Small Animal Critical Care Medicine PDF (XIX Miscellaneous Disorders)

820 PART XIX MISCELLANEOUS DISORDERS 3. Herring IP, Pickett JP, Champagne ES, et al: Evaluation of aqueous tear production in dogs following general anesthesia, J Am Anim Hosp Assoc 36:427, 2000. 4. Bojrab MJ, Birchard ST, Tomlinson JL, editors: Current techniques in small animal surgery, ed 3, Phil...

820 PART XIX MISCELLANEOUS DISORDERS 3. Herring IP, Pickett JP, Champagne ES, et al: Evaluation of aqueous tear production in dogs following general anesthesia, J Am Anim Hosp Assoc 36:427, 2000. 4. Bojrab MJ, Birchard ST, Tomlinson JL, editors: Current techniques in small animal surgery, ed 3, Philadelphia, 1990, Lea & Febiger. 5. Ofri R: Neuroophthalmology. In Maggs DJ, Miller PE, Ofri R, editors: Slatter’s fundamentals of veterinary ophthalmology, ed 5, St Louis, 2013, Elsevier. 6. Whitley RD, Gilger BC: Diseases of the canine cornea and sclera. In Gelatt KN, editor: Veterinary ophthalmology, ed 3, Philadelphia, 1999, Lippincott Williams & Wilkins. 7. Morreale RJ: Corneal diagnostic procedures, Clin Tech Small Anim Pract 18:148, 2003. 8. Morgan RV, Zanotti SW: Horner’s syndrome in dogs and cats: 49 cases (1980-1986), J Am Vet Med Assoc 194:1096, 1989. 9. Kern TJ, Aromando MC, Erb HN: Horner’s syndrome in dogs and cats: 100 cases (1975-1985), J Am Vet Med Assoc 195:369, 1989. 10. Scagliotti RH: Comparative neuroophthalmology. In Gelatt KN, editor: Veterinary ophthalmology, ed 3, Philadelphia, 1999, Lippincott Williams & Wilkins. 11. Slatter D: Neuroophthalmology. In Slatter D, editor: Fundamentals of veterinary ophthalmology, ed 3, Philadelphia, 2001, Saunders. 12. Canton DD, Sharp NJ, Aguirre GD: Dysautonomia in a cat, J Am Vet Med Assoc 192:1293, 1988. 13. Wise LA, Lappin MR: A syndrome resembling feline dysautonomia (Key-Gaskell syndrome) in a dog, J Am Vet Med Assoc 198:2103, 1991. 14. Guilford WG, O’Brien DP, Allert A, et al: Diagnosis of dysautonomia in a cat by autonomic nervous system function testing, J Am Vet Med Assoc 193:823, 1988. 15. Kenny PJ, Vernau KM, Puschner B, et al: Retinopathy associated with ivermectin toxicosis in two dogs, J Am Vet Med Assoc 233:279, 2008. 16. Houston DM, Parent J, Matushek KJ: Ivermectin toxicosis in a dog, J Am Vet Med Assoc 191:78, 1987. 17. Hopkins KD, Marcella KL, Strecker AE: Ivermectin toxicosis in a dog, J Am Vet Med Assoc 197:93, 1990. 18. Clarke DL, Lee JA, Murphy LA, et al: Use of intravenous lipid emulsion to treat ivermectin toxicosis in a Border Collie, J Am Vet Med Assoc 239:1328, 2011. 19. Epstein SE, Hollingsworth SR: Ivermectin-induced blindness treated with intravenous lipid therapy in a dog, J Vet Emerg Crit Care (San Antonio) 23:58, 2013. 20. Gelatt KN, van der Woerdt A, Ketring KL, et al: Enrofloxacin-associated retinal degeneration in cats, Vet Ophthalmol 4:99, 2001. CHAPTER 155 CRITICALLY ILL NEONATAL AND PEDIATRIC PATIENTS Maureen McMichael, DVM, DACVECC KEY POINTS Copyright © 2014. Elsevier. All rights reserved. There are significant differences in the biochemical, hematologic, radiographic, pharmacologic, and monitoring parameters in neonatal and pediatric animals. Dramatic elevations in alkaline phosphatase and γ-glutamyltransferase levels and very low values for serum levels of blood urea nitrogen, albumin, and cholesterol occur in the neonate and can mimic hepatic failure. The most common causes of dehydration in the neonate and pediatric patient are gastrointestinal losses and insufficient intake. There are several crucial differences in the diagnosis, monitoring, and treatment of critically ill neonates and pediatric patients compared with critically ill adult patients, and it is essential for veterinarians with a neonatal and pediatric patient base to become familiar with normal biochemical, hematologic, radiographic, and physical examination values for this age group. In veterinary medicine, the term neonate encompasses animals from birth to 2 weeks of age, and the term pediatric refers to animals between 2 weeks and 6 months of age. This chapter reviews the hematologic, biochemical, nutritional, imaging, fluid treatment, monitoring, and pharmacologic aspects of the normal and critically ill neonate and pediatric cat and dog. Also included is a brief review of sepsis in the neonate. Silverstein, D., & Hopper, K. (2014). Small animal critical care medicine. Elsevier. Created from purdue on 2024-02-04 21:23:55. PHYSICAL EXAMINATION FINDINGS Healthy neonates are lively and plump (Box 155-1). Illness is often recognized by incessant crying, lethargy, limpness, and poor muscle tone. Mucous membranes are often hyperemic during the first 4 to 7 days of life and may be pale, cyanotic, or gray in sick neonatal animals. The rectal temperature at birth is normally 35.2° to 37° C (95.4° to 98.6° F) and gradually increases to adult levels over the first 4 weeks of life. By pediatric stethoscope (ideally), many puppies and kittens will be found to have an innocent murmur until 12 weeks of age. However, other causes of a murmur include a congenital cardiac BOX 155-1 Clinical Values for Normal Puppies and Kittens Heart rate: 200 beats/min (puppy) and 250 beats/min (kitten) Respiratory rate: 15 breaths/min (birth) and 30 breaths/min (by 1 to 3 hours after birth) Temperature: 35.2° to 37° C (95.4° to 98.6° F) at birth, normalizing to adult values at 4 weeks Mean arterial pressure: 49 mm Hg at 1 month of age, 94 mm Hg at 9 months (puppies) Central venous pressure: 8 cm H2O at 1 month of age, 2 cm H2O at 9 months (puppies) CHAPTER 155 defect, stress, fever, sepsis, anemia, and hypoproteinemia. The heart rate in the normal neonatal puppy and kitten is 200 and 250 beats/ min, respectively. The heart rate decreases as the animal develops increased parasympathetic tone at 4 weeks of age. The respiratory rate following birth is normally 15 breaths/min but increases to 30 breaths/min within 1 to 3 hours. Because of the small tidal volume and increased interstitial fluid in the normal neonate, assessment of lung sounds is difficult. An increase or decrease in heart rate or respiratory rate should be assessed and rates should be monitored during treatment. LABORATORY VALUES The hematocrit (Hct) decreases from 47.5% at birth to 29.9% by day 28 in puppies (Box 155-2).1 By the end of the first month, the Hct starts to increase again. Kittens also have an Hct nadir at 4 to 6 weeks of 27%.2 Knowledge of this normal decrease in Hct is essential for BOX 155-2 Normal Laboratory Values for Puppies and Kittens Complete Blood Count—Pediatric Canine Hematocrit: 47% at birth, 29% at 28 days Leukocyte count: 12.0 × 103/mm3, day 7 Band count: 0.5 × 103/mm3, day 7 Lymphocyte count: 5 × 103/mm3, day 7 Eosinophil count: 0.8 × 103/mm3, day 7 Complete Blood Count—Pediatric Feline Hematocrit: 35% at birth, 27% at 28 days Leukocyte count: 9.6 × 103/mm3 at birth, 23.68 × 103/mm3 at 8 weeks Lymphocyte count: 10.17 × 103/mm3 at 8 weeks, 8.7 × 103/mm3 at 16 weeks Eosinophil count: 2.28 × 103/mm3 at 8 weeks, 1 × 103/mm3 at 16 weeks Biochemistry Profile—Pediatric Canine* Bilirubin: 0.5 mg/dl (range, 0.2 to 1; normal adult range, 0 to 0.4) Alkaline phosphatase: 3845 IU/L (range, 618 to 8760 IU/L; normal adult range, 4 to 107 IU/L) γ-Glutamyltransferase: 1111 IU/L (range, 163 to 3558 IU/L; normal adult range, 0 to 7 IU/L) Total protein: 4.1 g/dl (range, 3.4 to 5.2 g/dl; normal adult range, 5.4 to 7.4 g/dl) Albumin: 1.8 g/dl at 2 to 4 weeks (range, 1.7 to 2 g/dl; normal adult range, 2.1 to 2.3 g/dl) Glucose: 88 mg/dl (range, 52 to 127 g/dl; normal adult range, 65 to 100 g/dl) Copyright © 2014. Elsevier. All rights reserved. Biochemistry Profile—Pediatric Feline* Bilirubin: 0.3 mg/dl (range, 0.1 to 1 mg/dl; normal adult range, 0 to 0.2 mg/dl) Alkaline phosphatase: 123 IU/L (range, 68 to 269 IU/L; normal adult range, 9 to 42 IU/L) γ-Glutamyltransferase: 1 IU/L (range, 0 to 3 IU/L; normal adult range, 0 to 4 IU/L) Total protein: 4.4 g/dl (range, 4 to 5.2 g/dl; normal adult range, 5.8 to 8 g/dl) Albumin: 2.1 g/dl (range, 2 to 2.4 g/dl; normal adult range, 2.3 to 3 g/dl) Glucose: 117 mg/dl (range, 76 to 129 mg/dl; normal adult range, 63 to 144 mg/dl) *At birth except where specified. Silverstein, D., & Hopper, K. (2014). Small animal critical care medicine. Elsevier. Created from purdue on 2024-02-04 21:23:55. Critically Ill Neonatal and Pediatric Patients assessment of any neonate, and during this period a rise in the Hct is usually indicative of dehydration. Slight changes are seen in the biochemical profile of newborn puppies and kittens. In dogs there is a mild increase in bilirubin level (0.5 mg/dl; normal adult range, 0 to 0.4 mg/dl) and dramatic increases in serum levels of alkaline phosphatase (3845 IU/L; normal adult range, 4 to 107 IU/L) and γ-glutamyltransferase (1111 IU/L; normal adult range, 0 to 7 IU/L).3 In kittens, the alkaline phosphatase level (123 IU/L; normal adult range, 9 to 42 IU/L) is threefold higher than that seen in adults. Lower values of blood urea nitrogen (BUN), creatinine, albumin, cholesterol, and total protein are seen in neonates compared with adults (although the BUN concentration may be slightly elevated during the first week of life). Calcium and phosphorus levels are higher in neonates. Urine is isosthenuric in neonates because the capacity to concentrate or dilute urine is limited in this age group.4 This becomes important when prescribing fluid therapy because overhydration is just as much a concern as is underhydration. IMAGING Normal anatomic differences in the young may be significant and are reviewed briefly. The thymus is located in the cranial thorax on the left side and can mimic a mediastinal mass or lung consolidation on thoracic radiographs. The heart takes up more space in the thorax than it does in adults and can appear enlarged. The lung parenchyma has increased water content and appears more opaque in neonates.5 There is an absence of costochondral mineralization so that the liver appears to protrude further caudal from under the rib cage than expected, which makes a misdiagnosis of hepatomegaly more likely. There is loss of abdominal detail due to lack of fat and a small amount of abdominal effusion.5 Radiographic resolution may be improved by reducing the kilovoltage peak value to half of the adult setting and using detailed film or screens. INTRAVENOUS AND INTRAOSSEOUS CATHETERIZATION When venous access is required, use of the intravenous route is preferred and should be attempted first. Neonates often require very small-gauge catheters (e.g., 24 or 27 gauge), which can develop burrs easily when advanced through the skin. To avoid this, a small skin puncture can be made with a 20-gauge needle (while the skin is kept elevated), then the catheter can be fed through the skin hole. If attempts at intravenous catheter placement fail, an intraosseous catheter should be placed (see Chapter 194). An intraosseous catheter can be inserted in the proximal femur or humerus using an 18- to 22-gauge spinal needle or an 18- to 25-gauge hypodermic needle. An intraosseous catheter can be used for fluid and blood administration.6 The area must be prepared in a sterile manner and the needle inserted into the bone parallel to the long axis. Gentle aspiration will ensure patency, and the needle is secured with a sterile bandage. Intravenous access must be established as soon as possible, ideally within 2 hours, and the intraosseous catheter should be removed to minimize the risk of osteomyelitis or other complications. The incidence of intraosseous catheter complications correlates with duration of use.7 FLUID REQUIREMENTS Neonates have higher fluid requirements than adults because they have a higher percentage of total body water, a higher ratio of surface area to body weight, a higher metabolic rate, more permeable skin, a decreased renal concentrating ability, and less body fat. Both 821 Copyright © 2014. Elsevier. All rights reserved. 822 PART XIX MISCELLANEOUS DISORDERS dehydration and overhydration are concerns because neonatal kidneys cannot concentrate or dilute urine as well as adult kidneys can.4 A warm isotonic crystalloid bolus (30 to 40 ml/kg in puppies and 20 to 30 ml/kg in kittens) should be administered to moderately dehydrated neonates, followed by a constant rate infusion (CRI) of 80 to 100 ml/kg/day. A liter of fluid warmed to 104° F will cool down to room temperature (70° F) within approximately 10 minutes. A fluid warmer that is placed in line is also a good option. Lactated Ringer’s solution may be the ideal fluid because lactate is the preferred metabolic fuel in the neonate with hypoglycemia.8,9 Hypoglycemia in neonates commonly occurs as a result of inefficient hepatic gluconeogenesis, inadequate hepatic glycogen stores, and glucosuria. Urinary glucose reabsorption does not normalize until approximately 3 weeks of age in puppies.10,11 In addition, neonates have greater glucose requirements than do adults. The neonatal brain requires glucose for energy, and brain damage can occur with prolonged hypoglycemia.11 Fetal and neonatal myocardia use carbohydrate (glucose) for energy rather than the long-chain fatty acids used by the adult myocardium.12 In summary, neonates have an increased demand for, an increased loss of, and a decreased ability to synthesize glucose compared with adults. In adults, the counterregulatory hormones (i.e., cortisol, growth hormone, glucagon, and epinephrine) are released in response to low blood glucose levels and facilitate euglycemia by increasing gluconeogenesis and antagonizing insulin. Clinical signs of hypoglycemia can be challenging to recognize in neonates because of inefficient counterregulatory hormone release during hypoglycemia.11 Vomiting, diarrhea, infection, and decreased oral intake all contribute to hypoglycemia in neonates. A bolus of 1 to 3 ml/kg of 12.5% dextrose (i.e., 50% dextrose diluted 1 : 3 with sterile water) followed by a CRI of isotonic fluids supplemented with 2.5% to 10% dextrose is required to treat hypoglycemia. Any continuous supplementation higher than 5% dextrose must be given through a central line. To prevent a rebound hypoglycemia, any bolus should be followed by a dextrose CRI. In addition, some neonates may have refractory hypoglycemia and may respond only to hourly boluses of dextrose in addition to a CRI of crystalloids with supplemental dextrose. Carnitine supplementation may allow maximal utilization of glucose and may be considered as an additional therapeutic option. The recommended dosage is 200 to 300 mg/kg orally q24h for both puppies and kittens. The most common causes of hypovolemia in neonates are gastrointestinal (GI) disturbances (e.g., vomiting, anorexia, diarrhea) and inadequate oral intake. The most common cause of diarrhea in neonatal puppies and kittens is iatrogenic (owner) overfeeding with formula. In adults with hypovolemia, compensation occurs through an increase in heart rate, concentration of the urine, and a decrease in urine output. In neonates, compensatory mechanisms may not be adequate. Contractile elements make up a smaller portion of the fetal myocardium (30%) than the adult myocardium (60%), which makes it difficult for the fetus to increase cardiac contractility in response to hypovolemia. Neonates also have immature sympathetic nerve fibers in the myocardium and cannot maximally increase heart rate in response to hypovolemia. Complete maturation of the autonomic nervous system does not occur until after 8 weeks in puppies.13,14 Because neonates have higher fluid requirements and increased losses (less renal concentrating ability, higher respiratory rate, higher metabolic rate), dehydration can progress rapidly to hypovolemia and shock if not treated adequately. The difficulties associated with assessing hypovolemia in neonates require constant vigilance and continuous monitoring. One must assume that all neonates with severe diarrhea, inadequate intake, or Silverstein, D., & Hopper, K. (2014). Small animal critical care medicine. Elsevier. Created from purdue on 2024-02-04 21:23:55. severe vomiting are dehydrated and potentially hypovolemic, and treatment should be initiated immediately. Fluid therapy, monitoring of electrolyte and glucose status, and nutritional support are the mainstays of treatment. The patient should be weighed every 6 to 12 hours. Dehydration is likely when the urine specific gravity reaches 1.020, and this parameter should be monitored as an indicator of rehydration.15 In severely dehydrated or hypovolemic animals a bolus of 40 to 45 ml/kg (puppies) or 25 to 30 ml/kg (kittens) of warm isotonic fluids is given initially, followed by a CRI of maintenance fluids (80 to 100 ml/kg/day) and replacement of losses. Losses can be estimated (e.g., 2 tablespoons of diarrhea is equal to 30 ml of fluid). If the neonate is hypoglycemic or not able to eat, dextrose is added to the intravenous fluids at the lowest concentration that will maintain normoglycemia (treatment should start with 1.25% dextrose). TEMPERATURE CONTROL Neonates are basically poikilothermic for the first 2 weeks of life and are prone to hypothermia because of a higher ratio of surface area to volume, immature metabolism, and immature shivering reflex (this reflex develops at 6 days) and vasoconstrictive ability, and because their temperature is normally lower than that of mature animals. Hypothermic patients should be rewarmed slowly. Animals that are separated from the mother should be placed in a neonatal incubator at a temperature of 85° to 90° F and humidity of 55% to 65%. Heat lamps or heating pads and hot water bottles may also be used, but the neonate should be able to crawl away from the heat source. Heating pads should be covered with a towel to prevent burns. NUTRITION Nutrition is crucial to neonatal health, and inadequate caloric intake must be addressed promptly to prevent malnutrition. A surrogate dam is ideal if the biologic dam is unavailable, but this is often difficult to arrange. Weighing the neonate on a pediatric gram scale before and after each feeding can help the clinician to monitor intake. Bottle and tube feeding are other therapeutic options. Animals that are separated from the mother should be stabilized and rewarmed slowly before feeding because hypothermia prevents digestion and induces ileus. A human infant bottle is preferred for puppies because they often cannot latch onto the smaller kitten-size nipple supplied with most replacement formulas. Tube feeding is done using a 5 Fr red rubber catheter for neonates under 300 g and an 8 to 10 Fr catheter for larger neonates and should be performed only by experienced personnel.16 It is easy to improperly place the feeding tube in the trachea in neonates because the gag reflex does not develop until 10 days of age. Up to 10% of body weight may be lost within the first 24 hours following birth; additional weight loss or failure to gain weight is abnormal. Puppies should double their weight within 10 days of birth and gain 5% to 10% of their body weight per day. Nursing kittens should also double their weight within the first 10 days of life, and normal kittens gain 10 to 15 g per day. Formula-fed neonates grow at significantly slower rates, even with identical caloric intake. Although critically ill neonates and pediatric patients may not gain weight normally, weight loss should be prevented. Recently, the human microbiome project has begun to elucidate the critical nature of our symbiotic relationship with microflora.17 Intestinal commensal bacteria directly influence the development of the immune functions and differentiation of the epithelium of the GI tract.18 Microflora produce enzymes that aid in mucus secretion, CHAPTER 155 synthesis of certain vitamins, and absorption of calcium, magnesium, and iron. Protection against invading pathogens occurs via several mechanisms, including release of antibacterials (bacteriocins, lactic acid), competition for adhesion sites and nutrients, and the physical barrier itself.18 Critical illness combined with long-term medical therapy can disrupt the GI microbiome because of decreases in GI perfusion, antimicrobial drug administration, use of histamine-2 antagonists and proton pump inhibitors, administration of drugs that cause GI stasis, and lack of enteral nutrition. Supplementation with prebiotics (foods that sustain the growth of intestinal microorganisms) and probiotics (microorganism strains that may help recolonize the GI tract) has been shown to be safe and cost effective, in addition to having few known adverse effects. Unfortunately, very little research in this area has been done in veterinary medicine, particularly pediatrics, but this option should be considered in any animal that likely has a compromised GI flora. Copyright © 2014. Elsevier. All rights reserved. MONITORING Monitoring disease progression and efficacy of treatment can be challenging in neonates because the values of many parameters are significantly different from those in adults. Mean arterial pressure is lower (49 mm Hg at 1 month of age in puppies) and does not normalize (94 mm Hg) until 9 months of age.19 Central venous pressure is higher (8 cm H2O) at 1 month of age in puppies but decreases to 2 cm H2O by 9 months of age19 (see Box 155-1). Neonates cannot autoregulate their renal blood pressure with variations in systemic arterial pressure as adults do, so that the glomerular filtration rate decreases as the systemic blood pressure decreases.19 This makes restoration of intravenous fluid volume critical in neonates. Appropriate renal concentration and dilution of urine does not occur until approximately 10 weeks of age.20,21 Simultaneously, BUN and creatinine concentrations are lower in neonates than in adults, which makes monitoring for azotemia very challenging. The best way to monitor for underhydration or overhydration is to have an accurate pediatric gram scale and weigh the patient three or four times per day. Baseline thoracic radiographs are also helpful because normal neonate lungs have more interstitial fluid than adult lungs, and it can be difficult to diagnose fluid overload without a baseline. Other ways to monitor fluid therapy include checking Hct and total solids. It should be kept in mind that the Hct decreases progressively in normal neonates from day 1 to day 28, and total solids are lower than in adults (see the Laboratory Values section earlier). Neonatal skin has a lower fat and higher water content than does that of adults, and therefore skin turgor cannot be used to assess dehydration. Mucous membranes remain moist in severely dehydrated neonates and cannot be used for assessment. Lactate level, thought to be a good indicator of perfusion, especially when serial measurements are used, has been shown to be higher in normal puppies than in adult dogs (1.07 to 6.59 mmol/L at 4 days of age and 0.80 to 4.60 mmol/L from 10 to 28 days of age).22 Hypothermia 25.6° to 34.4° C (78° to 94° F) is common in neonates and is associated with a depressed respiratory rate, bradycardia, GI paralysis, and coma. Rectal temperature should be monitored using a normal digital thermometer. Temperatures above the normothermic range indicate fever or excessive external warming. A new therapeutic device that has great potential in veterinary pediatrics is currently being evaluated. Pulse oximetry–based determination of hemoglobin (Hb) level allows measurement of Hb noninvasively.23 The oximeter uses light absorption to determine levels of total Hb, oxyhemoglobin, and in some cases carboxyhemoglobin Silverstein, D., & Hopper, K. (2014). Small animal critical care medicine. Elsevier. Created from purdue on 2024-02-04 21:23:55. Critically Ill Neonatal and Pediatric Patients and methemoglobin as well. There are still significant issues with the currently approved devices and no published studies in human pediatrics or neonatology using the technology.23 The current studies reveal problems with accuracy and precision, particularly in patients that are hypotensive or hypoperfused. The benefits of noninvasive Hb measurement are substantial, particularly in the littlest patients. PHARMACOLOGY Drug metabolism in neonates differs significantly from that in adults because of differences in levels of body fat, total protein, and albumin (a protein to which many drugs bind). Renal clearance of drugs is decreased in neonates and renal excretion of many drugs (e.g., diazepam, digoxin) is diminished, which increases the half-life of the drug in circulation.4 Hepatic clearance is more complicated. Drugs requiring activation via hepatic metabolism will have lower plasma concentrations, and drugs requiring metabolism for excretion will have higher plasma concentrations.24,25 The oral route of fluid and drug administration should be avoided during the first 72 hours of life because absorption is significantly higher due to increased GI permeability. Intestinal flora is very sensitive to disruption by oral antimicrobial agents. Administration via the intravenous (or intraosseous) route seems to be the most predictable and is preferred over intramuscular or subcutaneous administration in this age group.4 One of the safest classes of antimicrobials in neonates is the β-lactam group (i.e., penicillins and cephalosporins), but the dosing interval should be increased to every 12 hours rather than every 8 hours.4 Metronidazole is the preferred drug for treatment of giardiasis and anaerobic infections. The dose and/or frequency should be decreased in neonates. Dosages of cardiovascular drugs (e.g., epinephrine, dopamine, dobutamine) can be quite difficult to determine in neonates because of individual variations in maturity of the autonomic nervous system. Assessment of response to treatment and continuous monitoring of hemodynamic variables are essential when these drugs are used. Elevations in heart rate after administration of dopamine, dobutamine, or isoproterenol cannot be predicted until 9 to 10 weeks of age, and response to atropine and lidocaine is decreased in the neonate.26-28 The blood-brain barrier is more permeable in neonates, allowing drugs to enter that do not normally cross over to the central nervous system.22 The normal neonatal respiratory rate is about two to three times higher than the normal adult rate as a result of higher airway resistance and higher oxygen demands. Drugs that depress respiration should be avoided in neonates. Neonates are very dependent on a high heart rate to increase cardiac output, so drugs that depress heart rate should be avoided. Opioids are a good choice for analgesia because of the reversibility of their effects, but the animal must be monitored closely because of the propensity of these drugs to depress heart and respiratory rate. Caution is advised when using heparinized saline flushes at the same volume (3 ml) used in adults. It is easy to overheparinize young animals; therefore a smaller volume of heparinized saline or plain isotonic saline should be used. SEPSIS Wounds such as those from tail docking or umbilical cord ligation as well as respiratory, urinary, and GI tract infections are most commonly implicated in neonatal sepsis. Common bacterial isolates include Staphylococcus, Streptococcus, Escherichia coli, Klebsiella, Enterobacter, Clostridium, and Salmonella. Additional possible 823 Copyright © 2014. Elsevier. All rights reserved. 824 PART XIX MISCELLANEOUS DISORDERS causes of sepsis include brucellosis, viral infections (distemper, panleukopenia, herpesvirus infection, feline infectious peritonitis, and feline leukemia virus infection), and toxoplasmosis. Clinical signs, as with hypovolemia, are often subtle or absent, which makes the diagnosis difficult in this age group. Some clinical signs that may be associated with sepsis are crying and reluctance to nurse, decreased urine output, and cold extremities. Studies of sepsis in children and several animal models have documented improved survival with rapid, aggressive fluid resuscitation.29 Large volumes of fluid are often needed in septic patients because of their increased capillary permeability (increased losses) and vasodilation. Resuscitation should be started immediately with a bolus of 30 to 45 ml/kg (puppies) or 25 to 30 ml/kg (kittens) of warm isotonic fluids, followed by a reassessment of the parameters of perfusion (see later in this section). If perfusion has normalized, a CRI consisting of maintenance fluids plus compensation for estimated dehydration and ongoing losses is begun. If perfusion has not normalized, repeated boluses may be required. Monitoring includes serial checks of perfusion indicators including mucous membrane color, pulse quality, extremity temperature, lactate levels, and mentation. Administration of a CRI of fresh or fresh frozen plasma or subcutaneous administration of serum from a well-vaccinated adult may help to augment immunity.30 One study in kittens showed that both intraperitoneal and subcutaneous administration of adult cat serum in three 5-ml increments (at birth and at 12 and 24 hours) resulted in immunoglobulin G concentrations equivalent to those seen in kittens that suckled normally.31 Frequent checks of electrolyte levels, blood glucose concentration, body temperature, and nutrition are done as indicated earlier. Septic neonates that have undergone adequate fluid resuscitation but that remain in a hypoperfused state (e.g., cold extremities, high lactate levels, low urine output, low blood pressure) may benefit from vasopressor or inotropic support, or both (e.g., dopamine, dobutamine, phenylephrine, norepinephrine). Because of variations in the maturity of the autonomic nervous system, all pressor and inotropic drug therapy needs to be tailored to the individual animal. Acceptable endpoints of therapy to normalize perfusion include increases in extremity temperature, decreases in lactate levels, increased urine production, and improvement in attitude. Ideally a sample from the area of possible infection is submitted for culture and susceptibility testing before antibiotic treatment is begun. Broad-spectrum antibiotics may be required if the source of infection cannot be identified. Penicillins or first-generation cephalosporins are good choices in the neonate. If oxygen therapy is needed, the inspired oxygen fraction should be kept at or below 0.4 to avoid oxygen toxicity, which can cause retrolental fibroplasia and lead to permanent blindness.32 Sepsis can be very difficult to detect in neonates. A high index of suspicion should be maintained for all neonates with risk factors, and treatment should be instituted rapidly and aggressively. The incidence of pediatric sepsis in humans is highest in premature newborns. Respiratory infections (37%) and primary bacteremia (25%) are the most common infections.33 CONCLUSION The unique anatomic and physiologic characteristics of critically ill neonatal and pediatric patients make diagnosis, monitoring, and treatment of these patients challenging. Parameters used in adults cannot be relied on in very young patients, and an awareness of their unique characteristics is essential. In addition, many laboratory and pharmacologic data differ dramatically in neonates compared with adults of the same species. Familiarity with these variations is Silverstein, D., & Hopper, K. (2014). Small animal critical care medicine. Elsevier. Created from purdue on 2024-02-04 21:23:55. essential in the monitoring and treatment of neonatal or pediatric patients that may be experiencing hypovolemia, shock, or sepsis. REFERENCES 1. Earl FL, Melveger BE, Wilson RL: The hemogram and bone marrow profile of normal neonatal and weanling Beagle dogs, Lab Anim Sci 23:690, 1973. 2. Meyers-Wallen V: Hematologic values in healthy neonatal, weanling and juvenile kittens, Am J Vet Res 45:1322, 1984. 3. Center S, Hornbuckle W, Hoskins JD: The liver and pancreas. In Hoskins JD, editor: Veterinary pediatrics: dogs and cats from birth to six months, ed 3, Philadelphia, 2001, Saunders. 4. Boothe DM, Tannert K: Special considerations for drug and fluid therapy in the pediatric patient, Compend Contin Educ Pract Vet 14:313, 1992. 5. Partington B: The physical examination and diagnostic imaging techniques. In Hoskins JD, editor: Veterinary pediatrics: dogs and cats from birth to six months, ed 3, Philadelphia, 2001, Saunders. 6. Otto C, Kaufman G, Crowe D: Intraosseous infusion of fluids and therapeutics, Compend Contin Educ Vet Pract 11:421, 1989. 7. Fiser DH: Intraosseous infusion, N Engl J Med 322:1579, 1990. 8. Levitsky LL, Fisher DE, Paton JB, et al: Fasting plasma levels of glucose, acetoacetate, D-beta-hydroxybutyrate, glycerol, and lactate in the baboon infant: correlation with cerebral uptake of substrates and oxygen, Pediatr Res 11:298, 1977. 9. Hellmann J, Vannucci RC, Nardis EE: Blood-brain barrier permeability to lactic acid in the newborn dog: lactate as a cerebral metabolic fuel, Pediatr Res 16:40, 1982. 10. Bovie KC: Genetic and metabolic diseases of the kidney. In Bovie KC, editor: Canine nephrology, Philadelphia, 1984, Harel. 11. Atkins C: Disorders of glucose homeostasis in neonatal and juvenile dogs: hypoglycemia: Part 1, Compend Contin Educ Vet Pract 6:197, 1984. 12. Textile D, Hoffman JIE: Coronary circulation and myocardial oxygen consumption. In Glickman PD, Heyman MA, editors: Pediatrics and perinatology: the scientific basis, London, 1996, Arnold. 13. Textile D, Hoffman JIE: Ventricular function. In Glickman PD, Heyman MA, editors: Pediatrics and perinatology: the scientific basis, London, 1996, Arnold. 14. Mace SE, Levy MN: Neural control of heart rate: a comparison between puppies and adult animals, Pediatr Res 17:491, 1983. 15. McIntire D: Pediatric intensive care, Vet Clin North Am Small Anim Pract 29:837, 1999. 16. Hoskins JD: Pediatric health care and management, Vet Clin North Am Small Anim Pract 29:837, 1999. 17. NIH Human Microbiome Project. Available at http://Hmpdacc.org. Accessed August 2013. 18. Papoff P, Ceccarelli G, d’Ettorre G, et al: Gut microbial translocation in critically ill children and effects of supplementation with pre- and pro biotics, Int J Microbiol 2012:151393, 2012. 19. Magrini F: Haemodynamic determinants of the arterial blood pressure rise during growth in conscious puppies, Cardiovasc Res 12:422, 1978. 20. Holster M, Keeler BJ: Intracortical distribution of number and volume of glomeruli during postnatal maturation in the dog, J Clin Invest 50:796, 1971. 21. Fetuin M, Allen T: Development aspects of fluid and electrolyte metabolism and renal function in neonates, Compend Contin Educ Vet Pract 13:392, 1991. 22. McMichael MA, Lees GE, Hennessey J, et al: Serial plasma lactate concentrations in 68 puppies aged 4 to 80 days, J Vet Emerg Crit Care (San Antonio) 15:17, 2005. 23. Holtby H, Skowno JJ, Kor DJ, et al: New technologies in pediatric anesthesia, Pediatr Anesth 22:952-961, 2012. 24. Short CR: Drug disposition in neonatal animals, J Am Vet Med Assoc 184:1161, 1984. 25. Peters E, Farber T, Heider A: The development of drug metabolizing enzymes in the young dog, Fed Proc Am Soc Biol 30:560, 1971. 26. Driscoll DJ, Gillette PC, Lewis RM, et al: Comparative hemodynamic effects of isoproterenol, dopamine, and dobutamine in the newborn dog, Pediatr Res 13:1006, 1979.