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Pediatric emergencies (Proceedings)
At birth, the autonomic nervous system and the baroreceptor reflexes are immature, with the ANS maturing by day 10 and the baroreceptor system maturing by 4 weeks. Due to this immature state, it is difficult for the neonate to respond to changes in blood pressure.
Respiratory Rate: 15-35 breaths/min until 4 weeks
- birth: 54/30 (40) mmHg
- 4 weeks: 70/45 (60) mmHg
- Adult: 130/80 (100) mmHg
At birth, the autonomic nervous system and the baroreceptor reflexes are immature, with the ANS maturing by day 10 and the baroreceptor system maturing by 4 weeks. Due to this immature state, it is difficult for the neonate to respond to changes in blood pressure. The cardiac function of a newborn is at a high resting function, which also makes it difficult for the heart to respond to acute changes in pressure by increasing stroke volume or heart rate. Instead of increasing cardiac output, the newborn increases oxygen extraction and redistributes blood flow to the heart, brain, diaphragm and adrenal glands, and away from the spleen, gastrointestinal tract, skin, and kidneys.
In the fetus, there is increased pulmonary vascular resistance, which causes blood to shunt through the ductus arteriosus to the aorta and the systemic circulation. The fetal alveoli are collapsed until the first breath taken by the neonate. With the expansion of the lungs, prostacyclins are released that increase pulmonary blood flow. The decrease in pulmonary vascular resistance causes closure of the ductus arteriosus. Additionally, type II epithelial cells in the lungs produce a large amount of surfactant in response to lung expansion and the stress of birth, and thus reduce the tension of the air-fluid interface in the alveoli. Normal neonatal respiratory rates are higher than adults, but with a lower minute ventilation and tidal volume.
Hypoxia will occur at birth if the lungs fail to expand or the pulmonary vascular resistance does not decrease adequately. The fetal response to hypoxia is to decrease respiratory movements, which may further delay spontaneous breathing at birth. Briskly rubbing the newborn with a clean, dry towel or administering Doxapram stimulates respiration.
Micturition should occur within the first 24 hours. Neonate urine specific gravity is 1.006 to 1.017, and neonates cannot fully concentrate urine until 8 weeks old. Glucosuria also occurs commonly in newborns.
Daily fluid requirements are up to 100 ml/kg/d. To treat hypotension or shock, a fluid rate of 50-100 ml/kg/hr can be given providing that cardiopulmonary and renal function are monitored frequently. Once a shock dose is administered, severely dehydrated puppies or kittens should be maintained at 100ml/kg/day.
Testicles should descend by 4-6 weeks in male puppies.
Neonates are born with a strong sucking reflex, but the swallowing reflex does not fully develop until they are 3 weeks old. Meconium is the neonate's first stools, comprised of amniotic fluid, mucous, bile, and cells shed from the intestinal tract. It is typically dark and thick and should be passed within the first 48 hours. Often, you will not observe neonatal feces if the mother is quick to clean her young.
Gastrointestinal contraction rates increase until 10 days after birth, and the normal flora colonizes the GI tract shortly after birth.
The liver goes through two periods of development—"rapid maturation" until 4 weeks old during which time the microsomal enzyme system develops, and "continued maturation" until 10 weeks old after which the liver is considered fully mature.
At birth the neonate's posture is primarily in flexion, much like the intrauterine fetus. Flexion is replaced by extension at 4-5 days. Hyperkinesia (fine body twitching) is normal for up to 3 weeks. A puppy should stand by 3 weeks, walk at 4 weeks, and trot or gallop at 6 weeks.
Eyes and Ears
The puppy's eyelids are closed at birth (ankyloblepharon), and open by 10-16 days. Symblepharon is the pathologic failure of the lids to open. Pupillary light reflexes are not normal until 4 weeks, and menace response takes 2-3 months to fully develop. To test retinal integrity in a neonate, you can look for the dazzle reflex (withdrawal or blink response to a very bright light such as a fiberoptic cable).
Neonates respond to sound from birth, but the external ear canal does not open until 12-14 days. Auditory ability is fully developed at 5 weeks.
The feline neonate's eyes and ears do not open at a definite time.
Newborns lose heat readily because of a high surface area:body mass ratio, reduced fat stores, and inability to shiver until 6 days old. The hypothalamus is also immature in newborns and cannot regulate heat well. Post-partum, ambient temperature should be maintained at 80-85F. Healthy newborns self-regulate their temperature by huddling with or separating from their littermates. A heat lamp or pad can also help the neonates to regulate their body heat as needed.
If the newborn is hypothermic, they should be warmed up slowly over 30 minutes or more, and then maintained at an ambient temperature of 90-95F. Warming a neonate too quickly increases oxygen demands and can cause hypoxia.
Neonates are able to absorb colostral antibodies through the intestine until 24 hours post-partum. The quantity of IgG in the colostrums decreases linearly for the first 2 days of lactation. Neonates that are risk of failure of passive transfer include those that are orphaned or rejected before nursing, small or weak neonates, and neonates from dams that fail to lactate on the first day of birth. (see Sepsis and Septic Shock for treatment of FPT).
The neonatal demand for glucose is very high given a large brain:body mass ratio. Neonates have few gluconeogenic precursors and low body fat. Therefore, when a neonate is fasted they rely primarily on liver glycogen stores that only provide glucose for 8-12 hours. Neonates are also predisposed to hypoglycemia as they lose an excessive amount of glucose through the immature kidneys. The normal blood glucose level for neonates can be around 40 mg/dl. Blood glucose levels less than 40 mg/dl should be treated for hypoglycemia.
Bitches and queens must be fed a high quality diet during pregnancy to prevent diseased or weak puppies. Taurine deficiency in pregnant queens can cause fetal resorption, abortion, stillbirths, and poor growing kittens. Post-parturition, malnutrition in the neonate can be directly related to malnutrition of the dam.
The caloric requirement for neonates is 130kcal/kg/day for the first week, 154kcal/kg/day for the second week, 176-198kcal/kg/day for the third week, and 220kcal/kg/week for the fourth week.
For the first week of life, the stomach capacity is about 50ml/kg of body weight. Esbilac (PetAg, Hampshire, IL) for puppies and KMR (PetAg) for kittens are commercial feeding formulas that are well balanced for orphaned neonates. Bitch's milk and queen's milk have differing amounts of protein, fat, calories, calcium, phosphorous and lactose, so do not interchange Esbilac and KMR. For the first week, the animal should be fed every 4 hours to ensure adequate daily caloric intake, and every 6 hours for the second week.
Low birth weights are associated with higher death rates. Most abnormally small puppies and kittens are born at full-term, and are underweight due to congenital anomalies or poor nutrition. Low birth weights are not related to sex, litter size, or weight of dam.
Puppies should double weight by 10-12 days. Kittens should double weight by 14 days. It is important to weigh neonates at frequent intervals until they are weaned, as puppies and kittens that die within the first few weeks of life are often born at a normal weight but fail to grow adequately after birth.
Interpretation of diagnostic tests
Complete blood count
The neonate hematocrit decreases from ~47% at birth to ~30% at 4 weeks old. There are many reasons for the "physiologic anemia of the newborn". First, the erythropoietic stimulus decreases in response to a rich oxygen environment post-partum. There is also an increased blood volume and a shortened red blood cell life span in the first few weeks after birth. Reticulocyte response starts around 21 days, and a marked response is seen at 6 weeks. Iron deficient neonates (microcytic, hypochromic) can be treated with iron dextran for 2-3 weeks.
Lymphocyte counts in puppies are highest at 3 weeks old (~5000 cells/mm3), and in kittens at 8 weeks old (~10,000 cells/mm3). This is due to the increased antibody formation
It is normal for neonates to have low glucose (see Glucose Metabolism). Neonates have low to low-normal Albumin levels and decreased globulins at birth. Globulin levels rise after ingestion of colostrum, but total protein decreases to a nadir around week 3. Adult protein levels are reached by about 6 months of age.
Neonates also have low creatinine values due to their anabolic state; low BUN and cholesterol, and slightly increased Bilirubin due to immature hepatic function; elevated ALP and GGT possibly due to increased intake via colostrum; and elevated calcium and phosphorous from bone growth.
Intravenous (IV) catheters are ideal, but can be difficult in dehydrated neonates. The jugular vein provides the best IV access for neonates. Intraosseous catheters (IO) can be placed if IV access is too difficult to obtain. The proximal femur or humerus should be prepared in a sterile manner, and a 18- or 22-gauge spinal needle or hypodermic needle can be placed IO and secured with a sterile bandage. IO catheters should be replaced with an IV catheter as soon as possible. Intraperitoneal fluid administration is recommended if neither IV nor IO access is obtainable. Subcutaneous fluid administration is not recommended for hypovolemic neonates due to minimal absorption.
Hypovolemic Shock and Dehydration
Responses to shock and dehydration can be more difficult to assess in neonates than in adults, as the compensatory mechanisms (e.g. tachycardia, prerenal azotemia, concentrated urine, and decreased urine output) are not as well developed in neonates. Gastrointestinal disturbances, inability to nurse, and competition for milk frequently cause dehydration and hypovolemic shock in neonates. Because it is difficult to use regular shock parameters for diagnosing neonates, the neonate's history is often used to suggest hypovolemia. Treatment of dehydration and hypovolemic shock includes an intial dose of 50-100 ml/kg/h of warm crystalloids, followed by a maintenance rate of 80-100 ml/kg/day.
While treating shock and dehydration, be sure to monitor for overhydration! Take baseline radiographs for comparison to indicate pulmonary edema or other signs of fluid overload; weigh every 12 hours with pediatric gram scale to determine fluid overoad. Can attempt to place a 3.5 or 5 French red rubber as a urinary catheter for more accurate monitoring of "outs".
Warming the neonate is a vital aspect of critical care. Hypothermia causes decreased suckle reflex, hypomotile bowels, and bradycardia and hypoglycemia as it becomes very severe. Rewarm the neonate gradually over 30 minutes or more to an ambient temperature of 90-95F.
Sepsis and Septic Shock
Diagnosis of septic shock is often based on history of failure of passive transfer, or of umbilical, respiratory, gastrointestinal, or tail docking infections. Clinical signs are again unreliable in the neonate but may include pale mucous membranes, decreased urine output, cold extremities, constant crying and reluctance to suckle. Treatment involves rapid fluid replacement (see above), antibiotics, oxygen therapy, and plasma or serum from well-vaccinated adults for neonates that may have experienced failure of passive transfer (FPT).
Antibiotic choice should be based on culture, but the animal can be placed on broad-spectrum antibiotics (e.g. cephalosporins) while culture results are pending. Oxygen concentration should not exceed 40% as higher levels have been associated with a retinopathy leading to permanent loss of vision.
Administering adult serum subcutaneously or intraperitoneally to kittens that have experienced FPT will increase IgG levels to protective levels. The recommended SQ or IP dose is 150ml/kg of serum, or 3,650 mg/kg of IgG within the first 24 hours after parturition. (Do NOT give type B serum to type A kittens!) It is best to administer serum as soon as FPT is realized, as it will not be as effective once sepsis occurs.
Hypoglycemic kittens and puppies can present with hypothermia, weakness, ineffectual nursing, crying, bradycardia, apnea, convulsions and death. A blood glucose measurement less than 40mg/dl is considered significant hypoglycemia and must be treated immediately. Treatment involves giving 1ml/kg or 25% dextrose IV or IO, followed by a CRI of isotonic fluids with 2.5% or 5% dextrose. Serial blood glucose levels should be taken to avoid prolonged hyperglycemia that can lead to osmotic diuresis and dehydration.
- Atropine—NOT RECOMMENDED. In the neonate, hypoxia is due to direct myocardial depression, not vagal effects and therefore atropine may not do any good. If atropine does increase the heart rate, the increase in myocardial oxygen demand may be detrimental.
- Doxapram—Acts as a central respiratory stimulant, but has little effect if brain is hypoxic already. May increase ventilatory efforts once they have started. Can be administered on the tongue, IV, or IM.
- Epinephrine—Drug of choice for cardiac arrest. Dose 10µg/kg IV.
Decreased liver and renal function in neonates causes decreased clearance and increased half-lives of many drugs. Oral drug absorption is much higher in the first 24-72 hours of life due to increased permeability of the gastrointestinal tract. Additionally, neonates have an imperfect blood brain barrier. Thus, toxic levels are reached more quickly and unpredictably
Some sources recommend for appropriate drugs reducing doses by 30-50% or increasing the treatment interval by 2-4 hours. Other sources recommend consulting with a veterinary pharmacologist for drugs in which a response to treatment is not easily evaluated.
Antimicrobials to Avoid in Neonates
- Chloramphenicol—Adverse effects on hematopoietic system.
- Tetracyclines—Cause fetal skeleton retardation and discoloration of teeth.
- Fluoroquinolones—Destroy cartilage of long bones.
Antimicrobials requiring dose-adjustment
- Potentiated sulfonamides—Induce bone marrow suppression. Avoid in anemic animals. Prolonged half-life in neonates requires dose adjustment or prolonged treatment interval.
- Metronidazole— Prolonged half-life and decreased rate of clearing in neonates requires dose adjustment or prolonged treatment interval.
- Beta-lactam antibiotics—Increase dose interval because of prolonged half-life in neonates.
Anticonvulsants, Sedative, and Analgesics
Avoid drugs that decrease heart rate or respiratory rate.
- Diazepam—Dose reduction recommended due to increased half-life.
- Barbiturates—Can have increased response due to decreased body fat stores and decreased hepatic clearance. Recommend dose reduction.
- Opioids are safe as they can be reversed easily. However, as they depress respiratory and heart rates, neonates should be monitored carefully.
It is difficult to dose cardiovascular drugs as maturation of α- and β-receptors has a wide degree of individual variation. Exogenous catecholamines can be used to increase heart rate, contractility, and blood pressure, but careful monitoring is essential in determining response to treatment. Neonates show a decreased response to atropine and Lidocaine.
Special circumstances for post-partum care
Anesthetic use in the dam has been shown to affect "puppy vigor" upon delivery. Inhalant anesthetics and ketamine decrease spontaneous breathing of the litter, and thiobarbiturates decrease movement of the litter after delivery. One should be aware that these neonates may require more intensive supportive care post-partum. However, these agents have not been associated with increased mortality. The only agents reported to increase neonatal mortality during a caesarean section are xylazine and methoxyflurane, and these agents should be avoided pre-caesarean section.
Neonatal care post-caesarean section:
- Remove all membranes from around the neonate's head.
- Stimulate breathing by rubbing neonate briskly with warm, dry towel.
- Fetal fluid will collect in the pharynx and should be aspirated routinely.
- Respiration in the neonate can also be stimulated with 0.1ml Doxapram on the tongue or intravenously into the umbilical vein. It is often easiest to place an umbilical vein catheter to facilitate IV administration.
- Oxygen should be supplied if the neonate demonstrates signs of respiratory distess.
- 20% glucose should be placed on the tongue of a neonate that is responding poorly.
- Keep neonates warm (85-90F).
- Reunite with mother as soon as she is awake.
- Temperature control, feeding schedules and weight monitoring are the most important guidelines for the first two weeks of an orphan's life.
- Ambient temperature should be maintained at 80-85F for the first 2 weeks.
- For the first week, the neonate should be fed every 4 hours to ensure adequate daily caloric intake. The neonate can be fed every 6 hours for the second week, and less frequently afterwards. Feed puppies Esbilac and kittens KMR. The maximum amount per feeding is 50ml/kg during the first week, and this decreases throughout the neonate period to 10-20ml/kg.
- If the neonate is not eating on its own, it must be bottle- or tube-fed. If bottle-feeding, the neonate must have a suckle reflex, and do not elevate the neonate's head as this can cause aspiration. Tube-feeding is preferred in neonates with poor suckle reflexes. Tube-feeding techniques involve premeasuring the tube from the nose to the last rib. After administering formula through the tube, kink the tube while removing it in order to prevent aspiration.
Immature neonates have shallow respirations, cyanosis, anemia, hypothermia, hypoglycemia, weak suckling and swallowing reflexes, and a very thin hair coat.
A relatively common congenital abnormality that should be checked at birth is a cleft palate. If the neonate has a cleft palate, they are often euthanized at birth. Other congenital anomalies include cranial deformities, agenesis of small or large intestines, cardiac anomalies, umbilical or diaphragmatic hernias, portosystemic shunts, etc.
This syndrome is rare among domestic shorthair kittens, and may be more common among purebred kittens. Kittens with blood type A that are born to a queen with blood type B develop NI. The queen's colostral anti-A alloantibodies bind to the kitten's erythrocytes and cause intravascular and extravascular hemolysis. NI can also be seen in kittens with blood type AB born to type B queens. As a result, the kitten develops severe anemia, nephropathy and other organ failures, and can develop disseminated intravascular coagulopathy.
There are three clinical courses that an NI kitten can follow:
1. Acute death on Day 1 with no other clinical signs.
2. Stop nursing over first 3 days and fail to thrive. May see clinical signs such as hemoglobinuria, icterus, anemia, fading and death.
3. Some kittens continue to nurse and thrive, and have no obvious clinical signs except for tail-tip necrosis. They do have a positive direct Coombs' test and moderately responsive anemia.
NI can also occur in puppies if the dam received an incompatible transfusion prior to her pregnancy.
High ambient temperatures and high humidity are related to increased incidence of neonatal mortality from lower respiratory infections. Aspiration pneumonia often occurs secondary to incorrect tube or bottle-feeding when hand-rearing. Bordetella pneumonia can develop in 8-16 week old kittens and puppies and can be life-threatening. Affected animals are characteristically febrile, lethargic, anorexic, and dyspneic. Puppies are at significant risk of dying if not treated. Culture and treat with appropriate antibiotic and supportive care.
Neonatal conjunctivitis develops in response to a staphylococcus or streptococcus infection, causing purulent exudate accumulates behind the eyelids before they open. Treatment involves gentle separation of the closed lids, flushing the conjunctival sac, and application of ophthalmic antibiotic ointment.
Dystocia, cannibalism, and maternal neglect are the most common forms of trauma to the neonate within the first 5 days after birth. Cannibalism often occurs as a maternal response to sickly puppies or kittens.
Toxoplasma obtained via transplacental transmission can cause born neonates to become weak and dyspneic, develop neurologic abnormalities, and die. Necropsy reveals pneumonitis, hepatitis, myocarditis, encephalitis and retinitis.
Roundworms (via transplacental infection) and hookworms (via transmammary infection) have been implicated in neonatal losses due to poor perinatal husbandry. Puppies and kittens can be dewormed with pyrantel pamoate at 2-3 weeks of age, and dewormed every few weeks afterwards for 12 weeks.
Canine neonatal diseases
Umbilical cord infections
Umbilical cord infections are typically the result of Streptococcus, and occur between the 1st and 4th day post-partum. Infected pups show a loss of vigor, discomfort and abdominal distention. The umbilicus is frequently edematous and inflamed, and peritonitis may or may not be present. Abscessed umbilical cords are lanced and flushed. A broad-spectrum antibiotic should be administered parenterally. When peritonitis is present, the abdomen should be drained.
Toxic milk syndrome
In this syndrome, the bitch appears healthy and lactation is usually adequate. However, an occult mastitis infection transfers pathogens to the pups. Typically, Staphylococcus, E. coli, Proteus, Streptococcus, or Klebsiella sp. can be cultured. The pups appear bloated, and have a yellow-green diarrhea and inflamed anus. Sepsis can follow (see below). Neonates should be separated from the mother and supported with fluids and antibiotics.
Juvenile cellulitis, also known as puppy strangles, is an immune-mediated disease of Dachshunds, Labradors, Golden Retrievers, and Pointers from 3 weeks to 12 months of age. Most occur in puppies younger than 16 weeks. Enlargement of the mandibular lymph nodes is the most consistent funding and occasionally a lymph node may rupture and discharge hemorrhagic purulent exudates. Cutaneous lesions are often first noticed by the owner, including papules and pustules involving the eyelids, pinnae, and the lips. A purulent otitis externa and conjunctivitis are seen with the majority of cases, as is facial edema. The disease may become generalized and may be fatal if untreated. The administration of corticosteroids at a dose of 2mg/kg for one to two weeks is required to resolve the condition. Broad-spectrum antibiotics should be administered concurrently.
Puppies are exposed to canine herpesvirus at birth if the dam is affected with the virus. The virus incubates in the neonate and clinical signs arise at 5-6 days old when the neonate's temperature is optimal for herpesvirus replication. Puppies that appear healthy often become acutely lethargic, stop nursing and die. If the neonate recovers, it will continue to shed the virus when immunosuppressed. Diagnosis is based on necropsy findings, including petechial and ecchymotic hemorrhages involving the lung, liver, and kidney, and sometimes the spleen, lymph nodes, and adrenal glands. Treatment is supportive care.
This syndrome becomes obvious at 3 weeks old when the neonate attempts to stand and walk and its legs slide to the side and cannot support him. The condition is seen most often in chrondrodystrophoid and short-limbed breeds. Although the cause is unknown, it may be related to decreased muscular and ligament strength in relation to the size and weight of the body. Pups should be given mats that provide traction for walking inside, and hobbles can be placed to prevent the legs from splaying to the side.
Feline neonatal diseases
Feline Streptococcus canis
Feline Streptococcus canis can cause kitten acute death between 7 and 10 days of age, with pneumonia being the primary clinical sign. Careful examination would reveal a drop in rectal temperature a few hours before death. Most of the deaths occur when the queens are first time mothers. Streptococcus canis exists in the vaginas of some queens and can cause umbilical abscesses on necropsy of the fetus. Other necropsy findings include peritonitis and thromboembolic hepatitis. Kittens from older queens do not die from the infection as older queens pass antibodies to the kittens. Verification that Streptococcus canis caused a neonatal septicemia and death requires that the organism be isolated from the blood or tissues of the puppy immediately after death.
Feline Herpesvirus infection is not a significant cause of neonatal kitten mortality. This infection, however, can cause abortion in pregnant queens, and kittens can acquire the infection from the carrier queen at birth. Purulent conjunctivitis, rhinitis, tracheitis, bronchopneumonia and hepatic necrosis have been associated with neonatal infection.
Feline Leukemia virus
Thymic atrophy is a common consequence of in utero or early postnatal infection of kittens with feline leukemia virus (FeLV). T-lymphocytes within the thymus and other lymphoid tissues are destroyed by the virus, which results in deficient cell-mediated immunity and increased susceptibility to secondary infections. FeLV infected kittens are usually small and often die of bronchopneumonia or enteritis within the first few weeks of life. At necropsy, the thymus is small or inapparent and lymph nodes are small. Kittens that survive the neonatal period often succumb to other FeLV-related diseases within the first year of life.
Abortions, stillbirths and the birth of weak, emaciated puppies and kittens have been associated with in utero transmission of salmonella. The bitch or queen usually has a prolonged vaginal discharge and delayed involution of the uterus. Salmonella organisms can be isolated from the vaginal discharge, placentas and meconium, and from the internal organs of puppies dying from the infection. Treatment of newborn animals with known salmonellosis is discouraged because of the poor prognosis and the public health hazard.
Dilated cardiomyopathy affects many purebred breeds of kittens, with the highest incidences in Abyssinians, Balinese, Burmese, Himalayans and Siamese. Anorexia, weakness and dyspnea are the most common signs. Physical exam often reveals cyanosis, abdominal distention with ascites, a cardiac murmur or gallop rhythms. Some kittens die acutely without previous signs. Thoracic radiographs show generalized cardiomegaly and frequently pleural effusion, pulmonary edema or both. Electrocardiographs may be normal or reflect cardiac enlargement and abnormal electrical activity. Echocardiography demonstrates poor cardiac contractility.
The prognosis for kittens with cardiomyopathy is very poor regardless of therapy. Affected kittens have a mean life span of two days once signs of congestive heart failure are apparent. An inherited cause of the disease is suspected and cats that have a repeat history of producing kittens with cardiomyopathy should not be bred.