Average reported canine and feline neonatal mortality rates (greatest during the first week of life) vary, ranging from 9%-26%. Prudent veterinary intervention in the prenatal, parturient, and postpartum periods can increase neonatal survival by controlling or eliminating factors that contribute to puppy morbidity and mortality. Poor prepartum condition of the dam, dystocia, congenital malformations, genetic defects, injury, environmental exposure, malnutrition, parasitism, and infectious disease all contribute to neonatal morbidity and mortality. Optimal husbandry impacts neonatal survival favorably by managing labor and delivery to reduce stillbirths, controlling parasitism and reducing infectious disease, preventing injury and environmental exposure, and optimizing nutrition of the dam and neonates. Proper genetic screening for selection of breeding animals minimizes inherited congenital defects.
Optimal neonatal resuscitation (if needed after birth or cesarean section) involves the same “ABC’s” as any cardiopulmonary resuscitation. Prompt clearing of airways (“A”) by gentle suction with a bulb syringe, and then drying and stimulation of the neonate to promote respiration (“B”) and to avoid chilling are performed. Neonates should not be swung to clear airways because of the potential for cerebral hemorrhage from concussion. The use of doxapram as a respiratory stimulant is unlikely to improve hypoxemia associated with hypoventilation and is not recommended. Spontaneous breathing and vocalization at birth are positively associated with survival through 7 days of age. Intervention for resuscitation of neonates after vaginal delivery should be done if the dam’s actions do not stimulate respiration, vocalization, and movement within 1 min of birth.
Cardiopulmonary resuscitation for neonates that do not breathe spontaneously is challenging yet potentially rewarding. Ventilatory support should include constant flow O2 delivery by facemask. If this is ineffective after 1 min, positive pressure with a snugly fitting mask or endotracheal intubation and rebreathing bag (using a 2-mm endotracheal tube or a 12- to 16- gauge IV catheter) is advised. Cardiac stimulation (“C”) should follow ventilatory support, because myocardial hypoxemia is the most common cause of bradycardia or asystole. Direct transthoracic cardiac compressions are advised as the first step; epinephrine is the drug of choice for cardiac arrest/standstill (0.2 mg/kg, administered best by the IV or intraosseous route). Venous access in neonates is challenging; the single umbilical vein is one possibility. The proximal humerus, proximal femur, and proximomedial tibia offer intraosseous sites for drug administration. Atropine is not advised in neonatal resuscitation. The mechanism of bradycardia is hypoxemia-induced myocardial depression rather than vagal mediation, and anticholinergic-induced tachycardia can actually exacerbate myocardial oxygen deficits.
Chilled neonates may not respond to resuscitation. Body temperature drops rapidly when a neonate is damp. Keeping the neonate warm is important during resuscitation and in the immediate postpartum period. During resuscitation, placing the chilled neonate’s trunk into a warm water bath (95°–99°F) can improve response. Working under a heat lamp or within a Bair hugger warming device is helpful. After resuscitation, neonates should be placed in a warm box (a styrofoam picnic box with ventilation holes is ideal) with warm bedding until they can be left with their dam. Neonates delivered by cesarean section should be left with the dam only after she is fully recovered from anesthesia and exhibiting good maternal behavior; otherwise, nursing should be directly monitored and permitted every 2 hr.
Neonates lack glucose reserves and have minimal capacity for gluconeogenesis. Providing energy during or just after prolonged resuscitation efforts becomes critical. Clinical hypoglycemia (blood glucose levels <30–40 mg/dL) can be treated with dextrose solution IV or intraosseously, at a dosage of 0.5–1 g/kg (0.0005–0.001 g/g body wt) using a 5%–10% solution, or a dosage of 2–4 mL/kg (0.002–0.004 mL/g body wt) of a 10% dextrose solution. A 500-g neonate would get 1–2 mL. Single administration of parenteral glucose is adequate if the hypoglycemic puppy can then be fed or nurses. If a neonate is too weak to nurse or suckle, 0.05–1 mL of warmed 5% dextrose can be administered orally by stomach tube every 15–30 min until the neonate is capable of suckling. If colostrum can be acquired from the dam, it can be administered in the same way. Dextrose solution (50%) should be applied to the mucous membranes only because of the potential for phlebitis if administered IV; however, circulation must be adequate for absorption from the mucosa. Neonates administered dextrose should be monitored for hyperglycemia because of immature metabolic regulatory mechanisms.
After resuscitation or within the first 24 hr of a natural delivery, a complete physical examination should be performed. Lack of cleft palate, a normal umbilicus, and functional urethral and anal openings should be established. A fontanelle, if present, should be small. The oral cavity, hair coat, limbs, umbilicus, and urogenital structures should be visually inspected. The mucous membranes should be pink and moist, a suckle reflex present, the coat full and clean, and the urethra and anus patent. A normal umbilicus is dry without surrounding erythema. The thorax should be ausculted; vesicular breath sounds and a lack of murmur are normal. The abdomen should be pliant and not painful. A normal neonate will squirm and vocalize when examined, and nurse and sleep quietly when returned to the dam. Healthy neonates will attempt to right themselves and orient by rooting toward their dam. Neonates are highly susceptible to environmental stress, infection, and malnutrition. Proper husbandry is critical and should include daily examination of each neonate for vigor and recording of weight.
Puppies and kittens lack thermoregulatory mechanisms until 4 wk of age; thus, the ambient temperature must be high enough to facilitate maintenance of a body temperature of at least 97°F (36°C). Hypothermia negatively impacts immunity, nursing, and digestion. Exogenous heat should be supplied, best in the form of an overhead heat lamp. Heating pads run the risk of burning neonates incapable of moving away from excessively hot surfaces.
Chilled neonates must be rewarmed slowly (30 min) to avoid peripheral vasodilation and dehydration. Tube feeding should be delayed until the neonate is euthermic. Hypothermia induces ileus, and regurgitation and aspiration can result.
Incompletely developed immune systems during the first 10 days of life make neonates vulnerable to systemic infection (most commonly bacterial and viral). Puppies must ingest adequate colostrum promptly after birth to acquire passive immunity. The intestinal absorption of IgG generally ceases by 24 hr after parturition. Colostrum-deprived kittens given adult cat serum at a dosage of 150 mL/kg, SC or IP, developed serum IgG levels comparable to those of suckling littermates. However, colostrum-deprived puppies given 40 mL/kg of adult dog serum orally and parentally did not match IgG levels of suckling littermates. Neonates should be encouraged to suckle promptly after resuscitation is completed; this usually necessitates close monitoring after a cesarean section, because the dam has not fully recovered from anesthesia. Maternal instincts (protecting, retrieving, grooming, nursing) usually return within 24 hr.
The umbilicus of neonates should be trimmed 1 cm from the abdominal wall, ligated, and treated with 2% tincture of iodine immediately after birth to reduce contamination and prevent ascent of bacteria into the peritoneal cavity (omphalitis-peritonitis).
Neonatal bacterial septicemia can cause rapid deterioration and result in death if not recognized and treated promptly. Predisposing factors include endometritis in the dam, a prolonged delivery/dystocia, feeding of replacement formulas, the use of ampicillin, stress, low birth weight (<350 g for a medium-size breed dog), and chilling with body temperature <96°F. The organisms most frequently associated with septicemia are Escherichia coli, streptococci, staphylococci, and Klebsiella spp. Premortem diagnosis can be challenging, because sudden death may preclude recognition of clinical signs. Commonly, a decrease in weight gain, failure to suckle, hematuria, persistent diarrhea, unusual vocalization, abdominal distention and pain, and sloughing of the extremities indicate septicemia may be present. Prompt therapy with broad-spectrum, bactericidal antibiotics; improved nutrition via supported nursing, tube feeding, or bottle feeding; maintenance of body temperature; and appropriate fluid replacement are indicated. The third-generation cephalosporin ceftiofur sodium is an appropriate choice for neonatal septicemia, because it alters normal intestinal flora minimally and is usually effective against the causative organisms. Ceftiofur sodium should be administered at a dosage of 2.5 mg/kg, SC, bid, for no longer than 5 days. Because neonates <48 hr old have reduced thrombin levels, presumptive therapy with vitamin K1 at 0.5–2.5 mg/kg can be used (0.01–1 mg/neonate, SC) if a coagulopathy is suspected (umbilical bleeding, hematuria, epistaxis).
Neonates have minimal body fat reserves and limited metabolic capacity to generate glucose from precursors. Glycogen stores are depleted shortly after birth, making adequate nourishment from nursing vital. Even minimal fasting can result in hypoglycemia. Hypoglycemia can also result from endotoxemia, septicemia, portosystemic shunts, and glycogen storage abnormalities. Oral fluid and glucose replacement may be preferable if the neonate has an adequate swallowing reflex and is not clinically compromised. The neonatal caloric requirement is 133 cal/kg/day during the first week of life, 155 cal/kg/day for the second, 175–198 cal/kg/day for the third, and 220 cal/kg/day for the fourth. Commercially manufactured milk replacement formulas are usually superior to homemade versions, but none is equal to the dam’s milk. The use of milk obtained from the dam can be considered and is superior if available. An osmotic diarrhea (usually yellow, curdled fecal appearance) can result from overfeeding formula, necessitating diluting the product 50% with water or a balanced crystalloid solution. Neonates should gain weight steadily from the first day after birth (a transient mild loss from birth weight is acceptable on day 1), with puppies gaining 1–3 g/day/lb (2.2 kg) of anticipated adult weight and kittens 50–100 g/wk. Neonatal weights should be recorded daily for the first 2 wk, then every 3 days until 1 mo old. Healthy, well-nourished neonates are quiet and sleep when not nursing. The normal neonatal weight gain is an increase of 5%–10% body wt/day.
Anesthesia of the neonate may be necessitated by an emergency or for an elective procedure. The distribution and metabolism of drugs are different in neonates than in adults. Neonates have decreased protein binding and increased permeability of the blood-brain barrier. Decreased protein binding is due to lower albumin levels with a lower affinity for drugs. Neonates have higher body water content and lower fat content than adults. This results in a greater initial volume of distribution for some drugs. In most neonates, the ability to metabolize drugs (via conjugation, hydrolysis, oxidation, and reduction) is reduced, as is renal clearance mechanisms. Nephrogenesis in puppies is not complete until the third week of life; the outer cortical nephrons are the last ones to become fully functional. The ability of the neonatal kidney to produce a concentrated urine is less than that of the adult, and so fluid balance is more labile in neonates. The differences in neonatal respiratory function mean that inhaled agents will have a more rapid onset and recovery. Neonates have immature central and peripheral nervous systems and immature neuromuscular junctions, such that less general/local anesthetic is required to produce anesthesia/local block than in adults.
Fluid support is indicated with neonates, but fluid overload is simply because of the capacity of the fluid lines used for larger animals. To avoid this problem, tubing with a much smaller internal diameter should be used. Care must also be taken to ensure that the lines do not contain any air, because these very small patients may still have communication between the left and right atrium, making it possible for IV air to result in coronary or cerebral emboli.
Core body temperature should be monitored, and hypothermia treated as soon as possible. A supplemental source of heat should be available (circulating water blanket or warm air blanket) to prevent hypothermia, because many of the anesthetic drugs eliminate the ability of the neonate to thermoregulate, and neonates are more prone to hypothermia than adults. Premedication with an anticholinergic is acceptable and usually sufficient by itself. Most neonates tolerate a simple mask induction with an inhalant such as isoflurane or sevoflurane. Propofol can be used as an induction drug in young animals. Maintenance by mask avoids the potential for trauma during intubation in tiny neonates, but less control of the airway is achieved.
During anesthesia of neonates, supporting and monitoring cardiopulmonary function is especially important. Cardiac output in neonates depends on heart rate; preventing bradycardia is more important than in adults. Monitoring blood pressure is also important. If hypotension is detected or tissue perfusion judged inadequate, treatment should be instituted. Initial therapy should include reducing the amount of anesthetic, if possible, and increasing the rate of fluid administration. If these treatments are ineffective, it is probably better to use a positive inotrope/chronotrope than a peripheral vasoconstrictor to try to increase blood pressure (unless it is very low, and a vasoconstrictor is needed to raise the pressure long enough to allow other therapies to work). Dopamine has been shown to increase blood pressure in puppies <10 days old at 5–10 mcg/kg/min but has little effect on heart rate or cardiac output. Dobutamine appears to have little effect at clinical doses.