially from foal to membranes if the foal is above the level of the placenta. Manual breakage of the umbilical cord is recommended if it remains attached for more than 8 minutes. The preferred method for manual cord breakage is to grasp the placenta side of the cord while holding the foal side of the cord with the other hand to prevent excessive traction on the abdominal wall. Gently twist and pull from the placenta side such that the breakage will occur at the natural site of detachment. The umbilical cord should not be cut, as this does not promote normal retraction of the umbilical structures. The cut umbilical stump usually remains prominent, often with detectable pulse, and is more likely to be associated with hemorrhage or patency of the urachus. Bleeding from the umbilicus can also occur after apparent closure if the foal is straining to either defecate or urinate. Clamping or tying off the stump again can reduce this. The exposed umbilical stalk is a portal for bacterial entry. Any manipulation of the cord should be performed with clean, gloved hands. Routine disinfection of the stump is strongly recommended during the first 2 days of postnatal life or until the stump has dried. Most hospitals use 0.5% chlorhexidine solution as the preferred dipping agent, but some advocate a 2% iodine solution for use by clients, as its use can be verified by the characteristic iodine staining.

The appearance of the umbilical stump changes over the first few days after birth. The external stump should be examined for size and moisture. A complete assessment of the umbilical remnants requires ultrasound. The most common problems of the umbilical stump are patency of the urachus and infection. Tearing of the urachus as it moves through the body wall can produce a circle of cellulitis around the stump because of leakage of urine into the tissues.

Umbilical hernias occur relatively commonly in foals. The condition is generally considered to be a congenital defect with a likely hereditary basis, although umbilical infection may be an important postnatal predisposing factor in some foals. In a study from the Netherlands 19 of 44 Dutch Warmblood foals had a palpable abdominal wall defect varying between 2 and 6 cm at the time of birth.⁴⁷ In all but one of these foals the defect had closed by 4 days of age. Of interest was that approximately 28% of the foals developed a defect at 5 to 8 weeks of age. These were considered to be true umbilical hernias in that a hernial sac with contents was palpable in addition to the abdominal wall defect. The group included both foals with and foals without a palpable abnormality at birth. In a retrospective study of hospitalized foals it was concluded that the defect was more likely to occur in fillies than in males and that the condition was more common in thoroughbreds than in standardbreds.⁴⁸ Most clinicians recommend delay in treatment, as some defects will close spontaneously. Several techniques have been described for repair and vary from external clamps to surgical herniorrhaphy. Rare complications are associated with umbilical hernias or their repair. These include enterocutaneous fistulas, umbilical abscessation, and intestinal incarceration.^49,50

Diagnosis of Umbilical Disorders Using Ultrasound

JOHN E. MADIGAN

Ultrasonography has been used to quantitatively correlate umbilical structural changes with age in foals. Mean diameters for selected umbilical structures derived from 13 foals ranging from 6 hours to 4 weeks of age have been reported.^50a Foals may be examined in a stall adjacent to their dams and near the stall door. Foals are made to lie down without sedation, using the method shown in Fig. 17-1. Foals will usually become quiet and still within a few minutes of recumbency. All ultrasound examinations are performed with the foal in left lateral recumbency with the ultrasound machine behind the examiner (Fig. 17-2).

Fig. 17-1 Procedure for placing neonatal foals in lateral recumbency for umbilical ultrasound. A, The foal is restrained by placing the arms around the neck area and rump and holding the tail. B, The left forearm of the handler is placed against the head of the foal, and the head is folded back toward the rump area while pressure is applied to the rear quarters with the other arm. C, The foal leans backward and sags toward the handler, becoming recumbent. D, The foal is allowed to sag to the ground and is kept in the folded position until completely recumbent and relaxed. E, The front legs are then grasped with left hand and the forearm is placed on the neck area. The rear legs are held with the right hand. F, The foal is held steady in this position until blindfolded and struggling stops. The foal is in left lateral recumbency.

Fig. 17-2 Ultrasound evaluation of equine umbilical structures. Diagram depicts the positioning of the ultrasonographer and the assistant and the selected anatomic locations recommended for ultrasound examination.

Fig. 17-2 includes a diagram of the anatomic locations of the structures examined during the ultrasound evaluation. A 5- to 8-cm-wide strip of hair can be clipped along the ventral midline, extending from the umbilical stump cranial to the xiphoid to facilitate examination of the umbilical vein. In addition, an area 5 cm by 5 cm caudal to the umbilical stump is clipped to visualize the umbilical arteries and urachus. The ultrasound examination is performed with a 7.5-MHz sector scanning transducer; a built-in standoff is preferred. Eight views of the umbilical vessels and linear measurements of the vertical and horizontal dimension of each vessel can be taken. This allows examination of the umbilical vein (three views) and umbilical stump (one view) (Fig. 17-3), and urachus/umbilical arteries (four views) (Fig. 17-4). The umbilical vein is visualized at a site approximately 1 cm cranial to the umbilical stump (view 1); another view taken approximately halfway between the umbilicus and the liver (view 2) and at a point where the vein curves away from the body wall and angles toward the liver (view 3). A single cross-sectional view of the external umbilical stump is made at the body wall. The combined urachus/left and right umbilical artery is visualized in a single cross-sectional view just caudal of the umbilical stump. The comparative mean umbilical vessel diameter normal data is summarized in Table 17-5. All but one of the ultrasound views demonstrated a significant reduction in mean vessel diameter over the first 7 days of life in normal foals; only the urachus and umbilical arteries in a single structure remain static during the first week of life. Enlargements in these structures are suggestive of inflammation, infection, or hematoma and should be correlated with clinical signs and laboratory findings for choosing an optimal treatment plan.

Fig. 17-3 Ultrasonogram images of four views of umbilical structures: umbilical vein views 1 (A), 2 (B), and 3 (C), and umbilical stump (D). Refer to the text for the definition of the views.

Fig. 17-4 Ultrasonogram images of four views of umbilical structures: urachus (A), umbilical arteries views 1 (B), 2 (C), and 3 (D). Refer to the text for the definition of the views.

Table 17-5 Comparative Mean Umbilical Vessel Diameters (mm) for 31 Clinically Normal Foals on the First and Seventh Days of Age (Mean ± SD)

Urogenital System

Urine is one of the most important indicators of health in foals. Normal neonatal foals produce a large volume of urine relative to their bodyweight; estimated at 148 mL/kg/day, this value is approximately fivefold to tenfold greater than that of a healthy adult horse on a per kilogram of bodyweight basis.⁵¹ The urine should be light in color and low in specific gravity. Any foal observed to pass thick, concentrated urine should be assessed closely. The first passage of urine after birth occurs around 8-9 hours of age.⁵² Colts will pass urine earlier than fillies, at approximately 6 hours of age in colts and 11 hours in fillies. Disruption to the urinary tract occurs relatively commonly and can be difficult to diagnose early in the clinical course. Rupture of the urinary bladder during delivery occurs more commonly in colts than in fillies, although postpartum disruption to the tract in sick or hospitalized foals has no gender bias.^53,54 Signs often include prolonged straining, passage of small volumes of urine, progressive abdominal distention, lethargy, and weakness.

In colt foals the inguinal and scrotal region should be palpated for swelling and testicular descent. Inguinal and scrotal hernias occur relatively commonly but rarely result in clinical signs. Preputial edema may be present. Most congenital hernias are indirect, unilateral, and easily reducible and spontaneously resolve by 3 to 4 months of age. Positioning the foal on its back facilitates manual reduction. A figure 8 support wrap can assist in keeping the hernia reduced. Surgical correction is recommended if spontaneous resolution is delayed, if the hernia increases in size, or if signs of colic develop. Certain breeds appear to be at increased risk for herniation, including Tennessee Walking Horses and standardbreds. A rent in the parietal vaginal tunic can lead to subcutaneous dissection of intestinal loops; this requires surgical reduction, herniorrhaphy, and unilateral castration.⁵⁵ Although such rents are extremely uncommon in foals, signs of colic can occur if herniated loops of intestine strangulate.

At the time of birth most testes lie within the inguinal canal. The extraabdominal gubernaculum typically limits movement into the scrotum. The mass of gubernaculum can easily be mistaken for the testicle. Monorchidism has been reported in foals, and affected colts are usually mistaken as cryptorchids.⁵⁶ Congenital abnormalities of the penis are rare. Failure to drop the penis during urination can occur as a consequence of preputial edema, a common complication in colts that are straining to defecate or urinate. The free part of the penis is normally fused to the internal lamina of the prepuce for up to 1 month of age. This can make exteriorization of the penis difficult. “Kinking” of the penis has been described, resulting in stranguria or pollakiuria.⁵⁷ Correction was achieved through manual straightening of the penis.

Musculoskeletal System

Supplementation of foals with selenium is recommended for those born in known selenium-deficient regions when mares have not been supplemented during pregnancy. Severe rhabdomyolysis has been reported in newborn foals, usually associated with selenium deficiency.⁵⁸ Glycogen branching enzyme deficiency is an inherited cause of mortality in quarter horse foals.⁵⁹ Clinical signs are variable and include seizure, persistent recumbency, respiratory failure, and cardiovascular collapse. Authors of the original report suggested that the generalized nature of the clinical signs would likely lead to a false diagnosis of other, more common neonatal diseases.

Because of the rapid growth that occurs in the first months of life, any orthopedic condition must be identified and immediately managed in order to achieve a successful long-term outcome. Palpation of synovial structures is a critical part of the foal physical examination, regardless of whether lameness or synovial distention is present. Persistent recumbency, a common feature of generalized sepsis, can make detection of joint infection difficult. Synovial sepsis is a common manifestation of bacterial infection, and most affected foals will be lame with obvious joint distention and heat on palpation. Diagnosis is confirmed through synoviocentesis. An elevated synovial fluid white blood cell (WBC) count (>20,000 cells/μL), a predominance of neutrophils (>90%), and an elevated protein concentration (>4 g/dL) all point toward sepsis. Osseous infection can also be difficult to identify in its early stages. Common sites include the stifle, hock, and distal physis of the cannon bone. Osteomyelitis should be suspected in any foal with lameness and edema, heat, and pain on palpation of the overlying tissues. Trauma by the mare is often suspected, but osseous infection should always be considered, particularly in foals with other manifestations of sepsis (e.g., omphalitis, diarrhea, uveitis). There may or may not be effusion in adjacent joints, and if present it could reflect either an extension of the septic process or a nonseptic “sympathetic” effusion. The management of synovial and bone infection is discussed elsewhere.

Contractural deformities of the limbs occur commonly in newborn foals. These are considered to be congenital and may result from a variety of causes including malpositioning within the uterus. If the foal is able to stand and ambulate, most mild deformities of the carpus, fetlock, and coffin joint will resolve within 4 to 5 days without specific treatment.⁶⁰ Moderately to severely affected foals often require splinting in combination with medical therapy in order to achieve a successful outcome in the shortest possible time. Foals with persistent or prolonged recumbency are very susceptible to secondary problems, the most important being sepsis and corneal abrasion. Medical therapy often includes judicious use of oxytetracycline and nonsteroidal antiinflammatory drugs. Rupture of the common digital extensor within the synovial sheath may occur in foals with contractural or flexural deformities. This should be suspected in foals with a soft, nonpainful swelling over the dorsolateral aspect of the carpus. Gait may appear stilted, and there may be knuckling of the fetlock. Most foals quickly regain extensor function, and the long-term prognosis is good.

Hyperextension or joint laxity is common in premature and dysmature foals. The most common presentation involves dropping of the fetlock, hyperextension of the pastern, weight bearing on the heel bulbs, and tipping upward of the toe. Again, most foals improve spontaneously over 3 to 4 days, but heel extensions and light padding to protect the heels from bruising will hel more severely affected foals. Hyperextension of the carpus is also observed in some foals.

Angular limb deformities are also frequently encountered in practice; the most common deviations are carpal and tarsal valgus and fetlock varus. Examination should include observation at rest from front and rear, paying careful consideration to any external rotation of the limbs, which may give a false impression of limb valgus. In weak or premature foals there may be limb deviation resulting from ligamentous laxity; this is best assessed through limb palpation including flexion and observation of the foal at the walk. If the limb can be straightened manually, then the deviation is due to ligamentous laxity or delayed ossification of the cuboidal bones.⁶⁰ There is a variety of conservative and surgical approaches to these foals.

Laminitis with sloughing of the hoof capsule can occur in neonatal foals; however, it is rare and is typically associated with significant systemic disease. Polydactylism is a duplication of all or part of the digit. This condition can occur as a single defect or as part of a group of congenital anomalies. Surgery may be indicated when the condition occurs as a single entity, not only to improve the cosmetic appearance but also to reduce the risk of lameness at a later age.

Neonatal Behavior

Calves and lambs normally have a head-righting reflex almost immediately after birth. Sternal recumbency is usually attained within 2 to 3 minutes, followed rapidly by attempts to stand, at 10 to 20 minutes for lambs and 15 to 30 minutes for calves.^61,62 Hypoxic neonates may struggle and appear bright initially but have difficulty maintaining sternal recumbency, have depressed or absent suck reflex, are slow to stand or remain recumbent, and develop a depressed mentation within hours. After experimentally induced hypoxia, nonviable hypoxic calves had heart rates (118 ± 36 bpm) and body temperatures (39.6° C ± 0.2° C) similar to those of viable calves but lower respiratory rates (14 and 18 versus normal 49 ± 12).⁶¹ In cattle the average time from birth to standing and nursing varies according to breed. The average time from birth to standing and nursing for beef calves is 35 and 81 minutes, respectively. Dairy calves take approximately twice as long.⁶³ Small ruminants are generally quicker to stand and nurse than calves, with most lambs standing within 30 minutes⁶² and nursing within 90 minutes of birth. Failure of the newborn to nurse may result from reduced neonatal vigor, poor mothering, poor maternal conformation, or adverse conditions such as slippery flooring. Calves have difficulty locating teats on low-slung udders (less than 45 cm from the ground)⁶⁴ and difficulty nursing from teats greater than 35 mm in diameter.⁶⁵ Observation of interaction between the newborn and dam in the immediate postnatal period allows early recognition of the compromised neonate and facilitates timely intervention if maternal conformation or behavior threatens to impede the neonate’s efforts to nurse.

Abnormal neonatal behavior in the immediate postnatal period is commonly secondary to perinatal hypoxia. Resuscitation of the newborn is discussed in Chapter 16. In utero infections and congenital neurologic abnormalities should also be considered as possible causes of abnormal neonatal behavior. Collection of sera before feeding colostrum is useful for diagnosing in utero infections. Precolostral serum immunoglobulin concentrations in calves are very low (IgM 0.126 ± 0.015 mg/mL, IgG 0.044 ± 0.003 mg/mL).⁶⁶ Elevated serum concentrations of immunoglobulins before ingestion of colostrum may be observed with in utero infections.⁶⁶ Specific serologic tests are available for Cache Valley virus, Akabane virus, bovine virus diarrhea (BVD) virus, Neospora species infection, Toxoplasma infection, and bluetongue virus.⁶⁷ Teratogens and inherited diseases that may cause the birth of weak neonates are listed in Box 15-3.

Tube-feeding colostrum during the first 12 hours of life is appropriate if free-choice consumption is questionable. Drying, warming, and tube-feeding colostrum may revive weak newborn lambs and kids. Tube-feeding dairy calves 3 L of colostrum at birth is recommended, as failure of passive transfer is high (61%) in dairy calves left to nurse their dams.⁶⁸

Maternal Behavior

Failure of maternal bonding is more common with primiparous dams, with multiple offspring, and after delivery via caesarean section. Restraint and patience often pay off. Reluctant dams will often accept the calf after several days of restrained feeding in which the dam is placed in a crush two or three times a day to allow the calf to nurse. Maternal bonding in sheep is mediated by an olfactory mechanism.⁶⁹ Parturition alters the release of monoamines, amino acids, and oxytocin within the olfactory bulb, stimulating an attraction to amniotic fluid and acceptance of the lamb.⁷⁰ Artificial vaginocervical stimulation with a gloved hand induces similar alterations in the release of monoamines, amino acids, and oxytocin within the olfactory bulb and is useful for triggering formation of maternal bonds to foster lambs for at least 27 hours postpartum.⁷⁰

Examination from a Distance

The physical examination begins with examination from a distance with assessment of behavior, body condition, and stance. Drooping of the head and ears is an early sign of illness. Sick calves spend increasing amounts of time recumbent and are less inclined to drink. In beef calves, lambs, and kids this may be reflected by udder distention in the dam. With dairy calves the calf feeder reports the calf requires stimulation to stand and fails to drink. Resting respiratory rate and effort are assessed before the calf is handled. Abdominal contour should be noted, with consideration of the neonate’s reported appetite; an apparently normal abdominal contour may be abnormal if the calf has not eaten for several days. Observing the neonate navigate its environment provides a simple assessment of vision.

Physical Appearance, Bodyweight, and Body Condition

Congenital disorders may cause subtle changes in physical appearance and behavior. For example, Saler calves with β-mannosidosis have moderately domed heads, mild superior brachygnathism, and a slight head tremor.⁷¹ Similarly, in utero infections that lead to growth retardation may be reflected by low birthweight and poor body condition.

Body Temperature

Rectal temperature in calves ranges from 99° F to 102° F (37.2° C to 38.9° C) during the first 4 days after birth. Calves with sepsis are often febrile; however, absence of a fever does not rule out sepsis. Calves in septic shock may have subnormal temperatures. Premature calves are prone to hypothermia.⁷² Hyperthermia during the first week of life has been reported to be common in cloned calves.⁷³

Cardiovascular System

Peripheral pulses in the tail and brachial arteries should be strong and regular, and the peripheral extremities warm. Mucous membranes should be moist and pale pink with a CRT of <2 seconds. Gray or cyanotic mucous membranes are associated with severe hypoxia (i.e., PaO₂ < 35 to 40 mm Hg) and/or circulatory collapse as seen with hypotensive, endotoxic, or hypovolemic shock. Cardiac and pulmonary causes of cyanosis must be distinguished. Cyanosis secondary to cardiac causes reflects right-to-left shunting of blood, as may be observed with tetralogy of Fallot or ‘Eisenmenger’s complex.

Dyspnea and coughing are often the predominant clinical signs of congestive heart failure in calves. Close examination may reveal distention of the jugular veins and brisket edema, but if heart failure is predominantly left sided these signs may be absent. Cardiomyopathy secondary to selenium deficiency or gossypol, monensin, or lasalocid toxicity may manifest as a syndrome of sudden death during periods of excitement precipitated by feeding or moving calves out of hutches into group pens.⁷⁴

Cardiac arrhythmias are observed sporadically in neonates, often associated with diarrhea. Metabolic acidosis secondary to losses of electrolytes and water causes a transcellular shift of potassium ions into the extracellular fluid in exchange for hydrogen ions.⁷⁵ As serum potassium increases (>5.5 mEq/L), aberrations in cardiac excitability occur and are manifested as progressive atrial standstill, progressing to ventricular fibrillation and asystole.⁷⁶ Tachyarrhythmias may be observed in calves with cardiomyopathies, ionophore toxicosis,⁷⁷ or hypomagnesemia.

The most common cardiac defect in the large animal neonate is a ventricular septal defect, but a variety of other malformations have been described and are discussed in Chapters 6 and 30. Ancillary tests for evaluating the cardiovascular system are discussed inChapter 30.

Respiratory Tract

The respiratory rate and effort of breathing in neonates are best observed from a distance so that the stress of restraint does not influence the assessment. Lung sounds of neonates are typically easier to hear than those of adults; however, lung sounds do not always correlate well with the severity of pulmonary pathology present. Thoracic percussion is also easier to perform in the neonate and can be useful to identify the presence of cranioventral consolidation. Animals with few or no audible thoracic abnormalities may have severe respiratory disease. The rate and effort of breathing are important to consider in the physical assessment of respiratory function. When available, chest radiology, thoracic ultrasonography, and arterial blood gas analysis are useful ancillary diagnostic tools.

Lung disease in the newborn is usually diffuse and is the result of infection acquired in utero or postpartum and/or lung atelectasis associated with immaturity, recumbency, or surfactant dysfunction. Signs of lung disease include increased work of breathing characterized by nostril flare, rib retractions, and increased abdominal effort. A cough and nasal discharge, salient features of respiratory disease in older neonates, are infrequent findings in newborns with lung disease.

Conditions that cause partial occlusion of the upper airway, such as necrotic laryngitis, often induce pronounced inspiratory stridor. Expiratory stridor and increased and prolonged expiratory effort are usually associated with lower airway disease. A malodorous breath may be present with necrotic pharyngeal injuries, necrotic laryngitis, or aspiration pneumonia. Age is an important signalment for respiratory disease in calves. Enzootic pneumonia is common in calves between 4 weeks and 6 months of age but uncommon in calves less than 4 weeks of age. Outbreaks of pneumonia in calves less than 4 weeks of age are occasionally observed in calves fed milk contaminated with Mycoplasma species.^78,79 This scenario is one of the risks associated with feeding calves unpasteurized “hospital milk.” Mycoplasma pneumonia in calves may be associated with arthritis, tenosynovitis, otitis media,⁷⁹ and decubital abscesses.⁸⁰ Clinical signs associated with mycoplasma otitis include cranial nerve 7 and 8 deficits, unilateral or bilateral ear droop, ptosis, epiphora, head tilt, and recumbency in severely affected calves. Aspiration pneumonia is common in calves less than a week of age, often reflecting inappropriate feeding practices (large holes in teat nipples or poor esophageal tubing technique) or pharyngeal dysfunction.

Periodic apnea and abnormally slow respirations are often the result of metabolic disturbances (e.g., hypoglycemia, hypocalcemia), hypothermia, advanced prematurity, or hypoxia-induced suppression of the respiratory center. Calves with metabolic acidosis usually have an increased respiratory rate with long, deep breaths reflecting respiratory compensation. Tachypnea may be a response to high ambient temperatures, pain, or stress. Congenital defects of the respiratory system in ruminants are rare.

Oral Cavity and Nasal Passages

Hyperemic membranes accompanied by scleral injection are the hallmark of early sepsis. Petechiae on the oral or nasal mucous membranes are consistent with sepsis or thrombocytopenia induced by type II BVD. Ecchymotic hemorrhages may be observed on the sclera with type II BVD infections, with DIC, or after birth trauma. Cleft palate is the most common congenital defect observed in ruminants. Calves with cleft palate may have milk run from the nose and are prone to developing aspiration pneumonia.

Eyes and Associated Structures

Eyes should be examined for the presence of entropion, ectropion, corneal abrasions or ulcers, uveitis and hyphema, congenital cataracts, microphthalmia, corneal dermoids, scleral injection, and scleral hemorrhage. Scleral hemorrhage is usually the result of birth trauma and can take several weeks to resolve. Icterus is uncommon in neonatal ruminants but may be observed with hemolytic or hepatic disease.

A common cause of corneal edema and ulceration, conjunctivitis, and lacrimation in lambs is acquired or congenital entropion. Acquired entropion is associated with self-trauma, dehydration, or prematurity and the lack of periorbital fat. Entropion should be corrected promptly before serious corneal ulceration and keratitis develop. Mild cases may respond to subcutaneous injections of procaine penicillin G into the lower eyelid. Refractory cases may require placement of vertical or horizontal mattress sutures in the eyelid to correct the problem. The affected eye should be stained to detect concurrent corneal ulceration. Varying degrees of miosis secondary to pain and ciliary body spasm is common. Treatment after correction of entropion includes topical administration of 1% atropine to dilate the pupil and relieve ciliary body spasm and topical antibiotics to prevent bacterial infection.

Uveitis may be observed in the newborn animal exposed to an infected uterine environment or may be a result of generalized infection acquired after birth. Scleral injection suggests and fibrin in the anterior chamber is highly indicative of sepsis.

Ears

Bilateral drooped ear carriage is a common observation in sick calves and should prompt a closer examination. Unilateral ear droop may be observed with otitis and facial nerve paralysis. Mycoplasma species, Pasteurella species, and Haemophilus species are reported to cause otitis in calves. Clinical signs may include facial and vestibular nerve deficits and a purulent discharge from the ear. Calves infected with Mycoplasma species may also have tenosynovitis and respiratory disease.

Poor perfusion is reflected by cold extremities. A high incidence of pinna abscesses usually reflects contamination of equipment used to place ear tags.

Neck and Back

Several congenital anomalies affect the alignment of the vertebral column. These include atlantoaxial malformations, scoliosis, kyphosis, lordosis, and combined anomalies such as kyphoscoliosis. Atlantoaxial malformations may occur with or without cervical scoliosis or signs of spinal cord compression. Holstein calves affected by the hereditary condition complex vertebral malformation may display a range of abnormalities that include retarded growth, malformation of the head (dysplasia or palatoschisis), bilateral symmetric flexion of the carpal and metacarpophalangeal joints, posterior arthrogryposis, and interventricular septal defects. Of these, growth retardation, vertebral malformation, and symmetric arthrogryposis are the most consistent findings.⁸¹

Gastrointestinal Tract

Much can be learned about gastrointestinal function by observing abdominal contour, appetite, and fecal consistency and volume. A normal abdominal contour and vigorous appetite associated with the passage of an appropriate volume of pasty stool suggest normal gastrointestinal function. Congenital defects of the gastrointestinal tract occasionally observed in ruminants include cleft palate, poor jaw conformation (brachygnathism, inferior and superior), atresia coli, atresia recti, and atresia ani. The spiral loop of the ascending colon (spiral colon) is the most commonly affected segment of intestine in calves.⁸² Neonates with atresia often have a distended abdomen and a history of a declining appetite. Astute owners may notice the lack of or reduced volume of feces.

In contrast to the adult, in the large animal neonate the rectal palpation of the abdominal structures is of limited value. External palpation of the abdomen can be more rewarding, depending on the cooperation of the individual and the tenseness of the abdominal musculature. In calves it is usually possible to palpate enlargement of the umbilical vein and arteries. The inguinal rings and umbilical area should also be palpated for hernias.

Infectious diarrhea is the leading cause of mortality in calves between 3 and 21 days of age. Typically more than one pathogen is involved and the physical examination provides no indication of the causative agent. Fecal pH may be used as an indicator to distinguish secretory diarrhea (enterotoxigenic E. coli) from diarrhea associated with malabsorption and maldigestion. Secretory diarrhea produces an alkaline pH, whereas malabsorption and maldigestion are associated with an acidic fecal pH.⁸³ Small amounts of blood may be observed in the feces of healthy calves. Passage of blood and fibrin is associated with inflammatory bowel disease induced by pathogens such as Salmonella and coronavirus that damage the gastrointestinal mucosa. Infectious agents that cause diarrhea and the ancillary tests available to establish an etiologic diagnosis are discussed in Chapter 20.

Abnormal forestomach function in neonatal ruminants, as in adults, is often reflected by altered abdominal contour as described in Chapter 32. Left and right abomasal displacement and abomasal torsion are observed sporadically in calves. Succussion (simultaneous auscultation and percussion) is useful for delimiting the boundaries of distended visci. Passage of a stomach tube helps distinguish rumen and abomasal distention and facilitates collection of a ruminal fluid sample. A putrid odor to neonatal ruminal fluid is common with putrefactive indigestion when milk is delivered to the rumen in greater quantities than normal by escaping the esophageal groove or via excessive backflow from the abomasum. Reflux of abomasal contents into the reticulum and rumen, independent of feeding, occurs in connection with abomasal inflammation and obstructions.⁸⁴ Evaluation of ruminal fluid pH and renin activity are useful for distinguishing abomasal reflux from esophageal groove overflow. Ruminal fluid pH is usually ≥7 with rumen putrefaction, and low to normal with abomasal reflux.⁸⁴ Chymosin (renin) is normally present in abomasal juice, and renin activity in ruminal fluid suggests abomasal reflux.⁸⁵ Renin activity is measured by adding 2 mL of ruminal juice to 2 mL of whole milk on a CMT (California Mastitis Test) plate. Presence of renin in the ruminal fluid causes coagulation of the casein in the milk. Chloride ion concentration in ruminal fluid from calves is higher than in adults (55 to 102 mmol/L in calves⁸⁶ and 25 mmol/L in adults⁸⁴), possibly reflecting the high chloride content of milk (45 mmol/L); therefore the chloride concentration of ruminal fluid is not useful for identifying abomasal reflux in calves.

Abdominal radiographs and/or ultrasound examination can be helpful in diagnosing abdominal problems in the neonate and in distinguishing causes of abdominal distention.^87-89 Transabdominal ultrasonography can be used to locate a suitable site for abdominocentesis. Normal peritoneal fluid from calves has a higher nucleated cell count than that of adult cattle (3350 cells/μl vs 1371 cells/μl). Total protein concentration in peritoneal fluid of calves is similar to that of adults (2.5 g/dL vs 3.1 g/dL).⁹⁰

Umbilicus

Umbilical cord remnant infections represent an important problem in neonates.⁹¹ The infection generally develops during the first 2 weeks of life. Complications associated with umbilical infections include septicemia, septic arthritis, and osteomyelitis.⁹² The umbilicus should be examined closely for patency, increased size, moistness or discharge, and tenderness. Abdominal palpation, using both hands and pressing together, is useful for evaluating the umbilicus of ruminants. Enlargement of the umbilical arteries can be palpated coursing caudally toward the bladder, and enlargement of the umbilical vein coursing cranially to the liver. Application of pressure caudal to the xiphoid often elicits a soft grunt from calves with a septic umbilicus and associated peritonitis. Extensive adhesion of bowel to inflamed umbilical structures produces a large, easily palpable intraabdominal mass. Common abnormalities of the calf umbilicus include umbilical hernias, omphalophlebitis, external umbilical abscess, urachal abscess, and omphaloarteritis. Patent urachus is uncommon in calves.

Ultrasound examination of the intraabdominal umbilical structures is a useful ancillary diagnostic tool. Ultrasonography of the umbilical structures of calves has been described by Watson and colleagues.⁹³ Ultrasound examination of the calf is performed with the calf standing; occasionally the umbilical vein is easier to identify with the patient in left lateral recumbency. The anatomy of the umbilicus of calves differs slightly from that of foals, necessitating alterations in ultrasound technique. In both species the umbilical vein courses from the umbilicus to the liver, which in the calf is located on the right side as opposed to midline in the foal. Also, in cattle the umbilical arteries and urachus retract into the abdominal cavity when the cord ruptures and thus cannot be identified in the external umbilical stalk in normal calves.⁹³ The umbilical vein of calves is scanned from the umbilical stalk to the liver along the right abdominal wall. The umbilical vein enters the liver caudoventral to the gallbladder. The umbilical arteries are most easily located adjacent to the urinary bladder and cannot normally be identified much beyond the apex of the urinary bladder unless they are enlarged and abnormal. Identification of a urachal remnant in calves is abnormal.⁹³

Literature on the efficacy of navel treatment at reducing calf mortality is divided. In a study of 104 dairy farms, a farm policy of navel treating newborn calves had no significant effect on calf mortality rates. A significant beneficial effect was observed when the navels of calves that had assisted deliveries were dipped with chlorhexidine; other navel treatments such as iodine tended to be associated with increased odds of dying.⁹⁴ Navel treatment with iodine was associated with significantly higher mortality in another study of 48 farms; however, the association of navel treatment with mortality on these farms may have reflected the response of producers to high neonatal mortality rather than indicating that iodine navel treatment is a risk factor for calf mortality.⁹⁵ Prophylactic administration of antibiotics to young calves has been associated with an increased incidence of diarrhea⁹⁶ and increased calf mortality.⁹⁷

Urogenital System

Neonates on a milk-based diet normally produce large volumes of dilute urine. Normal urine osmolarity in the 2- to 3-day-old calf has been reported to be 286 to 391 mOsm/L, and urine volume voided per day 34 mL/kg/day.⁹⁸

Congenital defects associated with the urogenital system in calves include ovarian aplasia, duplication of the cervix in Hereford cattle, persistence of the hymen (white heifer disease), and rectovaginal constriction in Jersey cattle. Congenital urolithiasis has been described in calves and lambs. Calcium oxalate is the most commonly reported congenital form of urolithiasis and may be associated with other congenital abnormalities.⁹⁹ A report of renal oxalosis in a number of Beefmaster calves suggests a possible recessively inherited metabolic defect resulting in primary hyperoxaluria in this breed.¹⁰⁰ Freemartins (XX/XY chimeras) occur in over 90% of bovine¹⁰¹ and 1% of ovine¹⁰² female heterosexual twins. Typically freemartins are sterile and have hypoplastic ovaries and internal tubal genitalia; the external genitalia normally are not affected. Males should be examined for cryptorchidism and male pseudohermaphroditism, and both sexes for evidence of hermaphroditism (gonads of both sexes).

Rupture of the urinary bladder at parturition is uncommon in ruminants. Clinical signs of a ruptured bladder include dysuria, stranguria, progressive abdominal distention, and depression. A percussion wave may be felt with ballottement of the distended abdomen. Ancillary tests including abdominal ultrasound, abdominocentesis, and assessment of serum and peritoneal electrolytes are useful to verify the diagnosis.

Hemodynamically mediated renal disease is observed sporadically in calves after chronic enteritis.¹⁰³ Prolonged reduced renal perfusion secondary to hypovolemia may lead to ischemia and acute tubular necrosis. Failure to thrive after apparent recovery from diarrhea may reflect compromised renal function.

Musculoskeletal System

The musculoskeletal system should be examined for evidence of birth trauma including fractured ribs, long bones, and mandibles, brachial plexus injuries, and soft-tissue trauma including an edematous head and tongue from prolonged compression in the pelvic canal. Strenuous manipulation during a dystocia can also result in Salter-Harris type 1 fractures characterized by disruption of the distal physis in one or more limbs. Femoral nerve paralysis occurs as a sporadic complication of dystocias associated with “hip lock” in calves.¹⁰⁴

All four legs should be examined for both flexural and angular limb deformities. Although most mild-to-moderate limb deformities correct themselves in a few days, others may need splinting for a successful result. In severe cases of congenital contracture, which are often associated with dystocia, even heroic measures, such as surgical resection of flexor tendons, may provide little or no benefit.

Any heat, swelling, edema, or pain around the joints or physes, or lameness, should be noted. A swollen joint should be considered infected until proven otherwise. In older neonates, metabolic bone disease should be considered as a differential diagnosis for lameness associated with flaring of the physis. Diets high in energy and protein that have low calcium and high phosphorus promote rapid weight gain, increasing the physical load on metabolically compromised growing bones. Damage to the growing physis may result in the subsequent development of angular limb deformities. Calcium deficiency in calves leads to reduced mineralization of bone. The transverse processes of the lumbar vertebrae become soft and bend when palpated. Copper deficiency causes metabolic bone disease that is manifested by physitis and brittle bones, reflected by a propensity to develop spontaneous fractures.

Skeletal muscle myopathy is an important differential diagnosis for lame neonatal ruminants. Lambs and kids with selenium and/or vitamin E deficiency are often mentally bright, are reluctant to stand, and walk with a stiff gait and cry when forced to move. Evaluation of serum creatinine phosphokinase, blood selenium, and plasma vitamin E concentrations is useful to confirm the diagnosis. In regions deficient in selenium, nutritional myodegeneration can be a major cause of death in neonates if the dam was not supplemented with selenium during pregnancy. Nutritional myodegeneration has also been observed when selenium levels are adequate but α-tocopherol levels are low.^105,106 The concentration of vitamin E in sheep colostrum is 5 to 11 times higher than in milk; sheep colostrum appears to be an important source of vitamin E for lambs, as vitamin E is transferred poorly across the placenta. Nutritional myodegeneration secondary to vitamin E deficiency is observed when pregnant ewes are maintained on forage low in vitamin E. Vitamin E–associated nutritional myodegeneration may be prevented by supplementing lambs and kids at birth with α-tocopherol (500 IU orally)* or by supplementing ewes during pregnancy either with a single dose of 500 mg IM 2 weeks before lambing or via dietary supplementation, delivering 150 mg daily for 3 to 4 weeks before lambing.¹⁰⁶ Neonatal nutritional myodegeneration associated with selenium deficiency may similarly be prevented by supplementing neonates at birth (2.5 to 3 mg of selenium per 45 kg) or by supplementing the dam during pregnancy and is discussed further in Chapter 42.

The skull should be examined for excessive doming of the forehead and symmetry. A moderately domed forehead is most commonly the result of intrauterine growth retardation rather than hydrocephalus. The entire vertebral column should be examined for scoliosis, kyphosis, and lordosis and other malformations. Arthrogryposis is characterized by multiple skeletal malformations, including severely contracted limbs and malformations of the vertebrae, and has been associated with the ingestion of toxins, such as locoweed and Sudan grass, by the pregnant mare.^107,108

Umbilical hernias are the most common congenital malformation. The greatest danger associated with a hernia is strangulation of a portion of the gastrointestinal tract outside the body wall, with compromise of its vasculature. Umbilical hernias in cattle do not tend to close spontaneously and are believed to be hereditary.¹⁰⁹ Dwarfism is a relatively common inherited problem in most cattle breeds. Osteopetrosis has been reported in Angus, Hereford, and Simmental breeds of cattle.¹¹⁰ Syndactyly is considered an inherited disorder in Holstein-Friesian cattle, and affected animals are also predisposed to hyperthermia.

Neurologic Examination of Neonatal Ruminants

Neurologic disease in neonates during the perinatal period often results from birth asphyxia, congenital disease, or sepsis. Congenital central nervous system (CNS) abnormalities in the large animal neonate may be inherited or may result from in utero infections, toxins, and other environmental factors. Hydrocephalus, hydranencephaly, and anencephaly may occur in calves. In the calf, both Akabane and bluetongue virus may cause hydranencephaly and other problems, including arthrogryposis and premature births. Hydrocephalus is fairly common and appears to be inherited as a simple autosomal recessive trait in many breeds. Internal hydrocephalus may result from a simple recessive gene or congenital BVD infection. Fetal infection with BVD virus may result in a number of other problems, including cerebellar dysplasia, ocular defects, hypomyelinogenesis, and intrauterine growth retardation. Cerebellar hypoplasia may also result from an autosomal recessive gene and is seen in a number of cattle breeds.

Disorders of amino acid metabolism that result in primarily neurologic signs include maple syrup urine disease^111,112 and citrullinemia.¹¹³ Maple syrup urine disease is analogous to branched chain keto acid decarboxylase deficiency and results in clinical signs of extensor spasms, weakness, dullness, recumbency, and opisthotonos shortly after birth. The most striking lesion of the CNS histologically is widespread spongy vacuolation in the white and gray matter of the brain. Citrullinemia, an inborn error of metabolism of the urea cycle, was reported in five neonatal Friesian calves.¹¹³ The calves appeared normal for a short period after birth, but at 24 hours to 5 days of age they developed progressive neurologic signs of depression, tremors, seizures, and opisthotonos, which were followed by death.

Congenital myoclonus (neuraxial edema) is an autosomally recessive inherited disorder of polled Herefords.¹¹⁴ Clinical signs included premature delivery, inability to stand after birth (with the majority remaining in lateral recumbency), normal mentation, and prominent sensory stimuli-induced myoclonic jerking of the whole body with extension of the head and limbs. The majority of affected animals also display traumatic hip lesions, presumably as a result of the severe myoclonic contractions. Severe alterations in spinal cord glycine-mediated neurotransmission result from a marked decrease or defect in glycine receptors and an increase in neuronal (synaptosomal) glycine uptake. Alterations are also present in the major inhibitory system (γ-aminobutyric acid [GABA] receptors) in the cerebral cortex.¹¹⁵ Storage diseases in cattle, usually inherited as autosomal recessive genes, include α-mannosidosis in purebred Angus, β-mannosidosis in Salers, GM-1 gangliosidosis in inbred Friesians, neuronal lipodystrophy in Beefmasters, and ‘“shaker calf syndrome” in horned Hereford calves. The last condition was recently recognized as an inheritable neurodegenerative disorder characterized by excessive accumulation of neurofilaments within neurons of the central, peripheral, and autonomic nervous systems. Clinical signs included a normal birth but inability to stand unassisted after delivery. Several hours later the calves developed fine generalized tremors, hyperesthesia to tactile stimulation, weakness, ataxia, and aphonia.¹¹⁶

Most acquired neurologic disease in neonates is associated with disease in other organ systems. Sepsis and diarrhea are both commonly associated with depressed mentation secondary to toxemia and/or metabolic derangements. Bacterial meningitis is common in neonates after bacteremia; diarrhea, septic arthritis, omphalophlebitis, and uveitis are frequent concurrent clinical problems. The clinical signs of meningitis in neonates—lethargy, anorexia, and recumbency—are nonspecific. Concurrent metabolic derangements may appear to provide an adequate explanation for the observed depressed mentation. In a retrospective study of 32 cases of bacterial meningitis in calves, concurrent metabolic derangements included hyperkalemia (15/25, 60%), respiratory acidosis (11/24, 46%), hypernatremia (3/20, 15%), and hypoglycemia (3/7, 43%).¹¹⁷ The more classical clinical signs described for bacterial meningitis in older animals—fever, opisthotonus, extension of the head, convulsions, hyperesthesia, and signs of neck pain—may not be evident or may not be perceived in neonates. Seizures in calves are often subtle, manifested as facial twitches or jaw champing. Common causes of cerebral disease in lambs and kids include polioencephalomalacia and focal symmetric encephalomalacia. Affected animals are typically depressed and blind but have normal pupillary light reflexes.

Posterior paresis is common in neonates; causes include border disease, enzootic ataxia, vertebral body abscesses, caprine arthritis encephalomyelitis virus, and vertebral body fractures associated with dietary copper deficiency or calcium phosphorous imbalance. These neurologic problems are discussed in Chapter 35.