key: cord-0040401-xqn7e5ni
authors: Whitehead, Claire E.; Cebra, Christopher
title: Neonatology and Neonatal Disorders
date: 2013-12-06
journal: Llama and Alpaca Care
DOI: 10.1016/b978-1-4377-2352-6.00042-0
sha: a7ee6b5bda582fca1dd0ce9e657a8e62f18931ab
doc_id: 40401
cord_uid: xqn7e5ni

nan

Claire E. Whitehead 

Management of the newborn alpaca or llama cria requires both the owner and the clinician to be familiar with the normal state to correctly identify abnormalities and to prevent or treat potential problems. Most crias in developed countries are born without complication and survive the neonatal period without incident. However, for the minority with problems, timely recognition and intervention maximize the chances of survival.

In South America, 20% to 80% of crias do not survive to weaning. Deaths occur for a variety of reasons, many of which have not been cataloged. In North American populations, the death rate is lower, but figures are not available. Well-managed farms should aim to lose fewer than 5% of their crias in a year. In general, crias suffer from the same maladies as other neonatal livestock. Dysmaturity, prematurity, dystocia, sepsis, and starvation are common problems and should be handled in the same way as in other species. In contrast, crias appear to have higher rates of certain problems such as those related to congenital malformations.

Abnormal neonates may initially show few overt signs of disease or may show signs that are vague. Given how rapidly sick neonates can deteriorate, even these small abnormalities may indicate the need for aggressive action. Abnormalities are best detected through a thorough postnatal checkup, routine, consistent monitoring of progress according to the timetable in Chapter 25, generally observing activities, including nursing, elimination, and physical activity, and charting changes in size and body weight. Even small changes such as failure to gain weight over a 24-hour period while all else appears normal could be significant, and any delay in investigating these changes and initiating treatment could result in more advanced clinical disease. Interventions may be anything from modest management changes to intensive medical care. Identifying the neonates that require interventions and determining the level are matters of experience and good diagnostic evaluation.

Crias born outside of the daylight birth window often have abnormalities and should automatically be considered to be at high risk from the start. It usually suggests either a prolonged delivery process or that a pathologic condition (sickness of the dam or fetus, abnormal placenta) triggered the birthing. Crias born following any difficult delivery likewise require greater attention. They typically take longer to achieve sternal recumbency and are slower to stand and nurse. Their suckle reflex may be depressed or absent, and they may appear depressed. Such crias require additional attention and supportive care to ensure that they acquire sufficient colostrum, oxygenate adequately, and avoid hypothermia.

Slow-starting crias may require little more than simple, but immediate, intervention. The most vital events of the first few hours of life are breathing, standing, and nursing. Breathing is the most urgent. Crias with overt dyspnea, including openmouthed breathing or stertorous respiration, should be maintained in sternal recumbency or assisted to stand. The airway should be assessed for obstruction. The external nares should be cleared. A bulb syringe may be used to blow mucus back into the oropharynx, and a soft rubber urinary catheter may be inserted past the level of the eye in each nares for a quick assessment of choanal patency. Rubbing the thorax and dorsum also may stimulate breathing efforts. Breathing function may be assessed by arterial blood gas (ABG) analysis and thoracic radiography, and endoscopy or imaging studies may be used to assess airway patency (see Chapter 37) . If hypoxemia is a concern, the cria may be placed on supplemental oxygen, and if ventilation is an issue, the cria may be intubated for mechanical ventilation. Face masks used for small animal patients may be tolerated in the short term but are hard to maintain. Nasal prongs used in human hospitals work well for crias and are self-retaining. Insufflation tubes or catheters placed in a nostril are also acceptable. When possible, supplemental oxygen should be warmed and humidified. Assessment of breathing function may be indicated even in the absence of dyspnea. Hypoxemia and hypercapnea are both important causes of neonatal obtundation, so supplemental oxygen or mechanical ventilation should be considered in any dull cria. Moribund crias are at risk of corneal ulcers because of reduced blinking reflexes. Ocular lubricants and common sense management to avoid eye trauma may be indicated.

During the period of initial assessment, after airway and breathing issues are sorted out, the cria should be examined for evidence of prematurity and external defects. Signs of prematurity are as follows: overt external defects such as facial malformations, cleft palate, limb abnormalities, a bleeding umbilicus or umbilical hernia, patent urachus, malformations of the external genitalia ( Figure 42-1) , and absence or atresia of the anus. Mucous membranes and sclerae should be examined for cyanosis, injection, vascularity and refill times, and the anterior chamber of the eye should be examined for hypopyon. Normal vital parameters and issues with cardiac auscultation have been discussed earlier in this text. It is important to realize that sepsis leads to hypothermia more commonly than fever. Pulmonary auscultation is the same as in other species. Some degree of "squeakiness" is normal in the immediate postpartum period, but this should resolve within an hour. Neurologic examination is difficult to interpret in the immediate postpartum period or in severely obtunded crias but may be useful in older crias.

Barring further concerns requiring more intensive management, standing efforts may be assisted. Just as good oxygenation increases mental acuity and the desire to move, ambulation assists in chest excursions and clearance of prenatal fluid from the lungs. The three best points of contact are the sternum and the two points of the hips. Placing a towel under the abdomen may increase intraabdominal pressure and restrict breathing and may even promote body wall hernias. Encouraging a newborn to stand every 10 to 20 minutes may eventually lead to it standing on its own.

Breathing and standing are usually prerequisites to nursing, but in their absence, some form of intervention to provide nutrition and immunoglobulin (Ig) is required. If the dam has colostrum, the cria should preferably be assisted to nurse or the dam milked out so that the cria can be fed via a bottle or tube. Dams may be restrained against stall walls to allow recumbent crias to nurse (personal communication, Dr. D. Mora). Colostrum or milk may be given via a tube, pan, or bottle, and intravenous (IV) nutrition or plasma transfusion may be initiated. If the dam's colostrum is not available, camelid or ruminant colostrum may be administered for the first 12 to 24 hours. Ruminant colostrum should be from Johne's free herds or flocks, if possible. Bovine colostrum has also been associated with immune-mediated hemolysis in rare cases.

If colostrum is not available within the first few hours after birth, administering milk or a milk replacer is likely to be beneficial in providing fluid volume, nutrition, and the impetus for gut closure. Warmed goat or cow milk or milk replacer may be used, and an initial volume equal to approximately 3.5% of body weight appears adequate. If milk is administered in the absence of colostrum, plasma transfusion should be strongly considered. Although it has not yet been studied scientifically, some think that camelid milk has metabolic effects beyond simple nutrition, so any cria fed milk or milk replacer from another species should be observed carefully for changes in attitude or activity that could reflect the onset of a hyperglycemic disorder (see Chapter 41, "Hyperosmolar Disorder"). It is also important to remember that antibody and nutrient absorption may be affected by tissue function and oxygenation; hypoxic or otherwise compromised crias may require plasma transfusion or parenteral nutrition in spite of adequate colostral or milk ingestion or administration.

If failure of passive transfer (FPT) is suspected or diagnosed after gut closure or colostrum is not available, Ig may be given in the form of camelid plasma. Llama, alpaca, and dromedary plasma appear to be interchangeable for this purpose, with the larger species often making better donors because of their size. Overall, cross-matching for a one-time transfusion is rarely necessary, and reports of transfusion complications are rare. Plasma may be administered by intraperitoneal (IP) or IV injection. One unit (300 milliliters [mL]) is often sufficient for an alpaca, whereas a large llama cria with complete FPT may require 2 units to reach the desired range.

Transfusions should be started at a slow rate and are ideally given using a filtered blood set over 30 to 40 minutes. Heart and respiratory rates should be monitored and the infusion rate decreased if either of those parameters rises more than 10%. If anaphylaxis is a concern, particularly in an animal that has previously received a transfusion, flunixin meglumine (1 milligram per kilogram [mg/kg], IV) may be give as a premedication 5 to 15 minutes before the transfusion.

Plasma may be administered by IV or IP (ventral midline or high right paralumbar) infusion. IP infusion is common as a field procedure in crias with uncomplicated FPT. Crias with other perinatal complications often have a jugular catheter for venous access, and this route is used preferentially. Rapid IP infusions (5-10 minutes) may cause abdominal discomfort, and nonsterile technique or accidental bowel perforation or laceration may result in peritonitis or intraperitoneal hemorrhage.

Typically, slow-starting or mildly dysmature crias respond quickly to these interventions. They usually learn to nurse and stand within 48 hours, and oxygen administration is rarely required beyond 72 hours and often less than 24 hours. Lack of satisfactory progress over that time usually indicates a severe congenital abnormality or an acquired disease. As such crias require aggressive treatment, it is often best to identify them from the start.

Some slow-starting crias are underdeveloped because of prematurity or dysmaturity. Because of the variability in normal pregnancy length in camelids, it may be difficult to define exactly what constitutes a "premature cria." However, on the basis of the available data, it seems reasonable to conclude that any cria born after less than 335 days of gestation could be considered premature. Dysmaturity further describes crias born at a normal gestational age showing evidence of prematurity. These crias are as much at risk of morbidity as are premature crias. Given the uncertainty with regard to what "normal" gestational age should be, dysmaturity is often considered the more appropriate term.

Clinical signs of dysmaturity are the same as those in other species and include obtundation, low birth weight, unerupted incisors, floppy ears or ears that are bent backwards ( Figure 42 -2), poor or absent suckle reflex, and silky haircoats. Tendon laxity (see later in this chapter and in Chapter 58) may result in overextension of the carpal and fetlock joints, so crias may be seen walking on their fetlocks ( Figure 42 -3). Crias may also have a rubbery covering on the nails of the feet and a thicker epidermal membrane that persists for longer than normal. The central incisors normally erupt 2 to 3 weeks prior to birth, so unerupted incisors suggest that a cria is underdeveloped at least to this extent. Dymature crias tend to be weak and may have difficulty standing or holding their heads up to nurse because of poor muscle development. Furthermore, dysmature crias may have incomplete structural and functional maturation of vital body systems, and this leaves them susceptible to a range of potential neonatal complications. These crias are at risk for hypothermia because their thermoregulatory control is poor, and they are prone to hyperglycemia or hypoglycemia. Respiratory system immaturity may result in poor lung expansion from lack of pulmonary surfactant, and this also reduces oxygen transfer across the alveoli. Poor oxygen diffusion together with bradypnea results in hypoxia. It is unknown when surfactant is produced in the lungs of camelids, but those with unerupted incisors are especially at risk. The intestinal mucosa may also be inadequately mature in premature crias, which results in inefficient absorption of colostral antibodies. More than half the dysmature crias presenting to one referral hospital had FPT. 1 Recognizing the clinical signs of dysmaturity is vital for newborn crias, as they may deteriorate rapidly. Early intervention is key to their survival. One report showed a 75% survival rate, and this was attributed to the fact that 87.5% of cases were presented within 24 hours of birth. 1 Therapeutic measures may include oxygen administration, IV fluid administration, and provision of warmth. The contents and rate of administered fluids should be tailored to the specific needs and blood abnormalities; nutritional support should not be neglected. Additionally, aminophylline (2 mg/kg, subcutaneously [SQ], q4h for 24 hours, followed by q6h for the next 24 hours and q8h for the next 24 hours) may be used proactively or therapeutically when concerns about breathing exist. Lung surfactants have also seen some use.

Tendon laxity in premature crias may resolve spontaneously once the newborn cria starts weight bearing and the ligaments and tendons strengthen from use. In severe cases, splinting of the forelimbs from the elbow to below the fetlocks may be necessary. However, splints must not be placed for too long, as they may create more laxity. All crias with splints should be evaluated daily for evidence of progress or development of complications.

The slow-developing cria that does not respond to conservative management, the severely obtunded newborn that never appeared vigorous, the healthy cria that acutely developed severe clinical signs, and any cria in respiratory distress all count as "critical crias." Crias born with low birth weight, after gestation of less than 335 days, outside of the daylight birth window, following a difficult birthing, or by cesarean section are overrepresented in this group. The critical nature of the disorder may be immediately apparent, or first recognized when conservative measures fail. Generally, the earlier the critical cria is recognized and treated, the better is the outcome.

Neonatal body systems are not as resilient as those of adult animals, and relatively minor events may have severe adverse effects. Fortunately, the same factors that promote these acute, severe presentations often allow for rapid, dramatic recoveries. Opportunistic bacterial pathogens may proliferate rapidly in the immunocompromised neonate but also respond quickly to the appropriate antimicrobials. Hypoxemia, or hypothermia all may rapidly improve with the initiation of treatment. Rapid recoveries are especially likely in crias that once were vigorous. Slow starters or those severely affected at birth are more likely to have a congenital defect, and in many cases those are irreparable.

The most common critical problems in neonatal crias less than 2 weeks of age relate to environmental conditions (hypothermia or hyperthermia), nutritional management (failure to nurse resulting in dehydration; hypoglycemia, FPT, or both; and subsequent sepsis), metabolic abnormalities related to organ dysfunction or general lack of well-being (hypoxemia, metabolic or respiratory acidosis, azotemia, hepatic lipidosis, or hyperglycemia), enteritis, and congenital morphologic impediments or organ dysfunction, including dysmaturity. Multiple mechanisms may contribute in individual cases, so a complete diagnostic evaluation is recommended. Some of this is warranted for some slow-starting crias as well before they reach the critical stage.

Components of this evaluation may include a more thorough physical examination, hematologic and biochemical blood evaluations, ABG analysis, culture of blood and potentially other abnormal body fluids, blood Ig determination, fecal investigations, and imaging studies.

Hematologic evaluation is mainly helpful for diagnosing infection or anemia. With neonatal sepsis, gram-positive organisms often evoke neutrophilia with a left shift, whereas gram-negative organisms often acutely lead to neutropenia, 2,3 which resolves over 3 to 5 days. Hyperfibrinogenemia, a leftshifted leukogram, and toxic changes in leukocytes both provide supportive evidence for sepsis but also may be absent in septic crias. The stress response, with its tendency to increase blood neutrophil counts, may mask neutropenia, so it is important to look for other evidence of stress (hyperglycemia, lymphopenia) and to mentally compensate for these: A normal neutrophil count in a stressed camelid, especially one with a left shift or toxic morphology of neutrophils may still be evidence of sepsis. Mycoplasma haemolamae infection has also been identified in newborns and may be identified on blood smear or by polymerase chain reaction (PCR). 4 Measuring plasma Ig concentrations also may provide indirect evidence of sepsis. Low immunoglobulin G (IgG) in a neonate may either be a predisposing factor to sepsis, often related to FPT, or reflect Ig consumption caused by infection. The longer after birth that IgG is measured, the less can be said definitively about passive transfer, especially in sick crias. Regardless, many hypogammaglobulinemic sick crias would benefit from a plasma transfusion.

Blood biochemical abnormalities of particular importance include changes in blood glucose, electrolyte abnormalities, azotemia, metabolic acidosis with or without hyperlactemia or a high anion gap, hypoproteinemia (particularly hypoalbuminemia or hypogammaglobulinemia), evidence of fat mobilization, and increased activity of liver or muscle enzymes. It with diarrhea and others with apparent renal tubular acidosis. Acidosis without dehydration has also been described. 6 The pathogenesis of this is not completely understood. Crias occasionally get lactic acidosis from grain overload or fermentation of milk, but hyperlactemia is more commonly the result of septic or hypovolemic shock. Ketoacidosis is also seen. Treatment of acidosis depends partially on the pathogenesis. With lactic acidosis or ketoacidosis, the primary strategies are to decrease production and increase elimination of the organic acid. Both these may often be achieved by rehydration. Ketoacidosis may also require the same treatment as that for hepatic lipidosis, and intestinal fermentative conditions may need to be treated in the same way as grain overload. If the blood pH is below 7.25, bicarbonate administration may be necessary as well. Sodium bicarbonate administration is also the cornerstone of treatment of bicarbonate-losing conditions, particularly when blood pH is less than 7.25. Multiplying the base deficit (or 24 mEq/L minus the observed bicarbonate value) by 0.5 by body weight in kilograms yields the total bicarbonate deficit. Half of this may be given within the first hour of fluids and the second half over the next 2 to 4 hours. Bicarbonate administration often temporarily corrects acidosis, but repeated monitoring is necessary to determine whether further doses should be given. Bicarbonate should also be avoided with respiratory acidosis, as hypercapnea may worsen.

Dehydrated or anorexic crias or those in shock should be treated with fluids. Although oral treatment is possible, the tubing procedure is often stressful for the neonatal cria, as its gastric capacity is only about 3.5% of whole body weight. Therefore, repetitions should be minimized. The quantity and type of fluids are often different from those for other species. Camelid babies are more prone to hypoproteinemia, hypernatremia, and hyperglycemia compared with calves or foals. They rarely are severely dehydrated but more frequently have septic shock or renal or hepatic compromise. In general, the initial bolus may be smaller (30 mL/kg), the subsequent rate may be slower (up to 100 mL/kg/day), and fluids containing glucose or lactate should be avoided without specific indication. A higher initial bolus (up to 90 mL/kg) may be given if the cria is overtly hypovolemic and has reasonably high or normal blood protein concentrations. If the cria is hypoglycemic, fluids may be spiked with glucose. If the cria is hyperglycemic and hypernatremic, mildly hypotonic fluids may be formulated by adding sterile water to isotonic saline or polyionic fluids; these fluids should be given at approximately 4 mL/kg/hour or slower and blood sodium and glucose carefully monitored.

Plasma is also a valuable adjunct, both because of failure of passive transfer and postnatal protein loss. On the basis of our laboratory equipment, we usually recommend a transfusion when total protein is less than 4 g/dL, when albumin is less than 2 g/dL, or when failure of passive transfer is confirmed or suspected. Synthetic colloids are being used in camelids with increasing frequency, but in crias, the provision of Ig is often as vital as the provision of a colloid, so plasma is usually preferable.

Plasma should be administered at 20 to 30 mL/kg. It is more effective than crystalloid fluids at expanding volume in is a dangerous misperception that the majority of sick neonates need supplemental glucose. Only 13% of sick crias in one unpublished study had hypoglycemia, including only 11% of crias less than 24 hours old, but 14% had blood glucose concentrations greater than 200 milligrams per deciliter (mg/dL; 11 millimoles per liter [mmol/L]). It is, therefore, imperative to measure glucose before supplementing it. The most likely causes for hyperglycemia are stress and administration of glucose or a glycogenic agent, often compounded by insufficient water intake. Camelid milk may also play a role in suppressing hyperglycemia. The most likely causes for hypoglycemia are inadequate milk intake, potentially compounded by shivering or seizures, sepsis, or liver failure. If hypoglycemia is identified, it should be addressed promptly. The seizure threshold in crias appears to be just under 40 mg/ dL (2.22 mmol/L) of glucose, so supplemental glucose is recommended for anything less than 70 mg/dL (3.9 mmol/L). Rapid infusion of 0.5 mL/kg of 50% dextrose, or preferably a slow infusion of 3 to 5 mL/kg of 10% dextrose over 5 to 10 minutes may be used.

High blood glucose concentrations become clinical through diuresis and dehydration of the brain and other tissues. 5 Serum sodium concentration is a good indicator of the severity of dehydration from glucose diuresis: When sodium climbs to greater than 165 milliequivalents per liter (mEq/L), aggressive measures to replace fluid volume and decrease blood glucose are indicated. Very high glucose concentrations may be combated with insulin (regular insulin, 0.2 units/kg, IV, as often as hourly) or less aggressively with subcutaneous insulin. The combination of hyperglycemia and hyperna tremia is termed hyperosmolar disorder. Its pathogenesis and treatment are discussed in Chapter 41. Hypernatremia and hyperchloremia are much more common in sick crias (roughly 14%) than hyponatremia or hypochloremia (roughly 1%), so salt loading should be avoided under most conditions. Hypokalemia (38% of sick crias) caused by anorexia is relatively common and may be addressed by IV supplementation or milk feeding. Vigorous supplementation is rarely necessary. Azotemia was found in 14% of sick crias in one unpublished study. The minority of these had renal failure or congenital abnormalities; most were in hypovolemic or septic shock and responded well to fluids. Evidence of fat mobilization was not uncommon, and hepatic lipidosis was found in 12% of nonsurviving, live-born crias, with the youngest being 2 days old. These findings highlight the need for nutritional support, and that factors beyond pregnancy-related or lactation-related negative energy balance may lead to disorders of fat metabolism in camelids. Hyperlipemia, high blood concentrations of nonesterified fatty acids (NEFAs) or β-hydroxybutyrate (BHOB) or high activities on liver enzymes all suggest such a disorder might be developing. Diagnosis and treatment of disorders of energy metabolism is covered in Chapter 41.

Acidosis is a relatively common finding in sick crias. It may be underdiagnosed in general practice because of lack of diagnostic capability. Neonates with fluid-filled lungs, severely obtunded crias, and those with pneumothorax, diaphragmatic paralysis, or hernia may have respiratory acidosis. Unless hypoventilation can be corrected by addressing the underlying condition, mechanical ventilation may be required.

Metabolic acidosis is more common. Simple bicarbonate loss is less common than in calves but is seen in some crias neonates more susceptible to the development of hypothermia. Additionally, premature neonates are likely to have inadequate reserves of brown adipose tissue, which develop late in gestation under the influence of NST inhibitors. Shivering generates additional heat, but the impact of this is small in neonates because of their small size and immature musculature. The presence of brown adipose tissue has not been specifically documented in camelids to date, so the extent of the role of NST in averting hypothermia in crias is uncertain. Thyroid hormones may also play a role in enhancing thermogenesis in the newborn. Neonatal llama crias have been shown to have very high blood thyroxine concentrations at birth, which decrease gradually over the first 90 days of life. 9 Crias born in cooler environmental temperatures, particularly in winter, are especially susceptible to hypothermia because of the greater temperature differential and the potential for increased heat losses from evaporation from a wet neonate. The epidermal membrane helps prevent some of this evaporative cooling but disintegrates soon after birth. Therefore, if females are expected to give birth during cooler periods of the year, they should be watched particularly closely or brought indoors so that parturition occurs in a warmer location. Ideally, matings in cold climates should be scheduled so that the birthing season occurs during the spring or summer months to minimize this problem.

Hypothermic neonates are depressed and lethargic and have reduced reflexes and poor ventilation. This, together with poor cardiac function, results in hypoxia, acidemia, and cardiac dysrhythmias. 10 Hypothermic neonates are susceptible to FPT because of decreased nursing activity and possibly gut function. Hypoglycemia, although uncommon, may develop concurrently as hypothermic neonates deplete their energy reserves. Additionally, prolonged hypothermia may result in damage to the intestinal epithelium because of hypoxia, predisposing the neonate to clostridial overgrowth and pathogen invasion. 11 Crias with hypothermia should be warmed. This involves placing them in a warmer environment away from drafts, drying them off if they are wet, and using external heat sources such as heat lamps, warmed towels and blankets, and hot water bottles. Forced-air warming blankets are particularly effective in crias because of the relatively larger surface area. If heating pads or lamps are used, appropriate insulation from direct heat should be used, and care must be taken to ensure that a recumbent cria is turned frequently to avoid overheating. Excessive heat may result in cutaneous vasodilation, which may be detrimental to the cria by reducing core temperature and resulting in further cardiovascular compromise. This is also true of warm water bathing, which is therefore not recommended. Caution must be exercised if heat lamps are used because some bulbs may pose a fire hazard. Bulbs should be positioned above the height of any potential kicks from the dam. Crias that have become hypoxemic as a result of hypothermia, and vice-versa, benefit from oxygen administration.

The rectal temperature for normal crias is 37.8°C to 38.9°C (100°F-102°F). 12, 13 Therefore, hyperthermia in a neonate would be defined by a rectal temperature of 39°C (102.2°F) or greater. The most common cause for hyperthermia is sick neonates, since such crias often have increased endothelial permeability from inflammation. Plasma should be administered using a filtered administration set. Larger volumes (30 mL/kg) should be given over at least an hour. Faster administration may result in tachypnea, dyspnea, and evidence of central nervous system (CNS) disease. In one recent study, 30 mL/kg of camelid plasma was administered to clinically healthy alpaca crias with FPT over 90 minutes. 7 This resulted in measurable plasma volume expansion, which appeared to be safe, and also a considerable improvement in arterial oxygen pressure. However, treated crias also showed a reduction in lung volume, and it was suggested that this may result in complications for those crias having preexisting cardiopulmonary compromise. Therefore, greater care would be advised in administering large-volume plasma transfusions to any cria with suspicion of cardiopulmonary issues or systemic disease. Monitoring changes in central venous pressures during a transfusion may be helpful in preventing such complications. Clinically, the observed response during a plasma transfusion may be quite rewarding.

Broad-spectrum antibiotics are usually indicated. Most injectable antibiotics used in foals or calves may be used in crias at similar dosage rates and intervals. Popular camelid regimens are covered under "Sepsis" later in this chapter. Nonsteroidal antiinflammatory drugs (NSAIDs) are similarly used. Taking into consideration fears about gastric ulceration, a reduced dose of flunixin meglumine (0.5 mg/kg, IV, q12-24h) is often used rather than the "full" dose.

By the time most crias present for evaluation, they often would benefit from IV fluids or other medications. Therefore, it is reasonable to place an IV catheter early in the evaluation (see Chapter 32) so that emergency treatment can be initiated while the examination is under way. Furthermore, blood samples can be collected from the catheter immediately after sterile placement for hematology, biochemistry, and culture, thereby reducing the number of venipuncture sites. Hematoma formation is even more common in crias than in adults, and each venipuncture increases the chance of introducing pathogenic bacteria into the bloodstream of the neonate. If venous access is not possible because of hypovolemia, intraosseous infusion may be achieved by placement of an 18-gauge spinal needle into the proximal femur. Fluids may be administered easily by this route and blood pressure restored, so that an IV catheter may be placed.

Hypothermia may be a routine finding in underactive crias or those subjected to harsh weather conditions or may be a sign of more severe disease. As such, it may indicate the need for increased management or intensive interventions.

During pregnancy, the fetal temperature is 0.3°C to 0.5°C higher than that of the mother because of higher fetal metabolic rates. At birth, neonates are subject to a rapid drop in external temperature and need to rapidly increase heat production to keep warm. For this, they are highly dependent on nonshivering thermogenesis (NST). 8 This process takes place in the mitochondria of brown adipose tissue and results in an uncoupling of fatty acid oxidation such that heat energy is produced instead of adenosine triphosphate (ATP). It is dependent on adequate oxygenation, making hypoxemic world, environmental temperatures may become extremely high and, especially when compounded with high humidity, may lead to hyperthermia. Neonates are particularly vulnerable if they are unable to seek suitable refuge, Furthermore, neonates that are suffering from underlying bacterial or viral infections are less able to thermoregulate and more susceptible to hyperthermia if unable to move to shade. High ambient temperatures may be focal as well, as in a stall with a heat lamp.

Fever is brought about by the production of pyrogenic cytokines, especially interleukin (IL)-1α, IL-1β, and tumor necrosis factor (TNF)-α, in response to a variety of conditions including infections, inflammation, trauma, or immunologic conditions. 10 The production of these cytokines results in a cascade of effects, including the production of acute-phase proteins and stimulation of the immune response while also resulting in behavioral changes such as increased sleep, reduced appetite, and separation from others that may allow recovery and reduced spread of infectious agents.

Hyperthermic neonates often develop tachypnea to increase evaporative heat loss. Heat loss from the body surface, aided by peripheral vasodilation, is limited to the small areas in the axillary and inguinal areas, where less hair coverage is present. When lying in closed sternal recumbency, heat loss from these areas is minimized because of lack of conductive loss from circulating air. Affected individuals are lethargic. At rectal temperatures higher than 41.5°C (106.7°F), the body's normal thermoregulation fails, peripheral vasoconstriction occurs, and cardiac output falls with reduction in blood pressure. 10 Organ failure, coagulopathy, and myocardial necrosis may develop subsequently. Seizures may occur at these temperatures because of alterations in the function of temperaturesensitive ion channels and also the production of the pyrogenic cytokine IL-1β that has been shown to enhance neuronal excitability. 14 Relatively small increases in brain temperature predispose the brain to hypoxic injury. 8 If hyperthermia is identified in a neonate, it is likely to be significant, and therefore the clinician should attempt to identify the underlying cause and provide the appropriate treatment. It is particularly important to rule out or identify bacterial infection, since mortality rates may be high if this is not treated early and aggressively (see "Sepsis" below). Neonates that are suffering from heat stress as a result of environmental conditions should be cooled. This may be achieved by removing the cria from the heat source, making use of fans, clipping of fleece, and using ice packs. Ice packs may be particularly effective if placed in the inguinal area close to the femoral arteries and veins; care should be taken, however, to wrap the ice packs in towels and not to place them directly onto the skin, as this may cause cold burns. NSAIDs are also indicated for neonates suffering from heat stress or seizures caused by hyperthermia. The use of NSAIDs for reducing fever from other causes is controversial because of the beneficial effects that fever may have, including stimulation of the immune response, as well as the potential harmful GI and renal effects of NSAIDs. They should therefore be used with care.

Sepsis is defined as systemic inflammatory response syndrome (SIRS) with either documented or suspected infection by fever related to infection. However, it is an inconsistent finding under those circumstances and should not be considered a prerequisite for a diagnosis of sepsis in camelids of any age. None of 21 crias with sepsis had a rectal temperature greater than 39°C (102.1°F) in one study, regardless of whether gram-positive or gram-negative bacteria were cultured from blood or tissue samples. 2 In fact, 7 (33%) were actually hypothermic. In another retrospective study, only 2 of 6 crias with gram-negative sepsis were pyrexic. 3 This compares well with findings in septicemic foals, in which only 30% of cases were pyrexic. 13 The differential diagnoses for a high body temperature in neonatal llamas and alpacas include bacterial or viral infections, high environmental temperature, muscle tremors, or seizure activity. Bacterial infections are a likely sequel to failure of passive transfer. Muscle tremors may result from cerebral edema or ingestion of tremorgens. Seizures may result from a variety of CNS disorders (Box 42-1). In certain areas of the identifying the nature and amount of fluid buildup in body cavities and for identifying tissue masses. Cross-sectional imaging studies may be used to assess any tissue but are currently used most to assess the CNS and other areas poorly imaged by other techniques.

A presumptive diagnosis of sepsis may be made by identifying compatible clinical signs and diagnostic test abnormalities, in some cases supported by historical evidence of increased risk such as a difficult birth or other factors associated with FPT. Confirmation requires seeing the organism on cytologic examination or growing it on bacteriologic culture. Cultures are usually performed on blood, but other suspect body fluids or possibly tissue samples collected postmortem may be used. Because of the rapidity with which neonatal sepsis can progress, aggressive treatment is usually warranted based on initial clinical suspicion. In many cases, simply recognizing that a cria is at risk for developing sepsis justifies treatment. Treatment follows the guidelines for critical crias, including fluid, environmental, and nutritional support, appropriate use of plasma to maintain oncotic pressure and provide Ig, antiinflammatory medications, and most importantly, antibiotics. Greater risk of capillary leakiness or body loss of protein exists in any animal with sepsis, so blood protein concentrations should be monitored and the animal frequently observed for clinical evidence of edema, particularly when on IV fluids.

A broad-spectrum antimicrobial regimen is usually appropriate, with particular consideration for gram-negative coverage. Combination therapy of a β-lactam agent (crystalline penicillin: 22,000 units/kg. IV, q6h; or ceftiofur: 8 mg/kg, SQ, intramuscularly [IM], or IV, q12h) with an aminoglycoside such as gentamicin (5 mg/kg, IV, q24h for 5 days) 17 or amikacin (15 to 18 mg/kg, q24h for 5 days) has seen widespread usage and resulted in many clinical cures. Other agents or combinations have not been as extensively used but may be supported by specific culture results. Antibiotics may have to be continued longer than suggested above, if sepsis persists. When using an aminoglycoside, monitoring of blood creatinine concentrations, preferably at least every 48 hours during treatment, may allow timely recognition of renal damage before it is irreversible.

Further management of septic crias involves regulation of body temperature, provision of oxygen in critical cases, provision of nutrition, and monitoring of hydration status and hematologic responses. Crias must be monitored for development of hypopyon, uveitis, conjunctivitis, or neurologic signs. If hypopyon is observed, administration of mydriatics such as atropine drops may minimize the risk of synechiae formation, which may subsequently result in glaucoma and necessitate enucleation. Prognosis of crias with sepsis is generally fair, if the condition is recognized and treated early and no preexisting morphologic defects such as dysmature lung or inadequate pharyngeal reflexes that promote continual compromise are present. Vertebral body or tissue abscesses may result in longterm or future complications.

Any evidence of insufficient respiratory function is usually considered the most urgent problem in a critical patient because of the potential for inadequate tissue oxygenation. Respiratory function may be affected by a variety of factors, bacterial, viral, fungal or rickettsial agents. 2 In crias, gramnegative and gram-positive bacterial sepsis appear to be the most common causes. 2,3,12,15 E. coli, Pseudomonas, β-hemolytic Streptococcus, Enterococcus spp., Listeria monocytogenes, and Citrobacter are the most common isolates, with gram-negative organisms making up 54% of diagnoses in one study and 72% in another review. 2, 16 Most organisms are considered opportunists and infect individual crias, as opposed to causing outbreaks of disease. Neonatal sepsis is a common sequel to FPT and hence is common in crias after difficult births and in those with agalatic dams or with other risk factors contributing to FPT. It may also occur in crias shown previously to have acceptable passive transfer.

Sepsis is characterized by weakness, lethargy, pyrexia or, more commonly, hypothermia, tachycardia, tachypnea, and failure to nurse or gain weight. 2,3 Evidence of dehydration, injected mucous membranes, or organ-specific signs, including diarrhea, colic, abdominal distention, hypopyon, seizures, blindness, ataxia, dyspnea, dysuria, lameness, or swollen joints, may exist. Signs may spread from one body system to another and may occur peracutely or gradually. When sepsis occurs before or soon after birth, it may be difficult to differentiate from dysmaturity, birthing complications, or disorders caused by birth defects, all of which may lead to severe obtundation or organ-specific signs. The greater the separation from the birth event, especially in crias that have shown days to months of normalcy, the more likely it is that local or systemic infection is the root of the problem. Generally, sepsis should be considered a possible cause or complication of almost any disease or disease sign in a neonate.

Initial physical examination findings are often relatively unremarkable, emphasizing the need for laboratory and possibly imaging evaluation of many sick neonates. Hematologic abnormalities often include leukocytosis or leukopenia, both often accompanied by a left shift and toxic changes in leukocytes. Neutropenia appears to be more common with gramnegative infections, whereas gram-positive infections are more commonly associated with neutrophilia, unless the infections are overwhelming. 2 Blood work may also reveal findings suggestive of FPT, including hypoproteinemia and hypoglobulinemia. Specific tests of blood Ig concentrations provide more specific evidence. Measurement of total blood protein is not a particularly good predictor of FPT in septic crias but still provides useful information on whether a sick cria is hypoproteinemic or not. 2 Additional blood abnormalities that may develop with sepsis include hypoglycemia or hyperglycemia, metabolic acidosis as a result of shock with or without diarrhea, azotemia as a result of dehydration, nephritis or kidney failure, hypoxemia or respiratory acidosis as a result of pulmonary infection or weakness-associated hypoventilation, electrolyte abnormalities, and increases in bilirubin and liver enzymes. Analysis of other body fluids, including peritoneal, pleural, joint, or cerebrospinal fluid (CSF), may also reveal local evidence of infection, if that part of the body is involved.

Imaging studies are not necessarily part of a routine evaluation but may provide useful information if a particular part of the body deserves further investigation. Conventional radiography is most useful for assessing the chest when abnormal lung tissue, masses, or fluid accumulation is suspected, or for identifying lytic bone. Ultrasonography is useful for excursions; in more vigorous crias, demonstration of respiratory acidosis, pneumothorax, poor coordination between the diaphragm and intercostal muscles, or inadequate chest movement may be necessary. Meconium aspiration may be inferred in a meconium-stained cria after a difficult birth, and milk aspiration is often the product of bottle-feeding the less vigorous neonate. Fluid overloading may be inferred from the treatment history, with further confirmation coming from the identification of hypoalbuminemia or hypoproteinemia on blood work. Infection is covered under "Sepsis" above.

More than one upper and lower airway problem may be present simultaneously. Factors which induce dyspnea facilitate feed aspiration, and anything that impairs early drinking promotes failure of passive transfer and secondary sepsis. Although one factor may be causative of the others, all may require specific treatments at the time of presentation.

South American camelids are known to have some unique adaptations that allow them to thrive in low oxygen environments such as those found at high altitude. Their oxyhemoglobin dissociation curve is shifted to the left of those of humans and many other mammals, so camelid hemoglobin (Hb) has increased affinity for oxygen in the lungs, allowing high oxygen saturation of Hb (≥90%) even at high altitude and low inspired oxygen concentrations. [18] [19] [20] However, the oxygen is released just as easily in the tissues, reflecting good oxygen extraction to meet the demands of tissue hypoxia. Fetal llamas have been shown to have even more efficient tissue oxygen extraction. 21 Llamas and alpacas have been shown to exhibit a much reduced pulmonary vasoconstrictive response to hypoxia such that they are resistant to the development of pulmonary hypertension at altitude. 22 Furthermore, the fetal llama, in contrast to lowland species, has been shown to respond to acute hypoxia with intense peripheral vasoconstriction and only a modest increase in cerebral blood flow with reduced oxygen consumption, indicating hypometabolism, even in the brain. 23 Presumably, the large decrease in peripheral oxygen consumption preserves available supplies for the brain. The fetal llama heart also receives an increase in blood flow in response to hypoxia. These fetal responses appear to be preserved into the neonatal period. 24 Therefore, the physiologic adaptations of these species may explain why neonates are better able to survive hypoxia in association with congenital heart defects compared with other domestic species.

Ventilation and oxygenation are best assessed via ABG analysis. If this is unavailable, or during the gap between presentation and confirmation of abnormalities, supplemental oxygen may be administered on the basis of suspicion of hypoxemia. If the patient is breathing poorly or has hypercapnea, mechanical or assisted ventilation may be required, if other treatments do not improve the respiratory effort. Generally, supplemental oxygen is recommended whenever partial pressure of oxygen (PaO 2 ) falls below 60 mm Hg and ventilation is recommended whenever partial pressure of carbon dioxide (PaCO 2 ) exceeds 60 mm Hg. Supplemental oxygen may be administered using oxygen tents or cages or more commonly via nasal catheter. It is usually sufficient to administer 2 to 4 liters per hour (L/hr) of 100% oxygen. This is effective or partially effective at combating hypoxemia caused by diffusion barriers and ventilation-perfusion mismatches but is not effective when blood is bypassing the lung because of a right-to-left shunt. Efficacy may be checked by comparing including respiratory tract or cardiovascular anatomy; the presence of abnormal fluids, tissues, or infection affecting areas of air movement or gas exchange; mental or physical impairment of ventilation; abnormal blood flow patterns through the lung; and other factors. Some of these factors are more likely to be identified during the neonatal period than in older animals, particularly those relating to anatomic defects or infection. Assessment of the airway and respiratory function requires a thorough physical examination, imaging studies of the upper airway or chest, and ABG analysis.

Abnormalities in respiratory function may lead to obvious or subtle signs. Obvious signs include tachypnea, dyspnea, flaring of the nostrils, open-mouth breathing, and loud sounds coincident with breathing efforts. More subtle signs include some degree of obtundation, poor growth, cyanosis, and a lower level of activity than expected.

Dyspnea, tachypnea, and open-mouth breathing are common in neonatal camelids with either an upper airway obstruction or fluid in their lungs but may be transiently present in healthy crias as well (Figure 42 -4). They should resolve within an hour in healthy crias. If pathologic, these problems are usually the most urgent and demand immediate attention. Simple obstructions have been described earlier in this chapter, and anatomic airway defects are covered in Chapter 37. Trying to pass a feeding tube or rubber catheter may quickly yield information about airway patency and may remove mucus. Imaging studies are necessary for more thorough assessment. Respiratory obstructions should be removed or bypassed, if possible. This may require surgical intervention.

Lower airway disease may be caused by pulmonary dysmaturity, atelectasis following prolonged recumbency, inadequate ventilation to remove fetal fluids, meconium or milk aspiration, fluid overloading, left-sided heart failure, or infection. Dysmaturity may be inferred from an early delivery date but is usually diagnosed by demonstrating hypoxemia and radiographic evidence of diffuse alveolar pathology in crias without other evidence of pneumonia, aspiration, or pulmonary edema. Inadequate ventilation may be readily apparent in severely obtunded crias in lateral recumbency with poor chest are likely to be infections, cerebral edema, and metabolic disturbances. In one unpublished study, out of 22 neonatal llamas and alpacas with neurologic disease, 50% had an infectious disease, with 64% of those cases involving meningitis or encephalitis.

Meningitis or meningoencephalitis are potential sequelae to neonatal sepsis but fortunately occur rarely. Cases involving Listeria monocytogenes, E. coli, Salmonella Newport, and Streptococcus bovis have been described. [26] [27] [28] [29] [30] Clinical signs may be remarkably variable and vague and may include weakness, depression, inability to stand or elevate the head, tremors, ataxia, opisthotonus, and seizures. In one case, the only clinical sign on presentation was abdominal discomfort; this progressed to signs of CNS depression within several days. Another cria was presented because it was spending increasing periods sleeping; meningitis with secondary hydrocephalus was subsequently diagnosed on the basis of CSF fluid analysis and CT evaluation of the brain. Blood work may be unremarkable unless sepsis has also developed, but low globulin concentrations may suggest FPT.

The chances of a CSF tap being diagnostic, with cytologic abnormalities, including leukocytosis, and possibly visible microorganisms, are reasonably good. 27, 28 Protein concentrations are also often high. Bacteriologic culture may yield the organism.

For noninfectious conditions, ABG analysis, blood biochemical analysis, and imaging studies are likely to be most revealing. CSF analysis may reveal inflammation and still not reveal the cause. ABG analysis is useful to diagnose hypoxemia. Blood chemistry analysis may reveal azotemia compatible with shock or renal disease, liver enzyme abnormalities or other indicators (hyperammonemia) compatible with hepatoencephalopathy, lactic acidosis, hypoglycemia, or hyperglycemia and hypernatremia. With the exception of the combination of hyperglycemia and hypernatremia (see "Hyperosmolar Syndrome" in Chapter 41), these abnormalities largely resemble similar disorders in other species.

Conventional radiography may reveal masses or gas pockets, evidence of trauma, or malformations of the spinal canal or skull compatible with hydrocephalus. MRI is particularly useful for diagnosing diseases of the meninges or brain parenchyma.

Generalized seizures should be controlled immediately. Diazepam (0.1 to 0.2 mg/kg, IV, as needed [PRN]) is usually effective and rapid. One dose may be sufficient to control the seizures until the underlying problem is corrected, although in some cases multiple doses are required. Beyond controlling the seizures, treatment should be directed at the underlying cause. Thiamine diphosphate (5-10 mg/kg, IV or SQ, q4-6h or added to IV fluids) is a useful adjunct. If cerebral edema is suspected, mannitol (0.5-2 g/kg in a 20% solution) may be helpful. Treatment of infection is the same as for neonatal sepsis; usually, disruption of the blood-brain barrier is sufficient for most antimicrobials to penetrate. Crias with meningitis or meningoencephalitis have a guarded prognosis even with aggressive treatment.

When auscultating the heart of healthy or sick crias, it is essential to listen to both sides of the chest over a number of ABG values on and off the supplemental oxygen; a good response suggests a more favorable prognosis. The flow rate may be decreased and oxygen finally discontinued when clinical response warrants it.

Mechanical ventilation is indicated for hypoventilating crias. Hypoventilation may be caused by pneumothorax or other causes of compressed lungs, damage to the diaphragm or thoracic wall, diaphragmatic paralysis, drug-induced respiratory suppression (e.g., following anesthesia of the neonate or dam for the purposes of dystocia resolution), head traumainduced respiratory depression, congenital or acquired airway obstruction, or neuromuscular weakness. A tidal volume of 4 to 8 mL/kg, at the rate of 20 to 30 breaths per minute (breaths/ min), and peak inspiratory pressure less than 20 centimeters of water (cmH 2 O) is usually adequate. Ventilation requires intubation with a cuffed endotracheal tube passed through the mouth or nasal passages or a cuffed tracheostomy tube.

Cyanosis is an additional sign of poor respiratory function. This bluish discoloration of the mucous membranes and the extremities is caused by accumulations of blood deoxyhemoglobin that exceed 2.5 grams per deciliter (g/dL). In addition to pulmonary and airway problems, cardiac defects causing blood to bypass the lungs are important contributors to cyanosis. These may include ventricular septal defect in combination with a right-sided obstructive lesion that results in right-to-left shunting, right-sided defects such as pulmonic stenosis with a patent foramen ovale, tetralogy of Fallot, transposition of the great vessels, or tricuspid atresia. These are covered in detail in Chapter 36.

Any neonate exhibiting seizure activity should be thoroughly evaluated to find the underlying cause. A thorough history should be taken to investigate any perinatal problems or the potential for trauma. In addition, a complete physical examination including neurologic evaluation should be performed. IV access should be acquired as soon as possible by placement of a jugular catheter, and blood samples should be collected and evaluated promptly for glucose concentrations, electrolytes, nitrogen compounds, and acid-base status. Further investigations include hematology, complete biochemistry, ABG analysis, blood cultures, CSF analysis, and radiography where required. Imaging may be extended to computed tomography (CT) or magnetic resonance imaging (MRI), if indicated, where these diagnostic modalities are available.

In neonates, seizure activity may be subtle. In human neonates and foals, seizure activity may not necessarily be convulsive and may include tremors and involuntary muscle activity, including lip smacking, rapid eye movements, and small limb movements. 25 This is also the case with alpaca and llama neonates. Seizures always indicate abnormal brain activity. In neonates, seizures may be caused by a number of factors, some of which may be intracranial in origin such as traumatic brain injury, cerebral edema, polioencephalomalacia, or encephalitis, whereas others may be extracranial, including electrolyte abnormalities, hypoglycemia, hypoxemia or ischemia, and hepatic or uremic encephalopathy (see . Hydrocephalus may be the result of an intracranial or extracranial lesion. The most common causes of seizures animals with cardiac problems may be helpful, if available. 33 Clinical signs of collapse, weakness, and cold extremities indicate reduced systemic perfusion, but these are not exclusive to cardiac problems. Occasionally, neonates with congenital heart disease present with signs of "exercise intolerance." Examples include a cria that struggles to keep up with its dam or one that finds nursing behavior exhausting and stands with its head down to the ground for long periods. Syncope may sometimes be a feature. Left-sided congestive heart failure (CHF) may result in signs such as coughing consistent with pulmonary edema or an increased respiratory rate and effort. Right-sided CHF may result in hepatomegaly or ascites. Abnormal blood flow to the GI tract may result in abdominal discomfort or colic in some cases, and pleural effusion may cause dyspnea. 31 Distension of the jugular veins may sometimes be evident in neonates with right-sided failure. For crias with slower developing failure, poor growth is the most common complaint.

Further evaluation of cardiac murmurs may involve ABG analysis, echocardiography, thoracic radiography, and advanced imaging studies. These tests are discussed in detail in Chapter 36. As with adults, electrocardiography does not consistently yield useful information about chamber enlargement but may aid in evaluating arrhythmias. The frequency of cardiac malformations with some form of right-toleft shunting makes ABG analysis highly useful. Active and growing crias are sometimes surprisingly hypoxemic; underweight or exercise intolerant ones and those with evidence of a significant murmur should be investigated in this way. Especially in the absence of echocardiography or other advanced imaging studies, ABG analysis before and during supplemental oxygen administration may be used to evaluate the likelihood or nature of a shunt, considering that oxygenation scarcely improves with a right-to-left shunt.

Most significant cardiac murmurs in crias are the result of congenital malformation. These are covered in Chapter 36. Heritability has been established for many types of defect in other species, but hard data for camelids are still lacking. Nevertheless, it is prudent to remove the affected animals from the breeding population, if they survive, and avoid mating the dam and the sire with each other again. Furthermore, although very few medical or surgical treatment options are available for camelids identified as having pathologic heart murmurs, it is recommended that camelids with persistent murmurs should be evaluated before reaching the breeding age.

Colic signs or abdominal distension in crias is somewhat different from these same issues in older camelids because crias are more likely to ingest foreign bodies, more likely to have clinically apparent congenital defects, and more prone to certain infectious and fermentative diseases. As crias mature from the immediate postnatal period, these differences begin to disappear. By 4 months of age, crias are essentially adults as far as most causes of colic are concerned. Major causes of abdominal distention are listed in Box 42-2.

Abdominal pain is generally caused by inflammation, ischemia, muscle spasms, or activation of stretch-pain receptors in the visceral serosa or mesentery. Crias are born with simple gastric digestion and hence are prone to aberrant fermentation intercostal spaces (ICSs). On the left side, the apex beat (fifth ICS) is found near the point of the elbow. Moving the stethoscope forward from there, medial to the elbow, allows evaluation of the aortic (fourth ICS) and pulmonic (third ICS) valves over the heart base. On the right side, the tricuspid valve (fourth ICS) and main murmur area are found medial to the elbow. The chest should be palpated for cardiac thrills over each valve. Heart rate in neonates is reported to have a mean of 108 ± 18 beats per minute (beats/min). 31 A normal range of 80 to 120 beats/min, depending on the level of excitement, seems acceptable. Normally, two or three heart sounds are audible. In crias, it is also easy to access the median (medial foreleg) or saphenous (medial hindleg) arteries to evaluate pulse quality. This may be done along with cardiac auscultation.

Pathologic arrhythmias are rare, so the primary goal of auscultation is to identify murmurs. These are relatively common in neonatal alpacas and llamas. Most are innocent or transient murmurs not associated with underlying pathology, but a few represent major flow abnormalities. 31 If a heart murmur is detected in a neonate, particularly in a critical cria, the clinician needs to decide whether the murmur is responsible for the clinical signs, is inconsequential, or is a consequence of the underlying problem and will resolve with treatment of that problem.

In the first few days of life, transient murmurs may be present prior to closure of the foramen ovale or ductus arteriosus. Grade 1 to 3 of 6 left-sided systolic murmurs may also persist for several months, potentially related to transient peripheral pulmonary artery stenosis. 31 ,32 This appears to cause turbulent blood flow in the distal main and branch pulmonary arteries, where they narrow. It resolves as pulmonary vascular resistance decreases. In healthy crias, suspected transient murmurs may be further evaluated when initially detected or reassessed in 3 to 4 months. In general, if the cria appears vigorous and is growing well, evaluation may be deferred.

Systolic ejection murmurs over the left heart base may become prominent in sick crias, especially those with hyperdynamic shock associated with hypovolemia or sepsis. These murmurs usually soften or resolve quickly with treatment of the underlying problem. In sick crias, unless they are likely to be causing the disease signs, they may generally be ignored until the primary disorder is cured.

Murmurs louder than grade 3 of 6, accompanied with signs typical of cardiovascular disease, or failing to resolve with appropriate therapy for potential underlying conditions should be investigated more thoroughly. Right-sided or diastolic murmurs are also more likely to be significant. Although many of these murmurs represent severe congenital abnormalities, signs are often subtle or nonexistent at birth, followed by weeks to months of progressive ill-thrift before final collapse. Some severe defects are also initially unapparent on auscultation or indistinguishable from transition murmurs. Definitive murmurs associated with defects and aberrant flow patterns may first develop or become identifiable when chamber enlargement leads to secondary valvular incompetence.

Historical and clinical information may increase suspicion of a cardiac abnormality. Some defects are suspected to be heritable, so breeding history and knowledge of related malformation if a good stream of urine has not been seen. Hospitalization appears to be a risk factor for spiral colon impaction. Duration of signs is important: transient distention or obstruction usually resolves within 1 day. Signs lasting longer than this are more likely caused by an anatomic defect or something that requires surgical repair.

Manifestations of abdominal pain in neonates vary considerably between individuals and may include nonspecific signs such as reduced appetite, separation, tachypnea with nostril flaring, lethargy, and weight loss or signs that are more suggestive of abdominal visceral involvement, including abdominal distention, obvious straining, sitting awkwardly with the legs out to the side, or rolling onto the side and possibly kicking. The severity of clinical signs does not necessarily correlate to the severity of the lesion or to the likelihood that a surgical lesion is present.

Physical examination is more helpful in determining severity than the nature of the particular lesion. Heart and respiratory rates are likely to be within reference ranges unless the animal is in shock or severe pain or if the distention physically obstructs venous return or lung expansion. Rectal temperature may not be particularly diagnostic if it is normal or low; fever is uncommon without an inflammatory lesion. All external orifices and genitalia should be examined carefully for evidence of patency or malformation. The presence of fresh feces in the rectum is usually a good prognostic indicator, suggesting that a surgical lesion is less likely. However, progressively drier and possibly mucus-covered feces may be continuously passed for 1 to 3 days following intestinal obstruction, particularly if the site of obstruction is more proximal. Loose feces suggest enteritis, peritonitis, or a partial obstruction. 35 If defecation is in doubt, it should be possible to determine the presence and quality of any feces in the rectum by careful digital examination using a well-lubricated, small finger.

Determining the nature of any distention is helpful. Gaseous accumulations tend to distend dorsally as well as ventrally and often make the skin tight. Gas tinkles may be heard on auscultation. Distension caused by fluid or feed material fills the ventral abdomen first, and succussion may yield sloshing sounds. In contrast to the abdomen of adults, the abdomen of neonates is more amenable to external palpation. Without the interference of a feed-filled first compartment, it is often possible to palpate specific enlarged organs or the intestinal loops distended by gas or fluid. Enlargement of organs may result in significant pain from stretching of the capsule; this is particularly true of the kidneys and ureters and, to a lesser extent of the liver and bladder. 35 Interpretation of blood and abdominal fluid follows the guidelines laid out in Chapter 40. Radiography and ultrasonography are also invaluable diagnostic tools, depending on the level of expertise in interpretation. Ultrasonography is particularly useful for detecting fluid accumulation within the forestomach, bowel, or peritoneal cavity and allows for assessment of intestinal contents, wall thickness, and motility, as well as examination of other abdominal organs, including the liver, the spleen, and the urinary tract. The small size and the lack of gas and fibrous feed material in the abdomen of neonates make them particularly suitable candidates for ultrasonography.

Radiography may be useful as well, particularly because of the neonates' small size and gastric fill compared with those of feedstuffs, either in the nascent forestomach or in the intestine. This "milk colic" is associated with overfeeding milk, especially goat's milk, and possibly bacterial overgrowth. Crias are also prone to foreign body ingestion, which may result in mucosal abrasions caused by sand or hair or trichophytobezoar obstruction. In very young neonates, obstruction from meconium impaction or atresia is possible. Peritonitis related to sepsis or umbilical infection is more common in neonates than older camelids.

History of diet, medications, and housing may be useful. Knowing whether the cria is nursing or is being supplemented, especially with goat's milk, is of particular relevance. Wood shavings, feed pellets, grain, di-tri-octahedral smectite, and hospitalization have also been associated with impaction. 34 Some enteric infections are possibly nosocomial as well. It is valuable to know whether defecation or urination has been observed, how recently, how frequently, and whether these occur without straining. In neonatal camelids, it is important to consider the possibility of a congenital intestinal defect such as segmental atresia, particularly if defecation or passage of meconium has yet to be observed, or a urinary tract • Aerophagia (common in crias with choanal atresia) • Enteritis • Organomegaly (e.g., liver/spleen secondary to heart failure) • Clostridial enterotoxemia performed for pregnancy diagnosis, particularly during early pregnancy.

Atresia ani may present in neonates without associated defects or, in some cases, may present in conjunction with other urogenital or digestive tract defects. Concurrent rectovaginal fistula may allow gas or fecal material to pass and possibly delay recognition. 38, 39 During embryologic development, a caudal growth of mesenchymal tissue (the cloaca) becomes divided into two chambers by the urorectal fold. These chambers later become the rectum and urogenital sinus. Failure of the anal membrane to open results in atresia ani, a rectovaginal fistula forms if the urorectal fold fails to develop properly. A rectovaginal fistula allowed atresia ani to remain undetected in a female alpaca until it was evaluated at 3 years of age for breeding soundness. 38 A 3-day-old alpaca cria with atresia recti and a small rectovaginal fistula, through which only air could pass, strained intermittently and had only mild abdominal distension with reduced intestinal sounds on auscultation. 37 Crias with atresia ani or recti typically present within the first 3 days of life. Earliest detection is by handlers seeking to give an enema or determine the rectal temperature. Clinical signs may vary, but typically a history of tenesmus exists, and with delayed recognition, abdominal distension or pain on palpation of the abdomen may develop. Affected individuals presenting later may have weight loss, lethargy, and a poor appetite. The diagnosis is fairly evident upon examination of the perineal region because of the presence of a bulge or lack of the anal orifice. It may be difficult to determine the depth of the defect and whether it is amenable to surgical correction. Gentle pressure applied to the abdomen while observing the perineal area may allow a bulge to appear, but this is not particularly reliable as a prognostic indicator. Radiographic images demonstrate whether gas is present within the pelvis or extends into the perineal area. Ultrasonography of the perineum may demonstrate the distance from the skin to the blind end of the bowel. In the absence of other complicating defects, atresia ani is amenable to surgical management, but it is important to discuss the potential for heritability with the owner. That being said, if the caudal pouch of the rectum is not too deep, corrective surgery is not overly challenging, and most corrected animals may be healthy, albeit nonbreeding, members of the herd. Surgical correction is performed by making either a linear or preferably a circular incision over the presumed site of the anus, blunt dissection to identify the caudal extent of the rectal pouch, and then a rectal pullthrough procedure (see Figure 40 -64). The rectal serosa is sutured to the perineal skin by using a simple interrupted pattern. Sutures are placed at the lateral margins first, then dorsally and ventrally, and finally in between until 12 sutures have been made around the margin. It is preferable to perform this surgery with the cria fully anesthetized and intubated, as sometimes it may take time to locate the rectal pouch. Sedation with epidural anesthesia is a less desirable option. Perioperative antibiosis should be continued for 5 to 7 days, when the incision site has healed. The cria should be monitored for normal defecation, GI function, and behavior. Some crias outgrow the correction and may require a second surgery later, if they start straining again. The same surgery is performed for atresia recti, provided the portion of atretic rectum is not too long to achieve adequate mobilization. of adults (see Chapter 40) . Lateral views of the standing cria are easier to interpret than views taken in lateral recumbency because of the movement of gas and fluid within the bowel. When possible, a ventrodorsal or dorsoventral image should be taken for comparison. Sedation is rarely required in neonates; neonatal crias tolerate positioning with sandbags and foam wedges well, even in dorsal recumbency. Timm et al. (1999) published a useful paper on the radiographic appearance of the normal GI tract of neonatal crias and also performed a barium study to evaluate transit times. 36 These investigators used barium sulfate at a dose of 11 mL/kg, diluted with water in a ratio of 1 : 3 and found that this dose provided good morphologic definition. In neonates that were fed barium diluted with water via an oroesophageal tube, contrast consistently entered C1 but emptied from C1 and C2 at a mean time following tubing of 11.25 hours (range of 4 to 22.5 hours). In bottle-fed neonates, contrast was transported directly into C3. They found that the total transit time of the barium through the GI tract was long compared with that in foals, with barium entering the ascending colon at a mean time of 25 hours (range 16-37 hours) and still remaining in the ascending colon at the end of the study for up to 48 to 72 hours. Contrast studies may be useful in investigating crias that are not defecating or have vague signs of abdominal discomfort, particularly if the clinical condition does not necessitate immediate surgery. Because of the long period before the emptying of the large intestine, it may not be possible to rule out suspected colonic atresia until contrast is seen clearly in the rectum. Furthermore, intestinal motility may also be impaired in neonates with GI problems, making interpretation problematic. From the results of their contrast study in neonatal crias, investigators recommended timing of radiography at every 20 minutes for the first 2 hours and then hourly for 12 hours until barium reaches the spiral colon. Thereafter, images are made every 6 hours until 36 hours after barium administration, followed by radiographs taken at 12 hourly intervals, if required. 36 Depending on the site of interest, this schedule could be modified to reduce the amount of radiation exposure.

Box 42-2 provides a list of some of the most common differential diagnoses for the painful or distended abdomen in neonatal crias.

Atresia of the jejunum, colon, rectum, and anus all have been identified in neonatal camelids, with atresia ani being the most common. [37] [38] [39] In other species, the origin of these defects is controversial. Both heritable and nonheritable factors may be involved. In cattle, atresia coli may be the result of damage to the embryonic colonic vasculature occurring during rectal palpation of the amniotic vesicle in early gestation; a genetic predisposition may exist among Holstein-Friesian cattle. 40, 41 Atresia coli is believed to be inherited in humans, whereas in horses, a pattern of simple recessive inheritance has been identified along with postulated sporadic cases. [42] [43] [44] [45] Atresia ani is believed to be inherited in cattle and pigs. 46, 47 In camelids, most intestinal malformations are thought to be heritable, although true data are lacking; atresia ani has been reported anecdotally in related llamas. Some cases may also be sporadic and arise from random mutations or unidentified environmental influences; rectal palpation is not commonly Prior to attempting surgical correction, it is important to discuss the possibility of atresia coli being heritable and that the animal should probably not be used for breeding. To improve the chances of a good outcome, it is essential that hydration, acid-base status, and electrolyte imbalances be corrected, as needed, and good postoperative care must be provided. One study in calves showed that almost a third of calves with atresia coli had concurrent FPT, so this should be addressed. 51 Preexisting sepsis makes a cria a more challenging candidate for surgery. The prognosis for calves undergoing corrective surgery is relatively poor, with discharge rates reported between 35% and 44%. [51] [52] [53] Information about survival rates in crias is not available. Surgery is optimally performed under general anesthesia via a ventral midline or right flank incision. After identification of the atretic portion of bowel, an end-to-side colocolic anastomosis is recommended to minimize postoperative ileus and stenosis at the site of anastomosis. 51, 53 Right midflank colostomy, a salvage procedure in calves, offers superior short-term survival but is not likely to be esthetically acceptable to camelid owners. 48 Umbilical, diaphragmatic, or inguinal hernias may potentially cause clinical signs of abdominal pain and distension if the herniated segment of bowel becomes entrapped or strangulated. 54, 55 It is the same case with intussusception. 56 The spiral colon or jejunum are most commonly involved. Affected crias present with clinical findings similar to those described above. Usually, it takes days to months for entrapment to develop. Older crias may have a history of normal passage of feces prior to the onset of clinical signs. External hernias should be palpable on clinical examination, whereas internal ones require imaging studies or surgical exploration.

Choanal atresia, although not normally considered a differential for abdominal pain and distension, may cause considerable aerophagia. The abdomen may become distended, and bowel motility may be compromised.

Meconium should be passed within 20 hours after birth. In crias, meconium is normally a sticky orange-colored semicylindrical lump, but it may also come in the form of rice grain-sized pellets coated with thick orange-colored mucus. Ingestion of colostrum is thought to aid in its passage, so meconium impaction may be more likely in crias that fail to nurse. Transient meconium impaction is fairly common. Affected crias typically exhibit nonproductive straining starting around 24 hours of age and worsening with time. The impaction may be relieved by instilling a 20 to 30 mL warm soapy water enema via a well-lubricated soft rubber catheter inserted 10 to 15 cm into the rectum. The cria should posture to defecate very shortly thereafter. Sometimes a second enema is required, but repeated enemas may promote tenesmus from mucosal irritation. Persistent impactions may be treated with retention enemas containing 4% acetylcysteine. This should be left in place for 15 to 45 minutes to allow better dissociation of meconium. If enema treatment is unsuccessful, especially when no fecal matter has been passed, the possibility of atresia should be considered.

Some bottle-fed crias occasionally exhibit a syndrome similar to "ruminal drinking" in calves, in which milk ends up in the Crias affected by atresia coli may not present initially with the suspicion of a GI tract anomaly, since the anus is usually present. 39 Straining is less of a feature than with more caudal defects. The one reported case was in a 10-day-old cria that had been doing poorly since 2 days of age. Calves with atresia coli have been reported to survive as long as 19 days before diagnosis, and one recent study showed that the age of presentation of calves with atresia coli ranged from 3 to 18 days, whereas those with atresia ani presented at less than 4 days old. 40, 48 Owners may report that they had not seen the cria pass feces and had seen straining, but occasionally some material may have been seen at the anus. This may be mucus and epithelial cells from the lining of the bowel mistaken for fecal material, particularly if the atretic portion of bowel is more proximal. Crias may initially be observed to do well for the first day or two of life and then start to do poorly, becoming dull and lethargic. Abdominal distension is progressive, and affected crias tend to exhibit a painful response on abdominal palpation. A gentle digital rectal examination may yield only mucus. Abdominal ultrasonography and radiographic studies ( Figure 42-5) should show loops of distended intestine, consistent with intestinal obstruction. Hematologic and biochemistry findings are initially normal but become abnormal with progression of cardiovascular compromise and secondary complications. Differential diagnoses for the clinical findings described would be other forms of intestinal atresia, intestinal impaction or volvulus, intussusception, and diffuse peritonitis. Other potential differential diagnosis for neonatal crias with abdominal distension and pain, as well as constipation and lethargy, would be coccidiosis or clostridial enterotoxemia. Only 27% of crias with clostridiosis in one report had diarrhea, and it also appears to be an inconsistent finding with coccidiosis. 49, 50 With clostridiosis, death usually followed within 1 to 2 days after the onset of clinical signs. accumulation is excessive or the result of inflammation or a compromised viscus, pain signs may be present as well. Intraperitoneal plasma transfusions also may cause mild, transient abdominal distension and discomfort. The nature of the fluid may be assessed by using ultrasonography or by collection and analysis. Abdominocentesis should optimally be performed under ultrasound guidance to avoid accidental laceration of fragile organs and the bowel.

Ascites may result from liver or kidney failure, right-sided heart failure, or hypoproteinemia. Organ failure may be suspected on the basis of clinical examination findings (e.g., cardiac murmur) or biochemistry results, and hypoproteinemia may be detected by blood analysis. On ultrasonography, ascitic fluid appears anechoic, and cytologic examination should suggest a modified transudate.

Urine may also appear anechoic. Unlike in foals, bladder rupture in neonatal crias is extremely rare. One case of ruptured bladder in a 6-week-old cria occurred secondary to urethral obstruction by a urate urolith. 58 In other crias, malformations of the urinary tract have led to intraabdominal, retroperitoneal, or subcutaneous leakage.

Blood in the peritoneal cavity appears more heterogeneous and may contain clots or fibrin strands. Clots may resemble hyperechoic soft tissue masses. Hemoperitoneum may result from ruptured intraabdominal blood vessels, although this appears to be rare. The source of hemorrhage should be identified and resolved, if possible, while intensive management of the patient is performed to maintain cardiovascular function, possibly including whole blood transfusion. Blood-tinged fluid is a more common finding and compatible with inflammation or strangulation. This fluid usually has moderately high concentrations of protein and cells, worsening with progression of the lesion.

A small increase in the amount of peritoneal fluid may also be observed with enteritis, which may also be associated with pain signs. Ultrasonographically, this fluid may surround mildly distended loops of bowel, which often have increased motility. Crias with enteritis often have, or soon develop, diarrhea. The presence of bowel contents in abdominal fluid carries a guarded to grave prognosis, and euthanasia is recommended. On ultrasonography, this would appear as free fluid of a mixed echogenicity.

Peritonitis is usually associated with abdominal pain. Other signs may include lethargy, depression, diarrhea, tenesmus, anorexia with weight loss, and signs of sepsis, including tachycardia, tachypnea, evidence of dehydration, and injected or tacky mucous membranes. 35 Palpation of the abdomen may elicit a pain response. Pyrexia may or may not be present. In younger crias, FPT is a predisposing factor. Peritonitis may result from generalized sepsis; an intraabdominal event such as enteritis, a perforating ulcer, ruptured bowel, or umbilical infection; or abdominal surgery. Intraperitoneal transfusions of plasma may cause peritonitis as a result of using nonsterile techniques, inadvertent perforation of the bowel, infusion of nonsterile plasma, or infusion without using a filter. IP transfusion may also create inflammation that facilitates bacterial colonization in crias with developing or ongoing sepsis. For this reason, IV transfusion may be preferable in cases already showing signs of disease.

Peritonitis may be suspected on the basis of clinical signs and hematologic findings suggestive of inflammation. first gastric compartment (C1) instead of the third. This is caused by failure of the esophageal groove reflex. The milk ferments in C1, and acidosis or bacterial overgrowth may result. Affected crias often exhibit ill-thrift, reduced appetite, lethargy, left-sided abdominal distension, and diarrhea. Splashing sounds may be detected on auscultation of C1. Ultrasonography clearly shows fluid swirling around in C1 where none should exist. Aspiration through a stomach tube passed into C1 may yield fermented milk; a small diameter tube should be used, such as a stallion urinary catheter with a 60-mL catheter-tipped syringe. Usually, affected crias either are overfed (more than 15% of their body weight in a 24-hour period) or drink large volumes of milk rapidly from the bottle. Feeding smaller volumes at a higher frequency and using a bottle with a small nipple orifice may help prevent this. This technique may also be employed to treat affected crias. Ideally, C1 should be emptied, but this may be difficult with a stomach tube and carries a risk of aspiration. Reduced milk feeding may also help in the short term, but it is important to continue to provide hydration and meet the energy demands with IV fluids and parenteral nutrition. In refractory crias over 2 weeks of age, it may be advisable to transfaunate them and encourage them to eat forage to prevent overgrowth of pathogenic bacteria.

Umbilical infections in neonatal camelids appear to be rare but must be considered among differential diagnoses for crias with failure to thrive, lethargy, depression, abdominal distention or pain, or reduced appetite or anorexia. 57 The umbilical stump may appear enlarged and tender (Figure 42-6) or may appear normal. In the latter case, ultrasonographic evaluation of the umbilicus may prove illuminating, particularly in crias with hematologic evidence of inflammatory disease. Resection or drainage may be necessary. 57

Free fluids leading to distension of the abdomen may include pus, urine, blood, bowel contents, or ascites. If fluid 

Postmortem examination of 87 llamas at one teaching hospital revealed that ulcers were the cause of death in 5% of cases and contributed to death or were an incidental finding in more than 20% of cases. 64 Although the prevalence is likely to be lower in less seriously ill, surviving camelids, this nonetheless indicates the importance of this disorder. Furthermore, the incidence of ulcers appears to be similar for crias and adults. Pathogenesis is covered in Chapter 40. In crias, stress related to death of the dam or to inadequate milk ingestion, particularly when a hungry cria prematurely ingests roughage, may be a contributing factor. Extreme weather conditions, accompanying the dam on its trip for breeding, and weaning may also cause stress.

Crias with C3 ulceration may grind their teeth, show a reduction in nursing behavior, fail to gain weight, or lose weight. They also may be quiet and depressed or colicky. Excessive salivation may be observed. Unfortunately, many nonruptured ulcers are clinically silent, and the more recognizable ruptured ulcer usually defies treatment. Ultrasonography of C3 may show focal thickening or cratering of the wall, and a localized increase in peritoneal fluid may occur around C3, particularly in the space between C3 and the liver. This fluid may be flocculent if the ulcer has ruptured. Confirmation of the diagnosis is difficult, since it is virtually impossible to pass an endoscope directly into C3 for direct visualization of ulcers. Fecal occult blood tests are unreliable in camelids.

Hospitalized crias are at risk of developing C3 ulcers, so prophylactic medications may be considered. However, this risk remains undefined, and progression of ulcers during hospital stays is poorly substantiated. Possible antiulcer medications include proton pump inhibitors (PPIs), histamine receptor (H 2 ) blockers, and mucosal protectants. Oral PPIs are poorly absorbed in adult camelids, but no data on crias are available. 65,66 SQ (2 mg/kg) or IV (1 mg/kg) pantoprazole is Leukocytosis or leukopenia may exist, with degenerative left shift and toxic changes in the neutrophils. Hyperfibrinogenemia may develop over the first few days. Hypoproteinemia may be present as a result of FPT and hypogammaglobulinemia or because of leakage of protein into the abdomen. Ultrasonography may show an increase in the volume of peritoneal fluid and may suggest a possible source for the peritonitis. Occasionally, the quality of the ultrasonographic image appears to be suboptimal and might appear granular, an appearance that may be replicated on radiography. Definitive diagnosis is obtained by analysis and culture of the peritoneal fluid. Cytologic abnormalities include increases in nucleated cell counts, particularly by cells of the neutrophil line; the appearance of immature neutrophils or cells with toxic changes, possibly the appearance of intracellular or extracellular microorganisms; and also possibly the appearance of feed material. Peritoneal fluid protein concentrations are also usually high. In healthy adult alpacas and llamas, peritoneal fluid was found to contain up to 3000 total nucleated cells per microliter (cells/µL), with fewer than 2000 neutrophils/µL and protein concentration less than 2.5 g/dL. 59 Normal values have not been established for camelid neonates, but in healthy foals, the total nucleated cell counts are considerably lower than those seen in adults. 60 The most common isolates in crias without a leaking bowel are Escherichia coli and Streptococcus spp. Peritonitis caused by a single type of bacteria and without major morphologic changes to abdominal viscera may respond quickly to appropriate treatment. Infections with mixed populations of bacteria and related to compromised or abnormal viscera usually carry a grave prognosis and may require surgical intervention as well as medical treatment.

Intensive monitoring and therapy is required in all cases and should include IV fluids, antibiotics, and antiinflammatories. IV plasma transfusion is likely to be required in crias with underlying FPT or consumption and may also provide improved oncotic pressure for cardiovascular support in the event of protein leakage into the abdomen. Peritoneal lavage may be considered, particularly when peritoneal fluid contains high concentrations of fibrin. Surgery and surgical lavage may be necessary to remove or oversew damaged tissue, drain abscesses, break down adhesions, or remove fibrin.

Differential diagnoses for intestinal obstruction in camelid neonates include intestinal atresia (discussed above), intraluminal obstruction by ingested or orally administered substances, entrapments or strangulations, intussusception, and spiral colon volvulus. Intussusception is rare, with only one reported case in a cria. 56 A high burden of coccidia may have been a predisposing factor in that case. Wood shavings, pellets, grain, hair, sand, plant fiber, and smectite have all been implicated in small intestinal or spiral colon impactions or bezoars in crias. 44, [61] [62] [63] Entrapment or strangulation may occur through the epiploic foramen, a mesenteric rent, or a hernial ring. Thorough examination and use of appropriate diagnostics including blood work, abdominocentesis, ultrasonography ( Figure 42-7) , and radiography (see The potential causes of diarrhea in llama and alpaca crias, the ages at which they are likely to be diagnosed, and the diagnostic tools available are listed in Table 42 -1. The most common causes are bacteria, viruses, and protozoa. Failure of passive transfer may predispose neonates to some of these infections. Nutritional factors such as feeding milk substitutes may promote diarrhea as well. Diarrhea caused by GI nematodes or cestodes rarely occurs in crias younger than 2 months of age, 69 presumably because young crias lack sufficient grazing behavior to ingest sufficient larvae and this also reflects the tendency of worms to cause ill-thrift but not specifically diarrhea.

Knowledge of the agents involved and at what age they are likely to cause disease is important in deciding on the appropriate diagnostic tests and the best treatment. Additionally, the clinician must realize that failure to reach a diagnosis and to institute effective treatment in a timely fashion may allow the disorder to become chronic and pathologic changes to become permanent. The individual infectious agents tend to have characteristic clinical presentations, which help guide the clinician. However, co-infections may blur these clinical distinctions and decrease the success of unimodal treatment. Therefore, it is preferable to perform a panel of diagnostic tests to identify all pertinent agents, as this ensures correct treatment or effective in adults and likely to be efficacious in crias as well. 67 Histamine receptor blockers have very short action in adults, even when given parenterally, and thus are unlikely to be effective at conventional doses in crias either. 65, 68 Gastric mucosal protectants have been used in camelids with the aim of aiding in healing of ulcers. Sucralfate (1 g, PO, q8-12h) binds to ulcerated tissue in the GI tract, thereby protecting the mucosa from further damage. The esophageal groove reflex may allow this drug to be carried directly into C3, particularly in neonates, and it therefore may have a role in treating suspected ulcers in crias.

Diarrhea is one of the most important neonatal diseases in South American crias and becoming a more recognized problem in North American and European herds. In a 5-year study of 250 crias on four different Ohio farms, diarrhea was identified as the most common cause of morbidity in the preweaning period, affecting some 23% of crias (Sharpe et al., unpublished data, 2000) . The increasing prevalence in the developed world coincides with the increasing popularity of raising llamas and alpacas, which has led to higher stocking densities and greater exposure of young stock to pathogens.

were determined at necropsy to enter directly into the caudal vagina. Ureteral duplication and hydronephrosis were reported in a young alpaca that developed dysuria at 7 months of age. 72 Unilateral nephrectomy and ureterectomy resolved the clinical signs. Ectopic ureters also lead to dysuria and dribbling.

Vulvar deformities have been reported in female crias in which the vulva is either totally or subtotally imperforate. 70 These are relatively common defects that have also been called labial fusion. 71 In cases of partial fusion, the defect may not be discovered until adulthood when females fail to become pregnant or appear to be uncomfortable during mating. In other cases, crias present with stranguria. If the vulva is totally imperforate, it protrudes as a fluid-filled swelling (see ; in some cases, a small hole may be present and allow urine to pass under pressure. Corrective vulvoplasty is a quick and simple procedure. Sedation or general anesthesia is not required. The cria is restrained in sternal recumbency and positioned with the hindlimbs over the end of a table; The region may be numbed by injection of a local anesthetic or topical use of an anesthetic gel, or regional anesthesia may be achieved through a sacrococcygeal epidural injection (approximately 0.1 mL of lidocaine is adequate). The site is prepared aseptically, and a dorsal to ventral incision is made on the midline of the vulva to create an approximately normal-sized vulvar opening (Figure 42-8) . Making the incision in this direction minimizes the chances of unintentionally creating a rectovaginal fistula. The vestibular mucosa may be sutured to the vulvar skin using an absorbable suture material, but suturing is not required and is not normally done. Postoperatively, the site should be treated with a topical antibiotic ointment with steroid once or twice daily for 5 to 7 days to prevent the wound from closing over again.

It has been suggested that vulvar deformities are heritable because 2 of 6 affected crias in one report were full siblings. 70 Furthermore, it has been reported as a familial trait in humans and marmosets. 76, 77 In marmosets, an autosomal recessive mode of inheritance was proposed, which suggests that the parents may perpetuate the defect in phenotypically unaffected individuals.

treatments being initiated in a timely fashion and allows more effective on-farm control measures to be instigated.

The specific agents of cria diarrhea, their diagnosis, and treatment are discussed in Chapter 40.

The main urinary system abnormalities of concern in neonatal crias are caused by congenital defects. This section also deals with renal failure and its potential causes in crias. The clinical signs exhibited by affected crias vary, depending on the actual problem, and may include abnormalities associated with urination (dysuria, stranguria, anuria, polyuria, hematuria) or nonspecific clinical signs of renal failure (lethargy, weakness, depression, anorexia, etc.). Thorough history taking, clinical examination, and use of appropriate diagnostic tests help in reaching a diagnosis.

A number of defects have been reported affecting the urinary system in camelids, including cystic kidneys, renal or bladder agenesis or hypoplasia, ureteral duplication, ectopic ureters, hypoplasia of the male or female genital tract, intersex variants, and vulvar deformities. [70] [71] [72] [73] [74] [75] With the exception of vulvar deformities, these defects are rare, and it is uncertain whether genetic or teratogenic factors are to blame. Both unilateral and bilateral renal agenesis have been reported. 73, 74 Bilaterally affected crias have progressive obtundation without evidence of urine production. Azotemia, hyperphosphatemia, and hyperkalemia may be detected on blood analysis and are refractory to fluid treatment. Ultrasonography should permit identification of neonatal kidneys with ease, so an inability to find either or both kidneys raises suspicion. Contrast radiography or cross-sectional imaging techniques may be useful as well. Crias with one relatively normal kidney may escape detection, unless that kidney has a progressive condition or is otherwise damaged. One reported cria was presented at 4 days of age for inappetence and was treated for failure of passive transfer and sepsis but was brought back within a month with azotemia. Agenesis of the right kidney was suspected, and acute renal failure was diagnosed. 73 The diagnosis was confirmed at necropsy. No nephrotoxic drugs had been administered, but it is possible that the initial septicemic episode resulted in damage to the normal kidney. Another llama cria was suspected to have unilateral renal agenesis and unilateral renal hypoplasia. In this case, only a nodule of hyperechoic soft tissue was found at the expected site of one kidney, and the other was very small and did not appear to have normal kidney structure on ultrasonography. Azotemia was identified on biochemistry, and the cria was treated symptomatically as a neonate, but the azotemia persisted even when the cria appeared clinically well. This llama lived for about 2 years before being euthanized as a result of renal failure (J. Lakritz, personal communication). Even when it appears normal, the kidney contralateral to the hypoplastic one may harbor a degenerative process, so affected crias should be monitored closely.

Agenesis of the urinary bladder was reported in one alpaca cria. 75 This cria presented at 10 days of age with a history of stranguria and urine dribbling. Bilateral hydronephrosis and dilated ureters were found on ultrasonography, and the ureters Fractional excretion of sodium is calculated by using the following formula:

where Cr is creatinine.

Ultrasonography is a convenient, noninvasive way to evaluate the kidneys and the bladder. Loss of renal corticomedullary contrast may be apparent in dehydrated animals, but it is hard to differentiate this from other renal pathology without other clinical information. Renal cysts are relatively common, and if small (up to a few millimeters), they are usually incidental findings. Large, hypoechoic or anechoic, well-circumscribed circular lesions may be cystic or neoplastic, even in quite young crias. Early identification of cystic or hypoplastic kidneys allows decisions to be made before too many hospital expenses have accrued. The ureters are easier to find if they are dilated; otherwise they are usually only seen as they exit the kidney. Plain or contrast radiography is likewise helpful (see . Renal biopsy may be indicated for further diagnostics and should be performed under ultrasound guidance.

Whatever the underlying pathology, treatment of azotemia involves IV fluids to restore fluid volume and cardiac output in cases of hypovolemia and to improve renal perfusion and excretion of metabolites. Sick neonatal camelids are often hypoproteinemic, so extra care must be taken when administering fluids to avoid potential complications such as pulmonary edema. Administration of colloids, especially plasma, helps prevent this and also addresses any underlying failure of passive transfer. With shock, initial crystalloid resuscitation may be achieved by using fluid boluses of up to 100 mL/kg over 15 to 30 minutes, but boluses greater than 20 mL/kg are rarely necessary, especially when followed by fluids at 2 to 4 mL/kg/hr. 79 Low sodium fluids are recommended in neonates with hypernatremia. Fluids may be administered continuously either as boluses every few hours or by continuous infusion, depending on what facilities are available. If a pump is not available, care must be taken not to underestimate the flow rate, particularly with positional catheters. Bolus administration is safer in this regard and allows the cria to stay with the dam. Allowing the cria to continue to nurse, if able, lowers stress and provides nutrition and water. Furosemide may be used to promote diuresis in cases with oliguria, preferably by constant rate infusion (0.66 mg/kg loading dose followed by 0.66 mg/kg/hr). However, its effects rely on furosemide reaching the lumen of the renal tubules, and this may be minimal in renal failure.

Neonatal crias may present with a variety of locomotor problems, including ligament laxity, flexural deformities, and angular limb deformities, similar to those encountered in other large animal neonates. Bone sequestra, a common issue in camelids of any age, are covered in Chapter 58.

On presentation of a cria with lameness, a thorough orthopedic evaluation should be performed. Carefully palpate each joint for evidence of swelling, laxity, inflexibility, angulation, crepitus or luxation, and along each long bone by pressing A similar defect has been seen in male or intersex crias in which a urine-filled swelling develops on the midline of the perineal area. The penis in affected crias appears smaller or overtly hypoplastic, and the entire penile sheath is situated more caudal than normal. The urethra does not appear to be intact such that affected crias have an inability to urinate normally and urine accumulates in the perineum. Surgical correction requires urethrostomy. A stoma is created over the swelling in a manner similar to that created in female crias. This defect may be similar to hypospadia in human males. 78 

Azotemia in neonates is most likely prerenal or renal in origin unless associated with a congenital urinary tract abnormality. Healthy neonates typically have low creatinine concentrations because of low muscle mass, but concentrations may be higher in the first 48 hours of life because of possible placental dysfunction, volume depletion, ingestion of creatinine-rich fetal fluids, or reduced renal clearance in premature crias. 79 Dehydration as a result of failure to ingest fluids or fluid losses from diarrhea are the most likely causes of prerenal azotemia, whereas sepsis, nephrotoxins, a congenital malformation, or poor perfusion may result in organ dysfunction. Diseases primarily affecting other organ systems often result in renal compromise, so it is important to identify underlying disease processes and treat them and azotemia appropriately. Toxic causes of renal failure in neonates include nephrotoxic drugs such as gentamicin and oxytetracycline or oversupplementation of vitamin D to prevent rickets. 80 Vitamin D toxicity was reported in two neonatal alpacas with anuric acute renal failure. Both had received toxic amounts of vitamin D orally over multiple consecutive days and developed soft tissue mineralization with hyperphosphatemia and hypercalcemia. These doses were estimated to be 3750 international units per kilogram per day (IU/kg/day) for 7 days and 12,987 IU/kg/ day for 5 days. Mineralization was evident as a continuous hyperechoic line on ultrasonography of the kidneys and as a grossly visible white line on the cut-section of the renal medulla at necropsy.

Since neonates dehydrate rapidly with fluid losses, early intervention with fluids may be necessary to preserve renal function. Blood samples should be analyzed from any sick neonate to aid in prompt recognition of biochemical abnormalities so that appropriate treatment can be given and fluid therapy adjusted according to requirements. Ideally, a urine sample should be evaluated for specific gravity in order to differentiate renal from prerenal azotemia. Urinalysis (dipstick, quantitative tests, and cytology) is also helpful in diagnosing renal failure. High protein on a dipstick test should be evaluated quantitatively and in the light of other findings on urinalysis. Increased protein with bacteria, increased white blood cells, hemorrhage, or all of these may occur with infections of the urinary tract, whereas increased protein without these suggests loss of protein at the glomerulus. Finding casts on cytologic evaluation suggests tubular damage. Assessment of urine output and fractional excretion (FE) of sodium may also aid in determining renal function. Fractional excretions are best calculated before the administration of fluids. Low FE of sodium is most often the case in prerenal azotemia because of angiotensin-mediated sodium resorption, whereas in true renal disease, FE of sodium is usually markedly increased. followed by postoperative splint application. The cria made a good recovery. These cases suggest that careful evaluation of the deformity with manipulation of the limbs prior to surgery guide the surgeon as to the most appropriate structures to transect.

Selenium deficiency may result in the birth of weak neonates that are unable to stand or raise their heads to nurse. Anecdotal reports of selenium deficiency resulting in this syndrome exist in camelids, and it is fairly common practice for owners of camelids to administer selenium-containing preparations to any weak crias, regardless of cause.

Angular limb deformities (ALDs) may be congenital or acquired (Figure 42-10) . They may be conformational in origin (genetic), associated with joint instability in premature crias because of trauma (in either the affected leg or the opposite one), or secondary to rickets. It is important to differentiate the causes so that the correct advice can be given to owners with regard to breeding choices. Severe deformities may result in abnormal weight-bearing, secondary subluxation of firmly along the entire length. Take care to also palpate the growth plate areas as pain or swelling in this area could indicate rickets or inflammation.

Ligament laxity associated with prematurity is usually mild and usually resolves over several days once crias begin to exercise. However, occasionally, it may be moderate to severe and result in pain and reluctance to stand or ambulate. In these situations, particularly where carpal valgus or hyperextension is occurring, support may be required in the form of splinting. Splints should be well padded to avoid pressure sores and they should only be placed for as long as necessary, with the legs being checked regularly.

Flexural limb deformities, more commonly termed "contracted tendons" or joint contracture, occur in cria neonates, but not as frequently as in foals and calves. [81] [82] [83] [84] They may affect the carpus, fetlock, or pastern, causing the affected joint to have limited extension. Various causes have been suggested in other species, including heredity, teratogens, and in utero positioning of the fetus. Arthrogryposis implies that flexural deformity is permanent and often affects multiple joints. In addition to the described causes for joint contracture, arthrogryposis may result from neurologic diseases or diseases that limit fetal movement. Arthrogryposis was found in only a small number of crias with congenital defects (21 of 895) in one study and was thought to be rare compared with the incidence in calves and lambs. 81 Most of the time, flexural deformity is relatively mild. If the pad of the foot continues to bear weight and the leg does not buckle with movement, contracture, like laxity, usually resolves as the animal walks around on it. If a cria has trouble standing or tries to walk on the dorsal aspect of the fetlock, manual stretching several times daily may resolve the problem. If physiotherapy alone is not successful, splinting the limb in as extended a position as possible may be required for up to 2 weeks. Padded gutter splints designed for dogs work well in crias, as do partial rounds of polyvinyl chloride (PVC) piping over cotton padding. Many affected crias are able to bear weight within a few days of splint application. The prognosis is worse for flexural deformities of carpus than for lower limb joints. If physical measures fail, radiography should be performed to ensure that the anatomy is normal before any more invasive and costly measures are undertaken. If arthrogryposis is suspected, diagnostic evaluation of the brain and spinal cord may be indicated as well. Suspensory ligament desmotomy was successful in one cria with bilateral flexural deformity of the carpal and fetlock joints. 82 Two earlier cases were less successful. One described bilateral transection of both superficial and deep flexor tendons, as well as the suspensory ligament in a 1-day-old llama that presented with severe flexural deformities of both metacarpophalangeal joints. 83 This resulted in ischemic necrosis of one distal limb at the level of the fetlock. In a second case report, wedge osteotomy of metacarpal bones III and IV was performed, but this resulted in luxation of the fetlock joint. 84 Another cria presented at 2 months of age with severe bilateral flexural deformities of the carpi (Figure 42-9 ). This cria was treated surgically by transection of the ulnaris lateralis and flexor carpi ulnaris tendons, back because of pain, and are typically smaller than agematched animals; herd mates may not be good comparators because they may also be affected. Some affected juveniles die with no other possible cause identified.

The two sources of vitamin D for herbivorous animals are (1) dietary vitamin D 2 (ergocalciferol) from plants and (2) endogenous vitamin D 3 (cholecalciferol) made in skin through the action of ultraviolet (UV) light on pro-vitamin D 3 . A small amount of vitamin D is also passed to offspring transplacentally and via the dam's milk. 90 Vitamin D 2 is found in higher concentrations in mature grass or hay; spring grass has relatively little. Therefore, spring is a high-risk time for recently weaned summer-born or fall-born crias put on fresh pastures without supplementary feeding. Vitamin D 3 production is also seasonal; blood concentrations drop during the winter months because of reduced UV light availability. [90] [91] [92] Heavy cloud cover reduces UV penetration to Earth's surface. It is believed that reduced exposure to UV radiation at low altitudes and nonequatorial latitudes (i.e., outside of South America) reduces vitamin D activation in skin. It has also been suggested that dark pigmentation and thicker fleece in sheep reduce photobiosynthesis of vitamin D and that darker unsheared animals are therefore more susceptible to rickets. 92 Similar findings were found in alpacas in two separate reports. 86, 91 Camelid breeders in high-risk areas are advised to supplement crias using injectable vitamin D-containing products 2 or 3 times during the winter months to provide 1000 IU/kg body weight. 86 Most products also include vitamins A and E. The effects last approximately 2 months. Three injections are recommended in areas or years where the winter is particularly long and cloudy. Oral multivitamin formulations are available, but these require a more frequent dosing interval of approximately every 4 weeks. Treatment regimens for animals with rickets are similar. Some oral preparations are made for larger animals and are not particularly conducive to delivering accurate cria doses. Dosing should be based on actual body weight and not "per cria" since weights of crias vary from 5 kg to 45 kg. Overdosing may lead to toxic effects, including soft tissue mineralization and renal failure. 80 Vitamin D toxicity should be suspected in camelids with compatible history of vitamin D supplementation above the recommended doses, along with hypercalcemia, hyperphosphatemia, and renal dysfunction apparent on clinical chemistry. fetlocks, joint pain, and arthritis later in life. Correction of angular limb deformities may be achieved but must not be used to mask bad conformation.

Rickets is a common condition affecting South American camelids residing outside of South America. [85] [86] [87] [88] It is characterized by stunted growth, increased recumbency, angular limb deformities, a hunched posture, lameness, and general illthrift; as such, it is of commercial and health significance to camelid breeders. The primary cause of rickets is believed to be a vitamin D deficiency; the most obvious abnormality on routine blood analysis is hypophosphatemia. Blood vitamin D analysis reveals the specific deficit, if a sample is obtained before exogenous supplementation.

Rickets in camelids has been reported in North America, New Zealand, Australia, and Europe. [85] [86] [87] [88] It is most severe in growing animals and is characterized by a failure of mineralization at the growth plates, resulting in increased depth of the cartilaginous growth plates and articular cartilage. These become distorted by the pressure of weight-bearing. 89 Changes are most obvious in sites where growth occurs rapidly, as in growth plates adjacent to the carpal and fetlock joints and the costochondral junctions of the ribs. Vertebral growth plates may be affected as well, possibly leading to secondary nerve impingement. Mineralization defects, including increased physeal and articular cartilage depth, irregular appearance of growth plates, metaphyseal flaring, and thinned cortices, may be seen readily on radiography (Figure 42-11) . Changes may be identified clinically as swollen, painful joints, pathologic fractures, and the classical "rosary bead" feel along the ribcage ( Figure 42-12) , which reflects enlargement of the costochondral junctions. Angular limb deformities may subsequently develop, and affected individuals show lethargy, have depressed appetites, may be lame and walk with a hunched ALD. Such procedures should be considered if required to improve quality of life for the patient. Bilateral wedge ostectomy of the distal radius was performed in one 14-month-old alpaca with severe bilateral carpal valgus of 40 degrees and 42 degrees and closed distal radial and ulnar growth plates. 93 The cria made a good recovery and was reported to be ambulatory 12 months postoperatively but with reduced carpal flexion. An 18-month-old llama had bilateral wedge ostectomy for a similar defect suspected to have been caused by premature closure of the distal ulnar physes. 94 For older crias with stunted growth and ALD caused by rickets, corrective surgery is likely to be less of an option. Vitamin D supplementation should be given to improve bone density before surgical options are considered. These crias are likely to remain stunted indefinitely.

Valgus deformity of the metacarpophalangeal joint was reported in a 1-month-old alpaca. 95 The deformity had been present from birth and its cause was not established. Transphyseal bridging of the distal metacarpal physes successfully corrected it.

Septic joints are less uncommon in crias than in calves and foals. When they do occur, they typically affect only a single joint. Affected crias often do not bear weight on the leg with the swollen joint, which is hot and painful on palpation. Radiography and arthrocentesis are indicated to confirm that the joint is infected and to rule out a sequestrum. Cultures and cytologic samples should also be submitted when joint fluid aspirates are suggestive of infection. Cultures are often negative in spite of infection because the bacteria are more commonly associated with the synovial membrane and the patient may already have been treated with antibiotics. Treatment for septic arthritis should be initiated as early as possible to improve the prognosis. Ideally, joint lavage should be performed using warmed saline through wide-bore needles inserted into the joint (through-and-through lavage). In chronic cases, needle lavage may be inadequate, and arthroscopy should be considered to remove large fibrin deposits. Systemic and intraarticular antibiotic therapy and antiinflammatory therapy are indicated. Affected crias should be evaluated for FPT and treated for this if it is suspected.

Carpal valgus is the most commonly encountered ALD. Although hindlimbs may also be affected, carpal valgus is more easily corrected. Premature crias with joint laxity may benefit from splint application, if the angulation is severe enough to interfere with ambulation. Radiography should be performed to assess the severity of the deformity and to determine whether lesions consistent with rickets are present. The earlier the ALDs are treated, the less invasive the method of treatment can be with fewer subsequent complications.

If ALD is mild in a cria aged less than 2 months, injection of vitamin D at 1000 to 2000 IU/kg body weight may improve the deformity or be curative in cases where hypovitaminosis D is the cause. This may be confirmed by preadministration determination of serum vitamin D concentration. Carpal valgus is the ALD most amenable to surgical management. For crias affected by rickets, corrective surgery to address this deformity, combined with vitamin D supplementation, is likely to improve corresponding deformities at other sites such as at the fetlocks, since the angulation of these joints is also improved. The least invasive technique and one that is appropriate at an advanced stage is periosteal stripping. This may be combined with partial ulna ostectomy. The cria is placed under general anesthesia and positioned in dorsal recumbency. A 5-cm incision is made on the lateral aspect of the carpus, starting immediately proximal to the distal physis of the ulna and continued proximally. The incision is made right down to the bone, and the periosteum is elevated from the radius and ulna as far as can be reached in a cranial and caudal direction. Care must be taken to avoid damaging nearby ligaments. A small section of the distal ulna may be removed using bone rongeurs. The skin incision is then closed and light pressure dressings placed postoperatively for 7 to 10 days to reduce swelling. Reevaluation should be done 30 to 45 days following surgery to assess the adequacy of correction.

As the affected cria becomes older, or if the carpal valgus is severe (>10 degrees), more invasive surgery is required. At this point, transphyseal bridging of the radial growth plates may be done. This technique is effective in young animals that still have open growth plates and are still growing. In this case, the incision is made on the medial aspect of the carpus. The position of the radial growth plate is estimated using radiography as a guide, and 18-gauge needles are placed into the bone above and below the growth plate. These mark the intended locations for screw placement. Intraoperative craniocaudal radiography allows the surgeon to place screws correctly using the needles as guides. One cortical bone screw (2.7-mm or 3.5-mm diameter) is placed proximal and one distal to the medial aspect of the distal radial physis. Before tightening down the screws, an 18-to 20-gauge orthopedic wire is placed around them in a figure-of-8 pattern. A light pressure bandage is again placed postoperatively for 7 to 10 days. The owner needs to monitor the cria closely so that the bridge can be removed just when the deformity has been corrected. This normally occurs in 3 to 4 weeks. It is possible that one leg may be corrected more quickly than the other in bilateral cases, leading to two separate surgeries for screw removal. If the bridge is left in too long, a varus deformity results.

In older crias, the ability to use compensatory growth diminishes. The radial growth plates close around 9 months; after that point, corrective osteotomy is required to correct the

The premature cria

Culture-positive sepsis in neonatal camelids: 21 cases

Gram-negative bacterial infection in neonatal New World camelids: six cases

Investigation of Mycoplasma haemolamae infection in crias born to infected dams

Cebra CK: Hyperglycemia, hypernatremia, and hyperosmolarity in 6 neonatal llamas and alpacas

Metabolic acidosis without dehydration in a llama cria

The association of lung function and plasma volume expansion in neonatal alpaca crias following plasma transfusion for failure of passive transfer

Evaluation of breed as a risk factor for atresia coli in cattle

Atresia coli inherited in Holstein cattle

Familial occurrence of congenital colonic atresia

Blind-end atresia coli in two foals

Segmental atresia of the transverse colon in a foal with concurrent equine herpes virus-1 infection

Intestinal atresia and stenosis in animals: a report of 34 cases

Intestinal malformations in calves and their surgical correction

Genomewide scan for anal atresia in swine identifies linkage and association with a chromosome region on Sus scrofa chromosome 1

Surgical repair and management of congenital intestinal atresia in 68 calves

Eimeria macusaniensis associated lesions in neonate alpacas dying from enterotoxemia

Eimeria macusaniensis infection in 15 llamas and 34 alpacas

Colonic atresia in cattle: a prospective study of 43 cases

Clinical management and surgical repair of atresia coli in calves: 66 cases (1977-1988)

Atresia coli in calves: 26 cases

Diaphragmatic hernia in a llama

Inguinal hernial repair in a llama (Lama guanicoe)

Ileocecocolic intussusception in a one-month-old llama

Abdominal pain associated with an umbilical abscess in a llama

Medicine and surgery of South American camelids

Collection and analysis of peritoneal fluid from healthy llamas and alpacas

Peritoneal fluid values from healthy foals

Clinical findings from 27 New World camelids with laparotomy for acute gastrointestinal disease

Fatal sand impaction of the spiral colon in a 1-month-old alpaca

Trichophytobezoar duodenal obstruction in New World camelids

Third compartment ulcers in the llama

Pharmacokinetics and pharmacodynamics of antiulcer agents in llama

Pharmacokinetics of oral omeprazole in llamas

Efficacy and pharmacokinetics of pantoprazole in alpacas

Effect of flunixin meglumine and cimetidine hydrochloride on the pH in the third compartment of the stomach of llamas

Potential pathogens in feces from unweaned llamas and alpacas with diarrhea

Congenital vulvar deformity in 6 alpacas

Labial fusion causing urinary tract obstruction in an alpaca cria

Hydronephrosis and ureteral duplication in a young alpaca

Renal agenesis in an alpaca cria

Fetal and neonatal thermoregulation

Serum triiodothyronine and thyroxine concentrations in neonatal llamas

Alterations in body temperature

Fowler ME: Medicine and surgery of South American camelids

Management of neonatal llamas and alpacas

Clinical and clinicopathological characteristics of the septicaemic neonatal foal: review of 38 cases

Febrile seizures: mechanisms and relationship to epilepsy

Neonatal diseases in llamas and alpacas

Antimicrobial use in New World camelids

Single intravenous and multiple dose pharmacokinetics of gentamicin in healthy llamas

Oxygen transport of hemoglobin in high-altitude animals (Camelidae)

Oxygen transport in the llama (Lama glama)

O2 transport in the alpaca (Lama pacos) at sea level and at 3,300 m

Cardiorespiratory functions in the fetal llama

Pulmonary circulation of the llama at high and low altitudes

The fetal llama versus the fetal sheep: different strategies to withstand hypoxia

Evolving in thin air-lessons from the llama fetus in the altiplano

Manifestations of disease in the neonate

Listeria monocytogenes and Escherichia coli septicemia and meningoencephalitis in a 7-day-old llama

Otitis media/interna and suppurative meningoencephalomyelitis associated with Listeria monocytogenes infection in a llama

Meningoencephalitis and brain abscessation due to Escherichia coli in a 2 week old alpaca cria

Meningitis associated with Salmonella newport in a neonatal alpaca (Lama pacos) in the United Kingdom

Streptococcus bovis biotype I meningoencephalitis in an alpaca (Lama pacos) cria

Camelid cardiology

Physiologic peripheral pulmonary artery stenosis in neonatal camelids

Atrioventricular septal defects in three llamas (Lama glama)

Spiral colon impaction in 10 alpaca crias

Abdominal discomfort in llamas and alpacas: causes and clinical characteristics

Radiographic contrast gastrointestinal study of the neonatal llama

Surgical correction of anorectal atresia and rectovaginal fistula in an alpaca cria

A case of atresia ani with rectovestibular fistulae in an alpaca (L. pacos)

Atresia coli in an alpaca cria

Vitamin D doses for alpacas (Lama pacos)

Vitamin D doses for alpacas (Lama pacos

Rickets in llamas and alpacas, Llamas Mar/Apr

Bones and joints

Perinatal 1,25-dihydroxycholecalciferol in the sheep and its role in the maintenance of the transplacental calcium gradient

Seasonal changes in serum calcium, phosphorus, and vitamin D concentrations in llamas and alpacas

Relative contributions of diet and sunshine to the overall vitamin D status of the grazing ewe

Surgical correction of carpal valgus deformity in three alpacas

Bilateral wedge ostectomy on an 18-month-old llama with severe bilateral carpal valgus

Surgical correction of metacarpophalangeal valgus deformity in an alpaca

Bilateral renal agenesis in an alpaca cria

Urinary bladder agenesis in an alpaca (Vicugna pacos) cria

Familial posterior labial fusion

Congenitally caused fused labia in the common marmoset (Callithrix jacchus)

Hypospadias in sons of women exposed to diethylstilbestrol in utero: a cohort study

Approach to the critically ill camelid

Acute renal failure and anuria associated with vitamin D intoxication in two alpaca (Vicugna pacos) cria

Congenital defects in the llama

Management of bilateral flexural deformity of the metacarpophalangeal joints in three alpaca crias

Arthrodesis for congenital flexural deformity of the metacarpophalangeal and metatarsophalangeal joints

Osteotomy for congenital flexural deformity of the metacarpophalangeal and metatarsophalangeal joints

Evaluation of vitamin D status of llamas and alpacas with hypophosphatemic rickets