Neonatology*



## S e c t i o n i i

## Neonatology
C H A P T E R 2 1 Neonatology*

## K. gary magdesian and pamela a. wilkins

## Physical examination of the newborn foal
Physical examination is the starting point for workup of the critically ill foal. To fully understand the subtle changes associated with disease, one must be familiar with the physical examination fi ndings and behavior of the healthy foal. Healthy, term foals are precocious neonates that can stand and nurse from the udder within 2 hours of delivery. An easy rule of thumb is the "1,2,3" rule: most foals should stand by 1 hour, they should nurse by 2 hours, and the placenta should be passed by 3 hours post partum. Vital signs change dramatically within the 24 hours of life. - At 1 minute of age the foal should have a heart rate and respiratory rate >60. By 1 to 2 hours after birth the heart rate should be 80 to 120 beats/min and the respiratory rate should be 30 to 40 beats/min. - At 10 minutes of age, a normal, healthy foal has an effective suckle refl ex, can sit sternally without assistance, and attempts to rise within 20 minutes.
- A fi nger inserted in the ear or nostril results in a head shake and a grimace refl ex. - Thoracolumbar stimulation performed by briskly running the thumb and forefi nger down either side of the foal's thoracolumbar spine elicits attempts to rise characterized by throwing the front legs forward, lifting the head and neck upward, and trying to push off with the hind limbs. - The foal's heart rate at this age approaches 100 beats/min, and the respiratory rate averages between 40 and 60 breaths/min. - A newborn foal that displays generalized hypotonia and an inability to rise, sit sternally, or suckle may be suffering from the following: - Peripartum hypoxia/asphyxia or other adverse peripartum challenge - In utero-acquired sepsis - Prematurity or dysmaturity - A thorough history of peripartum events and careful examination of the foal and placenta help differentiate these conditions. - Scleral injection and mucosal hemorrhages (petechiae) are consistent with sepsis in the neonate, and these fi ndings on physical examination warrant consideration of sepsis until proved otherwise. - Signs of hypovolemic shock in the neonatal foal include cold extremities, sunken eyes, We recognize and appreciate the contribution and original work of Wendy E. Vaala, VMD, in the fi rst edition, on which this chapter is based.

## Neonatology
obtundation, poor pulse quality, and pale mucous membranes. Unlike the adult horse, heart rate may not refl ect hypovolemia in the form of tachycardia.

## Placenta
A history of premature separation of placental membranes, prolonged delivery or dystocia, and meconium staining of the foal are periparturient events associated with acute or chronic hypoxia/ asphyxia. A maternal history of prepartum purulent vaginal discharge, precocious udder development and lactation, or evidence of abnormal discoloration of the placenta, particularly in the area of the cervical star, increases the index of suspicion for placentitis and in utero sepsis or fetal infl ammatory response syndrome (FIRS) associated with abnormal cytokine release. A normal placenta weighs approximately 10% to 11% of the foal's birth weight. Evaluate unusually heavy (or light) placentas by means of gross and light microscopic examination. Peracute cases of placentitis may produce only generalized edema without obvious areas of infection. Small placentas with large areas of abnormal villus formation have been associated with neonatal dysmaturity. Therefore, histopathologic examination of the placenta is strongly recommended if a neonate shows early abnormalities. Foals born with high serum creatinine concentration, especially when blood urea nitrogen (BUN) is normal or more normal than creatinine, should be suspected of having had abnormal placental function in utero.

## Prematurity
Foals from abnormally long gestations can exhibit signs of prematurity. The term dysmaturity rather than prematurity may be more appropriate in these cases. Unusually short (<320 days) or abnormally long (>360 days) gestation has been associated with the birth of foals with signs of prematurity, including the following:
- Small body size - Fine, silky hair coat - Generalized weakness - Increased passive range of limb motion - Flexor tendon and periarticular ligament laxity - Incomplete cuboidal bone ossifi cation - Domed forehead - Floppy ears - Inability to regulate body temperature Premature foals have inverted neutrophil to lymphocyte ratios, with a neutrophil/lymphocyte ratio <1 : 1. Hypoglycemia is common in such foals. Some foals born after a prolonged gestation have slightly different clinical features, characterized by a large frame size with poor muscle development, erupted incisors, and long hair coats. The physiologic fi ndings may be similar to those of dysmature foals, but the foals are considered "postmature."

## Mucous membranes and sclera
- At birth and during delivery, it is normal for mucous membranes of foals to appear cyanotic; however, this should resolve rapidly as the neonate makes the transition to extrauterine life. The mucous membranes of a healthy neonate quickly becomes pale pink with a capillary refi ll time of <2 seconds. Pale mucous membranes suggest anemia, whereas pale yellow mucous membranes are consistent with the presence of neonatal isoerythrolysis or hepatopathy. - Gray or slightly blue mucous membranes indicate shock, poor peripheral perfusion, or hypoxemia. Cyanosis appears only if the Pao 2 is <35 to 40 mm Hg and only when the packed cell volume (PCV) is within the normal range. Tissue damage may begin when Pao 2 is <60 mm Hg. - Do not rely on mucous membrane color to diagnose hypoxemia. - A birth, the normal foal is relatively tachypneic and tachycardic, but this should resolve with Of these two signs, increased or abnormal respiratory effort and pattern may be the most reliable indicators of respiratory diffi culty because foals with central respiratory depression due to hypoxia, hypothermia, hypoglycemia, or hypocalcemia may not have an appropriate increase in respiratory rate in response to pulmonary pathologic conditions. - Hyperemic, injected mucous membranes and hyperemic coronary bands may indicate sepsis or systemic infl ammatory response syndrome (SIRS) or be associated with FIRS. Petechiae on oral mucous membranes or inside the pinnas also are associated with sepsis and SIRS. Icteric mucous membranes may be observed with hemolysis, sepsis, equine herpesvirus (EHV-1) infection, meconium retention, and liver disease. NOTE: It is important to differentiate large-and small-vessel injection. Small-vessel injection imparts a generalized, bright red appearance to the mucous membranes and suggests more severe disease.
- The sclera should be white with only faint vessels apparent. Signifi cant injection is indicative of sepsis/SIRS. Prominent scleral hemorrhages can be observed after birth trauma. - Differential diagnoses for icterus in the neonatal foal include the following: - Liver or biliary disease: Examples are as part of multiple organ failure, resulting from sepsis, hepatitis/cholangitis, congenital malformation or dysfunction, glycogen branching enzyme defi ciency, Tyzzer's disease, toxic, and drug-induced. - Neonatal herpes viremia - Neonatal isoerythrolysis or other hemolysis

## Cardiovascular system
The cardiac rhythm of a neonate should be regular. However, nonpathologic sinus arrhythmia may be present for a few hours post partum. Heart rate averages between 70 and 100 beats/min during the fi rst week of life.

## Bradycardia
- Bradycardia is associated with the following severe conditions:
- Hypoglycemia: Use a stallside dextrometer, available in most human pharmacies, to monitor or measure blood glucose (see p. 561). Stallside dextrometers may be inaccurate under conditions of high humidity or extremes of temperature. See treatment of hypoglycemia. Avoid the temptation to give a bolus dose of 50% dextrose; rather, introduce 5% dextrose as a constant rate infusion beginning at 4 mg/kg per minute, increasing rate or concentration (no more than 15% dextrose) as needed to reach a target glucose concentration between 60 and 180 mg/dl. - Hypothermia: Carefully rewarm the foal. Be careful of direct heat application in the form of warming pads because they may thermally damage the skin. - Hyperkalemia: This condition is most common with anuric renal failure or ruptured bladder but also occurs with massive tissue damage resulting from severe shock, hypoxia, asphyxia, or muscular diseases such as white muscle disease (see p. 408 in the second edition). Hyperkalemic periodic paralysis is another possibility. - Tissue hypoxia: Perhaps the most common cause of bradycardia is hypoxemia or severe anemia leading to tissue hypoxia. Many foals respond readily to increased oxygen in the inspired air, administered by means of a mask, intranasal insuffl ation, fl ow-by oxygen, or nasotracheal intubation and ventilation. In cases of severe anemia, blood transfusion is indicated.

## Tachycardia
- Tachycardia occurs with the following: - Sepsis or SIRS: Fever often is absent at examination. - Hypovolemia - Hypoxemia - Anemia - Pain: abdominal or musculoskeletal - Stress - Cardiac failure or congenital cardiac anomalies - Hyperthermia - Hypocalcemia: occurs with severe asphyxia

## Murmurs
Many foals have physiologic fl ow murmurs that may persist for several days after birth. The typical patent ductus arteriosus (PDA) murmur is a continuous machinery murmur or a holosystolic murmur (most common) loudest over the left side of the base of the heart. Soft, blowing murmurs usually are Neonatology associated with blood fl ow and are exacerbated by anemia or alterations in hemodynamics. NOTE: Persistent or loud (> grade 2/6) murmurs, murmurs present for more than 5 to 7 days after birth that do not resolve or diminish in intensity, or murmurs associated with exercise intolerance or hypoxemia may be caused by persistent PDA, patent foramen ovale, ventricular septal defect, or another congenital heart anomaly and should be investigated further.

## Peripheral pulses
Peripheral pulses should be easy to palpate. The metatarsal artery is the easiest site to use. Bounding, hyperkinetic pulses are associated with early stages of compensated sepsis/SIRS. Weak, thready pulses indicate cardiovascular collapse and shock.

## Respiratory system
The resting respiratory rate of a newborn foal averages between 20 and 40 breaths/min (immediately after birth the respiratory rate should be >60 breaths/min). Because foals have a thin chest wall and a relatively rapid respiratory rate, thoracic auscultation often shows air movement throughout the chest even when there is lung disease, especially diffuse interstitial disease. Moist end-expiratory crackles and fl uidy large airway sounds are commonly auscultated immediately after birth as the normal foal expands its lungs. Unusually quiet adventitial lung sounds associated with large airway sounds auscultated immediately after birth can be compatible with incomplete alveolar infl ation and lung atelectasis. Signifi cant areas of ventral dullness on auscultation and percussion indicate areas of consolidation, atelectasis, or pleural effusion. Breathing effort should be minimal once the pulmonary liquid has been reabsorbed, which takes several hours. Areas of dorsal dullness when the foal is in sternal recumbency suggest pneumothorax. Neonatal foals rarely have signifi cant pleural effusion, but this should be ruled out in cases of ventral dullness. Pleural fl uid may occur in the neonatal foal with hemothorax, bacterial pneumonia chylous effusion, cardiac failure, and uroperitoneum.

## Respiratory distress
- Respiratory distress is exacerbated by recumbency and characterized by the following:
- Nostril fl are - Expiratory grunting - Rib retraction - Increased abdominal effort - Paradoxical respiration (chest wall collapses during inspiration) In some cases, respiratory distress is associated with congenital airway abnormalities such as choanal atresia and subepiglottic cysts, warranting endoscopic examination. Rule out rib fracture (gentle palpation, ultrasonographic evaluation of ribs) in all foals showing respiratory distress or abnormal respiratory function.

## Apnea
- Apnea and unusually slow or irregular respirations are abnormal and have been associated with the following:
- Central respiratory depression resulting from asphyxia or extrauterine maladaptationprobably the most common cause in neonatal intensive care units - Hypoglycemia - Hypothermia - Prematurity

## Diagnostic tests
Thoracic radiography and ultrasonography help identify rib fractures, hemothorax, pneumothorax, pulmonary consolidation, abscessation, and pleural effusion. Arterial blood gas analysis is the most accurate assessment of pulmonary function. These samples are most easily collected from the metatarsal artery or the decubitus artery . The artery can be used for repeated sampling. A small, subcutaneous, intradermal bleb of 2% lidocaine (without epinephrine) makes collection easier for foals sensitive to arterial puncture. Upper airway endoscopy is valuable in assessment for congenital anomalies and laryngeal dysfunction.

## Abdominal examination
Abdominal Auscultation - Auscultation should demonstrate bilateral borborygmi. Ingestion of colostrum and the act of sucking itself enhance gastrointestinal (GI) motility and passage of meconium and feces.

## Meconium
The fi rst manure a foal passes, meconium, is composed of cellular debris, intestinal secretions, and amniotic fl uid ingested by the fetus. Meconium is dark, blackish brown, or gray and is fi rm, pelletlike, or pasty. All meconium should be passed within 24 hours of birth and is followed by softer, yellow-tan "milk feces." Absence of manure passage can be associated with the following: - Atresia coli: This problem is suggested by lack of fecal staining in enema fl uid. - Meconium retention/impaction - Ileus - Intestinal obstruction - Ileocecocolic agangliosis in white homozygous overo foals (lethal white overo syndrome) Because of the foal's thin body wall, distention of the small or large intestine results in visible, generalized abdominal enlargement. Simultaneous auscultation or percussion of tympany indicates the presence of a gas-distended viscus. Tight, tympanic, dorsally distributed distention is compatible with gas accumulation. Turgid, ventrally distributed, pendulous distention can be seen with uroperitoneum and peritoneal effusion. Abdominal distention can contribute to cardiorespiratory failure by increasing intrathoracic pressure, a phenomenon known as thoracic tamponade associated with intraabdominal hypertension and abdominal compartment syndrome.

## Causes of colic (with or without abdominal distention)
- Meconium or fecal impaction: The impaction usually can be found by means of digital examination, although abdominal radiography or ultrasonography may be needed to fi nd more proximal impactions. Many foals allow abdominal palpation. In these cases, if abdominal distention is not severe, meconium may be palpated. Some foals have meconium retention without colic. In these cases, passage of meconium/feces is delayed because of primary GI dysfunction but does not result in colic and is common in foals with peripartum asphyxia or sepsis. Such foals may be less tolerant of enteral feeding because of this meconium retention. Foals with true meconium impaction may become uncomfortable because of proximal gas distention. occasionally, salmonellosis. If severe gastric distention is present, passage of the tube beyond the cardia may be diffi cult. Lidocaine applied to the nasogastric tube or injected down the tube helps relax the cardiac sphincter and facilitate entry into the stomach. Use the largest-diameter tube that can be passed in cases in which the presence of refl ux is suspected but no fl uid is obtained.

## Abdominal radiography
- Abdominal radiography can be used to determine the location, but not necessarily the cause, of gas or fl uid distention. Gaseous distention of the small intestine characterized by gas-fl uid interfaces within the lumen can be found in foals with ileus caused by enteritis, peritonitis, neonatal gastroenteropathy/ neonatal necrotizing enterocolitis, and smallintestinal obstruction (see p. 165). Concurrent large bowel distention is frequently associated with ileus caused by neonatal gastro enteropathy/neonatal necrotizing entero colitis or enteritis. Primary large-bowel distention occurs with obstruction caused by meconium impaction/retention, volvulus, or displacement. Sand or dirt accumulation can also be detected in foals with pica. - Radiographic settings on portable and stationary machines vary a great deal and depend on the model and brand of the unit, cassettes, fi lm-screen combinations, and focal distance. Consultation with a radiologist or radiologic technician is recommended for guidelines.

## Contrast studies
- Barium enema radiographic examination (barium mixed with warm water and administered by gravity fl ow through a cuffed Foley catheter inserted in the rectum) helps identify meconium impaction and may aid in the diagnosis of atresia. - Upper GI contrast radiography is used to document the delayed gastric emptying and prolonged transit time that occur with ileus, obstruction, and gastroduodenal ulcer disease. This is particularly helpful in foals with gastric outfl ow obstruction/dysfunction due to ulcers or strictures. - Contrast radiography of the upper GI tract is performed by administering 5 ml/kg barium sulfate suspension through a nasogastric tube. Serial radiographs are obtained 10, 20, 30, and 60 minutes and 2 and 4 hours after administration of the contrast agent. Contrast radiography is used to fi nd GI obstruction and ulceration. Normal fi ndings are as follows:
- Barium begins leaving the stomach immediately and is gone after 1 1 / 2 to 2 hours. - The cecum fi lls by 2 hours. - The transverse colon fi lls by 3 hours. Transabdominal Ultrasonography See p. 39. - Ultrasonography allows evaluation of the following:
- Small-intestinal motility - Bowel wall thickness - Degree of gastric or small-or large-intestinal distention - Volume and character of peritoneal fl uid Healthy foals have fl accid, motile, fl uid-fi lled loops of small intestine with a wall <3 mm thick and minimal amounts of peritoneal fl uid. Round, fl uid-distended loops of bowel can be seen with ileus, enteritis, and small-bowel obstructive disease. Enteritis results in a generalized increase in bowel wall thickness and edema. Severe neonatal gastroenteropathy/neonatal necrotizing enterocolitis bowel diseases can produce focal increases in bowel wall thickness with or without intramural gas accumulation (i.e., intestinalis pneumatosis). Small-intestinal intussusception has a doughnutshaped pattern ("target lesion") caused by the telescoping of one segment of bowel into another. The presence of an excessive volume of clear, nonechogenic peritoneal fl uid is compatible with uroperitoneum. An increase in peritoneal fl uid echogenicity is associated with increased cellularity, as in peritonitis (possibly associated with uroperitoneum if caused by ruptured urachal abscess), hemoperitoneum, chylous effusion, or ruptured abdominal viscus.

## Abdominocentesis
- Abdominocentesis is used to obtain peritoneal fl uid for analysis and cytologic examination. The procedure is best performed by means of sterile technique and ultrasound guidance with a 20-gauge needle or a teat cannula. CAUTION: Use care in performing abdominocentesis with a teat cannula: omental herniation can result. Any opening created by the procedure should be closed with a cruciate suture once the cannula is withdrawn. Needles can also penetrate the intestine and should be used cautiously.
- The fi nding of peritoneal fl uid with an increased nucleated cell count and protein concentration is consistent with peritonitis.
Peritoneal fl uid with a creatinine concentration greater than twice serum creatinine concentration establishes the diagnosis of uroperitoneum. If there is distended intestine, abdominocentesis can result in bowel perforation and peritonitis. Any obtained peritoneal fl uid should be tested for creatinine concentration, nucleated cell count, and total protein concentration and should be cultured. Sanguineous fl uid should be measured for PCV. Peritoneal lactate and glucose concentrations may be useful in assessing peritonitis and bowel ischemia when compared with plasma concentrations. Gastroscopy See p. 157, Gastric Ulcers. - Gastroscopy is used primarily to document gastric ulceration. It is also used to evaluate duodenal ulceration if the duodenum is entered. Withhold food and drink for a minimum of 3 to 6 hours before gastroscopy to ensure adequate gastric emptying.
- It is important that the stomach of the foal not be excessively fi lled with gas during the examination, because this exacerbates colic. Try to remove all gas before withdrawing the endoscope from the stomach. Refrain from performing gastroscopy just to "have a look" because many normal foals exhibit colic after the procedure because of the introduced gas in the GI tract.

## Urogenital system
Urination - Time to fi rst urination is approximately 8 to 12 hours, fi llies taking slightly longer than colts to void for the fi rst time. Because of a persistent frenulum, some colts do not drop the penis to urinate for the fi rst week after birth. Resist the urge to "pull the penis down" because this is uncomfortable for the foal and generally not necessary. The specifi c gravity of the fi rst urine produced usually is >1.035. Observe urination closely to be certain the foal does not have a patent urachus, in which case urine drips from the umbilicus. Colts urinating in their prepuce may appear to have patent urachus, as the urine runs down their ventral abdomen and drips off the external umbilical remnant or may create one because of the umbilical stump being wet with urine constantly. - Healthy, well-hydrated foals urinate frequently, often after nursing. Urine specifi c gravity is low in nursing foals (1.001 to 1.010) because of the high-volume liquid diet. Foals with peripartum asphyxia may have oliguria because of decreased renal blood fl ow and urine production (neonatal nephropathy), which warrants close monitoring of urine output. Dysuria can be observed with uroperitoneum, urachitis, patent urachus, cystic blood clots resulting from umbilical bleeding, or urachal diverticulum. Occasionally, foals with hypoxic ischemic injury (peripartum asphyxia) cannot urinate despite greatly distended bladders. Such foals require indwelling urinary catheterization for 1 or more days until the micturition refl ex normalizes, in order to prevent bladder rupture.

## Ophthalmic examination
- A pupillary light response is present and is more sluggish than in adult horses. - A consistent menace response often is not present until 2 to 3 weeks of age. Newborn foals have decreased corneal sensation and may not appear painful with corneal ulceration. - Ventral medial strabismus is common.
- Examine the foal's eyes for corneal cloudiness, congenital cataracts, microphthalmia, or entropion. - Ophthalmic examination may show a persistent hyaloid artery remnant coursing from the optic disc to spread on the posterior lens capsule, often resembling a spider's web. This is not an abnormality and should disappear with time. Suture lines frequently can be seen in the center of the lens. - Examine the retina for signs of detachment and hemorrhage. Scleral hemorrhage can be associated with sepsis, disseminated intravascular coagulation (DIC), or birth trauma. - The optic disc is round in foals compared with the elliptical shape in adults.
- Corneal ulcers are common in recumbent and weak foals. All septic and peripartum asphyxia foals should be evaluated for the presence of ulcers with fl uorescein stain. - Entropion is common in premature and dysmature foals. Most of these cases are transient and respond to temporary sutures for a few to 20 days. After local anesthesia, two to three single vertical mattress sutures are placed in the affected eyelid using 4.0 silk or nylon. Skin staples may also be used. - Congenital cataracts can be removed surgically if determined to be congenital and not resulting from infl ammation. Phacoemulsifi cation of the lens is highly successful and best performed in foals under 6 months of age.

## Neurologic evaluation
Healthy foals are bright, alert, and responsive to touch and sound. While being restrained in a standing position, foals often alternate between periods of hyperactivity and struggling and episodes of sudden, complete relaxation (fl opping). Foals should stand with an erect, angular head and neck carriage and a base wide stance in front. Their gait is exaggerated and limb refl exes are increased compared with adult horses. When recumbent, foals have strong resting extensor tone and a crossed extensor refl ex that persists for as long as 1 month. Foals normally spend approximately 50% of their time sleeping. When sound asleep, normal foals may be extremely diffi cult to arouse and may exhibit rapid eye movement, limb twitching, and irregular breathing patterns. To the untrained eye, this activity can be confused with seizure activity.

## Neurologic disease
The most common cause of neurologic disease among newborn foals is peripartum hypoxic/ ischemic damage or damage resulting from cytokine release associated with placental infl am mation/infection or sepsis. These perinatal injuries (neonatal encephalopathy) can produce the following: Hypertonic saline (3% to 7.5%) is an alternative to mannitol; however, serum sodium concentrations should be monitored closely. Dexamethasone is controversial and is no longer advocated in the acute treatment of head trauma. Dimethyl sulfoxide (DMSO), 1 g/kg IV diluted in 1 L of lactated Ringer's solution q12h or q24h is used by some, although its use and popularity are dwindling. It should be noted that neonatal foals may not eliminate DMSO as quickly as adult horses, and this can cause undesirable, persistent hyperosmolarity. DMSO solutions can cause hemolysis (rare in foals) and should be administered at no greater than 10% strength. The author prefers not to administer DMSO to neonatal foals. - Neonatal encephalopathy: Administer oxygen and improve cardiac function, polyionic crystalloids, colloids (plasma), dextrose in water (5% to 15% to provide 4 mg/kg per minute of dextrose) and positive inopressor drugs (e.g., dobutamine, 2 to 10 g/kg per minute; norepinephrine, 0.01 to 0.5 g/kg per minute) to normalize arterial pressure with hypoxia or head trauma. Magnesium may have some benefi t in reducing secondary or reperfusion injury. - Meningitis: antimicrobial therapy and other supportive therapy. Pharmacology of antimicrobials should be considered, especially blood-brain barrier penetrability. Third-generation cephalosporins, such as cefotaxime, ceftazidime, or ceftriaxone, are advantageous in terms of spectrum of activity and central nervous system (CNS) penetrability. Halicephalobus gingivalis nematode infection (older nomenclature: Halicephalobus deletrix, Micronema deletrix) has been documented as a cause of CNS disease in foals younger than 3 weeks. - Hypoglycemia: See previous discussion and p. 488. - Hypocalcemia: Administer 10% calcium gluconate, 1 to 2 ml/kg (Ca 2+ , 9 to 18 mg/kg), slowly IV over 5 to 10 minutes diluted in crystalloids. Slow or stop infusion if bradycardia develops. Follow with a maintenance infusion of calcium: 10% calcium gluconate, 5 ml/kg per day. - Hyponatremia: Give hypertonic saline solution, 1 ml/kg repeated-dose administration every 15 minutes until serum Na + concentration is raised by a few milliequivalents per liter (usually 2 to 5 mEq/L) and seizures stop, only if hyponatremia has been present for less than 12 hours and you are sure of this fact. Once seizures stop, the rate of sodium correction should be slowed (0.5 mEq/L per hour once at 120 mEq/L or greater). This emergency treatment is for seizures caused by hyponatremia and should not be used if seizure activity is not present. Sodium concentration in other cases of hyponatremia (longer duration or no seizure activity present) should only be increased at a rate of 0.5 mEq/L per hour. - Toxin or drug-induced: for example, aminophylline, cimetidine, imipenem, and doxapram - Idiopathic epilepsy: treated long-term with phenobarbital or potassium bromide

## Musculoskeletal system
- Examine the musculoskeletal system, including mandible, limbs, and ribs, for fractures resulting from birth trauma. Fractured ribs often are diffi cult to detect but frequently produce a clicking sound on auscultation, heard in synchrony with respiration. Keep foals with fractured ribs quiet, generally with the affected side down. Foals with multiple or medially displaced rib fractures may be candidates for surgical repair, particularly if there is any evidence of internal thoracic trauma or if the rib fractures are located over the heart. Foals normally have a mild carpal and fetlock valgus conformation in front; fetlock varus is more common behind. Examine limbs for more severe angular and fl exural deformities. Palpate joints and physes for signs of swelling and heat (see Chapter 15).

## Neonatology

## Dysmaturity, prematurity
- Musculoskeletal signs:
- Increased passive range of joint motion - Periarticular ligament and fl exor tendon laxity - Incomplete cuboidal bone ossifi cation (see p. 319; detectable only on radiographs) of carpus and tarsus (the navicular bone and epiphyses of long bones should also be evaluated in very premature foals): If incomplete ossifi cation is severe, restrict exercise and provide assistance as the foal attempts to stand. Tube casts and splinting are generally not recommended for these cases because they contribute to laxity of the supporting structures and may be associated with increased morbidity (cast sores). If used, they should be changed frequently. Casts can be stopped above the fetlock to minimize development of laxity.

## Severe flexor tendon laxity
- Treatment includes the following:
- Controlled exercise - Shoes with heel extension - "Light" protective wraps if weight bearing results in trauma to heel bulbs and fetlock, but keep in mind that wraps can compound laxity

## Septic arthritis
- Lameness is usually present, although septic arthritis/physitis can be diffi cult to identify in weak or recumbent foals. Careful, frequent palpation and visual assessment of all joints and growth plate regions are warranted in such foals. If a neonatal foal becomes acutely lame, septic arthritis should be the top differential diagnosis unless another cause is proved; too often an overly optimistic diagnosis of "the foal might have been stepped on by the mare" is made, and early and important treatment of septic arthritis may be delayed. - Fever is variable. - Painful, warm joint effusion is frequently accompanied by signifi cant leukocytosis and hyperfi brinogenemia. - Radiographs of affected joints are indicated to evaluate for concurrent septic physitis or osteomyelitis. Ultrasonography, computed tomography, or magnetic resonance imaging can aid in diagnosis of bone infections when equivocal results are obtained radiographically.
- Arthrocentesis reveals a neutrophilic pleocytosis and increased total protein concentration.
Neonatal foals with septic arthritis may not develop as great an elevation in white blood cell count as adult horses. Synovial fl uid leukocyte counts of 10,000 cells/l are indicative of sepsis. Synovial fl uid lactate and glucose concentrations and pH are helpful adjuncts in evaluating for sepsis; lactate increases, whereas glucose and pH decrease relative to serum concentrations. - Treatment is with systemic antimicrobial therapy and joint lavage using balanced electrolyte solution with 10 g DMSO added to 1 L. Small volumes of an antimicrobial (amikacin, <1 ml, or 250 mg per joint) can be instilled in the joint after lavage, but monitor total dose. Arthroscopic examination and lavage is indicated in joints where fi brin deposition or osteomyelitis is suspected. Regional limb perfusion, using one third the calculated total systemic dose of aminoglycoside, is indicated in many cases. Some severe cases may benefi t from debridement of affected bone or other more invasive techniques. If two or more joints are treated, the total daily dose of amikacin should be reevaluated and altered as required on the basis of peak and trough kinetics. Intraosseous perfusion is an alternative route when intravenous perfusion is not possible. - Continuous intrasynovial antimicrobial infusion has been studied recently for use in equine septic joints and appears to be an effective adjunct.

## Septic osteomyelitis
- Variable lameness - Fever - Painful swelling over physis or epiphysis proximal to joint, with or without sympathetic joint effusion - Radiographic evidence of periosteal osteolytic and proliferative changes - Leukocytosis and hyperfi brinogenemia usually accompanying the condition - Treat with long-term antimicrobial therapy; aspirate physis for culture and sensitivity; use nonsteroidal antiinfl ammatory drugs conservatively to provide analgesia and decrease infl ammation. Regional limb perfusion, using one third the calculated total dose of aminoglycoside, is indicated in many cases. Some severe cases may benefi t from debridement of affected bone or other more invasive techniques. Support unaffected limbs. The need for long-term nonsteroi-dal analgesia should prompt prophylaxis for gastric and duodenal ulcer disease in the care of these patients. Ketoprofen (1 to 2 mg/kg IV q24h) or carprofen (0.7 to 1.4 mg/kg IV or PO) may be safer for long-term use.

## Limb contracture/congenital flexural deformity
- Contracture and deformity can involve proximal (carpus, tarsus) or more distal (fetlocks, pasterns) joints. Tendon contracture has been associated with in utero malpositioning, toxins such as Sudan pasture, genetic causes (Norwegian Fjord horses), and neonatal hypothyroidism. Therapy for contracted tendons includes physical therapy, systemic analgesics, Robert Jones wraps or splinting, casting, controlled exercise to prevent extensor tendon rupture, and oxytetracycline, 1 to 3 g IV q24-36h for a maximum of three doses. Measure serum creatinine concentration before and after each treatment. CAUTION: Acute oliguric renal failure has been reported to occur after this treatment. Concurrent intravenous administration of fl uids is warranted.
- Casting and splinting have been associated with exacerbation of lateral laxity, promote rub and pressure sore development, and should be used with care.

## Nursing behavior
A healthy foal consumes between 15% and 25% of its body weight in milk daily with an average weight gain of 1 to 3 lb (0.45 to 1.35 kg) per day. Foals nurse at least several times an hour. Udder distention in the mare is one of the earliest signs of a "fading foal" that is no longer nursing effectively. Milk dripping from a foal's nose after nursing may be the result of the following: - Cleft palate: Although it has to be ruled out, cleft palate is one of the least common causes of dysphagia among foals. - Subepiglottic cyst - Persistent or restricted epiglottic frenulum - Dorsal displacement of the soft palate - Generalized weakness caused by sepsis/SIRS/ FIRS or dysmaturity (common) - Dysphagia associated with perinatal asphyxial syndrome (common) - White muscle disease: common in certain geographic regions - Esophageal pooling of milk (megaesophagus) - Idiopathic-may resolve in a few days

## Nutrition
The caloric requirements of the healthy, active foal are believed to be approximately 120 kcal/kg per day. Sick neonates, such as foals with sepsis or peripartum asphyxial injury, often have reduced caloric needs because of inactivity and recumbency. Feeding excessive calories is potentially harmful in septic human patients because these calories can be used to drive the infl ammatory response. Preliminary investigations using indirect calorimetry suggest that sick and nonexercising (orphan) foals have reduced resting energy requirements, as low as 43 to 55 kcal/kg per day.
Mare's milk is the optimal food source for foals. Mare's milk has approximately 500 kcal/L of milk. To provide 50 kcal/kg per day, a total of 2500 kcal is necessary for a 50-kg foal, equating to 5 L of milk. This is equivalent to 10% of body weight in milk. Alternatives for orphan foals include commercial milk replacers and goat milk. The author (KGM) prefers a 1 : 1 mixture of foal milk replacer and goat milk. Foals should be fed small amounts frequently, for milk serves as a buffer for gastric pH. Dividing the daily requirement into feedings every 2 hours or more frequently of small meals is optimal. Please see section on nutritional support and parenteral nutrition for more information (see p. 671).

## Catheterization and blood sampling
The jugular vein is the most common site for venipuncture in an awake, active foal. In more depressed foals, the saphenous and cephalic veins can be used. Sites for arterial blood gas sampling include the lateral metatarsal (fi rst choice), decubitus, transverse facial, facial, and less frequently, the brachial artery ; see p. 490).

## Triage of the critically ill foal (emergency stabilization) generalized weakness, loss of suckle
The most common causes of weakness and reluctance to suckle among newborn foals are the following: - Sepsis/SIRS - Peripartum asphyxia - Prematurity, dysmaturity

## Sepsis/sirs
Sepsis/SIRS is the leading cause of neonatal foal morbidity and mortality. The conditions are most commonly associated with gram-negative bacterial infections and endotoxemia, although grampositive microbes often are present concurrently. The clinical signs associated with sepsis are the result of unbalanced stimulation of the immune system after exposure to microbial toxins. During sepsis, release of endogenous proinfl ammatory and antiinfl ammatory mediators (e.g., tumor necrosis factor and interleukins-1, -2, and -6) precipitate a cascade of metabolic and hemodynamic changes that can fi nally result in multiple organ system failure. As septic shock advances, the patient dies of a combination of cardiopulmonary failure, generalized coagulopathy, disruption of metabolic pathways, and loss of vascular endothelial integrity.
The organisms most commonly associated with foal sepsis include Escherichia coli, Actinobacillus, Pasteurella, Klebsiella, Salmonella, and Streptococcus. Viral pathogens such as EHV-1 and equine arteritis virus also can produce sepsislike syndromes (SIRS), as can tissue damage associated with adverse peripartum events or severe hypoxia. <23 mEq/L because of poor peripheral perfusion and anaerobic metabolism. An increase in lactate concentration in these cases may contribute to the observed acidemia. Lactate concentration in neonates is higher than adults in the fi rst 24 hours of life. Neonates with high lactate concentrations may clear this rapidly with resuscitation; persistently increased lactate concentrations may carry a poorer prognosis.

## Clinical signs and diagnosis

## Neonatology

## Cultures for diagnosis
- Culture blood, synovial fl uid, CSF, peritoneal fl uid, and urine. Tracheal aspiration, although useful in the evaluation of foals with pneumonia, may be too stressful to perform on septic neonates with severe respiratory distress but should be considered if it can be rapidly and expertly performed. All samples obtained should be submitted for bacterial (aerobic and anaerobic), fungal, and viral isolation and identifi cation.

## Radiographs
- Obtain thoracic radiographs with the foal in lateral recumbency and the forelegs pulled forward to improve evaluation of the cranioventral lung fi elds. Obtain thoracic radiographs with the foal standing when possible, to reduce effects of recumbency-induced atelectasis. It may be desirable to image both sides of the thorax.
- Bacterial bronchopneumonia commonly is associated with an alveolar pattern and air bronchograms in the cranioventral and caudoventral lung fi elds . Acute bacterial pneumonia also can present as diffuse interstitial disease. Both patterns can be seen in acute lung injury and acute respiratory distress syndrome. - Viral pneumonia can be characterized by a diffuse interstitial pattern . - Aspiration pneumonia is associated with caudoventral and cranioventral infi ltrates.
- Surfactant defi ciency and hyaline membrane formation produce a diffuse, ground-glass appearance of the lung with prominent air bronchograms. This radiographic appearance also has been seen in foals with viral pneumonia . The ground-glass appearance can be mimicked in lateral thoracic radiographs of foals with hemothorax. - Radiographic abnormalities in the caudodorsal lung fi eld were more commonly associated with poor outcome in one study. - Serial radiographs of swollen joints or painful physes are recommended to detect signs of articular damage and osteomyelitis. These radiographs should be repeated in 2 to 5 days if swelling or pain persists.

## Figure 21-2
Recumbent lateral thoracic radiograph of a foal with bacterial pneumonia. The radiograph shows significant alveolar infi ltrate involving the caudal and ventral lung fi elds. This fi nding is compatible with consolidation resulting from bronchopneumonia.

## Figure 21-3
Recumbent lateral thoracic radiograph of a 24-hour-old foal. The pregnancy was complicated by severe bacterial placentitis. Radiograph shows an interstitial pattern most pronounced in the caudodorsal lung fi elds.

## Figure 21-4
Recumbent lateral thoracic radiograph of a premature foal. Cesarean section was performed at 322 days of gestation. A diffuse alveolar pattern in all lung fi elds is compatible with diffuse pulmonary atelectasis.
- Plain abdominal radiographs can help identify the location of gas distention. Ileus associated with enteritis or peritonitis is associated with generalized mild to moderate distention of the small and large intestines.

## What to do: general therapy for septicemia
goal is volume resuscitation but not overhydration or overloading with sodium.
- The minimum (dry) maintenance fl uid rate is administered as 5% dextrose, calculated as follows:
- 100 ml/kg per day for the fi rst 10 kg body mass - 50 ml/kg per day for the second 10 kg body mass - 20 to 25 ml/kg per day for the rest of the body mass - This provides the volume needed for a recumbent foal not consuming a milk diet for water maintenance and is about 94 ml/h for a 50 kg foal. If the foal is not receiving milk or total parenteral nutrition (PN) as an energy source, this rate, or the dextrose concentration, can be adjusted to provide 4 to 8 mg/kg per minute until dextrose needs are met. This rate needs to be adjusted upward accordingly to meet losses incurred by the foal because of increased insensible (increased respiration, fever, activity) or sensible (increased urine output, diarrhea) losses. Most foals actually begin at 1.5 to 2 times the calculated "dry" rate. Normal sodium need for a growing neonatal foal is 1.5 to 3 mEq/kg per day and can be generally met by the administration of a single liter of plasma or crystalloid containing 140 mEq/L. - Monitor blood pressure, central venous pressure (goal, 2 to 10 cm H 2 O), urine output, heart rate, peripheral pulses, and respiratory function. There is no "magic" number for mean blood pressure in foals, but a mean pressure between 45 and 50 mm Hg may be adequate if the pulse pressure difference is >30 to 40 mm Hg. Others prefer to maintain the mean pressure at 60 mm Hg or greater. Most important is the physical examination and clinical condition: Is the foal warm in its periphery? Are peripheral pulses easily found? Is the foal making urine, and what is the mental status of the foal? - Plasma may be needed to maintain oncotic pressure and intravascular fl uid volume. Minimum volume to administer is 20 ml/kg over 60 minutes, but foals with adequate fl uid volume should be administered plasma at a slower rate. One liter of plasma provides the equivalent sodium load of a normal milk diet in a normal foal in a single day. Hetastarch may also be used by some practitioners at an initial dose of 10 ml/kg body mass. Larger doses may induce or exacerbate coagulation abnormalities. - Volume expansion alone usually is sufficient to correct mild to moderate metabolic acidosis. Severe metabolic acidosis, especially when caused by a strong ion acidosis (i.e., hyperchloremia or hyponatremia) may necessitate sodium bicarbonate supplementation (generally diarrhea cases with ongoing bicarbonate losses), but be aware that for each milliequivalent of bicarbonate administered, a milliequivalent of sodium also is administered. Prefer isotonic (1.3%) solutions (150 mEq NaHCO 3 per liter). Bicarbonate should not be administered to patients in cardiac arrest or that need considerable resuscitation efforts. Ensure adequate ventilation before administering bicarbonate. Avoid rapid infusion: It is unnecessary and may lead to respiratory or paradoxical CNS acidosis. Sepsis-induced hypotension can be diffi cult to manage because some foals may be less responsive to adrenergic drugs. This may be simply a function of how they manifest sepsis or may be associated with developmental age. Treatment recommendations include the following:
- Isotonic fl uids as indicated before - Dobutamine: 2 to 15 g/kg per minute continuous infusion. Dobutamine is used to treat patients with adequate volume expansion as a beta-adrenergic, inotropic agent to improve cardiac output and oxygen delivery. Titrate dose to effect. Discontinue administration if severe tachycardia develops (>50% increase). - Norepinephrine: 0.01 to 3.0 g/kg per minute. Norepinephrine is an alpha-agonist pressor agent. Norepinephrine should be used with dobutamine to minimize splanchnic hypoperfusion. Norepinephrine is one of the least offensive pressor agents in terms of GI hypoperfusion in other species. - Vasopressin: 0.25 to 1.0 mU/kg per minute.
At this low dose, vasopressin provides support for adrenergic pressors, particularly in septic patients, without inducing renal effects. A potential concern with vasopressin is GI and splanchnic hypoperfusion.

## Neonatology
Vasopressin should therefore not be used in primary GI cases until studied further. - For unresponsive moderate to severe hypotension:
- Epinephrine: 0.1 to 2.0 g/kg per minute. Expect measured lactate concentration to increase substantially when this drug is used. - Phenylephrine: 1 to 20 g/kg per minute.
Although this pressor almost always increases measured pressure, the generalized vasoconstriction produced is probably counterproductive in the treatment of the patient because of severely diminished perfusion. Relative or absolute adrenal insuffi ciency may also exist in some septic foals, high adrenocorticotropic hormone, low or normal cortisol. If the septic foal is unresponsive (hypotensive) to fl uids and routine pressor drugs, 0.25 to 0.5 mg/kg hydrocortisone can be administered in hopes of improving the response. Combinations of the foregoing treatments are commonly used, and good fi rst-choice combinations include dobutamine-vasopressin and dobutamine-norepinephrine.

## Respiratory support
The aim of therapy is to minimize ventilationperfusion mismatching. Administer 10 mg/kg PO or per rectum as a loading dose, followed by 2.5 to 3 mg/kg PO once or twice daily as a maintenance dose. Therapeutic trough serum concentration is 5 to 25 g/ml. Toxicity (CNS signs) is associated with concentrations greater than 40 to 50 g/ml, but these concentrations are rarely achieved in foals.

## Nutritional support
- Hypoglycemia is managed initially with a glucose infusion best administered as a constant infusion of 5% or 10% solution at a rate of 4 to 8 mg/kg per minute. NOTE: At this rate, a 50-kg foal would receive 120 to 240 ml of 10% dextrose per hour. Do not give foals bolus infusions of 50% dextrose.
- Caloric requirements: A healthy foal consumes 10% to 20% of its body weight daily in milk, which equals 54 to 108 kcal/kg per day. Sepsis and fever are assumed to increase caloric requirements to 150 kcal/kg per day, although this may not be true in all cases and foals that are recumbent and weak likely Neonatology have reduced caloric requirements even when septic. Many ill foals gain weight on 10% body weight equivalent feeding (50 to 54 kcal/kg per day), likely because of decreased energy requirements associated with recumbency and lack of normal activity. - Enteral feeding: Use mare's milk, foal milk replacer, or goat's milk (or a combination). NOTE: The goal is 10% to 20% of body weight per day in milk administered in small volumes every 2 to 3 hours. If GI function is questionable, begin enteral feedings cautiously at 5% to 10% of the foal's body weight per day or less with gradual advancement of volume as it is tolerated. Supplement with PN if <10% of body weight in milk is fed daily for 2 consecutive days. Do not allow stuporous foals to nurse or drink from a bottle. Always feed foals in standing or sternal recumbency and maintain them in that position for at least 10 minutes after feeding is completed. CAUTION: Never feed a cold, severely hypotensive foal. - 10 g/kg per day of dextrose - 2 g/kg per day of amino acids - 1 g/kg per day of lipids - 5 to 10 ml/d of multivitamins - Add trace minerals if the foal needs prolonged parenteral nutritional support. - Potassium chloride can be added to the parenteral formula. - When fi rst starting PN, begin at one fourth the desired fl ow rate. Check blood for lipemia and blood and urine for hyperglycemia (blood glucose concentration, >180 mg/dl) at 3-to 4-hour intervals, and increase fl ow rate by one fourth until the fi nal rate is achieved. Sample calculation for 50-kg foal follows: - Dextrose: 10 g/kg per day = 500 g = 1 L of 50% dextrose - Amino acids: 2 g/kg per day = 100 g = 1 L of 10% amino acids or 1.2 L of 8.5% - Lipids: 1 g/kg per day = 50 g = 0.5 L of 10% lipids - Total volume: 2.5 L of PN.
Caloric content is approximately 1.14 kcal/ml - Another formula commonly used by others is the following:
- 1 L of 50% dextrose - 1.5 L of 8.5% amino acids - 0.5 L of 20% lipids

## Antimicrobial therapy
Broad-spectrum, bactericidal antimicrobials are indicated. Treatment should be based on culture and sensitivity results whenever possible. Administer antimicrobial therapy for a minimum of 10 to 14 days in foals with documented bacteremia, provided that no localized areas of infection develop requiring more prolonged treatment. Specifi c sites of infection (e.g., pneumonia, meningitis, arthritis, and osteomyelitis) necessitate prolonged antimicrobial therapy. Penicillin and aminoglycoside antimicrobials are a popular combination that provides coverage against gram-positive and gram-negative aerobes and anaerobes. Antimicrobial dosages (see references for expanded drug dosage lists) are as follows:
- Penicillin: 22,000 to 44,000 U/kg IV q6h; use in combination with aminoglycoside - Ampicillin: 22 mg/kg IV q8h; use in combination with aminoglycoside - Amikacin: 25 to 30 mg/kg IV q24h in foals <7 days of age combined with therapeutic drug monitoring (ideally peak should be >10 times the minimum inhibitory concentration [MIC]). Peak concentrations at 30 minutes should be >60 g/dl, and 23-hour trough concentration should be <1 g/dl. - Gentamicin: 6.6 mg/kg IV q24h, and up to 10 mg/kg IV q24h in foals <7 days of age. Peak and trough concentrations should be monitored, ideally peak should be >10 times the MIC and trough <1 g/ml. Gentamicin is thought to be potentially more nephrotoxic than amikacin in very young foals; use cautiously only in well-hydrated foals.
Many gram-negative organisms may be resistant to gentamicin. - Ceftiofur sodium: 2 to 10 mg/kg IV q6-8h; less nephrotoxic: 2 to 5 mg/kg IM q12h. One can use ceftiofur in combination with aminoglycoside coverage for increased gram-negative and Staphylococcus spectrum. - Ticarcillin/clavulanic acid: 50 to 100 mg/kg IV q6h; less nephrotoxic - Trimethoprim-sulfonamide: 25 to 35 mg/kg PO or IV q12h. Do not use with uncertain GI function. Many gram-negative organisms may be resistant. - Third-generation cephalosporins if meningitis is suspected: cefotaxime, 40 to 50 mg/kg IV q6-8h. Many other potential cephalosporin choices include ceftazidime (50 mg/kg IV q6h), ceftriaxone (25 mg/kg IV q6h), and ceftizoxime (50 mg/kg IV q6h). Cefepime is a fourth-generation cephalosporin that has been studied in foals (11 mg/kg IV q8h). - Imipenem-cilastatin sodium: broadestspectrum beta-lactam bactericidal antimicrobial. A recommended dose is 10 to 15 mg/kg slowly IV q6h. NOTE: Imipenem-cilastatin sodium is expensive, and seizure has been reported (rare) as an adverse effect.
- Fluconazole for fungal infections: 8.8 mg/ kg PO q24h loading dose, 4.4 mg/kg PO q24h maintenance dose

## Immune system support: colostrum administration
- Feed only foals with normal cardiovascular status and body temperature.

## General nursing care
- Provide warmth, using heating pads, warm fl uids, radiant warmers, forced hot air blankets, and fl uid jacket warmers (Intratherm, a a warm intravenous fl uid pouch, and Safe and Warm a reusable instant heat measuring 7 to 9 inches (17.5 to 22.5 cm). - Maintain sternal recumbency as much as possible. Frequent repositioning helps prevent decubitus sores and dependent lung atelectasis. - Apply sterile ocular lubricant to eyes of foals that spend most of their time in lateral recumbency to prevent exposure keratitis and ulceration. - Antiulcer medication can be administered if desired. Gastroduodenal ulcers in these patients may be associated with GI hypoperfusion. Critically ill foals may have an alkaline gastric milieu and a blunted response to inhibitors of acid production, thus the use of histamine 2 (H 2 )
- Ideally, foals should receive approximately 1 L of colostrum with a specifi c gravity >1.060 administered in three to four feedings during the fi rst 8 to 10 hours of life. This dose is equivalent to 1 g IgG per kilogram body mass.

## Coagulopathies in sepsis
- Foals with sepsis commonly develop coagulopathies. It has been shown that the prothrombin time/partial thromboplastin time, whole blood decalcifi cation, fi brinogen, fi brinogen degradation products, percent plasminogen, percent alpha-2 antiplasmin, and platelet activator inhibitor are increased in foals with septicemia. Protein C and antithrombin concentrations are decreased, consistent with hypercoagulation. In addition, there are a number of reports of digital, brachial, and aortoiliac arterial thromboses representing clinical evidence of coagulopathies such as DIC. Treatment of coagulopathies includes therapy aimed at sepsis (broadspectrum antimicrobials), as well as heparin and plasma. Low-molecular-weight heparin is currently used in human patients and adult horses, although it has not been studied in foals. Recommended doses for dalteparin in adult horses is 50 IU/kg SQ q24h.

## Plasma transfusion
- Use plasma to manage FPT to provide opsonins, to improve immune response, to support oncotic pressure, and to defend intravascular fl uid volume. Plasma can also provide for antithrombin and clotting factors for foals with coagulopathies. Fresh plasma contains platelets, an advantage for foals with neonatal alloimmune thrombocytopenia. - Administer hyperimmune plasma from donors negative for A and Q antigens and negative for red cell antibodies. - If orally administered, serum-derived commercial IgG products are used. They should be mixed with colostrum to improve absorption. The same dose of 1 g IgG per kilogram body mass is recommended. Absorption of these products can be erratic, and foals should be reevaluated after administration of these products. antagonists and proton pump inhibitors may be of little use in the care of these patients. Milk in the stomach is also alkalinizing to the gastric contents, and frequent feeding is also protective if the foal is tolerant of enteral nutrition. - Ranitidine, 6.6 mg/kg PO q8h, 1.5 mg/kg IV q8h (note that this is a mild prokinetic), and/or - Famotidine, 2.8 mg/kg PO q12h or 0.3 mg/ kg IV q12h - Omeprazole, 2 to 4 mg/kg PO q24h - Sucralfate, 1 to 2 g/45 kg PO q6h

## Shock
Shock is a pathophysiologic state of inadequate energy production for cellular function. Categories of shock include the following: 1.

## Peripartum hypoxic/ischemic/ asphyxia syndrome (neonatal maladjustment syndrome)
This syndrome can result from any periparturient event that impairs or disrupts uteroplacental perfusion or umbilical blood fl ow. Hypoxic/ischemic/ asphyxia produces multiple organ system damage in addition to the more commonly recognized behavioral and neurologic defi cits. This syndrome may also be associated with abnormal cytokine release in utero, a phenomenon currently under further investigation.
The following are periparturient events associated with this syndrome: - Dystocia: Supply more oxygen through an IN or nasotracheal tube for the mare to help reduce fetal hypoxia. - Induced delivery: Cervical dilatation is a prerequisite for induction to reduce the risk of dystocia.
- Cesarean section - Premature placental separation - Placentitis: fetal membranes greater than 11% of foal's body weight - Severe placental edema: uteroplacental thickness greater than 2 cm - In utero meconium passage with or without postpartum meconium aspiration - Twinning - Severe maternal illness, especially with hypoxia - Abnormally prolonged gestation - Pregnancy complicated by reduced fetal fl uid volume increases risk of umbilical cord compression during labor and suggests the presence of chronic placental dysfunction.

## Diagnosis
The syndrome produces a wide range of clinical signs. Asphyxia induces a critical redistribution of cardiac output. The result is preferential blood fl ow to the heart, brain, and adrenal glands and decreased perfusion of the lungs, GI tract, spleen, liver, kidneys, skin, and muscles. Diagnosis is based primarily on clinical signs. Mannitol may theoretically exacerbate cerebral hemorrhage. Questions remain as to the location of any edema that develops in neonatal encephalopathy. If edema has a role in the pathophysiology of this syndrome, most current evidence suggests that it is intracellular, not interstitial; therefore the use of osmotic diuretics is unwarranted in many cases. Some clinicians never use DMSO or mannitol in the management of cerebral edema and report no change in outcome. Others report that the antioxidant properties, with or without antiedema, of mannitol are of clinical benefi t. Some clinicians continue to use DMSO at 0.5 to 1.0 g/kg given as no more than a 10% solution IV over 30 to 50 minutes. Neonatal foals do not appear to eliminate DMSO as effectively as adult horses and can remain hyperosmolar for several days. Hemolysis is rarely observed in neonatal foals after DMSO administration unless administered at concentrations greater than 10%. - Protect the foal from self-trauma: Wrap legs. Apply a soft head helmet (Velcro foam leg wraps and helmet available at 702-851-1217). Pad walls and provide soft bedding. Apply ocular lubricant to reduce risk of traumatic corneal ulceration. - Keep the patient's head low during resuscitation. Keep the head elevated 30 degrees when the patient is in lateral recumbency, if cerebral injury is suspected, and after successful resuscitation. - Do not overhydrate, but aim to maintain appropriate cerebral perfusion.

## Signs associated with specifi c organ injury

## Renal failure
- Monitor fl uid in and urine out to evaluate renal function and avoid overhydration and to ensure adequate hydration. - Furosemide: Administer small amounts (0.25 to 0.5 mg/kg q30-60 min) to enhance diuresis, or begin continuous infusion (0.12 mg/kg per hour). Monitor for development of hypochloremic metabolic alkalosis and electrolyte abnormalities. - Mannitol: Administer 0.5 to 1.0 g/kg IV as 20% solution over 15 minutes (osmotic diuretic). Do not repeat if anuric. - Dobutamine (2 to 15 g/kg per minute):
Use dobutamine if cardiac dysfunction and secondary hypotension are contributing to poor renal perfusion; discontinue or reduce dosage if tachycardia develops. - Dopamine infusion: Administer 2 to 3 g/ kg per minute (or fenoldopam 0.1 g/kg/ min) if anuria or oliguria is present. Lower doses stimulate dopaminergic receptors and enhance urine output by natriuresis. Medium doses recruit beta-receptors and support cardiac function, which may further improve renal perfusion. Higher doses stimulate alpha-receptors and result in decreased splanchnic blood fl ow, renal blood fl ow, and urine production. Titrate the dose to the individual patient. Recommend bladder catheterization to allow accurate assessment of urine production. NOTE: The use of dopamine in renal failure is controversial in human patients and no longer commonly recommended. However, in cases of oliguria or anuria in foals, it is worth trying because hemodialysis is the only alternative when medical therapy fails.

## Caution:
If administering furosemide through the same intravenous line as dopamine, avoid prolonged mixing of solutions in the line by administering dopamine or furosemide solution as close to the catheter port as possible.
- Protect furosemide solution from light by wrapping the line in paper or foil.

## What not to do
- Although furosemide administration can result in diuresis, prolonged use is associated with electrolyte and acid-base disturbances. - The use of dopamine or furosemide in the management of oliguric renal failure does not control the underlying problem. Judicious use of intravenous fl uid, but protecting from dehydration, is indicated in these cases. - Close attention to matching "ins and outs" is important.
- Perform nasogastric decompression to check for refl ux. Discontinue or reduce the volume or frequency of enteral feeding if refl ux is present. - If abdominal exploration is delayed and abdominal distention is severe and causing signifi cant respiratory compromise and continuous colic, percutaneous large-bowel trocarization can be performed. Use a 16gauge, 3 1 / 2 -inch (8.75-cm) catheter-overstylet attached to 30-inch (75-cm) extension set. Sedate foal if necessary to keep it quiet in lateral recumbency. Clip and surgically prepare a site over one or both paralumbar fossae at the point of maximal bowel distention. Infuse a small bleb of lidocaine at the puncture site. Using sterile technique, advance the catheter and stylet through the skin and body wall into distended viscus. Remove the stylet and connect the extension set. Place the free end of the extension set into a small beaker of sterile water to monitor gas-bubble production. Once bubbling stops, a small volume of antimicrobial (e.g., amikacin diluted 50 : 50 with sterile water) can be infused as the catheter is withdrawn. Broad-spectrum systemic antimicrobial therapy is recommended for 3 to 5 days after trocarization. NOTE: There is a risk of peritonitis. - Administer prokinetic drugs for GI dysmotility. These drugs are not recommended for routine use because they can cause additional GI problems, such as intussusception or worsening colic, or neurologic complications. They may be indicated in foals with postoperative ileus.

## What to do: colic, reflux, abdominal distention
- Metoclopramide, 0.25 to 0.5 mg/kg as slow IV infusion or per rectum q6h; can also be used at 0.02 to 0.04 mg/kg/hr as a CRI; observe for excitement; stimulates gastroduodenal motility. This drug may be useful in the management of delayed gastric emptying associated with gastroduodenal ulceration in older foals. - Cisapride, 0.2 to 0.4 mg/kg q4-8h PO.
Cisapride stimulates small-and largeintestinal motility. Motility is not necessarily coordinated or progressive, and signs of colic may worsen. - Lidocaine, 1 to 1.3 mg/kg slowly IV followed by 0.05 mg/kg per minute. The pharmacokinetics of this drug have not been studied in neonates, and neonates are more susceptible than are older horses to toxicity. NOTE: Use lidocaine with caution. It may have several advantages with respect to analgesic and antiendotoxic effects, but it also has antiinfl ammatory effects that have unknown infl uences on natural protection against infection.
- Neostigmine: 0.005 to 0.01 mg/kg IM or SQ; has been used successfully to evacuate "gas"-distended large intestine - Antiulcer medication: (See p. 157, Gastric
Ulcers.) Foals with hypoxic or ischemic GI damage are at increased risk of GI ulcers because of poor GI perfusion and the primary disease process. Acid production is not necessarily the cause of the ulcers, and the gastric milieu is likely more alkaline than it is in normal foals; therefore, H 2 antagonists and proton pump inhibitors may not be needed. In addition, the neonatal foal has a blunted response to H 2 antagonists. - Ranitidine, 6.6 mg/kg PO q8h or 1.5 to 2 mg/kg slow IV q8-12h, to increase gastric pH (ranitidine has some motilityenhancing effects) - Famotidine, 2.8 mg/kg PO q12h or 0.3 mg/kg IV q12h - Sucralfate, 20 mg/kg PO q6h, as cytoprotective agent - Omeprazole, 4 mg/kg PO q24h. - Pantoprazole, 1.5 mg/kg slow, dilute IV q24h - Antacids, such as Maalox or Di-Gel: 30 to 60 ml q3-4h. Most antacids have a short half-life, produce minimal change in gastric pH, and may provide transient pain relief.
- Broad-spectrum, bactericidal antimicrobials to reduce the risk of sepsis resulting from translocation of luminal bacteria across compromised GI mucosa. Sucralfate also may decrease bacterial translocation. - PN: With mild GI compromise, reduce the volume or frequency of enteral feeding and support the foal with PN. In cases of severe asphyxia accompanied by hypothermia, hypotension, shock, or advanced prematurity, recommend delaying all enteral feeds and providing PN until GI function returns (passage of meconium, borborygmi present).

## Note:
Tolazoline therapy frequently results in severe tachycardia and hypotension because of the nonselective vasodilatation produced and is not considered a fi rst-choice approach.
- Nitric oxide (NO) is an important modulator of vascular tone needed to achieve neonatal circulatory patterns. Ventilation with NO in 100% oxygen reduces pulmonary vascular resistance. Inhalation of 5 to 40 ppm NO has been effective in reversing hypoxic pulmonary vasoconstriction in foals. Use approximately 5 : 1 to 9 : 1 ratio of O 2 : NO. (A special regulator/fl ow valve is needed to attach to NO tank.) - Future directions for management of PPHN include endothelin-1 receptor antagonists and specifi c phosphodiesterase inhibitors. Inhaled or nebulized prostacyclin is gaining favor in the human neonatal intensive care fi eld. - Monitor blood pressure. Support cardiac function with dobutamine if indicated. - Correct hyperthermia if present: Remove covers and heating pads.
- Control of hypoxemia in the neonate is vital because it is a consistent stimulus for pulmonary vasoconstriction. Control is accomplished through provision of a high concentration of oxygen, up to 100% oxygen delivered during mechanical ventilation if necessary.
- Administer oxygen intranasally, 5 to 10 L/min. The Fio 2 achieved with IN oxygen cannot be accurately predicted but can be high in the neonatal foal. - Acidosis accentuates hypoxic pulmonary vasoconstriction. Acid-base imbalances should be corrected. The goal is to achieve a pH of 7.4. Use of bicarbonate to correct acidosis cannot be recommended if Paco 2 is increased and the foal does not improve with mechanical ventilation with appropriate minute volumes. - Consider pulmonary vasodilators if other techniques fail:
- Tolazoline: infant dose, 1 to 2 mg/kg IV over 10 minutes; if there is a good clinical response with an increase in Pao 2 , follow with intravenous infusion at 0.2 mg/kg per hour for each 1 mg/kg pulse-dose administered. Tolazoline causes adrenergic blockade, peripheral vasodilatation, GI stimulation, and cardiac stimulation.

## What to do: persistent pulmonary hypertension of the neonate (pphn) and pulmonary vasoconstriction
- Mild hypoxemia (Pao 2 , 60 to 70 mm Hg; SaO 2 , 90%): Increase periods that the foal spends in sternal or standing position; turn every 2 hours if recumbent; stimulate periodic deep breathing to reinfl ate atelectic lungs; administer humidifi ed IN oxygen, 2 to 10 L/min. - Moderate to severe hypoxemia (Pao 2 , <60 mm Hg; SaO 2 , <90%) accompanied by hypercapnia (Paco 2 , >70 mm Hg): If not improved by treatment with a respiratory stimulant (e.g., caffeine) or if respiratory acidosis is affecting pH (<7.25) and is not associated with metabolic alkalosis and therefore not compensatory, provide positive pressure ventilation. Intubate nasotracheally, using a 7-to 10-mm diameter, 55-cm long, cuffed, silicone nasotracheal tube. c

## What to do: respiratory compromise
c Silicon nasotracheal tube (Bivona, Inc., Gary, Indiana).

## Neonatology

## Mechanical ventilation
- Ventilator modes:
- Controlled mandatory ventilation: All breaths are machine-triggered, and depth/timing are determined by machine settings. - Assist/control ventilation: In this mode the breaths can be patient-triggered or machine delivered or both. The patient may trigger the breath depending on the level of sensitivity, which can be varied. However, whether the breath is patient or ventilator delivered, the tidal volume, inspiratory time, and fl ow rate are machine determined and fi xed. - Synchronized intermittent mandatory ventilation (SIMV): This is an assistcontrol mode in which a minimum number of machine-delivered breaths are guaranteed, while the patient can trigger its own breaths in addition to this set number. The tidal volume, inspiratory time, and fl ow rate are determined by the patient with spontaneous breaths (i.e., are under complete control of the patient), whereas machine-triggered breaths are ventilator controlled. Pressure support ventilation can be combined with SIMV so that patient-triggered breaths are supported. - Pressure support ventilation: This is a "supported" means of ventilation for spontaneous breaths only. The inspiratory tidal volume and time are augmented by the machine, which decreases the work of breathing, but the control of tidal volume and inspiratory time are under patient control. Pressure support may be combined with SIMV mode, in which the spontaneous breaths are supported. - Continuous positive airway pressure (CPAP): This is a spontaneous breathing mode in which there is maintenance of positive airway pressures during inspiration, exhalation, and in between breaths. This mode results in increased functional residual capacity and improves ventilation-perfusion ratios. CPAP can be combined with pressure support ventilation.

## How to do mechanical ventilation and airway support
- Typical settings: Begin PPV with initial tidal volume of 6 to 10 ml/kg and PEEP of 4 to 6 cm H 2 O. Low tidal volumes (6 ml/kg) are associated with protective lung strategies in human critical care. A starting point for breath rate is 20 to 30 breaths/min, which should be adjusted using capnography and arterial blood gas analysis. The inspiratory/expiratory ratio should be set at 1 : 2. Providing pressure support (PS) without mandatory machine breaths may be suffi cient for many foals. PS should start at 8 to 12 cm H 2 O. In this mode, foals generate each breath and determine the depth, volume, and duration of the breath but are assisted by machine-generated pressure throughout each inspiration. CPAP is a weaning mode and may be useful for foals with milder respiratory compromise. - Use an Fio 2 of 60% to 100% initially and reevaluate arterial blood gas values within 30 minutes of initiating PPV. Adjust inspired oxygen concentration accordingly with the goal of rapidly reducing Fio 2 to <50% to 60% to minimize the risk of oxygen toxicity. - Attempt to maintain peak airway pressures below 30 to 40 cm H 2 O to reduce barotrauma. - Breath rate is determined by Paco 2 and the foal's initial breathing rate; some increase in Paco 2 is permissible and may be necessary to prevent barotrauma. Some foals respond best to PS only, with no mandatory machine-driven breaths. Foals seem to tolerate SIMV/PS modes best. - If meconium aspiration has occurred, attempt to treat the foal with IN oxygen alone. PPV can predispose to alveolar rupture and pneumothorax in these cases. Suctioning of the airways should be attempted, but do not perform prolonged suction without oxygen administration. - Intratracheal surfactant instillation may be benefi cial if surfactant dysfunction is suspected because of severe asphyxia, pulmonary hypoperfusion, sepsis, or meconium aspiration. - Apnea and irregular respiration may be caused by hypoxic-ischemic damage to the

## Prognosis
Between 60% and 80% of foals suffering from peripartum asphyxia recover fully and mature into neurologically normal adults. A poor outcome is associated with severe, recurrent seizures that persist for more than 5 days post partum, severe hypotonia that progresses to coma, and severe multiorgan system damage that includes unresponsive renal failure or hypotension. These foals should be monitored closely for development of concurrent septicemia. Dysmature and premature foals exposed to severe acute peripartum asphyxia have a poorer outcome than do term foals.

## Prematurity and dysmaturity
Prematurity is defi ned as the condition of a foal born after a gestational period of less than 320 days. Dysmaturity is defi ned as the condition of a foal born after a normal or prolonged gestation period in which there are signs of underdevelopment. Dysmaturity is associated with abnormal uteroplacental function, which can result in delayed fetal growth and maturation when chronic, and in varying degrees of fetal asphyxia when acute. Postmaturity is the term some clinicians apply to the foal born after a prolonged gestation with signs of dysmaturity, yet they have large frame size, poor body condition, and long hair coats.

## Clinical signs
In addition to generalized weakness and hypotonia, the following signs are characteristic of dysmaturity and prematurity: - Caffeine: This is the fi rst choice. Use a loading dose of 10 mg/kg PO initially and maintenance dose of 2.5 to 3 mg/kg PO q12-24h. Therapeutic range for caffeine is 5 to 20 g/L; toxic concentration is >40 mg/L. - Doxapram CRI: 0.01 to 0.02 mg/kg/min.
[formula] - [/formula]
Doxapram is also effective but may increase myocardial oxygen consumption; therefore, this agent should be used in the hemodynamically stable foal. Monitor the foal for hyperarousal or excitability, and reduce the dose if these occur. - Theophylline: loading dose of 5 to 6 mg/ kg administered slowly IV q12h. Therapeutic concentration is 6 to 12 g/L. CAUTION: Therapeutic and toxic concentrations are within a narrow range, and therefore this therapy cannot be recommended as a fi rst choice.
- Signs of toxicity: seizures, colic, hyperesthesia, tachycardia. Death occurs at concentrations >20 g/L. - Aminophylline, a precursor of theophylline, can be substituted; 1 mg aminophylline = 0.8 mg theophylline. Same warning as with theophylline. - If apnea persists, PPV may be needed. - If Pao 2 does not have a threefold to fi vefold or at least a signifi cant increase with 100% oxygen after 3 to 4 hours of treatment, suspect the presence of a shunt or primary cardiac anomaly, which is a poor prognostic indicator. Rule out PPHN by a trial with NO in the inspired gas.

## Secondary infection
- Evaluate serum IgG. If IgG is less than 800 mg/dl and the foal is younger than 18 hours and has a functional GI tract, administer good-quality colostrum (specifi c gravity, >1.060) enterally, or administer plasma transfusion, or both. If foal is older than 18 hours or has compromised GI function, administer plasma. Serum IgG should remain >800 mg/dl. Provide broadspectrum antibiotics if GI compromise is suspected, if the foal has signs of sepsis, or serum IgG is less than 800 mg/dl.
- Attempt to establish the cause of prematurity or dysmaturity. Examine the placenta. If evidence of placentitis is present, initiate broad-spectrum, bactericidal antibiotic therapy. Be on the look out for preterm deliveries associated with EHV-1 infection. - Observe closely for signs of respiratory distress and progressive respiratory fatigue.

## Hypothermia
- Maintain carefully controlled environmental temperature if foal shows poor thermoregulation. Provide external warmth using warm water pads, radiant heaters, forced warm air blankets, warmed intravenous fl uids, and insulated fl uid jacket warmers. Be careful of inducing hyperthermia because these foals cannot regulate body temperature effectively. Foals should be warmed slowly during the initial resuscitation phase to avoid compounding reperfusion injury, particularly in those having experienced peripartum hypoxia.

## Self-trauma
- Reduce risk of decubitus sores by providing soft bedding (e.g., synthetic sheepskin, pressure point pads, plenty of cushion) for recumbent foals.

## Metabolic disturbances
- Monitor serum electrolyte concentrations. Hyponatremia and hypochloremia are the most common disturbances associated with renal and endocrine immaturity. Hyperkalemia and hypokalemia may also be present. Hypocalcemia is common. Metabolic (organic and inorganic) and respiratory acidoses are also common in affected foals. Guidelines for correction include the following:
- Hypernatremia - Correct sodium slowly (0.5 mEq/h).
- Rapid correction results in brain edema.

## Evaluate serum immunoglobulin g concentration
- Check within 8 to 12 hours of birth. If IgG is <800 mg/dl, administer colostrum supplementation, plasma transfusion, or both.

## Secondary bacterial infection
- Premature and dysmature foals are at increased risk of infection. Administer broad-spectrum, bactericidal antibiotic therapy until the foal is up and nursing normally.

## Botulism (shaker foal syndrome)
- Botulism manifests as generalized weakness, dysphagia, muscle fasciculations, and hypoventilation in the neonatal foal (most affected foals are approximately 1 month of age

## Dysphagia
- Dysphagia in the foal is common. Dysphagia can manifest as nasal regurgitation of milk, an inability to prehend (suckle), and aspiration pneumonia. Differential diagnoses for inability to prehend include peripartum hypoxia, significant hyponatremia, botulism, white muscle disease, craniofacial malformations, and cranial nerve defi cits. Differential diagnoses for nasal regurgitation of milk include pharyngeal paresis associated with peripartum asphyxia or selenium defi ciency (white muscle disease; both of these are commonly associated with dorsal displacement of the soft palate), cleft palate, epiglottic entrapment or persistent frenulum, subepiglottic cyst, botulism, esophageal obstruction (choke), megaesophagus, and homozygous state of HYPP. Pharyngeal paresis associated with peripartum asphyxia or selenium defi ciency is usually a transient disorder that resolves with time and selenium supplementation in the case of selenium defi ciency.
- Preoperative treatment consists of hemodynamic and metabolic stabilization. - Treat with potassium-free fl uids, such as 0.9% saline or isotonic (1.3%) sodium bicarbonate. - Means of lowering potassium in addition to dilution include provision of glucose (4 mg/ kg per minute), sodium bicarbonate, and insulin therapy in more refractory cases. - Calcium is rapidly cardioprotective from the effects of hyperkalemia. - Removal of urine from the abdomen is an important feature of relieving hyperkalemia and in allowing improved ventilatory status. Peritoneal drainage can be performed using teat cannulas, abdominal drains, and even needles. These are best placed using ultrasound guidance because plugging with omentum is common. - Broad-spectrum antimicrobials should be given because a high percentage of foals with uroperitoneum have concurrent sepsis.

## What to do
- Do not administer aminoglycosides because they inhibit neuromuscular function.

## Colic

## Signs of colic in newborn foals

## What to do
- Gastroduodenal ulceration: This is uncommon as a primary cause of colic in the neonate but may be a primary problem in the older foal. Many gastric ulcers are clinically silent in neonatal foals. - Intestinal volvulus: This is a true surgical emergency. Diagnosis is suspected based on clinical signs of severe pain, refl ux, and abdominal distention. Ultrasonographic evaluation of the abdomen can confi rm the presence of multiple loops of turgid, distended small intestine with minimal motility. Abdominal distention is often rapid and severe.

## Meconium impaction
Meconium impaction is more common in colts than in fi llies. It is not unusual for the foals to also have FPT of immunity; perhaps colostrum ingestion aids in meconium expulsion, or failure to absorb ingested IgG indicates intestinal malfunction. In addition to colic, abdominal distention, and poor nursing behavior, affected foals may have tenesmus, tail fl agging, and an arched-back posture. If obstruction is complete, abdominal distention can develop rapidly.

## Diagnosis
- Palpation of fi rm meconium within the rectum and pelvic canal on digital examination - A history of unsuccessful straining to defecate - Firm fecal material within the pelvic inlet detected with abdominal palpation, plain radiography, or contrast radiography after a barium enema examination - Sonographic detection of echogenic material within the distal colon and rectum

## Warm, soapy (ivory soap) water, gravity enemas
- Use a soft urinary catheter or small feeding tube and enema bucket with 75 to 180 ml of the solutions. If repeated enemas are needed, alternate soapy water with warm water or water mixed with J-lube or rectal lubricant to minimize excessive mucosal irritation. Avoid dioctyl sodium sulfosuccinate (DSS) enemas because of irritation. Repeated enemas may lead to pathologic tenesmus.

## What to do

## Retention enemas
- Use Mucomyst or powdered N-acetyl-lcysteine. If Mucomyst is used, add 40 ml of 20% solution to 160 ml water to make a 4% solution. If using the powder, add 8 g of powder and 1 1 / 2 tbsp (22.5 g) of sodium bicarbonate (baking soda) to 200 ml of water. Insert a lubricated Foley urinary catheter (30F with 30-ml balloon in most average-sized foals) with a balloon tip approximately 2 to 4 inches (5 to 10 cm) into the rectum and infl ate the balloon. Slowly infuse 4 to 6 oz (120 to 180 ml) of acetylcysteine solution by gravity fl ow into the rectum. Occlude the catheter end for a minimum of 15 minutes (ideally 45 minutes). Defl ate the balloon and remove the catheter. The retention enema can be repeated several times.

## Oral laxatives
- Proximal (high) impactions require oral laxatives in addition to enemas. The safest, least irritating laxative is mineral oil (120 to 160 ml), administered through a nasogastric tube if the foal is >12 to 18 hours of age. Mineral oil lubricates around the impaction and reduces the risk of complete obstruction, which can rapidly result in severe and painful gas accumulation and abdominal distention. Milk of magnesia (60 to 120 ml) is an oral laxative that should be used conservatively. - Castor oil or DSS administered orally is not recommended because of excessive mucosal irritation and increased risk of severe diarrhea and colic.

## Intravenous fluid therapy
- Intravenous fl uid therapy is useful in cases of refractory impaction. Dextrose supplementation is recommended if nursing behavior is curtailed because of increasing abdominal distention and colic.

## Percutaneous bowel trocarization
- If severe abdominal distention develops before the impaction is resolved, enough to cause severe respiratory compromise, consider the technique described under Peripartum Asphyxia (see p. 608 of the second edition). Trocarization often provides immediate pain relief without excessive medica-tion and allows time for medical therapy and potential presurgical stabilization. Be aware of the serious potential for peritonitis. Broad-spectrum antimicrobials should be administered.

## Surgical management
- Surgical exploration and relief of the impaction may be indicated in foals with severe abdominal distention resulting in respiratory and cardiovascular compromise (intraabdominal hypertension with abdominal compartment syndrome).

## Analgesics and sedatives
- Analgesics and sedatives may be needed to prevent self-trauma in foals that are down and rolling. - Flunixin meglumine, 0.5 to 1.0 mg/kg IV q24-36h; avoid repetitive doses because of its ulcerogenic potential and effects on the kidney. Alternatively, ketoprofen can be used because it is safer (1 to 2 mg/kg IV q24h). - Butorphanol, 0.01 to 0.04 mg/kg IV. This is an excellent fi rst choice and usually is highly effective. Administration can be repeated as necessary for several doses at 1-to 4-hour intervals. - Xylazine, 0.1 to 0.5 mg/kg IV; use sparingly because of adverse effects on GI motility. Some debilitated neonatal foals experience signifi cant ileus or respiratory/hemodynamic compromise after use of this agent. Administering butorphanol and xylazine together decreases the dosage of xylazine needed.

## Ileus
Decreased GI motility is associated with ischemic and hypoxic bowel damage resulting from sepsis/ SIRS/septic shock or peripartum hypoxia and adverse events. Beware that intussusception can develop as a result of the ileus or prokinetic drugs used to promote motility. In addition, premature foals may have ileus and intolerance of enteral feeding. - Provide intestinal rest. Discontinue all enteral feeding until refl ux and diarrhea resolve and borborygmi return. Severe cases may necessitate up to 7 days of complete intestinal rest. Small amounts of enteral food (milk or commercial isotonic, easily digested products) support enterocyte and enzyme production. - Parenteral alimentation (see p. 503). - Broad-spectrum, bactericidal antibiotics are recommended (see p. 504). - Sucralfate, 20 to 40 mg/kg PO q6h.

## Clinical signs
- If a foal shows signs of endotoxemia, consider administering 20 to 40 ml/kg of hyperimmune plasma to provide opsonins and immunoglobulins to support the immune system. - Slowly reintroduce enteral feeding, beginning with small volumes of colostrum or fresh mare's milk. - Complications associated with necrotizing enterocolitis include septicemia, intussusception, peritonitis, anemia, and stricture formation. - Rule out C. perfringens and C. diffi cile infection.

## What to do
- Gastric refl ux (Bloody or dark brown to black refl ux suggests mucosal damage; consider administration of sucralfate in these cases.) - Diarrhea or constipation

## Diagnosis
- Based on results of physical examination and supported by several diagnostic techniques:
- Transabdominal ultrasound examination shows distended or hypomotile bowel and lack of propulsive motility. If necrotizing enterocolitis is present, ultrasound examination may show gas echoes within bowel walls. - Abdominal radiographs show generalized small-and large-bowel distention. Pneumatosis intestinalis, gas formation within the bowel wall, is observed with severe necrotizing enterocolitis.

## Mild to moderate ileus, mild colic associated with feeding, varying amounts of refl ux, and inconsistent manure production
- Decrease volume of enteral feedings temporarily (may require short-term discontinuation), and support with partial PN. - Allow controlled exercise, short periods of turnout with dam in a small paddock. - If constipation develops, treat with enemas, oral laxatives (mineral oil), and psyllium in small amounts, and maintain hydration with orally or intravenously administered fl uids. - Give oral probiotic agents: commercial products or 2 to 3 oz (60 to 90 ml) of active culture yogurt PO q12-24h.

## Intussusception
Colic caused by intussusception may be mild to severe, depending on the location and duration of obstruction and the level of mentation of the foal. Abdominal distention and refl ux usually develop. The diagnosis often is made with transabdominal ultrasonography. Sonography shows "bull's-eye" target lesions that represent a cross-sectional view of intussuscepted bowel. Contrast radiography may help identify the location of obstruction.

## Enteritis (with or without peritonitis)
Enteritis may be caused by a primary GI disorder or other systemic conditions, such as septicemia or peripartum hypoxia (see p. 506).

## Clinical signs

## What to do
- Maintain hydration using polyionic fl uids.
Monitor serum concentrations of electrolytes, glucose, and creatinine, acid-base balance, PCV, and total protein. If the foal is anorectic, administer parenteral alimentation. - Broad-spectrum, bactericidal, parenteral antimicrobial therapy is recommended for foals with severe diarrhea and toxic mucous membranes because of the increased risk of gram-negative septicemia. - Administer intestinal protectants: bismuth subsalicylate (Corrective Suspension g ), 0.5 to 1 ml/kg PO q4-6h; kaolin and pectin, 4 to 8 ml/kg PO q12h. - Nonsteroidal antiinfl ammatory drug therapy is used by some clinicians if the foal shows signs of endotoxemia. A "low dose" of fl unixin meglumine, 0.25 mg/kg IV q8-12h, is preferred, for short periods. - Conservative use of NSAIDs is advised because of their ulcerogenic potential and possibility of disrupting normal renal function (reducing mucosal and renal perfusion). - Plasma administration benefi ts foals with signs of endotoxemia and foals with FPT or hypoproteinemia. - Consider antiulcer medication: sucralfate, 20 to 40 mg/kg PO q6h; omeprazole 4 mg/ kg PO q24h. - Administer loperamide, 4 to 16 mg PO q6h, beginning with the low dose and increasing

## What to do
echoes and is associated with severe hypoxic intestinal damage. - Hematology, chemistry: Leukopenia and neutropenia are associated with endotoxemia. Secretory diarrhea usually results in hypochloremia, hyponatremia, varying degrees of metabolic acidosis, hemoconcentration, and variable potassium concentrations. - Perform abdominocentesis if peritonitis is suspected. Peritoneal fl uid contains increased protein concentration and nucleated cell count, although often it is not specifi c in the information provided. Be very cautious performing abdominocentesis in foals with enteritisenterocentesis can have fatal consequences.
in 2-mg increments every two to three doses. Because loperamide increases segmentation rate and slows transit time, it may enhance toxin absorption in cases of acute, infectious enteritis. Therefore, use of loperamide should be reserved for foals that do not have signs of severe endotoxemia or infectious enteritis. - Lidocaine may be useful for ileus and abdominal pain (see p. 509).

## Congenital malformations
Hernias: umbilical, scrotal,