PROCEEDINGS OF THE NEW ZEALAND VETERINARY NURSING ASSOCIATION ANNUAL CONFERENCE 2015 5

Management of the Patient with Canine Parvovirus

Philip R Judge BVSc MVS PG Cert Vet Stud MACVSc (Veterinary Emergency and Critical Care; Medicine of ) Senior Lecturer: Veterinary Emergency and Critical Care, James Cook University, Australia Director: Vet Education Pty Ltd (www.veteducation.net)

All documents are copyright to Vet Education Pty Ltd. Permission has been granted for inclusion in the NZVNA conference proceedings.

Canine Parvovirus is a highly contagious that aects typically causes symptoms of disease in tissue with rapidly dogs, resulting in severe gastrointestinal disease and dividing cells such as the and bone occasionally cardiac disease. €e virus itself is what is termed marrow: “non-enveloped”, and is made up of viral DNA. Canine - Cells of the intestines replicate rapidly on an ongoing parvovirus is a serious viral infection in dogs, basis, and are therefore aected by (and destroyed by) and as mentioned above, is highly contagious, being readily parvovirus infection, which results in diarrhoea and transmitted from one to another through contact with vomiting. infected faeces. - Cells of the of young dogs are replicating, producing red and white blood cells. Infection with €ere are some important facts about the virus itself that parvovirus aects production of white blood cells, and underpin some important aspects of patient management… can result in profound leukopaenia in infected patients. • Canine parvovirus is a stable virus that can survive for up - In young dogs that are born to unvaccinated parents, to ve to seven months in the environment. €is means, and that are infected within the rst two weeks of life, susceptible dogs can contract the virus simply by contacting the muscles of the may be aected as they replicate and ingesting virus in a contaminated environment. in the rst two weeks of life, causing . As • One gram of faeces from an infected, virus-shedding dog most dogs have some history of vaccination, cardiac is thought to contain enough viral material to infect over manifestation of parvovirus has become much less 10 million susceptible dogs by oral exposure! common – because maternal antibody usually provides • Canine parvovirus vaccination is very eective in protection against parvovirus infection in neonates preventing disease. However, young animals may still during the rst two weeks of life, during myocardial be at risk of contracting the disease despite vaccination, development. because antibodies in circulation from maternal colostrum • Symptoms appear when the virus infects cells within inactivate early puppy vaccinations in a number of puppies. the body. Intestinal cells become infected by day four In fact, a 12 week vaccination with a modied live canine of infection – and gastrointestinal symptoms of disease parvovirus vaccination will be inactivated by colostrum- usually appear over the subsequent two to three days. derived antibody in the puppy in approximately 8% of puppies. Vaccination protocols that stop at 12 weeks of Clinical Signs age can result in susceptible puppies. €e clinical signs of canine parvovirus are usually the result • €e virus initially infects the lymphoid tissue in the pharynx of intestinal and bone marrow cell destruction by the virus, before it enters the bloodstream, where it contaminates and therefore include the following: cells around the body, including the intestines, bone • Anorexia marrow and dividing cardiac cells in the very young. • Depression • Canine parvovirus replicates in dividing cells, and thus • Vomiting • Profuse haemorrhagic diarrhoea

Histopathology slides from a normal myocardium (le!) and myocardium infected with canine parvovirus (right). Note the Photographs of canine parvovirus. Being non-enveloped presence of large numbers of in"ammatory cells and the loss renders the virus extremely resistant to desiccation of pink muscle tissue in the infected section. 6 PROCEEDINGS OF THE NEW ZEALAND VETERINARY NURSING ASSOCIATION ANNUAL CONFERENCE 2015

• Abdominal discomfort possible; evaluate stool characteristics. Collect faeces • Cardiovascular for evaluation • g. Complete full physical examination • Pyrexia 3. Collect a Patient Data Base – for patients with diarrhoea • Infection – resulting from leukopaenia – or decreased as a presenting sign, the following samples should be count, and disruption to the intestinal collected at admission, or shortly following admission, to mucosal barrier, which allows intestinal bacteria to gain facilitate diagnostic evaluation of the patient: access to systemic circulation a. PCV/TP • Sudden death and congestive heart failure – may result if b. myocardial damage occurs in very young patients c. evaluation Diagnosis d. Blood gas analysis !e diagnosis of canine parvovirus is made on the basis of e. Serum biochemistry and complete blood count clinical signs and a history of poor vaccination protocol, or f. Urinalysis lack of vaccination history, along with con"rmation using g. Faecal evaluation – smear, faecal $otation, immunologic a faecal antigen test (parvovirus “snap” tests). In addition, assessment e.g. parvovirus, giardia, because there are many other diseases that may also result perfringens; culture if required e.g. spp., in similar clinical signs, a thorough evaluation of the patient spp. must be performed as outlined below… h. Abdominal radiography – preferably three views – right and le% lateral and ventro-dorsal recumbency views. !e diagnostic evaluation of the patient with acute Radiographic contrast studies may be carried out based gastroenteritis is critical to ensure that speci"c therapeutic on results of physical examination, blood tests, and modalities are not overlooked, and to ensure that inappropriate survey radiography. treatment is not administered to the patient. !e diagnostic i. Abdominal ultrasound evaluation usually follows the following format: A Note on Faecal Analysis 1. History – obtaining a complete and thorough history can !e diagnosis of acute infectious gastroenteritis is made aid in directing an appropriate diagnostic approach to the on the basis of history (including the health of in-contact patient. Pertinent questions to raise during history-taking animals and people); clinical examination, results of serum include: biochemistry, CBC and urinalysis, and faecal evaluation. a. Diet – current diet, any recent change, previously noted intolerances Faecal analysis should begin with faecal $otation – which will b. Behaviour of the patient - scavenging behaviour enable detection of organisms such as giardia, toxoplasma, c. Duration and progression of presenting signs and the whipworm Trichuris vulpis etc. Direct faecal smears d. Environment – does the patient have access o# the are useful for detection of intestinal parasites. A stained owners’ property etc? smear of faeces and immunological techniques can allow e. Parasite control detection of clostridium enterotoxin etc., and faecal culture f. Toxin exposure – are there herbicides, pesticides, can be useful in other . household products, human medications that the Staining of a faecal smear may allow detection of many patient has access to etc. organisms associated with infectious enteritis in dogs and g. Is the patient de-sexed? , as outlined below: h. Concurrent medical conditions i. Previous medical history 1. Wright’s Giemsa or Di# Quick stain – allows detection of a. White blood cells – the presence of neutrophils suggests 2. Physical examination – physical examination should in$ammation, commonly seen in Salmonella spp., reveal the presence of the following: campylobacter spp., or clostridium spp., and should a. Fluid de"cit – hydration status, evidence of blood prompt faecal culture to be performed volume depletion b. Bacterial morphology consistent with campylobacter b. Mentation spp., clostridium perfringens c. Abdominal evaluation c. Mononuclear cell examination – may reveal presence of i. Conformation Histoplasma spp. ii. Auscultation 2. Methylene Blue staining allows detection of d. Palpation – palpate the abdomen several times during a. Trophozoites of enteric protozoa the course of initial evaluation. Evaluate for the presence of pain; abnormal organ shape, size, or position; A Note on Faecal Elisa Tests for Parvovirus evidence of obstruction; palpation of unusual structures Enteritis e.g. tube-like thickening of intestines in intussusception !e faecal ELISA tests are very accurate, but can give etc. erroneous results on occasion – for example: e. Pain (nature, severity, location) • False positive results – where a dog does not have f. Rectal evaluation – palpate prostate or uterus if parvovirus, but tests positive for it – can occur between PROCEEDINGS OF THE NEW ZEALAND VETERINARY NURSING ASSOCIATION ANNUAL CONFERENCE 2015 7

Faecal analysis may reveal Whipworm (Trichuris) egg (le), Giardia cyst (centre) or hookworm (ancylostoma) egg (right)

ve and €een days following a vaccination - Hypochloraemia may be present, along with • False negative results – where a dog has parvovirus, but hypokalaemia +/- hyponatraemia does not test positive for it – can occur if a faecal sample - Urea and creatinine +/- phosphorus may be elevated is taken very early in the disease (within one to four days also of becoming infected). False negative tests should be • Platelets - numbers may be decreased in severe disease repeated one to days days later in individuals suspected of due to DIC, and reduced platelet production in the bone having parvovirus based on history and clinical signs. marrow • Coagulation prole – the ACT may be prolonged or A Note on Blood Test Results for Parvovirus normal depending on the degree of illness, with severe Enteritis illness commonly producing clotting abnormalities Blood test results in parvovirus-infected patients usually show secondary to extensive tissue damage and DIC non-specic changes, with the exception of the following… • Leukopenia – low white blood cell counts are common Other Tests for the Parvovirus Patient in parvovirus infection due to viral infection of rapidly Diagnostic imaging – such as radiography and ultrasound dividing white blood cell precursors in the bone marrow. can be useful in eliminating other causes of vomiting - Lymphopaenia – results from damage to and diarrhoea, and to determine if intestinal obstruction during the initial infection period or intussusception is present or not. "is is particularly - Neutropaenia and monocytopenia – result from damage important when evaluating patients with persistent or to precursor cells in the bone marrow recurrent vomiting and/or diarrhoea despite provision of • Biochemistry changes – usually re!ect loss of protein intensive care over several days in hospital. and into the gastrointestinal tract, as well as Treatment changes due to dehydration, and tissue hypoxia. "e treatment for parvovirus enteritis revolves around good - Albumin +/- globulin concentrations may be low supportive care of the patient with !uid therapy, analgesia, - enzymes may be slightly elevated transfusion therapy, !uid therapy, anti-emetics,

Photograph showing intussusception (le) and ultrasound image of intussusception (right) – a common cause of patient deterioration despite therapy for parvovirus enteritis. Surgery is required to remedy this condition. 8 PROCEEDINGS OF THE NEW ZEALAND VETERINARY NURSING ASSOCIATION ANNUAL CONFERENCE 2015 nasogastric suctioning and early nutritional support. In 1. Intravenous Fluid erapy – in most patients presenting addition, supportive care of the intestinal tract is required. to the veterinary clinic with vomiting and diarrhoea, the In order to be able to eectively care for the intestinal tract in presumption is that the patient will have lost su$cient such a severe illness, we must understand a little about what #uids to have become dehydrated, even if this is not the intestine does in health. By knowing this, we will be able to clinically apparent. Restoration of this #uid de"cit is more accurately assess, monitor and intervene appropriately required to prevent further gastrointestinal injury, and for our patients when their intestines are infected or diseased. patient hemodynamic compromise and renal injury. Fluid therapy is administered in the following manner: e Physiology of Intestinal Functions !e normal physiological functions of the intestine include: a. Correction of intravascular volume de"cits – • Intestinal motility – the intestine broadly moves in two ways for patients displaying symptoms of shock or - segmental or ‘mixing’ contractions that facilitate exposure haemodynamic compromise, such as those with weak of ingesta with the intestinal mucosa, and propulsive pulses, tachycardia, bradycardia, collapse, tacky mucous contractions that facilitate movement of intestinal luminal membranes etc., initial #uid resuscitation should begin contents distally within the gastrointestinal tract. with rapid intravenous administration of a balanced • Secretion – Normal intestinal secretion involves the isotonic crystalloid solution such as Lactated Ringers secretion of an isotonic solution of water and electrolytes Solution, or normosol-R. Initial #uid rates should into the intestinal lumen. Secretion may be stimulated by be su$cient to correct intravascular volume de"cits bacteria, bacterial toxins, osmotically active non-absorbed within one hour of patient presentation. !e authors’ solutes, drugs, and products of bacterial fermentation. preference is to administer an isotonic crystalloid in • Absorption – absorption of nutrients from the small boluses of 7-12 ml/kg IV over 10 minutes, followed intestine occurs through the cells of the villi. Most speci"c by patient reassessment, and for this procedure to be nutrients are absorbed by active means, using speci"c repeated until signs of haemodynamic compromise are membrane-bound transport mechanisms in the cells of no longer present – as evidenced by a return of normal the intestinal villi. !e movement or absorption of water pulse quality, improvement in capillary re"ll time, occurs either by passive transport along trans-mucosal improved mentation, normal heart rate etc. If signi"cant ionic or electrical gradients, by movement of water (solvent haemodynamic improvement is not noted within 30 drag) or by active, cell-membrane mediated transport minutes of #uid therapy, a bolus of synthetic colloid processes (ATPase pumps). such as hydroxy-ethyl starch (Voluven) or Pentaspan is • Digestion – digestion of food is facilitated by motility, but administered at a dose of 3-5 ml/kg, given intravenously primarily involves action of speci"c chemical reactions over 10 minutes to prolong the eectiveness of isotonic that facilitate degradation of food substances into small crystalloid therapy within the intravascular space. molecules that are able to be absorbed into the systemic b. Following correction of intravascular volume de"cits, circulation. Digestion begins in the oral cavity with secretion the patients hydration de"cit is calculated (hydration of the enzyme amylase, and continues in the stomach, with de"cit volume (ml) = % dehydration (e.g. 5% = 0.05) secretion of hydrochloric acid. Chemical reactions in the x bodyweight(kg) x 1000), and this volume of #uid is small bowel usually involve the action of cell membrane administered to the patient over 8-24 hours, in addition associated enzymes such as enterokinase; the action of to the patients’ normal daily #uid requirement (60 ml/ pancreatic enzymes, and the action of bile acids. kg/24hrs). Typically, #uid required to replace hydration !e structure of the intestine facilitates these key physiological de"cits is similar in composition to extracellular #uid, functions. For example, very large quantities of water and but should be supplemented with potassium, to replace electrolytes are cycled through the intestine each day. In renal and gastrointestinal loss of potassium. An ideal fact, a volume equivalent to approximately half of the body’s #uid for replacement of hydration de"cits is Lactated extracellular water is secreted and absorbed by the intestine Ringers Solution, supplemented with 20-30 mEq/L in each 24-hour period; yet the intestine loses only 0.1% of potassium chloride. this volume in faecal water. However, when normal intestinal c. Following correction of hydration de"cits, the patient secretory or absorptive capacity or function is disrupted, massive #uid and electrolyte losses may occur – as it does in diarrhoea or vomiting. Treatment of Parvovirus Enteritis in Dogs !ere is very little speci"c therapy that can be directed against the parvovirus virus itself by the time clinical signs of illness are evident. Treatment therefore remains supportive for the vast majority of patients clinically aected with signs of parvovirus gastroenteritis. In general, #uid therapy, Photograph showing intussusception (le) and ultrasound analgesia, intestinal support and nutrition form the basis image of intussusception (right) – a common cause of patient for successful patient management. A suggested treatment deterioration despite therapy for parvovirus enteritis. Surgery rationale follows… is required to remedy this condition. PROCEEDINGS OF THE NEW ZEALAND VETERINARY NURSING ASSOCIATION ANNUAL CONFERENCE 2015 9

requires uid therapy for maintenance of normal body complex nutritional formulations should be fed to the functions, PLUS replacement of ongoing uid losses patient – typically by nasogastric or oesophagostomy through the gastrointestinal tract, in patients that tube. On resumption of feeding, a low fat, high biological continue to have diarrhoea and/or vomiting. In most value protein, primarily carbohydrate diet should be fed. cases, a uid type such as Lactated Ringers Solution, ƒe carbohydrate present in rice is best because its starch with 5% glucose, and 20-30 mEq/L potassium chloride is is more completely assimilated than other carbohydrate required. In patients without signi€cant gastrointestinal sources. Select a lean protein source such as chicken. uid loss, 0.45% sodium chloride solution, 2.5% Veterinary prescriptions diets such as Hill’s i/d diet are glucose, and 20-30 mEq/L potassium chloride is usually ideal for this purpose. sucient to meet ongoing uid requirements. In patients 3. Motility modi!cation – narcotic analgesics – loperamide with signi€cant loss of gastrointestinal uid, blood (Imodium), Diphenoxylate (Lomotil) – increase segmental or protein, a combination of isotonic crystalloid and bowel contractions, and have been used for symptomatic colloid therapy, using hydroxy-ethyl starch, Pentaspan, management of acute diarrhoea. "ey should not however or blood or fresh frozen plasma transfusion is required, be used in patients with infectious diarrhoea caused by in order to maintain blood volume, hydration status, bacteria or , as they have been shown to prolong and colloid oncotic pressure necessary for tissue oxygen illness, and delay clearance of intestinal bacterial toxins. delivery to body tissues. 4. Protectants and absorbents – kaolin/pectin, charcoal, and d. Plasma and synthetic colloid use: Patients with barium sulphate – have questionable ecacy. Bismuth parvovirus enteritis are high risk, critically ill patients subsalicylate is the most useful, as is has anti-enterotoxin, that frequently su‚er from signi€cant losses of antibacterial, anti-secretory and anti-inammatory e‚ect, plasma proteins into the intestinal lumen. ƒis can and has been used as an adjunct to therapy, but is not lead to hypoproteinaemia, hypoalbuminaemia, and, considered essential in most cases. occasionally, coagulation abnormalities. ƒe use of fresh frozen plasma and/or synthetic in these 5. – are usually not indicated except in cases of patients is controversial, but it also has sound rationale. immunosuppression, fever, leukocytosis, leukopaenia, Hypoproteinaemia and hypoalbuminaemia are malena, haematochezia, and shock. Initial negative prognostic indicators in patients with severe choices for diarrhoea include antibiotics e‚ective against illness. ƒey are associated with decreased e‚ective enteric bacteria – usually a combination of mixed aerobic circulating blood volume, poor tissue perfusion, and and anaerobic, gram positive and gram negative bacteria. worse outcome. Administration of fresh frozen plasma First generation cephalosporin antibiotics are commonly can reasonably be considered in any patient with used at a dose of 22 mg/kg IV q 8 hrs. Alternatively, for parvovirus enteritis that is critically unwell. Optimum aerobic infections, enrooxacin at 5 mg/kg SC q 24hrs is bene€t from transfusion is obtained when transfusion is e‚ective. For anaerobic infections, is the administered early in the course of disease, at dose rates preferred agent, at 20 mg/kg IV q 24 hrs. of 10-30 ml/kg intravenously over four to six hours. 6. Anti-emetic therapy – anti-emetic therapy using Following plasma transfusion, synthetic colloids such as , , or hydroxy-ethyl starch or Pentaspan may be administered may be used in patients that have persistent vomiting not at a rate of 10 ml/kg/day in addition to uid therapy to caused by intestinal obstruction, in order to minimize provide for maintenance and ongoing losses. uid loss from the patient, and to improve patient comfort. 2. Dietary management – Nil per Os (NPO) for an initial Some clinicians insert naso-gastric tubes to remove gastric six to twelvehour period following admission to hospital secretions as an adjunct to the use of anti-emetics, and to may be bene€cial in most cases of diarrhoea in dogs and facilitate administration of micro-enteral nutrition. ƒe cats. NPO decreases the number of osmotic particles use of these tubes is associated with a dramatic reduction available in the intestinal lumen contributing to osmotic in nausea and vomiting – particularly in puppies with diarrhoea, and allows more rapid re-growth of intestinal parvovirus enteritis and in patients with pancreatitis. villi, and resumption of intestinal function. Following an 7. Analgesia – Opiate analgesics such as butorphanol or initial short period of bowel rest, micro-enteral nutrition fentanyl are preferred in most cases of acute infectious should commence. Micro-enteral nutrition, using glucose, gastroenteritis, and should be administered by continuous hydrolyzed proteins and isotonic electrolyte solutions, infusion for optimum bene€t for the patient. Non-steroid such as Lectade or Vytrate, have been shown to maintain anti-inammatory drugs or steroid anti-inammatory intestinal mucosal health, reduce atrophy of the intestinal drugs are contraindicated in most cases of acute infectious lumen cells, and improve recovery rates from diarrhoea. diarrhoea because they decrease blood ow to the gastric ƒe rate of administration is 1-2 ml/kg/hr. ƒese solutions mucosa, and can result in intestinal ulceration and acute may be used in the presence of ongoing vomiting and renal failure – particularly in dehydrated patients. diarrhoea, as they are readily absorbed by gastric mucosal cells, and enterocytes, even in the presence of disease. For the most part, this supportive care will ensure optimum Following 12 hours of micro-enteral nutrition, more conditions or opportunity for gut function to return to 10 PROCEEDINGS OF THE NEW ZEALAND VETERINARY NURSING ASSOCIATION ANNUAL CONFERENCE 2015 normal, once the underlying infectious cause resolves. during illness - none of which has been validated. Current Obviously, it is important in any patient to support airway, practice is to feed critically ill patients resting energy respiratory function, neurological function and renal requirements (RER) only, and to only multiply RER in perfusion with intravenous uid therapy, oxygen therapy and cases of severe malnutrition, and only then once the other supportive measures. patient is tolerating feeding Appendix 1: Nutritional Support of the Patient RER = Bodyweight (kg) x 30 + 70 (dog > 2kg) with Canine Parvovirus Enteritis RER = Bodyweight (kg) x 70 (dog <2kg) Step 1: Micro-Enteral Nutrition !e term micro-enteral nutrition was developed to de"ne RER = Bodyweight (kg) x 40 () the delivery of small amounts of water, electrolytes, and RER = Bodyweight (kg) 0.75 readily absorbed nutrients (glucose, amino acids, and small Step 3: Feeding the Patient peptides) directly to the gastrointestinal tract. !ese nutrients Enteral feeding should be initiated within 12-24hrs of may be given as a bolus infusion every one to two hours or admission to the ICU. If oral feeding is not possible or as a constant rate infusion directly into the oesophagus and feasible, a gastric feeding tube (nasogastric, oesophagostomy, stomach, duodenum, or jejunum via a feeding tube. Why do or gastrotomy tube) should be placed. Feeding may be by we give micro-enteral nutrition? – To improve blood ow to bolus feeding, or by constant rate infusion. !e residual the gut, improve gut function, and to improve the tolerance gastric volume should be monitored, and the feeding regime to more complex diets when we begin feeding them. adjusted as outlined below. Protocol for Micro-Enteral Nutrition In all cases, the target energy and protein requirements for • Begin within 2-12 hours of admission to the hospital • Solution - lectade, gastrolyte, OR 0.45% NaCl + 2.5% the patient should be met by the third day of feeding. If dextrose solution the protein content cannot be obtained by this time, a diet • Additives: containing higher protein content should be fed. - Potassium chloride- 20 mEq/L Bolus Feeding Protocol for Gastrotomy, Oesophagostomy, - Amino acids - 3% amino-acid solution. Addition or Nasogastric Tubes of amino acids promotes a protein-sparing e#ect If patient has had prolonged anorexia (2-3 days) use the in critically ill patients. Amino acids should not be following feeding protocol: supplemented in micro-enteral formulations for use in • Day 1 = feed 1/4 - 1/3 of daily feed requirement in several patients with pancreatitis small feeds - Glycine hastens the resolution of , improves • Day 2 = feed 1/2 - 2/3 of daily feed requirements in several intestinal morphologic characteristics in patients with small feeds diarrhea, and enhances the uptake of glucose. • Day 3-4 = feed entire feed requirements in several small - Glutamine is the preferred energy source of rapidly feeds dividing cells (GUT cells, lymphocytes, and "broblasts). Glutamine plays a role in the maintenance of the NB - if feeding via G – tube, oesophagostomy tube, or integrity of the GI mucosal barrier and preventing nasogastric tube, suction the tube "rst - if you suction a bacterial translocation volume greater than 1/3 of the previous volume of feed • Rate of administration: given, delay the next feed for 2-3 hours, and feed 1/3 - 1/2 the - CRI rate of 0.5 - 2.0 ml/kg/hr OR volume of the last feed. Consider the presence of intestinal - Bolus infusion of 1.0-4.0 ml/kg every 4 hours ileus, and manage with metoclopramide and/or cisapride. - Increase volume administered by 0.2-0.5 ml/kg/hr every 8-12 hours if patient is tolerating the solution Appendix 2: Feeding Tube Placement Guide • Begin feeding a commercial liquid diet if micro-enteral Nasogastric Feeding nutrition solution is being tolerated a$er 6-18 hours • Use silicone or polyurethane tubes (polyvinyl tubes can harden and be di&cult to remove) Step 2: !e Nutrition Formula – Beyond Micro-Enteral • Following placement of local anaesthetic in the nasal Nutrition cavity, pass tube in ventral nasal meatus, and pass to the When formulating a diet for the patient, the following are level of the distal esophagus – this reduces the chance of taken into consideration gastric contents ascending about the tube and causing a reux esophagitis. Note that when feeding patients with • Fluid Requirements - normal patient’s uid requirements nasal-esophageal tubes must be at a slow rate to avoid are between 60 and 80 ml/kg/day a rapid inux of food into the distal oesophagus, and • Energy Requirements - the energy requirements of subsequent regurgitation critically ill humans rarely approach normal maintenance • Following placement, apply suction to the tube – if air requirements, due to a reduction in physical activity is freely aspirated, or the animal is coughing, the tube is associated with illness. !ere are numerous methods and probably in the – relocation of the tube is necessary recommendations for estimating patient caloric needs • Radiography is desirable if doubt exists over tube location PROCEEDINGS OF THE NEW ZEALAND VETERINARY NURSING ASSOCIATION ANNUAL CONFERENCE 2015 11

and depth to the distance from the mid-cervical esophagus (insertion • Resistance is normally felt on passing tube through point) to the last rib (stomach) caudal nasal meatus due to narrowing caused by ventral • A curved Carmalt forceps (or similar instrument) is placed expansion of the maxilla-turbinate through the mouth down to a midpoint in the cervical • Following use, capping tube prevents gastric accumulation esophagus on the le! side of the neck, and pushed outward of air to tent the skin over the esophagus • Following use, ush the tube with water • "e skin is incised over the tip of the forceps; the skin • Complications: incision is extended through the subcutaneous connective - Gastric reux tissues, and through the wall of the esophagus. "e - Inhalation of food esophageal incision should be as small as possible – just - Patient intolerance of the tube large enough to allow the tip of the forceps to be pushed through Oesophagostomy Tube Feeding • Push the forceps through the skin incision. Grasp the tip • Select the appropriate tube: of the oesophagostomy tube with the forceps, and pull the - Polyurethane or red rubber tube tube through the mouth with the forceps. "e tip of the - Size 10-12 Fr (cats and small dogs); 16-22 Fr (dogs) tube is then re-directed down the esophagus to the pre- • Decide on location of distal tube – oesophagus vs. determined length – using the Carmalt forceps to direct stomach. Placement of the oesophagostomy tube in the the tube distal esophagus reduces the risk of gastric reux into the • Con#rm proper tube placement by suctioning the tube - if distal esophagus. However, placement of the tube into gastric contents are obtained on suction, the tube is in the the gastric lumen allows assessment of residual gastric stomach volumes, gastric suctioning, and hence reduced nausea. • "e tube is secured by placing an overlapping, interlocking Distal tube placement into the gastric lumen is considered suture pattern (Chinese Finger Trap), and bandaging to superior to distal esophageal placement the neck • Clip the skin over the LEFT side of the neck • Place a mark on the tube (measured from its tip) equivalent References available on request