{"id":1518,"date":"2016-08-29T09:00:02","date_gmt":"2016-08-29T13:00:02","guid":{"rendered":"http:\/\/phosdev.com\/todaysveterinarynurse\/?post_type=articles&p=1518"},"modified":"2022-05-03T18:54:51","modified_gmt":"2022-05-03T18:54:51","slug":"how-and-why-to-feed-canine-parvovirus-patients-right-away","status":"publish","type":"post","link":"https:\/\/navc.sitepreview.app\/todaysveterinarynurse.com\/nutrition\/how-and-why-to-feed-canine-parvovirus-patients-right-away\/","title":{"rendered":"How and Why to Feed Canine Parvovirus Patients Right Away"},"content":{"rendered":"

Canine parvovirus is a longstanding nemesis of veterinary professionals. It is a very common disease leading to a mortality rate of approximately 90% in untreated animals.1,2<\/sup> Even with aggressive treatment involving hospitalization, intravenous fluid replacement, antibiotics, antiemetics, gastroprotectants, and antiviral agents, the observed mortality rate is as high as 10%1<\/sup> to 36%.2<\/sup><\/p>\n

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Editor\u2019s Note:<\/strong> This article was originally published in August 2016. Please use this content for reference or educational purposes, but note that it is not being actively vetted after publication. For the most recent peer-reviewed content, see our issue archive<\/a><\/strong>.<\/p>\n

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Overview of Canine Parvovirus<\/h2>\n

Parvoviruses are nonenveloped, single-stranded DNA viruses. Canine parvovirus commonly infects young dogs 6 weeks to 6 months of age and unvaccinated adults. It is transmitted through the fecal\u2013oral or oronasal route by exposure to fecal material, vomitus, or fomites. In exposed animals, the virus has an incubation period (time between first exposure and appearance of clinical signs) of 3 to 14 days, and it is shed for as long as 3 to 4 weeks after onset of clinical disease.2<\/sup><\/p>\n

The hallmark clinical signs of parvoviral enteritis are vomiting and diarrhea resulting from enterocyte destruction, which is caused by the virus taking advantage of the high mitotic rate of intestinal crypt cells to replicate. The virus also localizes in the tongue, oral cavity, esophagus, bone marrow, thymus, and lymph nodes. Key signs of lethargy, inappetence, abdominal pain, and subsequent dehydration and hypovolemia are related to breakdown of the gastrointestinal mucosa and increased intestinal permeability; neutropenia can result from bone marrow involvement. Intestinal damage can lead to secondary bacterial infection, bacterial translocation, bacteremia, and sepsis. Sepsis can then lead to systemic inflammatory response syndrome and shock. Patients in shock may exhibit tachycardia or bradycardia, obtunded mentation, and poor pulse quality, and death may result.1,2<\/sup><\/p>\n

The mainstream treatment plan for canine parvoviral enteritis includes fluid therapy to replace deficits and keep up with ongoing losses, antimicrobial therapy against secondary bacterial infection, and isolation of the patient to prevent exposure of other animals. Electrolyte and dextrose supplementation through intravenous fluids should be adjusted according to regularly monitored blood glucose and electrolyte levels. Common electrolyte abnormalities include hyponatremia, hypochloremia, and hypokalemia. Antiemetics such as metoclopramide, ondansetron, dolasetron, or maropitant are provided to control vomiting and nausea.<\/p>\n

Traditionally, synthetic colloids (e.g., hydroxyethyl starch) have been used to augment colloid osmotic pressure, which is decreased when the protein-losing nature of the enteritis leads to hypoalbuminemia. Their use is now debated because of the potential for acute kidney injury, which seems greatest when they are administered as a constant-rate infusion (CRI).3<\/sup> Recombinant feline interferon omega has shown some beneficial effects in reducing mortality from canine parvovirus.4<\/sup> Other, less commonly used treatment options, such as human recombinant factors, equine lipopolysaccharide antitoxin, oseltamivir, and antibody-rich plasma, have not shown beneficial effects.3<\/sup><\/p>\n

The Traditional Nutritional Approach: NPO<\/h2>\n

Traditionally, interventions used in parvoviral enteritis patients include the practice of placing the patient on NPO, or nil per os (\u201cnothing by mouth\u201d), treatment for 24 to 72 hours, preventing any food from entering the gastrointestinal tract.5<\/sup> While the application of NPO treatment is common, growing evidence indicates that early implementation of enteral nutrition is beneficial for patients with a variety of gastrointestinal diseases, including canine parvoviral enteritis.6\u20138<\/sup><\/p>\n

A number of longstanding reasons advocate for an NPO strategy in a patient that is exhibiting gastroenteritis with signs of vomiting and diarrhea:<\/p>\n

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  1. It has been thought that the presence of food in the gastrointestinal tract can delay recovery by stimulating intestinal contractions and increasing frequency of defecation, thereby increasing patient discomfort, and that fasting allows the bowel to rest.<\/li>\n
  2. The introduction of food is thought to stimulate further vomiting in animals with gastroenteritis, which can lead to higher chances of aspiration.<\/li>\n
  3. Undigested food in the gastrointestinal lumen is thought to serve as nutrition for bacteria, leading to further proliferation of detrimental microbes.<\/li>\n
  4. The presence of food in the gastrointestinal lumen can draw exudate into the lumen through osmosis and exacerbate diarrhea.<\/li>\n
  5. Offering food to a patient that is nauseated and feeling ill can lead to food aversion, delaying the return of appetite when the patient is ready to eat.<\/li>\n<\/ol>\n

    While these reasons seem sound, evidence points toward various benefits of feeding and supports arguments against an NPO strategy.5\u20137,9,10<\/sup><\/p>\n

    Reasons to Feed<\/h2>\n

    Fasting Causes Contractions and Pain<\/h3>\n

    While the common belief is that fasting allows the bowel to rest, it seems to increase the degree of intestinal contractions instead. The lack of nutrients in the gastrointestinal lumen leads to vigorous contractions from the pylorus to the ileum, causing sensations described as \u201chunger pains.\u201d5<\/sup> These contractions are observed to be inhibited by the presence of food.9<\/sup> The presence of luminal nutrients also seems to promote contractions of normal intensity sooner, preventing the persistence of ileus related to gastroenteritis. Introducing food early thus prevents pain, promotes normal contractions, and shortens recovery time from impaired gastrointestinal motility.5<\/sup><\/p>\n

    Feeding Shortens Duration of Nausea<\/h3>\n

    Feeding animals with gastroenteritis is thought to stimulate vomiting. One study that evaluated the effect of early enteral nutrition on patients with hemorrhagic gastroenteritis observed that the chances of vomiting did increase, although the frequency subsided starting on the second day.6<\/sup> Similarly, another study evaluating dogs with parvoviral enteritis observed a shorter time to vomiting cessation in the group that was fed starting 12 hours after admission compared with the group that was fasted.7<\/sup><\/p>\n

    The presence of luminal nutrition is thought to help maintain the integrity of the gastrointestinal mucosa and promote healthier motility, leading to less vomiting. However, food containing high amounts of fat or poorly digestible starches causes maldigestion and gastrointestinal distention and promotes vomiting through afferent stimulation of the vomiting center in the medulla oblongata. When feeding is instituted, small, frequent meals of highly digestible foods are recommended to prevent excessive secretion of gastric acids and minimize gastric distention, which can stimulate emesis.5<\/sup><\/p>\n

    Feeding Reduces Bacterial Proliferation and Translocation<\/h3>\n

    While the presence of undigested food might lead to the proliferation of some species of microbes, the presence and production of volatile fatty acids such as proprionic acid and butyric acid acidify the environment and suppress pH-sensitive pathogens such as Campylobacter<\/em> and Clostridium<\/em> spp.10<\/sup> In addition, fasting seems to increase the chances of bacterial translocation and bacterial adherence, as seen in several experimental studies,5<\/sup> leading to worse consequences such as bacteremia and sepsis. Providing nutrition leads to a healthier mucosal barrier.5<\/sup><\/p>\n

    Feeding Maintains Digestive Function and Structure<\/h3>\n

    Changes are seen in the gastrointestinal system when an animal is fasted, even when the animal is healthy. First, fasting promotes negative changes in the intestinal mucosa, such as decreased villus height and crypt depth, decreased antioxidants within enterocytes, and increased enterocyte apoptosis. These changes lead to increased permeability of the mucosal barrier and higher chances of bacterial translocation. Negative changes such as small intestinal villous atrophy and infiltration of the lamina propria with white blood cells have been observed even in animals that were provided parenteral nutrition in the absence of oral nutrition, indicating that the presence of food in the gastrointestinal tract has beneficial effects beyond nutritional content in the blood.5<\/sup><\/p>\n

    Second, a fasted animal experiences reduced secretion of digestive enzymes. Lower levels of digestive enzymes impair an animal\u2019s ability to digest food, leading to less efficient use of nutrients when food is reintroduced. Basal and histamine-stimulated gastric acid levels and secretion of pancreatic exocrine enzymes (lipase, trypsin, and amylase) decrease when an animal is fasted, potentially contributing to diarrhea.5<\/sup> The presence of food is therefore important to both structural and functional soundness of the gastrointestinal tract.<\/p>\n

    Feeding Reduces Inflammation<\/h3>\n

    The number of neutrophils primed for activation through the expression of adhesion molecules increases when an animal is fasted. The adhesion molecules enable neutrophil sequestration in the microvasculature of the intestinal tract, where the neutrophils cause oxidative and enzymatic damage upon activation and degranulation. Fasting also leads to impairment in the interaction of T and B lymphocytes and, subsequently, reduced production of immunoglobulin A and cytokines, which are important in immunologic function and regulation of inflammation.5<\/sup> This dysfunction is seen even when total parenteral nutrition is provided,5<\/sup> further supporting the importance of enteral nutrition.<\/p>\n

    Enteral Nutrition Literally Feeds the Gut<\/h3>\n

    Normally, enterocytes of the small intestine are passively exposed to nutrients in ingested material and use them to their benefit. Glutamine, an amino acid derived in the intestinal lumen, serves as an antioxidant as well as the carbon skeleton and amino acid for DNA synthesis during enterocyte turnover.5<\/sup> Mucosal cells normally expire every few days; therefore, healthy mucosal turnover is vital to maintaining a functional gastrointestinal barrier. Deficiency in other nutrients, such as essential fatty acids, folate, zinc, vitamin A, and vitamin B12<\/sub>, decreases mucosal turnover. The presence of nutrients in the intestinal lumen allows enterocytes to directly acquire these nutrients.<\/p>\n

    Summary of Benefits<\/h3>\n

    Providing enteral nutrition early in the course of parvovirus treatment instead of applying an NPO strategy has significant benefits, including the following:<\/p>\n