CHAPTER 44 Clinical Approach to Pediatric Nutritional Conditions
Neonates may not receive the appropriate nutrition for a number of factors, including insufficient milk production, the mother’s death, an undeveloped gastrointestinal (GI) tract, or the inability to absorb nutrients. Neonates will not gain weight or may be unable to suckle normally as a result of a congenital defect or weakness.
Malnutrition can be caused by inadequate diet with poor quality ingredients, deficiencies, or excess supplementation. Inadequate protein and energy intake can lead to a decreased growth rate, inhibition of neural myelination and neurotransmission, decreased brain growth, and inhibited cognitive function. Patients with malnutrition may suffer from hypothermia, hypoglycemia, and dehydration.
Critically ill patients can receive nutritional support through a variety of routes, including enteral or parenteral feedings. Nutrition, both prenatal and postnatal, as well as during the first year of development, significantly influences the longevity and health of puppies and kittens.
At birth, the GI tract must transition from processing amniotic fluid to digesting milk. The release of hormones, digestive enzymes, activation of secretion, motility, and absorption are all adaptations that begin shortly after birth. These changes are critical to allow the GI tract to perform required functions.
Neonates have decreased pancreatic digestive enzymes, allowing the absorption of immunoglobulins from colostrum. Antibodies secreted in the mother’s colostrum are only absorbed during the first 12 to 24 hours after birth. Pancreatic enzymes begin to be produced in response to ingestion of solid food; therefore consuming solid food is important to facilitate the development of normal GI tract function. GI motility is minimal the first month, a condition which must be taken into consideration whenever a neonate requires supplemental feeding.
Excess dietary energy and caloric intake may support a growth rate that is too fast for appropriate skeletal development and may result in a higher incidence of skeletal abnormalities. Excess calcium affects the skeletal system by increasing the severity of osteochondrosis. The absolute value of calcium appears to be more significant than the calcium/phosphorus ratio. Subsequently it is contraindicated to supplement large breed puppies with calcium when they are fed a complete and balanced commercial diet.
Osteochondrosis dissecans (OCD) is a disruption in endochondral ossification that results in focal lesions. OCD occurs in the physis and/or epiphysis of the growth cartilage. Factors affecting OCD include age, gender, breed, rapid growth rate, and excess nutrients. Great Danes, Labrador Retrievers, Newfoundlands, and Rottweilers are at an increased risk. Overnutrition and/or excess caloric intake results in abnormal weight gain relative to skeletal structure and disruption of chondrocytes, leading to OCD. See Chapter 42 for more information about OCD.
Canine hip dysplasia (CHD) is a genetic disorder of large and giant breeds but can also be influenced by nutrition. Evidence suggests that rapid growth and weight gain in early development increase the risk for CHD. See Chapter 42 for more information about CHD.
Excess vitamin D is usually caused by inappropriate supplementation or rodenticide poisoning, and can be fatal. Increased levels of vitamin D can cause hypercalcemia and hyperphosphatemia, resulting in metastatic calcification. Symptoms may include vomiting, diarrhea, limb stiffness, increased respiratory rate, anorexia, muscle weakness, and polyuria/polydipsia. Diagnosis is generally made by questioning the history of the diet. Tests can be submitted to a laboratory to verify vitamin D toxicity and should include parathyroid-related hormone protein, phosphorus, and 25-OH-cholecalciferol. Treatment can be initiated by removing the excess vitamin D source. The prognosis can be guarded, depending on the severity of the condition. Dissolution of calcifications can be slow and generally incomplete.
Nutritional secondary hyperparathyroidism is a common skeletal disorder that occurs as a result of hypervitaminosis D and/or a mineral imbalance caused by an inadequate diet. Diets that are composed mostly of meat are deficient in calcium and/or have an inverse Ca/P ratio. Because of the deficient calcium in the diet, the parathyroid glands enlarge and release large amounts of parathormone. The elevated levels increase osteoclastic resorption, therefore increasing calcium release into the bloodstream. Puppies and kittens develop severe bony lesions that can be seen radiographically. Bones may appear “moth eaten” and have poor density. The cortex will appear thinned, and the medullary cavity is widened. Because of the increased calcium release, blood levels will appear low normal. However, serum alkaline phosphatase levels, as well as parathyroid hormone (PTH) levels, will increase.
Symptoms of nutritional secondary hyperparathyroidism may include lameness, fractures, inability to walk, incoordination, muscle twitching, and seizures. Fractured vertebrae are common in severe cases. Treatment consists of changing the patient to an Association of American Feed Control Officials (AAFCO)-approved diet, fracture support, and strict confinement for 4 to 8 weeks. Serial radiographs can be taken to monitor improvement. Calcium and vitamin D supplementation are not advised because the complete and balanced AAFCO diet will have appropriate levels. If blood samples are to be taken to check the PTH levels, samples must be taken before switching diets because the PTH levels can rapidly equilibrate. Once the diet has been changed and the fractures have healed, the patient can completely recover from the imbalanced diet.
Nutritional deficiencies appear when the patients’ nutritional requirements exceed the maintenance requirements. This can include periods during gestation, lactation, and growth. Deficiencies in protein, essential fatty acids, and zinc result in keratinization defects and are most commonly caused by generic foods that are low in fat and have excessive mineral supplementation. Low quality protein decreases the digestibility of the food. Essential fatty acids are generally deficient in low quality foods and can be damaged when overheated for a lengthy period. Deficiencies in vitamin A can lead to retinal, visual, and digestive problems.
Vitamin E deficiency is rare because the use of vitamin E (a natural preservative) to maintain fats that are poorly stabilized is common. Vitamin B deficiency is also rare and usually manifests as a dermatologic condition.
Deficiency in zinc is generally caused by foods that are high in phylates, which chelate zinc. These foods include those high in bran and are often oversupplemented with calcium. Copper deficiency is common in homemade diets that are not correctly supplemented and often also contain excess calcium, zinc, or iron. Calcium competes with the absorption of zinc, copper, and iodine. The percentage of absorption is often less than 30% but greatly improves when the trace elements are provided in inorganic form with chelated amino acids.
Thiamine deficiency is generally seen in cats that eat diets high in nonprocessed fish. The energy metabolism of the cat is compromised, resulting in weakness, blindness, head drop, and other neurologic disturbances. Cats may act interested in food but will not eat. Laboratory testing can determine thiamine deficiency; however, it generally takes an extended period to get results. Diagnosis can be made from history of diet, symptoms, and by the response to therapy. Response is generally observed after 1 to 2 days of treatment. Thiamine should be diluted 100 to 250 mg into 100 ml of NaCl fluids, which can then be administered subcutaneously daily. The pH of thiamine is approximately 5, necessitating diluting the product to increase the comfort level of the patient. The course of treatment continues until symptoms regress.
Hypokalemia is usually secondary to the depletion of potassium stores, either from loss through the GI tract or renal compromise. Symptoms include weakness and persistent ventroflexion of the neck, crouched posture, and muscular pain. Most symptoms resolve after the supplementation of potassium either orally or intravenously. Intravenous fluids with potassium supplementation should be mixed well before administration because sudden death can result from high levels of infused KCl. Oral supplementation is generally regarded as the safest method of administration. Patients should be monitored closely because potassium levels tend to rebound within 2 to 3 days of treatment. Supplementation may be lifelong as those who have experienced hypokalemia are at high risk of reoccurrence. Potassium gluconate can be administered orally to both puppies and kittens at 2 mEq/4.5 kg twice daily. The dosage can be adjusted as needed to maintain proper potassium levels.
Deficiency in taurine can be caused by an inadequate diet. AAFCO has minimum requirements for both dry and canned cat food as taurine bioavailability is decreased in canned food. Taurine is an essential amino acid for cats and is required for proper cardiac function and conjugating bile acids. Taurine is also lost in feces as a result of bacterial degradation in the intestinal tract. There is no evidence that suggests taurine is an essential amino acid in dogs; however, research shows that it may be conditional. Taurine is also necessary for bile acid conjugation in dogs, and dilated cardiomyopathy in Cocker Spaniels and Golden Retrievers has been associated with plasma taurine deficiency. Some lamb meal and rice diets have been suspected to have taurine deficiencies, but this suspicion has not been confirmed. Plasma or whole blood taurine levels can determine deficiencies. Dogs may be supplemented with taurine at 500 mg orally twice daily; cats can be supplemented with 250 mg orally twice daily.
Proper nutritional intake is key for neonates because they lack sufficient glycogen storage, fat reserves, and reduced precursors for gluconeogenesis. They are unable to maintain glucose levels for extended periods. Maintenance of glucose requires several interrelated factors, some of which neonates have marginal abilities, including digestive absorption, liver and muscle glycogenolysis, and liver gluconeogenesis.
Hypoglycemia can be caused by vomiting, diarrhea, intestinal parasites, sepsis, hypothermia, or inadequate nutritional intake. Hypoglycemia can also be secondary to a variety of conditions, including endotoxemia, septicemia, portosystemic shunts, and glycogen storage abnormalities.
Hypoglycemic symptoms can include lethargy, anorexia, depression, incoordination, muscle tremors, and seizures. Normal glucose levels are 80 to 140 mg/dl. Patients are considered hypoglycemic with glucose levels less than 50 mg/dl. Hypoglycemia most commonly occurs in toy breed puppies but can occur with any neonate.
Hypoglycemic patients should be treated with 10% to 25% dextrose intravenously at 1 to 2 ml/kg. Dextrose given orally rarely reverses a hypoglycemic crisis. Once the patient responds, a 5% to 10% dextrose drip can be initiated until the patient is eating normally. Neonates have an immature metabolic regulatory mechanism; therefore glucose levels should be carefully monitored, and dextrose administration should be adjusted accordingly. Any fluids that are administered should be warmed to 100° F (38° C) to prevent hypothermia.
Traditionally owners have been advised to keep some syrup on hand, and should hypoglycemic symptoms occur (or reoccur) they can apply a small amount to the neonate’s gum line while in transport to the veterinary clinic. This technique probably does no harm, but its effectiveness has been questioned recently. Often 50% dextrose solution is sent home for oral application if necessary. L-Carnitine increases the liver’s ability to convert fat to glucose and can be given to prevent hypoglycemic episodes from reoccurring. L-Carnitine can be administered at 50 mg/kg by mouth twice daily.
Hypothermic patients should not be fed until their temperature is 97° F (36.1° C) because hypothermia decreases GI motility and digestion. Decreased motility can cause curdling of milk in the stomach.
The purpose of dietary support either by enteral nutrition (EN) or parenteral nutrition (PN) is to provide adequate nutrition, promote health, and to prevent and treat deficiencies. Proper nutritional support can prevent deterioration of the immune system and improve wound healing. Many animals presented for veterinary care are in poor medical condition secondary to metabolic, infectious, or traumatic insults and are already suffering from decreased nutritional intake. This nutritional deficit could increase the adverse affects of previous and current underlying diseases. Administration of appropriate EN or PN to critically ill patients is an important part of their therapy. Each patient should be evaluated to determine which type of nutritional support would be appropriate. What is the physiologic state of the patient? What nutrients does the patient need? What formulas are available to meet those needs? How will the formula be administered?
Patients that are younger than 2 weeks and have lost weight or have not eaten for 3 or more days, have excessive losses through vomiting and diarrhea, or have an increased nutritional need as a result of trauma, surgery, or infection are candidates for nutritional support (Box 44-1). Parenteral support should be limited to paralyzed or comatose patients with severe GI dysfunction. When an adequate catheter is placed, either total PN or partial PN support can be administered.
From Tams TR: Handbook of small animal gastroenterology, ed 2, St Louis, 2003, Saunders/Elsevier.